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Nutrition 230 Exam 2 Study Guide

by: Juliana Bernard

Nutrition 230 Exam 2 Study Guide NUTRITN 230

Juliana Bernard
GPA 4.0
Basic Nutrition
Dr. Ronnenberg

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These are my detailed notes that cover the information on Exam 2. Studying these helped me get an A on the exam, so I hope they can help you too!
Basic Nutrition
Dr. Ronnenberg
Study Guide
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This 13 page Study Guide was uploaded by Juliana Bernard on Sunday January 18, 2015. The Study Guide belongs to NUTRITN 230 at University of Massachusetts taught by Dr. Ronnenberg in Fall. Since its upload, it has received 330 views. For similar materials see Basic Nutrition in Nutrition and Food Sciences at University of Massachusetts.

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Date Created: 01/18/15
Exam 4 Study Guide Respiratory System Respiratory Volumes Tidal volume volume of regular breath 500 ml at rest Inspiratory reserve volume volume of air that can be forcefully inhaled after a normal TV inspiration Expiratory reserve volume volume of air that can be forcefully exhaled after normal TV expiration Residual volume volume of air remaining in lungs after forced expiration used for values of hydrostatic pressure Respiratory Capacities Total lung capacity maximum amount of air contained in lungs after maximum inspiratory effort TLCTVIRVERVRV Vital functional capacity maximum amount of air that can be expired after a maximum inspiratory effort PC or VC TV IRV ERV Inspiratory capacity maximum amount of air that can be inspired after normal tidal volume expiration IC TV IRV Functional residual capacity volume of air remaining in the lungs after a normal tidal volume expiration FRC ERV RV VE minute ventilation volume of air exchanged per minute TV x R can reach up to 200 Lmin VE X R RR respiratory rate of breaths taken per minute 39VA alveolar minute ventilation volume of air getting to alveoli that is participating in exchange VA TV dead space x R 500 150 x 12 42 Lmin participating in ventilation which means almost 2 L are in tubes between nose and alveoli AVO2D1FF difference in oxygen concentration between what goes out of arteries and what returns in veins VO2 oxygen consumed by mitochondria V02 AVO2D1FF x CO Dalton39s Law of Partial Pressures total pressure exerted by a mixture of gases is the sum of the pressures exerted independently pressure exerted by each gas is a partial pressure In air Nitrogen 786 Oxygen 209 Water 5 CO2 04 Atmosphere Sea Level Alveoli Gas Approx Partial Press Approx Partial Press N2 786 597 02 209 159 137 104 mmHg CO2 04 03 52 40 mmHg H20 5 37 100 760 mmHg At atmospheric pressure of 760 P02 159 mmHg PaO2 104 mmHg aalveoli PaCO2 104 mmHg PVO2 40 mmHg Vveins PAO2 104 mmHg Aarteriole PP in alveoli lungs PP in veinsarteries PP in tissue PaOz 104 mmHg PVOZ 40 mmHg Pt022 lt40 mmHg PaCOz 40 mmHg PVCOZ 45 mmHg PtCOz gt45 mmHg PAOz 100 mmHg PACOZ 40 mmHg It39s excessively easy to exchange C02 with the room because there is so little in the air around us Oxygen is transported in 2 ways 1 98 is transported bound to Hb oxyhemoglobin deoxyhemoglobin 2 2 dissolved into plasma rst oxygen to be used Amount of oxygen that binds to Hb is dictated by concentration of oxygen in the plasma 02 saturation amount of Hb fully saturated with oxygen all 4 bound Not all Hb is always carrying full saturation capacity 9798 saturated Saturation can be affected by pH temperature PO2 CO2 transported in 3 ways 1 23 bound to Hb carbaminohemoglobin 2 7 dissolved in plasma based on amount produced by Krebs 3 39carbonic acid39 see below Transportation of CO2 If only 7 of CO2 can go in the plasma ut tissues are still making it CO2 from krebs muscle blood blood H2O from ETS CO2 H20 gt H2CO3 gt H HCO3 Acarbonic acid T A bicarbonate safe H to RBC HHb capillaries through membrane in alveoli of capillary into alveoli alveoli H HCO3 gt H2CO3 gt CO2 H2O then we exhale As altitude increases total air pressure decreases total air 760 mmHg 590 mmHg P02 159 mmHg 124 mmHg PaO2 104 mmHg A decrease in oxygen saturation will result in an increase unloading of oxygen off of Hb at the tissues saturation is an alveoli eventually unloading is a tissue event Oxyhemoglobin Saturation Curve As saturation decreases unloading increases Causes of reduction in internal P02 decrease of pH increase of temperature Changes in saturation happen to facilitate waste removal Everything you do during exercise is to facilitate waste removal Everything you do during rest is to facilitate nutrients in rest amp recovery Local control of respiration Chemoreceptors in bronchioles are stimulated by PC02 and induce bronchiomotion If there is an increase in PC02 in bronchioles induce bronchiodilation sign that you are producing more waste dilating allows more removal If there is a decrease in PC02 in bronchioles induce bronchioconstriction sign that there is not a lot of waste Neural Control Respiratory Centers in medulla Dorsal center dorsal respiratory group innervates nerves responsible for inspiration frenic nerve Ventral center ventral resp group innervations associated with all of accessory muscles for forced breathing inhalation and exhalation Atypically work in opposition of each other In PONS Apneustic center depth of breath eX yawning PhneumotaXic center rate of breath pheumotaXic center inhibits apneustic Acannot work at the same time Lymphatic System Functions 1 Productionmaintenancedistribution of lymphocytes 2 Identif1cationunderstanding of lymphoid tissue 3 Interchange between lymphocytes in blood gt tissues Lymphatic capillaries smallest vessels end of lymphoid vessels other end feeds into vena cava terminal capillaries branch all throughout peripheral tissues made up of endotheilial cells 1 layer thick mimic venous sysetm endotheilal layer overlaps like shingles on a roof overlapping held in place by collagen amp elastin fibers overlapping pattern allows formation of one way valves things go in but can39t go out very thin wall highly permeable roughly same diameter of regular capillaryvenule just smaller than RBC High oncotic pressure in lymphatic capillary pulls in water pitting edema amp any other cell waste Lymph intertitial uid that went into capillary via osmosis Lymphatic capillaries travel to 39collecting points39 and up to larger lymphatic vessels Maj or lymphatic collecting vessels units where many of these capillaries converge super cial located in subcutaneous layer of the skin collect from skin capillaries also in mucous membranes of respiratory system digestive system and urinary tract skin and mucous membranes deep much larger accompany all deep arteriesveins Lymphatic vessels do not have smooth muscle in walls Lymph is pushed up by skeletal muscle contractions like veins Lymph ows from Lymphatic terminal capillaries Maj or collecting vessels Lymphatic trunks 2 Lymphatic ducts Right lymphatic duct Thoracic lymphatic duct only collects from right side above diaphragm does greater job than right lymphatic duct merge into venous system just before vena cava Subclavian vein Brachiocephalic vein Lymphocytes main ghters of the immune system arise in red bone marrow from hemocytoblast mature into either T cells B cells or NK cells Tcells thymus dependent cells leave bone marrow gt thymus and mature there to become T cell 80 of lymphocytes become T cells 4 subdivisions helper Tcell analyzesdecides speci c or nonspeci c immunity cytotoxic Tcell phagocyte memory Tcell remember foreign invaders memorize antigens suppressor Tcell tell cytotoxic Tcells when to stop killing NK cells natural killer cell 510 of lymphocytes police our bodies and nd rogue cells B cells bone marrow derived cells don39t leave bone marrow to mature Lymphatic tissue vs organs Tissue Tissues dominated by lymphocytes Tonsils bundles of connective tissue packed with lymphocytes Mucosa associated lymphoid tissue MALT or peyers patches connective tissue packed with lymphocytes lining the mucosa in the digestive system in inner epithelium gt goblet cellsmucosa outside of digestive organs packed in connective tissue between organs omentum Organs Overdeveloped structures containing all 4 tissue layers Lymph nodes in large clumpy segments where larger collecting vessels start to merge together tend to merge in axillary region inguinal region cervical region Spleen regulates productiondistribution of lymphocytes houses largest of bacteria Nonspeci c defenses general to all foreign invaders Physical barriers skin mucous membrane nasal hairs cilia gastric juice saliva Phagocytes eats all nonself cells microphages bind to what they want to eat form vacule around it and then lysosome fuses to it and release digestive components to dissolve inside phagocytes xed attached to location they reside in free or roaming go wherever NK cells one of the lymphocytes responsible for nonspeci c defenses not phagocytic gt they lyse cells recognize sugars on outside of cell membrane 1 NK recognizes abnormal cell 2 Golgi changes position inside NK cell to line up with foreign inavader 3 NK makes and releases perforin from golgi perforin digestive enzyme that lyses outside of target cell 4 Perforin lysis pokes holes in membrane of foreign cell and it dies Complement group of 20 plasma proteins that circulate in inactive form active when you have a number of foreign bodies with antibodies attached complement lyses foreign invaders covered in antibodies also activates in ammatory response histamine releases vasodilators promotes chemotaXis which attracts other WBCs over to help creates opsonization makes outside of foreign cell membrane stickyadherent so phagocytes can easily stick to them Interferon protection gt send out chemical signal when a cell is taken over small proteins called interferons are released from the cell and taken up by receptors of neighboring cells and tells them to put up a shield so they don39t get taken over also Fever systemic response to foreign invader hypothalamus regulates temperature 36 C 986 F homeostasis WBCs release pyrogens when foreign cells are present pyrogens travel to hypothalamus and set thermostat to a higher temperature which means we can39t radiate heat until we hit that temperature this increases the speed the body can ghtrelease foreign invaders In ammatory response triggered whenever the body tissues are injured bene cial effects prevents the spread of damaging agents to nearby tissues disposes of cell debris and pathogens alerts the adaptive immune system sets the stage for repair begins with chemical alarm ood of in ammatory chemicals released by immune cells into extracellular uid chemicals include histamine complement kinkins prostaglandins EXAM TWO STUDY GUIDE Lipids Fatty acids in food are packaged as triglycerides or triacylglycerides TG or TAG consist of 3 fatty acids esteri ed to a molecule of glycerol carboxylic acid alcohol ester bond fatty acids glycerol triglyceride Monounsaturated fatty acids abundant in olive peanut and canola oils Omega6 polyunsaturated fatty acids abundant in saf ower corn and sun ower oils Omega3 polyunsaturated fatty acids abundant in sh and seafood salmon tuna mackerel nuts esp walnuts ax seeds and some vegetable oils Saturated fatty acids high in meats butter and regular dairy products and tropical palm and coconut oils Phospholipid glycerol in which one fatty acid has been replaced by a phosphatecontaining group phosphate group is hydrophobic tails are hydrophilic food sources egg yolks liver soybeans peanuts main building blocks of cell membranes Sterols family of molecules consisting of interconnecting carbon rings most common is cholesterol Cholesterol is synthesized in the liver from acetylCoA when there is no exogenous source endogenous synthesis is increased Cholesterol functions include component of cell membranes precursor to other substances Cholesterol is found only in animal foods organ meats gt egg yolk gt meat gt shell sh and sh gt dairy products Lipid Digestion l Triglyceride digestion begins in the mouth with lingual lipase 2 In the stomach gastric lipase continues the process breaking down the triglyceride into diglycerides and free fatty acids 3 Fat in the small intestine triggers the release of CCK and secretin from duodenal cells CCK causes the gallbladder to contract and release bile from the gallbladder into the duodenum Secretin causes the release of bicarbonate and pancreatic enzymes including pancreatic lipase Bile emulsi es fats breaking the fat globs into globules which increases the surface area for enzymes Pancreatic lipase breaks a triglyceride into a 2monoglyceride and 2 free fatty acids 3 Bile salts surround the products of digestion forming micelles can mix with water micellular lipids are passively absorbed across the brush border membrane of the duodenal and jejunal cells some fatty acids are absorbed by transport proteins Bile salts stay in the small intestine lumen and eventually are reabsorbed in the ileum returned to the liver and recycled into bile again enterohepatic circulation Lipid Absorption 1 In the ER of intestinal cells monoglycerides and free fatty acids reesterify into triglycerides triglycerides and other lipids cholesterol phospholipids join with protein molecules to form a lipoprotein known as a chylomicron which enter the lymphatic system through lacteals in the villi where they eventually will enter the bloodstream Lipids are transported through the circulatory system in lipoproteins Lipoproteins spherical bodies with a phospholipidprotein shell that contain food lipids Chylomicrons large lipoproteins that carry lipids from the small intestine first via the lymph system and eventually into the blood stream Chylomicr0ns carry lipids of dietary origin Lipoproteins chylomicrons formed in the gut and carry lipids of dietary origin lipoprotein lipase removes triglycerides cholesterolrich remnant left which liver uses VLDL formed in the liver from partially spent chylomicrons deliver lipids to body cells rich in triglycerides ultimately become IDL LDL formed in the liver from partially spent VLDLs deliver cholesterol to cells bind to LDL receptors on cells or to scavenger receptors can release cholesterol into blood vessel walls BAD LIPOPROTEINS HDL circulate through the body removing excess cholesterol from other lipoproteins and body cells pick up cholesterol from dying cells arterial walls and cell membranes for removal or recycling retum cholesterol to the liver GOOD LIPOPROTEINS Lipid Metabolism Fats are stored as triglycerides in adipose tissue Lipolysis hormones such as epinephrine and glucagon trigger the release of fatty acids from stored triglyceride in adipocytes by activating hormonesensitive lipase FFAs bind to albumin and circulate in the blood traveling to tissue to be used for energy lnside cells rst step in liberating the energy stored in the fatty acid is betaoxidation fatty acid is hydrolyzed into many 2carbon fragments that form acetylCoA which then proceeds through the citric acid cycle resulting in ATP and reduced coenzymes acetylCoA must have oxaloacetate to condense with in citric acid cycle otherwise they will condense and form ketone bodies Only the glycerol portion of a triglyceride enters the pathway as pyruvate or can be used to make glucose Wrong kind of fats saturated fats trans fatty acids oxidized fats may also contribute to heart disease and cancer 39Good39 fats monounsaturated fatty acids omega3s unhydrogenated fatty acids help prevent heart disease cholesterol intake 5 300 mg total serum cholesterol lt 200 mgdL serum triglyceride levels lt 150 mgdL serum LDL levels lt 100 mgdL HDL levels gt 50 mgdL Atherosclerosis narrowing and hardening of the medium and large arteries that result from chronic lipid deposition cell proliferation and in ammation in the artery wall Coronary Artery Disease CAD Coronary Heart Disease CHD atheroslerotic lesions occurring in the coronary arteries Cardiovascular Disease CVD disease of the heart and blood vessels HTN CAD angina stroke Somehow hypertension radiation cigarettes etc damage occurs to the endothelium of arteries causing immune cells to come to the area and squeeze through as monocytes Once they enter through the endothelium the monocytes mature to macrophages which ingest oxidized LDL and other lipids until they grow into foam cells which make up bulk of plaque Foam cells also secrete growth factors causing muscle cell proliferation so more muscle cell grows filling up the inside of these cells They also release enzymes that digest the stuff that holds everything inside of the artery which can get loose travel through the blood stream and block arteries causing potential heart attack stroke or poor circulation High serum cholesterol increases severity of atherosclerosis thus increasing risk of CVD Dietary saturated fat cholesterol and trans fats increase total cholesterol and serum LDL levels Polyunsaturated fatty acids and monounsaturated fatty acids decrease serum total cholesterol and LDL levels Polyunsaturated also decrease HDL levels monounsaturated may increase them Eicosanoids lipid mediators that are synthesized from 20c polyunsaturated FAs usually arachidonic acid Involved in wide range of activities in ammation pain and fever reproduction functional inhibition of gastric acid secretion regulation of BP through vasodilationconstriction platelet aggregation and thrombosis Eicosanoids can be synthesized from omega3 or 6 fatty acids and depending on diet they have different effects Linoleic acid derivatives omega6 family linoleic acid can be elongate and desaturated into arachidonic acid AlphaLinoleic Acid ALA derivatives omega3 family 1 Eicosapentaenoic acid EPA 2 Docosahexaenoic acid DHA Arachidonic Acid is the main 20c polyunsaturated fatty acid in tissues so it is the main eicosanoid precursor AA is often located in the 2 position on glycerol molecule of cell membrane phospholipids Once released from phospholipid AA is channeled into 1 of 3 pathways of eicosanoid synthesis depending on the enzymes expressed by the particular cell Each pathway involves addition of oxygen to one or more unsaturated double bonds forming oxygenated derivatives Pathway l Cyclooxygenase Pathway COX Liberated A2 goes through COX and results in prostaglandins PGs and thromboxanes TX COX has to isoforms COXl and COX2 COXl normal physiologic PG production COX2 PG production in response to in ammation after synthesis PGs are released into extracellular uid they bind to receptors initiating a response in target cells eicosanoids play important role in cell to cell communication have both autocrine and paracrine activity COX products play key but opposing roles in regulation of blood ow and vascular homeostasis PGI2 released from arterial endothelium acts on adjacent platelets inhibits aggregation and adherence prevents blood clotting also acts on underlying arterial smooth muscle to induce relaxation overall effect PROTECTIVE TXA2 is main eicosanoid product of platelets derived from AA triggers arterial contraction clamps artery BP up platelet aggregation also produced by monocytes and macrophages overall effect PROMOTES ATHEROSCLEROSIS Omega3 Fas and Eicosanoids ALA reduces synthesis of AA EPA and DHA compete with AA for incorporation into phospholipids that provide the fatty acid for eicosanoid synthesis and appear to suppress synthesis of AAderived eicosanoids Omega3 eicosanoids have less bioactivity than those from AA effects are GOOD reduced risk of cardiac arrhythmia improved lipoprotein metabolism decreased TG reduced BP DHA increases nitric oxide production Soluble ber may lower cholesterol Examples pectins and gums fruits vegetables oat and barley products soybean yeast Effects delays gastric emptying may slow glucose absorption lower total serum cholesterol levels Bile acids bind to ber in intestinal lumen decreasing enterohepatic circulation and increasing hepatic conversion of cholesterol to bile acids can reduce LDL Plant sterolsstanols may lower serum cholesterol levels by competing with dietary cholesterol for absorption Conjugated linoleic acid CLA family of trans polyunsaturated fatty acids derived from linoleic acid produced by bacteria in rumen of cattle conjugated because of double bond pattern Anticancer effects Prevention of atherosclerosis Modulation of immune functions Modulation of body composition Proteins and Amino Acids Proteins are most complex of all organic molecules consist of chains of 100 or so amino acids 20 different amino acids are used to form proteins the sequence of amino acids in a protein is speci ed by genes Polypeptides chains of more than 10 or so amino acids Amino Acids contain carbon hydrogen oxygen and nitrogen all consisting of a central carbon with an amino group a carboxylic acid group a hydrogen atom a variable side chain R group 9 Essential Amino Acids Pvt Tim Hall Phenylalanine Valine Tryptophan Threonine lsoleucine branchedchain amino acids Methionine Histidine Leucine Lysine Peptide bonds are formed when carboxyl group of one amino acid reacts with the amino group of another Peptide bond formation condensation reaction OH on carbon leaves with H on nitrogen releasing water Primary structure sequence of amino acids Secondary structure interactions hydrogen bonding between nearby amino acids in chain coils or sheetlike Tertiary structure bonding between more distant amino acids R group leads to folding of the molecule Quatemary structure nal structure of protein that is related to interactions among several peptide chains Shape of protein determines function Collagen in hair and nails consists primarily of long straight polypeptides Hemoglobin has 4 polypeptide chains folded into spherical structure adopted to hold oxygen atoms Enzymes are proteins specially shaped to hold two molecules together or to split a molecule apart Protein denaturation when proteins unfold bump into and bind to each other due to heat acid oxidation and other agitation they lose shape and can no longer carry out their normal function does not alter primary structure this is first step in protein digestion Functions of proteins Structure provide structure to all cells ex collagen keratin Motor proteins turn energy into mechanical work cell division muscle contraction swimming sperm Enzymes essential catalysts for virtually all reactions in the body Hormones formed in one part of body and are carried in the blood to a different location where they signal cells to alter activities ex CCK insulin glucagon Immune system Bcells of immune system secrete antibodies that bind to foreign materials and mark them for destruction by other immune cells Fluid balance blood proteins help maintain appropriate uid levels in the vascular compartment force of hearts beating pushes uid and nutrients into interstitial uid around cells proteins like albumin and globulin are too big to exit so they are trapped in capillaries and help draw uid back into vascular system Acidbase balance serve as buffers to resist detrimental changes in blood release or pick up H ions Energy gluconeogenesis can be degraded and use amino acids for energy but is last case scenario Nonprotein functions of amino acids Leucine is converted and used in ketone synthesis Thyrosine is a precursor of melanin thyroxine amp catecholamines dopamine norephinephrine epi Suff1cient tryptophan intake provides major portion of body39s niacin requirements Small intestine is the site of most protein digestion pH begins protein denaturation When polypeptidesamino acids enter intestinal lumen Secretin is released triggers release of bicarbonate by pancreas which raises pH 2 optimal for proteases CCK is releaseed by mucosal cells stimulates pancreas to release zymogens into small intestine Trypsinogen Chyotrypsinogen Procarboxypeptidase Enterokinase enzyme in BBM of enterocyte activates trypsinogen to trypsin trypsin then activates other zygmogens chyomtrypsinogen to chymotrypsin proelastase to elastase procarboxypeptidases to carboxypeptidases Endopeptidases hydrolyze internal peptide bonds Exopeptidases cleave off 1 amino acid at a time from end of the peptide carboxypeptidase active at Cterm Presence of peptides in small intestines triggers release of CCK which causes pancreas to release zymogens End products of pancreatic proteases are mostly dipeptides and oligopeptides with minor amount of free AA BBM of small intestine is equipped with exopeptidases that further hydrolyze small peptides into free amino acids and tri amp dipeptides at the N terminus Absorption at the Enterocyte Most amino acid absorption occurs in the jejunum 1 Speci c carrier proteins absorb AA and small peptides 2 Inside the enterocyte di and tripeptides are further hydrolyzed to free amino acids which are then transported out of the enterocyte and ultimately carried to the liver via the portal vein Di and tripeptides absorbed into enterocyte more readily than free AA Most AA absorption into enterocyte cross basolateral membrane and enter portal circulation Glutamine is extensively metabolized by enterocytes as their main energy source About 1 of rotein resists di estion can tri er aller ic res onses P g gg g P Amino acids are watersoluble and dissolve in blood uid those that are needed for protein synthesis or other functions are taken up by cells any excess amino acids cannot be stored and are dismantled by liver for energy glucose replenishment Amino acid pool the circulating amino acids available in blood and inside cells for protein synthesis Metabolism of Protein Hormones play important roles in protein and amino acid metabolism Anabolic insulinshort term growth hormonelong term Catabolic glucagongluconeogenesis from AA cortisolincreases muscle proteolysis Protein synthesis instructions from DNA are copied onto mRNA travels to ribosomes on rough ER where amino acids are attached to polypeptide chain with tRNA Nonessential amino acids can be synthesized through transamination Amino acids not needed for protein synthesis can be metabolized for energy or converted to glucose once amino group has been removed deaminatoin Transamination moving the alphaamino group from one carbon chain to another amino group of one AA is transferred to a keto acid to form another AA Most aminotransferases have preferred amino acidketo acid substrate amp use a alpha ketolutarate and glutamate Glucogenic catabolism yields citric acid cycle intermediary pyruvate Ketogenic carabolism yields acetylCoA or acetoacetate Regardless of their fate AA are first deaminated and the ammonia produced must be further processed to urea Deamination is the complete removal of the amino group from an amino acid in the liver NH2 group is removed becoming ammonia very toxic in the liver 2 ammonia molecules combine with CO2 to create less toxic urea Urea that is made in the liver is released into the blood and later removed by kidneys Essential AA are required for protein maintenance andor replacement of obligatory losses protein loss through bleeding urinary loss synthesis of nonproteins oxidation of AA as fuel Nitrogen balance assesses changes in body protein mass because thats where we get our nitrogen from Positive nitrogen balance intake gt output Negative nitrogen balance intake lt output Nitrogen Equilibrium intake output Protein Recommendations Adult RDA 08 gkg body weight Infants and children need considerably more protein per kg of body weight 06 months need the highest ratio of gkg Protein Quality ability of particular protein to meet body39s AA requirements based on Protein digestibility animal gt plant Amino acid composition Foods that contain essential amino acids in same proportion as required by human body high quality Assessing protein quality Amino acid score compares AA composition of protein to a reference pattern of AA Protein eff1ciency ration PER measures AA composition and accounts for digestibility Net protein utilization NPU measures percentage of ingested protein nitrogen that is retained Biological value determines extent to which protein in a food can be incorporated into body proteins Protein digestibilitycorrected amino acid score PDCAAS accounts for both AA composition of a food and the digestibility of protein Protein complementation combination of 2 food groups with certain AA groups provide balance of essential amino acids ex cereal grains and legumes rice and beans Protein Energy Malnutrition PEM Marasmus overall energy deficiency and wasting of the body Kwashiokor overall energy is sufficient but have chronic protein deficiency swollen belly Excess protein does no good excess proteinamino acid used for energy often related with animal fats in diet may lead to dehydration as body rids itself of waste ammonia can cause stress on liver and kidneys Alcohol Metabolism Alcohol ethanol CH3CH2OH caloric value is 7cal gram gt90 of ingested ethanol is metabolized healthy person can metabolize 57 grams of ethanol each hour Ethanol is readily absorbed from GI tract and is transported unaltered in the bloodstream to the liver 2 main metabolism systems 1 Alcohol Dehydrogenase Pathway ADH lowmoderate concentrations of ethanol ADH enzyme is in cytoplasm liver and requires zinc and NAD oxidized form ADH also found in gastric mucosa males gt females First Step ADH oxidizes ethanol to acetaldehyde also producing NADH H CH3CH2OH NAD gt CH3CHO NADHH ethanol ADH acetaldehyde Acetaldehyde is even more toxic to cells than ethanol and it is the cause of 39hangover39 symptoms It attaches to proteins and alters their function and structure cirrhosis in liver Second Step Acetaldehyde is further oxidized to acetate by acetaldehyde dehydrogenase ALDH CH3CHO NAD H20 gt CH3COOH NADHH acetaldehyde ALDH acetate Produces more reduced coenzymes Some drugs inhibit this reaction leading to elevated acetaldehyde Third Step Acetate is converted to acetylCoA AcetylCoA can then be oxidized in the citric acid cycle May be converted to fat or ketones Cannot be converted to glucose Conversion of ethanol to acetyl CoA requires niacin as NAD oxidized When enzymes oxidize ethanol they remove H atoms and attach them to NAD Thus NAD is used up and NADHH accumulates making lots of reduced coenzymes Both ADH and ALDH use NAD and both produce NADH metabolism of ethanol via this pathway depletes cells of NAD which leads to increased production of lactate from pyruvate via LDH reduced hepatic gluconeogenesis leading to hypoglycemia inhibition of the citric acid cycle with decreased oxidation of fatty aids and increased lipogenesis increased FA synthesis TG production fatty liver and hyperlipidemia Consumption of alcohol slows metabolic process and fosters accumulation of body fat Expression of both ADH and ALDH enzymes varies widely among individuals and ethnicities which affects responses to alcohol intake 2 Microsomal Ethanol Oxidizing System MEOS active with higher intakes of alcohol Associated with smooth ER Oxidizes many other compounds including steroids medications First Step CH3CH2OH NADPHH 02 gt CH3CHO NADP H2O ethanol reduced acetaldehyde Many MEOS enzymes are inducible by ethanol increasing metabolism of ethanol and leading to metabolic intolerance Enzyme induction can also in uence metabolism of other substances including drugs tylenol to hepatotoxic compounds DON39T TAKE TYLENOL AFTER DRINKING Chronic alcohol abuse can lead to pancreatitis fatty liver cirrhosis infertility micronutrient deficiencies Ethanol interferes with metabolism of all fatsoluble vitamins Folate is most common deficiency among alcoholics


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