NHM 365 Notes
NHM 365 Notes NHM 365
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Spath Study Guide M93 Diabetes during Pregnancy Part 3 Infant mortality rate is nearly twice as high for babies born to women with uncontrolled diabetes 80 want to have good glycemic control going into the pregnancy gtgt Describe MNT for a pregnant woman with preexisting diabetes MNT for Preexisting Diabetes and Pregnancy Preconception counseling Ideally nearnormal HbA1c hemoglobin A1 c levels should be achieved by 12 months prior to conception Hormonal changes in first trimester lead to erratic BG levels adjust meal plan Increased need for insulin in second amp third trimesters Adjust meal plan to provide additional kcals and insulin schedule as needed Avoid hypoglycemia and ketosis Preexisting DM and Pregnancy Nutrition Approaches Smaller meals with CHO spaced throughout the day Frequent snacks Late evening snacks to prevent overnight hypoglycemia Somogyi Effect Food intake records are essential and frequent monitoring of blood glucose Page1 of 10 gtgt Define Gestational Diabetes is diabetes that occurs during pregnancy in women who previously did not have diabetes gtgt When is GDM usually diagnosed Usualy diagnosed during the 2nd or 3rd trimester of pregnancy when hormonal changes cause insulin resistance Gestational Diabetes Mellitus GDM Glucose intolerance with onset or first recognition during pregnancy Does not include women who have diabetes diagnosed before pregnancy Usually diagnosed during the 2nd or 3rd trimester of pregnancy when hormonal changes cause insulin resistance the placenta provides the fetus with nutrients amp hydration but also produces a variety of hormones to maintain the pregnancy Some of those hormones are insulinantagonists which have a blocking effect on insulin As the placenta grows along with fetus the production of these hormones increases production really gets going in about the 2024 week of pregnancy See chart on next page May or may not require insulin treatment Standards of Medical Care in Diabetes Diabetes Care 20123581163 Page 2 of 10 gtgt Briefly describe the pathophysiology of GDM GDM Pathophysiology The cause is not exactly understood but major contributor seems to be the hormonal changes during pregnancy During pregnancy Increased mobilization of glucose to provide substrate for anabolic reactions for fetal growth and development Decreased insulin sensitivity due to increase in insulinantagonist hormones prolactin estrogen cortisol human placental lactogen have blocking effect on insulin l HyperglycemialR gt gtGDM These changes peak during the 2nd and 3rd trimesters due to rapid placenta growth to support growing fetus which result in increased production of hormones that cause insulinresistance THEM U IIIJVI Law I I DELIVERY I I I I I I I I I o 5 m 15 20 25 3 35 am 5 POSTquot WEEKS GESTATION PARTUM I C430 U VI I U o If the woman s body is unable to provide enough insulin to overcome insulin resistance caused by hormones and maintain normal glucose levels GDM is diagnosed Anesthesiology Clinics of North America 1998 16 2 441 458 gtgt What are some risk factors for GDM Gestational DM Who is at risk Pregnant women over age 25 Overweight and obese women Women with family hx of DM More prevalent in Asian Hispanic and Native American women Women with excessive weight gain during pregnancy gtgt GDM does NOT cause congenital amomalies birth defects Birth defects usually originate in the 1st trimester before insulin resistance has time to develop if a women is diabetic before pregnancy and has uncontrolled blood glucose during 1st trimester then elevated blood glucose could harm the fetus gtgtWhat are the major risks of uncontrolled GDM for the fetus Shortterm Risks to Fetus Fe fal macrosomia means a big baby baby s own insulin stores extra Fetal morbidity glucose from mom causing gt in weight Fetal hypoglycemia after birth baby is no High blood glucose quotLEWIL39E longer getting extra glucose from mom but miiihurlhe keep producing the same amount of insulin A which facilitates too much glucose into cells 39 M f leading to low blood glucose at E J W J Birth trauma due to the infant s larger size H quotf 7 Cause3 baby mput Emtr weirgift Longterm Risks Page 4 of 10 Increased risk for overweight amp obesity later in life Higher rates of prediabetes amp Type II DM later in life gtgtWhat are the major risks of uncontrolled GDM for the mother Risks to the Mother Shortterm HTN preeclampsia DVT s deep vein thrombosis or blood clots Preeclampsia is condition of high blood pressure amp increased protein in the urine If uncontrolled can lead to eclampsia which results in seizures that can cause permanent damage to vital organs Surgical deliveries and excessive blood loss Poor wound healing possible skin breakdown pressure ulcers Increased length of labor Longterm Increased risk of developing Type II DM within 510 years Increased risk for lipid abnormalities later in life Increased risk for recurrence of GDM Page 5 of 10 Diagnosing GDM The diagnostic criteria for GDM have recently changed 1 All women should be tested by an oral glucose tolerance test at 2428 weeks gestation using OGTT 2 Highrisk women should be screened for preexisting type 2 diabetes on the first prenatal visit blood glucose test using any of the 4 diagnostic tests Highrisk includes marked obesity previous dx of GDM glycosuria family hx of DM PCOS Polycystic ovary syndrome can affect a woman39s hormone levels If no GDM indicated test again at 2428 weeks gestation The oral glucose tolerance test OGTT at 2428 weeks gestation The OGTT Give 75 grams of glucose orally after an 8hr overnight fast A diagnosis of GDM when any of the following plasma glucose values equal or exceed Fasting glucose 2 92 mgdl At 1 hr glucose 2 180 mldl At 2 hrs glucose 2 153 mgdl Page 6 of 10 Nutrition Assessment Information to gather Physicianprescribed management plan PMH Past Medical History Labs and Meds Exercise guidelines per MD Anthropometrics Nutrition and social histories Mom s knowledge of DM GDM MNT Goals for GDM Manage blood glucose levels as near normal as possible without ketosis Provide adequate amounts of the nutrients needed for mother and baby gtgt Describe MNT for GDM MNT for GDM Individualize and adjust meal plan throughout pregnancy Usually involves 34 meals with 24 snacks daily Carbohydratecontrolled meal planning Evening snacks to prevent overnight ketosis SMBG is critical during pregnancy up to 8xday gtgt SMBG is especially important during pregnancy Insulin regimens may need to be tweaked and changed throughout the pregnancy gtgt Oral glucose lowering medications sometimes called Oral Hypoglycemic Agents OHAs are NOT approved for use during pregnancy if blood glucose is not controlled via diet may need to have insulin injections can t take OHAs during pregnancy Page 7 of10 Insulin requirements increase progressively throughout pregnancy this is normal amp expected Regular exercise gtgt What is the minimum CHO requirement during pregnancy Minimum CHO during pregnancy 175 gday Meal Planning with GDM 4O 45 of Kcal from CHO Minimum CHO during pregnancy 175 gday 14g1000 kcals fiber RDA for protein 11 gkg or additional 25 gd enough for appropriate weight gain No set energy requirements Minimum of 1700 1800 Kcal has been shown to prevent ketosis Set kcal limits with caution even in obesity Are feeding fetus too Insulin Tx in GDM May be required for GDM No onesizefitsall insulin regimen it must be individualized to fit mother s lifestyle Insulin needs T as pregnancy progresses so insulin regimens will need to be monitored and adjusted SMBG selfmonitoring of blood glucose is very important gtgt Oral Glucose Lowering Medications OHAs in GDM are Not approved by the FDA for use during pregnancy and are not generally recommended during pregnancy gtgt Insulin is the only medication that is 100 approved by the FDA for use during pregnancy gtgt some OHAs like Metformin have FDA Pregnancy Class B approval for use during pregnancy under close medical supervision Page 8 of 10 Mothers with preexisting DM and were on OHAs may have to switch to insulin injections Diabetic ketoacidosis DKA is an acute major lifethreatening complication of diabetes Ketoacidosis is a combination of ketosis overproduction of ketones and acidosis increased acidity of the blood that leads to accumulation of ketones in plasma Ketonemia and urine Ketonuria Ketonemia and Pregnancy Ketosis has been associated with t IQ scores in children of women with GDM This topic is a little controversial Ketone Testing The Academy EAL The Registered Dietitian should recommend ketone testing for women with gestational diabetes mellitis GDM who have insufficient calorie andor carbohydrate intake andor weight loss Page 9 of 10 Two of three studies regarding Ketonemia and Ketonuria with poor metabolic control during a diabetic pregnancy report a positive association with lower IQ in offspring gtpositive association shown but does not prove causation To play it safe avoid ketosis during pregnancy Follow Academy s recommendation that women with GDM test blood glucose in fasting state during ketones if ketones found in urine Ketonemia May by caused by Inadequate energy or CHO intake Allowing too much time between meals Omission of meals andor snacks Mothers should be instructed on testing urine for ketones gtgt Why are gestational diabetics advised to check urine ketones daily Ketones in the urine are a sign that your body is using fat for energy instead of using glucose because not enough insulin is available to use glucose for energy If ketones found in urine follow Academy s recommendation and have blood glucose test fasted levels to see if changes are needed to dietinsulin to avoid dangerous Ketoacidosis After Delivery Counsel moms on lifestyle changes to help prevent Type 2 DM later in life Breastfeeding benefits mom and baby Reduce weight if needed Increase physical activity Postpartum meal planning Page 10 of 10 I Spath Study Guide for Module 4 Cardiovascular Disease amp Hypertension PART TWO Dietary Factors amp CVD Modification in diet can be used to modify risk Fats Heart healthy diet people think of fat and cholesterol Gram of Fat 9 kcal provides the most calories Gram of Protein 4kcal Gram of Carbohydrates 4kcal CVD Dietary Factors AHA recommends less than or equal to 2535 kcals from total fat for healthy people to reduce CVD risk Pick and choose our fats wisely in a balanced diet Replacement of fat kcals with CHO especially refined CHO will result in T Serum TG in some persons but may also i total cholesterol Going on a low low fat diet but replacing that fat with refined carbs would be counter productive in preventing CVD Saturated fatty acids SFA limiting saturated fat in the diet Elevate total serum cholesterol all fractions but especially LDL In US the SFA most contributory to atherosclerotic CVD are in descending order of potency Myristic butterfat coconut amp palm kernel oil associated with atherosclerotic CVD Palmitic animal foods associated with atherosclerotic CVD Lauric coconut oil saturated fatty acid less atherosclerotic and is a medium chain Myristic and Palmitic are commonly consumed in people s diets From biochemistry Fatty acids are the building blocks of lipids They have a hydrocarbon chain with a carboxylic acid tail at one end Triglyceride glycerol backbone that has 3 fatty acids Fatty acids are saturated if they only have single bonds between the carbon atoms Unsaturated if the hydrocarbon chain contains one or more double bonds between the carbon atoms Monounsaturated one double bond Polyunsaturated 2 or more double bonds Polyunsaturated fatty acids PUFA s i serum chol primarily seen when SFA s are replaced with PUFA s Omega6 s Linoleic acid is predominant 182 omega 6 It is essential so we need some of it Common sources vegetable oils Not a more is better situation consuming large amounts of linoleic acid leads to oxidation via alternate metabolic pathways so T PUFA intake to gt current levels is not recommended High intakes of Linoleic acid seem to have adverse effects on vascular and stimulate production of proinflammatory Omega3 s cardio protective Most effective FA for lowering TG s i s cholesterol VLDL and LDL i s risk of MI stroke Sources eicosapentaenoic acid and docosahexaenoic acids inhibit EPA and DHA fatty cold water fish salmon mackerel herring trout and albacore tuna fish oils and capsules orlinolenic acid 183 omega 3 flaxseed walnuts Not as strong as the EPA and DHA can go undergo successful desaturations and elongations to yield EPA and DHA Goal would be to reduce saturated with polyunsaturated AHA recommends getting 235 oz of fatty fish Monounsaturated fatty acids MUFA s Cis forms oleic acid most common replacing SFA with MUFA lowers total chol LDL amp TG Sources peanut olive and canola oils Trans fatty acids stereoisomers of cis linoleic acid produced by hydrogenation T cholesterol and LDL and i HDL Dietary Cholesterol Increases serum total cholesterol amp LDL but less so than SFA T chol T SFA intake has greatest effect on serum cholesterol decreased LDL receptor activity and increased CVD risk Sources animal products If it didn t have a liver it doesn t have cholesterol When cholesterol intakes reach 500 mgday incremental rises in blood cholesterol get smaller threshold effect Varies from person to person There is variation among people in the response genetic variants gt hypo and hyper responders AHA recommends less than 300 mgday 200 mgday for people with diabetes and existing CVD and High LDL Plant stanols and sterols Isolated from soybean oil or pine tree oil wheatgerm some nuts seeds avocados certain vegetable oils Interferes with cholesterol absorption Consumption may significantly lower serum cholesterol Esterified versions have been made into margarines Benecol and Smart Balance Dietary Fiber Soluble Added to a lowfat diet appears to i total cholesterol Most effect on blood lipids attract water and form a gellike consistency in the gut Most effective appear to be pectins amp gums followed by psyllium oat bran oatmeal many dried fruits and nuts and dried beans and legumes Insoluble fiber cellulose whole grains nuts vegetables wskins Thought to have no direct effect on serum cholesterol Indirect replacement effect Recommended 14g fiber per 1000 kcals consumed per day AMA Dietary Guidelines Academy of Dietetics emphasize eating fruits vegetables legumes and whole grains Soy Protein Adding soy protein to lowfat diet has been shown to reduce total cholesterol in those with high serum cholesterol Food first supplement 2nd LDL TG and HDL are also affected positively Possibly related to phytosterol and phytoestrogens in SOY with isoflavones intact so soy protein isolate is not likely to have a comparable effect This may explain the disparity in research reports Alcohol cardio protective in small doses light to moderate consumption Moderate intake 2 drinksd for men 1 drinkd forwomen correlated with T HDL i oxidation of LDL amp anticoagulant properties However gt intake also T TG and risk of CHD in dose dependent fashion Antioxidants Dietary intake of antioxidant vitamins and carotenoids are inversely related to risk of CHD No benefit Overdosing of Vitamin E Flavonoids tea onions red wine red grape juice tomatoes grapefruit soy etc appear to have beneficial antioxidative effects CVD Other Risk Factors Plasma Homocysteine T levels positively associated with CVD Folic acid B6 and 812 decrease homocysteine levels optimal dosages unclear lf person follows a diet of fruits vegetables and whole grains they would get those B vitamins and low fat diary for Bf 2 Smoking Greatly T incidence of CVD and mortality from CVD l HDL T BP and damages endothelial lining of arterial walls Hypertension BP gt14090 mmHg causes vascular injury amp stresses myocardium Often present with T cholesterol amp obesity Result Coronary Artery Disease and Stroke Diabetes 80 of deaths among diabetic persons result of ASCVD Often present with hyperlipidemia obesity and HTN This combination metabolic syndrome Die from CVD Physical inactivity Sedentary individuals have greater risk of CHD compared to active people Menopause Loss of endogenous estrogen T s CHD risk Men had higher CHD until menopause when the levels evened out because of protective effects of endogenous estrogens Perimenopause associated with Ttotal cholesterol TG LDL and i HDL Obesity BMI gt300 As BMI increases CVD risk increases Exacerbated by coexisting conditions of insulin resistance Type 2 DM HTN and dyslipidemia Central adiposity VAT has greatest association with CVD morbidity amp mortality Oxidative stress Oxidation of LDL in vessel wall stimulates localized macrophage amp antibody activity leading to atherosclerosis Dietary factors that may i risk Vit E C Bcarotene calcium selenium magnesium flavonoids phytoestrogens in soy MUFA Monounsaturated Fatty Acids Too much iron copper zinc and SFA may T LDL oxidation Infectious Agents Viruses amp bacteria may trigger inflammatory response that harms coronary vessel walls resulting in scarring or narrowing Get your flu shot Psychosocial factors Timeurgent Type A personalities Depression Low education Familial Hypercholesterolemia Very rare genetic hyperlipidemia Monogenetic defect in LDL receptor Cholesterol of 250500 mgdL present at birth Very high LDL normal TG Heterozygotes 1500 are treated with diet amp drug therapy Homozygotes 11 million experience Ml or cardiac death in first or second decade of life prone to childhood heart attacks Require aggressive treatment eg biweekly plasmapheresis of LDL Genetic Hyperlipidemias cont Familial Combined Hyperlipidemia Characterized by T LDL andor TC in at least 2 family members LDL is often of small dense type Results in premature CAD Familial Dyslipidemia Pt and at least 2 family members have TG gt90th o percentile and serum HDL lt10th o percentile Both of these conditions frequently coexist with obesity HTN DM gout Tx TLC diet wt loss DM control exercise meds if lipidemia is resistant Lipid levels controlled with intervention patients likely will have myocardial infraction before age 60 Familial Dysbetalipoproteinemia Abnormal structure of ApoE resulting in delayed catabolism of VLDL lDL and chylomicron remnants Total cholesterol 300600 mgdL and TG 400800 mgdL are elevated Results in premature CAD and PVD Tx wt loss blood glucose mgt TLC Diet drug tx if condition iS resistant MNT for Cardiovascular Disease Referral to a RD for lifestyle changes should be initiated prior to initiating pharmacologic treatment and should continue during pharmacologic treatment Initial visit with RD 4590 minutes 26 followups of 3060 minutes each Academy of Nutrition and Dietetics Evidence Analysis Library Number of visits determined by complexity of changes number of changes and motivation of patient Diet can have a tremendous impact on primary prevention of CVD and on a disease management Managing CV Health NCEP National Cholesterol Education Program NHLBI 1988 National guidelines for detection evaluation amp treatment of hypercholesterolemia Established Adult Treatment Panels ATP s to classify risk based on serum cholesterol fractions Step 1 general public and Step 2 people that were at high risk for CVD diets ATP Ill 2001 eliminated Step 1 and 2 diets Established TLC Therapeutic Lifestyle Changes diet To prevent or reduce risk of CVD in all healthy persons gt2yo use the AHA Dietary Guidelines Major guidelines for all Americans Replaced the former Step 1 diet Emphasizes specific food choices and overall eating habits to improve health and decrease risk For medical nutrition therapy interventions for those with DM lipid disorders preexisting CVD etc use the TLC Therapeutic Lifestyle Changes Diet The TLC Diet replaced the Step 2 diet The DASH diet is an alternative diet that has also been shown highly effective AHA Dietary Guidelines for CVD Risk Reduction be familiar with these guidelines These guidelines are appropriate for all healthy Americans gt2yo Balance caloric intake and physical activity to achieve or maintain a healthy body weight Consume a diet rich in vegetables and fruits Consume fish esp oily fish at least 2xweek Limit sat fat lt7 of energy transfat lt1 and cholesterol lt300mgday Minimize intake of beverages and foods with added sugars Choose or prepare foods with little or no salt When consuming alcohol do so in moderation When eating food that is prepared outside the home follow the AHA Diet and Lifestyle Recommendations MNT with the TLC Diet Treats high LDL as a primary target for risk reduction Treats high cholesterol more aggressively Aggressively treats high TG levels Major Components of the TLC Diet be familiar with this Total fat 2535 SFA lt7 o total kcal PUFA up to 10 total kcals MUFA up to 20 total kcals CHO 5060 especially whole grains vegetables and fruits Protein 15 o Cholesterol lt200 mgd below regular guidelines Fiber 2530 gday Total kcals balanced to maintain desirable weight All adults gt20 yrs should have lipid profile every 5 yrs Pharmacology for CV Health Bile Acid Sequestrants Eg cholestyramine Questran binds up bile salts in the GI tract preventing them from being reabsorbed in the lower bowel Cholesterol medication Potential side effects Poor patient tolerance constipation bloating NVD May interfere with the absorption and digestion of fats and fat soluble vitamins May be necessary to supplement these vitamins as well as calcium and folic acid Diet is always a part of treatment even it is combined with medications But depending on a patient s risk category and LDL levels medicinal management may also be necessary Medical nutrition therapy should underpin all drug therapy most effective than medication alone Nicotinic acid form of niacin Bcomplex and is found in food available in high dosage prescription t s LDLamp T s HDL Least expensive Side effects limited compliance 2 poor pt tolerance skin flushing itching hyperglycemia hepatotoxicity A recent research study suggested that adding nicotinic acid or niacin to statin therapy was not associated with lower risk of heart disease Fibrates fibric acid derivatives EgGemfibrozil Lopid and Fenofibrate Tricor Primarily effective in i TG part due to inhibiting release of TG from fat stores with small increase in T HDL Not particularly effective for i LDL Side effects abdominal pain acute appendicitis constipation diarrhea eczema fatigue headache indigestion nauseavomiting rash vertigo may increase cancer risk Nutrition interaction should be taken with food increases absorption HMGCoA Reductase Inhibitors statins eg Simvastatin Lovastatin The mostprescribed lipidlowering agent Very effective in i LDL Generally welltolerated Side effects liver damage muscle myopathy peripheral neuropathy Nutrition interactions do not take with grapefruit or pomegranate juice some should be taken with food increases bioavailability may lower 0001 0 levels Medical Interventions PTCA percutaneous transluminal coronary angioplasty aka percutaneous coronary intervention or PCI Balloon is inflated within coronary artery to break up plaque CABG coronary artery bypass graft Vein from leg or artery from chest used to graft a resection of coronary vessels around an occlusion Spath Study Guide for DISORDERS OF THE SMALL AND LARGE INTESTINES M7Part 3 know gtgt Define Short Bowel Syndrome SBS small intestine Short Bowel Syndrome SBS is reduced absorption associated with reduced small intestinal length Common39y occurs if there is Surgical removal resection of 12 or more of small intestine May 33930 be caused by injuries or congenital defects present at birth Issues may depend on the location of the resection Associated with severe metabolic alteration and malnutrition There may not be enough absorption area left to absorb all of the nutrients from food people with 888 tend to have complicated fluid electrolyte amp nutritional management issues can have additional problems if the ileocecal valve sphincter is compromised gtgtDescribe how removal of the ileocecal valve may lead to Small Intestinal Bacterial Overgrowth SIBO SBS condition is more symptomatic with removal of ileocecal valve risk of small intestinal bacterial overgrowth SIBO The ileocecal sphincter valve separates the small intestine from the large intestine Normally the small intestine contains a low number of bacteria The small intestine environment with the bile amp pancreatic enzymes gutassociated lymphoid tissue immune cells amp rapid movement of material through via peristalsis is not friendly to bacteria The large intestine is much different The large intestine contains large numbers of bacteria our normal flora The ileocecal valve prevents backwash from the large intestine into the small intestine If the ileocecal valve is removed a person is at risk of SIBO Small intestinal bacterial overgrowth SIBO abnormally large numbers of bacteria present in the small intestine Can damage the small intestine mucosa and further impair absorption Page 1 of 21 Symptoms of SBS gtgtWhat are some other common symptoms and complications of SBS Malabsorption macro and micronutrients is a major concern know gtgtHow does SBS lead to gastric hypersecretion Why would this lead to diarrhea A reduction in the length of the small intestine means decreased production of secretions that inhibit the secretion of gastric acid in the small intestine Excessive acids inactivates pancreatic lipase amp trypsin leading to increased GI motility which results in diarrhea that will be acidic due to gtgastric acid Diarrhea 39 2 secondary to malabsorptionhyperosmolar intestinal contents weight loss amp fatigue acidic diarrhea secondary to gastric hypersecretion Hypersecretion of gastric acid in small intestine due to l inhibitory secretions that normally suppress gastric acid when food reaches the small intestine Excessive acid inactivates pancreatic lipase and trypsin T GI motility due to l CCK and secretin Results in acidic diarrhea Meds H2 Blocker Proton Pump Inhibitor Steatorrhea signals fat malabsorption Dehydration Electrolyte imbalance Weight loss Growth failure children Page 2 of 21 gtgtDescribe some special considerations for a jejunal resection An ileal resection RD needs to identify the ocations of patient s resections to determine possible effects on absorption of nutrients patient records patient interview output of stools Tends to be complicated Duodenal resections i5 Omy 10 long not much absorption happens here but is an important entry point for bile amp pancreatic juices Jejunal resections is the primary site for nutrient absorption lleal resections iS the Ohly site Of absorption for vitamin 312 ntrinsic Factor compex is the site for enterohepatic circulation or reabsorption of bile salts for return to Salivary amylase l 1 Mum Esophagus Stomach Gaslricjwce I d a H39Elfs39 g 7 New recyc e Pancreas Duodenum 7 7 L Pamruatlc iuicu H Clquot 504quot v iEicarbonate Iron a Enzymes Calm U m m o 7 Magnesium Gallbladder Bile F Zinc 7 Glucosegalacloselruclose i V Intestinal brush Amino acids dapeprides and tripeptldes 39 border enzymes Vilamin C 1 r Thiamln Water giblgtiavin soluble vHanuns lacIEMS 39 Pwmmmej Lelt subclawian Folnc aloud and left internal VuanunsADEwK quot jugular veins Fat Cholesterol Illeulm Erma vitamin K farmed g Bacterial action HgD Rectum nus 1 FBCES reabsorption the liver may not be able to produce enough bile for fat emulsification So there could be malabsorption of fat amp fatsoluble vitamins absorbs a good deal of water amp electrolytes After Jejunal resections ileal adapts over time to provide some additional nutrient absorption and so compensates for the missing Jejunal gtgtDescribe the possible MNT modalities for 333 Google Parenteral nutrition aka intravenous feeding through the veins While it is most commonly referred to as total parenteral nutrition TPN some patients need to get only certain types of nutrients Parental nutrition bypasses the digestive system altogether A person with Short Bowel Syndrome will likely need TPN initially to restore amp maintain nutritional status Some people with SBS are on longterm TPN Postop care Duration of TPN following resection depends on extent of removal Can require total bowel rest for several weeks Start enteral tube feeds through the intestine as soon as tolerated but introduce gradually Continue PN for nutritional adequacy Page 4 of 21 GI may never regain full absorptive capacity Maximum adaptation can take up to one year postresection Adaptation is improved by providing trophic stimulus to the gut ie enteral feeding gtgt Why would trophic feeds enteral feedstube feeding still be beneficial even if the TPN IV feeding is meeting a person s needs for macronutrients and micronutrients Trophic feeds enteral feedstube feeding are beneficial even if TPN is meeting 100 of person s nutritional needs because trophic feeds 1 prevent atrophy of the enterocytes intestinal lining cells 2 maintain gut integrity amp function and 3 prevent bacterial overgrowth Trophic feeds stimulate the gut Without trophic feed if we weren t stimulating the biliary tract to release bile the result could be bile sludge increased risk for gallstones etc Need to stimulate the gut know gtgtWhy may glutamine supplements or enteral formulas containing glutamine be beneficial Glutamine is a conditionally essential amino acid is the most abundant amino acid in the body amp is is the preferred fuel source for enterocytes the cells that line the GI tract Glutamine supplementation can help maintain the gut Google Conditionally essential amino acids are usually not essential except in times of illness and stress MNT for SBS continued 0 Oral nutrition will often support a pt with 23 in or more of small bowel remaining can usually be weaned from tube feeding amp lV nutrition but it could take a long time Begin oral feeds with clear liquids lnitial refeeding of solids should be bland low residue low fat lactosefree Progress in volume and concentration as tolerated AVerage reCOVery time 34 months before food by mouth is tolerated Liquid supplements or supportive PN may be required for life Page 5 of 21 gtgt Someone with 835 may require TPN to meet nutritional needs for a lifetime lt 23 inches of small bowel requires lifetime supportive PM or even TPN if gut function does not return Other considerations Drugnutrient interactions these patients will likely be on a lot of medications Drugs to retard gastric emptying slow motility and decrease secretions may improve absorption Loss of terminal ileum ileum resection requires B12 injections That person may exhibit more fat malabsorption because bile salts are not reabsorbed amp recycled as normal Some foods may never be tolerated by the SBS patient Some GI stimulants eg alcohol and caffeine may not be tolerated for a year if ever Distinguish food intolerances from GI side effects of narcotics amp other meds know gtgt What is Irritable Bowel Syndrome IBS Irritable Bowel Syndrome IBS a disorder not a disease Not the same as inflammatory bowel disease IBDCrohn s UC is a common gastrointestinal disorder involving an abnormal condition of gut contractions motility characterized by gtgtWhat are some common ss abdominal pain bloating flatulence mucous in stools irregular bowel habits with alternating diarrhea and constipation 0 Typical onset 2030 yrs old more common in young adults More common in women than men Page 6 of 21 Symptoms tend to be chronic and to wax and wane over the years Can cause chronic recurrent discomfort but does NOT lead to any serious organ problems gtgtWhy is this considered a functional disorder is a Functional GI disorder not explained by a known structural infectious or metabolic cause EtiOIOQY of IBS is unknown possible contributors stress inadequate rest caffeine or alcohol laxative abuse low fiberlow water intake heredity The enteric nervous system is the nerve plexus or network that innervates the GI tract Persons with Irritable Bowel Syndrome seem to have a heightened enteric sensitivity amp motility response to usual GI and environmental stimuli So foods like caffeine or alcohol stimulate peristalsis and persons with lBS may be particularly sensitive to those Google The enteric nervous system helps regulate digestion The enteric nervous system is sometimes referred to as a second brain because it relies on the same types of neurons and neurotransmitters that are found in the central nervous system brain and spinal cord Harvard Medical School Irritable Bowel Syndrome IBS continued Diagnosing IBS Because it is a functional disorder lBS can be tough to diagnose First rule out ro other illnesses World Congress of Gastroenterology s Rome Criteria for Diagnosis of IBS criteria are somewhat vague Symptoms of abdominal discomfortpain present 12 weeks 2 of the following Discomfort relieved by defecation Onset associated with change in stool patterns Page 7 of 21 Onset associated with change in stool form MNT for Irritable Bowel Syndrome IBS Goals 1 Provide relief management of symptoms 2 Restore nutritional balance know gtgtThe goals of MNT for IBS relate to symptomatic management Describe some possible treatment options for constipation and diarrhea MNT High fiber 2030 9039 institute slowly 68 glasses water daily Reduce Simple CH0 especially lactose amp fructose which tend to be more difficult to absorb anyway Consider limiting fermentable oligo dimonosaccharides and polyols FODMAPS in one s diet Other interventions Regular exercise Stress managementrelaxation techniques eating in a calm relaxed environment SSFil s Selective Serotonin Receptor Inhibitors Much of the serotonin in the body is found in the GI tract IBS has been correlated with serotonin levels that are either too high or too low SSRls are a class of antidepressants that help control serotonin levels MNT for Irritable Bowel Syndrome IBS continued gtgtDescribe some possible IBS treatment options for flatulence Flatulence excessive gas Flatusgas Prevent aerophagia swallowing air by chewing slowly not drinking through a straw not chewing gum Limit gasforming foods Page 8 of 21 Beans cabbage brOCCOIis asparagus etC cruciferous vegetables all contain a resistant starch resists digestion in small intestine called Raffinose that tends to produce gas production carbonated beverages Limit lactose amp fructose Limit sugar alcohols gtgtWould probiotics be helpful Probiotics have shown promise for IBS gtgtDescribe how you may initiate a trial of food elimination amp challenge with an IBS pt 0 Conduct a trial of food elimination amp challenge try removing certain foods from the diet monitoring symptoms and then slowly reintroducing foods one by one to determine which foods are triggers for IBS Start with foods to avoid identified in the FODMAPS diet next page Common fOOdS are poorly tOIGFated meaS5 caffeine5 food additives sorbitol and other sugar alcohols fructose and lactose Be careful about unnecessarily limiting large groups of food Start with these foods for trial of food elimination amp challenge Common Problem Foods for Irritable Bowel Syndrome IBS fermentable oligodimonosaccharides amp polyols FODMAPS Constipation is characteristic of IBS but can be a problem all its own is fairly common If food remnants remain in the colon too long then too much water will be reabsorbed and the stools will become hard amp difficult to pass older people can often complain of chronic constipation which can lead to anorexia amp poor intake Definition hard stools straining with defecation infrequent large bowel movements Page 9 of 21 Normal transit time through the GI tract is anywhere from 18 to 48 hours eg normal for one person may be a bowel movement every 3 days normal for another person may be 3 bowel movements each day know gtgtWhat are some common contributing factors to chronic cons pa on Most common causes in healthy people POOF bOWel habits ignoring need to defecate gt i muscle tone diverticula formation lowfiber diet inadequate fluid laxatiVe abUSG long term use of laxatives especially Stimulant laxatives may make constipation worse inactivity OPiOid medications for pain gt 80 of people on opioids experience cons pa on Complications of constipation A fecal impaction would be a large mass of dry hard stool that can develop in the rectum due to chronic constipation Straining can lead to hemorrhoids which are swollen inflamed veins in the anus and lower rectal area gtgtContrast stimulant vs osmotic laxatives gtgtWhy is longterm use of stimulant laxatives discouraged Page 10 of 21 know gtgtWhy isn t mineral oil recommended as a natural stool softener Types of laxative medications Stimulant stimulatetrigger rhythmic contractions of smooth muscle layers of the intestines to eliminate stool eg ExLax Ducolax is the harshest type of laxative long term use can damage the Structure and innervation of the colon Longterm use may worsen constipation Osmotic draw water into the bowel eg lactulose MOM are not as harsh as the Stimulant laxatives I 39H llhullllll ll Hf l39lnll HI hull 391 H39H39I39I Inl HI39HL lll LIHH EIUII 39 F DiMAP High F 39 DMAP food Fructose Fruits apples pea rs peaches mango suga r snap peas watermelon canned fruit in natural juice dried fru it fruit juice Sweeteners 11 oney39 high fructose corn syrup Lactose flaililk cow goat and sheep ice cream soft cheeses eg ricotta cottage cheese IUligosaccharides Vegetables artichokes asparagus beets brussel sprouts broccoli cabbage fennel garlic leeks okra Ifructans or onions peas shallots galactans Cereals wheat and rye large amounts Legumes chickpeas lentils kidney beans baked beans Fruits watermelon apples peaches rambutan persimmon Polyols Fruits apples apricots cherries longon l ychee pears nectarine peaches plums prunes watermelon Vegetables avocado cauli ower mushrooms snow peas Sweeteners sorbitol mannitol maltitol qtlitol and others ending in iE ol Low F lll il F Diet Instructions Avoid foods that contain fructose in excess of glucose unless fructose malabsorption is not demonstrated quot Try ingesting a source of glucose Twith Fructose containing foods lie sucrose contains equal amounts of glucose and Fructose quot Limit amount of fructose at any one meal quot avoid foods that contain signi cant amounts of fructans and galactans quot Restrict lactose containing foods unless lactose malabsorption is not demonstrated quot Avoid polyol containing foods Adapted from Gibson PR Shepherd SJ Evidence based dietary management of Functional gastrointestinal sym39iptoms the FUDMAP approach Gastricenterol Hepatol 252 52 21211121 FDDBLMP Femaentable oligro di and monosaecharides and polyols Mineral oil NOT recommended long term use may impede absorption of calcium and fatsoluble vitamins Page 11 of 21 a home remedy acts as a lubricant for easier passage of stool know gtgtDescribe some dietary recommendations that may be helpful for chronic constipation MNT for Constipation Ideally constipation for most people should be managed with diet and increased activity 0 Nutrition Adequate fruitvegetablewhole grain intake to provide appropriate soluble and insoluble fiber daily 14 g1000 kcal or 25 gday for women and 38 gday for men Daily Guideline Recommendations Very few people achieve that recommendation Fiber supplements are an Option take throughout day in smaller doses Watersoluble fiber eg pectin oat bran may soften and add bulk to stools commercial products like Metamucil Insoluble fiber eg cellulose can accelerate intestinal transit time Adequate UidS 39 2L daily especially warm fluids PrebiO EiCS amp Probiotics may help with bowel regularity Note incorporate over several weeks to diminish discomfort Bowel retraining program combination of nutrition exercises to strengthen pelvic floorrectal muscles consistent timing and medications Stimulants and laxatives caffeine prune juice erythromycin psyllium seed fiber lactulose gt prunes are rich in soluble and insoluble fiber are antioxidant are a natural source of sorbitol have a natural laxative compound amp are nutrient dense gt caffeine stimulates peristalsis Diarrhea is the opposite of constipation Any condition that rushes food remnants through the large intestine before the large intestine has had time to absorb enough water will result in diarrhea Page 12 of 21 Frequent evacuation of liquid stools Results from excessively rapid transit decreased enzymatic digestion of foods decreased absorption of fluids and nutrients mucosal damage know gtgtDiarrhea can have many many underlying etiologies Define osmotic secretory exudative medicationinduced and malabsorptive diarrheas Types of Diarrhea Patient may exhibit one or more types Osmotic Diarrhea osmotically active solutes are present in the intestinal tract and are poorly absorbed Eg dumping syndrome lactose intolerance lactase deficiency gtrelieved with fasting Secretory Diarrhea active intestinal secretion of electrolytes amp water by the intestinal epithelium 3939 bacterial infection gtN0T relieved with fasting Exudative Diarrhea mucosal damage gt outpouring of mucous fluid electrolytes blood andor plasma proteins 3939 Ulcerative colitis Crohn s Radiation therapy for cancer radiation enteritis Medicationinduced many kinds Can affect motility or decrease normal bacterial flora 3939 antibiotics may wipe out normal flora meds containing sorbitol Malabsorptive insufficient amount of absorptive area lack of bile or pancreatic enzymes Page 13 of 21 59 bowel resection inflammatory bowel disease villi atrophy Celiac Crohn s Short Bowel Syndrome MNT for Diarrhea 1 gt Diarrhea is not a disease but is a symptom of some other disorder Treatment should focus on identification amp treatment of the underlying cause antidiarrheal medications eg loperamide HCI sometimes slow down intestinal motility but motility could be the normal way the body gets rids of harmful bacteria or toxins in the intestine gt DO NOT treat with antidiarrheals without knowing the underlying cause 2 After determining cause next goal is to replace fluid amp electrolytes using dilute electrolyte solutions broth vegetable juices sodium amp potassium loss is very common with diarrhea know gtgtWhich foods would be indicated or contraindicated during diarrhea 3 As diarrhea subsides gt start lowfiber foods CHO then protein foods with moderate amounts of fat as tolerated 39 gt Limit lactose lactase production may be impaired fructose sugar alcohols egsorbitol fiber especially insoluble soluble fiber may be tolerated AICOhOIiC beVerages they increase GI secretions Hyperosmolar foods like simple CHO s caffeine stimulates motility Diarrhea should clear in 2448 hours In CHRONIC diarrhea monitor for absorptive deficiencies Infants and Children gt Greatest danger is dehydration gtgtWhat is an oral rehydration solution ORS REhYdra Eion With ORS or reduced osmolarity solutions Pedialyte Gatorade Page 14 of 21 gt Oral Rehydration solutions ORS typically contain glucose sodium amp potassium concentrations of glucose amp sodium optimal for sodium dependent glucose transport in the intestinal epithelium Prompt return to feed in the gut maintains GI integrity improves functional capacity gt resting gut for extensive periods can do more harm than good Children amp adU39tSi start with clear liquids but progress to full liquids gt low fiber foods gt advance as soon as tolerated gt The BRAT Bananas Rice Applesauce amp Toast diet is pretty popular These are not magic foods and by themselves do not provide sufficient nutrients long term Need to determine underlying cause of the diarrhea The American Academy of Pediatrics warns against using BRAT long term Diverticular Disease Diverticula are saclike herniations of the colon are abnormal small little pouches that protrude from the colon wall are multiple herniated areas of colon wall Diverticulum singular herniated pouch Diverticula plural herniated pouches Diverticulosis is fairly frequent with increasing age Incidence positively correlates with advancing age gtgtContrast diverticulosis and diverticulitis Diverticulosis presence of herniations small protruding pouches Diverticulitis herniations inflammation itis signals inflammation is inflammation amp infection of the diverticula occurs when bacteria become trapped in the pouches riSk 01 hemorrhage or perforation could spew bacteria into the peritoneum the membrane that lines the abdomen and that could lead to dangerous peritonitis Page 15 of 21 Symptoms of Diverticulitis distension nausea fever chills pain know gtgt How does MNT differ for diverticulosis vs diverticulitis MNT for Diverticulosis and Long Term Management of Diverticulitis is the same high fiber diet plenty of fluid know MNT for Diverticulitis during acute phase includes lowfiber diet May need complete bowel rest amp IV feeding parenteral nutrition MNT for Diverticulosis High fiber diet plenty of fluid gtAcademy says OK to eat nuts seeds strawberries raspberries corn etc an outdated recommendation says to avoid MNT for Diverticulitis Nutrition Care Acute Stage ie during inflammation low residue diet ABX complete bowel rest amp parenteral nutrition parenteral Utrition feeding a person intravenously Long term management high fiber same as MNT for Diverticulosis Encourage 68 glasses waterd High fiber diet gt if not tolerated as whole foods add fiber supplements eg Metamucil or Benefiber Colorectal Cancer Polyps Page 16 of 21 know gtgtWhat is the relationship between colon polyps and cancer risk Colon polyps mushroomlike growths are considered precursors of colon cancer MOST polyps DON T become cancer but if the doctor finds one during a colonoscopy preventive procedure heshe will remove it cauterization 3rd most common cancer after lung breast women prostate men Risks include family hx or genetic predisposition IBD Crohn s ulcerative colitis know gtgtList some dietary factors thought to decrease colon cancer risk Nutrition s role in prevention avoid foods that increase risk of cancer Balanced diet High intake of antioxidants Moderate to high fiber intake Low saturated fat red meat is postulated to reduce risk Decrease nitratenitrite containing foods Decrease intake of grilled or charred foods Colectomy A person with an intractable uncontrollable difficult case of IBD Crohn s Ulcerative Colitis or someone with colon cancer could have a partial or total colectomy Colectomy consists of the surgical resection of any extent of the large intestine colon know gtgt What is an ileostomy Colostomy When the total colon rectum amp anus are removed an ileostomy is performed and a stoma is placed at the ileum Consistency of stool is liquid When the rectum amp anus are removed a colostomy is performed and a stoma is placed at the colon Consistency of stool ranges from mushy to well formed lleostomy Colostomy involves creating an opening for waste discharge Page 17 of 21 ostomy an artificial opening stoma created surgically on the abdominal wall through which waste material passes out of the body from the bowel or urinary tract ostomy output depends on stoma location on the abdominal wall and on what the patient eats amp drinks lleostomy stoma placed at ileum Removal of colon rectum and anus op is liquid Colostomy stoma placed at colon Removal of rectum amp anus op ranges from mushy to formed There are various types of colostomies gtgtDescribe MNT for an ostomy patient know gtgtWhy would someone with an ileostomy have an above average needs for water and salt A person with an ileostomy has an above average need for water amp salt to compensate for those excessive losses drink a liter more of water than ostomy output each day Also needs more salt lleostomy Colostomy Nutritional Considerations Odor is major concern to pts educate regarding gas and odorforming foods and stoma care corn legumes onions cabbage fish vitamins garlic eggs can vary by person parsley amp buttermilk are thought to be natural deodorizers ileostomies usually have an acidic odor that is not unpleasant patients are trained in how to care for the stoma site by the ostomy nurse lleostomies need more water amp salt Supplement B12 for terminal ileum removal or small bowel overgrowth Chew foods well to avoid clogging Avoid fibrous vegfruits Don t overrestrict Regular meal times to normalize ostomy output Patient adapts to ostomy in about 6 weeks Sample PES statement for an ileostomy patient P Inadequate fluid intake E related to losses from ileostomy Page 18 of 21 S as evidenced by Input amp Output records intake 1200 mL output 1600 mLd know gtgtWhat is a fistula and what are some possible causes A fistula is an abnormal opening or passage between 2 organs or between an organ and the skin gtAn enterocutaneous fistula is an abnormal opening between the intestine and the skin Fistula Abnormal opening between two epithelial surfaces Internal 39 between 2 hollow organs External 39 between a hollow organ amp skin enterocutaneous intestineskin Types congenital birth defect spontaneous cancer IBD Crohn s UC infection Surgicallycreated With a fistula a person risks 1 losing large amounts of fluid amp electrolytes 2 infection High output gt 200 mLd of effluent Stomach duodenum pancreatic duct proximal bowel Usually require TPN may be needed until the fistula is surgically repaired If it s a small Low output fistula distal small bowel amp colon Tx with liquid diet or tube feeding Decreased absorptive area may lead to malabsorption Consider contamination potential gtgtDescribe MNT for a fistula patient MNT correct fluidelectrolyte imbalances T Kcal T protein diet to support healing patient may be slightly hyper metabolic expected healing time 12 months Additional Disorders to be aware of Page 19 of 21 Intestinal obstruction partial or complete blockage of the large or small bowel gtgtWhat are some possible causes of an intestinal obstruction Intestinal strictures Obstructions may occur in the small or large intestine due to a tumor fecal impaction in the colon or rectum or strictures Strictures one type of obstruction may occur in the small or large intestine Similar to what can happen in the esophagus inflammation from IBD Crohn s Ulcerative Colitis can cause scar tissue that could lead to narrowing or a stricture Causes of narrowing include radiation enteritis from radiation therapy People who are prone to obstructions are advised to chew food very well and to avoid excessive fiber intake lf person has a complete obstruction they will be intolerant of food intake and may be intolerant of their own GI secretions In that case surgery may be indicated and parenteral nutrition IV feeding may be the only option gtgtWhat is an ileus What is a pseudoobstruction What is the difference between the two Note many clinicians use these two terms interchangeably lleus is a lack of GI tract motility without evident mechanical obstruction involves both the small and large intestines symptoms are the same as for an obstruction or blockage but when intestines are examined no blockage is found A g Gallon l r 7 gt symptoms are actually due not to a blockage but to nerve or muscle problems that affect movement of food fluid amp air through the intestine may be common after abdominal surgery may take time for peristalsis to return after surgery may need TPN for nutrition support IV feeding Pseudoobstruction is colonic ileus technically a pseudoobstruction would be limited to the colon alone whereas an ileus involves both the small and large intestines Page 20 of 21 know gtgtWhat is a volvulus Volvuus abnormal twisting of the intestine causing obstruction Intestine twists on itself Is fairly rare Requires surgical intervention uri t I r r 391 quot v EEi39 L gamma inlllgJtigtm quothisquot EFiEIJJ Page 21 of 21 NHM 365 Module 92 Spath Study Guide Acute and Chronic Complications of Diabetes Part 2 Acute Complications severe amp sudden onset Hypoglycemia o is low is an acute complication is an acutely dangerous situation especially for someone on insulin or taking oral secretagogue meds Why is low blood glucose dangerous Glucose is the primary energy source the preferred energy source for the brain Red blood cells which carry oxygen to all other cells of body must have glucose for fuel 80 hypoglycemia could lead to coma or death Physiological response to I BG gt1st response to drop in blood glucose is from Autonomic Nervous System autonomicadrenergic symptoms shakiness sweating palpitations anxiety hunger Insufficient blood glucose to the brain causes Neuroglycopenic symptoms slow performance difficulty concentrating confusion and disorientation slurred speech irrational behavior extreme fatigue seizures unconsciousness What are some common causes of hypoglycemia Common Causes of Hypoglycemia Inadvertent or deliberate errors in insulin doses Excessive insulin or oral secretagogue medications Improper timing of insulin in relation to food intake Intensive insulin therapy Inadequate omitted or delayed food intake Unplanned or increased physical activities or exercise Alcohol intake without food Pagef of 12 IBlood Glucose quotSymptoms 90mgdl Endogenous insulin secretion inhibited 68mgdl Counterregulatory hormones released to bring blood nIurncn hat11 in nnrmnl 58mgdl Onset of symptoms shaky sweaty palpitations hungry 50mgdl Cognitive dysfunction inability to perform complex facizcl lt27mgdl Reduced conscious convulsions coma severe nan IrnnIIIrnnnniai gt gtWhat are the 55 of hypoglycemia Symptoms of Hypoglycemia Page 2 of 12 Need to Self Monitor Blood Glucose SMBG to maintain good control of blood glucose If blood glucose drops need to know what to do Treatments for Hypoglycemia blood glucose lt 70 mgdL gtgt Describe the rule of 15 for treatment of hypoglycemia lf lt70 mgdL amp responsive person should eat 15 gCHO After 15 min recheck blood glucose If blood glucose is still below lt70 person should eat another 15 gCHO Recheck blood glucose every 15 min amp eat another 15 gCHO until blood glucose is gt70 gtSo eat 15 gCHO every 15 min until blood glucose gt70 If BG is lt70 mgdL and pt is responsive use the Rule of 15 1 Administer 15gCHO Person ingests 15 9 CH0 simple CHO Glucose tablets work best Available at any pharmacy Keep on hand Or 12 cup juice or regular soda not diet 5 saltine crackers TBSP honey 78 lifesaver candies don t over compensate Glucose tablets are premeasured amp can prevent over treatment Recheck bg in 15 minutes Repeat until 15 min check is gt70 Then recheck at 1 hr 4 If next meal or snack is gt 30 min away person should have a more substantial snack a mixedmacronutrient snack like 12 sandwich or some peanut butter crackers 5 Be careful not to over treat saw gtgt What if someone experiencing hypoglycemia is unconscious or seizing How would the hypoglycemia be treated inject glucagon If pt is unresponsive or unable to swallow eg unconscious or seizing Page 3 of 12 Administer inject glucagon Kits are available that contain prefilled syringes of glucagon that can be injected Retest in 15 minutes Educa on Pathophysiology diet SMBG Reinforce with older patients Acute Complications Hyperglycemia amp Diabetic Ketoacidosis DKA Hyperglycemia blood glucose gt180 mgdL is an acute complication is an acutely dangerous situation gtgt What is diabetic ketoacidosis gtgt ls ketoacidosis primarily seen in type 1 or type 2 diabetes type 1 o More likely in type1 during illness such as a cold Usually see in type2 only during illness Diabetic ketoacidosis DKA inadequate insulin for glucose use results in the body switching to burning fatty acids and producing acidic ketone bodies Hyperglycemia gt250mgdl see chart on p6 so even if blood glucose is sky high without insulin to facilitate uptake of that glucose into the cells the cells are starved for glucose and resort to beta oxidation of fatty acids gt normally we maintain our blood pH right at around 74 but any type of acidosis is dangerous Primarily seen in T1 DM especially if they have an acute illness like a cold would only see in type 2 if that person were iii Page 4 of 12 gt so need to keep close watch if type1 or type2 are ill Symptoms gt fruity acetonesmelling breath vomiting dehydration deep gasping breathing or hyperventilation confusion and coma ls lifethreatening but reversible it treated Treatment IV fluids to correct dehydration insulin to suppress the production of ketone bodies treatment for any underlying causes such as infections and close observation to prevent and identify complications gtgt Describe the Hyperglycemic Hyperosmolar State HHS dehydration hyperglycemia gt 600 mgdL leads to hyperosmolarity to a point where it is acutely dangerous gtgt Recognize that this acute complication is typically seen in older adults with type 2 diabetes Acute Complications Hyperglycemic hyperosmolar state HHS acute complication acutely dangerous condition can lead to coma amp death HHS usually presents in older patients with T2DM Hyperglycemic hyperosmolar state HHS is characterized by dehydration hyperglycemia amp hyperosmolarity gt without significant ketoacidosis older persons are more prone to dehydration don t get thirsty signals don t get enough fluids are more likely to be on diuretics Page 5 of 12 dehydration hyperglycemia leads to hyperosmolarity to a point where it is acutely dangerous gt persons typically have extremely high blood glucose sometimes over a 1000 mgdL symptoms include hallucinations confusion Treatment Small incremental doses of insulin to bring blood glucose back down Fluid rehydration Correct Electrolyte imbalance Hyperglycemic Crisis DKA vs HHS Key differences DKA type1 HHS type2 usually elderly Page 6 of 12 lipolysis gt ketones dehydration Hyperglycemia gt250 mgdL lipolysis inhibited profound dehydration Hyperglycemia gt600 mgdL Most often with type 1 Severe insulin deficiency and T counterregulatory hormonesl Iipolysisl FFA releasel ketones Glycosurialjl diuresisl dehydration and electrolyte imbalance Hyperglycemia gt250mgdl ketosis dehydration electrolyte imbalance Rabid develonmenf lt24 hours 8amp3 ljpolyuria polydipsia polyphagia blurred vision vomiting abdominal pain dehydration weakness mental Most often elderly or undiagnosed type 2 t insulin T counterregulatory hormones but insulin adequate to inhibit lipolysis Glycosurialjl diuresisl profound dehvdration and electrolvte imbalance Hyperglycemia gt600mgdl no ketones profound dehydration gt320m0smkg altered sensorium to coma Evolves over several davs to weeks Altered sensorium most common presentation Exam will show dehydration weakness hypotension Treatment for DKA and HHS Both characterized by hyperglycemia Correct Fluid Electrolyte imbalance Page 7 of 12 Hypergycemia with appropriate insulin doses Educa on 8amp8 of hyperglycemia Sick day management How and when to contact MD Financial help Glycemic control can be more difficult during an illness gtgt What are the sick day guidelines for diabetics Sick Day Guidelines Self monitor blood glucose SMBG at least 34 timesday Take all medications including glucose lowering medications Illness can trigger the release of stress hormones that can raise blood glucose levels Hydration Nutrition eg 15 g CHO every 12 hours Call the doctor Vomitingdiarrhea gt46 hours Ongoing fever abdominal pains Uncontrolled BG andor ketones gtgt Contrast the Somogyi Effect with the Dawn Phenomenon Both present as high morning blood glucose amp both involve hormone action to raise blood glucose but have different causes amp treatments Page 8 of 12 Somogyi Effect rebound hyperglycemia is due to not enough CHO before bed OR too high pm insulinmeds Hormones respond to hypoglycemia So increase CHO before bed or lower pm insulinmeds Dawn Phenomenon is due to the body s normal hormone production while sleeping that leads to higher am blood glucose especially if person has inadequate insulin So opposite treatment lower CHO before bed or up pm insulinmeds gtgt How would you discern whether hyperglycemia in the morning is due to one or the other By testing blood glucose in the wee hours of the morning for a few days In Somogyi finding would be low blood glucose In Dawn finding would be normal or slightly elevated blood glucose Acute Complications Somogyi Effect vs Dawn Phenomenon Both present as high morning blood glucose elevated fasting glucose with different causes and different tx Somogyi Effect aka quotRebound hyperglycemiaquot that follows hypoglycemia in wee hours of morning blood glucose is very low in early am23 am due to not enough CHO prior to bed or too high insulinmeds if not enough CHO or too much of longacting meds blood glucose may drop in the early am body reacts by releasing counter regulatory Hormones SUCh as glucagon QFOWth hormone cortisol and catecholamines to T blood glucose Hormones help reverse the low blood sugar level by increasing hepatic glucose production but may lead to blood sugar levels that are higher than normal in the morning ie fasted blood glucose levels are elevated Tx T pm CHO intake or t pm med dosage Monitor Dawn Phenomenon Is not due to overnight hypoglycemia Blood glucose 23 am is normal or slightly elevated Hormones naturally produced while sleeping such as glucagon growth hormone cortical and catecholamines stimulate glygenolysis amp gluconeogenesis causing blood glucose to rise even higher in persons with inadequate insulin Tx tpm CHO do not eliminate or T pm meds Page 9 of 12 Exercise later in the day which may have more of a glucoselowering effect in the night Monitor gtgt Be familiar with chroniclongterm complications of diabetes due to high blood glucose 0 CVDMacrovascular diseases DM is an independent risk factor for CVD o Nephropathy DM most common cause of End Stage Renal Disease ESRD o Retinopathy DM is leading cause of blindness o Neuropathy autonomic nerve damage silent heart attack hypoglycemic unawareness o Gastroparesis delayed gastric emptying fairly common in diabetics Macrovascular diseases atherosclerosis when oxidized LDL lays down in the artery walls then atherosclerotic plaques form and form much more quickly in the presence of high blood glucose many type2 diabetics are already at risk of CVD because they already have Dyslipidemia high cholesterol Hypertension diabetes is an independent risk factor for CVD Microvascular diseases Nephropathy kidney disease 0 DM most common cause of End Stage Renal Disease ESRD Hypertension is also a leading cause so the combination of diabetes HTN is particularly dangerous nephrons are the functional units of the kidney Each kidney has millions of tiny little blood vessels that are constantly working to filter blood Chronically high blood glucose could damage those small blood vessels and eventually lead to renal failure Retinopathy damage to the blood vessels in the retina DM leading cause of blindness Think about the tiny blood vessels that supply the retina of the eye Chronically high blood glucose can damage those little capillaries Neuropathy nerve damage Peripheral eg foot ulcers amp poor wound healing Sensory deficits decreased sensation or numbness and spontaneous acute pain Autonomic autonomic nerve damage Bladder and sexual dysfunction gastroparesis postural hypotension cardiac denervation Page 10 of 12 hypoglycemic unawareness many signs are autonomic responses if autonomic nerve damage person may not experience the red flag warnings of hypoglycemia can put diabetes at higher risk of silent heart attacks person may not feel warning pain eg radiating up amp down arm or may not feel pressure to the chest Gastroparesis is delayed gastric emptying in the absence of a mechanical obstruction diabetic gastroparesis is fairly common will likely be prescribed a prokinetic medication SS lweight T early satiety irregular BG control MNT Stable and optimal BG control to stop Neuropathy damage to nerves Small frequent meals with consistent CHO Limit high fat foods because they empty the stomach more slowly Avoid high fiber foods to prevent risk of bezoar formation Eat slowly and sit up 1 hour after eating Lose weight if overweight gtgt Describe MNT for hypoglycemia of nondiabetic origin Hypoglycemia of Nondiabetic Origin Hypoglycemia in person who is not a diabetic Symptoms usually with BG lt65 mgdl Postprandial reactive hypoglycemia occurs after eating is the most common type of hypoglycemia in nondiabetics person may have an exaggerated insulin response person may have increased incretin hormones that are released from the small intestine Alimentary hyperinsulinemia person may have dumping syndrome with rapid delivery of nutrients into the small intestine that could lead to a rapid release of insulin from the pancreas that causes hypoglycemia Page 11 of 12 Idiopathic reactive hypoglycemia Fasting fooddeprived hypoglycemia is rare eg due to eating disorder Factitious hypoglycemia artificially created is even more rare person deliberately uses insulin to induce a low serum glucose level can be detected with a blood test for insulin to cpeptide ratio Cpeptide is cosecreted with insulin MNT 5 or 6 small mixed macronutrient mealssnacks each day consistent CHO intake spread throughout the day too much at one time could cause a spike and then a crash of blood glucose eat as though you have diabetes Page 12 of 12 Sieath Study Guide for DISORDERS OF THE SMALL amp LARGE INTESTINES M7Part 1 gtgt Review the normal anatomy and physiology of the small and large intestines including functions secretions sphincters etc Small Intestine The Duodenum is about 10quot long and it receives chyme from the stomach through the pyloric sphincter valve Then ducts that empty into the duodenum deliver pancreatic juices and bile from respectively the pancreas liver and the gallbladder The middle section of the small intestine is the Jejunum which is about 8 long This is where most of the absorption of nutrients takes place The terminal portion of the small intestine is the lleum The lleum is about 12 long It ends with the ileocecal sphincter valve which regulates movement of material into the large intestine and prevents backward movement of material from the large intestine to the small intestine Large Intestine Right below the ileocecal sphincter valve is the cecum The appendix is a small projection attached to the cecum Movement is from the ascending colon to the transverse colon to the descending colon to sigmoid portion of the colon to the rectum where waste is excreted from the body Functions of Intestinal Tract Motility Secretion of enzymes hormones etc Secretin signals the pancreas to release bicarbonate rich fluid and some enzymes into the duodenum CCK signals the pancreas to release most of its enzymes signals the gallbladder to contract and release bile into the duodenum Digestion amp absorption Chemical digestion of CHO PRO amp FAT and their absorption 3quot occur in the smaquot intestine Absorption of water amp electrolytes takes place in the arge and smau intestine Protection physiologic barrier and immune function gut associated lymphoid tissue GALT Payers PatCheS unencapsulated lymphatic cells that protect the mucous membranes of the small intestine the ileum from infection the normal flora bacteria of the large intestine produce some vitamin K and a few oi the B vitamins They also ferment nondigestible CHO to short chain fatty acids that nourish the colonocytes Page 1 of 8 Excretion the main job of the large intestine is to absorb water amp electrolytes and transport solid waste out of the body Disorders of the Small Intestine Celiac Disease know gtgt What are other common names for Celiac Disease aka glutensensitive enteropathy aka nontropical sprue aka Celiac Sprue gtgt What is gluten Gluten glutenin gliadin Guten is a composite of the proteins gluten and gliadin It is the gliadin that causes the flare up and autoimmune response in a person with Celiac Disease know gtgt Which fraction of gluten is responsible for the abnormal immune response that causes the 55 of Celiac Disease Giadin is the fraction of gluten responsible for the abnormal immune response that causes the 55 of Celiac Disease know gtgt Describe the pathophysiology of Celiac Disease Ceiac Disease a lifelong adverse autoimmune response in the proximal small intestine to gliadin a protein in gluten People with Celiac Disease have an abnormal Tcell response to gladden in gluten that leads to inflammation of the small intestinal mucosa gtgtHow does the damage to the intestinal mucosa lead to malabsorption and secondary malnutrition The autoimmune response damages small intestinal mucosa causes inflammation scarring and gtvilus atrophy Villi amp microvilli which make up the brush border of the small intestine increase the absorption area and secrete several enzymes eg peptidases sucrase lactase maltase Page 2 of 8 gtAtrophy of villi decreases the absorption area and decreases the amount of enzymes Primary manifestation malabsorption and secondary malnutrition Person also experiences pain PPT includes Photomicrographs of Duodenal Mucosa Biopsy Normal human duodenal mucosa long thin villi Patient with glutensensitive enteropathy loss of villi amp heavy infiltrate of white blood cells in the lamina propria know Celiac Disease continued Prevalence 1133 persons in US strong Genetic component More common in Caucasians More common in people with other autoimmune disorders such as lupus or type 1 Diabetes Wide range in SGHSitiVity to gliadin a protein in gluten Diagnosed anytime between infancy and older adulthood There may be delay in diagnosis due to the wide variety of symptoms or silent presentation May be triggered by trauma stress a viral infection or even by pregnancy It is not understood why such things trigger Celiac Disease know Presenting Symptoms Weight loss Increased appetite Generalized fatigue Abdominal bloating amp pain Symptoms associated with micronutrient deficiency eg anemia Diarrhea steatorrhea gt Children growth failure projectile vomiting Can diagnose Celiac Disease with a blood test results will show antibodies for gliadin Then results would be confirmed by a small intestine biopsy to examine the tissue and the damaged villi MNT for Celiac Disease There is no cure for Celiac Disease There is no medication that will make it go away Page 3 of 8 Treatment Goals Relieve symptoms Once on a strict glutenfree diet patient can expect improvement within 45 days Prevent or treat nutritional deficiencies Prevent recurrences requires a lifelong glutenfree diet even tiny amounts of gluten can cause relapse RD needs to provide intensive education to the patient on glutenfree diet RD can refer patient to a local support group RD need to provide longterm follow up AcaGlemy s EAL has an evidence analysis report for Celiac Disease gtgtContrast Celiac Disease with Gluten Sensitivity or Gluten Intolerance Sensitivity vs Disease Glutenfree diets are fashionable right now and many people in Hollywood are strong proponents of a glutenfree foods There is evidence that some people are gluten intolerant or gluten insensitive For those people excess gluten can be associated with irritable bowel syndrome or abdominal discomfort and can cause headaches or difficulty concentrating It may help those people to limit gluten in their diet They are usually able to tolerate small amounts But for people diagnosed with Celiac Disease even a tiny amount of gluten can cause an immune reaction with symptoms that last 45 days gtgt What foods commonly contain gluten Gluten is naturally present in wheat rye amp barley But it is in many foods and hidden in many foods you would never suspect eg ketchup Gluten gives elasticity to bread dough When you knead dough you are working the gluten know gtgt Discuss common sources of hidden gluten and cross contamination MNT Gliadinfree diet Eliminate gluten or gliadin wheat rye barley also buckwheat spelt durum semonlina kamut couscous and triticale and their derivatives as they may contain gluten Beware of crosscontamination person with Celiac disease would not only use glutenfree bread they would use separate toaster to avoid crosscontamination via crumbs must ensure clean utensils and containers know gtgtAre oats allowed on a glutenfree diet Pure Cats can be included in a glutenfree diet Formerly 0quot the avoid list now there is Fair evidence that moderate amounts of pure uncontaminated Oats may be included in a glutenfree diet Page 4 of 8 The Academy s EAL says Inclusion of GlutenFree Oats as Tolerated quotThe registered dietitian RD should advise individuals with celiac disease who enjoy and can tolerate glutenfree oats to gradually include them in their glutenfree dietary pattern Research on individuals with celiac disease reports that incorporating oats uncontaminated with wheat barley or rye at intake levels of approximately 50g dry oats per day is generally safe and improves compliance with the glutenfree dietary patternquot aPPVOXimate39y 509 per day of dry oats uncontaminated with wheat barley or rye newly diagnosed Celiac patients should avoid Oats at first try adding it later on know gtgtWhy is a glutenfree diet so difficult to follow Gluten is in everything OK not everything but a lot of foods you wouldn t suspect Including modified food starch stabilizing agent for ketchup ice cream and salad dressings MSG textured vegetable protein or seiten emulsifierslecithins soy sauce most of it contains wheat you have to use wheatfree tamari instead prescription and overthecounter drugs even some vitamins quotnatural flavoringsquot Beers ales lager wine and distilled hard liquors are glutenfree even if a liquor is made from a grain containing gluten the distillation process destroys the gliadin Gliadin beers made from sorghum are now on the market Malt Vinegar distilled Vinegars are glutenfree vegetarian meat substitutes processed foods MNT Gliadinfree diet continued Eat simply Substitute allowed grains uncontaminated potato rice corn soy tapioca beans sorghum millet quinoa arrowroot Eg Bob s Red Mill Natural Foods Whole Foods Glutenfree bakeries etc quotGlutenfree labels are helpful but vary in definition There is evidence that the Mediterranean diet pattern rich in olive oil fruits amp vegetables may be beneficial to patients with Celiac Disease Lifelong compliance required to maintain remission Page 5 of 8 It may be difficult to eat out NEW FDA Labeling Law August 2013 if a food says quotglutenfree on the label it must contain less than 20 ppm gluten THIS SLIDE IS NOT IN POSTED PPT ppm parts per million gt Companies required to come within that standard by August 2014 standard does not apply to alcoholic beverages since the FDA39S scope of authority does not extend to alcoholic beverages Company could try to get around the standard by saying quotno gluten products usedquot Celiac patients should be wary of these products since there could be cross contamination Celiac patients should look for the quotgutenfreequot abe But quotglutenfree does not mean that it is healthier than other products People could have the health halo perception of quotglutenfree labeled products So a company could put a quotglutenfree label on soda or Crisco but that does not make those products healthy The National Foundation for Celiac Awareness and the Gluten Intolerance Group of North America 33950 certify TOOdS as quotglutenfree The Celiac Sprue Association have been putting their label on foods for years certifying those foods as quotgluten freequot So it is easier to navigate in the grocery store than it used to be MNT for Celiac Disease Other Considerations know gtgtWhy might a Celiac patient present with anemia Assess Biochemical Data Someone with Celiac disease would be prone to micronutrient deficiencies if the small intestinal mucosa is inflamed and the villi atrophied So that person might be prone to anemias from iron 312 or folate deficiencies Vitamin D insufficiency is common anyway so that is another thing to assess The registered dietitian RD should assess the biochemical data and review the results of medical procedures in individuals with celiac disease regardless of presentation and clinical symptoms including but not limited to the following 1 Nutritional anemia profile eg folate ferritin and vitamin B12 2 Vitamin profile eg thiamin vitamin BG and vitamin D 3 Mineral profile eg copper and zinc Page 6 of 8 Untreated celiac disease results in villous atrophy and malabsorption The use of effective techniques to assess nutritional status is essential to prevention and treatment of malnutrition and the presence of iron deficiency anemia gtgtWhy is a bone density screening recommended for Celiac patients Bone Density Screening Calcium absorption is complex Someone with Celiac may have impaired calcium absorption especially if they have lactose intolerance which is common with Celiac disease because of lack of lactase enzyme But Calcium deficiency would not necessarily show up in a blood test for serum Calcium Rather Calcium would be leeched from the bones over time The Academy recommends bone density screening for Celiac patients quotThe registered dietitian RD should recommend bone density screening for adults with celiac disease within the first year Clinical trials and crosssectional studies have reported reduced bone mineral content and bone mineral density in untreated adults with celiac diseasequot Nutritional side effects of corticosteroid medications know Celiac patients with acute inflammation may be taking a corticosteroid medication which have many nutritional side effects Hypercalciuria loss of Calcium in the urine that may make bone weakening even worse Sodium and fluid retention Other electrolyte imbalances eg potassium loss in urine Must be taken with food Hyperphagia Hyperglycemia know gtgtWhy might a Celiac pt be intolerant to lactose andor large amounts of fructose Lactose and Fructose Intolerance may occur secondary to celiac disease as a result of villus atrophy and insufficient brush border enzymes Lactose and fructose intolerance is common among patients with Celiac disease Lactase is a brush border enzyme Fructose tends to be more difficult to absorb than the other monoglycerides Low lactose low fructose diet may help control symptoms Page 7 of 8 If a person has signssymptoms of fat malabsorption then products with medium chain triglycerides may be used Many supplement shakes and tube feeding formulas have medium chain triglycerides as a fat source Most commercial supplement shakes such as Boost or Ensure are glutenfree already Other Resources Celiac Disease and GlutenFree Diet Support Group wwwceliacoom Celiac Disease Foundation wwwceliacorg Krause page 625 Box 297 Academy of Nutrition and Dietetics Evidence Analysis Library eatrightorg Page 8 of 8 Spat StUdV GUide 39 II3392 39 Diseases 0f Biliary System amp Exocrine Pancreas Biliary Tract Disease gtgt What is bile Bie cholesterol bilirubin bile salts amp electrolytes eg sodium potassium chloride Bilirubin is a pigment produced from the breakdown of red blood cells gtgt Why is Bile important Bile is primary excretion route for bilirubin copper Cu amp manganese Mn Bie emulsifies fat Dietary fat triglyceride is not watersoluble so in the aqueous environment of the human intestine big fat globules tend to clump together Bile acts like a detergent to emulsify break up those large globules into smaller fat globules so that pancreatic lipase can hydrolyze the ester bonds and chemically digest the fat gtgt Where is Bile made in the Liver in hepatocytes liver cells gtgt Where is Bile stored in the Gallbladder Gallbladder function concentrate store amp excrete bile The Gallbladder is located right under the liver The main stimulus for contraction of the Gallbladder and release of bile is Cholecystokinin CCK When food reaches the small intestine especially FAT amp PRO it will stimulate release of hormone CCK CCK signals the Gallbladder to contract and release bile and signals the pancreas to release digestive enzymes milsadder E i Bil E39JIJET The biliary tract or biliary tree is a system of ducts that connects the liver the gallbladder amp the small intestine There are also ducts that connect to the pancreas This interconnectedness may explain why diseases of the liver gallbladder amp pancreas are interrelated L erepahcvmn 39 iHepEME away Fiarucreatic duct Parcel vein of Dddi Bile is made in hepatocytes liver cells and it flows from the liver through ducts to the Left amp Right Hepatic ducts which drain into the Common Hepatic Duct that connects with the gallbladder Bile leaves the gallbladder through the Cystic Duct to the Common Bile Duct The Pancreatic Duct also brings juices from the pancreas gtgt The Common Bile Duct amp the Pancreatic Duct converge at which muscular sphincter to empty their contents into the duodenum Sphincter of Oddi a smooth muscle sphincter that surrounds the end portion of the Common Bile Duct amp the Pancreatic Duct relaxes after a meal to allow bile amp pancreatic juices to flow into the small intestine Terminology Page 2 of 12 know gtgt Define biliary dyskinesia Biliary Dyskinesia describes spasms of the Sphincter of Oddi that prevents bile release into the duodenum as if there were a communications disconnect between the gallbladder amp the sphincter treated with antispasmodic medications possible surgery no MNT for it know Cholelithiasis gallstones Risk factors obesity rapid wt loss pregnancy DM some idiopathic gallstones are made of cholesterol bilirubin amp calcium salts gallstones may not be a problem no ss unless they obstruct a bile duct Choledocholithiasis condition when gallstones obstructing a bile duct abdominal pain amp cramping other ss intolerance for fatty foods sieatorrhea Obstruction of bile flow affects digestion of fat amp may lead to fat malabsorption evidenced by fatty stools stools may also be light gray due to decreased bilirubin can cause jaundice or lead to liver damage if obstruction is in the distal part of the Common Bile Duct where the pancreatic duct converges it could result in a blocked pancreatic duct pancreatitis 39ncltag39e of the wlila nail Valuer ill1339 Mme know gtgt How does choledocholithiasis differ from Cholelithiasis choledocholithiasis is when gallstones obstruct a bile duct chole doc ho lithiasis need to call doc Cholelithiasis is gallstones which may or may not be problems gtgtWhat are some possible complications of choledocholithiasis Jaundice Liver damage pancreatitis Page 3 of 12 Terminology continued know gtgt Define cholecystitis itis inflammation Cholecystitis is gallbladder inflammation with total obstruction of bile or blockage by gallstones can be acute or chronic usually caused by gallstones that are obstructing bile ducts know gtgt Define cholestasis Cholestasis involves disturbance of bile flow and sludge buildup in the gallbladder might be caused by a viral or autoimmune hepatitis hemochromatosis primary sclerosing cholangitis Bilary Tract Disease cholecystitis choledocholithiasis amp cholestasis all involve impaired bile secretion which impairs fat digestion micelle formation amp fat absorption because that fat has to be emulsified by bile in order to be digested by pancreatic lipase Fat malabsorption is common in these patients who may benefit from lowfat diet medium chain triglyceride oil gt medium chain triglycerides don t need emulsification amp micelle formation for digestion amp absorption watersoluble forms of fatsoluble vitamins if chronic fat maabsorption know gtgt What is MNT for cholecystitis Acute cholecystitis may need MPG to stop gallbladder contractions Page 4 of 12 PN indicated if pt is malnourished or NPO will be longterm Resume feeding with a lowfat diet 3045 gfatday Chronic cholecystitis Lowfat 2530 kcalsfat to reduce gallbladder work Provide watersoluble forms of fatsoluble vitamins gtgt What is a cholecystectomy Cholecystectomy is surgical removal of the gallbladder in the absence of a gallbladder adaptation occurs the ver secretes bile directly into the small intestine Pt may slowly progress to regular diet as tolerated fat restricted at first to allow the liver to adapt amp compensate for loss of gallbladder fat gradually reintroduced back into diet Pancreas The Pancreas is a glandular organ having endocrine glands amp exocrine glands endocrine cells amp exocrine cells gtgt Differentiate the endocrine and exocrine functions of the pancreas Endocrine glands endocrine cells secrete substances hormones directly into the bloodstream are ductless glands Hormones are chemical messengers secreted by endocrine glands into the blood Hormones travel through the blood to their target tissues eg CCK amp secretin insulin glucagon SomatOStatin can inhibit secretion of insulin amp glucagon Page 5 of 12 Exocrine glands exocrine cells secrete substances into ducts secrete digestive enzymes amp bicarbonate rich fluid into ducts which lead to the Pancreatic Duct which merges with the Common Bile Duct amp then through the unified opening the Sphincter of Oddi to the duodenum amp intestinal lumen Factors that Affect Pancreatic Secretions secretions of digestive juices into the ducts 1 Cephalic phase mediated through the vagus nerve Sightsmelltastethought of foods triggers some secretion of bicarbonate and pancreatic enzymes 2 Gastric distension gastric phase the presence of food in the stomach stimulates a little bit of enzyme secretion 3 Intestinal phase most potent effect on pancreatic secretions when food reaches the duodenum mediated mainly by the release of CCK Secretin also released CCK amp Secretin travel through the bloodstream to the pancreas Secretin stimulates the pancreas to release bicarbonate rich uid to neutralize acidic chyme from the stomach amp to release some digestive juices gtgt Describe 3 factors that stimulate secretions from exocrine pancreas 1 Sightsmelltastethought of foods Cephalic phase mediated through vegas nerve 2 Presence of food in the stomach Gastric phase Page 6 of 12 3 Food reaches the duodenum Intestinal phase mediated by release of CCK gtgtWhat is the most potent stimulus of secretions from exocrine pancreas CCK Tests of Pancreatic Function Pancreatic Disease Pancreatitis is inflammation of the pancreas itis inflammation Acute Pancreatitis gt is activated by premature activation of zymogen enzymes in the pancreas instead of the duodenum where they should be activated zymogen is the inactive form of the enzyme gt when activated in the pancreas the enzymes can begin to digest the pancreas itself Page 7 of 12 90 cases due to excessive alcohol intake gallstones amp idiopathic etiology lt10 from gt hypertriglyceridemia high triglycerides trauma drugs peptic ulcers Blood test that shows elevated levels of serum amyase amp lipase in Pan EfEat i Pancreatic duct Bile duct Duodlenum circulation signifies damage to the pancreas Condition is hypermetabolic and proteinwasting PtS Often haVe l alb transferrin and lymphocytes signs of malnutrition Pts often present with sudden severe abdominal pain May also experience nausea vomiting amp diarrhea most cases are selflimiting 14 of patients experience chronic pancreatitis MNT for Acute Pancreatitis Should be supportive with fluid electrolytes and pain control Nutrition goals Page 8 of 12 1 gt Reduce pancreatic stimulation pancreatic enzymes are activating in the wrong place in pancreas instead of duodenum 2 Match kcal amp pro needs 3 Energy BEE x 15 pro 1820 gkg 4 But do not overfeed Monitor for ss of overfeeding Test Significance Secretin stimulation Measures pancreatic secretion particularly bicarbonate in test response to secretin stimulation Glucose tolerance test Assesses endocrine function of the pancreas by measuring insulin response to a glucose load 72hr stool fat test Assesses exocrine function of the pancreas by measuring fat absorption that reflects pancreatic lipase secretion know gtgt Describe MNT for acute pancreatitis Severe eases NPO with TPN support if NPO is protracted If Te 2 400 mgdL do not include lipid in the TPN Monitor glucose Somatostatin can be added to inhibit pancreatic secretion of digestive enzymes ask physician Somatostatin can also inhibit endocrine secretion of insulin amp glucagon so could cause problems for a person who is having difficulty managing blood sugar use enteral route as soon as possible not using GI tract can result in complications amp longer hospitalization once inflammation calms down Enteral nutrition refers to any method of feeding that uses the GI tract to deliver part or all of a person39s caloric requirements eg oral tube feeding Parenteral nutrition refers to the delivery of calories amp nutrients into a vein Page 9 of 12 Mild to moderate cases most use enteral route Decrease pancreatic stimulation by using 1 Jejenunal tube feedings 2 Elemental or hydrolyzed formulas gtgtHow can jejunal tube feedingselemental MCT formula be beneficial Jtube feedings with an elemental medium chain triglyceride formula use the enteral route amp bypass the Cephalic amp gastric phases minimizing pancreatic stimulation MCT s require no bile acid amp less pancreatic enzyme to digest amp are more easily absorbed Decreased pancreatic stimulation means decreased release of bile amp pancreatic enzymes Bile is needed for digestion of dietary fat long chain triglycerides MNT for Acute Pancreatitis continued Milder cases should be able to progress to lowfat oral feedings 5 days after onset Start with small meals throughout the day May need to supplement fatsoluble vitamins if absorption is impaired know gtgt Why use a lowfat diet w supplemental pancreatic enzymes MNT includes decreasing pancreatic stimulation Because CCK is the most potent stimulator for the release of pancreatic enzymes we want to initiate a lowfat diet because fat is the most potent stimulator for CCK release Supplement pancreatic enzymes with food intake because decreased pancreatic stimulation likely results in decreased secretion of enzymes Page 10 of 12 Pancreatic Disease Chronic Chronic pancreatitis is chronic inflammation of the pancreas that results in permanent impairment of pancreatic function endocrine amp exocrine gtgt How could chronic pancreatitis lead to diabetes Damage to the pancreas frequently leads to diabetes because it destroys the beta cells of the pancreas chronic persisting for a long time or constantly recurring gtgt What is the most common cause of chronic pancreatitis Most common cause excessive ETOH intake alcohol abuse heavy consumption of alcohol other causes include hereditary disorders eg cystic fibrosis Associated with permanent damage amp loss of endocrine amp exocrine func on Presenting symptoms pain after eating NV malabsorption diabetes pts are often depleted of fat stores amp muscle mass inflammation amp duct obstruction can cause debilitating pain Some patients may become dependent on pain medications Will be at higher risk for protein kcal malnutrition because they may have a combo of insufficient pancreatic enzymes poor PC by mouth intake it hurts to eat MNT Goals to provide optimal nutrition support while minimizing pancreatic inflammation gtgt Describe MNT for chronic pancreatitis Page 11 of 12 lnflammation resulting in decreased pancreatic function may lead to decreased bile secretion which impairs dietary fat digestion amp absorption because dietary fat has to be emulsified by bile in order to be digested by pancreatic lipase So Patients may benefit from lowfat diet lt40 gd for symptomatic fat intolerance medium chain triglyceride oil MCT don t need emulsification amp micelle formation for digestion amp absorption oral pancreatic enzymes taken before meals help digest dietary fat watersoluble forms of fatsoluble vitamins ADEK if chronic fat malabsorption Other monitor for 312 deficiency if pt on antacids H2 receptor antagonists or proton pump inhibitors to reduce stomach acid diet higher in CHO Small frequent meals gtgt Why would someone with chronic pancreatitis likely be on antacids H2 blockers or PPls Antacids H2 receptor antagonists or proton pump inhibitors may be needed to reduce stomach acid if bicarbonate secretion is impaired due to decreased Secretin Erldocrine hormone Secretin stimulates the pancreas to release bicarbonate rich fluid to neutralize acidic chyme from the stomach amp to release some digestive juices Counsel pts to avoid alcohol If DM Diabetes mellitus Type 2 present treat as a comorbidity Page 12 of 12 Spath Study Guide for NHM 365 Module 5 Digestion Absorption amp Transport Part Two Digestion and Absorption of Specific Nutrients Part One Overview of Digestion and Absorption gt Part Two Digestion and Absorption of Specific Nutrients gt Key Points definitions gtgt Key Pointdefinition is on SelfStudy Guide gt Tricky Question Alert Contents Substrate Digestion Carbohydrates CHO Digestive enzymes secreted by the brush border microvilli Major enzymes involved in CHO digestion End products of CHO digestion Proteins PRO Major enzymes involved in PRO digestion End products of PRO digestion Intestinal absorption of end products CHO digestion vs PRO digestion Absorption by diffusion or active transport diffusion simple amp facilitated vs active transport Fat Lipid Role of bile in fat digestion prepares the way for the enzymes IVIicelles Enzymes involved in fat digestion End products of FAT digestion Digestion FAT vs CHO vs PRO Digestionabsorption of medium chain triglycerides MCT vs digestionabsorption of longchain triglycerides typically consumed in our diets Absorption of vitamins vs absorption of minerals Unique absorption of vitamin B12 Page 1 of 32 Substrate Digestion Chemical digestion involves hydrolysis reactions that break chemical bonds in food molecules CHO glycosidic bonds join monosaccharides together to form disaccharides amp polysaccharides those bonds will be broken PROTEIN peptide bonds between amino acids will be hydrolyzed FAT ester bonds that join fatty acids to glycerol to form triglycerides will be hydrolyzed Hydrolysis occurs with the aid of enzymes Page 2 of 32 Substrate Digestion Carbohydrates gtgt Key enzymes for digestion of CHO Ptyalin salivary amylase Pancreatic aamylase especially important for starch digestion Sucrase lsomaltase Maltase Lactase secreted by brush border microvilli in small intestine gtgt What are digestive enzymes secreted by the brush border microvilli in the small intestine Sucrase lsomaltase Maltase Lactase O Pancreatic enzyme I Intestinal enzyme STAPEH DEXTFlIN O Maltese molecules 1 MOLECULE MOLECULE Smaller dextrin molecules salivary enzyme l J GluesSe molecules Elseuier items and derived items 2012 2008 200 by Saunders an imprint of Elseuier Inc Page 3 of 32 Figure 17 The gradual breakdown of large starch molecules into glucose by digestion enzymes Substrate Digestion Carbohydrates Continued gtgt What are the major enzymes involved in CHO digestion Key enzymes for digestion of CHO Ptyalin salivary amylase Pancreatic uamylase especially important for starch digestion Sucrase lsomaltase Maltase Lactase secreted by brush border gt Pancreatic uamylase is especially important for starch digestion because most of the starch we eat is in the form of amylase or amylopectin amylase amp amylopectin are polymers of glucose so the pancreatic aamylase will break alpha14 glycosidic bonds of amylose amp break alpha16 bonds in amylopectin So the pancreatic amylases are necessary for starch digestion What we don t have are amylases to break some other bonds such as beta 14 glycosidic linkages eg in cellulose so those fibers would pass undigested gt Sucrase lsomaltase Maltase Lactase Brush border enzymes finish off the job by breaking down disaccharides amp oligosaccharides to monosaccharides Page 4 of 32 Substrate Digestion Carbohydrates Continued gtgt What are the end products of CHO digestion Monosaccharides glucose fructose amp galactose are the end products of carbohydrate digestion that will be absorbed into the blood So pancreatic amylases digest polysaccharide starch amylose amp amylopectin to smaller polysaccharides called dextrins and then to maltose Starch via pancreatic amylases gt dextrins gt maltose Isomaltose is a disaccharide very similar to maltose but it has an alpha 16 glycosidic linkage instead of an alpha 14 glycosidic linkage Brush border enzymes of the epithelial cells lining the small intestine release additional enzymes maltase isomaltase sucrase lactase that hydrolyze dissacharides into monosaccharides Maltose and isomaltose gt glucose Page 5 of 32 Sucrose gt glucose fructose Lactose gt glucose galactose So Monosaccharides glucose fructose amp galactose are the end products of carbohydrate digestion that will be absorbed into the blood Substrate Digestion CHOs Continued polysaccharides gt dextrins gt maltose 1 Starch digestion begins in the mouth via salivary amylase ptyalin food is not in the mouth long enough for much to happen there No digestion happens in the Esophagus Not much CHO digestion happens in the stomach HCL halts action of ptyalin stomach empties before there is time for much digestion gt Greatest digestion chemical digestion of CHO occurs in the duodenum top section of small intestine pancreatic amylase sucrase maltase lactase isomaltase dextrins amp maltose Page 6 of 32 l glucose fructose galactose monosaccharides gtgt Contrast diffusion simple amp facilitated with active transport Absorption In absorption end products of digestion pass through the intestinal mucosal cells and make their ways into capillaries that feed into veins that take them to the liver Or In the case of fat chylomicrons are absorbed into lacteals those little lymphatic vessels and those enter lymphatic circulation first 3 Absorption Mechanisms 1 Simple Passive Diffusion going with the flow ATP Energy not needed 2 Facilitated Diffusion Needs Carrier Protein but ATP Energy not needed 3 Active Transport Needs Carrier Protein AND ATP Energy Diffusion random movement of nutrients through mucosal cells to bloodstream ATP The energy molecule of cells energy from breakdown of ATP drives many important reactions in the cell Page 7 of 32 Simple passive diffusion is sort of like going with the row Molecules flow back amp forth as needed to maintain osmotic equivalency on either side Some small nutrients pass through membrane channels Driven by concentration gradient molecules will always move down their concentration gradient from high to low concentration No ATP no energy input needed Facilitated diffusion involves a carrier protein as a vehicle to move molecules too large to diffuse easily Molecules still diffusing down their concentration gradient but need to hitch a ride across the cell membrane No ATP no energy input needed Active Transport input of energy is required to move nutrient amp carrier protein across membrane Some nutrients share same carrier protein causing competition for absorption Transport Pathways through the Cell Membrane Substrate Digestion CHOs Transport Diagram below shows how monosaccharides glucose fructose galactose are ABSORBED INTO epithelial cells lining intestinal lumen active transport glucose galactose amp facilitated diffusion fructose gt Glucose amp galactose are absorbed from gut lumen into the enterocyte by secondary active transport with a Nadependent carrier Na is the transport protein lt transports both sodium amp glucose into the cell It will not transport one of those without the other This is one reason for Na in sports drinks This why Gatorade has a mixture of sodium amp glucose active transport requires ATP energy Diffusion Active transport Channel Carrier protein proteins l i Facilitated Simlple diffusion dif usion gt Fructose is absorbed from gut lumen into the enterocyte by facilitated diffusion using another carrier protein facilitated diffusion does not require ATP fructose is absorbed more slowly than glucose amp galactose Then they are transported OUT of the enterocyte via facilitated diffusion Monosaccharides glucose fructose galactose are then transported out of the enterocyte by facilitated diffusion by another transport protein and from there they move into capillaries within the villi The capillaries eventually feed into the hepatic portal vein that takes them to the liver In the liver galactose amp most of the fructose are converted to glucose Substrate Digestion Protein Key Enzymes Substrate Digestion PRO We also rely on enzymes for digestion of proteins the hydrolysis of peptide bonds gtgt What are the major enzymes involved in PRC digestion see chart on p 14 The picture below shows some of the key enzymes for protein digestion Rennin Pepsin Trypsin Chymotrypsin Carboxypeptidase Enterokinase amp Brush border peptidases gt Rennin also called the milkcurdling enzyme It is produced by chief cells of the stomach in infants It is found in the gastric juice of human infants before pepsin formation Rennin curdles the milk when it empties the stomach allowing it to stay in the k WWW h stomach longer so there is maximal quot3 maximum protein sucrose dextrins maltotriose maltose lactose FRUCTYOSE GLUCOSE GALACT39OSE 39 an Enterocyte interior Eznterocyte interior FRUCTOSE GLUCOSE GALACTOSE digestion Without Rennin the milk would remain liquid and pass through the stomach too quickly Rennin gradually goes away amp is replaced by Pepsin Rennin is not found in adults Rennin is found in ruminant animals eg cows gt Caution do not confuse Rennin with Renin part of the renin angiotensin system These are completely different molecules Substrate Digestion Protein Key Enzymes Continued Rennin Pepsin Trypsin Chymotrypsin Carboxypeptidase Enterokinase amp Brush border peptidases Pepsin a proteolytic enzyme in the stomach begins chemical digestion of protein in the stomach secreted from chief cells begins as inactive pepsinogen which is activated by hydrochloride acid HCL Page 10 of 32 HCI pepsinogen inactive gt pepsin active Proteolytic breaking down of proteins into smaller polypeptides or amino acids Trypsin pancreatic protease Chymotrypsin pancreatic protease Carboxypeptidase pancreatic protease Enterokinase is an intestinal enzyme secreted by the duodendum or duodenal mucosa small intestinal cells Brush border peptidases they finish off protein digestion Substrate Digestion Protein Continued Stomach gt Digestion really gets Digestion of protein stomach HCI pepsinogen active 77 Jrquot 7 i f w er iffr quotquotl5 going in the Stomach really begins in I inactive gt pepsin Aminoacids t g a r ammonia h ae ti1ia If flu IWI OL Z ng 7 7 i a Small Intestine gt Most digestion in the Duodenum Most protein digestion occurs in duodenum in the small intestine gt Absorption by end of Jejunum Almost all protein is absorbed as amino acids amp small peptides amp tripeptides by end of the jejunum middle section of small intestine Most protein is digested amp absorbed Only about 1 of dietary protein exits in feces Substrate Digestion Protein Pancreatic Enzymes How Pancreatic Enzymes Work in small intestine to digest Protein Proteolytic Pancreatic Enzymes Page 12 of 32 Proteolytic breaking down of proteins into smaller polypeptides or amino acids Stimulated by gastrointestinal hormones Secretin amp CCK gt Acidic chyme in duodenum stimulates hormones secretin amp CCK which stimulate release of proteolytic pancreatic enzymes Secretin When acidic chyme enters the duodenum it stimulates the secretion of hormone Secretin Secretin travels through the blood to target cells in the pancreas The pancreas secretes bicarbonate to the duodenum to neutralize acid To some extent Secretin also stimulates the pancreas to release some digestive enzymes into the duodenum CCK Food especially fat amp protein in the duodenum will signal the secretion of CCK into the blood CCK is the most potent stimulus for the pancreas to secrete digestive enzymes through the pancreatic duct into the small intestine chyme gt secretin amp CCK hormones gt proteolytic pancreatic enzymes Substrate Digestion Protein Pancreatic Enzymes Continued How Pancreatic Enzymes Work in small intestine to digest Protein Page 13 of 32 Pancreatic Proteases Proteases enzymes that cleaves breaks peptide bonds that link amino acids in protein molecules Zymogen an inactive substance that is converted into an enzyme when activated by another enzyme Pancreatic proteases are secreted as zymogen into the small intestine eg trypsinogen and will be activated in the small intestine Enterokinase an intestinal enzyme secreted by the duodenum activates pancreatic trypsinogen to trypsin it trips trypsinogen which in turn activates trips chymotrypsin elastase amp carboxypeptidase directing hydroloysis to small polypeptides and amino acids Pancreatitis very dangerous amp painful condition If trypsinogen was inappropriately activated in the pancreas itself rather than the small intestine it could active the other proteases and begin to digest the pancreas itself Brush Border Peptidases of the small intestine As small polypeptides reach the brush border brush border peptidases of the epithelial cells lining the small intestine will digestbreak those down complete the hydrolysis to gt dipeptides tripeptides amp amino acids and those are what are absorbed across the intestinal epithelium gtgt What are the end products of PRO digestion dipeptides tripeptides amp amino acids gtgt What are major enzymes for PRO digestion Page 14 of 32 Major Enzymes for PRO digestion Secreted by Acts by Notes Rennin quotmilkcurdling enzymequot secreted from chief cells in stomach found in infants gradualy replaced by Pepsin Pepsin secreted from chief cells in stomach begins as inactive pepsinogen which is activated by HCL Pancreatic Proteases Trypsin Chymotrypsin Carboxypeptidase secreted by pancreas after pancreas is stimulated by gastrointestinal hormones Secretin amp CCK secreted as zymogen inactive into the small intestine amp will be activated in the small intestine eg secreted as trypsinogen If trypsinogen was inappropriately activated in the pancreas itself Pancreatitis Enterokinase intestinal enzyme is secreted by the duodenum activates pancreatic trypsinogen to trypsin quottrips trypsinogenquot Domino effect trypsin in turn activates quottripsquot Chymotrypsin elastase amp carboxypeptidase CEampC CEampC direct hydroloysis to small polypeptides amp amino acids Brush Border Pep dases Sucrase Isomaltase Maltase Lactase Brush Border microvilli in the small intestine Finishes the job breaks small polypeptides amp amino acids to End product dipeptides tripeptides amp amino acids Page 15 of 32 Substrate Digestion Protein Pancreatic Enzymes Continued Mechanisms of amino acid amp water absorption The mechanisms of amino acid absorption are conceptually identical to that of monosaccharides So the epithelial cells that line the intestinal lumen have sodium dependent amino acid transport proteins for secondary active transport of amino acids across the lumen Requires ATP energy When we have the absorption of amino acids amp monosaccharides along with sodium that will set up a osmotic gradient that drives water absorption So while we have absorption of nutrients we also have absorption of water by osmosis as well We have the absorption of those small dipeptides amp tripeptides amp also amino acids into the enterocytes cells of the intestinal lining and from there they are further digested to amino acids Amino acids will enter the capillaries that take them to the hepatic portal vein and on to the liver gtgt Describe the intestinal absorption of the end products of CHO amp PRO digestion see p 78 Absorption of CHO end products Absorption of PRO end products Monosaccharides glucose fructose amp amino acids amp some peptides galactose dipeptides amp tripeptides gt Glucose amp galactose are absorbed from gut gt amino acids are absorbed from the gut lumen lumen into the enterocyte by secondary active by secondary active transport with a Na transport with a Nadependent carrier dependent carrier Requires ATP energy Requires ATP energy gt Fructose is absorbed from gut lumen into the enterocyte by facilitated dittusion using another carrier protein no ATP energy required Page 16 of 32 absorption of monosaccharides sodium gt absorption of amino acids sodium gt absorption of water by osmosis as well absorption of water by osmosis as well Substrate Digestion Lipid Fat Fat digestion is a little more high maintenance Mouth negligible insignificant digestion of fat Stomach very little fat digestion gt Small Intestine most fat digestion occurs via 2 pancreatic enzymes Lingual lipase mouth gt negligible fat digestion l Gastric lipase stomach reduces shortchain TG s gt FA glycerol l Pancreatic lipase and cholesterol esterase SI primary fat digestion gtgt What enzymes are involved in fat digestion oPancreatic lipase is the main enzyme which hydrolyzes triglycerides to monoglycerides glycerol amp free fatty acids Cholesterol esterase a pancreatic enzyme that liberates dietary cholesterol from other components of food to make it bioavailable for absorption Pharmaceutical companies are working hard on cholesterol inhibitors that would have the opposite effect Page 17 of 32 Substrate Digestion Lipid Fat Continued The problem with fat digest is that it is a fat It s a lipid It s lipid soluble lipophilic lt s not hydrophilic It s not water soluble Iipophilic capable of dissolving of being dissolved in or of absorbing lipids hydrophilic of relating to or having a strong affinity for water So when you have fat in the aqueous environment of the small intestinal lumen then lipid molecules will tend to coalesce together Pancreatic lipase can t get in there and hydrolyze the bonds coalesce come together to form one mass If you poured oil or grease into a glass of water all of the droplets would coalesce together and float on the top of the water quot If you added a detergent would droplets into drop of dish detergent the break down the big fat little fat droplets Page 18 of 32 Substrate Digestion Lipid Fat Continued Fat digestion Before pancreatic lipase can hydrolyze the bonds of triglyceride molecules large fat globules must be broken down into smaller fat molecules by a process called emulsification Emulsification the process of breaking down large fat globules into smaller fat molecules gtgt What is the role of bile in fat digestion Bile salts break down large fat globules into small fat molecules in the small intestine in a process called emulsification This allows pancreatic lipase to hydrolyze the smaller fat droplets Bile salts emulsify fat in the small intestine Bile is produced in the liver amp stored in the gallbladder Bile consists mainly of cholesterol phospholipids bilirubin and several electrolytes to make bile salts Page 19 of 32 When food especially fat reaches the duodenum CCK signals the gallbladder to contract and release bile into the small intestine for emulsification of fat Substrate Digestion Lipid Continued 1 Bile salts emulsify fat in the small intestine 2 Pancreatic lipase is able to hydrolyze the smaller fat droplets triglyceride TG molecules are digested to monoglycerides glycerol amp free fatty acids FFAs gtgt What are micelles 3 Tiny water soluble Micelles are formed from a combination of bile salts monoglycerides amp free fatty acids FFAs Page 20 of 32 gt By orienting the polar ends facing out the hydrophilic portion to the outside and the hydrophobic portion to the inside Micelles allow end products of fat digestion to be soluble and to travel to the brush border transit the lumen to the intestinal mucosa See picture 4 So Micelles travel to the brush border where the tats are released and taken up by the brush border for absorption 5 Bile salts are reabsorbed in the distal ileum for return to the liver where they are recycled to reenter the gut in bile secretions via enterohepatic circulation gt Exception Shortchain amp medium chain 39 fatty acids lt12 carbons are directly absorbed via portal vein Ems Explained on p 20 Absorption of Lipids 1 So Micelles uequotquot ydr P bi aquot deliver monoglycerides amp free fatty acids FFAs to the brush border 2 At the brush border monoglycerides amp free fatty acids FFAs detach from micelles and enter intestinal epithelial cells Page 21 of 32 3 Inside intestinal epithelial cells monoglycerides amp free fatty acids FFAs reassemble into newtriglyceride molecules Then these new triglycerides along with cholesterol fat soluble vitamins and phospholipids are packaged into particles called chylomicrons Chylomicrons are a type of lipoprotein lipid protein gt The hydrophilic protein portion surrounds the hydrophobic lipid portion allowing transport in the aqueous environment like the blood or the lymph This is why lipids have to travel as lipoproteins in the blood or lymph The water soluble hydrophilic protein is like a taxi for the lipid gt Unlike the end products of carbohydrate and protein digestion chylomicrons do NOTenter hepatic portal circulation gt Chylomicrons are absorbed into lacteals which enter lymphatic circulation Lymphatic vessels empty into venous circulation so chylomicrons enter the bloodstream amp deliver fat to tissues They don t go to the liver first gt Exception Shortchain amp medium chain fatty acids lt12 carbons are directly absorbed via portal vein Explained on p 20 See RECAP amp Diagram on next page RECAP Micelles MampFFAs gt brush border MampFFAs detach amp enter intestinal epithelial cells MampFFAs reassemble into new TGs packaged in Chylomicrons Chylomicrons are a type of lipoprotein Page 22 of 32 Chylomicrons are absorbed into lacteals Lacteals enter lymphatic circulation Lymphatic vessels empty into venous circulation Chylomicrons via lacteals enter bloodstream where they deliver fat to ssues Chylomicrons via lacteals enter Lymphatic Circulation Fat Digestion Exception Shortchain amp medium chain fatty acids o Bile salts O O LIPID gt ntestinal lumen o O O o O Bile salts Pancreatic lipase G O 3 0 7 3 0 3 ts WATER O 0 0 39 U m SOLUBLE O 0 g a w y lMllCELLES O Q 0 U 0 U l 0 IN UNSTlFllRED V G a 0 0 WATER LAYER 0 U r a U u UWL U r r r 39 WM Fatty acids and BRUSH 3 r l monoglycerides BORDER IJTriglyceride I BASEM ENT l synthetic enzymes MEMBRANE in endoplasmic s 33 Q reticulum quotI 3 Droplets or P I jy triglycerides n KO cholesterol l ntesti rral cell wall EPITIHELIAL CELLS 39w 7 sear 3 I BASEMEth MEMBRANE Clhylomicron Page 23 of 32 gtgt How does digestionabsorption of medium chain triglycerides MCT differ from digestionabsorption of longchain triglycerides we typically consume in our diets Medium chain fatty acids can be absorbed without Micelles without bile enter the hepatic portal vein to the liver Most of the fatty acids we consume in our diet are long chain fatty acids In the typical diet we eat very little medium chain TGs gt Exception Shortchain amp medium chain fatty acids lt12 carbons are directly absorbed via hepatic portal vein to the liver Medium chain fatty acids TGs of 812 carbons are an EXCEPTION to normal fat absorption Medium chain fatty acids can be absorbed without Micelles without bile enter the hepatic portal vein to the liver gtgt How does FAT digestion differ from that of CHO amp PRO Page 24 of 32 CHO Digestion PRO Digestion FAT Lipid Digestion Hydrolysis reactions with aid of enzymes will break bonds formed by glycosidic bonds monosaccharides gt disaccharides amp polysaccharides chyme prompts hormones to stimulate pancreatic enzymes Hormone Secretin stimulates pancreas to secrete bicarbonate amp some digestive enzymes Hormone CCK main stimulus for pancreas to secrete digestive enzymes Hydrolysis reactions with aid of enzymes will break peptide bonds between amino acids Before hydrolysis fat needs to be emulsified CCK signals gallbladder to release bile CCK esp reacts to fat Bile salts emulsify fat in small intestine Hydrolysis reactions with aid of enzymes will break ester bonds that join fatty acids to glycerol to form triglycerides Key enzymes for digestion of CHO Ptyalin salivary amylase o Pancreatic aamylase especially important for starch digestion Most CHO consumed are starches Sucrase lsomaltase Maltase Lactase secreted by brush border Key enzymes for digestion of PRO see Details on chart at p 12 Rennin infants Pepsin pancreatic proteases Trypsin Chymotrypsin Carboxypeptidase Enterokinase Brush border peptidases Key enzymes for the digestion of fat Pancreatic lipase is the main enzyme which hydrolyzes triglycerides to monoglycerides glycerol amp free fatty acids Cholesterol esterase a pancreatic enzyme that liberates dietary cholesterol from other components of food to make it bioavailable for absorption Most protein digestion occurs in the small intestine duodenum Most protein digestion occurs in the small intestine duodenum Most protein digestion occurs in the small intestine End Product of CHO Digestion Monosaccharides glucose fructose amp galactose 39 are carried by the hepatic portal vein to the liver End Product of PRO Digestion amino acids amp some peptides dipeptides amp tripeptides 39 are carried by the hepatic portal vein to the liver End Product of FAT digestion ch ylomicrons Chylomicrons via lacteals enter Lymphatic Circulation amp deliver fat to tissues gt Unlike the end products of CHO amp PRO chylomicrons do NOT enter hepatic portal circulation Page 25 of 32 Vitamins amp Water Water is absorbed by osmosis all along the GI tract A good deal of water is absorbed in the small amp large intestines A lot of water is absorbed in the ileum lower part of the small intestine A good deal of water is absorbed in the large intestine too Water Soluble Vitamins eg Vitamin C Most water soluble Vitamins pass unchanged from the small intestine into the bloodstream via passive diffusion A few enter the bloodstream by active transport so most of our water soluble vitamins are pretty bioavailable There are a few exceptions like B12 gtgt Describe the unique absorption of vitamin B12 312 in food HCL amp gastric juices IF 312 in fortified foods amp supplements IF Absorbed in the ileum of the small intestine Vitamin B12 gt 312 in food is bound to protein It requires hydrochloric acid HCL amp gastric proteases to release 312 from the protein Then Intrinsic Factor IF must bind to 312 IF is secreted by parietal cells in stomach gtThe B12 IF complex is absorbed in the ileum of the small intestine gt Compare B12 found in fortified foods or supplements is NOT BOUND TO PROTEIN so it may be easier to absorb no HCL amp gastric proteases needed to release it from protein Page 26 of 32 STILL REQUIRES THE INTRINSIC FACTOR Vitamins amp Water Continued Fat Soluble Vitamins A D E amp K The A D E amp K are absorbed with fat They are carried by Micelles to the intestinal lumen where they are absorbed and then they are packaged into the Chylomicrons and absorbed into lymphatic circulation Fatsoluble vs Watersoluble Bioavailability The Bioavailability of most vitamins water soluble amp tat soluble is pretty good Absorption could be impeded by the presence of phytates in grains amp legumes or oxalates in spinach So Bioavailability can be affected by pH andor presence of phytates or oxalates Absorbed in the small intestine B12 IF Complex is absorbed in the ileum of small intestine gt Enter Bloodstream Watersoluble Vitamins from the small intestine enter into the bloodstream via passive diffusion Page 27 of 32 Fatsoluble Vitamins from the small intestine enter into the bloodstream via Lymphatic Circulation See diagram on p 23 Fatsoluble vs Watersoluble Continued o gt Enter Bloodstream SEE Diagram below Watersoluble Vitamins from the small intestine enter into the bloodstream via passive diffusion Fatsoluble Vitamins from the small intestine enter into the bloodstream via Lymphatic Circulation Salivary V amylaaa l mam Eacphagua Stcmach Gaatl39icjuic r Papain I HG Alcchal r Fancrcaa l uiadanm Pancreatic julaa l A El 591 a icarbcnata i A I v i Enzymes 1 r Iran 39 Calcium a Magaaaium 1 Gallbladch Ella i39 am l l l I Gluccaa galactc axa iructcaa Intaatinal hruah r tlc rclar anagma 1 Ariana a da papiiclaa and t paptidaa Vilar aia I 1 Thiamin Water Jairmnurn a b quot Fiibctlamn quot ED39UWE39 A V vitamina 39Laataal a Pyl39llmlm lymphatic I 39 Laltaubclawlan FE am W laymani andlatlintamai j 1Ii39ilarruiria A D E I llTn jugularaaina39 Fat quot r i Eihclaatraral 7 IIELIi 1 IEila aalla and vitamin B12 Ir Grch Vitamin tarmac by bacta rial aclicri Ham A Haaalia 39 panital U aini39 39 Rectum r Anua Facaa Primary Sites of Absorption diagram Most nutrients are absorbed in the jejunum of small intestine Minerals Absorption of most minerals is more complex Complex absorption driven by pH amp food composition eg tannins For some minerals like iron or zinc the efficiency of absorption depends on our needs for that mineral For example if we have low iron stores our body will upregulate transcription of transport proteins for iron absorption If iron stores are low we absorb iron more easily from food Calcium absorption is pretty complex Vitamin D acts as a transcription factor amp upregulates expression of genes that code for calcium transport proteins So Vitamin D enhances calcium absorption in the gut Some minerals compete with one another for transport proteins so too much of one mineral may impede the absorption of another Example copper amp zinc Tzinc gt i copper absorption Minerals are absorbed into the blood Most travel in the blood bound to gttransport proteins Metals are transported bound to protein carriers eg transferrin carries iron in the blood ceruloplasmin carries copper in the blood Albumin plasma protein binds a variety of minerals So you can do a blood test for ionized calcium to see calcium that is not bound to Albumin Most Protein carriers are undersaturated which is thought to be a buffer against mineral toxicity if there is an excessive amount of the mineral Page 29 of 32 gtgt Contrast absorption of vitamins with absorption of minerals Vitamins Minerals watersoluble amp fatsoluble absorption is more complex absorbed in the Jejunum of the small absorbed in the Jejunum of the small intestine intestine Excep on B12 IF Complex is absorbed in the ileum of small intestine Most Watersoluble Vitamins from the small efficiency of absorption may depend on intestine enter into the bloodstream via body s needs for that mineral Body will call passive diffusion for transport proteins as needed Fatsoluble Vitamins from the small from small intestine absorbed into intestine enter into the bloodstream via bloodstream Lymphatic Circulation most travel bound to transport proteins A D E amp K gtprotein binding can be specific eg transferrin binds with iron or general eg Albumin which binds with a variety of minerals competition for transport proteins gt too much of one mineral may impede the absorption of another Most Protein carriers are undersaturated likely a buffer against mineral toxicity Page 30 of 32 bioavailability is generally good but can be bioavailability can be affected by various affected by various factors factors First it may depend on whether body needs it or not Drug Absorption Interactions Many drugs compete with nutrients for absorption some antibiotics may compete with calcium so person may be advised not to take them with dairy foods some meds need to be taken on an empty stomach 12 before a meal or 2 hours after a meal sometimes in a hospital setting when a patient is supposedly receiving tube feeding of a specific amount of food every hour continuously for 24hours that could be thrown off if tube feeding is stopped for a few hours each day or several times a day in order to provide medications 80 it is very important to review the medication list along with nutrition assessment Primary Sites of Absorption diagram on p 23 Most nutrients are absorbed in the jejunum of small intestine People who have had bariatric surgery will need micronutrient supplements for the rest of their lives Bariatric surgery is increasingly popular and we are seeing more vitamin amp mineral deficiencies especially B12 folate iron amp Vitamin D in people who had bariatric surgery and did not continue to take sufficient micronutrient supplements Drug absorption by passive diffusion amp active transport Many drugs also absorbed via passive diffusion Page 31 of 32 Drugs requiring active transport may compete with nutrients for absorption eg alcohol inhibits active transport of thiamine Drugs may also can chelate with minerals eg tetracycline amp calcium calcium can interfere with the body39s ability to absorb tetracycline antibiotics Page 32 of 32 NHM 365 SPATH STUDY GUIDE FOR MODULE TWO Nutrigenomics Chapter 5 LecturePPT Self Study Guide for Module 2 Academy AOND Position Paper on Genomics and httpIearndeneticsutahedu REVISED 7 JUNE 2015 gt Key Points definitions gtgt Key Pointdefinition is on SelfStudy Guide Contents page in Spath Study Guide Nutrigenomics p 2 Genome Nutrigenetics Epigenome above the genome p 4 Epigenetics Power of Food p 6 bioactive food components phytochemicals Functional Foods Nutraceuticals Agouti gene in mice Identical Twins Genetics Basics p 10 DNA amp DNA decoding bioactive food components Inheritance Basics p 14 Mendelian mitochondrial Mother mtDNA epigenetic singlegene and complex polygenic diseases Genetic Technologies Microarrays DNA chips p 17 Ethical Concerns p 18 privacy amp genetic testing Genetic Information Nondiscrimination Act GINA Genetic Testing Singlegene disorders v Complex disorders clinical Scenario Krause p 159 Jared amp Matthew identical twins p19 Academy s position paper on Nutritional Genomics Use of nutrigenetic testing to provide dietary advice is NOT ready for routine dietetics practice p 20 Genetic Testing amp DTC Genetic Testing Regulation amp Oversight of Genetic Tests US agencies chart p 23 Page 1 of 26 Nurtrigenomics Genomics describes interactions of various genes amp their protein products with each other and the environment gtgt Genome the entire set of genetic instructions found in a cell In human beings the genome consists of 23 pairs of chromosomes found in the nucleus as well as a small chromosome found in the cells mitochondria These chromosomes taken together contain about 31 billion bases of DNA sequence Academy p 302 The human genome contains 20000 25000 genes which is only 2 of the total genome Human Genome Project an international effort over 20 years to determine the sequence of human genome and identify the genes it contains The full sequence of human genome was completed and published in 2003 Human beings differ from each other in only in about 01 of the total sequence of nucleotides that compose DNA These variations in genetic info are thought to be the basis for the physical and functional differences between individuals gtgt Genotype a person s genetic makeup genetic potential what person can be what person will be may depend on environmentlifestyle choices from PPT gtgt Phenotype physical traits observable characteristics resulting from genotype and environmental influences from PPT Nutritional Genomics can be used as a broad term that encompasses nutrigenetics nutrigenomics and nutritional epigenomics Academy 301 gtgt Nutrigenomics examines the role of nutrients amp bioactive food components in gene expression gene interactions and geneenvironment interactions PPT gt quotgene x environmentquot GxE premise focus on how interactions between genetic variations and environmental factors influence the genetic potential of individuals In GxE environment broadly encompasses the typical toxins to which humans are exposed as well as diet and lifestyle Nutrigenomics will likely play big role in disease prevention Disease is genetically based connected to the information in the genes Based on genetic variation some individuals may benefit from gt amounts of certain nutrients while others because of genetic makeup may require less of those nutrients for optimal health Page 2 of 26 Unlike most other healthcare professionals RD has solid foundation in food amp nutrition sciences but will need to develop genetics expertise to play key role in nutrigenomics Major change in the role of the RD are ahead in 1individualized dietary recommendations 2 increasing the effectiveness of therapy for existing disease 3 preventing disorders from developing 4 decreasing incidence of dietrelated disease What RDs can do now 1 take detailed family histories as pedigrees and use to determine risk 2 take thorough diet histories 3 take a functional medicine nutrition approach gt Genetic Markers Today s markers are blood lipids etc Next step is Genetic markers but they are not yet ready for prime time Examples of Genetic markers APOE 24 associated with coronary heart disease responsive to lowfat diet coupled with oat branfiber CETP variants moderate amounts of alcohol increases HDL AGT variant responds to decrease in saltsodium gt Nutritional Genomics in a Nutshell Use nutrition to solve problems caused by genes to maximize genetic potential Use of Bioactive food components in the diet is KEY to influence genetic outcomes and thereby physiological function Lifestyle will trump genetic disposition Nutrigenetic Influences on Health and Disease gt Nutrigenetics is the study of the impact of individual s genetic variants on their metabolic and physiological function eg on levels of nutrients required ability to digest and absorb food and susceptibility to various diseases from PPT gtgt In the future we mav be able to tailor recommendations for nutrients based on a person s genetic variants Explain once we know Mthe genetic variants impact a person s metabolic and physiological function RDs can use nutrition to solve problems caused by genes Each individual may require a different level of nutrient because of hisher particular set of genetic variations Levels needed may be significantly higher or Iowerthan the usual recommended nutrient level PKU a singlegene metabolic disorder is best known example of how nutrigenetics can help Academy 303 PKU causes an inability to convert phenylalanine to tryrosine Lifelong dietary restriction of phenylalanine enables individuals to live into adulthood Interplay between nutrition and genetics varies from being straightforward to being complex Most straightforward direct correlation between faulty gene defective protein deficient level of metabolite and a resultant disease state passed on through Mendelian inheritance and responsive to nutrition therapy eg inborn errors of metabolism IEM that are characterized as rare mutations that result in protein dysfunction that leads to metabolic disorders Page 3 of 26 all human beings have mutations that result in protein dysfunction that leads to metaboIic disease Humans require certain nutrients that must be supplied by diet to prevent dysfunction and disease eg if dietary vitamin C intake is below needed levels individuals are at risk for developing scurvy which can be fatal More complex is the interplay between nutrition and complexchronic diseases gt Epigenome quotabove the genomequot quoton top of geneticsquot gt Nutritional Epigenomics concerns the influence of diet on changes in gene expression without changing the DNA sequence Academy 301 last sentence continued on 303 Folate methionine choline vitamin B12 vitamin B6 play a critical role in maintaining DNA methylation Too much or too little of these nutrients can disrupt DNA methylation patterns which has been linked to increased cancer development gtgt Epigenetics concerns heritable changes that influence gene expression without altering the sequence of nucleotides in DNA gt DNA contains the instructions for building all the parts of the body but DNA is only half the story Epigenetics provides an addition set of instructions beyond that contained in the DNA nucleotide sequence gt Genetic Code amp Epigenetics Nature s quotPen amp Pencil Setquot The sequence of the genetic code is like an indelible ink that with rare exceptions is faithfully transcribed from cell to cell and from generation to generation But on top of this code lies another one literally epigenetic which is represented by methyl groups added to the DNA as well as changes in histone proteins around which the DNA is coiled This epigenetic information is more like a code written in pencil in the margins around the DNA gt Both the DNA and histones are covered with chemical tags This second layer of structure is called the Epigenome gt The Epigenome shapes the physical structure of the genome It tightly wraps inactive genes making them unreadable It relaxes active genes making them easily accessible gt The DNA code remains fixed for life but the Epigenome is flexible Epigenetic tags react to signals from the outside world such as diet and stress The Epigenome adjusts specific genes in our genetic landscape in response to our rapidly changing environment Page 4 of 26 gtgt Study guide provides 3 websites that provide quotgreat informationquot on epigenetic Info from these websites included in Spath Study Guide but view short videos gtgt httpearngeneticsutaheducontente geneticsintro Epigentics at a glance gtgt httpearngeneticsutaheducontentemgeneticscontrol Epigenetic Tags effects on genes 1 Methyl Tags Green Florescent Protein 2 MethylationDemethylation Cancer gtgt httpswwwvoutubecomwatchvM4boKud1MRk Agouti gene and mice experiment identical twins study gtgt Describe the three most common mechanisms of epigenetic control epigenetic modification gtgt DNA methylation epigenetic mechanism in which methyl groups are attached to DNA Methylation generally silences gene expression and demethylation promotes gene expression gt Bioactive food components mayinfluence epigenetic modifications Diet has been found to influence at least one epigenetic mechanism DNA methylation and the effects can be inherited as demonstrated in the agouti gene experiment in mice that is discussed below gt Agouti mouse model demonstrated some of strongest evidence that diet plays a role in epigenetics gtgt Histone modifications epigenetic mechanism which relaxes DNA structure so DNA is available for transcription into mRNA OR condenses DNA structure so DNA is unavailable for transcription gtgt RNA interference RNAi posttranscriptional epigenetic mechanism whereby short pieces of singlestranded RNA attach to DNA or mRNA Attaching to DNA leads to Egigenetic Gene Silencing the silencing of whole regions of chromosomes Attaching to mRNA interferes with gene expression Inappropriate gene expression can have serious consequences eg uncontrolled cell growth and cancer Page 5 of 26 Dietary factors can act via epigenetic mechanisms throughout the lifespan even across generations eg exposure to famine Academy 305 gt POWER OF FOOD food first supplements second gt Bioactive Food Components include integral food parts amp food contaminants Nutrients vitamins minerals Omega3 fatty acids Flavonoidsother polyphenols Live active cultures probiotics Soluble fibers Soy protein isolate Stanolsterol esters Additives hormones pesticides preservatives so some bioactive food components may be harmful Phytochemicals are a major source of bioactives that occur naturally in plants Many have positive effects on health How they work remains to be defined They are classified by their chemical structure into categories eg carotenoids phenolics of particular interest for possible protection against heart disease and cancer Nutritional value of Phytochemicals conveyed to consumers by stressing the dominant food color each color contributes different valuable phytochemicals 3 types of food under investigation 1 existing food known to have bioactive components that promote health 2 commonly eaten foods to which key bioactive components can be added 3 foods specifically developed to promote a particular type of health eg heart joint immune system diabetesmetabolic syndrome gtgt Know Examples of bioactive food components correlated with heart health immune function and diabetes risk see lecture slides PPT 8 9 gt Bioactive food components food source correlated with heart health Omega3 fatty acids coldwater oily fish antioxidants fruits amp vegetables folate B6 Bf 2 dark green leafy vegetables mineral rich foods nuts soy protein gt Bioactive food components food source correlated with immune function Page 6 of 26 Detoxification cruciferous vegetables Fiber beans Vitamin D fortified dairy gt Bioactive food components food source correlated with diabetes risk Low glycemic index foods The glycemic index or GI measures how a carbohydrate containing food raises blood glucose Low GI foods include all nonstarchy vegetables some starchy vegetables like sweet potatoes most fruit Fiber beans vegetables whole grains High fiber foods lower the GI of a food httpwwwdiabetesorgfoodandfitnessfoodwhatcanieatunderstandingcarbohydratesglycemicindex anddiabeteshtml gtgt Functional Foods Nutraceuticals A functional food is commonly defined as a food that provides benefits beyond the basic nutrition provided by that food Food contains a component that offers physical or biological benefits Example Tomatoes are considered a functional food because they go beyond basic nutrition providing additional health benefits because it contains the phytochemical lycopene Lycopene has been shown to promote prostate health Other examples plant stanol amp stanolcontaining foods bioactive peptides for high blood pressure probiotics yogurt 2 categories 1 functional foods that naturally contain a componentthat offers additional benefits to the consumer 2 foods in which a component is added to the food to give it additional benefits Example Omega3 may occur naturally in a food fish or be added eggs milk juice So functional foods possess attributes of both foods and dietary supplements Apply Nutrigenomics in 3 stages 1 Move away from today s generic dietary approaches eg a bioactive food component seems to help many people so recommend moreless for everyone eg more Omega3 enriched less salt Group people by genotype and develop base diet to their predominant risk susceptibilities 3 Finely tailor diet prescriptions and lifestyle recommendations I EXPERIMENTS Epioenetic Tags effects on genes Methvl Taqs Green Florescent Protein Green Florescent Protein GFP was isolated from the bioluminescent jellyfish GFP is encoded by the GFP gene the segment of DNA that contains instructions for making Green Florescent Protein GFP mRNA is a singestranded copy of the GFP gene in the form of messengerRNA mRNA Ribosomes read translate GFP mRNA to produce Green Florescent Protein It is possible to place the GFP gene inside virtually any cell type where it will produce the glowing green protein The GFP glows bright green under nearultraviolet light gt In this experiment GFP provides a readout of gene activity Since DNA and genes are not visible even under a microscope the amount of glowing GFP tells us whether gene is active inactive or somewhere in between Researchers placed the GFP gene into cells growing in culture dishes Then they added different compounds AdoMet Valproic acid to the cells analyzed the GFP genes from these cells and confirmed that the compounds changed the number of methyl tags attached to Page 7 of 26 the DNA Adding methyl tags decreased GFP output turned gene off removing methyl tags decreased GFP output turned gene on Epidenetic Tads effects on genes MethvlationDemethvlation Cancer Cancer develops when a cell becomes abnormal and begins to grow out of control Cancer can begin when mutation changes a cell39s DNA sequence But cancer cells also have abnormal epigenomes In many cancers some genes are turned up and some are turned down often in the very same cells gt Cancer cells have a lower level of methylation more active DNA than healthy cells If less methyl genes ON Too little methylation causes Activation of genes that promote cell growth Chromosome instability highly active DNA is more likely to be duplicated deleted and moved to other locations Loss of imprinting gt Cancer cells can also have genes that have m methyl are less active than normal If more methyl genes OFF The types of genes that are turned down in cancer cells Keep cell growth in check Repair damaged DNA Initiate programmed cell death gtgt httplearngeneticsutaheducontente geneticscontrol gt Geneticallv Identical Mice Experiment Aqouti Gene LANDMARK EPIGENETICS STUDY gt Important findings diet found to influence DNA methylation an epigenetic mechanism effects found to be inherited Researchers bred genetically identical female mice with two copies of the normal wildtype agouti allele which causes coat to be brown with genetically identical male mice with two copies of the agouti viable yellow allele A vy mutation which causes coat to be yellow Researchers fed 12 females on regular diet and 12 on a methylrich diet folate vitamin B12 etc Most regular diet females had children With yellow coats Most methylrich diet females had children with mottled coats mix of yellow amp brown pseudo agouti This demonstrated a correlation between mottled coat and degree of mytheaticn of the agouti gene suggesting that the methylrich diet led to epigenetic silencing of the Avy allele Researcher found that if they fed female mice of the grandmother generation a methylrich diet this epigenetic fix was inherited by the next generation of mice grandchildren regardless of what their own mothers ate Page 8 of 26 So you what eat can affect your future generations You are what you eat what your parents ate and possibly what your grandparents ate As shown in the video clip In the yellow mice the agouti gene stays on all the time causing obesity Brown mice are thin because a tiny chemical tag called a methyl group has affixed to the agouti gene shutting it down Living creatures have million of tags some like methyl groups attach to genes directly inhibiting their function other types grab the proteins called Histones around which genes coil and loosen or tighten them to gene expression Distinct Methylation and Histone patterns exist in each cell constituting a second genome the epigenome quotabove the genome The genome is like the computer hardware The Epigenome is the software that tells the computer when to work how to work and how much gt The Epigenome tells the cells what sort of cells they should be eg skin hair heart Cells have the same genes but their Epigenome silences the unneeded ones to make cells different from each other Epigenetic constructions pass on as cells divide but they39re not necessarily permanent Researchers think they change especially during critical times eg puberty pregnancy gt Epigenome and Identical Twins YouTube Epignome NOVA Identical twins have identical genes Why does only one of them get cancer gt Human Identical Twins Geneticallv identical Experiment To find out if the epigenomes of identical human twins might account for their differences in developing disease researcher collected cells of 40 pairs of identical twins aged 3 to 74 Dissolved cells down to DNA and amplified fragments of DNA until genes became detectable Overlaps of gene results suggest that as twins age epigenome differences accumulate especially when lifestyles differ eat drink smoke As chemical tags that control genes change cells can become abnormal triggering diseases Epigenetic Therapy It is easier to rearrange epigenetic tags than to fix brokendamaged genes Already have some drugs that work to change the instructions of the cancer cells by reactivating genes Page 9 of 26 gt It is easier to fix the epigenome than the genome but it is also easier to mess it up The genome is inherited but you can alter the epigenome Source httpswwwyoutubecomwatchvM4boKud1MRk link in study guide did not work discussed in Krause at p 150 gt Genetics Basics Tour of Basic Genetics view the short clips on DNA Chromosomes and Proteins httpearnqeneticsutahedu The CELL gt Each cell of a living organism contains a nucleus containing instructions to the cell on its role in the body instructions are in the form of a molecule of Deoxyribonucleic acid DNA WhiCh GHCOdeS plans for cell DNA is is wrapped around proteins called Histones and tightly packaged in chromosomes gtgt Chromosome a molecule of DNA tightly coiled around histones Defintion on PPT Page 10 of 26 gtgt Histones proteins that form a scaffolding around which DNA is wrapped to create the nucleosome similar to thread wrapped around a spool gtgt Genes are located on chromosomes All human cells except for gametes sperm and egg cells which each have one pair of 23 chromosomes have 46 chromosomes 2 pair of 23 chromosomes So we inherit 2 copies alleles of each gene 1 from mom amp 1 from dad gt Mitosis process of a parent cell dividing into two genetically identical daughter cells All 46 chromosomes are duplicated and distributed to each new cell gt Meiosis process in which a cell duplicates its DNA and divides twice to produce four gametes or reproductive cells Most cells in the body have two copies of each chromosome but gametes because they have gone through meiosis have one copy of each chromosome During sexual reproduction two gametes called the egg and sperm join together and form a cell called a zygote with 46 chromosomes one copy of each chromosome from each parent can contain chromosomes from both of parent s two sets but only one of each chromosome that will eventually become an individual organism 80 each child has a unique set of chromosomes and a unique combination of traits some like dad some like mom some may be a unique combo The appearance or phenotype of the new individual will depend on whether it inherited recessive or dominant copies of various alleles from its parents Sources include httpeducationseattlepicomeXplanationmendelsthreelawsthrouqh discussionmeiosis3838html The DNA molecule comes in the form of a quotdouble helixquot a twisted ladder The ladder s rungs are built with a 4letter DNA alphabet and uses basepairing rules A adenine always pairs with T on a rung AT pair T thymine C cytosine always pairs with G on a rung CG pair G guanine The DNA strand is made of letters ATGCTCGAATAAATGTCAATTTGA that make words ATG CTC GAA TAA ATG TCA ATT TGA that make sentences lt ATG CTC GAA TAAgt ltATG TCA ATT TGAgt Page 1 1 of 26 These sentences are called genes which tell the cell to make other molecules called proteins gtgt Gene a sequence of nucleotides on a DNA molecule that determines the sequence of a polypeptide chain Definition on PPT nucleotide one of the structural components or building blocks of DNA and RNA A nucleotide consists of a base one of four chemicals adenine thymine guanine and cytosine plus a molecule of sugar and one of phosphoric acid polypeptide chain of amino acid Different sets of genes are active in different cell types gtgt Allele one of two forms of a gene one allele is inherited from mom the other from dad Definition on PPT All living organisms are composed largely of proteins Proteins are large complex molecules made up of long chains of subunits called amino acids 20 different kinds of amino acids are usually found in proteins gt Each gene in the DNA encodes information on how to make an individual protein When a cell needs to make a specific protein DNA info in cell must be decoded to be useful gtgt Gene Expression the flow of information from DNA to RNA in the process of transcription and translation in which proteins are formed Academy 301 gtgt Silencing prohibiting expression of a gene DNA Decoding takes 2 steps Transcription and Translation Step 1 gtgt Transcription process in which RNA polymerase converts DNA into an intermediate molecule messenger RNA mRNA Page 12 of 26 gt Control Regulatorv Region of gene controls transcription Within this region are response elements DNA sequences that serve as binding sites for regulatory proteins such as transcription factors It is through the binding of transcription factors to response elements that environmental factors eg bioactive components in food essentially quottalkquot to the gene conveying info that moreless of a protein product is needed gtgt Transcription factors are molecules that bind to the control region and control gene expression from PPT gtgt Explain how bioactive food components influence gene expression Bioactive fOOd components can either act as transcription factors eg vitamin A or interact with transcription factors to exert control over gene expression from PPT gt Promoter Region of gene controls binding of RNA polymerase gtgt Coding informational Region of gene region where RNA polymerase converts DNA into mRNA gene expression contains Exons and Introns Exons are sequences of nucleotides that correspond to the order of amino acids in the gene s protein product A Codon is specific sequence of 3 deoxyribonucleic acid bases that directs the cells proteinsynthesizing machinery to add specific amino acids gt Genetic Code is a series of condons each one a specific sequence of 3 DNA bases that specify which amino acids are required to make up specific proteins gt Compare Introns are sequences of nucleotides between eons that do NOT code for amino acids do NOT code for proteins Introns compose most of the DNA in humansThey perform structural and regulatory functions and are NOT quotjunk DNAquot Following transcription mRNA must be processed so that introns are removed before the protein is synthesized Step 2 gtgt Translation process in which mRNA moves from the nucleus into the cytoplasm of the cell where the Ribosome reads the message and produces a protein that matches the specifications set out by the gene gtEach time a cell divides into 2 daughter cells its full genome is duplicated In humans and other complex organisms the duplication occurs in the cell s nucleus The base pair of strands Page 13 of 26 separate and each strand directs the synthesis of a new strand Each daughter cell receives one old and one new DNA stand Adherence to basepairing rules ensures that the new strand is an exact copy Mutations are changes within a gene that alter the amino acid sequence of the DNA protein All changes to DNA are technically mutations only some have measurable outcomes Compare gt Mutation is usually applied to those changes that sufficiently influence function such that a measurable outcome results gt Genetic variation or gene variant is applied to mutations with an effect on function that is NOT strong enough to lead to a disease or other measurable outcome by itself gt Not all mutations are harmful and some may be helpful eg increased resistance to malaria but a single nucleotide change could cause a debilitating disease Outcome depends on the mutation s effect on the functioning of the encoded protein Some variations in a person 5 genetic code Will have no effect on the protein that is produced others can lead to disease or an increased susceptibility to a disease gtgt Genetic Polvmorphism a difference in DNA sequence from a reference sequenceDefintion on PPT A gene can exist in slightly different forms due to even a minor change eg a single nucleotide substitution As a result genes have protein products with differing amino acid sequences isoforms and often different functions gt Even though people are 999 alike genetically the 01 difference is enough to explain obvious physical variations amp nonobvious differences that may explain inconsistencies in therapeutic outcomes amp nutritional intervention research gtgt SNP Single Nucleotide Polvmorphism quotSNIPSquot is gene variation ata single base pair Defintion on PPT SNP is the most common type of gene variation in human beings amp the structural gene variant best studied to date SNPs are considered normal variations in DNA and account for differences in human eye color hair color and blood type Some SNPs may influence the risk of developing certain diseasesdisorders FTO SNP genotype has been associated with obesity Academy 301 304 The most widely investigated common SNPdisease association is the relationship between the apolipoprotein E apoE genotype and coronary heart disease CHD risk There is insufficient evidence at present on which to base dietary fat recommendations based on apoE Academy 304 Hot area of biomedical research developing SNP quotSNIPquot MAPS a single map of the human genome containing all possible SNPs There are an estimated 10 million SNPs in human genome Page 14 of 26 gt Inheritance Basics Traits are transmitted from one generation to the next in 3 ways Mendelian mitochondrial epigenetic gtgt Mendelian Inheritance the transmission of singegene traits from parent to offspring in humans according to a predictable set of rules governing distribution of chromosomes during mitosis and meiosis Since genes are carried on chromosomes rules can be used to predict the probability of a genetic change or a disease caused by a change being transmitted pedigree to a particular family member Each gene in a individual is present in 2 copies alleles one on each chromosome gt when two alleles are different one common one variation the individual is said to be Heterozygous gt when two alleles are the sameboth common or both variations the individual is said to be Homozygous gtgt Phenotype Traits see Spath Study Guide p 2 An individual s genotype obeys the laws of inheritance but the phenotype may not The terms dominant and recessive describe the inheritance patterns of certain traits That is they describe how likely it is for a certain phenotype to pass from parent o spnng gtgt Dominant variant allele is said to be dominate if a trait is expressed in a heterozygous individual when only a single copy of a variant allele is present ie the phenotype of the variant allele is the predominant one Heterozygous individual also called a carrier gtgt Recessive alleles that do not dominate the genotype when only a single copy is present are said to be recessive The variant allele is present in the genome but the trait is not expressed unless two copies of the variant alleles are present gt Penetrance A gene is said to have reduced penetrance when a individual has the gene but the gene is not expressed in measurable form Penetrance is of interest to nutrition professionals because it reflects the inability of a genetic variation to impair function and cause disease unless the person is exposed to specific environmental triggers e g diet amp lifestyle Mendelian Transmission of genetic changes can be autosomal or sexlinked dominant or recessive Page 15 of 26 5 classic modes autosomal dominant autosomal recessive Xlinked dominant Xlinked recessive and Ylinked gt Mitochondrial or Mother Inheritance In addition to the genetic material in the nucleus the mitochondria in each cell also contains DNA that codes for a limited number of proteins As with nuclear DNA changes in mtDNA can lead to disease Traits resulting from mitochondrial genes changes in mitochondrial DNA mtDBA typically pass from mother to child gt Egigenetic inheritance involves at least 3 mechanisms histone modification relaxes DNA so genes can be transcribed into mRNA OR condenses so genes are silenced DNA modification attachment of chemical tags eg methyl groups agouti gene experiment RNA interference RNAi posttranscriptional mechanism whereby short pieces of single stranded RNA attach to DNA or mRNA Attaching to DNA leads to epigentic gene silencing silencing whole regions of chromosomes Attaching to mRNA interferes with gene expression gt Genomic Imprinting unusual phenomenon in which only one of two alleles is expressed either the one contributed by the mother or by the father Histone modification and DNA modification can contribute to genomic imprinting gtgt A key difference between singlegene and complex polygenic diseases is the ability to predict risk of transmission In singlegene diseases the Mendelian rules of inheritance can be used to predict the probability of a disease being transmitted to a particular family member But most commonchronic diseases eg CHD obesity inflammation are polygenic involving more than one gene with an unknown number of genes contributing in a small way to the symptoms The risk of transmission can be estimated but not calculated httplearnoeneticsutaheducontenthistorvoeneticrisk gtgt Susceptibility to many conditions not typically considered quotgenetic diseasesquot eg cancer obesity metabolic syndrome may be influenced by genetic variants However genetics may account for only a very small percentage of attributable risk BECAUSE diet and lifestyle can minimize a person s susceptibility Examples Cardiovascular disease CVD dietary interventions must be matched to genotype to accomplish the intended lipidlowering response Page 16 of 26 Cancer dietary interventions should increase endogenous internal detoxification activity neutralization of potentially harmful molecules Studies suggest that consuming plant foods may be cancerprortective Type2 Diabetis Mellitis T2DM healthy diet that controls blood sugar Susceptibility to increased body fat restrict dietary fat vigorous exercise More than 20 genes are associated with obesityrelated anthropometric measures Academy 30 INHERITANCE AND DISEASE Disease at the Chromosomal level change in number of chromosomes or the arrangement of DNA within a chromosome or the loss of portion of a chromosome detected by karyotype visualization of chromosomes in picture form eg Down syndrome Nutrition professionals play an important role in therapy of those with chromosomal disorders Disease at the Mitochondrial level mutations in mtDNA which is passed by mother to offspring that are typically degenerative Mutations can manifest at any age More than 60 diseases resulting from changes in mtDNA have been identified eg neurologic diseases gt Disease at the Molecular level the majority of disease conditions associated with nutritional genomics involve changes at the molecular level Because most human genes reside on nuclear chromosomes gene variations are transmitted according to Mendelian inheritance and are subject to modification from epigenetic markings It is possible to track a mutationgene variation with the Mendelian Rules of Inheritance The transmission pedigree may be used to predict the probability of a genetic change being inherited by a particular family member When the change causes a disease a pedigree can be helpful in predicting whether another family member will inherit the disease Family History Initiative implemented by US Surgeon General to help people construct their family pedigree Autosomal chromosome is a chromosome that is not an allosome ie not a sex chromosome autosomal dominant singlegene disorders that have nutritional implications autosomaI recessive more common include metabolic disorders Detected because of effect on newborn infants that led to serious developmental consequences or death and designated inborn errors of metabolism IEM IEM disorders are earliest known examples of nutritional genomics dietary modification is primary treatment Classic example of an IEM of amino acid metabolism is PKU Hereditary fructose intolerance prevents fructose from being converted from glucose Page 17 of 26 Xlinked dominant fragile X syndrome characterized by developmental delays mental impairment behavioral problems affects nutritional status Xlinked recessive conditions include Duchenne muscular dystrophy DMD Ylinked inheritance disorders involve male sex determination To date NO nutritionrelated disorders are assigned to the Y chromosome GENETIC TECHNOLOGIES Recombinant DNA technology researchers used restriction endonucleases restriction enzymes to cut DNA in precise reproducible locations along nucleotide chain and polymerase chain reaction PCR technology to make unlimited copies of DNA for various applications Recombinant DNA technology paved the way for DNA sequencing which is used to identify the sequence of nucleotides within a gene pinpoint the exact location of any change and identify each of the nucleotides in an individual s genome gt whole exome capture promises to be an efficient way to identify the DNA sequences that constitute genes Microarray Technology gt Microarrays are also called DNA chips that are used to determine which genes are expressed at a particular time under particular conditions Can be used to determine which genes are turned on or off in response to environmental factors such as nutrients Useful clinical application compare gene expression between normal and diseased cells like cancer Interference with Gene Expression to determine function of gene and its encoded protein Transgenic animals animals most commonly mice that have had a foreign gene deliberately inserted into their genome gt Knockout Mouse a gene is altered quotknocked outquot so that the usual protein is no longer made This permits research on effects of overexpressing or under expressing a gene Learn more about the role of protein Page 18 of 26 NUTRITIONAL GENOMICS ETHICAL LEGAL amp SOCIAL IMPLICATIONS Genetic Testing Nutritional genomics has the potential to be a valuable tool but it involves genetic testing an essential component of identifying genetic variations in individuals There is some controversy over the use of genetic testing Consumers don t like insurers and employers having access to their personal genetic information and worry that it could be used against them to deny insurance coverage or employment gt Genetic Information Nondiscrimination Act GINA A 2008 federal law that 1 defines genetic testing and genetic information 2 bans discrimination based on genetic information and 3 penalizes those who violate the provisions of this law Consumers also are concerned that because of the cost of genetic testing only the wealthy will be able to afford it and be able to benefit As the use of genetic testing increases cost should decrease Genetic testing laboratories should have 1 appropriate credentials and state licensing if required At a minimum labs should have gt Clinical Laboratory Improvement Amendment certification 2 appropriately credentialed health professionals to interpret genetic test results 3 privacy policies how privacy of person tested will be protected if DNA sample is retained or destroyed 4 transparency inform consumers about 13 Read the questions Important amp Ethical Questions related to Genetics Testing Box 51 Krause p 160 Page 19 of 26 CLNCAL SCENARIO Krause p 159 Jared and Matthew identical twins Should we compare notes on answers Answers to Nutritional Care questions 16 1 Similar health profiles As identical twins Jared and Matthew are genetically identical 2 Different diets Twins live apart and may have very different diets 3 Same genetic susceptibilities Same phenotype Think about DNA environmental influences epigenetic markings Jared and Matthew inherited the same susceptibilities to disease but susceptibilities are affected by epigenomic changes lifestyle and environment 4 How would you confirm that Jared is genetically predisposed to type 2 diabetes Family history 5 What would you advise Jared to do to decrease his susceptibility to diabetes I would advise Jared to watch his weight eat low glycemic index foods and foods high in fiber which tends to lower the GI of a food 6 What do findings of chronic inflammation mean for Jared Chronic inflammation is recognized as an underlying factor in chronic disorders including heart disease cancer and obesity Variants of L1and L6 genes have been discovered to increase susceptibility of humans to be in a proinflammatory state which increases the risk of developing a chronic disorder Krause 157 Can he decrease his susceptibility to chronic disease Certain diet bioactive food components and lifestyle approaches can minimize susceptibility and dampen existing inflammation Page 20 of 26 POSITION OF THE ACADEMY OF NUTRITION amp DIETETICS NUTRITIONAL GENOMICS Key Points in Abstract gt Nutritional genomics provides insight into how diet and genotype interactions affect phenotype but its practical application to complex chronic disease is an emerging science gt Use of nutrigenetic testing to provide dietary advice is NOT ready for routine dietetics practice Would require registered dietitian nutritionists to understand interpret and communicate complex test results in which the actual risk of developing a disease may not be known gt Most chronic diseases are multigenetic and multifactorial so genetic mutations are only partially predictive of disease risk Registered dietitian nutritionists need basic competency in genetics as a foundation for understanding nutritional genomics but advanced knowledge amp skills are required to be proficient DirecttoConsumer genetic testing is not closely regulated in US and may not come with access to health care practitioners who could explain test results gt Family history biochemical parameters and the presence of risk factors in individuals are relevant tools for personalizing dietary interventions Page 21 of 26 The practical application of nutritional genomics in dietetics practice requires an evidencedbased approach to validate that personalized recommendations result in health benefits to individuals and do not cause harm Key Points in Article Genotyping alone will not be sufficient to personalize diet for improved health Must understand and manipulate how diet affects the phenotype of an individual gt Most genes are the same from person to person but lt1 of genes are slightly different between people which translates to a difference of 3 million bases gt Family History Family history is an important screening tool to determine risk of inherited diseases eg type 2 diabetes mellitus colorectal cancer and to guide decisions on use of genetic testing but FHs are of limited use for assessing risktargeting interventions for chronic disease Generally health care practitioners are NOT obtaining FHs or NOT doing FHs thoroughly Genetic Testing Singlegene disorders v Complex disorders Singlegene disorders Currently there are about 2000 genetic tests available for use in clinical settings most of which test for singlegene disorders Testing for singlegene disorders occurs primarily within the traditional medical testing In singlegene disorders a defective gene may confer as high as 100 probability of the disorder eg Huntington s disease Breast cancer genes BRA1 amp BRA2 are associated with a significant increase in probability of developing breast cancer Complex disorders Genetic tests for complex disorders which look to mutations in SNPs Single Nucleotide Polymorphism are only predictive of an altered risk associated with disease development Since not all SNP associations amp other factors that contribute to development of a particular complex disease are known testing does not provide enough info to alter standard of care at this time gt Validity amp Usefulness of Genetic Tests Centers for Disease Control and Prevention CDC Office of Public Health Genomics developed the ACCE model that defines whether the genetic test has 1 analytical validity accuratelyreliably detects if specific genetic variant is present or absent Page 22 of 26 2 clinical validity accurately detectspredicts the presence of a disorderdisease 3 clinical utility likely improves patient outcomes 4 ethical legal social considerations associated with genetic test gt CDC categorizes genetic tests and their application in practice by LEVEL OF EVIDENCE Genomic Tests recommended by CDC for clinical use having achieved analytic validity clinical validity and clinical utility Genomic Application that has demonstrated analytical amp clinical validity but has insufficient evidence for clinical utility Genomic Applications NOT recommended by CDC for routine practice because they lack analytic validity clinical validity and clinical utility newborn screening panel of 31 core conditions 39 Family History for common diseases usually complex diseases 39 genetic risk factors for common diseases 39 BRCA12 analysis for women with specific history of breast or ovarian cancer whole genome sequencing to assess risk for common diseases gt400 emerging genomic tests Two categories of genetic tests used in clinical practice 1 In vitro diagnostic tests manufactured for distribution to multiple laboratories eg kits 2 Laboratorydeveloped tests uses solely in test developer s lab DTC direct to consumers genetic tests are considered laboratorydeveloped tests but their classification is unclear because they use a gene chip a tool that identifies variations in genes bought from a 3d party DTC direct to consumers Genetics Testing and Nutrigenetic Testing gt DTC Genetics Testing refers to genetic tests that are marketedsold directly to consumers health care providers are usually not involved in ordering testsinterpreting results value of this testing is questionable because the test results returned to consumers are interpretation of risk of developing a disease and the accuracy of the interpretation depends on many factors eg panel of risk SNP used by the company environmental factors that contribute to the risk of developing disease In 2006 the General Accounting Office released a statement on directtoconsumer nutritional genetic testing They concluded that the tests they evaluated mislead consumers by quotmaking predictions that are medically unproven and so ambiguous that they do not provide meaningful information to consumers At this point the state of the science simply does not allow nutritional genetic testing on a public scale to provide clinically useful information DTC Nutrigenetics Testing Page 23 of 26 In the early 2000s many companies offered tailored diets and advice on dietary supplements based on SNP analysis But some companies provided nutrition advice based primarily on medical amp family history FTC action caused many of these companies to go out of business Regulation and Oversight of Genetic Tests gtREVEW CHART OF AGENCIES BELOW Federal and state government entities share responsibility for oversight of genetic tests Comprehensive info is in US System of Oversight of Genetic Testing A Response to the Charge of the Secretary of Health amp Human Services Federal Agency Genetic Testing Activities Notes More Notes Food amp Drug Administration FDA Regulates in vitro ND and laboratory developed tests LDT Recently recommended that some DTC genetic tests sold online no longer be readily available to consumers Some OTC over the counter tests should not be used without involvement of physiciangenetic specialist Regulates genetic tests based on riskdegree of harm of inaccurate test results Regulates genetic tests as medical devices if they provide medical info used to diagnose treat or prevent disease Some companies marketing their tests as lifestyle behavior approaches rather than disease diagnosis to avoid regulations on selling medical devices Centers for Medicare amp Medicaid Services CMS Regulates US clinical laboratory testing pursuant to Clinical Laboratory Improvement Amendments of 1988 CLIA Ensures analytical validity of genetic tests Does NOT address the clinical validity or utility of genetic tests Federal Trade Commission FTC FTC can take action against DTC direct to consumers genetic testing companies to enforce consumer protection laws eg can get companies on misleading advertising FTC can enforce action to prohibit DTC companies claims of clinical validity if insufficient scientific evidence for claims Page 24 of 26 National Institutes of Central location for Does NOT Health NIH Genetic voluntary submission of independently verify info Testing Registry GTR genetic test info by or endorse tests or labs CLlAcertified labs FEDERAL LAW Law s purpose Law defines genetic info Law does not cover Genetic lnfo Prohibits discrimination Law defines genetic info Does NOT cover life Nondiscrimination Act of by health ins cos and as info about an disability or longterm 2008 GINA employers on basis of individual s genetic care insurance genetic info tests genetic tests of family members and manifestation of diseasedisorder in family members Ethical Legal and Social Issues Nutritional Genomics Research Genetic Testing amp Clinical Practice Research Regulations that apply to using human subjects in research also apply to nutritional genomic research gt Genetic Exceptionalism refers to genetic information that 1 identifies family relationships 2 can predict future health events 3 may be of interest to third parties eg insurers employers and 4 can be recovered from stored biological specimens in future Genetic Testing Disclosure of genetic test results should be the responsibility of primary care physicians in conjunction with geneticistsgenetic counselors RDN s should not have this responsibility Clinical Practice RDNs may have basic knowledge of genetics but a required degree of proficiency has not been determined RDNs generally have low knowledge of nutritional genomics and have limited ability to discuss probability and risk with patients especially when the actual risk of developing a disease may or may not be known The Future of Nutritional Genomics Nutritional genomics holds promise for tailoring diet to a person s genotype and influencing chronic disease development but the science is still developing gt Standards of Professional Practice for genetic metabolic dietitians published 2008 RDN s with expertise in managing genetic metabolic disorders through nutrition interventioncounseling may lead the way They have specialized knowledge and are well trained for complex multifactorial disorders Page 25 of 26 Models being developed for personalized medicine may be applicable to nutritional genomics in the future eg Intergrative Personal Omics Profile uses a various data including genomic data to understand healthy states and monitor the onset and progression of disease states 20122022 Dietetics Workforce Supply amp Demand Future Scan identifies the evolution of personalized nutrition as a quotchange driverquot Page 26 of 26 Spath Study Guide for Module 3 Obesity Part TwoAssessment amp Treatment LecturePPT SelfStudy Guide Krause Chapter 22 Nutrition in Weight Management gt Key Points definitions gtgt Key Pointdefinition is on SelfStudy Guide Assessment of Body Weight Assessment of Body Fat Assessment of Disease Risk Assess Patient Readiness Evaluation of MNT for Obesity Optimizing MNT Strategies of Calorie Reduction Very Low Calorie Diets VLCD Other Therapies Exercise Behavior Modification Pharmaceutical Management FDAapproved weight loss meds Surgical Procedures Bariatric surgery chart with prof s comments Calculating Energy Needs for obese adult EAL recommendations for critically in obese adult EAL recommendations pregnant mothers Childhood Obesity Pediatric Weight Management Guidelines Energy Restricted Diets Calculating Energy Needs for overweight youth NIH recommendations Pagel of 19 Assessment of Body Weight How do we determine if weight loss is indicated gt BMI is primary classification method height amp weight Some nonBMI definitions for Overweight v Obese Overweight body weight standard based on height Obese condition of excessive fatness or adiposity Hamwi Formula Ideal Body Weight IBW o men 106 for 1st 5 ft then 6 for each additional inch o women 100 for 1st 5 ft then 5 for each additional inch for small or large body frame Commonly used method but NOT VALIDATED Assessment of Body Fat BMI generally correlates well for body fat Some people may be gtmuscular amp has a gtBMI but low body fat Some people may appear small in size but have high body fat General rules for calculating BMI always use metric equation weight kght m2 don t round until final answer must be given to one decimal place Assessment of Disease Risk Waisttohip ratio WHR provides NO assessment advantage over waist circumference alone Waist Circumference alone is best predictor of disease risk Predicts risk for dyslipidemia HTN amp CVD because of excess abdominal visceral fat Waist Circumference is strongest negative predictor of insulin sensitivity Page 2 of 19 gtgt Why is Waist Circumference a good indicator of obesityrelated disease risk Because high amount of fat around the waist indicates a higher risk for heart disease amp type 2 diabetes NIH web site gtgt Know criteria for healthy waisttohip ratios amp waist circumferences for men amp women Men Women Waisttohip ratio healthy ratio ltorto10 ltorto 08 if higher than 10 08 associated with gt risk for CVD amp DM2 Waist Circumference some recommend measure at smallest diameter below the rib cage some measure at umbilicus WC alone is best predictor of disease risk gt40quot 102 cm indicates disease risk above that determined by BMI gt35quot 88 cm indicates disease risk above that determined by BMI Useful for assessing risk in people categorized as normal or overweight Not necessary to measure waist circumference in people with BMIs gt or 350 Health Risk According to Waist Circumference amp BMI BMI Normal 185 249 BMI Overweight 250 299 BMI Obese gt300 Waist Circumference Page 3 of 19 Men lt 40quot 102 cm Women lt 35 88 cm least risk increased risk high risk Men or gt 40quot 102 cm Women or gt 35 88 cm increased risk high risk very high risk Assess Patient Readiness The decision to attempt weightloss treatment should also consider the patient s readiness to make necessary lifestyle changes reasons amp motivation to lose weight previous attempts to lose weight support expected from family amp friends understanding of risks amp benefits attitudes towards physical activity time availability eg for physical activity potential barriers including financial limitations Examples of Nutrition Diagnosis NI NC amp NB N113 Excessive energy intake NC34 Unintended weight gain N122 Excessive oral intake NC33 oveweightobesity Nl563 Less than optimal intake of types of fat specify Nl583 Less than optimal intake of types of carbohydrates specify Page 4 of 19 Nl562 Excessive fat intake Nl582 Excessive carbohydrate intake NBf 3 Not ready for dietlifestyle change NB16 Limited adherence to nutritionrelated recommendations Obesity Treatment Pyramid from base up options for weight management Base lifestyle modification diet physical activity Middle Ms pharmacotherapy treatment to lifestyle changes 39 Top peak surgery amp individualized lifestyle plan Evaluation of MNT for Obesity gtgt What s the M choice of obesity treatment Review EAL guidelines for adult weight management MNT always includes lifestyle changes at the base first choice is low calorie diet physical activity amp lifestyle modification Medical Nutrition Therapy MNT MNT is a specific application of the Academy39s Nutrition Care Process in clinical settings that is focused on the management of diseases MNT involves indepth individualized nutrition assessment and a duration and frequency of care using the Nutrition Care Process to manage disease Guidelines for Adult Weight Management recommend comprehensive program including changes in intake diet with exercise behavior modification nutrition education amp psychological support If warranted medication and possibly surgical intervention can be added to the regimen Page 5 of 19 Adult Weight Management Guideline 2014 httpwwwandealordtODiccfm cat4688amphiohlidhtadult20weioht20manaoement oo20Cluidelinesamphome1 Goals of treatment weight management ie attaining best weight possible in context of overall health Academy of Nutrition amp Dietetics 510 body weight loss in obese is often beneficial Guide for Selecting Obesity Treatment BMI 250269 270 299 300 349 350 399 gt or 400 within within overweight overweight Obesity 1 Obesity 2 Obesity 3 range range Treatment Diet Exercise Behavior Pharmacotherapy if with co if lifestyle changes morbidities eg over 6 mos hypertension unsuccessful diabetes Surgery bariatric if with 00 morbidities Optimizing MNT for Obesity Page 6 of 19 gt Rate of weight loss slow steady loss enhances adipose loss and minimizes 1 lean body mass LBM loss amp 2 RMR decline Setting goals Lose at Optimal rate 12 lbs per week for first 6 mos Achieve initial weight loss of up to 10 from baseline mild weight loss can make a big difference Once goal is achieved need to focus on Weight Maintenance To spare lean body mass exercise important component of weight maintenance Compare drastic kcal reduction mimics starvation response which can lead to decreased RMR If person loses lean body mass the primary determinant of RMR the RMR could decrease even further Could also see increases in hormones eg ghrelin and lipoprotein lipase and other alternatives that may predispose person to gaining back the weight Extent of loss must be individualized consider obesity type Hyperplastic obese amp those with gynoid distribution have greatest difficulty maintaining a large weight loss ldeal Body Weight Hamwi not evidence based so may not be ideal goal for everyone even BMI of 250 may be unobtainable unreasonable goal MNT for Obesity gt EAL recommends caloric deficit of 5001000 kcal below estimated energy needs which should result in weight loss of 12 lbs pre week One practical way to achieve this is to reduce dietary fat andor carbohydrates May need to individualize to person Total caloric intake should be distributed throughout day with the consumption of 45 mealssnack per day including breakfast Consumption of greater energy intake during the day may be preferable to evening consumption Page 7 of 19 MNT LowCalorie Diet Guidelines Nutrient Recommended Intake Total Fat 2030 of total calories Cholesterol lt 300 mgday Protein 1035 of total calories Carbohydrate 4565 of total calories Calcium 10001200 mgday Fiber 2030 gday Strategies of Calorie Reduction Counting calories gives patient freedom to distribute energy freely through the day encourages ownership of the process appeals to some but not for everybody For most people total kcal from fat must also be considered gtgt What are different MNT strategies for moderate kcal reduction Exchange Meal Replacement Commercial Comprehensive 1 Exchange system popular easy to manage eg Weight Watchers 2 Formula or meal replacement systems Jenny Craig Nutrisystem usually provide 10001600 kcalday liquid or bar meal replaces 12 meals each replacement supplies 20 protein 30 fat 50 CHO RDA for vitmin PROS easy substitutes for meals when difficult to obtain appropriate foods for wt reduction plan CONs don t support development of appropriate eating behavior can instill dependence on a product amp can be boring 3 Commercial programs Page 8 of 19 Among the best Weight Watchers UAB s Eatright TOPS Taking Off Pounds Sensibly 4 Comprehensive program is best comprehensive changes in intake diet exercise behavior modification Good resources for caloric reduction weight management NIH ShapeUp America Federal Trade Commission FTC RD4111com Fad Diets not often recommended by health professionals typically emphasize fast results with minimal effort usually promote loss of muscle mass which promotes weight regain based on unscientific principles frequently make claims not supported by research health risks minimized because person is unlikely to stick with the fad diet for long can set person up for failure promoting cycle of selfdefeating feelings of guilt selfloathing amp hopelessness Very Low Calorie Diets VLCD gtgt Describe the general features of a VLCD Rapid weight loss typically provide m kcal daily no evidence to support benefits of caloric restriction below 800 kcal daily prof corrects Krause MUST be Medically Supervised because people have died in the past Usually provided as commercial liquid supplements based on milk or soy protein Completely replaces normal food intake for 812 weeks 100 need for micronutrients electrolytes amp EFAs essential fatty acid Typical weight loss is approximately 20 kg in 1216 weeks Followup has shown a high rate of weight regain within 1 yr gtgt What are some potential side effects of VLCD Potential Side Effects Page 9 of 19 cardiac complications syncope potassium losses Gallstones liver secretes more cholesterol into bile Gout ketones produced during VLCD diet interfere with kidney S clearance of uric acid gtgt When may a VLCD be prescribed Should be reserved for those with 1 BMls gt300 who have tried amp failed with other diet programs 2 BMls 270300 if comorbidities exist obesityrelated diseases amp have triedfailed with other diet programs 3 Medical need for rapid weight loss VLCD do result in rapid weight loss comparable to bariatric surgery but weight regain is common Longterm effectiveness of VLCD is no greater than any other diet plan but is improved with lifestyle modifications exercise and nutrition counseling for wt loss maintenance Other Therapies Exercise extremely important for maintaining weight loss increases proportion of LBM to fat offsets decrease in RMR with weight loss strengthens cardiovascular integrity increases sensitivity to insulin expends more energy 6090 minday recommended for weight loss at least 30 min at moderate intensity Optimal aerobic resistance training Behavior Modification Strategies include selfmonitoring stress management stimulus control problemsolving contingency management Page 10 of 19 cognitive restructuring social support hypnosis amp acupuncture Pharmaceutical Management of Obesity gtgt When may pharmacotherapy be indicated For persons with BMI gt300 or BMI gt270 significant risk factors who tried diet amp lifestyle modifications for 6 mos with no success Not all patients respond If 2 kg has NOT been lost after 4 weeks it is unlikely pt will benefit from drug Drug augments diet exercise amp behavior therapy these all should continue while person is taking drug gtgt What are the FDAapproved weight loss medication on the market now How does each one work 3 FDAapproved weight loss meds How they work Orlistat Xenical Lipase Inhibitor inhibits gastric amp pancreatic lipase which digests 12 strength OTC orlistat Alli fat so Orlistat inhibits fat digestion which in turn inhibits fat absorption OTC over the counter side effects may be unpleasant amp are worse aftera high fat meal flatulence etc so people may avoid high fat meals forces a behavior change Orlistat could impede absorption of fatsoluble vitamins so supplements may be needed Long term treatment would be necessary Page 11 of 19 Phentermine topiramate stmia came on the market in 2014 Combo drug is a CNS stimulant that suppresses appetite Phentermine is a central nervous system CNS stimulant that suppresses appetite combined with Topiramate an antiseizure med that reduces appetite less food less pleasurable Combo drug targets multiple brain pathways that trigger overeating Lorcaserin HCI Belviq newest drug CNS stimulant that suppresses appetite amplifies the brain s response to serotonin Another drug mentioned in Krause has been taken off approved list due risks eg stroke Watch out for dietary supplements which escape FDA regulation May contain high doses of caffeine or other herbal stimulants Surgical Procedures final treatment option gtgt Describe the criteria for determining when an individual may be a candidate for bariatric surgery Recommended as an adjuncttherapy for those with BMI or gt 400 or BMI or gt 350 with other risk factors Person must demonstrate that other methods of weight control failed Person must have psychological analysis prior to surgery Decreases amount of food entering andor absorbed in GI tract RestrictiveMalabsorptive Provides medically significant sustained weight loss for gt 5 yrs in most patients Dangerous side effects reflux dumping syndrome tearingsuture loss septicemia obstruction plugging vitaminmineral losses Page 12 of 19 gtgt Comparecontrast the following weight loss surgeries Weight loss surgeries Type Key Points Adjustable gastric banding LapBand Restrictive surgeon forms a small gastric pouch that limits amount of food entering the stomach at one time doctor can adjust size of pouch gives immediate feeling of fullness fully reversible no cuttingstapling of stomach leads to more gradual weight loss but total amt of weight loss is comparable to the other surgeries RouxenY gastric bypass Restrictive amp Malabsorptive very common popular surgery option that creates small stomach pouch about size of an egg that restricts amt of food person can eat in one meal and attaches pouch to small intestine Page 13 of 19 biliopancreatic diversion with duodenal switch the switch surgery Restrictive amp Malabsorptive least popular surgery most invasive most complications usually reserved for people with BMI of or gt 50 bypass is gt extensive surgeon actually removes a portion of the stomach sleeve gastrectomy Restrictive most popular surgery rapid weight loss fewer complications than Roux enY amp switch surgeon removes 75 of stomach leaving a sleeve sleeve remains connected to intestine no bypass of intestines as found in RouxenY amp switch aids weight loss by 1 restricting the amount of food the stomach can hold 2 reducing the hunger hormone Ghrelin people report feeling full quickly Good descriptions of surgeries with animations at httpwwwstvhscombariatricsbariatricsuroervaso Typical diet progression after gastric bypass surgery Post op clear liquids as tolerated likely sugar free to avoid dumping syndrome Stage 2 1st 23 weeks full liquid diet High protein liquid supplement 2 oz every hour when awake Noncarbonated room temperature lowkcal liquids 2 oz every 15 min after the houn Sample Meal Schedule 800 am 2 oz Boost High Protein 815 am 2 02 water 830 am 2 oz broth 845 am 2 oz diluted juice Page 14 of 19 Stage 3 Next 68 weeks soft diet as tolerated focus on highprotein foods limit fat sugar fiber avoid dry sticky stringy fibrous foods bread peanut butter popcorn tough meats Stage 4 1012 weeks postsurgery Regular diet as tolerated DAT lowfat low sugar Eat slowly and chew well Limit fluids with meals drink fluids between meals micronutrient supplements for life Calculating Energy Needs gtRMR measured by indirect calorimetry is the gold standard gtgt If you don t have access to indirect calorimetry which prediction equation would you use to estimate energy needs Don t need to memorize equations but be able to apply assessment data to calculate energy needs using equations gtgt for an overweightobese adult MifflinSt Jeer equation Page 15 of 19 EAL Recommendation is that if indirect calorimetry is not available the MifflinSt Jeer equation using actual weight is the most accurate equation for estimating REE in overweight amp obese individuals REEresting energy expenditure gtgt for a critically ill obese adult on a mechanical ventilator EAL Recommendation is that if indirect calorimetry is not available use PSU 2003b or PSU 2010 depending on age of person gtgt PSU 2003b validated in 2009 also referred to as Penn State Equation If indirect calorimetry is not available use for critically ill mechanicallyventilated adults with obesity who are lt 60 yrs of age RMR Mifflin096 vE 31 Tmx 167 6212 gtgt PSU 2010 validated in 2010 also referred to as Modified Penn State Equa on If indirect calorimetry is not available use for critically ill mechanicallyventilated adults with obesity who are or gt 60 yrs of age RMR Mifflin071 vE 64 Tmx 85 3085 Tmx is maximum body temperature in the previous 24hours dgrees Celsius VE is minute ventilation liters per minute at the time of measurement read from the ventilator Can obtain from flow sheets from the ventilator settings Calculating Energy Needs for pregnant mothers Prepregnancy weight Recommended weight gain Underweight BMI less than 185 28 to 40 lbs about 1318 kilograms Normal weight BMI 185 249 25 to 35 lbs about 1116 kilograms Overweight BMI 25 299 15 to 25 lbs about 711 kilograms Obese BMI 30 or more 11 to 20 lbs about 59 kilograms Page 16 of 19 If overweight at time of conception then weight gain goals are lower If underweight at time of conception then weight gain goals are higher Childhood Obesity Nearly onethird of US children are overweight or obese gtgt How do you assess the weight status of children Growth charts are used to assess the weight status of children whether a child is overweight or obese The curves on the growth charts show patterns of growth Track BMI on age amp sex specific CDC growth carts Growth charts available at httbwwwcdcoovdrowthcharts and in Krause appendix gtgt Review the EAL guidelines for pediatric weight management currently under review Multicomponent intervention including diet PA and nutrition counseling Family involvement is critical Page 17 of 19 Weight stabilization is the goal for children 25 yrs old No data supports safetyefficacy of weight reduction For all children individualized treatment is crucial Energy Restricted Diets in children 612 yrs old If appropriate balanced macronutrient diet no fewer than 900 kcal Per day recommended range is 9001200 amp medically monitored Energy Restricted Diets in children 1318 yrs old If appropriate balanced macronutrient diet no fewer than 1200 kcal Per dayamp medically monitored Pediatric Weight Management Guideline 2007 httpwwwandealordtODiccfmcat2721amphidhlidhtpediatric20weidht20manaoement 20Ciuideineamphome1 Executive Summary httpwwwandealorCltODiccfmcat3013 link found at beginning of Major Recommendations document Page 18 of 19 gtgt If you don t have access to indirect calorimetry which prediction equation would you use to estimate energy needs for an overweight child Don t need to memorize equations but be able to apply assessment data to calculate energy needs using equations gtgt if indirect calorimetry is not available NIH recommends equa onsfon Overweight Boys Ages 3 18 yrs of age TEE 114 509 at age y PA x 195 x weight kg 11614 x height m Overweight Girls Ages 3 18 yrs of age TEE 389 412 at age y PA x 150 x weight kg 7016 x height m Source 2005 US Institutes of Medicine quotDietary Reference Intakes for Energy Carbohydrate Fiber Fat Fatty Acids Cholesterol Protein and Amino Acids Macronutrients Formulas posted at httpwwwandealordtcbiccfmcat3060 Note that the equation gives total energy expenditure so already takes into account physical activity PA so we don t multiply by a PA factor like we do in some other equa ons Page 19 of 19 Spath Study Guide DISORDERS OF THE SMALL amp LARGE INTESTINES M7 Part 2 gtgt What are the two major types of Inflammatory Bowel Disease IBD Crohn s Disease Ulcerative Colitis gtgtWhat do these two disorders have in common Crohn s Disease amp Ulcerative Colitis have many things in common inflammation of intestinal mucosa hence the name Inflammatory Bowel Disease abdominal pain diarrhea fever food intolerance weight loss anemias people with these conditions may have periods of remission amp periods of fareup etiology is unknown likely genetic amp involving an inappropriate immune system response to certain environmental triggers not fully understood unable to identify trigger foods that cause IBD most common in younger people ages 1530 yo seems to strike men amp women equally gtgt Clinical defining features that distinguish Crohn s Disease from Ulcerative Colitis Crohn s can affect any part of the small or large intestine U0 is limited to the large intestine Crohn s causes inflammation that can skip sections of the intestine inflamed segments of the bowel may be separated by healthy segments of bowel It is a mystery why some sections are inflamed and not others UC s inflammation is continuous Crohn s is transmural it affects all layers of the mucosa including submucosa amp deeper tissue U0 is generally limited to the mucosal layer innermost lining Page 1 of 9 Crohn s has no cure Sometimes portions of the bowel are resectioned surgically removed and the healthy portions reconnected anastomosis UC s only cure is a partialtotal colectomy Crohn s more commonly involves fistulas abnormal tunnels through mucosa Crohn s can cause additional problems outside the GI tract know gtgt What are some defining features of Crohn s Disease IBD Crohn s Disease Chronic amp progressive GI ulceration Affects all layers of the mucosa lncurable resection to remove affected sections can provide relief gt May involve any sections of the GI tract 5060 of cases involve distal ileum terminal ileum amp colon large intestine gtgtWhat are the most common ss Symptoms Ulceration of the small andor large intestines weight loss anorexia fatigue abdominal pain andor mass diarrhea may have a long period of remission followed by a relapse can be debilitating know gtgtWhat are some possible complications of Crohn s Disease Complications Page 2 of 9 StriCture or obstruction 2 secondary to scar tissue formation due to repeated inflammation amp healing Malabsorption deficiencies and anemias related to malabsorption StU39a depending on location can produce significant nutrientfluid losses can cause ulcers or sores that tunnel through all the layers of the GI tract especially around the anUS 0r rectum These abnormal tunnels are called fistulas Fistulas are fairly common with Crohn s disease More common than in UC at increased risk for colorectal cancer can cause additional problems outside the GI tract A variety of immunologically related systemic complications can occur in Crohn39s disease including ulcerations of the tongue skin rashes or joint problems kidney stones gallstones inflammation of the eyes IBD Ulcerative Colitis know gtgtWhat are some defining features of Ulcerative Colitis Chronic inflammation amp ulceration of intestinal mucosa Usually starts in rectum or sigmoid colon and can spread to other areas of the large intestine limited to large intestine Inflammation is generally limited to the mucosal layer Inflammation is continuous Total colectomy only cure know gtgtWhat are the most common 55 of Ulcerative Colitis Symptoms Bloody diarrhea pain Weight 39033 anorexia Ulcerative lesions of large bowel mucosa Page 3 of 9 Anemia due to blood loss from diarrhea since there is no appreciable nutrient absorption in large intestine gtgtWhat are some possible complications of Ulcerative Colitis Complications 39933 SEVere Malabsorption since food nutrients are absorbed in the small intestine But there can be major water amp electrolyte losses since these are absorbed in the large intestine gtgtPrimary Sclerosing cholangitis chronic liver disease characterized by inflammation destruction and fibrosis of the intrahepatic and extrahepatic bile ducts leading to cirrhosis of the liver strong correlation 12 people with UC also develop primary sclerosing cholangitis possibly due to an autoimmune response Toxic colitis Toxic megacolon gtgtWhat is toxic megacolon and why is this a very serious disorder Toxic megacolon a rare but serious complication of UC the inflamed colon becomes immobilized unable to pass gas or stool and distended Could rupture and spew bacteria into the abdominal cavity This would be lifethreatening may be more prone to colorectal Cancer Rarely stricture formation or fistulas know gtgtldentify the most common medications used to treat acute flareups of IBD Pharmacology for IBD There is no cure for Crohn s or Ulcerative Colitis but medications may help to control symptoms and reduce inflammation Three most common types of meds to reduce inflammation amp control symptoms 1 Antiinflammatories can cause GI irritation 2 Corticosteriods eg prednisone Suppresses immune response and inflammation Page 4 of 9 Side effects include T susceptibility to infection electrolyte imbalances weight gain hypercalciuria loss of calcium in the urine so weak bones over time sodium amp fluid retention 3 lmmunosuppressants block the immune reaction that contributes to inflammation Side effects NVD and l immune function making them more susceptible to all types of infection so food safety becomes important for that person Medications prescribed after inflammation subsides Antidiarrheal medications know gtgtWhat are the nutritionrelated side effects of these meds Fluidelectrolyte replacement Micronutrient replacement especially iron RD would review the lab results amp look for hemoglobin hematocrites serum ferritin and other indications of iron deficiency anemia due to blood loss Goals of IBD MNT 1 induce amp maintain remission 2 improve nutrition status Diet is one of the environmental factors that triggers relapses of IBD Identify food intolerances these often include T sucrose inadequate FV intake t fiber intake Page 5 of 9 T red meat andor alcohol intake altered omega6omega3 FA intake During an acute flareup stay on low residue diet lowfiber avoid lactose avoid excessive fructose avoid greasy high fat foods Eliminate the foods identified as triggers Prevent malabsorption deficiency parenteral nutrition intravenous or IV or tube feeding may be needed Supplement Ca Vit D folate Fe B12 Mg Zn as needed Monitor fooddrug interactions Energy needs not greatly increased unless pt is malnourished amp weight gain is desired 3040 kcalkg gtgtWhat are the recommendations for PRO during acute inflammation of IBD gtgtWhy are PRO needs elevated 115 g prokg depending on severity of illness Protein needs T to 1 support tissue healing in the inflamed areas amp 2 because steroids used to treat flareups can increase protein needs know gtgtWhy would someone with IBD likely be lactose intolerant Lactose intolerance may be found with Crohn s disease if the brush border is inflamed causing decreased secretion of lactase Monitor for lactose intolerance Page 6 of 9 IBD MNT continued know gtgtWhat would you recommend regarding fiber intake for IBD Fiber Acutely restrict during inflammation lndividualize addition during remission know gtgtWhy is MCT beneficial for someone who presents with steatorrhea For steatorrhea decrease dietary fat to lt 25 of kcal add medium chain triglycerides MCT to increase energy intake Most of our dietary fat is in the form of long chain fatty acids or long chain triglycerides but medium chain triglycerides are much more easily digested and absorbed For bowel resection Crohn s disease requires individualized evaluation Determine probable deficiencies based on which sections are removed and by how much functional area is left gt May need MNT for shortbowel syndrome gtgtDiscuss how prebiotics and probiotics may be helpful or harmful for IBD gtgtPrebiotics help support growth of and maintain friendly bacteria in the gut are not bacteria but are natural compounds found in plants that help fuel the bacteria to ferment short chain fatty acids and those may nourish intestinal cells eg pectin fructooligosaccharides FOS inulin oats banana flakes fermentable fibers resistant starches helpful anytime gtgtProbiotics sources of bacteria live active cultures used to reestablish beneficial gut flora acidophilus bifidum lactobacillus Page 7 of 9 may be helpful when pt is in remission may not be helpful when pt experiences acute attack due to risk of inflammation know gtgtWhy may fish oil supplements be helpful Omega3 fatty acids Recent evidence suggests that omega3 fatty acid supplements in the form of fish oil DHA and EPA may reduce acute inflammation and maintain remission of Crohn s Disease However studies have yielded mixed results gtgtWhy may some patients have difficulty tolerating fish oil If a person is having a problem with fat absorption they may not tolerate fish supplements well Fish oil supplements may cause side effects that are similar to symptoms of IBD such as flatulence diarrhea etc Support groups Crohn s and Colitis Foundation of America wwwccfaorg Page 8 of 9 Page 9 of 9 Spath Study Guide for Module 3 Obesity Part One Physiology amp Etiology LecturePPT SelfStudy Guide Krause Chapter 22 Nutrition in Weight Management gt Key Points definitions gtgt Key Pointdefinition is on SelfStudy Guide Classification of Overweight amp Obesity US Demographics of Obesity BMlassociated Disease Risk Etiology of Obesity Body Weight Components Andipose Tissue Fat Storage Enzymes amp Hormones Regulation of Body Weight 3 components of energy expenditure shortterm amp longterm regulation of energy intake hunger amp satiety role of neurotransmitters corticotropin releasing factor role of hormones Environmental Influences Tissue Changes with Caloric Restriction amp Weight Loss Page1 of 19 Classification of Overweight amp Obesity BMI is the most common classification of overweight amp obesity Based on NIHWHO proposal to define overweight amp obesity based on the risk of morbidity diseasedeath It is how the CDC defines overweight amp obese status It is what we use for diagnosis gtgt Calculation for BMI WH2 weight in kg by height in meters2 gtgt NIH classifications for weight status based on BMI It is important to report BMI to one decimal place 299 and 30 are close but are different classifications NIH Classification Body Mass Index kgm2 Underweight lt185 Normal 185249 Overweight 250299 Obesity Class 1 300349 Obesity Class 2 350399 Extreme Obesity Class 3 400 Other weight assessment tools waist circumference gt40quot men amp gt35quot women signifies gt risk equivalent to BMI of 25 4O waisttohip ratio WHR ratio of gt1 0 men amp 08 women is associated with high risk for cardiovascular events Deurenberg equation uses BMI age amp gender to predict body fat percentage Body fat of 2025 men amp 2532 women considered excessive amp associated with risk of obesity Optimal BMI with least risk of mortality 23249 Optimal range for longevity appears to be 205249 Page 2 of 19 Balancing energy intake amp energy expenditure is the basis of weight management throughout life As you age prevent gradual weight gain by making small decreases in overall calories amp increasing physical activity The Calorie Restriction CR Society International members believe that cutting calorie intake reduces aging and chronic disease development Prevalence of Obesity International amp US Internationatrend towards obesity quotglobesityquot US has the highest prevalence of obesity among the developed nations US Demographics of Obesity 692 of US adults ages 20 are overweight or obese 359 are obese Source 20092010 National Health amp Nutrition Examination Survey NHANES conducted by Centers for Disease Control amp Prevention CDC NHAN ES obesity rates have climbed since the 19603 CDC obesity trends among US adults have nearlv doubled since the 19803 Racialethnic disparities in US prevalence of obesity is higher among black and Hispanic populations especially among MexicanAmerican men amp women African American women The lower the socioeconomic status the higher the prevalence of obesity BMIAssociated Disease Risk NIH Classification Disease Risk Underweight Increased Normal Normal Overweight Increased Obesity Class 1 High Obesity Class 2 Very High Extreme Obesity Class 3 Extremely High Additional Risks that may influence BMI amp disease risk large waist circumference increase of 5 kg weight or more since 1820 yrs of age poor aerobic fitness Page 3 of 19 specific race amp ethnic groups Jshaped curve morbiditydeath associated with obesity but also with underweight J on graph morbiditydeath rate is high for underweight low for normal amp very high for obese Medical Complications of Obesity see drawing at Krause p 470 Chronic diseases tend to worsen with gt obesity Health costs of overweightobese adults several thousand higheryr especially for women Etiology of Obesity Obesity occurs when energy intake exceeds energy expenditure but influences on energy intake amp energy expenditure are complicated Obesity is a multifactorial chronic disease that results from a variety of factors Obesity is poorly understood influenced by genetic amp environmental variables including cultural psychological amp physiologic mechanisms no singe theory applies need careful assessment of each individual S medical amp social histories and energy balance Body Weight Components gtgt Components of body composition Fat Mass FatFree Mass Fat Depots adipose tissue gtgt Most commontraditional Body Weight Model divides body into 1 Fat Mass fat from all body sources 2 FatFree Mass FFM which includes water protein and mineral components Lean body mass LBM LBM includes skeletal muscle water bone small amount of essential fat higher in men increases with exercise decreases with age Water 6065 of body weight is most variable component of LBM LBM is major determinant of resting metabolic rate RMR resting energy expenditure To achieve longterm weight loss lose fat mass while maintaining FatFree Mass FFM and Resting Metabolic Rate RMR maintaining muscles gtgt Body FatAdipose Tissue Essential body fat Essential body fat necessary for normal physiologic functioning about 3 men about 12 women to support reproductive process breasts pelvic region thighs Page 4 of 19 Storage body fat Storage body fat energy reserve stored primarily as triglycerides TGs in adipose tissue Accumulates under the skin and around internal organs to protect them from trauma Most storage fat is expendable In Total body fat quotessentia storage fat usually expressed as o of total body weight Total body fat for optimal health 1025 men 18 30 women elite men athletes 12 o18 o elite female athletes 16 o25 o Theoretical Body Composition Model slide on p 8 Adipose Tissue stored in different depots places in the body Visceral Adipose Tissue VAT fat that lies beneath the abdominal muscle and surrounds the internal organs Excess VA associated with gt risk for type2 diabetes and CV Subcutaneous Adipose Tissue SAT fat right underneath skin Liposuction is cosmetic does not address VAT fat associated with health risks Adipose Tissue Composition primarily fat but contains small amounts of protein and water Adipose Tissue Structure gtgt White adipose tissue main storage form of triglycerides for energy Carotene gives it a slight yellow color gtgt Brown adipose tissue much higher amounts in infants heat production but new PET scans show it is also found in adults neck abdomen scapula people who have it tend to be lean amp have better metabolic profiles so may be involved with energy regulation amp be important for weight control More research is needed Coldinduced brown adipose tissue activation in adult men used PET scans brown color due to mitochondria amp blood vessels Fat Cell Development Size amp Number Main job of adipose tissue is to store fat gtgt Fat cell development Page 5 of 19 Birth to 6 mos the greatest level of body fat about 25 occurs with normal growth 6 mos 6 yrs fat cell size decreases in lean children but not in obese children 6 yrs of age lean children s body fatness increases again adiposity fat rebound gt in girls than boys If this increase fatness occurs before 55 yrs of age it iS predictive of greater adiposity by age 16 and in adulthood If this increase occurs later than 6 yrs of age it correlates with normal adult weight For obese children increase in w is faster throughout childhood gtgt Contrast Hypertrophy amp Hyperplasia in relation to storage of triglyceride in adipocvtes mature fat cells Hypertrophy amp Hyperplasia both increase the storage of triglycerides in adipocytes Hypertrgphy increases the size or volume cell expands uo to 1000x original size of adipocytes and can happen at any age Mature fat cells adipocytes can store fat equal to 80 o95 o of their volume Weight gain increases the size of the fat cells and if the maximum cell size iS reaChed can also increase the number of fat cells Weight loss of at least 5 is required to decrease fat cell size Hyperplasia increase the number of adipocytes fat cells This happens mostly in infants amp adolescents as part of the growth process but can happen in adults if maximum cell size is reached due to weight gain cell number is unlimited the adipose reservoir can reach very large dimensions If there is weight less fat cell size decreases but the cell remains the same 80 a hyperplastic obese person who loses weight may find it more difficult to maintain weight loss due to high number of fat cells waiting to store more triglycerides Fat Storage Page 6 of 19 Fat composition is determined by diet fatty acids in adipose are identical to dietary triglycerides consumed Lipogenesis creates fatty acids from excess dietary carbohydrate amp protein at triple the energy cost 25 so it is very inefficient 3 x more energy is needed to convert excess energy from carbohydrate to fat storage We eat less fat today but overweightobesity rates keep going up It is not enough to reduce dietary fat Body can store any excess micronutrient as a triglyceride in adipose tissue Total reduction of calories is needed for weight loss to occur Semivolatile organic compounds svocs accumulate in adipose tissue from exposure to toxins chemicals and pesticides Exposure to toxins comes from 2 main sources 1 environment external toxins amp 2 gut breakdown products of our metabolism internal toxins When toxins overwhelm the body s endogenous detoxification mechanisms the toxins are stored in the body s depot adipose fat Toxins interfere with key weight control mechanisms in the body by 99 altering metabolism disrupting endocrine function damaging the mitochondria increasing inflammation amp oxidative stress lowering thyroid hormones and altering circadian rhythms amp the autonomic nervous system Semivolatile organic compounds SVOCs continued Life style choices as well as medical detoxification can reduce exposure to toxins and enhance mobilizationelimination of stored and external toxins When adipose tissue is mobilized during weight loss SVOCs are released Obese women should lose weight before becoming pregnant because the effects of SVOCs on the developing fetal brain is not yet known gtgt Key Enzymes in Fat Storage LPL amp HSL play opposite roles gtgt Lipoprotein Lipase LPL facilitates triglycerides storage in adipocytes fat cells enzyme that facilitates removal of dietary triglycerides TG from the blood and into the adipose cells Endogenous triglycerides TG synthesized in liver from free fatty acids FFAs travels in the very lowdensity lipoprotein VLDL amp is broken down to glycerol FFAs by low density lipoprotein LPL so these can enter adipose cells to be reesterified amp stored as lipid Increase during periods of weight gain some evidence that LPL activity remains elevated in a weightreduced formerly obese individual May make it easier to regain weight Page 7 of 19 Elevated LPL activity enhances one s ability to store circulating triglycerides TG and contributes to efficient weight regain gtgt HormoneSensitive Lipase HSL a fat burning enzyme enzyme in the adipose cell that is responsible for the hydrolysis of triglyceride into FFAs and glycerol which then leave the adipose ll and enter circulation HSL is inhibited by the insulin hormone Hormones in Fat Storage gtgt How do estrogens and progesterone influence fat storage Estrogens and progesterone stimulate Lipoprotein Lipase LPL activity in gluteotemoral buttocks amp thighs adipocytes and thus promote fat storage in these areas for childbearing and lactation breastfeeding 39 In the presence of sex steroid hormones a normal distribution of body fat exists women tend to pearshape fat distribution men to appleshape As sex steroid hormones decrease as with aging gender distribution patterns decrease and central adipositv increases especially in women Regulation of Body Weight Energy Expenditure gtgt 3 components of total energy expenditure TEE EE RMR voluntary activity thermogenesis of food 1 Resting Metabolic Rate basic energyburning rate to maintain basic bodHytunc ons explains 6070 of total energy expenditure TEE decreases with age loss of muscle lean mass is prime determinant of RMR decreases with energy restriction increases with stress may vary among people of same age size sex Page 8 of 19 2 Activity thermogenesis energy expended in voluntary activity normally 1530 of energy expenditure most variable component all activity counts Nonexercise activity thermogenesis NEAT is the energy expended for everything that is Msleeping eating or sports like exercise Includes work chores fingertapping fidgeting standing NEAT and a sedentary lifestyle may play a big role in weight management NEAT varies as much as 2000 kcalday between individuals To reverse obesity individuals should standambulate walkmove about for 25 hrsday 3 Dietary thermogenesisthermic effect of food TEF energy expended to digest metabolize amp store food 10 of energy expenditure rise of metabolic rate above basal level after eating measured as the loss of heatcreated during intermediary metabolism use amp formation of adenosine triphosphate ATP Regulation of Body Weight Energy Intake shortterm amp longterm regulation of body weight shortterm regulation controls factors affecting hunger appetite amp satiety GI hormones ex ghrelin cholecystokinin Gastric nerves fire during hyperextension to signal satiety to the brain 39 physical triggers for hunger are much stronger that those for satiety and it iS easier to override the signals for satiety Page 9 of 19 longterm regulation involves feedback mechanism from adipocytokins gt Adipose tissue stores triglycerides but can also act like an endocrine organ adipocytes fat cells can secrete hormones called adipoctokins or adipokines chemical messengers that may have protective effect like Adiponectin or be nonprotective eg be pro inflammatory gtgt adipocytokins or adipokines are proteins released from the adipose cells into the bloodstream that act as signaling molecules eg adiponectin leptin gtgt Adiponectin a regulatory peptide hormone produced by adipose cells that modulates glucose regulation amp fatty acid catabolism Levels of this hormone are inversely correlated with BMI Plays a role in preventing metabolic disorders eg type2 diabetes amp obesity is protective Levels drop for up to 6 mos post gastric bypass surgery gtgt Lthin a regulatory hormone produced mainly by adipose cells that contributes to longterm fullness by sensing the body s overall energy stores Suppresses food intake in normal weight people Younger people are more responsive to adipocytokinsadipokine feedback Signals from Hormones Our hunger and satiety centers are localized in the hvpothalamus of the brain Regulatory hormones communicate with the hypothalamus to control a person s intake and weight Several regulatory neurotransmitters amp hormones determine satiety amp feeding activity Table 221 Regulatory Factors in Feeding amp Weight Management Krause 467 Influence dietary intake establish primary fat patterning maximal fat cell growth etc Page 10 of 19 Neurotransmitters that influence dietary intake are the target of pharmaceutical therapy eg Phentermine an appetite suppressant that stimulates the release of norepinephrine and dopamine The stomach communicates with the brain via the vagus nerve part of the autonomic nervous system that travels from the brain to the stomach When filled with foodliquid the stomach s stretch receptors send a message to the brain indicating satiety Neurotransmitters chemical substances that transmit nerve impulses across synapses gt How do the these neurotransmitters influence hungersatiety gtgt dopamine high levels suppress appetite deficiency of dopamine or dopamine receptors results in overeating Exercise may increase the release of dopamine amp increase of receptors gtgt norepinephrine high levels suppress appetite Page 11 of 19 gtgt serotonin a decrease in serotonin has been associated with an increase in appetite especially an appetite for carbohydrates gtgt neuropeptideY NPY an increase in NPY has been associated with an increase in appetite especially an appetite for carbohydrates NPY increases during food deprivation amp may be a factor leading to an increase in appetite after dieting gtgt endorphins neuropeptides that bind to opiate receptors in the brain eliciting an analgesic effect May be responsible for increased cravings for sweet highfat foods especially after food deprivation in obese or bulimic individuals gtgt How does corticotropinreleasing factor CRF affect appetite CRF is a powerful appetite suppressant secreted by the hypothalamus that overpowers appetite stimulating hormones amp neurotransmitters Produced in brain controls adrenocorticotropic hormone ACTH from the pituitary gland an anorexic agent Released during exercise levels increase with depression or starvation Summary chart Highincreased levels suppress Exercise may increase levels to Increased levels associated with Decreased levels associated with Appetite stimulant especially after appetite suppress appetite increased increased dieting gt appetite CHO gt appetite CHO gt Overeating Overeating Overeating dopamine dopamine neuropeptideY serotonin neuropeptideY gt levels of NPY NPY levels receptors increase during food deprivation norepinephrine exercise releases corticotropin a powerful appetite suppressant endorphins may gt cravings for sweet highfat foods especially after dieting Page 12 of 19 gtgt List hormones secreted from the gastrointestinal tract that travel through the blood to the hypothalamus to signal hunger amp satiety The ones discussed in the lecture gtgt Describe the role of each on hungersatiety Gut HormonesPepetides Role in signaling hungersatiety Cholecystokinin CCK Gut hormone released in small intestine in the presence of fats amp proteins reach the small intestine CCK receptors found in GI and brain 39 causes contraction of gallbladder to release bile stimulates pancreas to release enzymes so is important for digestion signals brain to inhibit food intake Signals satiety amp decrease food intake short term regulation of energy intake GLP1 amp GIP Gut hormones released from small intestine after food intake amp are lncretins so stimulate insulin secretion from pancreas Signa satiety amp decrease signal satiety amp decrease food intake food intake short term regulation of energy intake Ghrelin GutPeptide hormone secreted in the stomach Signals hunger to the brain Signas hunger Acts on hypothalamus to stimulate feeding Regulatory hormone that tells the brain when the stomach is empty h hn rhrmn t e u ge O 0 e prompting hunger pangs andadrop in metabolism short term regulation of energy intake Ghrelin levels are highest in lean peonle Ghrelin levels increase in people who are dieting making it Note the levels info low in difficult to maintain reduced weight obese people but increase obese person Ghrelin levels decrease after a meal goes on a diet Ghrelin levels are low In obese peonle amp decrease after RouxenY surprising gastric bypass surgeries Gastric bypass surgery reduces the stomach to the size of an egg and triggers a sharp drop in ghrelin levels which lessens hunger and oral intake There are many more eg gt30 neuropeptides secreted in GI track that stimulate hunger or gt30 Neuropeptides satiety via peristalsis direction of gastric emptying regulation of blood flow etc Page 13 of 19 Other Hormones Thyroid Insulin Leptin Thyroid How does T3 active thyroid hormone affect body composition Hormone gtgt Low levels of T3 active thyroid hormone lower adaptive thermogenesis amp may result in increased body weight Common symptoms of hypothyroidism underactive thyroid unintended weight gain feeling cold feeling lethargic Flip side hyperthyroid symptoms anxious fidgety has unintended weight loss Modify tissue responsiveness to neurotransmitters eg dopamine norepinephrine Page 14 of 19 Insulin Primary action is to stimulate glucose uptake by cells Response especially after eating carbo CHO Peptide hormone released from the pancreatic betacells of the islets of Langerhans in response to the rise of serum glucose from food intake mainly carbohydrate CHO Impaired insulin activity may lead to impaired thermogenesis rise of metabolic rate above basal level after eating Also gt glycogen synthesis storage of glucose in liver amp muscle cells in the form of glycogen gt fatty acid synthesis fat cells take up blood lipids amp convert to triglycerides lack of insulin causes the reverse lt proteolysis reduced protein degradation reduced lipolysis reduced breakdown of fat cell lipid stores gtgt What is glucostatic theory Debatable theory that excess insulin causes peripheral hypoglycemia which in turn is a potent stimulator of appetite spike in insulin gt drop in blood glucose gt perception of hunger Leads to vicious cycle Impairment of insulin signaling may reduce sympathetic nervous system SNS activity and thus reduce thermogenesis So Insulin resistance decreased SNS activity ltthermogenesis amp gtweight gtgt How does insulin affect fat storage Insulin promotes anabolic storage processes and inhibits catabolic breakdown ones It signals a quotfed statequot and instructs the body to store fuels for use later Insulin promotes uptake amp storage of glucose in muscle amp fat cells In fat cells the glucose is used to make fat Page 15 of 19 Lep n correlates with of body fat low levels may stimulate appetite long term regulation of energy intake an Adipocytokin hormone secreted from adipose tissue that informs the brain about the amount of adipose tissue in the body Contributes to longterm quness Leptin level correlates with percent of body fat rise amp fall with fat mass As fat cells enlarge they secrete more leptin In healthy normalweight people leptin increases satiety amp energy expenditure Obese people produce gt amounts of leptin due to fat mass so maybe they have quotleptin resistancequot possibly due to leptin s inability to reach the brain defect in bloodbrain barrier transport system or defect in leptin receptors in central nervous system CNS Mice experiment did not hold true for obese people Com re Increased Leptin levels decreased weidht in mice obob mice with genetic defect producing deficiency or absent levels of leptin are obese When injected with leptin mice food intake drops thermogenesis increases amp weight decreases Weight loss reduces leptin levels which seems to coincide with gt desire to eat may be involved with body fat mass regulation Rare genetic expression of a leptinleptin receptor deficiency results in massive spontaneous obesity that begins in early childhood Set Point Theory fat storage in nonobese adults appears to be regulated in a manner that preserves a specific body weight In both animals and humans deliberate efforts to starve or overfeed are followed by a rapid return to the original body weight a set point Obesity Genes With completion of Human Genome Project are being identified Gene mutations singlecell disorders that directly cause obesity are rare 40 known candidate genes are currently associated with obesity phenotypes eg FTO gene May increase person s susceptibility to obesity Page 16 of 19 Environmental Influences on Regulation of Body Weight Diet amp Activity evidence strongly suggests that diet amp activity have major influence on US obesity levels we have an obesogentic environment People eat more when offered a variety of choices SensorySpecific Satiety phenomenon Normally as foods are consumed they become less desirable Can lead to excess energy intake Overriding this is the all you can eat buffet in which the dinner reaches satiety for one food but has many choices for the next course Large portion sizes contribute to active overeating One fast food meal can exceed a person s energy needs for the entire day sleep patterns the hypothalamus which regulates satietyhunger also regulates circadian rhythms Sleep deprivation may trigger increase in hormones that promote excessive energy intake 39 exposure to viruses amp pathogens infeCtObeSitY 39 microbiome our normal large intestine bacteria 39 ambient temperatures 39 stress cortisol released under stress simulates insulin release to maintain blood glucose levels in the fight or flight response Thus appetite increases Cortisol levels are typically high in the early morning and low around midnight gtgt obesogens chemical compounds foreign to the bodythat disrupt normal metabolism eg bisphenol A amp phthalates found in plastics can migrate to foods stored in them Compare Pima Indians similar genetically living in 1 Mexico and 2 Arizona Study found ageadjusted prevalence of diabetes amp obesity higher in Arizona group May be due to westernized fast food etc amp more sedentary lifestyle of Indians living in Arizona Page 17 of 19 gtgt Review the tissue changes with caloric restriction amp weight loss gtgt In starvation substate utilization shifts Used first glycogen stores will be used up in about a day Next 10 days 812 of energy derived from endogenous protein muscle catabolism with the rest 8892 from breaking down fat stores gt10 days adaptation occurs and only 5 from endogenous protein sparing muscle and 95 of energy expenditure is from stored triglyceride gtgt During weight loss 1st 2 wks Resting Metabolic Rate RMR deLases by as much as 15 during first 2 weeks of weight loss RMR will rebound somewhat once a new stable weight is achieved gtgt What is the plateau effect The plateau effect occurs when weight loss results in 1 a decrease in lean mass with a subsequent decrease in Resting Metabolic Rate RMR 2 a decrease in Thermic Effect of Food TEF as food intake is restricted further reducing Total Energy Expenditure TEE 3 and less energy expenditure is required to move around 4 Eventually equilibrium of enerav intake and output is reached and weight loss stops or plateaus gtgt After weight loss A majority of patients who lose significant amounts of weight will regain that weight because of tissue changes resuming old preweight loss habits Page 18 of 19 Tissue Changes with Weight Loss Loss of muscle mass ie lower RMR After a lowcal diet hypocaloric diet tissues are highly responsive to nutrients enhancing the repletion of losses Hormonal changes following weight loss may persist for years Can lead to Weight Cycling yoyo dieting increasing the efficiency of weight gain with every cycle Yoyo dieting is correlated with health risks eg cardiac risks Page 19 of 19 Spath Study Guide for Module 4 Cardiovascular Disease amp Hypertension PPT Heart Failure This is 4 of 4 parts of Module 4 Part 1 Pathophysiology amp Assessment Part 2 Dietary Factors amp CVD gt Part 3 Heart Failure Part 4 Hypertension HTN LecturePPT SelfStudy Guide Krause Chapter 34 Medical Nutrition Therapy for Cardiovascular Disease gt Key Points definitions gtgt Key Pointdefinition is on SelfStudy Guide NEW gt Tricky Question Alert Contents Chart some key HF points Heart Failure Medical Nutrition Therapy MNT for Heart Failure HF Classes amp Stages Comparison Chart Key Nutrition Considerations for Heart Failure HF Patients ANDEAL amp DASHTLC amp AHA Guidelines Sodium Chart Salt amp Sodium Measurement Equivalents Chart Food Labeling Guide Fluid Energy Needs Assessment indirect calorimetry vs Predictive Equation Cardiac Cachexia Protein Micronutrients Page1 of 19 Heart Failure Chart About HF Medical Nutrition Therapy MNT Classification amp Stages HF aligns with lCD1O Diagnosis Codes for medical diagnoses Diseases of the heart can lead to HF ANDEAL strong evidence that MNT can reduce HF symptoms amp reduce hospitalizations Assessing HF patient s energy needs ANDEA specifies Indirect Calorimetry an accurate measure as best choice If IC is not possible ANDEA does NOT specify a predictive equation Class lIV based on symptoms amp ability to do physical activity Class 1 HF most mild Class 4 HF most severe HF condition in which the heart is weakened and has lost the ability to pump enough blood to the body39s tissues MNT guidelines often individualized for HF patients MNT for HF patient pulls from ANDEAL DASHTLC amp AHA ANDEAL EvidenceBased Nutrition Practice Guidelines for diet HF patients aligns with DASHTLC amp AHA Guidelines Like DashTLC recommends wellbalanced diet rich in vegetables fruits amp whole grains MUFA over SFAs AHA Guidelines on 2 servings of fatty fishweek may improve heart function blood oxygen levels amp exercise capacity in HF patients MNT will be tailored to how serious the HF is So sodium amp fluid restrictions will be more strict for Class 4 HF than for Class 1 HF HF symptoms include edema dyspnea shortness of breath amp fatigue Shortness of breath is the earliest symptom Sodium Typically 2gday or less but individualized level of sodium restriction will depend on the severity of HF Studies show direct correlation between excess dietary sodium and repeat hospitalizations for HF patients Stages AD based on structural heart disease with and without symptoms failure is NOT sudden silent disease can be asymptomatic phase Fluid Typically 2Lday but individualized restriction will depend on the severity of HF Fluids include foods that are liquid at room temperature Stage of HF determines medical amp pharmacologic therapy Page 2 of 19 Heart Failure Chart About HF Medical Nutrition Therapy MNT Classification amp Stages Most likely cause hypertension or atherosclerosis which make it harder for heart to pump blood and heart muscle weakens over time HF risk gt with age eg people who have HTN andor atherosclerosis over long period of time Incidence of HF in US has increased due to aging population Protein 1 Clinically stable depleted HF patients daily intake of at least 137 g proteinkg eg HF patients with loss of lean body mass due to Cardiac Cachexia may need more than 137 g 2 Normally nourished HF patients daily intake of 112 g proteinkg HF patients have gt need for protein as measured by negative nitrogen balance Heart may weaken on one or both sides systolic failure left ventricle can t pump well gt pulmonary edema left ventricle may hypertrophy enlarge in an effort to pump cardiac remodeling dystolic failure right ventricle can t pump well gt peripheral edema Micronutrients HF patients usually on diuretic medications which can lead to deficiencies in important micronutrients Ensure intakes to meet the DRls for Folate B6 and 312 Thiamine Magnesium Page 3 of 19 Heart Failure Chart About HF Medical Nutrition Therapy MNT Classification amp Stages About 1020 of HF patients will suffer from Cardiac Cachexia which may increase Resting Energy Needs REE resting energy expenditure Cardiac Cachexia unintentional severe weight loss caused by heart disease which may be masked by concomitant edema fluid retention Loss of Lean Body Mass LBM Weight loss may be masked by edema fluid retention If Indirect Calorimetry is not available and a predictive equation is used to measure energy needs may need to tweak equation to allow for increased energy needs Page 4 of 19 Heart Failure HF gtgt Heart Failure and Congestive Heart Failure are often used interchangeably but gtgt Heart Failure is the preferred term gt Heart Failure aligns with lCD10 Diagnosis Codes for medical diagnoses gtgt Heart Failure is a condition in which the heart is weakened and has lost the ability to pump enough blood to the body39s tissues gt the heart s main job The heart gradually weakens overtime gt failure is NOT sudden Can result from many things eg a mechanical defect Iike vane disease alcoholdrug abuse PreViOUS Mild myocardial infarctions MI heart attacks have not been fatal but some of the myocardiocytes cardiac muscle cells have been replaced with scar tissue so the heart loses its ability to pump blood as efficiently Most likely if a Person has hypertension or atherosclerosis amp the heart has been constantly pumping against that resistance for a long period of time then over time the heart muscle can weaken gt Most likely cause of Heart Failure HF Page 5 of 19 Heart Failure Krause Figure 3410 p 769 provides a good visual picture The Heart has two sides One or both sides may be weakened gt It is possible for one side to fail independently of the other Normally the left amp right ventricles are contracting together amp they are pumping blood out left ventricle pumps oxygenated blood out into systemic circulation right ventricle pumps deoxygenated blood up through the pulmonary circuit for gas exchange in the lungs gt Systolic Heart Failure Left V weakened but Right V is fine gt pulmonary edema If left ventricle can t pump blood sufficiently is weakened but the right ventricle is working fine then blood will back up in the lungs and cause pulmonary edema as the fluid leaks out through the capillaries gt left ventricle may hypertrophy enlarge in an effort to pump cardiac remodeling gt Dystolic Heart Failure Right V is weakened but Left V is fine gt peripheral edema eg feet If right ventricle can t pump blood sufficiently is weakened but the left ventricle is working fine then fluid may build up in systemic circulation causing peripheral edema of the feet or ankles or maybe puffy fingers gt Edema is one symptom of Heart Failure Page 6 of 19 gt Edema abnormal fluid accumulation for any reason accumulation of interstitial fluid in the tissues definition 1 on slide definition 2 from lecture Reduced blood flow can stimulate the release of hormones aldosterone or vasopressin in compensation which can lead to even further fluid retention So in most cases a Heart Failure patient will be on diuretic medications increase urine Medical Nutrition Therapy MNT for Heart Failure gtgt Heart failure symptoms include edema dyspnea shortness of breath amp fatigue hallmarks of HF Rehospitalization is common for heart patients who are sometimes called frequent flyers Rehospitalized is usually needed due to problems with edema or breathing gt ANampD EAL Goals of MNT for Heart Failure Reduce the workload of the heart Decrease edema Decrease fatigue Decrease dyspnea shortness of breath usually the first symptom Reduced hospitalizations Maintain quality of life Academy of Nutrition and Dietetics Evidence Analysis Library gt Heart Failure EvidenceBased Nutrition Practice Guidelines httpwwwandealorgtoloiccfmcat2800 MNT and Heart Failure Referral to a registered dietitian for Medical Nutrition Therapy MNT is recommended whenever an individual has heart failure A planned initial visit lasting at least 45 minutes and at least one to three planned followup visits at least 30 minute each can lead to improved dietary pattern and quality of life Page 7 of 19 and decreases in edema and fatigue Along with optimal pharmacological management MNT may also reduce hospitalizations gt According to the EAL there is strong evidence that MNT can reduce those symptoms and reduce hospitalizations Classifications and Stages of Heart Failure HF Physicians diagnosis Heart Failure in Classes amp Stages depending on the structural damage to the heart itself amp how bad the symptoms are and how they impact daily activities gt Classifications to IV based on symptoms and ability to do physical activity gt Stages A B C D based on structural heart disease with and without symptoms gt Stage of HF determines medical amp pharmacologic therapy Krause chapter 34 Table 347 on page 770 Nice description of Heart Failure classifications Don t need to memorize table but know gtgt Class 1 HF most mild gtgt Class 4 HF most severe gtgt MNT will be tailored to how serious the Heart Failure is So sodium amp fluid restrictions will be more strict for Class 4 HF than for Class 1 HF Comparison Chart on next page Page 8 of 19 Classification Class of HF based on symptoms amp ability to do physical activity Goes from low to high Stages of HF based on structural heart disease with and without symptoms determines medical amp pharmacologic therapy Goes from low to high Class 1 most mild no undue symptoms associated with ordinary activity no limitation of physical activity Stage A at high risk for HF but without structural heart disease or symptoms of HF Class 2 slight limitation of physical activity patient comfortable at rest Stage B structural heart disease but no symptoms of HF Class 3 marked limitation of physical activity patient comfortable at rest Stage C structural heart disease with prior or current symptoms of HF Class 4 most severe symptoms of cardiac insufficiency or chest pain at rest inability to carry out physical activity without discomfort Stage D Refractory difficult to treat HF requiring special interventions Page 9 of 19 Key Nutrition Considerations for Heart Failure HF gt Academy of Nutrition and Dietetics Evidence Analysis Library Heart Failure EvidenceBased Nutrition Practice Guidelines Sodium Likely Restricted to address edema Typically Zgday or less but individualized Fluid Likely Restricted to address edema Typically 2Lday but individualized Energy and Protein high quality protein eg lean meats lowfat dairy Micronutrients Adequate intake of B6 B12 folate thiamine and magnesium Alcohol If not contraindicated ie if not related to the etiology cause of HF eg if alcoholic cardiomyopathy need to avoid alcohol maximum of 1 drink per day for women and 2 drinks per day for men may need to education patients on what is considered a drink ANDEAL Guidelines align with some DASH TLC recommendations AHA Guidelines recommendation on fatty fish benefits HF patients gtgt like DASH TLC diets recommends wellbalanced diet rich in vegetables fruits amp whole grains picking amp choosing MUFA eg olive oil over SFAs gtgt AHA Guidelines recommends 2 servings of fatty fishweek benefits especially for HF patients supported by one recent study that found that Omega3 fatty acids in the diet may improve heart function blood oxygen levels amp exercise capacity in heart failure patients Page 10 of 19 Key Nutrition Considerations for Heart Failure HF Sodium Intake and Heart Failure gtgt The level of sodium restriction will depend on the severity of the Heart Failure HF Although ANDEA general guideline of 2000 mg of sodium 2 g per day is a common diet order in most hospitals there is NO blanket recommendation for HF patients gtgt ANDEA General Guideline for Sodium For patients with heart failure sodium intake should be less than 2000 mg 2 g per day Source Academy of Nutrition and Dietetics Evidence Analysis Library Heart Failure EvidenceBased Nutrition Practice Guidelines gtgt Guideline may not be right for a specific patient HF patient may require even less sodium eg 1500 mg Consult the physician amp medical team about the severity of the heart failure Like sodium restriction for the management of Hypertension sodium restriction can be very important for the management of HF gt Several studies have shown a direct correlation between excess dietary sodium and repeat hospitalizations for HF because HF patients are so prone to fluid retention and edema Page 11 of 19 gt something Krause Sodium amp Salt Measurement Equivalents p 775 teaspoon to NaCl to Na Sodium in mEq amp mmol Sodium to Salt grams To convert Sodium is also measured in To convert sodium specific weight milliequivalent mEq to sodium chloride grams to mg of NaCL to salt multiply by sodium To convert mg of Na to mEq 254 equivalent divide by atomic weight of 23 multiply weight by 0393 Salt 1 teasp salt 6096 mg NaCL NaCl approx 6 g x 0393 2396 Sodium NaCL 6096 mg Na approx Chloride mg NaCl 2400 393 approx 40 sodium amp 60 chloride Sodium 1 teasp salt 2400 mg Na23 104 mEq Na Na 2400 mg Na approx 2400 approx 2400 Sodium 1 g Na 1000 mg Na23 43 mEq or Na 1000 mg Na mmol millimoles mmol amp milliequivalents mEq of sodium are the same Page 12 of 19 Food Labeling Guide for Sodium Box 3410 Krause 776 Food Labeling Guide for Sodium What it means gt Sodium free less than 5 mg of sodium per standard serving cannot contain any sodium chloride Very low sodium 35 mg or less of sodium per standard serving Low sodium 140 mg or less per standard serving gt Reduced sodium at least 25 less sodium per standard serving than in regular food gt Light in sodium 50 less sodium per standard serving than in regular food Unsalted without added salt no salt added No salt added during processing gt Lightly Salted 50 less added sodium than is normally added could still be high amount If less than 50 must say quotnot a lowsodium foodquot Page 13 of 19 Fluid Intake and Heart Failure gtgt As with sodium ANDEAL suggests a general guideline but RD will work with physician amp medical team to tailor recommendation for the individual gtgt ANDEAL General Guideline for Fluid For patients with heart failure fluid intake should be between 14 and 19 L 4864 oz per day depending on clinical symptoms ie edema fatigue shortness of breath gt Academy of Nutrition and Dietetics Evidence Analysis Library Heart Failure EvidenceBased Nutrition Practice Guidelines Fluids gt The goal is adequate fluids to maintain hydration while avoiding excess liquid that could lead to a volume overload Fluid management gt Generally capped at 64 oz per day Individualized recommendations if tighter fluid restriction is indicated fluid intake depends on symptoms of fatigue edema shortness of breath Page 14 of 19 If fluid restriction is indicatedtranslate to a patientfriendly ounces amp cups patients usually don t think in terms of mL Translate mL to ounces and cups gt 30mL 1 ounce Consider foods that are liquid at room temperature gt all foods liquid at room temperature count toward daily fluids Water including water with meds milk juice coffee tea etc Ice cream sherbet frozen yogurt popsicles gelatin soups ice Energy Needs in Heart Failure It can be tricky to assess energy needs in HF patients Indirect Calorimetry accurate vs Predictive Equations ANDEA Guideline In assessing energy needs for patients with heart failure the majority of studies indicate that gtgt use of indirect calorimetry best determines energy needs gtgt When indirect calorimetry is not possible consider starting with usual predictive equations and adjusting for increased catabolic state gt Academy of Nutrition and Dietetics Evidence Analysis Library Heart Failure EvidenceBased Nutrition Practice Guidelines gtgt Gold Standard according to studies indirect calorimetry accurate measurement as opposed to predictive not always an option not always feasible time consuming to do gtgt The ANDEA does NOT specify one particular predictive equation for energy needs but it does state that we may have to adjust equation for increased catabolic state Page 15 of 19 gtgt Tricky question alert ANDEA specifies Indirect Calorimetry an accurate measure as the best choice If IC is not possible ANDEA does NOT specify a predictive equation Energy Needs in HF continued ANDEA states in energy intake guidelines for HF patients we may have to adjust predictive equation for increased catabolic state gtgt What does this mean About 1020 of HF patients will suffer from Cardiac Cachexia amp with Cardiac Cachexia Resting Energy Needs REE resting energy expenditure may be increased gtgt Cardiac Cachexia unintentional severe weight loss caused by heart disease which may be masked by concomitant edema fluid retention gt Cardiac Cachexia similar to other cachexia states is characterized by unintentional weight loss gt LBM loss loss of lean body mass driven by increased circulating proinflammatory cytokines hypermetabolism gt So with Cardiac Cachexia Resting Energy Needs may be increased This can be difficult Several factors can contribute to compromised intake in HF patients dyspnea shortness of breath with eating Page 16 of 19 fatigue sense of taste amp smell tends to decrease with age medications low sodium diet salt can enhance the flavor of food Recommendations for patient to do gt Daily weights weigh to monitor edema amp unintended weight loss Each morning after voiding but before eating Wear minimal clothing when weighing Keep a written log of daily weights gt Daily written weight log may be best way to identify gt dry weight what person weighs when not retaining water weight without edema unintended weight loss amp fluid build up edema gt Small frequent meals 1 HF patient may find it tiring to eat amp breath at the same time amp become fatigued 2 with large meals a person may have abdominal distention that pushes up on the diaphragm amp makes the dyspnea shortness of breath even worse Energy Needs in HF continued Protein Needs in Heart Failure gt RDA for most normally nourished adults is 08 g proteinkg day Compare with ANDEAL guidelines for HF patients In assessing protein needs for patients with heart failure gtgt clinically stable depleted HF patients should have a daily intake of at least 137 g proteinkg to limit effects of hypercatabolism Excessive metabolic breakdown of a specific substance or of body tissue in general leading to weight loss and wasting gt tricky question alert at least 1 37 g proteinkg so a depleted HF patient could need more protein than that Page 17 of 19 HF Patient with Cardiac Cachexia may require more protein in diet gt normally nourished HF patients should have a daily intake of 1 12 g proteinkg to preserve their actual body composition In lecture Prof rounds 112 closer to 11 g proteinkg gt Research indicates that HF patients have significantly higher protein needs than those without HF as measured by negative nitrogen balance Academy of Nutrition and Dietetics Evidence Analysis Library Heart Failure EvidenceBased Nutrition Practice Guidelines Energy Needs in HF continued Micronutrients and Heart Failure Most HF patients will be on diuretic medications increase urine to help them get rid of excess sodium amp fluid which may lead to some deficiencies Ensure intakes to meet the DRls for Folate B6 and 312 Thiamine Magnesium Page 18 of 19 gt Compare ANDEAL guidelines do NOT state an evidence base for supplementation of these nutrients above the DRls but we want to encourage intake to meet the DRIs for those micronutrients gt Academy of Nutrition and Dietetics Evidence Analysis Library Heart Failure EvidenceBased Nutrition Practice Guidelines Krause p 776 Caffeine Studies indicate that moderate intake of coffee or tea may reduce CHD deaths amp may reduce heart rhythm disturbances Also antioxidant effects may be beneficial Page 19 of 19 Spath Study Guide for Module 4 Cardiovascular Disease amp Hypertension Part 4 Hypertension HTN Revised 62115 This is 4 of 4 parts of Module 4 Part 1 Pathophysiology amp Assessment Part 2 Dietary Factors amp CVD Part 3 Heart Failure Part 4 Hypertension HTN LecturePPT SelfStudy Guide Krause Chapter 34 Medical Nutrition Therapy for Cardiovascular Disease gt Key Points definitions gtgt Key Pointdefinition is on SelfStudy Guide gt Tricky Question Alert Contents Hypertension HTN persistently high arterial blood pressure Silent killer Etiology EssentialPrimary HTN amp secondary HTN Risk Factors associated with essential HTN Classifications for Blood Pressure BP MEMORIZE Morbidity amp Mortality Possible consequences of uncontrolled HTN Physiology Cardiac Cycle Cardiac Output Blood Pressure Vascular System Blood Pressure Measurement sphygmomanometer systolic and diastolic BP cardiac output amp peripheral resistance Major Regulators of Blood Pressure Nervous Systems Autonomic NS sympathetic NS amp parasympathetic NS Kidney ReninAngiotensin system Memorize pathway Page 1 of 40 Vasopressin Contents continue on next page Contents continued Other Factors Influencing Blood Pressure Nicotine Caffeine Sodium Obesity Atherosclerosis Chronically elevated BP HTN harms the body silent killer Intervention amp Management of HTN Longterm Goal Lifestyle Modification Other than diet Diet Modification Nutrition Therapy Sodium Restriction Sodium Restriction Recommendations Dietary Guidelines lOM Academy EAL Educating the HTN Patient about the ReducedSodium Diet Salt Substitutes Dietary patterns of the DASH Diet Role of K Ca and Mg in HTN management Avoid black licorice natural licorice is a natural hypertensive Pharmacologic Therapy ReninAngiotensin system ACE Inhibitors ARBs Loop Diuretics Thiazide Diuretics Potassiumsparing Diuretics Nutritionrelated side effects or interactions of those meds Page 2 of 40 HYPERTENSION HTN gt Hypertension is persistently high arterial blood pressure the force exerted per unit area on the walls of the arteries Epidemiology 67 million people 319 in the United States age 2 20 years old have high blood pressure HTN Of those people with HTN 776 were aware of their condition So about 14 of people with HTN are NOT aware that they have HTN gt HTN a silent killer because person may not experience symptoms or acclimate so that it feels normal to have high blood pressure It blood pressure really high may have some symptoms dizziness flushing headaches gt HTN occurrence 1 in 3 Americans are hypertensive 1 in 3 American adults have mehypertension Page 3 of 40 Rates of HTN by Ethnicity Gender Health disparity higher rates among African Americans than among other racial groups Male gtAA 430 EA 339 Mexican 278 American All 341 Female gtAA 457 EA 313 Mexican 289 American All 327 Prevalence of HTN by Geography Southeastern states tend to have the highest rates of HTN in US CDC 2014 Page 4 of 40 Etiology of HTN gtgt Contrast essential HTN and secondary HTN Most people with HTN have essential or primary HTN which means that HTN can t be pinpointed to a specific cause You may be able to identify several underlying risk factors It may be due to an interaction of a number of factors and there seems to be a genetic predisposition In contrast secondary HTN means that the HTN is directly linked to another disease It is a straightforward cause amp effect If you can control the disease HTN may go away Essential or Primary HTN 9095 of persons with HTN gt idiopathic unknown etiology but may be affected by lifestyle factors appears to have a strong genetic component ie genes have been identified which contribute to sodium balance inflammatory responses and other metabolic controls of bp Secondary HTN results from another condition often renal or endocrine disease may be curable gtgtWhat are some risk factors associated with essential HTN Page 5 of 40 Risks Factors for Essential HTN many are modifiable Heritability Smoking impairs endothelial relaxation and vasodilation Hyperinsulinemia relationship unclear Diet Tsodium SFA ipotassium magnesium calcium Stress Inactivity Obesity Classification of Blood Pressure gtgt MEMORIZE the classifications for BP andOR gt If either the Systolic top number OR the Diastolic bottom number is above range it would meet the criteria Page 6 of 40 So if a person had a blood pressure of 14278 that person would be classified as HTN stage 1 based on the systolic pressure of 142 gt Person would be given a based on 3 blood pressure readings Classificati SBP DBP mmHg Treatment on of BP mmHg Diastolic BP Systolic BP top bottom number number Normal lt 120 and lt 80 PreHTN 120139 and 8089 Diet amp Lifestyle changes or HTN 140159 and 9099 Diet amp Lifestyle changes stage I or antiHTN medication SBPsystolic blood pressure DBPdiastolic blood pressure Ref 7th Rpt of Nat Comm on Prevention Detection Eval amp Treatment of High Blood Pressure Treat BP according to classification Page 7 of 40 Morbidity amp Mortality Even if person feels fine amp has no symptoms doctor will want to get HTN under control because of the damage it is likely doing Uncontrolled HTN is like a ticking time bomb gtgtDescribe the possible consequences of uncontrolled HTN Chronically elevated BP is detrimental to many systems gtgt Can cause Heart failure HF myocardial infarction MI arrhythmias sudden cardiac death aneurysms Cerebrovascular accident stroke peripheral vascular disease and ischemic injury Kidney failure Vision problems from ruptured blood vessels Page 8 of 40 Physiology gt Cardiac Cycle mechanical events of one complete heartbeat 2 major phases Systole period of ventricular contraction amp ventricles pumping blood out Diastole period of ventricular relaxation amp ventricles are filling with blood gt Cardiac Output Cardiac Output Stroke Volume x Heart Rate CO SV X HR Stroke Volume volume of blood ejected with each heartbeat in other words the volume of blood pumped out from a ventricle during systole Heart rate beatsmin gt So cardiac output is the volume of blood flowing through each ventricle per minute Page 9 of 40 Blo BP I f X l x R II gt Stroke Volume x Heart Rate X peripheral resistance od Pressure cardiac output X peripheral resistance Cardiac Output BP volume of blood flowing through each ventricle per minute X peripheral resistance Page 10 of 40 Decreased vessel diameter increased resistance eg atherosclerosis gtgt Blood pressure measures hydrostatic pressure exerted on the walls of arteries Vascular System Blood from the ventricles gets pumped into the two big arteries pulmonary trunk amp aorta Arteries carry blood awayfrom the heart From the two big arteries smaller arterias branch arterias feed into tiny capillaries small thinwalled blood vessels those capillary beds branching network of capillaries that provide exchange of gases amp nutrients to the cells feed into Venules very small blood vessels which feed into veins which feed into bigger veins which eventually empty into the great veins Superior Vena Cava amp Pulmonary Vein which return blood back to the atria gt So blood pressure measurement is actually measuring the pressure in the arteries Page 1 1 of 40 Capillaries are only one cell layer thick gt All other blood vessels in the body have 3 layers 1 endothelium the innermost layer allows blood to flow through smoothly 2 smooth muscle middle layer innervated supplied with nerves by by sympathetic amp parasympathetic nerve fibers so blood can constrict or dilate 3 connective tissue outer layer Arteries are a lot thicker amp stronger than veins Vascular System continued Blood through pulmonary amp systemic circulation is dependent on pressure gt hydrostatic pressure is the pressure that moves blood through the blood vessels Pulmonary circulation is the portion of the cardiovascular system which carries deoxygenated blood away from the heart to the lungs and returns oxygenated oxygenrich blood back to the heart Systemic circulation is the part of the cardiovascular system which carries oxygenated blood away from the heart to the body and returns deoxygenated blood back to the heart Page 12 of 40 The pressure in arteries is much higher than in the veins if you cut a vein blood will trickle out slowly if you cut an artery blood will spurtgush out due to the higher pressure The laws of physics says that blood will always flow from a high pressure area to an area of lower pressure So when we talk about blood pressure we are talking about that hydrostatic pressure that moves the blood through the arteries gt Blood pressure hydrostatic pressure exerted on the walls of arteries Blood Pressure Measurement mm Hg Because hydrostatic pressure in the arteries rises and falls with each cardiac cycle the Systole amp the Diastole we can do an easy blood pressure measurement to determine the efficiency of circulation gtgt When we take a blood pressure measurement with a sphygmomanometer what are we actually measuring gtgt When we take a blood pressure measurement with a sphygmomanometer we are actually measuring hydrostatic pressure exerted on the walls of arteries during one cardiac Page 13 of 40 cycle which consists of the Systole phase and the Diastole phase We measure blood pressure with a sphygmomanometer or the blood pressure cuff and we report it as two numbers Systolic over Diastolic gtgt What does systolic and diastolic BP represent gtgt Systolic Blood Pressure is the hydrostatic pressure in arteries when the ventricles contract during systole gtgt Diastolic Blood Pressure is the hydrostatic pressure in arteries when the ventricles relax during diastole gt Blood Pressure is reported as millimeters of mercury because it was initially determined as the force that could support a column of mercury So you place the sphygmomanometer or the blood pressure cuff around the upper arm of the person and inflate it until blood flow through the brachial artery ceases Then deflate the cuff and listen with a stethoscope When the pressure of blood is greater than the pressure in the cuff the you would hear the first sounds and that corresponds to systolic pressure When the sounds disappear and blood is flowing freely that would be the diastolic pressure Blood Pressure Measurement mm Hg continued gtgt BP cardiac output x peripheral resistance What is cardiac output What is peripheral resistance gtgt Blood pressure in the arteries is dependent upon two factors 1 Cardiac output volume of blood flowing through each ventricle per minute Stroke Volume x Heart Rate Page 14 of 40 2 Peripheral resistance resistance the blood encounters as it flows through the vessels So anything that influences cardiac output or peripheral resistance through the arteries is going to influence blood pressure Physiology Major regulators of Blood Pressure gtgt Describe the normal physiological regulators of BP including the roles of gtgt Autonomic nervous system sympathetic amp parasympathetic divisions gtgt The reninangiotensin system know this pathway well We said that the smooth muscle layer middle layer of the arteries is innervated supplied with nerves by by sympathetic amp parasympathetic nerve fibers of the autonomic nervous system so blood can constrict or dilate The autonomic nervous system controls involuntary actions of the smooth muscles the heart and the glands Physiology Major regulators of Blood Pressure gtgt Nervous systems Autonomic Nervous System has 2 big divisions Page 15 of 40 1 gtgt Sympathetic NS epinephrine amp norepineprhine increase heart rate so increase BP the fight or flight nervous system in a sympathetic response epinephrine amp norepineprhine release increasing heart rate amp BP amp constrict blood vessels to gut so more blood flows to skeletal muscles Type A personaIities may be more prone to sympathetic responses Some people experience a white coat syndrome when visiting the doctor They get so nervous that is actually induces a sympathetic response that raises BP 2 gtgt Parasympathetic NS decreases heart rate through vagus nerve and so causes BP to decline the rest amp digest nervous system increases intestinal amp glandular secretions and slows heart rate through actions of the venus nerve Person practicing meditation may invoke the parasympathetic response which is more likely to lower BP Physiology Major regulators of Blood Pressure Page 16 of 40 gtgt Kidney BeninAngiotensin System KNOW PATHWAY WELL Read with the diagram on the next page 1 Drop stimulates release of Benin from the Kidneys The RA system kicks in when there is a drop in 1 serum sodium 2 plasma volume or 3 arterial blood pressure BP which stimulates the release of renin from the kidneys 2 Renin acting as an enzyme converts angiotensinogen to Angiotensin l 3 ACE angiotensin converting enzyme converts Angiotensin l to its active form of Angiotensin II 4 Angiotensin II 1 causes blood vessels to constrict 2 stimulates adrenal cortex to secrete aldosterone which causes Na and Cl reabsorption in kidneys resulting in water retention increased blood volume amp increased blood pressure BP Pathway Summary i serum sodium i plasma volume or i arterial BP stimulates release of renin from the kidneys Renin catalyzes conversion of angiotensinogen to Angiotensin Angiotensm I is converted to its active form of Angiotensin II by ACE angiotensin converting enzyme Angiotensin II Causes blood vessels to constrict Causes the adrenal cortex to secrete aldosterone which causes Na and Cl reabsorption in kidneys resulting in water retention and T blood volume and T blood pressure BP Page 17 of 40 gtgt MEMORIZE ReninAngiotensin System Kidney PATHWAY a 1 ma kd T It ratan y Almat mnaa HWI E EEH II ngi tamEiHIv Waning Enzyme Angima ainll Page 18 of 40 Physiology Major regulators of Blood Pressure continued gtgt Vasopressin aka antidiuretic hormoneADH A drop in blood pressure or a drop in blood volume associated with a water deficit in the body would signal the release of Vasopressin from the posterior pituitary gland Vasopressin causes vasoconstriction amp retention of water by the kidneys which increases blood volume amp blood pressure BP Summary Vasopressin is released from the posterior pituitary gland when there is a water deficifin the body ie l BP Causes vasoconstriction and retention of water by the kidneys gt increasing blood volume and BP Physiology Other Factors Influencing Blood Pressure Nicotine transiently briefly increases BP Caffeine transiently briefly increases BP Sodium Intake can have a big effect on BP especially for some people Obesity increases BP if heart has to work harder to pump blood to adipose ssue Atherosclerosis increases peripheral resistance in the arteries which increases BP Vicious cycle increased BP injures endothelial walls of arteries amp worsens atherosclerosis which increases BP If the heart is constantly having to pump against chronically elevated peripheral resistance Page 19 of 40 that can weaken heart muscle and lead to heart failure HF Ml or lschemic stroke due to blood clot Morbidity amp Mortality Chronically elevated BP is detrimental to many systems a silent killer Can cause Heart failure HF myocardial infarction MI arrhythmias sudden cardiac death aneurysms Cerebrovascular accident stroke peripheral vascular disease and ischemic injury Kidney failure Vision problems from ruptured blood vessels Aneurysms gt Uncontrolled Hypertension HTN can lead to an aneurysm a weakened artery wall A weakened artery can balloon out and potentially rupture gt If the blood vessel ruptures in the brain that could cause a Hemorrhagic stroke Slide 1700 shows picture of an abdominal aortic aneurysm Kidney Failure Think about the intricate blood supply through the kidneys and the tiny blood vessels in the kidney nephrons filtering units of the kidney Page 20 of 40 gt Uncontrolled HTN is one of the leading causes of kidney failure Vision We have a very delicate vasculature blood vessels that supplies the eyes gt Uncontrolled HTN retinopathy disease of the retina that results in impairment or loss of vision Intervention amp Management of HTN gt MNT is a science amp an art Keep in mind that RDs treat the patient and not just the numbers That is why MNT is a science amp an art RDs will always look at the lab numbers will always look at things like blood pressure but will treat in the context of the entire clinical picture So the goal is NOT necessarily just about getting the blood pressure within normal range just so we can say it is normal gt The GOAL is to reduce the morbidity amp mortality that is associated with HTN gt Longterm MNT GOAL Reduce morbidity amp mortality from stroke heart disease and renal disease For children prevent adoption of risky lifestyle factors including wt gain increased salt intake sedentary habits Lifestyle Changes Cornerstone of prevention amp management for HTN even if someone is on HTN medications Page 21 of 40 MNT encompasses a comprehensive approach to lifestyle modifications diet being cornerstone in that along with pharmacotherapy therapy using pharmaceutical drugs It a person is overweight or obese even a 510 weight reduction can have a dramatic effect on lowering blood pressure Intervention amp Management of HTN continued gtgt HTN management includes a comprehensive lifestyle approach What are some of the components in addition to diet Lifestyle modification to manage HTN gtgt Physical activity 3060 mind 56 daysweek reduces BP and decreases relative workload of heart by improving cardiorespiratory fitness gtgt Smoking cessation benefits BP almost immediately gtgt Stress management decreases sympathetic nervous system activity Diet Modifications Nutrition Therapy to manage HTN Page 22 of 40 Sodium restriction is the cornerstone of dietary treatment for HTN gtgt ANDEAL American Heart Association AHA amp Institute of Medicine IOM all recommend sodium restriction for prevention amp management of HTN Recommendations are based on studies showing the positive relationship between dietary sodium and blood pressure ie as sodium goes up blood pressure goes up There are some inconsistencies in research results primarily regarding magnitude of effect Studies in both animal models amp humans Diet Modification Nutrition Therapy to manage HTN continued gt Clinical Trials Support Sodium Restriction and Weight Loss DO NOT HAVE TO KNOW DETAILS OF STUDIES TONE Trial of Nonpharmacologic intervention in the Elderly 700 participantS aged 6080 yo Na restriction allowed the majority of patients to be removed from pharmacoloaic tX for HTN after 3 months TOHP Trial of Hypertension Prevention 4500 participants Na restriction with or without weight loss can reduce incidence ie initial onset of HTN by 20 Controversy over Sodium Restriction Recommendations When the US Dept of Health amp Human Services came out with the Dietary Guidelines for Americans there was great debate over what the recommended level of sodium intake should be Part of that controversy stems from the observation that some people are more saltsensitive and their bodies retain sodium more easily leading to fluid retention and HTN Page 23 of 40 Sodium may not have as dramatic an effect on blood pressure for people who are not saltsensitive and who have healthy kidneys So this may be an area where nutrigenomics will help us in the future to pinpoint who is more saltsensitive and who would best benefit from sodium restriction in the diet Sodium restriction to healthful levels is suggested to benefit blood pressure across the population regardless of the presence of salt sensitivity gt Salt sensitivity is genetic and will require a more aggressive salt restriction A large portion of the US population appears to be somewhat saltsensitive so the Dietary Guidelines recommend that we ALL limit our sodium intake gt Since we do not yet have practical methods to identify a saltsensitive person it makes sense for the population in general to limit sodium intake gtgt Sodium restriction is recommended for HTN prevention and management What are the recommendations for sodium intake by the Dietary Guidelines IOM Academy EAL MEMORIZE THIS CHART Comparison Chart Most Americans Americans 51 Persons with of Americans 50 and and older or HTN who are Sodium Intake younger African not meeting Na American or treatment goal Recommendations those with with 2300 diabetes mgday sodium hypertension or chronic kidney disease Page 24 of 40 Dietary 2300 1500 Guidelines for mgday mgday Americans US Dept of Health amp Human Services Institute of 1500 Medicine IOM mgday issues the Dietary Reference Intakes DRI Academy EAL 2300 1600 mgday and0r diet gt1 tsp table salt 2300mg Na gtgt Dietary Guidelines for Americans for Sodium US Dept of Health amp Human Services Recommended Na Intake Dietary Guidelines for Americans gt 2300 mgday for those 50 years and younger gt 1500 mgday for those 51 African American or those with diabetes hypertension or chronic kidney disease Another viewpoint Maillot M and Drewnowski A A Conflict Between Nutritionally Adequate Diets and Meeting the 2010 Dietary Guidelines for Sodium American Journal of Preventive Medicine February 2012 422 174179 Page 25 of 40 The authors argue that recommendations for sodium intake are too stringent They argue that it is not possible to adhere to 1500 mgday AND still meet the other dietary guidelines for Americans gt The American Heart Association s recommendations for sodium intake To lower blood pressure aim to eat no more than 2400 milligrams of sodium per day gt Reducing daily intake to 1500 mg is desirable because it can lower blood pressure even further Choose and prepare foods with little or no salt Nutrition Therapy Limit Sodium Page 26 of 40 Average Na intake for Americans age 2 and up is over 3000mgd mostly from processed foods gt Our bodies need only 180500 mg of sodium each day This less than 14 teaspoon EU UIIUIIH F l igi UIIUEU FLiZ ly l Average daily eedinm nteke age 2 and up 39IFeellen39aiielle Upper intake Le ee quot J y 213 iing Het em mended quotquot 53 Adequate Ilntake Leee t 5 E1 I i d L me me Hear meet daily gem it a emanatesneed T1 1mg eereaing eedinm intake eanidi prevent thaueande ef deatke annuallyf Beeaeee neariy eti ttl l tieatria eaeh year are attribute in l39iih bleed preeeure gtgt 2011 Institute of Medicine IOM DRI Recommendations for Na lt1500 mg Nad Page 27 of 40 No or very little salt added to cooking No added salt at table Avoidance of salty snacks amp processed foods Avoid foods with gt300 mg Naserving gt The IOM puts out the Dietary Reference Intakes DRI gtgt Academy of Nutrition amp Dietetics EAL Recommendations for Na Hypertension HTN Dietary Sodium HTN Sodium Intake Dietary sodium intake should be limited to no more than 2300 mg sodium per day Reduction of dietary sodium to recommended levels lowers systolic blood pressure by approximately 2 8 mmHg HTN Sodium lntake Monitoring and Evaluation If the patient demonstrates adherence to a 2300 mg sodium diet but has not achieved the treatment goal then the dietitian should recommend the DASH dietary pattern andor reduction in sodium to 1600 mg to further reduce blood pressure Page 28 of 40 So the consensus is that sodium restriction is indicated for HTN gtgt If you are instructing a pt on a reducedsodium diet what are some things you would include in your education gtgt The following are teaching tools to share with patients during an educational session to help them reduce sodium intake 1 tsp table salt 2300 mg Na Just one teaspoon of table salt is 2300 mg Na so maybe a good start is to take the salt shaker off the dining table A preference for saltiness is an acquired taste so as we reduce salt our tastes will adjust Also we may discover good flavors in food that have been hidden by salt Beware of hidden sodium The AHA notes that Americans get gt 34 of dietary sodium every day from packagedprocessed foods amp restaurant food Some foods with the highest sodium content Canned foods frozen entrees with gt600mg Na each frozen veggies with added sauces picklespickled foods cured meatsluncheon meats seasonings amp spice blends that include salt boullion cubes steak sauce marinades soy sauce 1 TBL of soy sauce has 1000 mg of sodium Added flavor without added salt Consider ways to enhance the flavor of food eg lemon juice This is especially important for older persons because the sense of taste amp smell diminishes with age gt Onions garlic spices rosemary basil citrus juices vinegars Page 29 of 40 Teaching Tools to Share with Patients continued gt Caution with salt substitutes Some antiHTN medications 99 thiazide diuretics amp loop diuretics can promote urinary loss of electrolytes including potassium so a person who is on these medications may need additional potassium in the diet But some other antiHTN medications like the potassiumsparing diuretics amp ACE inhibitor medications can promote potassium retention Table salt is sodium chloride Some salt substitutes in the grocery store are potassium chloride eg No Salt A person who is on a potassiumsparing or ACE Inhibitor medications would NOT want to use a salt substitute made of potassium chloride because those people are retaining more potassium already and that combination could lead to dangerous hyperkalemia Page 30 of 40 Teaching Tools to Share with Patients continued Include reading the food label as part of patient education gt The first place to look on a food label is the top line the number of servings per container Then ask yourself how much of this product do I usually eat at one time to determine if this is a good choice Sodium is listed in milligrams on food labels so patient can ignore the Daily Value which does not help much If someone wants to cap daily sodium intake at 2300 mg then they need to decide whether this is a good choice This food label for Chili with beans shows that it contains 2 servings at 1010 mg of sodium per serving If the patient were to eat the entire container this would come to over 2000 mg for just this one food so this may not be the best choice NUtf l Facts Tiaralam re 1 my Sirl1 cg Ecru 11M a l ai tf E galleries EEUZ Klimt hum Fa E if ally UEIHE Tiatall Fat an i EHEJEEEEE Fat Eli i 32 ihuestem r I sea2 7 HIE If Fig 1 fatal Earb hydrate 33g Fir Eastern Ejil39llg39i39 Ga A ngers rt Protein ESQ Teaching Tools to Share with Patients continued Don t be misled by sodium claims on food labels gt Food labels are standardized by the US government s National Labeling amp Education Act but some claims can be misleading The first three claims below may be pretty helpful but ReducedSodium can be confusing to consumers ReducedSodium just means that the food contains 25 less sodium than the regular version of that food So for the can of chili with beans that had 1010 mg of sodium per serving a reduced sodium version would still have more than 750 mg of sodium for serving Food Label Claim What it means Sodium or Saltfree lt 5 mg sodium per serving LOW SOdium 5 140mg sodium per serving Very IOW SOdium 5 35mg sodium per serving Page 32 of 40 gt DASH Diet Dietary Approaches to Stop Hypertension There are important dietary recommendations for HTN that extend beyond sodiumreduction The DASH diet has been shown to be very very effective in reducing blood pressure The DASH diet limits sodium but also relies on T minerals T fiber amp lower fat It is not your typical lowsodium diet gt The DASH Diet is considered the ideal diet for most adults But it is not for everyone The DASH diet would NOT BE ADVISABLE for someone with end stage renal disease because it is rich in potassium and someone with kidney failure would have a difficult time regulating potassium gt The DASH diet for preventing amp treating HTN is endorsed by the ANDEAL AHA National Heart Lung amp Blood Institute The DASH Diet started as a research study back in the 1990s The study results repeatedly showed that a diet rich in fruits vegetables whole grains lowfat dairy emphasizing nuts amp legumes moderating calories amp sugar amp added fats would significantly reduce blood pressure gtgt Describe the dietary patterns of the DASH Diet Dietary Approaches to Stop Hypertension DASH dietary pattern is rich in fruits vegetables lowfat dairy and nuts low in sodium total Page 33 of 40 fat and saturated fat and adequate in calories for weight management The DASH Diet continued For a 2000 kcal diet 78 servings of whole grains 810 servings of fruits amp vegetables 23 servings of fatfree or lowfat dairy products No more than 6 oz of lean meat 12 1 serving of nutsseedslegumes 23 servings of fatsoils Sweets s5week Transition to this diet slowly to avoid gastric discomfort gtAcademy of Nutrition and Dietetics EAL Recommendations Hypertension HTN Dietary Approaches to Stop Hypertension DASH Dietary Pattern Individuals should adopt the Dietary Approaches to Stop Hypertension DASH dietary pattern which is rich in fruits vegetables lowfat dairy and nuts low in sodium total fat and saturated fat and adequate in calories for weight management The DASH dietary pattern reduces systolic blood pressure by 814 mmHg There is a strong evidence base that this is a favorable eating pattern for preventing amp treating HTN gt The DASH diet pattern would easily fit within the AHA Guidelines the TLC Diet or even the Mediterranean Diet Page 34 of 40 Nutrition Therapy for HTN Limit Alcohol It is a good idea to practice moderation with alcohol intake Intakes above the recommended amounts have been shown to transiently briefly increase blood pressure and chronic heavy intake over a long period of time is associated with chronic HTN HTN persisting for a long time or constantly recurring HTN risk increases in a dosedependent fashion as alcohol intake exceeds 2 drinksday for men 1 drinkday for women gt A drink 5 oz wine 12 oz beer 15 oz distilled spirits Nutrition Therapy for HTN Increase Dietary Sources of Specific Minerals Other minerals besides sodium have been shown to have important effects on blood pressure gtgt What is the role of K Ca and Mg in HTN management Potassium K Calcium Ca amp Magnesium Mg have been shown to be protective against HTN Potassium has a natriuretic effect promotes excretion of sodium in urine inhibits renin release amp relaxes smooth muscle lining of arterioles The mechanisms of the protective effects of Calcium amp Magnesium are not as well understood but intake of Page 35 of 40 foods rich in Calcium amp Magnesium have shown inverse associations with blood pressure gt The DASH diet not only is low in sodium but it is rich in K Ca amp Mg This may explain why DASH is so effective in preventingtreating HTN Potassium K Calcium Ca amp Magnesium Mg continued Potassium strong inverse relationship between intake and blood pressure DASH diet provides 46 9 potassiumday Has a natriuretic effect inhibits renin release relaxes smooth muscle lining of arterioles Calcium DASH diets provided 3 cups lowfat dairy productsday Specific intake recommendations beyond the DRI have not been established for HTN Magnesium DASH diet also high in Mg similar inverse relationship with BP as K A note on KCaMg gt Food First The effects of these minerals on BP as demonstrated by the DASH studies were a result of dietary patterns not a result of mineral intake from supplements So eat foods rich in KCaMg It is also important that there may be an important synergy with other aspects of DASH such as Na restriction exercise low saturated fat and high fiber gtgtWhy would someone who is hypertensive want to avoid black Hco ce Page 36 of 40 gtgt Avoid natural licorice a natural hypertensive Hypertensive causing high blood pressure Pharmacologic Therapy If a person is diagnosed with stage 1 HTN then that person will likely be prescribed an antiHTN medication major classes of BP meds listed below gt If lifestylediet modification does not produce results win 2 weeks consider short or longterm pharmacologic tx AngiotensinConverting Enzyme ACE Inhibitors Wider used for treating HTN prevent kidneys from retaining sodium in the water by deactivating AngiotensinConverting Enzyme the enzyme in the Renin Angiotensin System that converts inactive Angiotensin to its active form of Angiotensin II Angiotensm quot Receptor Blockers Antagonists ARBS also work on the BeninAngiotensin System They block the action of Angiotensin II at the receptors so they prevent the release of aldosterone BGtaBIOCKGI S Interact with beta receptors on the cells of the heart Normally when epinephrine attaches to beta receptors in the heart cells then that increases heart rate amp increases blood pressure but beta blockers will block that receptor action Page 37 of 40 CaChanne blOCkel S Slow the flow of calcium into smooth muscle cells of the heart Central adrenergic inhibitors Diuretics very common water pills the oldest amp least expensive class of drugs used to treat HTN They help kidneys eliminate sodium amp water from the body and in the process they lower blood pressure Loop diuretics act on the loop of Henle in the kidneys They help kidneys eliminate sodium amp water from the body and in the process they lower blood pressure They permits the excretion of potassium Thiazide diuretics They work in the kidney to help kidneys eliminate sodium amp water from the body and in the process they lower blood pressure They permits the excretion of potassium Potassiumsparing diuretics They help kidneys eliminate sodium amp water from the body and in the process they lower blood pressure gt They promote the RETENTION of potassium Typically need to monitor Na K supplement or restrict Page 38 of 40 gtgtDescribe the action of each of the following medications for HTN gtgtWhat are the nutritionrelated side effectsinteractions of those meds gtgtACE Inhibitors ACE Inhibitors prevent kidneys from retaining sodium in the water by deactivating AngiotensinConverting Enzyme the enzyme in the Renin Angiotensin System that converts inactive Angiotensin I to its active form of Angiotensin II gt Increases potassium retention by the kidneys May need to restrict potassium intake Avoid salt substitutes that are potassium chloride gtgtARBs Angiotensin II Receptor Blockers ARBS work on the ReninAngiotensin System They block the action of Angiotensin II at the receptors so they prevent the release of aldosterone gt Increases potassium retention by the kidneys May need to restrict potassium intake Avoid salt substitutes that are potassium chloride gtgt Loop Diuretics Act on the loop of Henle in the kidneys They help kidneys eliminate sodium amp water from the body lowering blood pressure gt They permit the excretion of potassium May need to supplement dietary Potassium Page 39 of 40 gtgt Thiazide Diuretics They work in the kidney to help kidneys eliminate sodium amp water from the body lowering blood pressure gt They permit the excretion of potassium May need to supplement dietary Potassium gtgt Potassiumsparing Diuretics They help kidneys eliminate sodium amp water from the body lowering blood pressure gt They promote the RETENTION of potassium May need to restrict dietary Potassium Avoid salt substitutes that are potassium chloride RD Role in Pharmacologic Therapy Encourage compliance with drug therapy in order to consistently control blood pressure and minimize endorgan damage Assess foodmedication interactions eg need for Na restriction and K supplement with diuretics effect of alcohol side effects on appetite other side effects eg dry mouth constipation taste changes Page 40 of 40 Spath Study Guide for Module 4 Cardiovascular Disease amp Hypertension PART ONE Pathophysiology and Assessment This is 1 of 4 parts of Module 4 gt Part 1 Pathophysiology amp Assessment Part 2 Dietary Factors amp CVD Part 3 Heart Failure Part 4 Hypertension HTN LecturePPT SelfStudy Guide Krause Chapter 34 Medical Nutrition Therapy for Cardiovascular Disease gt Key Points definitions gtgt Key Pointdefinition is on SelfStudy Guide Contents Prevalence of CVD Diseases in CVD Cardiovascular system Pulmonary Circulation amp Systemic Circulation Ventricles amp Atria Arteries Veins gt quot LECTURE ADDS GOOD DES CRIPTI 0N CVD Physiology amp Etiology 39 Atherosclerosis Cerebrovascular Accident CVA Cerebrovascular Events CVD Assessment Standard fasting lipid panel TC LDL HDL TG 39 5 Classes of Lipoproteins 4 Major Classes 39 National Cholesterol Education Program N CEP values tested scope of testing Page 1 of 23 Other Biomarkers for CVD 39 Metabolic Syndrome aka Syndrome X Prevalence amp Mortality Heart disease is leading cause of death in the US CDC 2009 gt CVD is the 1 killer of men amp women in US 1 of every 29 deaths It is wrong to think that CVD is more prevalent in men gt Most CVDrelated deaths result from Myocardial Infarction Ml a heart attack CVD accounts for 752000 deaths annually CDC 2009 47 of cardiac deaths occur before emergency services or transport to a hospital In 2006 heart disease cost gt258 billion including health care services medications and lost productivity gt NIH 2007 2010 Prevalence of CVD is over 70 for men amp women ages 60 CVD affects all racial amp ethnic groups gtgtWhat types of disorders would be classified as quotcardiovascular disease quot CVD The Cardiovascular system is made up of the heart blood vessels amp the blood CVD includes the following interrelated diseases that often coexist Hypertension HTN Coronary Heart Disease CHD aka Coronary Artery Disease CADIschemic Heart Disease IHD Atherosclerosis Cerebrovascular Accident CVA aka Stroke Heart Failure ie Congestive Heart Failure Congenital Heart Disease and Rheumatic Heart Disease The majority of deaths from CVD relate to Coronary Artery Disease Page 2 of 23 A lot of what we know of CVD risk factors comes from the Framingham Heart Study but study continues today Many risk factors such as diet can be modified Framingham Heart Study 1948 and continuing 39 Started in Framingham Massachusetts in 1948 Epidemiological longitudinal prospective study setup to identify risk factors for CHD in a large group of participants who had not yet developed overt symptoms of CVD or suffered a heart attack or stroke 5209 men and women ages of 30 and 62 39 Came in every 2 years for physical exams lab tests and lifestyle questionnaires Added 5124 quot2nd generationquot participants in 1971 Now recruiting the 3rd generation Major Findings CVD risk was increased by Cigarette smoking 1960 0 Elevated cholesterol BP 1961 Obesity 1967 Menopause 1976 0 Elevated homocysteine 1990 CVD risk was decreased by Physical activity 1967 0 Elevated HDL 1988 Page 3 of 23 gtgt Be familiar with the basic anatomy amp physiology of the cardiovascular system Atria Ventricles Arteries Veins Systemic Circulation Pulmonary Circulation gtgtThe main function of the cardiovascular system is to move blood around the body Blood transports oxygen nutrients hormones amp other chemical messengers to all the body s tissues Blood carries oxygen for cellular respiration Blood carries carbon dioxide amp other waste products away from cells so they can be removed from the body The heart is divided into two halves Each half is divided into two chambers an atrium and a ventricle So we have a right atrium and a right ventricle and a left atrium and a left ventricle The atrium on each side empties into the ventricle on that side The main job of the heart is to pump blood Blood is pumped into 2 circuits gtgt in pulmonary circulation blood is pumped from the right ventricle to the lungs and then it comes back to the left atrium right ventricle gt lungs gt left atrium gtgt in systemic circulation blood is pumped from the left ventricle to all the tissues in the body except the lungs and comes back to the right atrium left ventricle gt body tissues except lungs gt right atrium 0 gtVentricles 2 chambers of the heart that pump blood out Page 4 of 23 o gtgtAtria 2 chambers of the heart that receive blood back In both the pulmonary amp systemic circulation systems gtgtArteries vessels that carry blood away from the heart gtgtVeins vessels that carry blood to the heart Cardiovascular System continued gtgt The blood circulation cycle So oxygenated blood leaves the left ventricle and passes through systemic circulation delivering oxygen to all of our cells Then deoxygenated blood is returned by venus circulation to the right atrium Where it passes to the right ventricle and is then pumped to the lungs pulmonary circulation Where it gets rid of the carbon dioxide and picks up oxygen That oxygenated blood comes back from the lungs to the left atrium Where it is passed to the left ventricle Where it can be pumped out again to all the tissues Shortened version of cycle oxygenated blood leaves left ventricle systemic circulation gt oxygen to cells deoxygenated blood via venus circulation gt right atrium gt right ventricle gt pumped to lungs dumps C02 picks up 0 amp oxygenated blood passes to left atrium pulmonary circulation gt passes to the left ventricle and cycle starts again gt Blood ow through these circuits is determined by pressure blood pressure Page 5 of 23 CVD Physiology amp Etiology gtgt Coronary Artery Disease CAD or Coronary Heart Disease or CHD and ischemic stroke can result from atherosclerosis The heart cells the cardiomyocytes receive oxygen amp nutrients from the coronary arteries that branch off from the aorta The aorta is the largest vessel in the body It transports oxygenated blood from the left ventricle of the heart If one of those arteries gets blocked with a clot it causes a heart attack aka MI aka coronary Usually this happens due to the process of atherosclerosis the build up of waxy plaque on the insides of blood vessels Atherosclerosis Greek deriv athero gruelpaste sclerosis hardness Progressive narrowing of the arterial tree can affect any artery in the body including arteries in the heart brain arms legs and pelvis i 395 blood ow Atherosclerosis is a silent disease Arterial changes begin in infancy and progress asymptomatically throughout adulthood if the person has risk factors is susceptible to arterial thrombosis or has a genetic susceptibility Atherosclerosis is a quotsilentquot disease because many individuals are asymptomatic until the first often fatal myocardial infarction heart attack Plaques atheromas build inside coronary arteries result from endothelial injury from sources such as these modifiable risk factors Page 6 of 23 T Cholesterol particularly LDL cholesterol 39 HyperglycemiaDM HTN Obesity 39 Cigarette smoking T Homocysteine Diet high in saturated fat Atherosclerosis Stages 1 Fatty Streak 2 Intermediate Lesions 3 Fibrous plaques 4 Advanced plaquesocclusion gtgt Describe the process of Atherosclerosis Prof recommends Krause description gtgt Atherogenesis the process leading to the development of atherosclerosis is a chronic local in ammatory response to risk factors such as lowdensity lipoprotein LDL cholesterol that leads to the development of plaques atheromas inside arteries 1 Inflammation stimulates a response by immune cells white blood cells called monocytes 2 Once in the tissue monocytes evolve into microphages that ingest oxidized cholesterol amp become foam cells and then fatty streaks in blood vessels 3 Intracellular microcalcification occurs forming deposits within the vascular smooth muscle cells of the surrounding muscular layer 4 A protective brin layer atheroma or plaque forms between the fatty deposits and the artery lining gtgt Know how Prof describes the process of atherosclerosis in her lecture 39 Low density lipoprotein LDL delivers cholesterol into cell walls The predominant theory is that LDL cholesterol in circulation can intact with free radicals amp reactive oxygen species and that LDL can become oxidized Key step in inflammatory process Page 7 of 23 Oxidized LDL accumulates at the endothelium of artery walls any artery e g coronary carotid causing fatty streaksf lt When immune cells white blood cells called monocytes are attracted to that site they develop into Macrophages Macrophages engulf the oxidized LDL fatty material and become foam cells Krause says macrophages become foam cells and then fatty streaks Smooth muscle cells at the site proliferate connective tissue forms at that site and the fatty streaks become intermediate lesions and then fibrous plaques Plaques can harden amp calcify and form scar tissue Blood ow becomes increasingly turbulent in that area which can cause platelets to rupture and form a clot Krause Atheromas can rupture or break off forming a thrombus activating the clotting system in the body which can result in blocking or restricted blood ow If oxidized LDL accumulates at the endothelium of artery walls in a person who is diabetic with uncontrolled blood sugar it is even worse because molecules of glucose can stick to other molecules in the lining of the vessel and that can amplify atherosclerosis WebMD video of process httpwwwwebmdc0mheartdiseasevideoatherosclerosis Video provides more detail than you need to know but includes the process as described above This url is not from the lecture Atheromas plaques Aneurysm Atheromas produce enzymes that cause the artery to enlarge over time to compensate for the narrowing caused by the plaque This change in shape amp size of the blood vessel may lead to an aneurysm An aneurysm is a weak area in the wall of a blood vessel that causes the blood vessel to bulge or balloon out gtThe clinical outcome of impaired arterial function due to arteriosclerosis depends on the location of the impairment So the effect of a clot depends on where it is located Page 8 of 23 Clot in Brain Ischemic stroke Transient ischemic attack Clot in Heart Myocardial infarction Angina pectoris chest pain stable unstable sudden death Clot in Lower body Intermittent claudication a pain in the leg caused by ischemia critical limb gangrene necrosis Clot can dislodge maybe becoming an embolism obstruction of a blood vessel traveling to the lung and leading to a pulmonary embolism blockage in one of the pulmonary arteries in your lungs gtgt Ischemia insufficient supply of blood delivery of insufficient oxygen to a part of the body e g hear brain that is due to obstruction of the in ow of arterial blood gtgt Contrast ischemic stroke and hemorrhagic stroke What are some risk factors for each gtgt What is a TIA Transient ischemic attack TIA is a quotministroke Cerebrovascular Accident CVA 0 gtgt Ischemic stroke caused by a blood clot occluding an artery that supplies the brain atherosclerosis in clot formation that blocks off an artery supplying blood to the brain 85 of strokes are this type Transient ischemic attack TIA quotmini strokequot caused by temporary decrease in supply of blood to the brain Last less than 5 minutes gtgt Hemorrhagic stroke occurs when a blood vessel to the brain ruptures uncontrolled HTN is a common cause Page 9 of 23 lschemic Stroke 85 of strokes Transcient ischemic attack TIA Hemorrhagic Stoke caused by a blood clot occluding an artery that supplies the brain caused by temporary decrease in supply of blood to the brain Last less than 5 minutes occurs when a blood vessel to the brain ruptures Risk Factors Risk Factors Risk Factors atherosclerosis atherosclerosis uncontrolled Hypertension HTN a frequent cause atherosclerosis gtgtBe able to define any terms we discussed in class eg ischemia angina bradycardia tachycardia Afib Vfib MI apolipoproteins next page etc Cardiac Events gtgt Ischemia insufficient supply of blood delivery of insufficient oxygen to a part of the body e g hear brain that is due to obstruction of the in ow of arterial blood gtgt angina chest pain or pressure caused by reduced blood ow to the heart Angina pectoris can be a preliminary sign of MI gtgt Cardiac Arrhythmia abnormal heart rate or rhythm Page 10 of 23 gtgt Bradycardia abnormally slow rate lt60 bpm ok in athletes but for non athletes could signal inadequate circulation gtgt Tachycardia abnormally rapid rate gt100 bpm if quotracing heartquot is prolonged could signal problems with the electric activity in your heart Measure heart rate by taking pulse on radial artery wrist or on carotid artery in your neck Electrical Activity of the Heart The S inoatrial node is the pacemaker of the heart which sends action potentials or nerve impulses across the two atria and they contract in unison That depolarizes the atrioventricular node that sends nerve impulses down the walls of the 2 ventricles so they contract in unison Whenever there is damage to the heart the coordination of contraction becomes dysregulated and you can get uncoordinated contractions or fibrillations gtgtFibrillation is a rapid uncoordinated contraction of the heart Automated external devices AED sometimes an electric shock can reset the contractions gtgtAfib Atrial fibrillation rapid irregular amp incomplete contractions of atria Can be mild Some people live with atrial fibrillation and may have an artificial pacemaker put in May lead to cardiac arrest gtgt Vfib ventricular fibrillation rapid irregular amp incomplete contractions of ventricles Much more serious amp can make heart a useless pump for supplying oxygen to the body May lead to cardiac arrest Cardiac Events continued gtgt MI Myocardial infarction MI quotheart attackquot due to occlusion of 1 or more coronary arteries A medical emergency CVD Assessment Page 1 1 of 23 Medical assessment of atherosclerosis includes use of angiogram or cardiac catheterization or MRI CT scan of arteries All of these procedures are expensive and some are very invasive The most basic amp the most common tool we have for assessing CVD risk is a blood draw for fasting lipids To be meaningful has to be fasting to eliminate the contribution of any food you recently ate Dyslipidemia or Hyperlipidemia refer to a lipid profile that increases the risk for CVD When we get a lipid panel we are actually measuring lipoproteins in the blood Lipids like triglycerides and cholesterol are not water soluble so they don39t travel well through the aqueous blood all by themselves they are carried as part of lipoprotein particles Lipoproteins consist of varying amounts of triglycerides cholesterol some phospholipid and protein gtgtWhat are lipoprotein particles gtgtLipopr0tein Particles A group of molecules consisting of both lipid and protein portions that are the principal way lipids are transported in the blood gtgtApolipoproteins The protein portions of lipoprotein particles They carry lipids in the blood CVD Assessment continued Lipoproteins Page 12 of 23 gtgt Describe the major classes of lipoprotein particles including Where each one comes from and What it does Lipoproteins are classi ed according to their density The ratio of fat to protein determines the density Particles with higher levels of protein are the most dense eg HDLs gtgtThere are 5 Classes of Lipoproteins C VLDL Intermediate IDL amp HDH gtgt 4 Major Classes of Lipoproteins C VLDL LDL HDL from low to high density 1 Chylomicrons Low density because they are almost all triglycerides 90 Largest particles carry dietary fat TG amp cholesterol from intestine to bloodstream Once in the bloodstream the TG within the Chylomicrons are hydrolyzed by lipoprotein lipase LPL on the endothelial cell surface in muscle and adipose tissue so that the free fatty acids can enter the cells When about 90 of the T G is hydrolyzed the Chylomicron particle is released back into the blood as a remnant The liver metabolizes these Chylomicron remnants but some remnants deliver cholesterol to the arterial wall and thus are considered atherogenic gtSo not only do we have fat amp cholesterol that we consume in our diet we also synthesize TG amp cholesterol endogenously from within our body mainly in the liver gt Chylomicrons are not generally specifically measured unless looking for a metabolic disorder Not usually reported as part of a routine cholesterol screen 2 Very low density lipoproteins VLDL Low density but not as low as Chylomicrons containing mostly T G along with some cholesterol amp phospholipid The TG and cholesterol that is made in the liver is packaged into VLDLs VLDL particles are sent out from the liver to deliver endogenous TG to cells As VLDLs particles unload TG to cells via lipoprotein lipase they are converted to intermediate density lipoproteins IDL and then to low density lipoproteins LDL Some of the remnants of VLDL are taken back up by the liver but over half 50 of the VLDL remnants become circulating LDL gt VLDL amp IDL not usually reported as part of a routine cholesterol screen 4 Major Classes of Lipoproteins continued Page 13 of 23 3 Low density lipoproteins LDL quotthe bad cholesterolquot when the cholesterol content of VLDL particles becomes greater than the content of TG we say they are LDL particles LDL particles consist mainly of cholesterol and their primary role is to transport cholesterol to cells and therefore positively correlate with T cholesterol LDL particles will bind to specific cell receptors on the cell surface and they are taken up by receptor mediated endocytosis High levels of LDL in particular have been associated with atherosclerosis amp CVD Called the quotbad cholesterol because LDL becomes oxidized and creates fatty streaks in artery walls 95 of protein in LDL is Apo B Strong predictor of CHD gtgt LDL may be our best measure of CVD health risk Interpreting levels of LDL lt 100 mgdL Optimal 100 129 mgdL Nearabove optimal 130 159 mgdL Borderline high risk 160 189 mgdL High risk gt 190 mgdL Very high T LDL related to diet amp obesity genetics aging DM low postmenopausal estroger progestins hypothyroid renal disease liver disease steroid drugs Diets high in SFA amp cholesterol gt T LDL makes it a prime target for diet tX Trans fatty acids gt T LDL and l HDL 4 Major Classes of Lipoproteins continued Page 14 of 23 4 High density lipoproteins HDL quotthe good cholesterolquot Most dense contains the most protein amp least lipid acts to remove cholesterol from blood amp tissues and return it to the liver where it can be reprocessed and excreted into bile salts Called the quotgood cholesterol because high levels of circulating HDL are associated with reduced risk of CHD gtThe protective mechanism of HDL is not fully understood The protein portion of HDL appears to have antiin ammatory amp antioxidant properties HDL also interacts with LDL and prevents LDL from becoming oxidized gtgt HDL levels are also a good measure of CVD health risk 39 Values gt60 mgdL are considered protective Values lt40 mgdL for men amp lt50 for women are considered a risk factor for CHD Factors that T HDL estrogen endogenous amp exogenous exercise wt loss moderate alcohol consumption Estrogen increases HDL levels so up until menopause women have fewer heart attacks than men Before menopause women have higher estrogen levels Factors that l HDL many factors are to some extent modifiable risk factors obesity inactivity cigarette smoking anabolic steroids high TG genetics Major Classes of Lipoprotein Chart by density lowest to highest density Page 15 of 23 Class of Lipoprotein Density the gt the fat the gt the density Other Chylomicrons Low Density 90 TG some Chylomicron remnants deliver cholesterol to the arterial wall and thus are considered atherogenic Very low density lipoproteins VLDL Intermediate IDL forms from catabolism of VLDL precursor to LDL Low Density not as low as Chylomicron 5565 TG sent from liver to deliver TG to cells when unloading TG to cells VLDL particles convert to intermediate density lipoprotein IDL then to LDL 50 of VLDL remnants become circulating LDL Low density Low Density lipoproteins LDL quotBad Cholesterolquot is strong predictor of CVD primary transporter of cholesterol to cells ApoB the primary apolipoprotein 90 in LDL indicates the number of potentially atherogenic LDL particles High density lipoproteins HDL quotGood Cholesterolquot is good predictor of CVD health Most Dense contains most protein acts to remove cholesterol ApoA1 the primary apolipoprotein in HDL reflects antiatherogenic HDL particles LDL amp HDL Comparison Chart LDL vs HDL Levels increase Levels in Body Levels decrease Low density increases related to lt 100 mgdL Optimal Diets low in lipoproteins diet amp obesity 100129 mgdL Nearabove optimal SFA amp cholesterol LDL genetics aging DM 130159 mgdL Borderline high risk low postmenopausal 160189 mgdL High risk quotBad estrogen gt 190 mgdL Very high Cholesterolquot progestins hypothyroid renal disease liver disease steroid drugs High density estrogen gt 60 mgdL considered protective obesity inactivity lipoproteins endogenous amp cigarette smoking HDL exogenous lt 40 mgdL for men amp anabolic steroids exercise wt loss lt 50 for women are considered a risk high TG genetics quotGood moderate alcohol factor for CHD Cholesterolquot consumption Page 16 of 23 gtgt The National Cholesterol Education Program N CEP a consensus group NCEP is an expert panel from the National Heart Lung amp Blood Institute the American Heart Association and NIH They recommend that 1 the llstandard lipid panel values are the values that should be tested and 2 everyone aged 20 amp older should be tested every 5 years more frequently if person is at risk Standard fasting lipoprotein profile cholesterol screen Total cholesterol LDL LDL C is calculated LDL TC HDL TGSgtXlt gtXltnote this formula is accurate only if TG lt400 HDL TG gt gt Chylomicrons VLDL amp IDL are NOT usually reported as part of a routine screen gtgt What are the components of a standard fasting lipid panel Be able to describe What each lab value measures TC LDL HDL TG Total Cholesterol Provides a picture of cholesterol contained in all of the lipoprotein particles LDL HDL TG It measures all fractions of lipoprotein but about 70 of the cholesterol comes from LDL fractions so a high total cholesterol like LDL is associated with CVD gtgtHow is LDLcholesterol calculated from other measures of a standard lipid panel LDL is a calculated value from other measures If total T G is skyhigh then that calculation is skewed gtgt Total Cholesterol does not provide full picture because high HDL is good TG measurement would include the TG rich lipoproteins e g Chylomicrons Chylomicron remnants VLDL If it is a fasted blood draw the Chylomicrons should be virtually absent or very few gtSo clinically T G levels is a measure of VLDLs and their IDL intermediate density remnants gt Chylomicrons amp VLDL not generally reported as part of a standard fasting lipid panel Page 17 of 23 Total Cholesterol is l a cheap amp easy assessment and 2 the first measure of risk amp strong predictor of CHD potential Total Cholesterol continued Factors related to T cholesterol age T with age genetics T SFA diet saturated fat trans fat anabolic steroids meds glucose intoleranceuncontrolled DM physical inactivity Interpreting Total Cholesterol Results for Adults American Heart Association gt gtEvery 1 reduction in total serum cholesterol predicts a 2 decrease in CHD incidence Interpreting Total Cholesterol Results for Adults according to the American Heart Assn Value mgdL Interpretation lt 200 Desirable 200 239 Borderline high 2 240 Hypercholesterolemia Page 18 of 23 Total Triglycerides part of routine fasted lipid panel TG reading includes Chylomicrons Chylomicron remnants VLDL amp IDL Highly variable postprandial after eating a meal values are pretty useless If not fasting the Chylomieron levels can be all over the place Best results with 2 fasting samples 1 week apart Inversely related to HDL gtgtcombination of T TG l HDL is better predictive of CVD risk than TG alone The National Cholesterol Education Program N CEP defines these classi cations Interpretation lt 150 mgdL Normal 150 199 mgdL Borderline high 200 499 mgdL High gt 500 mgdL Very highgtXlt associated with T risk of pancreatitis Factors contributing to T TG Lipoprotein lipase deficiency very rare genetic disorder Familial dyslipidemiagtXlt Obesity DM Hypothyroidism Renal disease Liver disease Estrogens Alcoholism Discussed 0n the next page Diets vegetarian l fat T refined CHO T cholesterol amp SFA gtXltDyslipidemia blood lipid profile that increases risk of developing arteriosclerosis amp typically shows T LDL and i HDL gtgtEstrogen can raise TG but they also raise HDL so there is a balance It is the consensus that normal estrogen levels before menopause are protective But there is disagreement over hormone replacement for heart health after menopause The evidence base for this is yet to be defined Page 19 of 23 One study the Women39s Health Initiative showed mild increased risk for CVD in women on hormone replacement therapy but other studies have found lower risk or no association Effects of diet on TG levels is interesting Diets vegetarian lfatT refined CHO T cholesterol amp SFA gtgtEven lowfat diets even vegetarian diets can possibly increase serum triglycerides TG if they are high in re ned carbohydrates simple sugars which can increase serum triglycerides by stimulating fatty acid biosynthesis in the liver 39 heavy alcohol intake can do the same thing Treatment for elevated TG Weight loss if appropriate Diet 39 reduce simple amp refined CHO add high fiber low glycemic index foods 39 less alcohol 0 reduce saturated fat SFA amp cholesterol in the diet Exercise Smoking cessation Optimize DM management Drug therapy gtgtKn0w the normal ranges for total cholesterol LDLC HDLC amp TG standard fasting lipid panel Normal Ranges Component Total Cholesterol lt 200 mgdL LDLC lt 100 mgdL HDL gt 60 mgdL Triglycerides TG lt 150 mgdL Page 20 of 23 gtgtAlternative serum biomarkers of CVD risk include ApoAl ApoB and CRP What does each lab value tell you There are other biomarkers in the blood that are associated with risk of CVD These are additional tests used to assess CVD risk The tests are a little more expensive and not as routine gtgtApolipoproteins are the protein portions of lipoprotein particles They carry lipids in the blood Alternative serum biomarkers of CVD risk gtgt ApoAl the primary apolipoprotein in HDL re ects anti atherogenic HDL particles The protein portion of HDL appears to have antiin ammatory amp antioxidant properties It helps remove cholesterol from artery walls and take it back to the liver High level is good gtgt ApoB the primary apolipoprotein in LDL indicates the number of potentially atherogenic LDL particles On a standard fasted lipid panel LDL is calculated The Apo B test is a direct measure of LDL High level is bad B is for Bad gtgt Creactive protein CRP a biomarker of in ammation high serum CRP is associated with increased risk of MI and stroke High levels higher risk There is a little controversy as to how predictive CRP is Blood Biomarker Level Assessment Key info As are good Bs amp Cs are bad ApoA1 High is good HDL helps remove Cholesterol from artery wall primary apolipoprotein in HDL Page 21 of 23 ApoB High is bad A direct measure of LDL primary apolipoprotein in LDL Creactive protein CRP High is bad gt risk of MI amp stroke biomarker of inflammation Risk factors tend to travel in packs in clusters gtgtDescribe how an individual would be diagnosed with Metabolic Syndrome aka Syndrome X gtgtMetabolic syndrome is present if a pt has 3 OR MORE of the following signs 39 Blood pressure equal to or higher than 13085 mmHg 39 Fasting blood glucose gt than 100 mgdL 39 Large waist circumference length around the waist Men gt 40 inches Women gt 35 inches 39 Low HDL cholesterol Men lt 40 mgdL Women lt 50 mgdL 39 Serum triglycerides gt 150 mgdL Page 22 of 23 Page 23 of 23 Spath Study Guide for DISEASES OF THE LIVER M81 gtgtBe familiar with the following major functions of the liver Functions of the Liver the Liver is the gatekeeper of metabolism Lots of blood flow through the liver gt Blood is supplied to the liver by the Hepatic artery that branches off from the aorta and by the Hepatic portal vein that brings blood to the liver from the stomach the small intestine the large intestine amp the spleen the Liver affects macronutrient amp micronutrient metabonsm the Liver filters wastes amp toxins so Liver disease can result in a waste amp toxin build up in the blood gtgtMajor Metabolic Functions of the Liver The Liver is integral to over 500 metabolic functions in the body Prof assumes that everyone in the class has taken Nutritional Biochemistry and is familiar with the major functions of the liver Because Liver plays so many roles in metabolism Liver disease presents some of the most complex cases for MNT gtgt Recognize how these metabolic pathways may be impaired in someone with chronic liver disease gtgt Glycogenesis gtgt Glycogenolysis gtgt Gluconeogenesis gtThe Liver plays a major role in CHO Metabolism Meheeaeehartdee glucose fructose amp galactose are byproducts of CHO metabolism Monosaccharides are absorbed into capillaries that lead to venules and then to veins that feed into the Hepatic portal vein gtThe Hepatic portal vein delivers the monosaccharides to the liver the Liver cells hepatocyctes convert galactose and most fructose to glucose What happens next to that glucose depends on what the body needs if ATP is needed that glucose can be metabolized through 3 pathways glycolysis Krebs cycle or the electrontransport chain to provide energy those 3 pathways take place in hepatocytes but the liver will also send out glucose into the bloodstream for uptake by other cells to use as energy too Glycogenesis Metabolism amp Storage takes place in the liver t3 the geheete 0t gthogen glucose is converted to its storage form of glycogen Glycogen is the storage form of glucose is stored in muscle and in the liver Glycogenolysis Taps into Storage as Body needs Releases into bloodstream for cells to use takes place in the liver breaks down the stored glycogen in the liver to glucose that can be used by the Liver cells or released by the Liver into the bloodstream for other cells to use Glycogen is stored in the Vet and the mUSCteS but It is glycogenolysis in the Iiverthat releases glucose into the bloodstream for other cells to use the Liver maintains blood glucose by this process Page 2 of 39 Gluconeogenesis Synthesis 90 takes place in the liver Also occurs in the kidneys is the PathWay that makes new glucose out of other substrates like lactic acid glycogenic amino acids and TCA cycle intermediates CHO Metabolism We eat CHO lt s digested lt s absorbed gtThe end products of CHO go first to the liver and that is why the Liver is the gateway of metabolism PRO Metabolism It is the same for end products of PRO digestion Amino acids are absorbed into capillaries gt venules gt veins gt Hepatic portal vein gt Liver gtThe Liver is the primary site of amino acid catabolism gtgt Know Transamination and oxidative deamination in amino acid catabolism steps in protein metabolism or breakdown Step 1 Transamination occurs when the amino group from the amino acid is transferred to a Keto acid usually alphaketoglutaric acid is catalyzed by transaminase enzymes enzymes are present in the Liver Step 2 Oxidative deamination is removal of that amino group is catalyzed by oxidase enzymes enzymes are present in the Liver Remaining carbon skeletons can be burned for energy converted to fat or converted to non essential amino acids Page 3 of 39 Excreted in urine gtgt Know Synthesis of nonessential amino acids this page amp next page know gtgt Albumin Synthesis in the Liver Made in the Liver Synthesis of nonessential amino acids occurs mainly in the liver 0 Synthesis in the liver of other important vital plasma proteins such as albumin transferrin RBP fibrinogen lipoproteins Synthesis of Albumin Albumin is the most abundant plasma protein in the body Albumin is made in the liver Albumin is important because it A binds to several minerals like calcium for their transport in the blood B helps maintain osmotic balance in the body If circulating albumin becomes too low excess leak from blood into interstitial space The combination of high pressure in the portal vein hypertension and low albumin leads to fluid accumulation in the peritoneum ascites Page 4 of 39 Ascites is often seen in patients with liver failure gtgt Know Synthesis in Liver of important plasma proteins continued transferrin retinol binding protein RBP fibrinogenprothrombinother clotting factors ipoproteins VLDL and HDL The following are made synthesized in the liver Transferrin transports iron in the blood Retinol Binding Protein RBP is important for transport amp metabolism of vitamin A FibrinogenProthrombin are blood clotting factors Liver disease could lead to defects in blood clotting Lipoproteins VLDL amp HDL triglycerides amp cholesterol are made in the liver and packaged into VLDL particles VLDL particles will deliver that triglyceride to all of the cells of the body HDL is also made in the liver HDL picks up excess cholesterol from the cells and tissues and takes it back to the liver for excretion in the bile Page 5 of 39 gtgt Know Synthesis of bile We also have synthesis of bile in the liver Bile is made in the liver The principal components of bile are cholesterol bile salts and a pigment called bilirubin know gtgt What is bilirubin Bilirubin is a component of bile and is the pigment that gives bile its color Bilirubin is the product of red blood cell breakdown Normally after red blood cell breakdown Bilirubin is passed on to the Liver and incorporated into bile Bile is then passed from the liver to the gallbladder and then secreted into the duodenum gtgt Describe how inadequate removal of bilirubin in bile can lead to jaundice Page 6 of 39 Jaundice yellow staining of the skin mucous membranes and the sclerae the whites of the eyes by abnormally high blood levels of the bile pigment bilirubin Jaundice can be a red flag for some sort of hemolytic disorder eg excessive red blood cell destruction liver damage or disease gallbladder disease obstructed biliary duct We have a system of ducts in the liver and these bile ducts will exit the bile and they increase in size and merge into the common bile duct Bile is stored in the gallbladder until it is needed to emulsify fat When bile is needed the gallbladder will contract and release bile to the duodenum Liver Functions continued gtgt Know Biosynthesis of fatty acids TG and cholesterol Cholesterol triglycerides amp phospholipids are also synthesized made in the liver Fatty acid biosynthesis can occur in some other cells as well eg the kidney the mammary glands but gt main site of fatty acid biosynthesis is in the liver gtgt Know Beta oxidation and formation of ketone bodies Lipid FAT Metabolism Fatty acids can be broken down to acetylCoA by Boxidation Boxidation takes place in most cell types not just hepatocytes liver cells Page 7 of 39 When the amount of acetylCoA produced by Boxidation exceeds the capacity of the citric acid cycle then that acetylCoA will be converted to ketone bodies in the liver gt So the synthesis of ketone bodies takes place primarily in the liver gtgt Know Conversion of betacarotene to active vitamin A retinol and activation hydroxylation of vitamin D to its active form The Liver is also a site of activation for some important vitamins AampD Conversion of provitamin A carotenoids to active i Vitamin A 39 I i Vitamin D to active 39 form 1 has to undergo 2 W hydroxylations to be activated the 1st one occurs in w the liver the 2nd one occurs in the kidneys Folate is converted to tetrahydrofolate in the liver Liver Functions continued know gtgt Know Storage of fatsoluble vitamins vitamin B12 and certain minerals Page 8 of 39 The Liver stores Fatsoluble vitamins ADEK Fe Zn Cu Copper Mg B12 gtgt Know Detoxification of many drugs amp potential toxins Detoxification is a critical function of the Liver gtgt Know Conversion of toxic ammonia to urea via the urea cycle Liver converts Ammonia to urea When amino acids are broken down by Oxidative deamination that removes an amino group which becomes ammonia or the ammonium ion Ammonia is very toxic to cells so we need to get rid of it We do that by the urea cycle which gt takes place exclusively in the liver gtgt Know Breakdown of ETOH The Liver also detoxes by metabolizing steroid hormones filtering amp removing bacteria amp potential toxinspoisons gt breaking down ethyl alcohol drinking alcohol amp many drugs medications know gtgt Be familiar with the most common lab tests to assess liver func on Page 9 of 39 You don t need to know any normal ranges but gt recognize what highlow values of each one could signify Alanine aminotransferase ALT and aspartate aminotransferase AST Liver Enzymes involved in hepatic amino acid metabolism High elevated level of liver enzymes ALT amp AST may indicate ver damage Low Alkaline Phosphatase ALP Enzyme present in the liver bile ducts and bone High e39eVated IGVel 0quot ALP may indicate liver damage or a blocked duct Low Bilirubin Produced from the breakdown of RBCs normally passed on to liver where it is excreted in bile High Elevated IGVel 0quot BiliI Ubin may indicate liver damage liver fails to remove Bilirubin Low Albumin The most abundant plasma protein One of several plasma proteins synthesized in the liver High gtLOW may indicate liver damage Prothrombin Time International Normalized Ratio PTINR are coagulation factors synthesized in the liver PTINR is a test to measure how long it takes blood to clot High gt1 0 could signify inadequate hepatic synthesis of clotting factors Low Page 10 of 39 The next page shows slide amp lecture information know Liver Function Tests LFTs aka Liver Panel gtthese are common blood tests used to assess liver damage Alanine aminotransferase ALT and aspartate aminotransferase AST Liver Enzymes involved in hepatic amino acid metabolism lf Liver cells are inflamed or damaged Liver enzymes ALT amp AST will leak out of the hepatocytes and into the bloodstream Elevated blood levels may indicate liver damage Alkaline Phosphatase ALP Enzyme present in the liver bile ducts and bone Elevated blood levels of ALP may indicate liver damage or a blocked duct eg gallstone Bilirubin Produced from the breakdown of RBCs normally passed on to liver where it is excreted in bile Elevated blood levels of Bilirubin may indicate liver damage because the liver is failing to remove Bilirubin Albumin The most abundant plasma protein One of several plasma proteins synthesized in the liver gt Lowerthannormal blood levels may indicate liver damage Prothrombin Time International Normalized Ratio PTINR Prothrombin and several other coagulation factors are synthesized in the liver PTINR is a test to measure how long it takes blood to clot A high PTINR means that it takes blood longer than normal to clot This could signify inadequate hepatic synthesis of clotting factors PTINR is the standard unit used to report the result of a PT test Page 1 1 of 39 a normal PTINR is 10 a higher result indicates that is taking the blood longer to clot than normal This indicates that there are not enough blood clotting proteins Liver Diseases Hepatitis gtgt Give the general definition of hepatitis Hepatitis is widespread inflammation of liver itis signals inflammation gtgt List some possible things that could cause hepatitis Widespread inflammation of liver 2 secondary to 1 Toxins or drugs alcohol amanita toxin in mushrooms gtMedications most commonly causing druginduced Hepatitis are Nonprescription pain relievers acetaminophen 1 druginduced cause ibuprofen antituberculosis medicines tetracyclineminocycline etc 2 Infections viral hepatitis mainly A B and C mumps virus rubella virus cytomegalovirus EpsteinBarr virus herpes viruses toxoplasmosis Rocky Mountain Spotted Fever gtMain causes of viral hepatitis are Hepatitis A Hepatitis B amp Hepatitis C and to a lesser extent Hepatitis D and Hepatitis E 3 Autoimmune processes know gtgtWhat are the 55 of acute hepatitis headache muscle aches anorexia NVD RUQ right upper quadrant pain dark urine jaundice pale stools fatigue elevated LFT s abdominal discomfort with Chronic Hepatitis a person may NOT have any signssymptoms but liver cells may remain inflamed for years causing liver damage May lead to End Stage Liver Disease ESLD or liver failure May progress to cirrhosis formation of scar tissue in the liver Page 12 of 39 gtThe most common causes of Chronic Hepatitis are Hepatitis B virus Hepatitis C virus or autoimmune Hepatitis Acute lt6 mos vs Chronic gt6 mos may lead to ESLD amp liver failure gtgtContrast acute and chronic hepatitis In Acute Hepatitis the inflammation goes away in about 6 months The person experiences signs symptoms such as headache muscle aches anorexia NVD RUQ right upper quadrant pain dark urine jaundice pale stools fatigue elevated LFT s abdominal discomfort ln Chronic Hepatitis inflammation persists for 6 months or more but the person may NOT experience any signssymptoms The most common causes of Chronic Hepatitis are B C autoimmune Hepatitis B virus Hepatitis C virus or autoimmune Hepatitis know gtgtComparecontrast Hepatitis Viruses A B C D and E Hepatitis viruses A amp E are spread by fecaloral infection sewage contaminated food or drinking water HAV acute fecaloral highly infectious usually resolves itself in a few days without treatment has incubation period of 1 month or more Hep E acute fecaloral has incubation period of 810 weeks more common in Asia Africa Mexico US travelers to these countries may return home before showing symptoms Hepatitis viruses B is spread by bloodsemensaliva Hep C by blood Page 13 of 39 HBV chronic bss highly infectious HBV vaccine can survive outside the body for 7 days or more can resolve on its own but may progress to chronic Hepatitis antiviral drugs but no certain cure HCV chronic blood most common chronic blood borne infection in US NO vaccine blood banks started screening for Hep C in 1992 can take decades to manifest amp progress may not have symptoms for years some people with Hep C never develop chronic damage other people with Hep C develop cirrhosis of the liver liver cancer or end stage liver disease requiring a transplant antiviral drugs but no certain cure Hep D must have Hep B in order to develop Hep D Very rare Major forms of Viral Hepatitis A B C D and E Hepatitis viruses A amp E are spread by the fecaloral infection sewage contaminated food or drinking water gt HAV acute highly infectious fecaloral is a food borne illness spread by food or water that s contaminated by the feces of someone who has HAV gtNot typically fatal usually resolves itself in a few days without treatment More dangerous for very old very young or someone with a compromised immune system gtcan have an incubation period of a month or more so it can be tricky to pinpoint the source of an outbreak know gt Hep E acute fecaoral infection seen more often in Asia Africa amp Mexico has long incubation period of 810 weeks US travelers to these countries could return home before exhibiting symptoms know Hepatitis viruses B C D are spread by bloodsemensaliva gt HBV Hep B Page 14 of 39 chronic highly infectious bIOOd semen saliva transmission usually sexual contact or contaminated needles gt Hep B vaccine all hospital workers must have gt Hep B can survive outside the body for 7 days or more HBV infection can resolve on its own but may progress to chronic Hepatitis antiviral drugs are available but there is no cure that is certain gt Chronic blood transmission gtmost common chronic blood borne infection in US gt NO vaccine for Hep C gtcan take decades to manifest amp progress may not have symptoms for yrs person who had a transfusion before 1992 when bood banks began screening for Hep C could be at increased risk gtsome people with Hep C never develop chronic damage other people with Hep C develop cirrhosis of the liver liver cancer or end stage liver disease requiring a transplant antiviral drugs are available but no certain cure Hep D chronic occurs only in patients with Hep B Hep D attaches itself to Hep B typically chronic uncommon in US except among illicit drug users Fulminant Hepatitis aka Acute Liver Failure is scary is rare but often fatal fulminant means to strike suddenly like lightening person with a previously normal liver experiences Hepatitis symptoms but Hepatitis progresses very rapidly very aggressively Syndrome in which severe liver dysfunction acute liver failure is accompanied by hepatic encephalopathy and hepatic necrosis ver ceIIs die amp are replaced by scar tissue within 8 weeks of onset Causes are similar to hepatitis however liver regeneration is absent Page 15 of 39 Complications include cerebral edema coagulopathy bleeding renal failure cardiovascular complications pancreatitis frequently leads to multiorgan failure and death Mortality rate wo tx gt70 know necrosis is death of cells in tissues Hepatic necrosis liver cells die amp are replaced by scar tissue Hepatic encephalopathy is a disturbance in central nervous system function that occurs when the liver is no longer able to remove toxic substances from the blood Characterized by altered mental status amp neuromuscular problems Medical Treatment for Hepatitis Medical Treatment for Hepatitis will depend on its underlying etiology eg Hep A usually resolves itself in a short while Hep B amp Hep C will be treated with antiviral drugs autoimmune Hepatitis will be treated with corticosteroids which will dampen the immune response know gtgt Describe the general MNT guidelines for Hepatitis well balanced diet Intake may be poor for short time nausea or vomiting gtgt With any chronic liver disease the liver can have a hard time storing glycogen a main job of the liver Due to inadequate glycogen stores muscle protein is broken down amp oxidized to provide blood glucose during times of fasting In other words glycogenesis amp glycogenolysis may be impaired so the body may break down muscle protein for gluconeogenesis Frequent meals amp snacks with a little CHO at each mealsnack can help spare muscle protein Objectives Page 16 of 39 Promote liver regeneration and rest Prevent further injury Prevent or correct weight loss gtgt Spare muscle protein by providing adequate kcals primarily from CHOs T fluid to prevent dehydration unless contraindicated infection fluid needs may increase with any infection gtgt Person With ascites may need fluid restriction gt Oral diet provided as frequent small meals to help prevent hyperglycemia amp compensate for liver not storing glycogen as it should gtgtTube feeding as necessary gt TPN only in case of ileus or obstruction tube feeding is preferred gtgt Provide 3035 kcalkg energy needs of person with acute Hepatitis are likely normal or slightly elevated varies by person depending on severity of disease Oral supplements eg Boost or Ensure may be helpful if regular food is not optimal May contain medium chain triglycerides as a fat source gtgt Protein 1012 gkgday during acute stages DRI during chronic stages gtgt 5055 kcals from CHO ie adequate CHO to prevent hyperglycemia amp spare muscle protein gtgt Fat up to 30 of kcals Most cells the body can oxidize fat but monitor for gtfat malabsorption may be due to decreased bile production If fat malabsorption evidenced by steatorrhea a lowfat diet is needed LIVER DISEASE End Stage Liver Disease ESLD Diagnosed when the liver is severely and irreversible damaged Liver is severely dysfunctional The only option at this point is to get a liver transplant Can be caused by any other liver disease Page 17 of 39 gt Many complications that can be made better or worse by diet know gt Major complication hepatic encephalopathy Hepatic encephalopathy is a disturbance in central nervous system function that occurs when the liver is no longer able to remove toxic substances from the blood Characterized by altered mental status amp neuromuscular problems Other complications gt Portal hypertension T bp in the portal venous system gt Ascites accumulation of fluid in the peritoneum caused by T pressure from portal htn and l hepatic albumin production ESLD Complications discussed on the next few pages 1 Hepatic Encephalopathy Major Complication 2 Portal Hypertension 3 Ascites 1 Hepatic encephalopathy is a common complication of ESLD gt Hepatic Encephalopathy is an alteration in someone mental condition that occurs when the liver is no longer able to convert toxic ammonia to urea and can no longer detoxify other substances ammonia is very toxic to the central nervous system Page 18 of 39 ammonia is normally processed in the urea cycle to less toxic urea that can be excreted through the urine Pathogenesis of hepatic encephalopathy HE gtgtWhat are the two major factors involved in the pathogenesis of hepatic encephalopathy Excess ammonia is a major contributor to HE amp an imbalance of amino acids can exacerbate HE gtgt 1 Accumulation of ammonia in serum amp Cerebrospinal Fluid CSF Cerebrotoxic effects of ammonia results in range of symptoms Grade I mild confusion poor coordination Grade II asterixis slurred speech gt asterixis is a tremor of the wrist that occurs when the wrist is extended or dorsiflexed aka liver flap because it is said to resemble a bird flapping its wings Grade lll somnolence confusion incomprehensible speech Grade IV loss of consciousness coma gtgt 2 Altered neurotransmitters 2 secondary to abnormal plasma amino acids BCAA s l leucine isoleucine valine as they are used as energy substrate AAA s T phenylalanine tyrosine and tryptophan and other amino acids cross bloodbrain barrier inhibiting brain function Liver damage can result in a higher ratio of aromatic amino acids AAAs to branch chain amino acids BCAAs in circulation The heart amp skeleton muscles will use up BCAAs quickly but AAAs will be released from muscle proteolysis breakdown The Liver is the main site of degradation of most amino acids but BCAAs are an exception to that rule BCAAs are mainly used amp degraded by muscle cells The Liver has very little BCAAs aminotransferase enzyme but muscle has lots of those enzymes 80 BCAAs that we ingest from food will for the most part will do a first pass through the Liver and be passed to muscle where they are catabolized So liver damage skeletal muscle breakdown leads to an imbalance More AAAs are in circulation than BCAAs This can exacerbate the encephalopathy MNT for ESLD Prevent malnutrition which is very common in ESLD patients Page 19 of 39 Manage symptoms know gtgt Why is lactulose commonly prescribed for patients with hepatic encephalopathy to lower ammonia Lactuose hyperosmotic laxative which increases excretion of ammonia aso prevents production of ammonia by gut bacteria in the large intestine gut bacteria normally produce a little ammonia gtgt What are the side effects of this medication diarrhea gtgt Specialty tube feeding formulas are available for hepatic patients Those formulas are rich in BCAA s but low in AAA s How could this be helpful There are mixed opinions as to whether the hepatic formula of lactulose is better for liver patients than the standard formula for enteral feedings hepatic formulas have gtBBCA amp lt AAAs are more expensive gtgt ls protein restriction generally warranted for ESLD gtgt When may a short period of protein restriction be necessary Dietary protein restriction is unnecessary in majority of cases gtgt May be needed restriction in rare cases of refractory encephalopathy know gtgt For a person with severe or problematic encephalopathy we may need to withhold oralenteral intake for 2448 hrs while giving lV dextrose to prevent hyperglycemia Then may have to restrict protein to 5 6 g per kilogram of dry wt Vegetable proteins like soy amp dairy proteins like whey are higher in BBCAs amp are good sources of protein for the liver patient lmprove BCAAAAA ratio by T oral intake of BCAA T vegetable protein low in methionine high in BCAA s T dairy protein casein is low in AAA high in BCAA Possibly consider oral supplements enriched with BCAA s and low in methionine amp AAA s eg HepaticAid gtgt Why would specialty enteral formulas enriched in glutamine be contraindicated for someone with ESLD Page 20 of 39 Avoid glutamineenriched TF formulas because they gt ammonia levels even more 2 Portal Hypertension is a common complication of ESLD The Hepatic portal vein brings blood to the liver from the stomach the small intestine the large intestine amp the spleen If that blood flow to the liver is obstructed that will result in a rise in venus portal pressure The body responds by diverting blood to smaller collateral blood vessels like those in the esophagus Those little veins in the esophagus can balloon out causing esophageal varices If those veins break open the patient could bleed severely Someone with ESLD will likely have inadequate synthesis of clotting factors so bleeding would be a severe risk Portal hypertension T bp in the portal venous system Portal HTN can lead to esophageal varices If there is decreased hepatic albumin production as well Portal HTN can lead to ascites Albumin is synthesized produced in the liver MNT for esophageal varices would be a soft lowresidue diet 5 113 Fl I39LEIE LI LEI 39I L 39l l IaJ39 Effort Left right gastric veins portal trains 7 l Left riht l gastric trains gm l l a i39 51 w 1 34 r Portal treein l a Epl nm WI i My 39 z Eaatr w urging fr m 39 4i i n ilpl i 39ti39Eil i pancreas all T 7 39 duodenum i Inferior i 47 frmesenteric 1 rein veins from amending an SUDEFIULI Eli jun LnTQEE I ErIG in trains from Hazins from descending jejunum E ileu m E sigmoid colon aw 3 Ascites is a common complication of ESLD gtgt Why does liver failure lead to fluid accumulation in the peritoneal cav y gtgt Describe how the combination of low albumin and portal HTN from advanced hepatic disease can lead to ascites Ascites is the accumulation of fluid in the peritoneum caused by T pressure from portal htn and i hepatic albumin production Albumin is synthesized produced in the liver fi V E W H 39 I39 d Jfr lcterlr sclerae lad if if I If H ZI r 7 Encephalopathy at 39 2 t NODECia Spider angiioma 75 Aster ixris 7 39 Vquot quot W quot ll i 33 v H a WWW a 39 3 if Jaundtce 39 ewthema 39 I I39 n II Esophageal r vanices It39s Bruitsth 7 39 i ll Gyintecomastia I 39 Caput med Lil5EI e a t Muscle 39 Ascites ff 2 y I WWW i Altered hair quotV quotu PD n istri39w 39 39 39 r s 5 rta d button NJ if hypertension Testicular atrophy ti I 39 r t quot l xquot i39 C r t iirrlnosis r39 f Jude 39 3 r c r I I 39 E l 5 t I Hepatrorenat 355 a f 2quot 7quot ILL Syndrome l u 39l in r I 39 II it I V 39I39I I39v39 quot i ll cg t r 392quot a 239 II I Edgma i 9 Teacoored urine t Ctaycolored stool 71 quot3 EXTERNEL SYMPTOMS INTERNAL SYMPTOMS lEIserier items and derived items 2012 2008 200 by Saunders an imprint oi Elsevier Inc gtgt Describe the appropriate MNT for ESLD Page 22 of 39 gtgt Recognize that ESLD cases can be very complicated MNT may differ depending on whether or not the pt has ascites encephalopathy esophageal varices micronutrient deficiencies or proteincalorie malnutrition Avoid fasting Provide frequent small meals helps prevent hyperglycemia amp spare muscle protein breakdown Energy needs will depend on how malnourished a person is Energy at 3035 kcalkgday if a person is severely malnourished start nutrition repletion slowly to avoid gt refeeding syndrome Refeeding Syndrome occurs when a person who has adapted to starvation and calories especially CHO calories are introduced too quickly or too aggressively gtThis may cause serum potassium magnesium amp phosphorus can be taken up too quickly into the cells and levels of these electrolytes in the blood can bottom out This can be an acutely dangerous even fatal situation for a severely malnourished person start low amp go slow maybe 1520 kcalkgday for that person 1015 gprokg 3035 fat liberal fat in this context means a good amount of fat unless there is fat malabsorption evidenced by steatorrhea and then a lowfat diet is needed gt Fat malabsorption may be due to decreased bile production gtgt MNT for Portal Hypertension During acute bleeding in portal hypertension pt will be NPO If gt5 days provide TPN gtgt Describe the appropriate MNT for someone with ascites MNT for Ascites May be treated with paracentesis Protein needs will be elevated as plasma proteins eg Albumin are lost paracentesis needle is used to remove fluid accumulated in the abdominal cavity Fluid restriction to 1 15Lday Lowsodium diet Restrict Na to 2 gday Monitor K serum potassium during diuretic use pt will likely be on diuretics May only be able to tolerate small meals because pt will feel satiety fullness quickly Page 23 of 39 Estimate dry weight tricky to do when person has Ascites Whenever a patient is on diuretics we need to closely monitor serum potassium micronutrient deficiencies some physical signssymptoms are glossitis stomatitis amp dermatitis MNT for ESLD continued gtgt Normally fat intake can be liberalized for a pt with ESLD unless the pt has ss of fat malabsorption know gtgt Why would a person with liver disease be prone to fat malabsorption know gtgt How could MCT help Fat malabsorption may be due to decreased bile production It helps to replace some long chain triglycerides or dietary fat with medium chain triglycerides MCT Because MCTs do not require bile salts amp micelle formation for absorption they are readily taken up via the portal route some nutrition supplements contain MCTs which can be used in addition to MCT oil gtgt Why are patients with ESLD more prone to muscle proteolysis during fasting gtgt What MNT modalities can be used to minimize catabolism of muscle in these patients With any chronic liver disease the liver can have a hard time storing glycogen a main job of the liver Due to inadequate glycogen stores muscle protein is broken down amp oxidized to provide blood glucose during times of fasting In other words glycogenesis amp glycogenolysis may be impaired so the body may break down muscle protein for gluconeogenesis M NT Frequent meals amp snacks with a little CHO at each mealsnack can help spare muscle protein gtgt Alcoholic liver disease is the leading cause of cirrhosis in US but it is NOT the only cause of cirrhosis Cirrhosis can be caused by many chronic liver diseases hepatitis autoimmune disorders drug toxicities etc Page 24 of 39 Alcoholic Liver Disease 50 of US chronic liver disease cases Ethanol is absorbed from the GI tract into the blood and travels to the liver It is in the liver that Ethanol is metabolized Metabolic pathways that take place in the liver will prioritize Ethanol above everything else Ethanol is broken down in the liver by a series of oxidation reactions 1 enzyme alcohol dehydrogenase ADH catalyzes the conversion of Ethanol to acetylaldehyde is highly toxic circulating levels are normally low would cause damage to cells so 2 Acetylaldehyde is quickly metabolized by aldehyde dehydrogenases ALDH to acetylCoA ADH amp ALDH activity may differ from person to person Notice in these 2 reactions that when Ethanol is oxidyzed NAD is reduced to NADH Excessive Ethanol intake will lead to an excessive build up of reduced NADH in the cytoplasm solution that fills cells Excessive NADH inhibits fatty acid oxidation amp will favor fatty acid biosynthesis but actually interferes with incorporation amp export of those fatty acids by VLDL gtThis can lead to a condition called steatosis aka fatty liver develops in nearly any individual who consumes gt 60 g of Ethanolday on a regular basis 60 g 212 oz chronic heavy consumption of alcohol So that means drinking gt 10 oz of a wine that is 13 ethanol varies by wine by volume gtSteatosis aka fatty liver is reversible gtgt Recognize how excess acetylaldehyde from ETOH oxidation as well as excessive NADH can lead to liver damage Acetaldehyde a byproduct of ETOH metabolism is highly toxic amp can damage the liver Excessive NADH interferes with incorporation amp export of fatty acids by VLDL amp can lead to a condition called steatosis aka fatty liver CH3CH20H NAD ADH CH3CHO NADH H gt Ethanol Acetylaldehyde CH3CHO NAD ALDH CH3COO NADH H gt Acetylaldehyde Acetate Page 25 of 39 know gtgt What are the 3 stages of alcoholic liver disease know gtgt Which of these stages is reversible Alcoholic Liver Disease progresses in 3 stages 1 Hepatic steatosis fatty liver gtreversible by reducing ETOH intake 2 Alcoholic hepatitis swelling of the liver hepatomegaly inflammation of the liver T bilirubin or transaminase levels abdominal pain NVD weight loss can damage the liver amp lead to Cirrhosis but gtmay resolve with discontinuation of EtOH intake 3 Cirrhosis Liver cells die amp replaced with scar tissue Diffuse fibrous scar ssue Liver is NOT ABLE to remove toxins from the blood regulate CHO metabolism synthesis hepatic proteins convert ammonia to urea gtIrreversible damage Prognosis depends on liver involvement and abstinence from EtOH Can lead to End Stage Liver Disease and then a liver transplant would be the only treatment option The process amp progression of alcoholic liver disease seems to be influenced by genetic factors Steatosis fatty liver gt 90 of people who drink heavily on a chronic basis day after day develop Steatosis Acohoic hepatitis Not all heavy drinkers develop alcoholic hepatitis Cirrhosis about 1 in 4 heavy drinkers develop Cirrhosis According to the National Institute on Alcohol Abuse amp Alcoholism Advanced Alcoholic Liver Disease or Alcoholic Hepatitis is often synonymous with End Stage Liver Disease know One unique feature found with Alcoholic Liver Disease is Wernicke s Encephalopathy aka WernickeKorsakoff syndrome Caused by thiamin deficiency Common in alcoholics Page 26 of 39 know gtgt What is Wernicke s Encephalopathy Wernicke s Encephalopathy aka WernickeKorsakoff syndrome is a brain disorder caused by thiamin deficiency in alcoholics It is characterized by unsteady gait mental confusion lack of fine motor skills same symptoms are found with beriberi amp frank thiamine deficiency medical dEfinition of frank unmistakeable obvious know gtgt How does alcoholism lead to this condition Alcohol interferes with absorption amp metabolism of thiamine Alcoholic Liver Disease Clinical features Compression of blood lymph and bile flow gt Portal Hypertension Diverted blood flow increases pressure in smaller vessels gt Varices of esophagus amp stomach Accumulation of fluid in peritoneal cavity from portal HTN amp low serum albumin gt Ascites Tx paracentesis know Malnutrition in Alcoholic Cirrhosis Alcoholics are prone to may micronutrient deficiencies Malnutrition in the alcoholic due to Replacement of nutrients with calories from alcohol 71 kcalg digestion amp absorption due to pancreatic insufficiency and changes in gut mucosa gt steatorrhea l hepatic amino acid uptake and protein synthesis Page 27 of 39 impaired fat OXidation gt fat accumulation in the liver elevated serum triglycerides and insulin resistance Vitamin amp mineral deficiencies Cirrhotic Liver Disease Secondary Causes of Cirrhosis in addition to alcoholic liver disease gt R side HF repeated bouts of rightsided heart failure with fluid backing up in the liver Chronic hepatitis Biliary disorders gt Cholangitis inflammation of the bile ducts walls of bile ducts inside amp outside the liver harden amp thicken is an autoimmune disorder correlated with gt Ulcerative Colitis is a rare form of liver disease Chemical Drug toxicity other inherited disorders eg hemocromotosis body absorbs too much iron glycogen storage diseases Nutrition Assessment in Cirrhotic Liver Disease cont Cirrhosis can lead to End Stage Liver Disease so adequate nutrition becomes very complicated ProteinEnergy Malnutrition PCM common in advanced disease Malnutrition positively correlates with T morbidity and mortality Some traditional nutritional assessment parameters can be misleading in patients with liver failure a person could have substantial loss of lean body mass but actually present as weight gain if he has ascites so the numbers on the scale could indicate overweight or obese but the person is clearly malnourished Assessment must include a careful review of patient s oral intake Page 28 of 39 Use all of the best tools for physical assessment Assessment must consider energy protein fluid electrolytes vitamin amp mineral status Appetite amp eating habits including EtOH intake Assessment should consider signs amp symptoms of malabsorption eg fat malabsorption is common diarrhea steatorrhea GI bleeding person with heavy ethanol intake is prone to GI amp stomach bleeds tarry stools anemia vomiting blood encephalopathy mental confusion poor coordination asterixis liver flap fluid retention ascites peripheral edema vitamin deficiencies physical signs of cheilitis glossitis anemia night blindness bruising esophageal varices bleeding risk muscle mass subjective assessment gtgt Pts with ESLD are susceptible to many micronutrient deficiencies Vitamin and Mineral Deficits in Severe Hepatic Failure ESLD patients are at risk for deficiencies for all of the following Vitamin A Niacin Careful High doses of preformed Vitamin A can be toxic to the liver Vitamin D Thiamin Vitamin E Zinc Vitamin K Magnesium Vitamin B6 Iron Vitamin B12 Potassium Folate Phosphorus Page 29 of 39 know gtgt Which micronutrient deficiencies are particularly prevalent in alcoholic patients Patients with ongoing EtOH ingestion are at increased risk for thiamin magnesium and folate deficiencies know gtgt Two trace elements are normally excreted in bile Hepatic excretion may be impaired with liver disease so supplementation of these two minerals would be contraindicated for ESLD Which ones Avoid excessive copper amp manganese as these are hepatically excreted NTR Assessment in Cirrhotic Liver Disease cont gtgt How could assessment of body weight be misleading for hepatic patients Which weight would you use for your calculations Anthropometrics Body weight can be skewed with fluid amp Na retention It can be difficult to determine the dry weight of a person with ascites With ascites as with heart failure fluid retention can mask hide weight loss In this case use dry weight guesstimate for calculations TSF and MAMC will reasonably estimate fat reserves amp muscle mass TSFtricep skinfold estimates stored body fat Page 30 of 39 MAMCmid arm muscle circumference estimates skeletal muscle mass gtgt Review the lab values you would assess for a liver disease patient Chemistry Liver Function Tests LFTIS AST ALT ALP Anemias hypochromic microcytic OR macrocytic Thrombocytopenia body does not produce enough platelets Ieukopenia low white blood count Prolonged PT l albumin may be skewed low 2 to edema or low following paracentesis MNT for Cirrhotic Liver Disease Cirrhotic Liver Disease amp End Stage Liver Disease are often one and the same so goals amp intervention strategies are the same for both Goals of MNT Support remaining liver function amp enhance liver s ability to regenerate Strategy Page 31 of 39 Provide adequate energy amp protein to maintain nitrogen balance without precipitating encephalopathy Energy Indirect calorimetry is always the best bet for estimating energy needs amp is recommended if edema or ascites is present but that option in not always available In general energy needs are not elevated in cirrhotic liver disease gt 3035 kcalkg dry weight based on a guesstimatequot of dry weight if person has significant ascites may need to ask person about their usual weight lecture slide info is not the same as info in posted PPT gt Protein is the most controversial macronutrient in liver failure not a good evidence base lot of debate about protein recommendations 08 10 gkg or up to 15 gkg in uncomplicated nonencephalopathic 15 gkg if mUSde WaStings GI bleed 0r paracentesis fluid removal with needle 0507 gkg dry wt if encephalopathic increasing as tolerated protein restriction Encephalopathy may warrant trial of BCAA S some enteral formulas have gt ration of BCAAs to AAs MNT for Cirrhotic Liver Disease continued know gt The primary role of the liver is CHO metabolism so when that is compromised other cells of the body may more easily use fat as an energy substrate Fat Moderate to Liberal fat intake unless fat malabsorption is present Page 32 of 39 gt When malabsorption is present medium chain triglycerides MCT can be given in divided doses as an energy source Na and fluid often restricted with edema or ascites VitMin supplementation required gt monitor Copper Cu amp Maganese Mn levels since they are hepatically excreted Will not want to supplement these lecture slide info is not the same as info in posted PPT Small frequent meals for pts w ascites maximize intake prevent hyperglycemia compensate for inadequate glycogen storage Prevent EXCESSWG proteolysis breakdown of muscle protein Anorexia amp nausea are common Serve attractive amp appetizing meals Cold foods may be better tolerated Maintain oral route if possible Use oral liquid supplements Enteral tube feedings may be given with esophageal varices if needed Beware of Refeeding Syndrome in severely malnourished patients sharp decline in serum phosphorous magnesium amp potassium if malnourished patients are refed too quickly especially CHO start low amp go slow lecture slide info is not the same as info in posted PPT Other Liver Diseases Wilson s Disease know gtgt What is Wilson s Disease Page 33 of 39 Hereditary disease characterized by excessive copper storage in tissues and organs primarily liver amp brainCNS impaired biliary copper excretion allows excessive copper to build up copper build up causes cirrhosis liver damage cognitive impairment Always fatal wo lifelong chelation treatment is a rare autosomal recessive disorder so a person would need 2 affected alleles variant form of a gene for the condition to manifest copper is a trace element and we need a little bit of copper excess copper is usually excreted through the bile gtgt How is it treated lifelong chelation therapy even with treatment liver damage is common know MNT for Wilson s Disease Krause has a good table of foods that are low in copper gt Want to avoid copper for anyone with advanced liver failure Vegetarian diet minus soy amp meat substitutes may be helpful as Cu is less bioavailable Cu restriction used only when chelating agents are unsuccessful Restrict lamb pork organ meats soy meat substitutes shellfish avocado chocolate dried beans etc Krause 303 Other Liver Diseases Hemochromatosis gtgt What is Hemochromatosis Hemochromatosis is Page 34 of 39 sometimes called iron overload results from a genetic abnormality that causes the intestines to absorb too much iron excessive iron builds up in certain organs especially the liver and can cause liver damage the Liver normally stores iron but excessive amounts can cause liver damage people have problems if they are homozygous for the gene ie have two of the same allele people who are heterozygous for the gene have just one copy amp usually have no problems gtgt Identify two lab values that may be a red flag for hemochromatosis Hemochromatosis is usually diagnosed by a blood test called transferrin saturation 1 T serum Ferritin saturation or 2 elevated Ferritin would indicate Hemochromatosis Hemochromatosis would be confirmed by genetic testing Toxic condition of T Fe absorption resulting in excessive deposition as ferritin and hemosiderin in liver spleen and bone marrow Major organ involvement if untreated cirrhosis pancreas DM cardiomyopathy heart failure pituitary failure Iron is a prooxidant so hemochromatosis increases colon Ca risk Affected labs T serum Ferritin saturation or transferrin saturation Patients with Hemochromatosis usually have their blood drawn several times a year to prevent iron from building up Pts may be anemic 2 bone marrow involvement Do not treat anemia with Fe supplementation wo knowing the cause Page 35 of 39 Fatigue is a symptom of Hemochromatosis So if a person complains of fatigue don t be too quick to recommend iron supplements Treatment Phlebotomy IV chelating agents gtgt Describe MNT for hemochromatosis MNT for Hemochromatosis avoid iron Avoid EtOH and Vitamin C supplements these increase Fe absorption Avoid Fefortitied foods or supplements Avoid cooking in castiron cookware intake of hemeiron protein sources and T intake of nonheme iron protein sources hemeiron is derived from hemoglobin the protein in red blood cells that delivers oxygen to cells Hemeiron is found in animal foods that originally contained hemoglobin like red meat fish or poultry iron in protein plant foods is arranged in a chemical structure called non heme gt Hemeiron protein foods are more easily absorbed than nonheme iron protein foods gt a person with Hemochromatosis would be better off consuming non heme iron protein plant foods like lentils or beans instead of heme iron protein foods to limit hemeiron ie more plant protein than animal protein Liver Resection and Transplantation For a patient with cirrhosis of the liver or End Stage Liver Disease a liver transplant is the only option for a cure Page 36 of 39 gtgt How would the nutrition needs of a liver transplant patient differ before transplant immediately after and longterm Nutrition recommendations both pre amp post transplant would be customized for each patient The dietitian would be an integral member of the transplant team Malnutrition common in liver transplant candidates Pretransplant attempt to resolve malnutrition Posttransplant PO post op intake important to stimulate liver function Immediately first 2 months Needs are slightly elevated to allow for healing and liver cell regeneration BEE x 11513 12175 gprokg Longterm Weight maintenance moderate protein 10 gkg may have weight gain due to medications MNT should be adapted based on immunosuppressant drug regimen used Nonalcoholic Fatty Liver Disease NAFLD gtgt What is NAFLD Nonalcoholic Fatty Liver Disease Accumulation of TG fat in the livers of people who drink little or no EtOH gtgt What is NASH NAFLD can progress to nonalcoholic steatohepatitis NASH The liver would become inflamed NASH can lead to permanent liver damage irreversible liver damage or it could progress to cirrhosis of the liver NAFLD amp NASH appear to have genetic underpinnings but are much more common in obese persons Could be an example of ectopic fat deposits or fat where it shouldn t be Normally we store fat in adipocytes fat cells If we exceed the capacity of adipocytes in some people fat could be deposited in liver cells or other cells of the body So NAFLD is more common in people who are obese especially if the person has visceral adiposity VAT or central obesity Page 37 of 39 The same MNT modalities for weight management amp CVD would most likely be beneficial for these patients Page 38 of 39 jl39im39I Er Ilii SSHIlii39ili i i fartEa Erwinail r mam m Han Emmi er nubII lrmr 5 maimeme ii39w l nailmu arra1 mum I Eu magiminis Page 39 of 39 Spath Study Guide for NHM 365 Module 5 Digestion Absorption amp Transport Part One Overview of Digestion Absorption amp Transport of Nutrients gt Part One Overview of Digestion Absorption amp Transport of Nutrients Part Two Digestion and Absorption of Specific Nutrients gt Key Points definitions gtgt Key Pointdefinition is on SelfStudy Guide gt Tricky Question Alert Contents Anatomy of the digestive system the gastrointestinal tract muscular sphincters amp accessory organs GI Tract from the mouth to the anus MOUth aspects of digestion that begin in the mouth StOmaCh types of digestion that occur in the stomach Major gastric secretions HCI IF pepsin gastric lipase gastrin Sphincters circular muscles at various points along GI tract Small Intestine Villi and microvilli increase surface area 3 segments Duodenum Jejunum amp ileum Absorption Mechanisms Role of organs in digestion the pancreas the liver the gallbladder Large Intestine Anatomy Colonic Bacteria Colonic Salvage Roles of Endocrine System hormones in digestion gastrin secretin cholecystokininCCK motilin somatostatin Summary Chart Page 1 of 25 The Digestive System gtgt Review the anatomy of the digestive system including the gastrointestinal tract muscular sphincters and accessory organs The main components of the digestive system rillU CLllS am algesuve enzymes 39 a SlJblinlgual Tbotlllahahj quot Slmeaxillary Tongue Epiglcttis open V 39 closed Esophagus Tracrlea V U gEsophagus L Stonlachl Dialpl lraglm a Spleen llver bile l Liver ducts lw 39l 7 Z HClias Gallbladder f d a J L r Pancreatic duct DuodenLlllm Transverse colon Descending colon Bile dLlct opening 7 39 V Ascending colon r g gt 7 77 Cecullrl l 39 l Appendix Jejunlum Sigmloid colon ileum Reclllm Anus Gastrointestinal GI Tract or Alimentary Canal a long tube that starts at the mouth and ends at the anus gt GI Tract includes the mouth the pharynx the esophagus the stomach the small amp large intestine Serves as a physical amp immunological barrier The health of the GI tract will affect overall health Major Layers of GI Tract Inside layer lumen lined with Mucosa epithelial cells Submucosa layer blood vessels lymph vessels glands Muscularis layer smooth muscles innervated by nerve plexuses Outer Surosa layer connective tissue Page 2 of 25 Pharynx throat the intersection between the respiratory tract amp the GI tract Esophagus connects the throat to the stomach GI Tract aka Alimentary Canal GI tract continuously renews its lining Most of cells lining the gut lumen have a high turnover rate the life span of Enterocytes is 72 hrs Lumen inner layer is lined with Mucosa epithelial cells gt Enterocytes absorptive cells are the predominant epithelial cell type lining the lumen The Nervous System helps regulate digestion The Nervous System via neural mechanisms controls movement contraction mixing and propulsion through the GI Tract Muscularis layer smooth muscles innervated by nerve plexuses 90 to 97 of the food consumed is digested amp absorbed gt Digestion is primarily by enzymes Chemical digestion gt Mechanical Digestion breaking up big food particles into small particles amp mixing them with digestive juices gt Chemical Digestion breaking of chemical bonds by hydrolysis reactions depends on enzymes Hydrolysis is a reaction involving the breaking of a bond in a molecule using water gt Enzymes are secreted by cells of the GI tract but many enzymes come from the pancreas The liver amp gallbladder supply bile for the emulsification break down of fat Appendage organs play a role in digestion pancreas liver and biliary tree Page 3 of 25 GI TractAlimentary Canal The Mouth gtgtWhat aspects of digestion begin in the mouth gtgt The Mouth readies the food for swallowing deglutition mostly by mechanical digestion chewing but also by some chemical digestion starch breakdown by a salivary amylase called ptyalin and a small amount of fat breakdown by lingual lipase No appreciable amount of absorption occurs in the mouth gt Most of the digestion in the mouth is Mechanical We chew masticate with teeth food into pieces and then mix it with saliva into a small bolus small mass of food that can be swallowed gt Process of swallowing deglutition Peristalsis moves bolus down the esophagus to stomach gt A small amount of digestion is done by saliva chemical digestion 3 pairs of salivary glands secrete 115 L salivaday into the mouth gt Saliva contains a salivary amylase enzyme that hydrolyzes starch into sugars called ptyalin which begins starch breakdown gt Saliva contains some lingual lipase but there is minimal fat digestion in the mouth hydrolyses break down by chemical reaction with water Page 4 of 25 Starch is not in the mouth long so salvia only has time to break down a few polysaccharides so only a small amount of digestion demo leave a piece of bread on your tongue and after awhile it would begin to taste sweet due to action of ptyalin Saliva also contains antibodies amp other antimicrobial agents neutralizes acid in the mouth and helps prevent dental cavities Digestive System After swallowing peristalsis moves bolus down the esophagus to stomach Page 5 of 25 gt NO mechanical or chemical digestion NO absorption occurs in esophagus At end of esophagus is the lower esophageal sphincter which opens to allow bolus into the stomach Submaxillary and Sublingual Glads 1 oesophagus Liver Gall Bladder Duodenum Transverse Colon Ascending Colon V LeumSmal Intestine Caecum Rectum 7 i rrrrrrr quot Vermiform Appendix Anus Biology Digestive System Digestion in the Stomach gtgt What types of digestion occur in the stomach In the stomach there is a mechanical amp chemical breakdown of large molecules Wavelike contractions mix food with gastric secretions amp hydrochloric acid to breakdown protein Very little fat digestion occurs in the stomach Review Overview of Gastric Juices Page 6 of 25 gt Two systems regulate digestion 1 Endocrine System via hormones amp 2 Nervous System Nervous System Two large plexuses of nerves innervate the GI tract the gut brain Endocrine System Food in the stomach will signal the release of a hormone called gastrin from G cells gastrinproducing cells of the stomach mucosa Gastrin stimulates parietal cells epithelial cells to secrete hydrochloric acid HCI and intrinsic factor IF When food reaches the stomach it stimulates stretch receptors of enteric neurons and those stimulate muscle contraction so there is a mixing amp churning of the hydrochloric acid with the food allowing proteins to begin to be denatures destroys the characteristic properties of Intrinsic Factor IF a glycoprotein will be important for B12 absorption in the small intestine gt Chief Cells in the stomach secrete pepsinogen a zymogen an inactive enzyme that is activated by hydrochloric acid in the stomach to its active form of Pepsin Pepsin will hydrolyze and break Peptide bonds Chief Cells secrete a small amount of gastric lipase but there very little fat digestion occurs in the stomach gt Goblet Cells secrete mucous The churning of the stomach mixes the food with the hydrochloric acic and the gastric juices into a creamy paste called chyme Acid reduces number of microorganisms ie protectiveimmunological effect Long term acidinhibitors used by some people with acid reflux which could put them at increased risk for infection or achlorhydria the absence of hydrochloric acid in gastric secretions Digestion in the Stomach Continued gtgt Review major gastric secretions amp their functions HCI IF pepsin gastric lipase gastrin together they form chyme gtgt Gastrin Food in stomach signals release of hormone Gastrin from stomach mucosa Gastrin stimulates parietal cells to secrete hydrochloric acid HCL Stretch receptors of enteric Page 7 of 25 neurons respond to stimulate muscle contraction Food mixes with HCL allowing proteins to be denatured ie broken down Parietal cells also secrete Intrinsic factor IF a glycoprotein that will be important for 812 absorption in the small intestine gtgt Pepsin Chief cells in the stomach secrete pepsinogen a zymogen activated by HCL to the active enzyme pepsin Pepsin catalyzes the hydrolysis of peptide bonds gtgt Gastric lipase is secreted from chief cells but very little fat digestion occurs in the stomach Gastric juices From Acts by Causes Causes Causes in form chyme in stomach in stomach Small Intestine Gastrin G cells in stimulates HCL activates HCL mixes with IF glycoprotein hormone stomach parietal Pepsinogen food amp breaks important for mUCOSEI cells to inactive down protein B12 secrete TO absorption in HCL chief active enzyme Pepsin below Ileum small cells to Pepsin intestine secrete IF Pepsinogen chief cells zymogen or stomach inac ve enzyme Pepsin HCL gt hydrolyzes amp Pepsin breaks Peptide active bonds helps enzyme digest protein Hydrochlori Gastrin gt c Acid HCL parietal cells gt HCL Intrinsic Gastrin gt Factor IF chief cells glycoprotein gt IF Gastric chief cells lt fat digestion Lipase stomach in stomach Digestive Process Stomach Continued Page 8 of 25 Semiliquid Chyme passed from stomach to small intestine Emptying from the stomach into small intestine The pyloric sphincter aka pyloric valve regulates opens amp closes to allow passage of semiliquid chyme from the stomach to the small intestine A small amount a few milliliters of chyme enters the small intestine with each wave of contraction The emptying time of the stomach gastric emptying is 14 hours depending on what you eat and how much you eat Most rapid through the stomach liquids CHO isotonic mixtures empty fastest sowest solids fats or foods containing large particles such as fibergristleconnective tissue take longer to empty gt So these provide satiety longen Solid mixed meal 2 to 3 h varies by composition Pyloric value slightly open IDFI39G 3 value closed P yloric r value closed rat in M Page 9 of 25 Digestive Process Stomach Continued Sphincters Muscles made of circular smooth muscle Sphincters along the GI tract control flow of material into amp out of the stomach Esophagus connects pharynx to stomach upper esophageal sphincter closed except when swallowing Lower esophageal sphincter LES closes entrance to stomach prevents reflux of acidic chyme back into esophagus Stomach can handle acidic chyme but esophagus can t Some foods that decrease l LES pressure relax LES can allow acidic chyme back into the esophagus Gastroesophageal reflux or acid reflux painful eg alcohol fat peppermint spearmint chocolate caffeine This is a common problem pyorus sphincter pyloric valve Closes exit from the stomach to the small intestine Prevents reflux of small intestine back into stomach Less common Sphincters can spasm amp malfunction very painful Sphincters can be excessively stimulated by stress causing spasm IL FIT E I I I I Sphincter 1n ML l 391 Fr 1 L Eccphaguc E39lcrnachj in Eld39 1 3553 I r F39 a l 5 39 quot quotLcwcr Eccphageal Sphincter l llcwing Reflux A 5quot 4 5 d L l39 A A 4 A H I r 4 a I A n u A n Avil a 2 l L A a39 l Eff n 2 v 39 me u l39 J 391 if r aquot l lt 39 n n 1 A A K r I A L 9 y 1 H are Elm Page 10 of 25 Digestion so far gt Mouth a little digestion of starch via mechanical chemical ptyalin salivary amylase gt Stomach small amount of digestion of protein via HCL Pepsin chemical gt Small Intestine most chemical digestion amp nearly all of the absorption Small Intestine Primary site of chemical digestion amp absorption hydrolysis of molecules into absorbable entities amp absorption of nutrients The Small Intestine is the primary site of chemical digestion hydrolysis of molecules into absorbable entities and absorption of nutrients and water across brush border The Small Intestine consists of 3 sections duodenum jejunum amp ileum gt To be used by cells end products of digestion need to be absorbed from the lumen of the GI tract and delivered to cells by the circulatory system so the small intestine primarily the jejunum is the principal site of absorption The Surface area of the small intestine is huge about the size of a tennis court It is the anatomy of the small intestine mucosa that make that possible Page 1 1 of 25 The Surface area of the small intestine is huge about the size of a tennis court It is the anatomy of the small intestinal mucosa that makes that possible Con nuedquot Absorptive cell ViIILis Goblet cell Larnina proipria iacteal iyimpnaiiq Capillary Cirypii oi quotLieberkulnn 5 2 iVlucosa Glandular secreiing cells of Paneth as y Muscularis mucosae l Vein Lymph vessel Artery l 39i39ela subimLicosa l gtgt How do villi and microvilli increase the surface area for small intestinal absorption The surface area of the small intestine is increased by length folds villi and microvilli the brush border Page 12 of 25 Villa are a fingerlike projections of the small intestinal mucosa Each villus is supplied by a capillary bed and a Iacteal a lymph capillary Tiny projections of the plasma membrane called microvilli form the brush border of the small intestine Diagram of Intestinal Villi Digestive Process Small Intestine 3 Segments of the small intestine Duodenum 25 cm long begins at the Pylorus sphincter amp ends at the Ligament of Treitz Chemical digestion really begins here when food mixes with duodenal juices pancreatic amp biliary secretions Jejunum 25 meters long Primarily absorptive MOST ABSORPTION HERE lleum 36 meters long Primarily absorptive ABSORPTION OF Vitamin B12 Sphincter between small amp large intestines ileocecal valve Chart includes info provided in later slides Small Intestine Sections Length Key Info Page 13 of 25 Top Duodenum shortest section 25 cm Chemical digestion Pancreas secretes 05 meters really begins digestive enzymes into begins at Pylorus duodenum sphincter amp ends at Ligament of Gallbladder releases Treitz bile into the duodenum aids digestion of fat Middle Jejunum 25 meters MOST of the ABSORPTION occurs here Bottom or terminal longesti Shtion 36 lleum quot ends at the ileoceca junc on ileocecal valve sphincter separates ileum from large ABSORPTION OF VITAMIN B12 occurs here Reabsorption of BILE Water amp ions absorbed Any end products not processed in the Jejunum Vitamin B12 combines with intrinsic factor for absorption in the ileum Bile salts are reabsorbed amp returned to liver to be recycled again into more bile gt Enterohepatic intestine Circulation gtgt What is the role of the pancreas in digestion The livergallbladder Pancreas F secretes digestive enzymes into the 00 h duodenum of the small intestine Liver produces bile which is stored in the gallbladder Gallbladder releases bile into the duodenum of the small intestine to aid digestion of fat Page 14 of 25 The pancreas is a glandular organ that secretes digestive enzymes into the small intestine The liver produces bile which is stored in the gallbladder The gallbladder releases bile into the small intestine to aid fatdigestion Digestion gt Digestion is the process of breaking down food into molecules small enough to be absorbed across the intestinal epithelium into the blood or the lymph Digestion breaks down polysaccharides amp disaccharides sugarscarbohydrates into monosaccharides glucose fructose amp galactose Proteins are broken down into amino acids dipeptides amp tripeptides Fats are broken down into triglycerides gt free fatty acids amp glycerol After food is digested it is absorbed Absorption Page 15 of 25 gt Absorption is the process by which the end products of digestion enter the cells lining the small intestine and then pass into the blood or lymph for delivery to the body s cells via the circulatory system Water vitamins minerals amp ethanol alcohol used in drinks which do not need to be digested are also absorbed Most of the absorption of nutrients occurs in the jejunum so we can feed people using a J tube using digested food or tube feeding formula The small intestine has a huge surface area for absorption Villi amp microvilli In the terminal ileum bile salts are reabsorbed and returned to the liver to be recycled again into more bile Enterohepatic Circulation Vitamin B12 combines with intrinsic factor for absorption in the ileum Most water is absorbed by osmosis in the small intestine as well Digestive Process Small Intestine Time to travel length of small intestine 310 hrs Some patients may have their small intestine partially resectioned surgically removed due to trauma radiation therapy etc gt Loss of part of the jejunum would lead to nutrient losses more than fluid gt Loss of part of the ileum would make person prone to dehydration amp loss of electrolytes Page 16 of 25 gt The ileum is able to compensateadapt over time for jejunum func ons Practice point patients kept NPO gt 3 days have ldigestive enzyme activity may exhibit food intolerance when refed It is important to initiate feeding slowly for better tolerance NPO NPO nothing by mouth NOS is an abbreviation for the latin phrase non per os or nil per os meaning nothing by mouth Sphincter between small amp large intestines ileocecal valve Absorption In absorption end products of digestion pass through the intestinal mucosal cells and make their ways into capillaries that feed into veins that take them to the liver Or In the case of fat chylomicrons are absorbed into lacteals those little lymphatic vessels and those enter lymphatic circulation first 3 Absorption Mechanisms 1 Simple Passive Diffusion going with the flow ATP Energy not needed 2 Facilitated Diffusion Needs Carrier Protein but ATP Energy not needed 3 Active Transport Needs Carrier Protein AND ATP Energy Page 17 of 25 Diffusion random movement of nutrients through mucosal cells to bloodstream ATP The energy molecule of cells energy from breakdown of ATP drives many important reactions in the cell Simple passive diffusion is sort of like going with the flow Molecules flow back amp forth as needed to maintain osmotic equivalency on either side Some small nutrients pass through membrane channels Driven by concentration gradient molecules will always move down their concentration gradient from high to low concentration No ATP no energy input needed Facilitated diffusion involves a carrier protein as a vehicle to move molecules too large to diffuse easily Molecules still diffusing down their concentration gradient but need to hitch a ride across the cell membrane No ATP no energy input needed Active Transport input of energy is required to move nutrient amp carrier protein across membrane Some nutrients share same carrier protein causing competition for absorption Transport Pathways through the Cell Membrane Large Intestine Anatomy The large intestine Frames the small intestine on three sides cecum appendix ascending colon transverse colon descending colon sigmoid colon rectum amp anus see labels on left diagram below Has quite a larger diameterthan small intestine Is 15 m long less than half as long as the small intestine Diffusion Active transport Channel Carrier protein proteins Facilitated Simiple diffusion diffusion Has many goblet cells which secrete mucus which ease the passing of feces amp protect the colonocytes colonic epithelial cells from gases produced Mucosa lines the inner lumen layer but there is NO villi or microvilli The ileocecal spinchter or valve keeps content that has reached the large intestine from backing up into the ileum of the small intestine Large Intestine Anatomy Continued The large intestine frames the small intestine on three sides cecum appendix ascending colon transverse colon descending colon sigmoid colon rectum amp anus End of Small intestine The ileocecal spinchter or valve keeps content that has reached the large intestine from backing up into the ileum of the small intestine Large Intestine no sagas enzymes Pa rotid I Sublingual T DUlthlh xq F v 7E I g quotSubrnaxillary Tongue Epiglo is opeu u closed Esophagus Tracnea Esophagus Stornacn Iapnraglm Splee n Liver bile Pa cweas Liver ducts 39 f Cystic duct digestive enzyrnes Gangladdew and Insulin l uodennm Bile duuct opening Pancreatic duct Transverse colon Descending colon Ascending colou Jejunun39l Ceculrn Appendix Sigmoid colon Rectum Anus The cecum is the first part of the large intestine right below the ileocecal valve The appendix is a fingerlike projection attached to the cecum It is about the size of your little finger It contains masses of lymphoid tissue It appears to serve no critical purpose but if it were to become blocked amp inflamed appendicitis it could even burst and spew bacteria over the peritoneum thin membrane that lines the abdominal wall amp covers the organs inside which could be lifethreatening An inflamed appendix is generally surgically removed Peristalsis amp Mass Movements are the two major propulsive movements occurring in the large intestine but peristalsis here is sluggish amp slow Mass movements are long powerful contractile waves that move over large areas of the colon You typically have 34 Mass Movements per day which move the contents of the colon toward the rectum gtWater and electrolytes are absorbed all along the way Along with a little absorption of vitamin K this is the only appreciable absorption that occurs in the large intestine Finally what is excreted is the feces which is mainly water bacteria mucous sloughed off cells some undigested food amp pigment Any condition that rushes food residue through the large intestine before it has sufficient time to absorb all the water would cause diarrhea On the flip side if food remnants remain in the colon too long then too too much water is absorbed and the stool could become hard and difficult to pass So dietary fiber and fluids can be very beneficial for bowel regularity Role of the Large Intestine Most of the nutrients from food have been extracted gt NO additional digestive enzymes are secreted into the large intestine The primary job of the large intestine is to concentrate and excrete waste products as feces The large intestine absorbs most of the remaining water all but 50200 mL and electrolytes Colonic salvage more on next page Page 20 of 25 colonic salvage colonic bacteria ferment undigested fiber amp resistant starch residual substrates in chyme to form shortchain fatty acids SCFA Fecal matter is 75 water and 25 solid organic matter comprised of 13 dead bacteria 2040 inorganic materials and fats 23 protein and the rest pigment undigested food undigested fiber amp resistant starches amp sloughed cells cells of the gut have a high turnover rate Recap of Gut Cell Turnover Rate Life span of Enterocytes is 72 hrs Enterocytes absorptive cells are the predominant epithelial cell type lining the gut lumen inner layer Large Intestine Colonic Bacteria Colonic Salvage Benefits of Colonic Bacteria Gut Bacteria Page 21 of 25 1 Colonic Salvage process Gut bacteria normal flora amp Organic Acids SCFA Undigested food material could present an overwhelming osmotic load into the large intestine but it doesn t because there are hundreds of species of microorganisms colonized in the large intestine good gut bacteria that make up our normal flora There is a symbiotic relationship between bacteria amp SCFA colonic bacteria can ferment certain types of undigested fiber amp resistant starch to form short chain fatty acids SCFA amp gases some have strong odor but SCFA will nourish normal flora amp colonocytes colonic epithelial cells So that is why a high fiber diet is thought to be a good thing Some forms of fiber like lignines aren t fermented but with adequate fluid intake will soften amp add bulk to stool making it easier to pass Lecture Points on Gut Flora ASCGDding 00 0quot where most fermentation occurs as colonic salvage Normal flora of colonic bacteria digest materials that resist degradation higher in the gut gt almost everything of nutrient value is absorbed by the end of the colon Bacteria consume residual CHO S and amino acids gt SCFAs SCFAs mostly absorbed with residual water providing 510 of energy 2 Good Colonic Bacteria colonize to keep out bad bacteria A decrease of good colonic bacteria can allow C Diff bacteria to colonize Clostridium difficile often called C difficile or C diff is a bacterium that can cause symptoms ranging from diarrhea to lifethreatening inflammation of the colon Illness from C difficile typically occurs after use of antibiotic medications 3 Colonic bacteria synthesizes a significant amount of vitamin K NOT enough to meet our needs also synthesizes a small amount of B12 thiamin riboflavin Probiotics are live microorganisms like those found in yogurt or kefir Prebiotics are carbohydrates like inulin or oligosasaccharide that aren t digested but they are fermented by those colonic bacteria Synbiotic food is a functional food that provides both probiotics amp prebiotics This is a hot area of research right now to see if probiotics amp the Page 22 of 25 optimal balance of bacteria in the gut could be good for GI health amp overall health and immune function too Hormones and GI Function The Digestive System is regulated by Nervous System amp Endocrine System Organs of the Endocrine System secreterelease hormones SEE SUMMARY CHART ON NEXT PAGE more info on chart gtgt Describe the roles of the following hormones in digestion gastrin secretin cholecystokininCCK motilin somatostatin gtgt Gastrin hormone released by g cells in the stomach stimuates gastric secretions amp motility GI muscle contraction stimulates parietal cells to secrete HCL amp chief cells to secrete IF Secretion initiated by Distension of antrum of the stomach lmpulses from vagus nerve as from sight or smell of food Presence of secretogues substance that promotes secretion partially digested proteins alcohol caffeine etc Inhibited by high acidity gtgt Secretin hormone released by cells in the proximal small intestine Acts as a traffic signal to regulate digestion Opposes the action amp secretion of gastrin Stimulates pancreas to release bicarbonate amp water into the duodenum Bicarbonate helps neutralize the acidic chyme Secretion initiated by Gastric acid amp digestive products in the duodenum gtgt Cholecystokinin CCK hormone released by cells in the small intestine in response to presence of HCI and food especially fat reaching the duodenum Stimulates pancreatic to release enzymes Signals gallbladder to contract amp secrete bile Increases satiety gtgt Motilin hormone released by cells in the upper small intestine in response to bile amp pancreatic secretions Page 23 of 25 T s gastric emptying amp stimulates gut motility also during fasting Erythromycin binds to motilin receptors used to treat delayed gastric emptying as for postanesthesia gtgt Somatostatin hormone produced throughout body abundant in GI tract Decreases GI motility Inhibits secretion of other GI hormones Endocrine System From Acts to some key hormones Gastrin g cells in stomach mucosa stimulates gastric secretions Secretion started by amp motility Distension of antrum of stomach Impulses from vagus nerve Sightsmell of food stimulates parietal cells to secrete HCL amp chief cells to Presence of secretoguesi partially secrete IF digested proteins alcohol caffeine etc HCL activates Pepsinogen inactive Inhibited by high acidity TO active enzyme Pepsin Secretin cells in the proximal small intestine Opposes the action amp secretion of gastrin traffic signal Secretion initiated by Stimulates the pancreas to Gastric acid amp digestive products release bicarbonate amp water stop to gastrin amp go in duodenum into duodenum Bicarbonate to bicarbonate helps neutralize the acidic chyme Cholecystokinin CCK released by cells in the small intestine 39 Stimulates pancreatic in response to presence of HCI amp enzyme release food especially fat Signals gallbladder to contract amp secrete bile Increases satiety Page 24 of 25 Motilin motility released by cells in the upper small intestine in response to bile amp pancreatic secretions also released during fasting every 100 min to stimulate gastric emptying amp gut motility housekeeping clears undigested material control of motilin is largely unknown perhaps stimulated by alkaline PH in duodenum T s gastric emptying and stimulates gut motility Erythromycin used to treat delayed gastric emptying as for postanesthesia Erythromycin binds to Motilin receptors Somatostatin lt motility produced throughout the body abundant in the GI tract Decreases GI motility Inhibits secretion of other GI hormones Page 25 of 25 NHM 365 SPATH STUDY GUIDE FOR MODULE ONE Nutrition Care Process and Documentation in the Medical Record Chapter 11 LecturePPT Self Study Guide for Module 1 NCP Review REVISED 7 JUNE 2015 gt Key Points definitions gtgt Key Pointdefinition is on SelfStudy Guide Contents Spath Study Guide page Nutrition Care Process amp Model p2 Evidencebased practice 4 Step Process PES Statement p 3 Three Domains of Nutrition Diagnosis Good PES Statement Medical Records p 6 Protected Health Information PHI Health Insurance Portability amp Accountability Act of 1996 HIPPA Documentation in the Medical Record p 7 The Joint Commission Do Not Use List Forbidden Abbreviations Nutrition Care Process Progress Notes amp the Medical Record p 8 Progress Notes most common formats for documentation PES Statement from Krause p 10 see Sample PES Statements Krause p 263 Page1of11 gtgt NUTRITION CARE PROCESS systematic process for applying evidencebased practice established by the American Dietetic Association gtgt EVIDENCEDBASED PRACTICE is the conscientious explicit and judicious use of current best evidence in making decisions about the care of the individual patient Integrates individual clinical expertise with the best available external clinical evidence from systematic research RDS use American Dietetic Association s Evidence Analysis Library to find best available evidence to answer questions regarding nutrition care gtgt Nutrition Care Model graphical representation of Nutrition Care Process Study Model at Krause p 254 2 items outside Model one with an arrow pointing in and the other arrow pointing out Screening amp Referral System nutrition screening may be done by health care professional as part of admissions process Persons quotat riskquot are referred to the RD for nutrition assessment Outcomes Management System monitor success of NCP implementation PatientClient amp RD relationship is at CENTER of the Model Model has 3 Rings Ring 1 Client s ability to access RD services Practice Settings Health Care Systems Social Systems Economics Ring 2 RD Resources Evidencebased Practice Code of Ethics Dietetics Knowledge Skills amp Competencies eg ADA S Standards of Professional Performance quotSOPPquot Krause p 258 Critical Thinking Collaboration Communication Ring 3 RD s 4 NCP Steps document each step 1 nutrition assessment amp reassessment use ADA Evidence Analysis Library 2 nutrition diagnosis PREPARE PES STATEMENT 3 nutrition intervention planning set goals implementation the quotwhat where when howquot of the care plan to address nutritionrelated causes of the problem food amp nutrition therapies nutrition edcounseling coordination of care referrals eg meals on wheels program 4 monitoring and evaluation determine what indicators eg weight to monitor Indicators should be based on signssymptoms and must be measurable evaluate indicators frequently to see if goals are being met and modify intervention as needed on a timely basis Page20f11 gtgt IDNT Reference Manual Snapshots p 17 35 49 63 know key into about each of 4 NCP steps gtgt PES Statement Problem Nutrition Diagnostic Label gtgt MUST USE phrasing from International Dietetics amp Nutrition Terminology IDNT Ref Manual Standardized Language for the Nutrition Care Process by the Academy of Nutrition and Dietetics Not every patient has a nutrition problem Address present problems only note any concerns about he patient developing a problem in the monitoring section of the note Etiology cause of or factors contributing to the problem COMPARE m USE phrasing from IDNT Manual eg swallowing difficulty Guides the intervention will nutrition intervention will improve problem Problem may not be clear no guessing Signs and Symptoms evidence that the problem exists how you know there is a problem There may be several signssymptoms Basis for monitoringevaluating gtgt Three Domains of Nutrition Diagnosis Nutrition Diagnostic Terminology 1 Intake NI excessive or inadequate intake compared to requirements 2 Clinical NC medical or physical conditions that are outside normal 3 Behavioralenvironmental NB knowledge attitudes beliefs physical environment access to food food safety Use phrasing for PES documentation NumbersIDNT Codes are used for billing purposes Class materials include numberscodes as a learning aid The Fewer number of PES Statements for a patient the Better Look for a nutritional diagnosis that combines problems gtgt What makes a GOOD PESStatement And how does it relate to intervention plan and to monitoring amp evaluation There is no one right way to write a PES but a good PES one should use an Intake domain diagnosis when possible since the intake domain is most specific to the RD role Page3of11 guide intervention so that it addresses the etiology or Signs amp Symptoms Intervention should be specific the what where when how of the care plan to address nutritionrelated causes of the problem use measurable Signs amp Symptoms so you can evaluate whether or not the problem is resolved or improved Hallmarks of a WELLWRITTEN PES Statement follows format Problem RELATED TO Etiology AS EVIDENCED BY Signs amp Symptoms Exception quotNo nutrition diagnosis at this timequot each PES statement relates to one problem short g 25 words amp simple gt See PES Statements chart on page 9 Important info from lecture in Things to Know column NUTRITION INTERVENTIONS Krause 269272 The RD is the only licensed provider who can reliably offer food and nutrition services that are credible amp individualized continuing education competency review evert 5 yrs to maintain certificate indepth knowledge of nutrients in foods nutrientdense foods vitaminminerals supps INTERVENTIONS FOOD amp NUTRIENT DELIVERY Compare Nutrition Prescription written by RD after diagnosis of nutrition problem designates the type amount and frequency of nutrition based on a person s disease process and disease management goals Diet Order in most states must be written by a licensed independent health care provider physician physician assistant advance practice nurses Some facilities may authorize the RD to write a DO Diet Planning Resources MyPlate Food Guidance System Dietary Guidelines for Americans Dietary Reference Intakes DRIs MODIFICATIONS OF THE NORMAL DIET Normal diet is the foundation for therapeutic diets The purpose of diet is to supply nutrients to the body in a form it can handle Modifications may be needed change in consistency high fiber gt or lt in energy value gainlose weight gt or lt in type of food or nutrient sodium restricted lactoserestricted elimination of specific foods allergy diet gluten free rebalance of amount of protein fat carbohydrate diet for diabetics Change in how nutrients delivered enteral nutrition within the intestinevia digestive system parenteral intravenous intramuscular Page4of11 DIET MODIFICATIONS IN HOSPITALIZED PATIENTS Regular or General Diet Serve as foundation for more diversified therapeutic diets In some institutions a diet that has no restrictions is called the regular or house diet basic diet of 16002200 kcal 6080 g of protein 80100 g fat 180300 g carbohydrate Some institutions provide healthy regular diet lowfat etc some focus on foods the patient is willing to eat some allow patient to choose from a selective menu 2 Consistency Modifications Modification of consistency for patients with chewing or swallowing difficulties Use of Clear Liquid Diet or Liquid Diet There is little scientific evidence supporting use of clear liquid diets as transition diets after surgery Usually 500600 kcal 510 g protein min fat 120130 carbo small amounts of sodium amp potassium Inadequate in calories fiver essential nutrients Also fuII liquid diets not recommended for a prolonged time FOOD INTAKE Need to consider both food served AND amount of food actually eaten meals amp snacks caloriecontaining beverages to accurately determine patient s energy amp nutrient intake Calorie counts even if inaccurate may justify need for enteral digestive tractintestine or parenteral intravenous intramuscular nutrition ACCEPTANCE amp PSYCHOLOGICAL FACTORS pleasant surroundings eating with others independence control over sequence of foods to be eaten participate in eating personal selection from menu room servicestyle menu attitude of caregiver INTERVENTIONS NUTRITION EDUCATION amp COUNSELING RD may only have a short time with patient but can teach quotsurvival 3kiSquot 99 types of foods to eatavoid timing of meals portion sizes INTERVENTION COORDINATION OF CARE when patient leaves facility the RD needs to prepare discharge nutritional summary for patient393 caregiver include patient in planning process play essential role in referrals and followup NUTRITION FOR TERMINALLY ILL HOSPICE PATIENT Page50f11 Nutrition support should be continued as long as patient wants it if patient is unable to communicate directly heshe may have prepared an Advance Directive that addresses end of lHeissues Person has the right to request or refuse nutrition Dietary restrictions rarely appropriate Food plan should fit the individual quotComfort feeding onlyquot may be a better alternative to tube feeding MEDICAL RECORDS permanent legal documents As of 2014 all health care facilities receiving MedicareMedicaid reimbursement required to use electronic health records Trend towards use of electronic medical records spurred by Institute of Medicine reports recommending use of technology to improve health care quality amp safety tech helps to avoid medical errors Clinical Info Systems used by Health Care Providers Electronic Health Record EH R describes info system that contains ALL the health information for a patient including the Medical Record Contains all info usually found in a paperbased system Eiectronic Medical Record EM R describes clinical info system used to document patient care Compare Personal Health Record PHR system used by consumer to maintain health info gtgt Medical Record includes Protected Health Information PHI gtgt The Health Insurance Portability amp Accountability Act of 1996 HIPPA protects the privacy of PHI HIPPA violations are serious civil amp criminal penalties grounds for termination Page60f11 PHI NoNos no use of thumb drives don t leave voice mail messages containing PHI social media never share your password never access PHI of person who is not your patient do not discuss PHI in public areas or where you may be overheard DOCUMENTATION IN THE MEDICAL RECORD 1st Rule of Documentation If it isn t documented it didn t happen gtgt The Joint Commission TJC formerly called Joint Commission on Accreditation of Healthcare Organizations is an independent not forprofit organization that accredits and certifies more than 20500 health care organizations and programs in the United States httpwwwiointcommissionordabout usabout the ioint commission maina3px gtgt requires RD to documentation of Nutrition Care Process gtgt requires use of DO NOT USE list forbidden abbreviations created in 2004 to help avoid misinterpretation of abbreviations acronyms symbols can result in Sentinel Events unintended events that are unanticipated and need to be prevented Must document any sentinel events Compare at present not required for preprogrammed health tech systems eg electronic medical records Applies to handwritten and freetext computer entry and to preprinted forms Page7of11 Accreditation Manual for Hospitals provides standards some standards apply to RDs requires institutions to complete nutrition screening with 24 hrs of admission to acute care but does NOT mandate a method to accomplish screening Documentation Must be done at the time of service not ahead of time or afterwards Entries must be signed with credentials Note Actual date and time If you forget to make an entry and do it later must provide 1 date and time that it should have been done 2 date and time that it was done If you make a correction draw a thin line through the incorrect statement Many health facilities use Problemoriented medical records POMRs that are organized according to the patient s primary problems There are many styles of entry eg ADIME SOAP but it is the content not style that is important All RD entries should address issues of nutrition status and needs be accurate amp complete and convey important info to other health care professionals involved with the patient gtgt RD documents the NCP in the PROGRESS section of the medical record Other health care professionals enter their progress notes here too RD reviews a Patient s complete medical record gtgt Most common formats for documenting progress notes in the medical record ADIME assessment diagnosis PES statement intervention monitoring evaluation Aligns with the Nutrition Care Process NCP SOAP subjective objective assessment PES statement plan Narrative brief summary of progress data action in a paragraph format often used to document brief interventionsfollowups to initial assessments NCP can be applied to this format Page8of11 Compare In the ADIME medical record format the PES Statement is included in the diagnosis In the SOAP format the PES Statement is included in the assessment Guidelines for documentation in a hospital setting for PAPERBASED SYSTEM Black pen or typewritten Entries should be legible Add DateTimeService signature credentials AT THE TIME OF ACTUAL SERVICE Late entries identify that entry is late enter 1 the actual daytime of entry AND 2 the daytime when entry should have been made Info accidentally omitted 1 write see addendum by the original entry date your initials 2 enter info label as Addendum datetime of original entry Patient namehospital number on each page Chronological amp consecutive First word of each statement capitalized and period placed at the end Complete sentences NOT necessary Correct grammar amp spelling NONOs No personal opinions or criticism of professionalism of others Never erase a word statement etc If correction needed draw a single thin line through the error and initial Never add notes after the fact without accurately authenticating dating and referencing the original entry Never remove an original and replace with a copy PES Statement Things to know Inadequate energy intake related to poorly fitted dentures and hoarding of oral supplement as evidenced by observation and pt report of pain when chewing food with dentures Uses Intake diagnosis label Uses bridging phrases related to as evidenced by Inadequate energy intake related to chewing difficulty and poor appetite as evidenced by diet history and recent unintentional weight loss Chewing difficulty related to illfitting denture as evidenced by diet history and pt report Uses 2 PES statements for this patient Uses bridging phrases Page90f11 Excessive energy intake related to frequent intake from fast food restaurants as evidenced by BMI of 30 and pt report of 25 wt gain over the past year OR Excessive fat intake related to high intake of fried foods and bakery goods as evidenced by diet history and hyperlipidemia OR Excessive energy intake related to high intake of fried foods and snack items as evidenced by diet history and BNI of 30 PES statements may be written different ways Foodnutrition related knowledge deficit related to lack of education on cholesterollowering diet as evidenced by new dx of hyperlipidemia and patient selfreport quotFoodnutrition related knowledge deficitquot diagnosis should be used with caution but here it is appropriate for 2 reasons 1 there is a new medical diagnosis hyperlipidemia and 2 the patient reports lack of knowledge Foodnutrition related knowledge deficit related to lack of prior exposure to information as evidenced by client having no prior information of need for lowresidue diet quotFoodnutrition related knowledge deficitquot diagnosis is appropriate because the patient reports lack of knowledge No nutrition diagnosis at this time Not all patients have a nutrition problem Bridging phrases not needed Malnutrition related to unknown etiology as evidenced by low body weight Don t guess It is ok to say quotunknown etiologyquot but is rarely used Increased nutrient needs related to increased nutrient needs as evidenced by potential effects of chemotherapy General rule is to deal with the here and now Exception patient is about to undergo chemo Diagnostic abel quotincreased nutrient needsquot is used for etiology PES STATEMENT taken from Case study at Krause 263 Intervention MonitoringEvaluation Page 10 of 11 Foodnutrition related knowledge deficit related to lack of prior exposure to information as evidenced by client having no prior knowledge of need for low residue diet Compare PES for liquid diet post bariatric surgery Foodnutrition related knowledge deficit related to lack of information as evidenced by bariatric surgery pt having no prior knowledge of need for full liquid diet postop Education will provide pt with written and verbal instruction on lowresidue diet Goals Pt will be able to develop 1day menu using dietary restrictions Pt will be able to identify good sources of calcium and protein from list of foods appropriate for lowresidue diet Pt will ask appropriate questions and verbalize understanding of dietary modifications Follow up with pt regarding questions about diet indicated no further questions good comprehension Evaluation anticipate no problems following diet at home Gave business cardphone contact Sample PES Statements Krause p 263 Look over sample language Page11 of11 Spat Study Guide for NHM 365 Module 6 Disorders of the Oral Cavity Esophagus amp Stomach Part One MNT for Disorders of the Oral Cavity gt Part One MNT for Disorders of the Oral Cavity 45 slides Part Two MNT for Upper GI Disorders 41 slides gt Key Points definitions gtgt Key Pointdefinition is on SelfStudy Guide gt Tricky Question Alert Contents Anatomy of a tooth enamel dentin amp pulp Fluoride s effect on tooth enamel Pathophysiology of dental caries Saliva is protective against dental caries Pathophysiology of periodontal disease Cariostatic foods vs Cariogenic foods Considerations for patients who are endentulous fullpartial loss of teeth Stomatitis Glossitis amp Cheilosis common causes Head amp neck cancer patients Stomatitis Xerostomia Dysphagia Xerostomia Underlying causes MNT modalities Dysphagia oropharyngeal vs esophageal Dysphagia signssymptoms Dysphagia cases amp complications Dysphagia problem consistencies RD Role for dysphagia management National Dysphagia Diet Levels National Dysphagia Liquid Viscosities Page 1 of 27 Nutrition amp diet play key roles in tooth development integrity of the gingiva gums and mucosa bone strength amp preventionmanagement of diseases of the oral cavity gtgt Describe the anatomy of a tooth including the enamel dentin amp pulp gt Enamel Hard white tooth enamel is made up of Hydroxyapatite a naturally occurring form of calcium amp phosphorus Hydroxyapatite calciumphosphate crystals that make up tooth enamel just like the bones Fluoride stabilizes these crystals Calcium amp vitamin D are important for bone amp tooth health gt Dentin is the main part of the tooth It is mostly collagen surrounds pulp and is covered by the enamel Vitamin C is important for collagen formation Scurvy is a disease that occurs due to a severe lack of vitamin C ascorbic acid in your diet One signsymptom is painful bleeding gums gt Pulp the soft part of the tooth that is supplied by the nerves lFlGURE 251 Anatomy of a tooth Elsevier items and derived Items 91 2006 2004 by Saunders an ilnnri l 0f EISEVieV E Page 2 of 27 gtgt Describe the pathophysiology of dental caries Pathophysiology of Dental Caries takes 5 simultaneous things Dental Caries is a medical term for tooth decay cavities It is an infectious disease because it involves bacteria know Dental Caries is an oral infectious disease in which organic acid metabolites lead to a gradual demineralization of tooth enamel followed by rapid proteolytic destruction of the tooth structure from Krause gt 5 factors must be present simultaneously for dental caries to occur 1 Susceptible host or tooth surface composition of enamel amp dentin location of teeth pits amp fissures in teeth saliva usually protects surface of teeth gt Normally alkaline saliva with lysozymes microbacterial protective agents protects tooth enamel from acid above pH 55 2 Microorganisms Bacteria eg Streptococcus mutans most prevalent bacteria in mouth metabolize fermentable CHO in mouth producing acid as a byproduct 3 Fermentable carbohydrates CHO susceptible to the actions of salivary amylase 4 pH lt 55 drop in pH is caused by acids from fermentable CHO metabolism acids produced by metabolism of fermentable CHO causes drop to lt 55 5 Time to produce acids takes only minutes gt Plaque a sticky film that accumulates on teeth in the pH lt 55 environment consists of food debris amp bacteria amp acid amp saliva Plaque can combine with calcium amp harden into tartar which is removed by a dental hygienist gt Acid in plaque can cause demineralization of tooth enamel Eventually the dentin amp pulp can become exposed Acid amp bacteria can continue into pulp amp cause an abscessed tooth Page 3 of 27 gt Plaque is the primary cause of periodontal disease It produces toxins that destroy tissue amp permit the loosening of teeth more on p 5 gtgt How is saliva protective against dental caries Normally saliva acts as a buffer Saliva is 1 alkaline which offsets lactic acid amp keeps mouth pH gt55 2 has Iysozymes which are microbacterial protective agents Fluoride F Topical Fluoride amp Drinking Water Fluoride are protective against dental caries know gtgt How does fluoride affect enamel Two ways 1 Topical Fluoride stabilizes the enamel Applying Fluoride to the teeth stabilizes hydroxyapaptite crystals in tooth enamel eg fluoride rinse fluoride toothpaste 2 Drinking water Fluoride prevents demineralization by making enamel stronger Fluoroapatite Fluoride in the water protects tooth enamel from demineralization by making the enamel more resistant to acid Fluoride interacts with calcium phosphate crystals of hydroxyapatite to form Fluoroapatite a compound more resistant to acid than hydroxyapatite Fluoride is the ionic form of the element fluorine Fluoride has one extra ion that gives it a negative charge which allows it to interact with calcium phosphate crystals of hydroxyapatite to form Fluoroapatite Fluoride is a trace element and is found naturally in a few foods Fluoride is toxic at high doses Level of fluoride in drinking water is very low gt Fluorosis occurs when there is excess fluoride in the diet during tooth development while the teeth are under the gums and can cause dark spots to develop on teeth enamel May also cause pitting of tooth enamel Page 4 of 27 Children younger than 68 yo should not use fluoridated mouthwashes Should use only a small amount of fluoride toothpaste Toothpaste should not be swallowed Periodontal Disease and Nutrition The relationship of periodontal disease and nutrition is reciprocal Good nutrition helps ward off periodontal disease and keeps teeth healthy Healthy teeth ward off decreased intake of certain foods of high nutritional value due to chewing difficulties gtgt Describe the pathophysiology of periodontal disease gt Periodontal disease is the inflammation of the gingiva gums aka gingivitis that affects the tissues that support and anchor teeth Can lead to edentulism loss of some or all of the teeth gt Plaque is the primary cause of the development of periodontal disease Factors in the defense of the gingiva from bacterial infection oral hygiene integrity of the immune system gt optimal nutrition to protect gingival tissue epithelial barrier amp saliva Healthy epithelial tissue prevents the penetration of bacterial endotoxins into subgingival tissue SaliVa s bicarbonatecarbonic acid and phosphate buffering system neutralizes bacterial acid metabolism Saliva also clears food from around teeth Page 5 of 27 know gtgt Contrast Cariogenic and Cariostatic foods Cariostatic foods tending to inhibit the formation of dental caries Cariogenic foods producing or promoting the development of tooth decay Relativer T protein Moderate fat minimal CHO T concentration of Ca and phosphorus pH gt6 Stimulates saliva secretion cheese peanuts meat milk eggs some vegetables T fermentable CHO content starch sugars or a mixture Sticky consistency Breaks into small particles in the mouth Causes pH to fall lt 55 Carbonated beverages even sugar free Highly processed crackers pre sweetened cereals breads muffins dried fruits cookies potato chips chewable vitamin C Dairy products are alkaline amp have calciumand phosphorusbuffering potential High fiber foods with few or no fermentable CHO such as popcorn or raw veggies are cariostatic diet soft drinks may not contain sugar but they are acidic by nature and can cause pH to fall Page 6 of 27 Other cariostatic foods nuts oils chewable vitamin C supplements provide margarine butter amp seeds an acidic substance that directly contacts tooth surfaces amp causes pH to fall xylitol a 5carbon sugar alcohol artifical sweetener found in chewing gum bacteria eg Streptococcus mutans can t metabolize 5carbon the way they do 6carbon sugars eg glucose sucrose amp fructose xylitol is non fermentable not broken down by salivary amylase xylitol stimulates saliva xylitol inhibits Streptococcus mutans xylitol replaces fermentable CHO in diet thought to be protective against caries Page 7 of 27 Sample Cariostatic Diet Plan El eu er ilenns and derived i39tE 39 lE E 212 RUDE1 2 by Sundem iEi39I impr li Eff EIlEE39uriEI39 uric Page 8 of 27 Management of Periodontal Disease Dental Brush at least 2 x day preferably after meals Rinse mouth after meals and snacks when unable to brush Chew sugarless gum 1520 min after meals and snacks Xylitol in sugarless gum is cariostatic Floss twice daily Use fluoridated toothpastes Nutrition Pair cariogenic foods with cariostatic foods When snacking choose cariostatic foods Limit betweenmeal eating and drinking of fermentable CHO Nutritional Deficiencies Increase the Risk of Periodontal Disease Protein needed for collagen formation Vitamin C needed for collagen formation antioxidant Folate tissue repair Zinc tissue repair gingival permeability Micronutrient deficiencies are often first detected by changes in the oral cavity Because oral mucosa cells have a rapid turnover rate you can see signs of micronutrient deficiency in the oral cavity before other places Page 9 of 27 Treatment of Periodontal Disease MNT importance of pre and postsurgical diet Adequate kcals energy and protein Adequate intake of Ca Zn Phos F and vitamins C A amp D micronutrients gt Maintain appropriate blood glucose levels Hyperglycemia poorly controlled blood sugar is associated with periodontal disease dental caries and Thrush Oral Candidiasis a fungal infection Texture modification of diet Soft diet may be warranted Oral supplements as needed Timing of meals and snacks to decrease tissue exposure to bacteria and acids Severe periodontal disease may require surgery Hyperglycemia an excess of glucose in the bloodstream often associated with diabetes mellitus Page 10 of 27 Tooth Loss and Dentures o More common in older adults with chronic disease social isolation and use of multiple medications Edentulism loss of teeth full or partial should be part of the assessment Dentures may not fit properly Increased tooth loss results in an inadequate intake of dietary fiber vitamins and minerals Can impact Dietary habits Masticatory function Nutritional adequacy of diet Dentures Foods causing the greatest problem for persons with complete dentures gt Fresh whole fruits and vegetables Hardcrusted breads Steak Page 1 1 of 27 Sticky foods White breads Chewy candies Chewing gum Have a handout for older persons that lists soft protein foods eggs yogurt amp cottage cheese amp soft fiber foods gtgt List some considerations for patients who are edentulous having full or partial tooth loss MNT for Tooth Loss and Dentures Importance of balanced diet Peel cut and chop fruits and vegetables to minimize need for biting and to reduce the amount of chewing Cook foods to a softer consistency Fresh amp frozen vegetable may have more nutrients and less sodium than a canned variety but applesauce and canned vegetables are often very soft and inexpensive So rinsing canned vegetables to get rid of sodium may be a better option for someone who wears dentures Canned carrots are better than no carrots at all Blended smoothies Liquid supplements like Boost or Ensure Cut meats and vegetables across the fibers into bitesized pieces Page 12 of 27 Avoid sticky foods know gtgt Define stomatitis glossitis and cheilosis What are some common causes of each oral cavity disorder stomatitis glossitis cheilosis itis inflammation itis inflammation Inflammation of the oral mucosa Causes severe pain and ulceration of the gingiva oral mucosa and palate gt painful ea ng inflammation of tongue amp lips fissuring amp scaling at the corners and angles of the mouth Page 13 of 27 Common causes HNAMS lupus Radiation therapy for cancer very frequently Autoimmune disease eg Common causes o Iron deficiency anemia 39 pernicious anemia B12 deficiency other Bvitamins deficiency Common causes Signature sign of Riboflavin deficiency may also indicate iron deficiency MNT for Stomatitis Glossitis amp Cheilosis eating can be painful with any of these conditions using a straw for liquids might help direct fluids away from painful areas numbing the mouth with ice chips or sugar free popsicles Good oral hygiene AVOId very hot or cold foodsbeverages carbonated beverages caffeine alcohol and tobacco products acidic or spicy foods Treat oral lesions caused by candidiasis thrush with antifungal meds gtTreat micronutrient deficiencies Consider using oral topical agents and anesthetics gtPossibly oral glutamine supplementation glutamine is a conditionally essential amino acid amp has some antiinflammatory properties amp may help with these conditions It helps with the rapidly turning over oral mucosa cells Xerostomia know gtgt What is xerostomia Xerostomia is Dry Mouth little or no saliva gtgt What are some of the underlying causes of xerostomia dehydration poorly controlled diabetes mellitus several autoimmune diseases consequence of radiation therapy Page 14 of 27 Cel tain medications DO NOT HAVE TO MEMORIZE LIST BUT HAVE AN APPRECIATION OF THE MANY TYPES OF MEDS THAT CAN CAUSE DRY MOUTH Antianxiety agents Anticonvulsants Antidepressants Antihistamines Antihypertensives gt Diuretics Narcotics Sedatives Serotonin uptake inhibitors Tranquilizers gtgt What are some MNT modalities not sure what Prof means by modalities but must be info on p 1314 know Common Problem Foods Associated with Xerostomia gt Lack of saliva impedes all aspects of eating Moistening amp swallowing food the water amp egcoproteins in saliva moisten food amp make it easier to swallow Tasting Food in order to taste the chemoreceptors on our tongue need to be stimulated by particles in solution so without saliva taste may be compromised Prone to dental caries without alkaline saliva and its antimicrobials a person is more prone to dental carries know Persons with Xerostomia usually have problems eating these foods Chewy steak Crumny cake crackers rice Dry chips crackers Sticky peanut butter gtgt What are some MNT modalities more MNT for Xerostomia Consume moist foods without added spices T fluid intake sip on liquids throughout the day Page 15 of 27 Sucking on sugarfree items frozen tart grapes berries sugarfree candy or ice chips Add extra sauces and gravies to foods Good oral hygiene habits Some overthecounter saliva substitutes may interact with medications Alcoholfree mouthwash may be helpful know gtgt Many head and neck cancer patients experience compromised nutrition Why Radiation or other cancer therapy may cause Page 16 of 27 1 Stomatitis Inflammation of the oral mucosa which causes severe pain and ulceration of the gingiva oral mucosa and palate gt painful eating p12 radiation therapy 1 Xerostomia p13 radiation therapy 2 Dysphagia p 17 trauma to swallowing structures gtgt What are some specific nutrition problems of head and neck cancer patients How would you address each one know MNT for Stomatitis p 12 use a straw for liquids to direct fluids away from painful areas numb the mouth with ice chips or sugar free popsicles Avoid very hot or cold foodsbeverages carbonated beverages caffeine alcohol and tobacco products acidic or spicy foods Treat micronutrient deficiencies know MNT for Xerostomia p 14 Consume moist foods without added spices T fluid intake sip on liquids throughout the day Sucking on sugarfree items frozen tart grapes berries sugarfree candy or ice chips Add extra sauces and gravies to foods know MNT for Dysphagia p 21 Avoid Thin Liquids like water are most commonly aspirated because they require a lot of muscular control amp coordination for a safe swallow Particulate Foods crackers foods that crumble in the mouth Stringy Foods Mechanically Intensive Foods baguette tough meats Mixed Consistencies vegetable soup cereal in milk Page 17 of 27 Polypharmacy Regular use of multiple prescriptions or overthecounter meds gt Medications can alter the integrity of the oral mucosa gt impairs taste dysgeusia amp alters saliva production gt altered taste dysgeusia Several medications cause a metallic taste Ways to alleviate metallic taste are to use plastic utensils when eating instead of stainless steel drinking out of a glass instead of a can eating food at room temperature or eating cold food instead of hot gt don t confuse dysgeusia with dysphagia gtgt What is dysphagia Contrast oropharyngeal with esophageal dysphagia gt Dysphagia is difficulty with swallowing Person may have one or both of these 2 swallowing difficulties gt Oropharyngeal dysphagia Difficulty with swallowing in the mouth and throat or pharynx gt Esophageal dysphagia Motility and structural disorder of the esophagus Complication of Dysphagia Swallowing difficulty can result in food going down the wrong way gt Aspiration entry of a foreign substance into the respiratory tract For example food or fluid even water goes down the wrong way and enters the air pipe This could result in a person having aspirational pneumonia Page 18 of 27 Causes of Dysphagia gtgtWhat are some possible causes of dysphagia What are some potential complications Dysphagia is generally a secondary diagnosis or a symptom of an underlying disease as shown below Neurological disordersconditions Multiple Sclerosis Muscular Dystrophies Stroke Parkinson s Disease AIzheimer S Disease ALS Swallowing requires a lot if neuromuscular control A person with demential of impaired pathways could silently aspirate food could enter the lungs without the person having a gag reflex Diseases or conditions affecting head and neck gtgtHead and Neck Cancer trauma to the swallowing structures Pharyngeal diVertiCUla diverticula little out pouches of mucosa Aging process Combined Chronic diseases Gastro Esophagea Re ex Disease Developmental problems Premature birth Cerebral Palsy Medication Antipsychotic or neuroleptic therapy Anticonvulsant antiemetic antihistamine Cardiac meds and steroids Page 19 of 27 Swallowing Occurs in 3 Phases Oral all actions are voluntary food is manipulated into a bolus amp propelled to the rear of oral cavity Pharyngeal involuntary reflexive actions food passes from the mouth to the esophagus The soft palate will elevate and close off the nasal pharyngeal area which prevents regurgitation The larynx and the hyoid bone will elevate Vocal cord closes to prevent foodliquid from entering the airways avoids aspiration Breathing stops very very briefly during this phase llar39d Bolus Soft Posterior palate of food palate nares lPharynx lEpiglcttis Tongue V Vocal 39 ESOPNEQUJS cords 39 Perlstaltic wave llLarytnx 39 39 Bolus of food irt esophagus ESOPHAGEAL PHASE 1 ORAL PHASE voluntary 3 involuntary Page 20 of 27 Esophageal involuntary reflexive actions final transit of food from esophagus to stomach gtgt Describe the signssymptoms of dysphagia Red Flag Signs and Symptoms of Dysphagia Difficulty managing oral suction Drooling of secretions or food Delayed swallowing initiation Coughing or choking during or after swallowing Prolonged eating timeinability to finish a meal Food avoidance Weight loss or dehydration Nasal regurgitation oropharyngeal regurgitation Wet gurgle voice after swallowing URls or pneumonia MNT the RD will evaluate the person s nutritional intake Tube feeding may be needed gtgtWhat are some potential complications of dysphagia Complications of Dysphagia Malnutrition Caused by anorexia Dehydration Resulting from decreased fluid intake Respiratory problems and infection Liquidsfoods aspirated into lungs Page 21 of 27 Aspiration pneumonia Diagnosis of Dysphagia The Speechlanguage pathologist or speech therapist leads the medical team in evaluation of dysphagia The first and most important evaluation is a thorough interview of the patient and caregivers Then speech therapist then commonly gives what is called a bedside swallow test by observing the patient eat amp drink to see how well they handle different food consistencies Diagnostic tests that allow visualization of person s swallowing Barium Xray Modified Barium Swallow Test very common test different consistencies of food amp fluids are labeled made radioactive with barium so they can be tracked after the person swallows them Can see visual images of swallowed foodfluid on a video monitor Can see aspiration EndOSCOpy fiberoptic endoscopic evaluation of swallowing FEES test not as common as the Barium Xray test Treatment Based on the evaluation amp test results the speech therapist would recommend compensatory strategies Exercise help coordinate swallowing muscles and restimulate the nerves that trigger swallowing Positioning of head when eatingdrinking Environment Page 22 of 27 Diet modifications small frequent meals so as not to fatigue muscles involved in swallowing cold food or liquid may be easier to handle Cold can bring the sensory nerves into the game to facilitate the swallow gtgt What are some common problem consistencies for dysphagia patients Problem Consistencies gt Thin Liquids like water are most commonly aspirated they require a lot of muscular control amp coordination for a safe swallow Particulate Foods crackers foods that crumble in the mouth Stringy Foods Mechanically Intensive Foods baguette tough meats Mixed Consistencies vegetable soup cereal in milk Pills crush pills or take them with a food like applesauce or pudding which are safer than taking a pill with water gtgt Review the role of the RD for dysphagia management including diet modification oral PROkcal supplements and enteral nutrition support gtgt The speech therapist amp the RD often work together as a team to identify foods that the patient enjoys that meet the patient s nutritional needs and that are also safe and easy to swallow Page 23 of 27 MNT for Dysphagia Oral feeding related to quality of life maintain it possible Determine swallowing abilities and provide appropriate modified diet With modified diets sensory appeal becomes more important Aroma Seasoning Plate Presentation gt Provide enteral nutrition via tube feeding support it The gut works but pt is at high risk of aspiration from oral intake Patient cannot eat enough nocturnal feedings The National Dysphagia Diet NDD Published in 2002 American Dietetic Association which is now the Academy of Nutrition amp Dietetics Aim to establish standard terminology amp practice applications of gt dietary texture modification in dysphagia management know gtgt Know the 3 levels of the National Dysphagia Diet details on the next page Level 1 DysphagiaPureed homogenous very cohesive puddinglike requiring very little chewing ability Level 2 DysphagiaMechanical Altered cohesive moist semisolid foods requiring some chewing Page 24 of 27 Level 3 DysphagiaAdvanced soft foods that require more chewing ability know gtgtNDD 1 Dysphagia Pureedquot Foods of quotpuddinglikequot consistency that are smooth or pureed with no lumps Not included are JellO fruited yogurt peanut butter unblenderizedunpureed cottage cheese scrambled fried or hard cooked eggs Jeo turns into a thin liquid in someone s mouth peanut butter is too sticky cottage cheese needs to be blended or pureed scrambed fried or hard cooked eggs why not Sample menu pureed chicken mashed potatoes with gravy pureed carrots pureed broccoli and chocolate pudding know gtgtNDD 2 Dysphagia Mechanically Altered aka Mechanical Soft Page 25 of 27 Foods that are moist and softtextured such as tender ground or finely diced meats softcooked vegetables without skin soft ripe or canned fruit without skin and some moistened cereals Not allowed on this diet bread dry cake rice cheese cubes corn and peas Sample menu diced tender chicken with gravy carrots moist cake with icing know gtgt NDD 3 quotDysphagia Advancedquot Most regular foods except very hard sticky or crunchy items Bread rice cake shredded lettuce and tender moist meats are allowed Not allowed are hard difficult to chew fruit amp vegetables corn skins nuts and seeds Sample menu vegetable soup shredded lettuce salad with dressing turkey sandwich with mayonnaise fresh ripe melon and chocolate chip cookie with no nuts NDD and Liquid Viscosity Thickening a liquid can make it easier to swallow know gtgt Know Liquid Viscosities as defined by National Dysphagia Diet 1 Thin water milk juice coffee tea carbonated drinks gelatin ice cream sherbet sorbet and brothbased soups 2 Nectarlike aka Nectar Thick fruit nectars maple syrup Ensure eggnog tomato juice and creambased soups 3 Honeylike aka Honey Thick consistency of honey Page 26 of 27 4 Spoonthick aka Pudding Thick pudding gt The speech language pathologist would tell the RD what the liquid viscosity should be for a specific patient How are liquids thickened Many commercial thickeners are available They can make swallowing much easier amp safer Make sure patient is getting enough fluid to avoid dehydration There are two types of food thickeners 1 Starch thickener made out of modified starch or maltodextrin powdered form Brand names Thick It and Thicken Up 2 Gelbased thickener premeasured packets based on desired consistency Brand names Simply Thick Hormel Beware Health care personnel sometimes believe thicker is better and do not follow thickening instructions Commercially prepared thickened liquids are available Page 27 of 27 Spat Study Guide for NHM 365 Module 6 Disorders of the Oral Cavity Esophagus amp Stomach Part Two MNT Therapy for Upper GI Disorders Revised page 8 Part One Overview of Digestion and Absorption gt Part Two MNT Therapy for Upper GI Disorders gt Key Points definitions gtgt Key Pointdefinition is on SelfStudy Guide gt Tricky Question Alert Contents Esophageal Strictures Achalasia GERD GERD Meds Antacids PPIS Histamine receptor antagonists H2 Blockers Prokinetic agents GERD Nissen fundoplication Stretta procedure Barrett s Esophagus Hiatal Hernia Eesophageal varices portal HTN cirrhosis MNT Dyspepsia amp functional dyspepsia Gastritis acute amp chronic atrophic gastritis amp achlorhydria ulcer peptic ulcer PUD What are the ss and goals of MNT for peptic ulcers Total gastrectomy vs Partial Subtotal gastrectomy ZollingerEllison Syndrome Billroth I amp Billroth II RouxenY gastric bypass procedure bariatric surgery Sleeve Gasterectomy Vagotomy Pyloroplasty Gastric Surgery postop amp complications Dumping Syndrome other complications Gastroparesis bezoars Page 1 of 26 Crisepharyngeus museie upper Iv esophageal sphincter iiherseis pairt ANNE amh st esophagus with negative E intratheraeie pressure r Lsit hrehehus Diaphragm Positive intrsahdominai a pressure 39 Stemsth Medi ed Frem Prise SA Wisen LM Fethephysierogy clinical concepts er disease processes ed a Si Leuis 20GB Messy Epidemiology Digestive disorders most common problems in health care 3040 elderly gt swallowing problems Page 2 of 26 20 adults gt frequent indigestion 44 adults gt heartburn at least once a month gtgt Define esophageal strictures What are some 55 of esophageal strictures Describe the appropriate diet choices for someone with this condition Disorders of the Esophagus Strictures Motility Disorder The esophagus really doesn t do too much in the way of digestion amp absorption It is really just the conduit to get the food from the mouth down to the stomach and intestines where the real work gets done During a normal swallowthe upper esophageal sphincter relaxes and the food moves from the mouth into the esophagus Then peristalsis propels the food forward towards the stomach and the lower esophageal sphincter relaxes to allow the food into the stomach gt So the job of the esophagus is motility People can have motility disorders that cause a lot of grief eg strictures Esophageal strictures narrowing of the esophagus Can be caused by many different things may be idiopathic etiology unknown gt One common cause is repeated Gastro Esophageal Reflux GERD If acid from the stomach continuously refluxes back into the esophagus it can cause inflammation of the lower esophagus Scarring can occur and cause a stricture or narrowing of the esophagus SymptomsSigns Regurgitation Dysphagia Food gets stuck in my chest frequent burping or hiccups Tx Esophageal dilation works if there is a blockage may not work if the esophagus is just spastic or weakened Soft dietwellchewed foods small bites Page 3 of 26 Good posture while eating Small frequent meals Plenty of fluids with meals Room temperature foods if esophagus is spastic very hot or very cold foods may trigger spasm gtgtWhat is achalasia What are some 55 of achalasia Describe the appropriate diet choices for someone with this condition Disorders of the Esophagus Achalasia Motility Disorder gt Achalasia means failure to relax it is the failure of the LES lower esophageal sphincter to relax and let food pass into the stomach Achalasia Motility disorder involving the smooth muscle layer of the esophagus and the LES Iower r f esophageal sphincter HgL f Emormgua 31quot i 2 gt More common in younger adults than older Dita adults gt Is a fairly rare disorder fw 3 Cumtraoted muscle x Elevated LES pressure Impaired relaxation of LES Aperistalsis absence of peristalsis of the esophagus May be idiopathic or secondary SignsSymptoms initially choking sensation food gets stuck o Dysphagia vomiting substernal pain Body of esophagus loses muscle tone and stretches Poor oral intake weight loss malnutrition inflammation of the esophagus Complication aspiration pneumonia if someone is regurgitating food Page 4 of 26 MNT for Achalasia Alter diet COHSiStenCY Semisolid pureed or liquid foods Increase nutrient qualitydensity Avoid extreme temperatures or spicy foods Small frequent meals i fiber intake Emsbww Disorders of the Esophagus Gastroesophageal Reflux Disease GERD or Heartburn GERD reflux of gastric contents chyme into the esophagus because the esophageal sphincter relaxes too much Fluid pH of most of our body fluid is 74 Chyme can have a pH of around 2 the stomach has a lot of hydrochloric acid so the chyme is very acidic The stomach has plenty of goblet cells to produce mucus and the stomach is protected by the thin layer of bicarbonate that is secreted by the epithelial cells of the mucosa gtgtName some factors that may predispose a person to GERD Dysregulation of LES causing it to relax too much can be caused by Increased secretion of gastrin estrogen progesterone eg hormone secretions associated with pregnancy Hiatal hernia Cigarette smoking Use of medications Esophagus Lower Esophageal Sphincter Open allowing Reflux Diaphragm Lower Esophagus Sphincter Closed Fquotrorus ur 7 l vquot 39 I 7 quotZf Stomaoh zoos h edioineNet inro gtgt What are some common problem foods for someone with GERD Common trigger foods Foods high in fat empty food the most slowly chocolate spearmint peppermint alcohol caffeine o Alcohol amp caffeine relax the LES amp stimulates gastric acid production GERD SignsSymptoms Heartburn Dysphagia Increased salivation Belching Pain radiating to back neck or jaw Aspiration Ulceration Barrett s esophagus gtgt Describe other aspects of MNT for GERD GERD MNT Identify and avoid foods that worsen symptoms trigger foods vary by person A lot of GERD management is trial amp error to determine which foods worsen a person s symptoms the pH of food is not of major importance unless the person already has lesions or erosion in the esophagus Then low pH acidic foods could be painful Chyme will have a much lower pH than any of the foods Avoid acidic and highly spiced foods When inflammation exists gt Avoid foods which decrease LES pressure highfat foods chocolate EtOH alcohol caffeine mint Cho39eCYStOKinin CCK stimulates relaxation of LES ie lowers LES pressure CCK especially responds to fat Fat takes longer to pass through the stomach so relaxation of LES may last longer after a large highfat meal Page 6 of 26 DFOtein fOOdS don t seem to decrease LES pressure as much fiber also passes through the stomach slowly but guidelines do not say to restrict the amount of fiber in the diet Consume small frequent meals Avoid lying down bending over straining immediately after meals Avoid eating 23 hrs prior to bedtime Sleep with torso elevated 46 inches Lose weight if warranted GERD Lifestyle tx Avoid tightfitting clothes Assess smoking and physical activity Incorporate regular exercise but avoid vigorous exercise immediately after ea ng GERD Medications acid suppression is mainstay of tx gtgt Medicinal management is the mainstay of GERD tx Briefly describe how these classes of medications work to reduce symptoms Antacids PPls Histamine receptor antagonists H2 Blockers Prokinetic agents Antacids neutralize chyme i acidity of gastric fluids amp T LES pressure Aluminum hydroxide Mg hydroxide calcium carbonate Mylanta Maalox AlkaSeltzer is sodium bicarbonate Tums is calcium carbonate Calcium amp aluminum based antacids may cause constipation Magnesium based antacids may cause diarrhea Proton pump inhibitors PPls Page 7 of 26 gt l Gastric acid production by parietal cells they block an enzyme in parietal cells that is necessary for pumping out stomach acid so less hydrochloric acid is produced most effective amp most common type of medication for GERD Eg Lansoprazole Prevacid esomeprazole Nexium Omeprazole Prilosec pantoprazole Protonix Histamine receptor antagonist H2 blockers gt l Gastric acid production by blocking histamine receptors in the parietal cells Eg Ranitidine Zantac Cimetidine Tagamet Famotidine Pepcid AC Prokinetic agents dopamine antagonists T LES pressure amp speed GI emptying rate Metoclompramide Reglan GERD Surgery gt Note Nissen fundoplication and Stretta procedure both directly improve the lower esophageal sphincter LES gtgt If medicinal management and lifestyle changes for GERD fail Nissen fundoplication is a surgical option Describe the procedure and how it alleviates ss Nissen fundoplication shown at right The upper part of the stomach or the fundus is wrapped around the lower esophagus to create an improved valve mechanism Page 8 of 26 gtReinforces the lower esophageal sphincter gtgtThe Stretta procedure is another option for GERD tx Describe this procedure and how it alleviates ss Stretta procedure balloon is minimally invasive uses endoscopy to treat the tissues of the lower esophagus sphincter with highfrequency radio waves threads a catheter with a balloon on the end down the esophagus The balloon is inflated exposing four sharp probes on the outside of the balloon The probes then discharge highfrequency radio waves into the LES After several treatments the LES becomes thickertighter due to shrinking of collagen strands Disorders of the Esophagus Esophagitis gt itus inflammation Usually Inflammation of the lower end of the esophagus due to gastric reflux Can be caused by other things as well gtgt GERD is one common cause of esophagitis List some other possible causes Causes GERD lm ection such as Candida or Herpes Vomiting eg bullemia Surgery Medications such as aspirin and NSAIDS non steroid anti inflammatory drugs Taking a large pill with too little water or just before bedtime Swallowing a toxic substance Hernias Radiation injury ex radiation for cancer treatment MNT gt Same as GERD Complications of Prolonged EsophagitisGERD gtgtDescribe Barrett s Esophagus Barrett s Esophagus Acid damages lining of esophagus due to chronic esophagitis Damaged area heals but abnormal columnar cells replace squamous cells columnar cells are similar to the intestinal lining squamous cells form the normal epithelium lining the esophagus Can increase risk for adenocarcinoma slide 13 includes color photos showing progression of condition gtgtWhat is a the esophageal disorder of hiatal hernia How does this condition cause GERDesophagitis Hernia is the outpouching at arrow of portion of stomach into chest thru esophageal hiatus of diaphragm where esophagus penetrates diaphragm Causes reflux of gastric contents into esophagus gt GERDesophagitis Page 10 of 26 Potential causes weakness of muscles in diaphragm excess abdominal fat mass heavy lifting and pregnancy SS GI discomfort after large meal heartburn discomfort when lying down or bending over following a meal Hiatal Hernia MNT gt Same as GERDesophagitis Weight loss if warranted Hiatal Hernia Medical Tx Medications to decrease acidity and reduce gastroesophageal reflux Surgical repair may be necessary if not W responsive to other treatments Diaphragm gtgt Describe esophageal varices gtgtWhat is portal HTN and how does it cause esophageal varies How are these conditions related to cirrhosis Esophageal Varices will talk more about this in the module on liver disease Hallmarks of cirrhosis of the liver and portal hypertension HTN gtgtEsophageal Varices occurs when esophageal veins small and large in the lower part of the esophagus become distended gt bleeding risk Caused by Hepatic Portal Vein HTN Rise in blood pressure may be due to obstruction of blood flow to the liver caused by cirrhosis scarring gtgtWhat are the goals of MNT for esophageal varices What are some appropriate dietary choices ll l quot allfif f f39if e L t I39 llmp mgrri Swimgut I quotKWquoti I UTE l l i l 39I i E J Hrn ml Esophagus Ell ii g Parnennpmrgenl and E39linmtl h HIELIJE39 H ir l Him lus Hamlin gt The MNT goal is to prevent bleeding gt MNT 56 small soft textured lowresidue mealsd prune juice or soluble fiber supplement for bowel regularity amp to prevent straining can cause bleeding There is a high risk of malnutrition gt Hepatic Portal Vein carries blood from the small intestine to the liver It also carries blood from the stomach the large intestine and the spleen to the liver It blood flow to the liver is obstructed eg by cirrhosis it may cause a rise in blood pressure gtportal hypertension HTN in the hepatic portal vein The body would respond by diverting blood into the smaller collateral vessels like those in the esophagus Increased blood flow may cause those tiny vessels to balloon out become distended If the vessels break open they could bleed severely Stomach Disorders Dyspepsia know gtgtWhat is dyspepsia What does it mean if someone has functional dyspepsia gt Dyspepsia is a fancy word for indigestion or upper GI discomfort Causes gastric irritation reflux 33 of derangement of some other organ gallbladder disease kidney stones chronic appendicitis DM rapid eating poor mastication overindulgence in rich foods poor diet psychoneurosis etc gastric veins gt Functional Dyspepsia recurrent upper GI discomfort of unknown etiology It is a functional disorder SS Abdominal pain fullness gas bloating belching nausea reflux MNT for Dyspepsia determine underlying cause treat accordingly Stomach Disorders Gastritis itis signals inflammation gtgt Contrast acute gastritis and chronic gastritis Inflammation of the gastric mucosa 2 types 1 Acute sudden onset of inflammation of gastric mucosa associated w dietary indiscretions abXchronic medication useaspirinNSAIDS overeating ETOH tobacco ingestion of certain toxins spoiled food etc MNT Page 13 of 26 NPO 2448 hrs with IVF PRN NPOnothing by mouth IVF PRN intravenous feeding as needed Start with clear liquids Advance as tolerated to regular diet 2 Chronic prolonged inflammation of gastric mucosa that can lead to atrophic gastritis atrophy of parietal cells and achlohydria inadequate hydrochloric acid secretion Prevalence increases with age gtgtWhat is the primary cause of chronic gastritis What are some other possible causes gt Primary cause H pylori bacteria a gram negative bacteria that does not mind the acidic environment of the stomach at all gtOther causes alcohol food poisoning NSAle or other viralbacterial infection gtgt Chronic gastritis frequently results in atrophic gastritis and achlorhydria What does this mean gtgt Absorption of which micronutrients may be affected by this condition B12 Iron Fe amp Calcium Ca Tx Acid suppression or buffering andor antibiotics gtgtDescribe MNT for chronic gastritis Page 14 of 26 Gastric MNT Soft bland diet w adequate nutrition Small meals avoid distension Avoid irritating foods eg onion garlic pepper alcohol Avoid smoking gt Assess B12 statuscalciumiron gt Prolonged inflammation of gastric mucosa can cause Atrophic gastritis atrophy of parietal cells amp Achlorhydria loss of HCL gt Achlorhydria loss of HCL I absorption of Fe and Ca the body may leach some Calcium from bones to meet daily needs This could lead to osteopenia gtAtrophic Gastritis atrophy of parietal cells I IF gt B12 malabsorption Parietal cells secrete Intrinsic Factor so atrophy of the parietal cells decreases Intrinsic Factor IF amp can cause B12 malabsorption because B12 must be bound with IF to be absorbed in the ileum Could increase risk for stomach cancer Peptic Ulcer Disease Gastric Ulcers amp Duodenal Ulcers gtgtWhat is an ulcer What is a peptic ulcer What causes PUD gtgtWhat are the 55 and goals of MNT for peptic ulcers An ulcer is a lesion that is eroding away the skin or mucous membrane Page 15 of 26 gt Peptic ulcers are open sores or ulcerations of the gastric mucosa that penetrate the mucosa layer to the submucosa of the stomach gastric ulcer or the upper part of the duodenum duodenal ulcer usually just before the pyloric sphincter Perforation if the ulcer goes all the way through the submucosa it is called a perforation this would be a medical emergency gt H pylori is the usual cause of peptic ulcers but not everyone who has H pylori in the stomach develop peptic ulcers It is a myth that spicy food can cause peptic ulcers Things that increase the risk of developing a peptic ulcer NSAms alcohol smoking regular use of aspirin or ibuprofen may also be a genetic link Increased risk of gastric cancer gtSymptoms abdominal epigastric pain burning sensation Pain may be relieved with eating or antacids but after eating there is a rebound of gastrin gt more pain viscous cycle Presence of blood in the vomit coffee ground vomitushematemesis or stool Peptic Ulcer Disease Treatment Objectives relieve pain heal ulcer reduce tendency to recur maintain good nutrition status Medical tx Antacids histamine H2 receptor antagonist sucralfate Carafate antibiotics If med tx fails or with additional complications gastric surgery Elsev ier items and derived ll gt MNT Restrict only those foods known to aggravate ulceration or T acid secretion Black and red pepper caffeine coffee ETOH individually non tolerated foods Consider timing and size of meal eg Carafate medication must be take QID on an empty stomach Small frequent meals Assess for anemia that could result from blood loss Gastric Surgery gtgt Contrast a total gastrectomy vs a partial subtotal gastrectomy Gastrectomy removal of part or all of the stomach Partial subtotal gastrectomy Page 17 of 26 gt may be done to treat stomach cancer gt uses Billroth or II gtTotal Gastrectomy if all of the stomach is removed the surgeon will attempt to make a new stomach using some intestinal tissue So the end of the esophagus would be attached to the small intestine and a Jejunal reservoir would be created know gtgt What is ZollingerEllison Syndrome Total gastrectomy is less common but is used to treat gt ZollingerEllison Syndrome disorder characterized by T gastrin gt T HCI Results in severe peptic ulcers People with this syndrome secrete way too much gastrin Gastrin is mostly secreted in the stomach but the duodenum and the pancreas also secret a little gtgt The Billroth l and Billroth II are two types of partial gastrectomies What s the difference between the two Which one would be associated with higher risk and more side effects Billroth 1 duodenum Billroth ll jejunum gtcomplications gtrisks Page 18 of 26 risk of dumping risk of dumping QUHIU IH quotI resecled Stomach gt Subtotal or Partial 9 39 gastrectomy resection of the stomach a part of the stomach is removed followed with Emma rm a reconstruction procedure gt anastomosis means a surgical connection between 2 structures gtGastroduodenostomy Billroth l anastomosis of distal portion stomach to proximal duodenum gt bypasses pyloric sphincter gt risk of dumping gtGastrojejunostomy Billroth ll anastomosis of stomach to side of jejunum gtbypasses pyloric sphincter amp creates blind loop gt risk of dumping bacterial overgrowth amp fat malabsorption Page 19 of 26 Gastric Bypass food bypasses most or all of stomach eg RouxenY procedure or esophagojejunostomy Risks include dumping malabsorption of Fe B12 gtgt Review the RouxenY gastric bypass procedure This bariatric surgery is both restrictive and malabsorptive what does that mean RouxenY is a common bariatric surgery for weight loss It is both restrictive amp malabsorptive gtlt is Restrictive because it limits the amount of food intake by reducing the size of the stomach gtlt is Malabsorptive because it limits the absorption of foods in the intestinal tract by quotbypassingquot a portion of the small intestine In the RouxenY procedure a small portion of the stomach about the size of an egg is stapled off from the rest of the stomach The new egg portion is attached directly to the jejunum bypassing the rest of the stomach and the upper portion duodenum of the small intestine A biliopancreatic limb is created to connect the duodenum to the jejunum so that bile and pancreatic enzymes can enter the jejunum So the food is able to mix with digestive juices in that common channel or the y gtSleeve Gastrectomy is a second common bariatric surgery for weight loss Page 20 of 26 In the sleeve gastrectomy a portion of the stomach is removed but the gtpyloric sphincter remains intact and no intestines are bypassed gtgt What is a vagotomy What are the effects of a vagotomy gtgt What is a pyloroplasty gt Vagotomy is a surgical cutting severing of portions of the vagus nerve to reduce acid secretion usually to reduce HCI secretion into the stomach It is a surgical method for treating peptic ulcer disease if medicinal management does not work Can decrease peristalsis solids may empty slower liquids may empty faster in undiluted state gt The vagus nerve one of the largest nerve systems in the body stimulates gastric acid secretion is the 10th cranial nerve It originates in the medulla oblongata a part of the brain stem amp extends from the brain stem to the colont innervates the pharynx lungs heart esophagus stomach amp most of the abdominal viscera Picture below shows innervation of the stomach by the vegas nerve The vegas nerve splits into branches that go into different parts of the stomach lt stimulates gastric motility and stimulates hydrochloric acid HCL secretion So by severing part of the vegas nerve fibers in the stomach you can reduce the secretion of stomach acid Because this severing may also decrease stomach motility which delays gastric emptying a gtpyloroplasty is often done with a vagotomy gt Pyloroplasty surgery to widen the opening of pylorus to compensate for the decrease in stomach motility caused by the Vagotomy so the stomach can empty its contents into the duodenum more easily Vagotomy Pyloroplasty 39l at at w 39 39lrquotllr n1ii15i lg3939lfgI39r39lglrD tment fr39 quot I g l stimul39em Ir 4 w tefthu stow3h h 39l know gtgt Describe the postop MNT and advancement of the diet for a gastric surgery pt MNT for Gastric Surgery Immediately PostOp NPO with NGT suction NPO nothing by mouth NGT Nasogastric tube suction to empty gastric content When peristalsis returns as evidenced by return of bowel sounds gurgling noises heard in the abdomen with a stethoscope that can be heard every 5 15 seconds start ice chips small sips water gt Postop water amp other fluids should be sugarfree to avoid potential dumping syndrome More fluids may be offered as vomiting diminishes clear liquids gt full liquids often lactosefree Soft low residue Advance to high protein low CHO moderate fat amp often lactosefree diet as patient tolerates volume amp consistency Usually back to regular food by 57 d postop If a person is not able to tolerate an oral diet then they may be fed with a feeding tube into the jejunum for a period of time The tube is placed int the jejunum because the jejunum is where most of the nutritional absorption occurs Complications Complications are variable There can be a risk of obstruction Page 22 of 26 gt The most common complication is dumping syndrome Reduced capacity t intake Changes in gastric emptying amp transit time know gtgt What is dumping syndrome What are some possible causes of this condition What are the 55 gt The most common complication of gastric surgery is dumping syndrome About half of people undergoing gastric surgery experience it gt Dumping Syndrome is when the contents of the stomach empty too quickly into the small intestine gt Causes occurs w alteration or bypass of pyloric sphincter Partially digested food draws excess fluid into the small intestine with signssymptoms gtEarly dumping 1015 mins NVD nauseavomitingdiarrhea gtLate dumping 13 hrs can cause an insulin spike that leads to reactive hyperglycemia weaknessfainting palpitations gt blood rate Most people with dumping syndrome experience Early Dumping Some people experience both early and late dumping gt Dumping usually occurs after the consumption of too much hypertonic foodsfluids so sugary foods are a key trigger for the dumping syndrome in a few months the patient be able to consume sugary foods without dumping Tx small frequent meals no liquids with meals avoid simple sugars avoid lactose consume T protein moderatefat diet fat triggers dumping in some people gt avoid foods that are very hot or very cold Page 23 of 26 kn gtgt Describe MNT for Dumping Syndrome Nutritional Care Guidelines for Patients with Dumping Syndrome 1 gt Small meals spread throughout the day are likely to result in improved net absorption and less dramatic fluid shifts 2 Highprotein moderatefat foods are recommended with sufficient calories for weight maintenance or gain as needed Complex carbohydrates are included as tolerated 3 Intake of fibrous foods slows upper GI transit and increases viscosity However to avoid obstruction caution should be used with large particles and fiber supplements especially with esophageal or gastric outlet narrowing or dysmotility 4 gt Lying down and avoiding activity an hour after eating may help slow gastric emptying gt Compare if patient has GERD they should not lie down right after ea ng 5 gt Do NOT take liquids with meals Consume liquid throughout the day small amounts at a time 6 Avoid only very small quantities hypertonic concentrated sweets These include soft drinks juices pies cakes cookies and frozen desserts unless made with sugar substitutes 7 Lactose especially in milk or ice cream may be poorly tolerated because of rapid transit and thus may need to be avoided Cheeses and yogurt are likely to be better tolerated Page 24 of 26 Gastric Surgery Complications cont know gtgt Besides Dumping Syndrome identify some other possible complications of gastric surgery gt Malabsorption occurs with bypass of duodenum resulting in l hormone amp enzyme production RouxenY gastric bypass surgery is a forced malabsorption as a weight loss mechanism But weight loss can be an unwanted side effect for people having other gastric surgeries gtWith RouxenY amp Billroth II where the duodenum is largely bypasses malabsorption of fat is common gtMost frequent is malabsorption of fat producing steatorrhea excretion of abnormal quantities of fat with the feces owing to reduced absorption of fat by the intestine weight loss and possibly fatsoluble vitamin deficiency Tx Supplement with digestive enzymes MVImineral supplementation may need for life know gtAnemia potential causes 1 interrupted conversion of iron to ferrous form l HCI Tx supplement ferrous sulfate more easily absorbed 2 reduced iron absorption due to decreased absorptive area Tx supplemental iron Under medical supervision 3 Decreased lF production may result in pernicious anemia Tx IM injections of B12 gt A person with a total gastrectomy would need intramuscular injections of 312 because that person would not have any intrinsic factor gtgt What is gastroparesis What are some possible causes of this condition Upper GI Disorder Gastroparesis Page 25 of 26 gtGastroparesis is delayed gastric emptying is a complex condition associated with chemical and neurological factors gtCauses include surgery delayed return of peristalsis nerve damage from prolonged blood sugar is a common cause of gastroparesis in diabetics other causes smooth muscle disorders neuropathic disorders psychological disorders and obstruction 30 are idiopathic Metoclopramide or erythromycin are common medications used to stimulate gastric emptying motility for gastroparesis gtgt Describe the most appropriate dietary choices for gastroparesis Gastroparesis Diet Small frequent meals Lowfat because fat delays the emptying of the stomach Lowfiber fiber can delay gastric emptying amp contribute to bezoars gtgt Gastroparesis patients are at risk for formation of bezoars What are bezoars gt Bezoars mass of undigested material in the stomach eg hairballs in cats gtgtDrink liquid with the meal gtgtWalk around after eating Chew food well or consider liquid supplement shakes Possibly consider jejunostomy tube feeding Page 26 of 26 Spath Study Guide Diabetes M91 Diabetes Part One Just like there are different types of Cancer there are also different types of diabetes Diabetes Mellitus is a blanket term that includes different types of diabetes Diabetes Mellitus is a group of diseases characterized by high blood glucose blood sugar concentrations resulting from defects in 1 insulin secretion from the pancreas 2 insulin action at its target cells 3 both insulin secretion insulin action gtgt Know definitions gtgt Hyperglycemia elevated blood glucose or blood sugar gtgt Hypoglycemia lower than normal blood glucose Both are acutely dangerous situations Blood glucose Glucose from CHO We eat CHO which are digested to monosaccharides which are absorbed into hepatic portal circulation for transport to the liver In the liver galactose and most fructose are converted to glucose The hepatocytes liver cells can use that glucose or they can release the glucose into the blood for the use of all the other cells in the body to use Glucose from nonCHO substrates via gluconeogenesis We also get some hepatic endogenous glucose production That is the liver produces some new glucose out of nonCHO substrates like lactaid or certain amino acids in a process called gluconeogenesis Glucose is the universal fuel source for every single cell in the body gt Red blood cells which deliver oxygen to all of the body s cells can only use glucose for fuel Page 1 of 43 Major Complications of Diabetes Dangers of Hyperglycemia elevated level of blood glucose include Increased risk for atherosclerosis heart disease stroke cerebrovascular disease microvascular complications damage to little blood vessels in the eyes Retinopathy kidneys nephropathy damage to nerves neuropathies nerve damage poor circulation in extremities may lead to amputation eg toes or feet Having elevated blood glucose can be like having high blood pressure hypertension HTN a person can have elevated blood glucose andor HTN and feel fine but these conditions can result in complications that are dire extremely serious a r i i Cerebretraeeular tilieeaee Retinapathf Cerenary heart dieeaee Nephrepatl39tryr 4 MiELJIFDpEthly Peripheral vaaeular dieeaee in the le39wer limbs Llleeratieri and arnpurtatierl i fer diabetic teat Page 2 of 43 Hormonal Control of Blood Glucose Our bodies normally adapt to maintain blood glucose depending on whether we are in a fed or fasted state So after an overnight fast a normal blood glucose concentration for a person Without diabetes would be 70 99 milligramsper deciliter Then it would normally be below 140 milligramsper deciliter a couple of hours after a meal We maintain that homeostatis because of gtTwo peptide hormones insulin amp glucagon which are the key regulators of blood glucose They are secreted by endocrine cells of the pancreas homeostasis any selfregulating process by which biological systems tend to maintain stability while adjusting to conditions that are optimal for survival Source Britannicacom gtgt What types of cells produce insulin and glucagon in the body Insulin is synthesized and secreted by betacells of the pancreas glucagon is synthesized and secreted by alphacells of the pancreas Page 3 of 43 gitesge39teake by cells insulin Stimub glycogen formation Blood glucose falls to normal range Stimulus Rising blood glucose level I Homeostasis Normal blood glucose level about 90 mgltl u ml I 39 Stimulus Declining blood glucose level Bloodl glucose rises to normal range Stimulates glycogen breakdown Glucagon Copyright 2006 Pearson Education Inc publishing as Benjamin Cummings The picture above ties it all together Stimulus Rising Blood Glucose Level blue box midway on the left side After CHO ingestion fed state 1 glucose levels rise stimulating pancreatic beta cells to secrete insulin into blood 2 Insulin stimulates cells mainly skeletal muscle cells to take up glucose from the blood 3 blood glucose levels return to normal Without insulin glucose can t enter those cells resulting in hyperglycemia Page 4 of 43 Stimulus Declining Blood Glucose Level blue box midway on the right side When blood levels drop fasting state 1 2 3 glucose levels fall stimulating pancreatic alpha cells to secrete glucagon glucagon stimulates the liver to break down glycogen glycogenolysis amp release glucose into the blood glucagon also stimulates the liver to make glucose from nonCHO substrates gluconeogenesis gtgt Describe normal insulinmediated glucose uptake into cells After CHO ingestion fed state 1 2 glucose levels rise stimulating pancreatic beta cells to secrete insulin into blood Insulin stimulates cells mainly skeletal muscle cells to take up glucose from the blood When insulin binds to its receptor it s like insulin is knocking on the door of the cell That signals the Glut4 transporter to come to the door and let glucose in Glucose enters the cells by facilitated diffusion Glucose requires Glut4 transporters to come to the cell surface amp let glucose inside the cell Glut4 require insulin to come to the cell surface into taken from p 4 amp p 12 Page 5 of 43 You do not need to know the following statistics but they are staggering Prevalence Rates of Diabetes are through the roof In 2011 258 million children and adults in the US 83 of the population had diabetes Diagnosed 188 million people Undiagnosed 70 million people Prediabetes 79 million people New Cases 19 million new cases of diabetes are diagnosed in people aged 20 years and older each year Prevalence T with type2 diabetes the most common form Age Overweight amp obese Lower education lower socioeconomic status Prevalence is influenced by ethnicity health disparity Higher in African Americans amp Native Americans Obesity Trends In 1990 no state had an obesity rate over 14 By 2008 several states exceeded an obesity rate of 30 or more lan Colorado is the only quotblue statequot in 2008 Diabetes Trends have mirrored the obesity trends Obesity is a major risk factor for type2 diabetes Two good resources American Diabetes Association sets Standards of Care for diagnosis amp treatment of diabetes updates info annually wwwdiabetesorg National Guideline Clearinghouse Page 6 of 43 updates amp guidelines on diabetes and other diseases amp health conditions wwwguideinegov gtgtWhat is prediabetes Prediabetes is a stage of impaired glucose homeostasis not diabetes yet persons with prediabetes have IFG or IGT indicating high risk for developing diabetes do not yet meet the diagnostic criteria for diabetes gtgt Identify the lab values for impaired fasting glucose amp impaired glucose tolerance that would be used to diagnose prediabetes Impaired fasting glucose IFG fasting plasma glucose FPG above normal gt100 mgdL and lt126 mgdL Impaired glucose tolerance IGT plasma glucose elevated after 75 g glucose load gt140 and lt200 mgdL Impaired glucose tolerance is diagnosed by an oral glucose tolerance test quotOGTTquot person comes in fasted ingests 75 g glucose sample plasma glucose tested 2 hrs later Source Standards of Medical Care in Diabetes Diabetes Care 20123581163 Types of Diabetes I main types of diabetes I el l 03 I DDO EE CIOI id CID 9amp69393393EE5I 4035E2 DIAEEl V E l l 0 gtI CICIOEEE CIOI r z ik CID ltgt gtI OOV DIA EEEV E I AVVDIO V E A 035E500gtIltV A ltgt WlkE kV i EEE CI AEI35l gtlltgtIlt I gtIltgtllt VIDEEE AI DltgtC3EE l l l l V kal 1 gtIltACICI gt1 E CIA alslsztzals gtIltCICIAgtIltA 9 lgtl DIDVVA 0VOCH4VI V E A DIA3 V his V i l IDOI l 9 3DVltgtDIE n 0 his V 3 A33 035k DltgtC3EE VIDEEE A I Gestational diabetes mellitus GDM Page 7 of 43 develops only during pregnancy affects 210 of all pregnancies mainly due to the hormones produced during pregnancy that cause insulin resistance hormones increase the amount of insulin needed to control blood glucose levels amp if the mother s body can t meet that increased need the mother will develop GDM Usually presents in the later stages of pregnancy Goes away once baby is born but a mother who has had GDM is at much greater risk for developing Type 2 down the road Babies born to mothers who had GDM during pregnancy are also at increased risk for developing Type 2 as they grow up I Type 1 formerly insulin dependent diabetes IDDM or juvenile onset represents about 510 o of all diagnosed cases of diabetes typically begins before age 20 that s why it used to be called quotjuvenile onsetquot diabetes is caused by a destruction of the insulin secreting beta cells of the pancreas usually due to an autoimmune dysfunction type 1 diabetics need endogenous insulin to live That s why it is sometimes referred to as quotinsulin dependent diabetesquot but the most appropriate term is Type 1 gtgt Insulin may be injected by mechanical pump or syringe Why can t insulin be taken as an oral pill Page 8 of 43 Insulin is a peptide hormone If you took insulin as a pill it would be digested just like any other protein So endogenous insulin must be administered by injection Pictures below show how glucose is taken into cells when insulin binds to its cell surface receptor When insulin binds it triggers the cell signaling cascade inside the cell that brings glucose transporters to the cell s surface so that the glucose can enter the cell by facilitated diffusion If insulin does not bind then glucose transporters stay in vesicles sacs inside the cells The cell would be starved for glucose Blood glucose levels would remain elevated because glucose is not being taken up into cells The discovery of insulin was an absolute landmark in medicine A hundred years ago a diagnosis of type 1 diabetes would be virtually a death sentence Children would become skeletons and die Two scientists discovered that injections of insulin could treat diabetes and save lives They tried it first in dogs They induced diabetes in dogs by knocking out pancreatic beta cells In the 19203 just one year after the test injection insulin became widely available and has saved countless lives since then Frederick G Banting and John Macleod were awarded the Nobel Prize in Physiology or Medicine in 1923 quotfor the discovery of insulinquot The Discovery of Insulin N Engl J Med 2008 358975976February 28 2008 DOI 101056NEJMbkrev58827 Type 1 Diabetes Pathophysiology EIUEDEE Iithllilll Fieee r H Intulin In the human eell ineulin i ilLliiat tint Ijlith rere triters H heiferre gluenee green enter tit e eellt WITI39IIII39LI I eneugh lrntiliri iiE39iji little gfueete t in trernperteti tn the cell Initial onset Affected persons are usually lean have abrupt onset of symptoms before age 30 Honeymoon phase After diagnosis and correction of hyperglycemia and metabolic derangements need for exogenous insulin may drop dramatically for up to a year the diabetes may appear to go away for months maybe even up to a year lnsulin needs are minimal during this time Some patients find they can maintain normal or near normal blood glucose levels with very little insulin type 1 diabetics present with symptoms only after most of their beta cells have been destroyed and eventually the remaining beta cells will wear out and the honeymoon phase will end Complete Bcell loss 8 to 10 years after onset gtgt Sometimes type 1 diabetics experience a honeymoon phase immediately after diagnosis What does this mean Type 1 diabetics present with symptoms only after most of their beta cells have been destroyed After diagnosis and correction of hyperglycemia amp metabolic derangements need for exogenous insulin may drop dramatically for up to a year Eventually the remaining beta cells wear out and the honeymoon phase ends What would cause pancreatic beta cells to fail The cause appears to be immune response but may be idiopathic cause unknown Type 1 Diabetes 2 forms 1 Immunemediated Genetic predisposition is Autoimmune reaction which may be triggered by environmental factors eg viral infection toxins body destroys its own Bcells in pancreas that produce insulin 2 Idiopathic cause unknown Strongy inherited Page 10 of 43 African or Asian ancestry gtgt What are the 55 of type 1 diabetes Type 1 Diabetes Symptoms Hyperglycemia Excessive thirst polydipsia when blood glucose is elevated then blood osmolality increases triggering sensory receptors in the hypothalamus to make a person think he s thirsty to maintain glucose homeostasis Frequent urination polyuria gtgt glycosuria the body is trying to get rid of all the extra glucose in the blood by excreting it through the kidneys into the urine Normally when kidneys filter blood glucose is reabsorbed by the renal tubules so there is not a significant amount of glucose in urine If blood glucose is too high the transport proteins for reabsorption become saturated glucose exceeds the renal threshold for absorption and glucose spills over into the urine So the presence of glucose in the urine is sign of abnormal glucose homeostasis Significant weight loss Electrolyte disturbance Ketoacidosis without insulin cells resort to burning fat for fuel Excess beta oxidation of those fatty acids leads to formation of ketone bodies Two of the three ketone bodies are acidic Normally we maintain our blood pH at a very tight range at about 74 but excessive ketone bodies can lead to ketoacidOSiS WhiCh can lead to coma or death if untreated I Type 2 formerly non insulin dependent diabetes NIDDM or adult onset formery caIed quotnon insulin dependent diabetesquot but some Type 2 diabetes do need insulin formerly called quotadult onsetquot diabetes but with the rise in childhood obesity Type 2 diabetes is increasing found in teenagers and even younger children Most common form of diabetes accounting for 90 to 95 of diagnosed cases Combination of insulin resistance beta cell failure insulin deficiency E39 39f 399 393 E39 H E EHEH EI39 Hall I EH2 C III 3 2 CH3 I EH3 acetuacetate hgdrnaghutgrate acetone Progressive disease Ketoacidosis rare usually arises in illness Prof s comments when discussing risk factors for type 2 p 14 type 2 all of the causes haven39t been elucidated explained genetics plays an underlying role 12 different SNIPS are associated with type 2 multifactoral gtgt Define Glycosuria Glycosuria is the presence of glucose in the urine is a sign of abnormal glucose homeostasis is a ss of type1 diabetes discussed on previous page gtgt Describe normal insulinmediated glucose uptake into cells See p 5 Diabetes Type 2 Pathophysiology Glucose enters the cells by facilitated diffusion ie glucose moves down its concentration gradient from a high concentration to a low concentration Glucose does not require ATP but does require transport proteins for entry into cell Those transmembrane proteins Glut4 transporters that facilitate the glucose uptake into muscle amp fat cells are inside the cell amp require insulin to come to the cell surface Page 12 of 43 The number of Glut4 transporters in plasma proteins increase rapidly in the presence of insulin When Insulin binds to its receptor that initiates a cell signaling cascade that brings Glut 4 transporters from the cytoplasm to the plasma membrane cell surface amp glucose is allowed to enter the cell by facilitated diffusion Simplified version When insulin binds to its receptor it s like insulin is knocking on the door of the cell That signals the Glut4 transporter to come to the door and let glucose in gt type 2 starts with insulin resistance cells not responsive to insulin Unlike type 1 diabetes where there is destruction of beta cells amp insulin deficiency in type 2 diabetes some people have a higher level of insulin in their blood at least in the beginning But then beta cells wear out and the person becomes insulin deficient ln type 2 diabetics cells are not responsive to that hormone insulin insulin resistance Insulin resistance decreased tissue sensitivity or responsiveness to insulin gt Type 2 results from a combination of insulin resistance and Bcell failure In type 2 endogenous insulin levels may be normal depressed or elevated but are inadequate to overcome insulin resistance Resistance to insulin increases over time When the pancreas is no longer able to produce enough insulin to overcome insulin resistance blood glucose levels begin to rise at first after meals and eventually in the fasted state too at that point type 2 diabetes is present type 2 insulin resistance continued 1 gt insulin resistance begins the progression that results in type 2 diabetes 2 pancreatic beta cells increase insulin secretion to compensate for resistance 3 blood glucose levels remain normal 4 resistance to insulin keeps increasing 5 gt pancreatic beta cells no longer able to produce sufficient insulin 6 As insulin production fails T postprandial blood glucose hyperglycemia 7 Liver production of glucose increases resulting in T fasting blood glucose type 2 is now present i i nsulin 7 i i i 39 quot39 H r y H39 1 1 quotquot h E Page 13 of 43 must bind with UEEEI J EIJT vEr ItjEr Wm QEII Willaquot EJEEEIIFI IE w tj h EH 2 Ellaiii man tj hr am Er lr uflgh lllf llllnlll hill 1 n r EDEDIUUE H ENE r ElEt l lt 13 UMSWIIITS EJETUDU39D 8 Glucotoxicity and lipotoxicity further impair insulin sensitivity and insulin secretion gtgt What is insulin resistance Insulin resistance is decreased tissue sensitivity or responsiveness to insulin gtgt What are the 55 of type 2 diabetes type 2 has some of the same 35 as type 1 hyperglycemia polydipsia polyuria type 2 53 includes polyphagia excessive hunger Unlike type 1 type 2 55 unlikely to include ketoacidosis WGith loss only occasionally a symptom person is more likely to be overweight gtgt How could someone have type 2 diabetes without realizing it Symptoms for type 2 are more subtle than those for type 1 A person could have insulin resistance for years without presenting with hyperglycemia Other symptoms not always present Even if present symptoms may not be noticed Diabetes Type 2 Symptoms Insidious onset estimated type 2 dm can begin 7 years prior to diagnosis Often goes undiagnosed for years Hyperglycemia may not present for years insulin resistance increases over time Excessive thirst polydipsia Frequent urination polyuria Polyphagia hyperphagia not always Weight loss occasionally present Symptoms not always present and even if they are may not be noticed As we age our thirst mechanism tends to diminish so an older adult may not feel thirsty may not notice the symptom of polydipsia If a person is taking a diuretic that person may not notice the symptom of polyuria Polyphagia is excessive hunger or increased appetite May not connect this with type 2 Obesity is a risk factor for type 2 and weight loss is not a common symptom gtgt There are several wellrecognized risk factors for type 2 diabetes Name the 7 we highlighted in class 1 Family history of diabetes Page 14 of 43 Older age Obesity particularly intraabdominal obesity Physical inactivity sedentary lifestyle Prior history of gestational diabetes during pregnancy Impaired glucose homeostasis prediabetes Highrisk ethnic groups African American Latino Native American Asian America Pacific Islander N9191sz gtgt Know differences between type 1 amp type 2 diabetes in regard to 0 Typical age of onset o Pathophysiology 0 Prevalence o Medicinal management 0 Former names gtgt Prof Know this table well Type 1 vs Type 2 Summary gtgt Contrast the pathophysiology of type 1 amp type 2 diabetes mellitus I Typical Age at Onset Childhood or early Adults older than 30 Pathophysiology Absolute insulin deficiency Combination of insulin resistance and beta cell failure insulin deficiency Prevalence 510 of DM cases 9095 of all diagnosed DM Management Dependant on exogenous Lifestyle modifications insulin oral medications andor injectables including insulin Former Name JuvenileOnset or Insulin Adult Onset MaturityOnset Dependent Diabetes IDDM or Noninsulin Dependent Diabetes NIDDM Page 15 of 43 Type 1 Diabetes Pathophysiology is caused by a destruction of the insulin secreting beta cells of the pancreas usually due to an autoimmune dysfunction but may be idiopathic affected persons are usually lean have abrupt onset of symptoms before age 30 0 after diagnosis may experience a honeymoon period for up to a year until remaining beta cells wear out Complete Bcell loss 8 to 10 years after onset need endogenous insulin to live Type 2 Diabetes Pathophysiology starts with insulin resistance that develops over time Results from a combination of insulin resistance and Bcell failure Insidious onset can begin 7 years prior to diagnosis affected persons are generally adults over age 30 but with a rise in childhood obesity is increasingly found in teenagers obesity is a risk factor not all type2 diabetics need to be on insulin but they may progress to adding it p 12 23 Page 16 of 43 Prediabetes Impaired Glucose Homeostatis is an Independent Risk Factor for cardiovascular disease so people with diabetes are at elevated risk for things like myocardial infarction amp stoke Metabolic Syndrome Individuals diagnosed with the metabolic syndrome have 3 or more of the following abnormalities waist circumference of more than 40 men 35 women serum T63 of at least 150 mgdL highdensity lipoprotein HDL level less than 40 mgdL men 50 mgdL women blood pressure13585 mm Hg or higher fasting glucose 100 mgdL or higher Krause p 471 gtgt Review the characteristics of Metabolic Syndrome Metabolic Syndrome Characteristics Insulin resistance Compensatory hyperinsulinemia Abdominal obesity Dyslipidemia elevated TG low HDL Hypertension Insulin resistance which may precede the development of T2DM and macrovascular disease by many years induces numerous metabolic changes known as the metabolic syndrome Krause p 704 Page 17 of 43 The American Diabetes Association defines how we diagnose diabetes standards of care for treatment of diabetes gtgt Know the diagnostic criteria for a diagnosis of diabetes ie fasting plasma casualrandom plasma glucose OGTT glucose amp Hb A1 C Methods of DM Diagnosis gtgt 4 diagnostic methods 1 Fasting plasma glucose FPG measured after No calories for at least 8 hours 2 Casual Random plasma glucose CPG measured any time of day less reliable because more variable 3 Oral glucose tolerance test OGTT 2 hour Plasma Glucose 2 hour blood draw after oral glucose load of 75 grams glucose not generally recommended for clinical use a little more time consuming amp labor intensive 4 Hemoglobin A1C Hb A1 C a new diagnostic method This blood test has been used for years to monitor persons already diagnosed as diabetic but it only recently became sufficiently standardized amp reliable to be used as a diagnostic method is blood test for glycosylated hemoglobin or Hb A1 C measures how much glucose adheres to hemoglobin of red blood cells the higher a person s blood glucose the higher his Hb A1C used to assess person s average blood glucose over the previous few months average life span for red blood cells is 120 days so Hb A1 C gives an estimate of long term glycemic control Used to assess a person s average blood glucose over the previous few months more convenient than the OGTT Page 18 of 43 person does not have to be fasted for this blood test has become a very common method of assessment Normal lt 100 lt 140 lt 57 Prediabetes 100125 140199 5764 Diabetes gt 126 gt 200 2 200 gt 64 symptoms gtgt PROF SAYS KNOW THESE RANGES Diagnostic Criteria for Prediabetes amp Diabetes In the absence of unequivocal hyperglycemia criteria should be confirmed by repeat testing Standards of Medical Care in Diabetes Diabetes Care 20123581163 Page 19 of 43 People may not realize that they have diabetes Screening for DM recommended by American Diabetes Association Screen all persons 45 years amp older repeat every 3 years Screen at earlier age amp more frequently for High risk persons o risk factors 39 Overweight BMI gt25 Firstdegree relative with diabetes Highrisk ethnic population Delivered baby gt9 lb or diagnosed GDM Hypertensive HDL lt35 mgdl or TG gt200 Prediabetes Polycystic ovary syndrome Page 20 of 43 gtgt What are the treatment goals for diabetes in terms of Hb A1 C preprandial capillary glucose amp peak postprandial capillary glucose Diabetes Treatment Goals Recommendations for Glycemic Control for Adults With Diabetes Modified from American Diabetes Association Standards of Medical Care in Diabetes Diabetes Care 20123581163 Referenced to a nondiabetic range of 4 o6 o using a DCCTbased assay TPeak levels in patients with diabetes There is no cure for diabetes but these are manageable diseases gtgt Describe the management of prediabetes Management of PreDiabetes the emphasis is on lifestyle changes Goal of interventions amp MNT Decrease risk of diabetes amp CVD by promoting healthy food choices amp physical activity leading to moderate weight loss Lifestyle changes Increase physical activity Glycemic Control Treatment Goal A1 C aka glycated hemoglobin lt70 Preprandial capillary plasma glucose 70130 mgdl 5072 mmoll a finger prick test when fasted or before a Peak postprandial capillary plasma glucose1 lt180 mgdl lt100 mmoll Reduced fat and energy intake as appropriate nutrient dense heart healthy diet controlled CHO Whole grains and dietary fiber Page 21 of 43 Moderate weight loss maintain a healthy weight Educationsupport Regular participant followup Management of type1 amp type2 amp gestational diabetes MNT is cornerstone Self management is key Medical management of type1 amp type2 amp gestational diabetes focuses on medical nutrition therapy MNT is the cornerstone of treatment Management also involves physical activity monitoring medications amp education for selfmanagement Goals of MNT for type1 amp type2 amp gestational diabetes Achieve and maintain normoglycemia optimal lipid and lipoprotein profile and lowrisk blood pressure To prevent or at least slow the rate of development of the chronic complications of diabetes To address individual nutrition needs taking into account personal and cultural preferences and willingness to change To maintain the pleasure of eating by only limiting food choices when indicated by scientific evidence Be adaptive for special situations Strive for selfefficacy an ability to selfmanage to maintain good glycemic control is key to successful management of diabetes Want to avoid high amp low blood glucose Diabetes Care January 2008 vol 31 no Supplement 1 861878 gtgt Describe MNT for type 1 diabetes including meal patterns and insulin regimens MNT for Type 1 Diabetes type1 patients are Insulin dependent for life so MNT will always involve food amp meal planning with patients to coordinate with insulin regimens Page 22 of 43 patients should eat at consistent times synchronized with the time action of their insulin preparation especially if not using an insulin pump insulin pump multiple injections allow more flexibility with meal times snacks amp amount of food eaten insulin pump delivers longacting continuous 247 subcutaneous infusion of basal or background insulin when patient eats he uses buttons on pump to deliver an additional dose of rapid acting amp shortacting insulin called a bolus that would cover the CHO intake at that meal or snack Total energy intake and CH0 intake to avoid weight gain If not using an insulin pump follow meal patterning lnsulin required for all pts with type 1 DM Less common Insulin sensitizing agents may be required for those with additional peripheral insulin resistance unlike in type2 insulin resistance does notprecede onset of type1 diabetes but a type1 diabetic could develop insulin resistance 80 it is important to maintain a healthy weight amp stay physically active Integrate insulin regimen into usual eating habits and physical activity schedule Multiple injections 3day for better control insulin pump with buttons to use for bolus doses Half of daily insulin given as basal or background other half given before meals Mealtime or bolus dose rapidacting or shortacting insulin is given before meals to mimic normal insulin response to a meal Insulin is adjusted based on the CHO content of meal Starting points 1 unit of insulin for every 15 g of CHO for an adult 1 unit for every 2030 g CHO for school aged child these are estimates amount of insulin would vary from person to person Can establish an insulintocarbohydrate ratio for an individual MNT for Type 1 Diabetes continued Page 23 of 43 gtgtThere are different types of insulin that differ in their onset peak and duration Contrast longacting insulin with rapid and short regular insulin Longacting insuIin is a continuous 247 subcutaneous infusion of insulin Referred to as Basal or background insulin Rapidacting amp shortacting insulin regular insulin is given before meals or snacks to mimic normal insulin response to a meal Referred to as a mealtime or bolus dose of insulin Only covers the CHO intake at that meal or snack gtgt Describe a typical insulin regimen Half of daily insulin given as basal or background the other half given before meals amp snacks If using insulin pump which provides longacting continuous insulin need to use buttons on pump to deliver a mealtime or bolus dose Have more flexibility with meal times If not using insulin pump injections need to follow meal patterning Will need to be careful to eat at consistent times synchronized with the time action of their insulin preparation gtgt What would be a starting point for an insulinCHO ratio for type1 lnsulin is adjusted based on the CHO content of meal Starting point is o 1 unit of insulin for every 15 g of CHO for an adult 1 unit for every 2030 g CHO for school aged child These are estimates the amount of insulin would vary from person to person Page 24 of 43 gtgt Describe MNT for type 2 diabetes MNT for Type 2 Diabetes type2 diabetes is much more common than type1 not all type2 diabetics are on insulin but they may progress to adding it gtFor many type2 diabetics management consists of diet lifestyle or oral medications Because type2 diabetics are at increased risk for heart disease we need to focus on the entire metabolic profile blood lipids hypertension HTN etc in addition to glycemic control Progressive tX 1 MNT 2 Medication typical 3 May progress to adding insulin Blood glucose control improve food choices increase physical activity moderate energy restriction to promote weight loss as appropriate Teaching carbohydrate sources serving sizes number of servings meal planning limiting fats SMBG the emphasis is on selfmanagement Selfmonitoring of blood glucose SMBG Lifestyle interventions to improve metabolic abnormalities glycemia dyslipidemia hypertension dyslipidemia elevated TG low HDL and hypertension are correlated to obesity if a person is overweight or obese even moderate weight loss can have a dramatic effect on glycemic control blood lipids amp blood pressure gtgt All type 1 diabetics are dependent on exogenous insulin while only some type 2 diabetics require insulin Why type1 diabetes is caused by a destruction of the insulin secreting beta cells of the pancreas type2 diabetes starts with insulin resistance cells not responsive to insulin In type 2 endogenous insulin levels may be normal depressed or elevated but are inadequate to overcome insulin resistance gtFor many type2 diabetics Page 25 of 43 management consists of diet lifestyle or oral medications eg glucose lowering meds gtgt What are special MNT considerations for type 2 diabetes in youth MNT for Type 2 Diabetes in Youth Goals for glycemic control are the same as for adults Accompanies childhood obesity Cessation of excessive weight gain promote normal growth and development achieve blood glucose and A1 C goals don t want the child to develop an eating disorder so it may work best to have the child maintain existing weight and then grow into that weight Address comorbidities hypertension and dyslipidemia Behavior modification strategies Metformin oral glycemic agent medication often used when lifestyle changes alone are not effective gtgt What are special MNT considerations for type 2 diabetes in older adu s MNT for Older Adults with diabetes Goals for glycemic control are the same but may be relaxed if a person is at risk for inadequate nutrition due to comorbidities the presence of other diseases or conditions poor dentition teeth problems diminished taste etc Increased prevalence of diabetes and IGT impaired glucose tolerance with age Similar recommendations to younger population Concern for malnutrition gt may be at increased risk of complication of hyperglycemic hyperosmolar state HHS Page 26 of 43 is a condition that occurs in a type2 diabetic usually an older adult occurs when Hyperglycemia combined with dehydration leads to a very high blood glucose level amp high blood osmolality blood glucose levels may be above a 1000 mgdL deciliter Common Diabetes Myths that are NOT true quotNo more sugar ever againquot quotCarbs are evilquot quotFruit is healthy so it s okay to eat as much as I wantquot quotDiabetics need to purchase special 39diabetic foodsquot Truths The American Diabetes Association ADA does NOT endorse any one particular diet The ADA recommends that everyone with diabetes receive a referral to a Registered Dietitian to learn consistent CHO meal patterns 80 there is no diabetic diet but the meal pattern amp food choices good for diabetics are good for everyone There is no need to buy special foods or prepare special meals for the diabetic person in your family American Diabetes Association Dietary Guidelines quotAlthough numerous studies have attempted to identify the optimal mix of macronutrients for the diabetic diet it is unlikely that one such combination of macronutrients existsquot The message of the ADA s broad statement is that we tailor the diet to the individual diabetic person IOM s Acceptable Macronutrient Distribution Ranges AMDR are a good place to start AMDR Recommendations from the IOM 4565 of kcals from CHO 1035 of kcals from protein 2035 of kcals from fats Page 27 of 43 Standards of Medical Care in Diabetes Diabetes Care 20123581163 MNT for DM Carbohydrate The primary focus of MNT for DM is on CHO which ultimately convert to glucose CHO foods will drive blood glucose the most We want a balance of macronutrients with appropriate types amp amounts of CHO spaced throughout the day CHO should be included in the diabetic s diet but need a consistent CHO meal pattern It is all about how much and when Once this is figured out managing diabetes does not seem so overwhelming Teach the patient what foods contain CHO Determine how many grams of CHO patient should have at each meal amp snack Patient determines how many CHO servings to have at a meal amp What CHO Wll be Prof s local diabetes center recommends 34 CHO servings at each meal amp 12 CHO servings for snacks for most of their patients Figure out how to space out those CHO throughout the day gtgt What is the recommended range for percent kcals from CHO for diabetics 0 DRI 4565 CHO LowCHO diets lt45 of kcals are not recommended Sugars do not increase glycemia more than isocaloric amounts of starch Manipulating glycemic index GI and glycemic load GL may be helpful in controlling bg Main focus of diet interventions Page 28 of 43 Carbohydrate counting portions of food that each contain 15 g carbohydrate Exchange lists Plate method gtgt Diabetics and their wellmeaning friends amp relatives often think they can never eat sugar again Why is this not true Sugar amp sweets can be incorporated into the meal plan Sugars do not increase glycemia more than isocaloric amounts of starch gtgt How can sugarssweets be incorporated into a diabetic diet Be aware of how much CHO in portion size Substitute as needed Sugary foods pack a lot more simple CHO in a small volume of food so need to be aware of portion sizes Need to substitute as appropriate to offset a sugary food For example if a diabetic planned to have a slice of pie after dinner he would forgo having eg bread or potato or pasta salad at that meal The American Diabetes Association does not give a formal recommendation for or against incorporating glycemic index into MNT for diabetes because to calculate the glycemic index for each meal would be a tedious process and would make for a complicated diet education For example the glycemic index for a ripe banana is higher than for a banana that is a little green glycemic index is higher for cooked vegetables than for raw vegetables gtgt Why would CHO foods with a lowglycemic index be beneficial in the diet of a diabetic CHO foods with a lowglycemic index are beneficial in the diet of a diabetic because they lead to a slower more gradual rise in blood glucose They would not raise blood glucose levels as quickly as highglycemic index foods gtgt Define glycemic index and glycemic load Glycemic Load and Glycemic Index Glycemic Index an index indicating the effects of various foods on blood sugar the relative area under the postprandial blood glucose curve of a food compared to the glucose curve of glucosestarch Glycemic Load glycemic index g of CHO 100 Page 29 of 43 The complete list of the glycemic index and glycemic load for more than 1000 foods can be found in the article quotInternational tables of glycemic index and glycemic load values 2008quot by Fiona S Atkinson Kaye FosterPowell and Jennie C BrandMiller in the December 2008 issue of Diabetes Care Vol 31 number 12 pages 22812283 MNT for DM Fiber gt A food higher in fiber has a lower glycemic index gtgt What are the fiber recommendations for a diabetic Recommendations are the same as for general public 14 g1000 kcal Consume a variety of fibercontaining foods such as legumes fiberrich cereals gt5 gserving fruits vegetables and whole grains gtgt How would you account for fiber when teaching CHO counting For CHO counting purposes or for purposes of insulintoCHO ratios if a serving of a food contains more than or equal to 5 grams of dietary fiber you can subtract half the grams of dietary fiber from the total carbohydrate serving of that food So if a portion of food equivalent to 15 9 contains 6 g of dietary fiber the CH0 count for that food would drop to 12 g 15 12 of 6 MNT for DM Sweeteners Sucrose table sugar in diet should be counted as a carbohydrate source in a food plan or covered with insulin or glucoselowering medications It can be substituted for other CHO at a Page 30 of 43 meal Sugary foods are usually caloriedense rather than nutrientdense You would not want to substitute sugary CHOs for healthy CHOs at every meal Fructose does not appear to have benefit vs sucrose Reduced calorie sweeteners sugar alcohols and tagatose gtgt What are the proscons of sugar alcohols as reducedcalorie sweeteners PRO Sugar alcohols are incompletely absorbed in the digestive tract so they provide sweetness without excess calories Like fiber affects CHO counting CON Excessive amounts at one meal can cause gas bloating diarrhea For CHO counting purposes or for purposes of insulintoCHO ratios if a serving of a food contains more than or equal to 5 grams of sugar alcohol you can subtract half the grams of sugar alcohol from the total carbohydrate serving of that food gtgt How much CHO do nonnutritive sweeteners eg aspartame saccharin etc provide an insignificant negligible amount Nonnutritive sweeteners saccharin aspartame neotame acesulfame potassium sucralose stevia Tend to be hundreds of times as sweet as sucrose they provide very few calories and have a negligible effect on blood glucose MNT for DM Protein Does not affect blood glucose levels in wellcontrolled diabetes with insunn insufficiency gluconeogenesis could proceed rapidly and contribute to elevated blood glucose But in general gt the major determinate of glycemic response is CHO Does NOT slow absorption of carbohydrate but if it replaces displaces CHO in a meal it decreases glucose load Protein does seem to be the most satiating feeling full macronutrient Including lean protein in a meal or snack may improve glycemic control Recognize that the ADA s guidelines for dietary fat mirror those of the National Cholesterol Education Program NCEP for CVD risk reduction MNT for DM Fat Page 31 of 43 gt Fat has the smallest effect on raising blood glucose but diabetics are at a higher risk for cardiovascular disease CVD gt People with diabetes have similar risk to those with past history of CVD So all of the American Heart Association Recommendations come into play Total fat 20 to 35 of total kcals Saturated fatty acids lt7 o Minimized or eliminate trans fat Omega3 polyunsaturated fatty acids Dietary cholesterol lt300 mgday lower with evidence of T CVD riSk 0r T LDL39S Plant sterol and stanol esters 2 to 3 gday gtgt Why would a mixedmacronutrient meal or snack with CHO PRO FAT be beneficial for the diabetic CHO has the greatest effect on blood glucose and substituting PRO and FAT for some of the CHO in meals amp snacks can help control blood glucose PRO does not affect blood glucose levels in wellcontrolled diabetes and is the most satiating micronutrient so it will help satisfy hunger FAT has the smallest effect on blood glucose but heart healthy fats should be used to lessen the risk of CVD gtgt What are the lipid and blood pressure goals for diabetes Page 32 of 43 Lipid and Blood Pressure Goals for Diabetes Modified from Standards of Medical Care in Diabetes Diabetes Care 20123581163 Measure LDL cholesterol lt1OO mgdl HDL cholesterol Men gt40 mgdl Women gt50 mgdl Triglycerides lt150 mgdl Blood Pressure lt13080 mm Hg MNT for DM Alcohol Page 33 of 43 Small amounts of alcohol can increase sensitivity to insulin Moderate amounts of alcohol with food have minimal effect on glucose control Excessive alcohol 3 drinksday contributes to hyperglycemia May be due to reduced sensitivity to insulin in pancreatic beta cells gtgt Although chronic heavy ETOH intake can lead to chronic hyperglycemia diabetics are prone to hypoglycemia if they drink on an empty stomach Why Drinking without eating in a fasted state can cause hyp0gycemia lower than normal blood glucose because the liver will prioritize the metabolism of ETOH above all else even glycogenolysis amp guconeogenesis This can lower blood sugar alcohol does not require insulin to be metabolized alcohol should be an addition to the meal plan not a substitution for a food serving don t apply CHO counting to alcohol since it can lower blood glucose Lecture amp Krause p 687 gtgt Hyperglycemia elevated blood glucose or blood sugar gtgt Hypoglycemia lower than normal blood glucose Both are acutely dangerous situations gucagon stimulates the liver to break down glycogen glycogenolysis gucagon stimulates the liver to make glucose from nonCHO substrates guconeogenesis gtgt What are the ADA s recommendations for alcohol and diabetes ADA position for type1 amp type2 If individuals choose to drink alcohol the type doesn t make a difference daily intake should be limited to 1 drink for adult women and 2 drinks for adult men to reduce risk of hypoglycemia alcohol should be consumed with food Never drink on an empty stomach Have glucose tablets as a source of CHO on hand Page 34 of 43 Physical Activity Exercise May preventtype 2 diabetes in highrisk individuals Integral part of treatment plan for diabetes Ts insulin sensitivity Regular physical activity is recommended for all diabetics because it increases insulin sensitivity in type2 diabetics this means exercise ls insulin resistance is CVD risk factors Weight control Improves wellbeing Exercise Prescription The American Diabetes Association recommends planned structured exercise as part of their Standards of Care Min150 minweek of moderateintensity aerobic physical activity OR 90 minweek of vigorous aerobic exercise Distribute over at least 3 daysweek with no more than 2 consecutive days without activity Resistance exercise 3gtltweek Modified from American Diabetes Association Standards of Medical Care in Diabetes Diabetes Care 20123581163 American Diabetes Association s General Guidelines for Exercise Ensure metabolic control before exercise Avoid exercise if ketosis is present Use caution if glucose gt300 mgdL wo ketosis Ingest additional CHO if glucose lt1OO mgdL Monitor BG before and after exercise Identify when changes insulin or CHO are necessary ii on insulin or medS Stimulating insulin production Learn individual glycemic responses to different exercise conditions Food intake Consume added CHO as needed to avoid hypoglycemia Keep CHObased foods readily available HypOglycemia is a risk for diabetics treated with insulin or insulin secretagogues meds that stimulate insulin production Page 35 of 43 gtgt What are the ADA s general guidelines for SMBG with exercise Selfmonitor blood glucose before amp after exercise If on insulin or insulin stimulating meds learn to identify when changes to insulin or CHO are necessary Learn your own glycemic response to different exercise conditions Problemsolving with Exercise Hypoglycemia possible if using insulin or insulin secretagogues Due to T insulin sensitivity Strenuous exercise may lead to Hyperglycemia due to acute shifts in counterregulatory hormones Insulin I Glucagon T However diabetics on insulin or insulin secretagogues are prone to hypoglycemia gtgt What would diabetics on insulin or insulin secretagogues do to prevent hypoglycemia during exercise Adjust CHO amp insulin see below 1 Adjusting CHO for Insulin or Insulin Secretagogue Users During Exercise gt No supplementary carbohydrate if not receiving insulin or secretagogues Add 15 g carbohydrate for every 30 to 60 minutes of activity depending on intensity No adjustment for moderate exercise lt30 mins Add carbohydrate before exercise if preexercise glucose level is lt100 mgdl CHO ingestion during prolonged exercise improves performance CHO ingestion after exercise may optimize repletion of muscle amp liver glycogen 2 Insulin Guidelines for Exercise to prevent hypoglycemia Moderate to strenuous activity gt45 to 60 minutes decrease rapidacting shortacting insulin 1 to 2 U Prolonged vigorous exercise may need 15 to 20 decrease in total daily insulin dose if using insulin pump need to adjust both backgroundbasal amount amp bolus doses effects of prolonged exercise can last for hours afterwards may need to monitor blood glucose during prolonged exercise Page 36 of 43 gtgt Know main mechanisms of action for major oral glucoselowering meds Prof This is an important slide Be familiar with major classes of Glucose Lowering Medications sometimes called Oral Hypoglycemic Agents OHAs used for type2 diabetes management OHAs are the first line of treatment for type2 diabetes Some type2s need insulin Oral GlucoseLowering Medications taken in a pill form used for type2 only used alone or in combination to achieve euglycemia in type 2 DM work to lower blood glucose in different ways Insulin secretagogues Sulfonylureas and meglitinides Stimulate or promote insulin secretion by Bcells poses risk of hypoglycemia Insulin sensitizers Biguanides metformin and Thiazolidinediones TZDs Enhance insulin action ie enhance muscle amp fat cells ability to take up glucose decrease insulin resistance suppress hepactic glucose production gt Metformin is probably most common diabetes med amp is 1 st line of treatment for type2 diabetes especially for adolescents it does not have weight gain as a side effect like some other meds it does not pose risk of hypoglycemia Enzyme inhibitors ocglucosidase inhibitors Inhibit enzymes that digest carbohydrates in small intestine delay carbohydrate absorption and lower postprandial glycemia Acarbose Precose and miglitol Glyset Prof does not see these in her practice probably because they have pretty noxious side effects DPP 4 Inhibitors Januvia Works indirectly to increase insulin release by pancreas Inhibits enzyme that breaks down natural gut hormones incretins that stimulate the pancreas to secrete insulin after a meal Prevents break down of incretins so incretins stay in circulation longer and stimulate more insulin release Page 37 of 43 sometimes used in combination with some of the other meds o it does not pose risk of hypoglycemia like the insulin secretagogues Canagliflozin Invokana NEW FDA approved March 2013 o works by flushing blood glucose out in the urine Sodium glucose cotransporter 2 SGLT2 inhibitor Blocks reabsorption of glucose from the kidneys baCk into the blOOd SO it iS expelled in the urine may become popular because it does not have weight gain as a side effect and is a once a day pill Some side effects found in trials yeast infections urinary infections due to extra glucose in urine Injectable GlucoseLowering Medications Exenatide Byetta incretin mimetic or incretinlike agent agonists for incretin lncretins are hormones released during nutrient absorption which increase glucosedependent insulin secretion slow gastric emptying decrease glucagon production and decrease appetite Pramlintide Symlin synthetic form of amylin to compensate for deficiency of amylin found in diabetics Amylin is a peptide Hormone normally cosecretion with insulin from pancreatic beta cells in response to food intake Inhibits glucagon secretion Slows gastric emptying improves satiety Page 38 of 43 Insulin Always prescribed for type1 diabetes Essential to survive in type 1 diabetes The pancreatic beta cells are destroyed and no longer producing insulin Sometimes prescribed for type2 diabetes as needed to restore glycemia 3 characteristics of insulin to consider onset peak and duration there are different types of insulin depending on onset peak amp duration how quickly insulin works when insulin peaks Page 39 of 43 how long insulin lasts Individualize type amp timing of insulin regimen based on eating amp exercise habits amp blood glucose levels Insulin pump continuous basal dosage with boluses to quotcoverquot food intake gtgt PROF KNOW DIFFERENCES BETWEEN RAPID SHORT INTERMEDIATE amp LONGACTING Types Action Times of Human Insulin Preparations Adapted from Bode BW Medical management of type 1 diabetes ed 4 Alexandria Va 2004 American Diabetes Association Action of Rapid vs LongActing lnsulins Want person s insulin regime to mimic the normal physiological response in which plasma glucose and insulin concentrations increase rapidly after eating and then return to basal concentrations within 23 hours Onset of lA eak Usual Type of Insulin 1quotquot A A39rrnT AN B yjsla sti gMealtime bolus lt15 min 12 hr 34 hr Intel necliateActinggNPH 24 hr 410 hr 1016 hr 39I39In39I39Iquot 391 quot TA an n m39quot IIIIRA Mixtures remixed doses often 05 to 1 hr Dual 10 to 16 hr usecl fog 0 er ergsons with ntrnoIquot n17 nI IItr IFFInrllIIno AAA AA AAA 7030 70 neutral protamine aspart lITPAl 2004 nqhnr Page 40 of 43 Half of daily insulin given as basal or background other half given as rapidacting or short acting before meals Mealtime or bolus dose rapidacting or shortacting insulin is given before meals to mimic normal insulin response to a meal rapidacting lt 15 min before eating shortacting 30 60 mins before eating longacting is used for basal or background insulin coverage over 24hrs The picture below shows a proportionate division of rapidacting doses but you could also use an insulintoCHO ratio depending how much CHO he plans to consume at each meal Sometimes a little more effort is needed to cover the breakfast meal because of counter regulatory hormones present in the morning Calculating an Insulin CHO Ratio Because CHO drives blood glucose the most the focus is on matching the insulin to the CH0 intake at each meal Only used for DM 1 An IC ratio tells how many units of insulin needed as a bolus dose to quotcoverquot a specified number of carbohydrate grams Rapidacting Rapidacting RaniaElecting Lenrgaecting t e L llnenlin effect to THE B Meale 5 Breakfast L lunch D dinner HS bedtime enact1 amen time ef insulin iniecticn Schematic representatien nniy ril39ifee39 39iee39 frem Em Medical management ef type 1 diabetea ee39 4 Mexem39rie 39Lt39e MAmeneee Diabetes Aeeeei fen for example if the IC ratio is 112 1 unit of insulin is needed for every 12 grams of carbohydrate eaten Typically begin at 115 and finetune prescription over time patient keeps food log and record of selfmonitored blood glucose for use at follow up visit gtgt What is SMBG and why is it important Selfmonitoring of blood glucose SMBG needed to adjust insulin doses amp food Monitoring Selfmonitoring of blood glucose SMBG up to Type 1 diabetic may monitor up to 8 X day gt 3 conventional 8 intensivexday Type 2 14xday 34 dayswk Training and recordkeeping critical Used to adjust insulin doses and food gt Treatment goal A1C aka glycated hemoglobin at lt 70 see p 17 amp 19 A1 C used to assess a person s average blood glucose over the previous few months Continuous ambulatory blood glucose monitoring is available but rarely used Urine and blood ketones testing is not routine woud Check for ketones during illness and when blood glucose levels regularly exceed 240 mgdl pregnant women also checked if gestational diabetes When would someone with diabetes other than gestational diabetes monitor urine ketones during illness and when blood glucose levels regularly exceed 240 mgdl Curing DM 1 Page 42 of 43 There is NO cure for diabetes but some type1 diabetics may be candidates for Pancreas transplant or Islet cell transplant Islets ces from islets of Langerhans clusters of alpha amp beta pancreatic cells These transplants are not common due to lack of donors and side effects of procedure Usually done only in cases of brittle type1 diabetes in which there are wild swings from hyperglycemia to hypoglycemia Both require Intensive bg monitoring and insulin adjustments Immunosuppressants and Corticosteroids Longterm complications atered metabolism and fat deposition osteoporosis hyperlipidemia MNT Acute T protein to offset steroid catabolism Monitor electrolytes Weight management Fat intake emphasize MUFA s and PUFA s minimize SFA Longterm increase calcium intake Page 43 of 43
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