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Exam 4 Study Guide

by: SunDevil_21

Exam 4 Study Guide HCR 240

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Study guide for chapters 44-49
Human Pathology
Study Guide
pathophysiology, patho
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This 24 page Study Guide was uploaded by SunDevil_21 on Saturday February 20, 2016. The Study Guide belongs to HCR 240 at Arizona State University taught by Fortier in Spring 2016. Since its upload, it has received 7 views.


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Date Created: 02/20/16
Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. Chapter 44  1. Describe the following types of movement in the gastrointestinal tract and their unique  role in controlling movement of digesta: a. Tonic i. Continuous movements that last for minutes or even hours ii. Contractions occur at sphincters iii. Constant without period of relaxation iv. Found in the sphincters, lasting minutes to hours, used to blocking motility beyond key  points in the GI tract either to facilitate further digestion of defecation before we are  prepared to do so b. Rhythmic i. Intermittent contractions responsible for mixing and moving food along the digestive  tract  ii. Peristaltic movements are rhythmic propulsive movements. c. Peristaltic i. Rhythmic waves of contraction with rest periods ii. Not the same as constant constriction 2. Describe the phases of swallowing, and give one example of a potential complication of  dysfunction at each phase. a. Oral i. Bolus collected at the back of the mouth; tongue lifts food upward until it touches the  posterior wall of the pharynx. b. Pharyngeal i. Soft palate pulled upward, palatopharyngeal folds pull together to block nasopharynx,  vocal cords pull together, and epiglottis covers the larynx, this prevents the food from  going down only in the esophagus ii. Respiration is inhibited. iii. The bolus is moved backward into the esophagus by constrictive movements of the  pharynx. c. Esophageal i. Esophageal stretching triggers local and central reflexes for peristalsis down into the  stomach Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. 3. Describe briefly the conditions and systems influencing control of secretory functions in  the digestive tract.  Local Control: Act as stimuli for neural and humoral mechanisms for stimulating or suppressing  secretions pH osmolality chyme humoral mechanism(s)  Response of endocrine cells to changes in the concentration of substances in the ECF Neural mechanism(s)  Mediated through the ANS  Increased with parasympathetic stimulation   Inhibited with sympathetic activity 4. Define the function(s) of the following and/or how they affect rate of gastric emptying: Cholecystokinin:  Stimulates contraction of the gall bladder, secretion of pancreatic enzymes, slows gastric  emptying Secretin  Stimulates secretion of bicarbonate­containing solution by the pancreas and liver Gastrin  Stimulates secretion of gastric acid, pepsinogen  Increases gastric blood flow  Stimulates gastric smooth muscle contraction  Stimulates growth of the gastric, small intestine, and colon mucosa Trypsin Released as trypsinogen and activated by enterokinase in alkaline environment Chymotrypsin  catalytic enzyme for protein hydrolysis Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. Carboxypeptidase  cleaves proteins at the carboxyl end of the molecule Elastase  hydrolyzes elastin, meat digestion bc most of the proteins are contained in an elasatin  envelope Lactase  hydrolysis of lactose to glucose and galactose Sucrase  brush border enzymes hydrolyzing sucrose to fructose and glucose Amylase  catalyze hydrolysis of starch, glycogen, and polysaccharides to maltose and glucose Maltase  hydrolysis of maltose to glucose α­dextrinase  complexes with sucrase to hydrolyze maltose and isomaltose 5. Describe the role of the following in digestion: a. Acid production i. Parietal cells ii. Chief Cells iii. Produces pepsin, protein specific hydrolytic enzyme b. Enzyme cleavage i. Brunner’s glands c. Fat emulsification i. Liver/gallbladder 6. Describe briefly the immunologic support mechanisms of the gut flora.  Natural habitat of large, diverse bacterial community.  a. Major functions of the gut microflora: i. Salvage energy and absorbable nutrients  ii. Trophic effects on intestinal epithelial cells iii. Protection against pathogenic organisms Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. 7. Describe the etiology and symptoms associated with Steatorrhea.  Fatty stools  Lab tests involve measuring the amount of fat contained in a 72hr stool collection during  which time the person is to consume 50­150g of fat per day Chapter 45  1. What are the common signs and symptoms of gastrointestinal disorders? Briefly describe  them.   Anorexia – loss of appetite  Nausea – sickness with inclination to vomit  Retching – rhythmic spasm of diaphragm, chest wall, and abdominal muscles  Vomiting (emesis) – forced expulsion of stomach contents, can remove certain agents from the GI  tract  Gastrointestinal bleeding – presence of blood in the stool or vomitus from damage to gut 2. Describe the system responses controlled by the Vomiting center and the chemoreceptor  zone with respect to vomiting.   Vomiting involves functionally distinct medullary centers o Vomiting center o Chemoreceptor trigger zone.  Vomiting is thought to be a reflex integrated in the vomiting center located in the dorsal reticular center  of the medulla near the sensory nuclei of the vagus 3. GERD: a. Signs/symptoms  HEART BURN, 30­60 mins after eating  Belching and chest pain  Avoiding large meals   Avoiding alcohol use and smoking  Eating meals sitting up  Avoiding recumbent position several hours after a meal  Avoiding bending for long periods   Sleeping with the head elevated   Losing weight if overweight b. Complications Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. i. children 4. Esophageal Diverticulum:  a. Diverticulum: herniation of the esophageal wall caused by a weakness of the muscularis layer i. ESOPHAGEAL DIVERTICULUM: 1. Tends to retain foods b. Signs/symptoms i. The food stops before it reaches the stomach.  ii. Gurgling iii. Belching iv. Coughing v. Foul­smelling breath c. Complications i. Trapped food may cause esophagitis and ulceration  ii. Correction requires surgical intervention 5. Esophageal cancer: Squamous cell a. Risk factors i. Alcohol and tobacco use b. Signs/symptoms c. Complications i. Dysphagia 1. Weight loss 2. Anorexia 3. Fatigue 4. Painful swallowing Adenocarcinoma a. Risk factors i. Barrett esophagus ii. GERD b. Signs/symptoms i. Erosion of lower esophagus as a result of chronic GERD c. Complications i. Dysphagia 1. Weight loss 2. Anorexia 3. Fatigue 4. Painful swallowing 6. Describe the relationship between NSAIDS and H. pylori in developing ulcers. Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts.  Aspirin or nonsteroidal anti­inflammatory drugs (NSAIDs) o Irritate the gastric mucosa and inhibit prostaglandin synthesis – regulation of bicarbonate  production  Infection with H. pylori o Thrives in an acid environment of the stomach  o Disrupts the mucosal barrier that protects the stomach from harmful effects of its digestive  enzymes 7. Peptic ulcers : group of ulcerative disorders that occur in areas of the upper GI tract that are exposed to acid­pepsin secretions  Most common are duodenal and gastric ulcer a. Risk factors/cause i. More prevalent among middle aged and older adults ii. Duodenal: more male predominance iii. H. pylori and NSADIS b. Signs/symptoms i. Discomfort and pain ii. Periodicity  iii. Hemorrhage iv. Perforation v. Outlet obstruction c. Complications i. Surgery d. Treatment i. Eradicate the cause and promote a permanent cure for the disease  1. Eradicating H. pylori­ complex process, infection must be cleared which could  cause more problems 2. Relieving ulcer symptoms 3. Healing the ulcer crater  a. Antacids b. Proton pump inhibitors 8. Gastric cancer: a. Risk factors/cause i. Genetic predisposition ii. Carcinogenic factors in the diet: alcohol, smoking, processed meats  iii. Autoimmune gastritis iv. Gastric adenomas or polyps b. Signs/symptoms i. Asymptomatic until late in their course ii. Indigestion, weight loss, vague epigastric pain, vomiting, and an abdominal mass Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. c. Complications i. Surgery 9. Irritable bowel disease: a. Risk factors/cause i. Functional GI disorder characterized by a variable combo of chronic and recurrent  intestinal symptoms, not explained by structural or biochemical abnormalities  b. Signs/symptoms i. Persistent or recurrent symptoms of abdominal pain ii. Altered bowel function­ constipation of diarrhea  iii. Varying complaints of flatulence, bloating iv. Nausea and anorexia v. Constipation or diarrhea vi. Anxiety or depression c. Complications i. Pharmacologic agents  10. Inflammatory bowel disease Crohn disease  A recurrent, granulomatous type of inflammatory response that can affect any area of the  gastrointestinal tract from the mouth to the anus a. Risk factors/cause b. Signs/symptoms i. Lesions surrounded by mucosal tissue  ii. Diarrhea, abdominal pain, weight loss, fluid and electrolyte balance disorders, malaise,  and low grade fever c. Complications i. Can result in: perineal fistula, intestinal obstruction, malabsorption, infection Ulcerative colitis  A nonspecific inflammatory condition of the colon a. Risk factors/cause I. Very common in US II. Disease may arise at any age, peak incidence between 15 and 25 yrs old b. Signs/symptoms I. Affect continuous areas rather than sporadic areas II. Diarrhea, stools with blood and mucus, abdominal cramping, fecal incontinence,  anorexia, weakness, fatigability c. Complications I. Colon cancer  Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. 11.Intestinal polyps: a. Risk factors/cause i. Increase with age, greatly after 60y.o. b. Signs/symptoms c. Complications i. Colorectal cancer 12.Diverticulitis: a. Risk factors/cause i. Western society, 60 years old = 40% of population, 60% by age 80 b. Signs/symptoms i. Pain in lower left quadrant ii. Nausea and vomiting iii. Fever iv. Elevated wbc count, result of increased presence of pathogens c. Complications i. Hospitalizations, surgical treatment 13.Appendicitis a. Risk factors/cause i. Very common, 12% risk in males, 25% risk in females ii. Appendix is inflamed, swollen, and gangrenous, can perforate if not treated iii. Intraluminal obstruction with fecalith, gallstones, tumors, parasites, or lymphatic tissue  b. Signs/symptoms i. Pain is a result of stretching due to swelling during the onset of inflammation  ii. Pain is vague can gradually increase and can become colicky c. Complications i. Peritonitis, localized periappendiceal abscess formation, septicemia  14.Diarrhea: a. Risk factors/cause i. Frequent passage of loose or unformed stools  b. Large­Volume­ noninflammatory in nature i. Osmotic­ ex) lactose intolerance ii. Secretory – ex) incr. secretion or inhibited absorption of electrolytes c. Small­Volume –inflammatory  i. Inflammatory bowel disease ii. Infectious disease iii. Irritable colon 15.Intestinal obstruction  Mechanical obstruction from post operative causes such as external hernia and postoperative  adhesions.  Paralytic, or adynamic, obstruction results from neurogenic or muscular impairment of  peristalsis. Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts.  Abdominal distension   Dehydration and electrolyte depletion a. Risk factors/cause i. Impairment of movement of intestinal contents in cephalocaudal direction b. Signs/symptoms i. Pain, absolute constipation, abdominal distention, sign of fluid volume deficit, vomiting  ii. Restlessness, weakness, perspiration, anxiety c. Complications i. Necrosis of tissues  16.Peritonitis  Permits rapid absorption of bacterial toxins  Favors the dissemination of contaminants   Great inflammatory response  Thick, fibrinous protective substance a. Risk factors/cause i. Causes: perforated peptic ulcer, ruptured appendix, perforated diverticulum, gangrenous  bowel, pelvic inflammatory disease, and gangrenous gallbladder b. Signs/symptoms i. Perforated peptic ulcer ii. Ruptured appendix iii. Perforated diverticulum iv. Gangrenous bowel v. Pelvic inflammatory disease vi. Gangrenous gallbladder vii. Abdominal trauma and wounds c. Complications 17. Celiac disease:  Presents in infancy o Abnormal t cell response to gluten protein components   Manifests as o Failure to thrive o Diarrhea o Abdominal distention o Occasionally, severe malnutrition a. Risk factors/cause Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. i. Immune mediated disorder triggered by ingestion of gluten containing grains ii. Type 1 diabetes individuals b. Signs/symptoms i. Bloating , diarrhea, constipation, flatus, belching c. Complications Chapter 46  1. How is jaundice categorized, and what features are unique to each category?  Prehepatic o Major cause is excessive hemolysis of red blood cells due to injury or toxins. o Unconjugated bilirubin   Intrahepatic o Caused by disorders that directly affect the ability of the liver to remove bilirubin from  the blood or conjugate it so it can be eliminated in the bile o Conjugated bilirubin  Posthepatic o Occurs when bile flow is obstructed between the liver and the intestine o Conjugated bilirubin 2. Describe the reactions in the liver that detoxify and metabolize substances from the body. a. Phase 1 reactions i. Involve chemical modification or inactivation of a substance b. Phase 2 reactions i. Involve conversion of lipid­soluble substances to water­soluble derivatives c. Phase 3 reactions i. Involve substances, metabolites, or conjugates secreted as bile  3. Differentiate between the sub­types of drug­induced liver damage. a. Direct hepatotoxic injury – toxic metabolites cause necrosis, causes damage while being  metabolized b. Idiosyncratic reactions – allergic­like reactions, no dose or length of use  c. Cholestatic reactions – decreased or blocked bile movement  Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. d. Chronic hepatitis – long­term use damage, cirrhosis  4. Hepatotropic viruses (Complete for all 5 strains): a. Hepatitis A virus (HAV)­  i. self limiting, unenveloped single strain RNA virus  ii. contracted from fecal contamination of food and water, or as result of immature hygiene  habits or behaviors from children in daycare centers iii. asymptomatic in children under 6, symptoms worsening with age iv. S/S: fever, malaise, nausea, dark urine, jaundice v. Symptoms persist for about 2 mos, chronic hep and carrier status do not occur vi. Ab appear w/in a wk of exposure vii. Immunization b. Hepatitis B virus (HBV) i. Double strand DNA virus that can be acute, chronic, progressive, and result in carrier  status and participates in the development of HDV ii. Incubation is several wks, S/S similar to Hep A iii. Virus is common in IV drug users, can be transmitted via oral and sexual contact iv. Vertical transmission to infants born to infected mothers occurs 10­85% depending on  prenatal care v. Vaccination is recommended in childhood series vi. Ig therapy c. Hepatitis B–associated delta virus (HDV) i. Single strand RNA virus ii. Causes coinfection, dependent on preexisiting infection w/ Hep B iii. Hep B infected individuals are the most at risk for developing HDV d. Hepatitis C virus (HCV) i. Most common cause of chronic hepatitis, cirrhosis, and hepatic cancer ii. Single strand RNA virus w/ notorious instability, results in genotypes and subtypes  making it highly pathogenic iii. Difficult to treat and no vaccine Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. iv. Incubation is 6­12wks, 85­90% developing chronic hep v. Most are asympto. Jaundice is rare vi. Ab are not protective, are used as markers e. Hepatitis E virus (HEV) i. Unenveloped single strand RNA virus ii. Transmitted by fecal oral route iii. High mortality rate iv. Not endemic in US, those who have it usually contract it abroad v. Treatments are limited 5. Intrahepatic biliary disease: primary and secondary a. Risk factors/cause i. Women 40­60 y.o. ii. Familial occurrences b. Signs/symptoms i. Unexplained pruritus or itching, weight loss, fatigue, dark urine and pale stools ii. Osteoporosis in 51% of women iii. Jaundice  Primary biliary cirrhosis o Caused by damage to bile ducts from autoimmune actions causing cholestasis o Liver enlarges and becomes greenish in hue due to the accumulation of bile  o Dark urine, pale stools o Diagnosis: destruction of bile ducts, presence of nonspertive cholengitis, cholestasis with  alkaline phosphate for at least 6 mos, presence of antimicrobial Ab  Secondary biliary cirrhosis o Long term blockage of extra biliary tree 6. Describe the progression of alcohol­induced liver disease: pg 1227 a. Fatty liver: accumulation of fat in hepatocytes, aka STEATOSIS.  i. Liver becomes yellow and enlarges  b. Alcoholic hepatitis: intermediate stage between fatty changes and cirrhosis i. Common in “spree” drinkers ii. Inflammation and necrosis of liver cells iii. Hepatic tenderness, pain, anorexia, nausea, fever, jaundice, ascites, and liver failure,  some may be asymptomatic  c. Cirrhosis: end result of repeated bouts of drinking related liver injury  i. Fine, uniform nodules on the surface of liver Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. ii. Nodules can compress hepatic veins, curtailing blood flow out of the liver and producing  portal HTN, extrahepatic portosystemic shunts, and cholestasis iii. Manifestations: weight loss, weakness, anorexia, hepatomegaly, jaundice, abdominal  pain, esophageal varices, splenomegaly 7. Describe the manifestations of liver failure: a. Hematologic disorders: i. Can cause anemia, thrombocytopenia, coagulation defects, leukopenia ii. Changes in lipid composition of RBC increase hemolysis iii. Thrombocytopenia often occurs as result of splenomegaly  iv. Person w/ liver failure is subject to purpura, easy bruising, hematuria, abnormal  menstrual bleeding, vulnerable to bleeding from esophagus and other segments of GI b. Endocrine disorders: i. Liver metabolizes steroid hormones ii. Endocrine disorder, particularly disturbances in gonadal (sex hormone) function are  common of cirrhosis and liver failure iii. Women: menstrual irregularities, loss of libido, sterility iv. Men: testosterone levels fall, testes atrophy, loss of libido, impotence, and gynecomastia  occur c. Skin disorders: i. Lesions called vascular spiders, telangiesctases, spider angiomas, and spider nevi  ii. Palmar erythema iii. Finger clubbing  iv. Jaundice d. Hepatorenal syndrome: i. Functional renal failure sometimes seen during terminal stages of liver failure when no  functional causes of renal disease exist  ii. Characterized by: progressive azotemia, incr. serum creatinine levels, oliguria e. Hepatic encephalopathy: i. Totality of CNS manifestations of liver failure ii. Characterized by: neural disturbances ranging from lack of mental alertness to confusion, coma, convulsions iii. Early sign is a flapping tremor called asterixis 8. What differentiates hepatocellular carcinoma from cholangiocarcinoma?  Hepatocellular carcinoma o Arises from the liver cells  o Viral hep infections  Cholangiocarcinoma Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. o A primary cancer of bile duct cells 9. Differentiate between forms of pancreatitis: PAGE 1238 Acute pancreatitis  Gallstones (stones in the common duct)   Alcohol abuse  Hyperlipidemia  Hyperparathyroidism  Infections (particularly viral)  Abdominal and surgical trauma  Drugs such as steroids and thiazide diuretics Chronic pancreatitis  Chronic calcifying pancreatitis  Chronic obstructive pancreatitis­ abnormal dilation of pancreatic duct  10.Pancreatic Cancer a. Risk factors/cause i. The cause of pancreatic cancer is unknown. ii. Smoking appears to be a major risk factor.  iii. The second most important factor appears to be diet. 1. Increasing total calorie intake  2. High intake of fat, meat, salt, dehydrated foods, fried foods, refined sugars, soy  beans, and nitrosamines iv. Highest mortality rate v. Adrenal carcinoma of ductal epithelium vi. Asymptomatic until duct blockage creates symptoms of pancreatitis  b. Signs/symptoms i. Depend on size and location of tumor ii. Dull epigastric pain, back pain, jaundice Chapter 47  1. Describe the role in appetite control of: Arcuate nucleus –center for hunger and satiety    Brain stem – centers in the hypothalamus also control the secretion of several hormones (ex­ throid and  adrenocortical hormones) that regulate energy balance and metabolism Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. 2. Describe briefly the four types of energy expenditure.  a. Basal metabolic rate or resting energy equivalent i. Amt of energy used at rest in neutral temp, with inactive digestive system b. Diet­induced thermogenesis i. Energy needed to digest food above and beyond BMR c. Exercise­induced thermogenesis i. Energy extended above the BMR for exertion exercise d. Nonexercise activity thermogenesis i. Energy expend doing everything else  3. Differentiate the prevalence and functions of white and brown fat.  White fat o Constitutes 10% to 20% of body weight in adult males and 15% to 25% in adult females o Exists as an oil at body temperature o Consists of triglycerides   Brown fat  o The site of diet­induced thermogenesis and nonshivering thermogenesis o Fat assoc. w/ newbies ||emergency thermoregulation 4. What is the function of the adipokines? a. Adipokines­ chemokines responsible for communicating the state of adipose tissue  i. Leptin­ primary appetite suppressing hormone ii. “satiety hormone” iii. Growth factors­ insulin growth factor 1­ white adipose tissue depositing iv. Adiponectin­ initiates metabolism of fat deposit 5. Obesity pg. 1254 a. Risk factors/cause a. Hypertension b. Hyperlipidemia c. Type 2 diabetes d. Coronary heart disease e. Other health problems b. Signs/symptoms a. Weight gain c. Complications a. Diabetes b. Shorter life expectancy c. Increased risk of cardiac disease, HTN Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. 6. Kwashiorkor­like secondary protein­energy malnutrition: a. Risk factors/cause i. Deficiency in protein in diets high in carbohydrates b. Signs/symptoms i. Edema, desquamating skin, discolored hair, anorexia, extreme apathy  c. Complications i. Hepatomegaly, distended abdomen, cold extremities, decreased CO, tachycardia  7. Marasmus­like secondary protein­energy malnutrition a. Risk factors/cause i. Chronic illnesses like COPD, congestive heart failure, cancer, HIV 8. Anorexia nervosa: a. Anorexia nervosa, mental illness i. Refusal to maintain normal body weight ii. Intense fear of gaining weight or becoming fat iii. Disturbance in the way body is perceived iv. Causes amenorrhea in girls 9. Bulimia nervosa a. Recurrent binge eating b. Inappropriate compensatory behaviors c. Self­evaluation unduly influenced by body shape and weight Chapter 48  1. Describe the mechanisms of action of autocrine and paracrine hormones.  a. Paracrine Actions i. Hormones acting locally on cells other than those that produced the hormone ii. For example, the action of sex steroids on the ovary b. Autocrine Actions i. Hormones exerting action on the cells from which they were produced ii. For example, the release of insulin from pancreatic beta cells can inhibit its release from  the same cells. Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. 2. Describe some situations in which alteration to typical availability of hormone receptors may alter  hormone/tissue action: Number of receptors:  Up­regulation  Down­regulation Affinity of receptors:  Affected by a number of conditions  For example, the pH of the body fluids plays an important role in the affinity of insulin receptors. Level of product regulated by hormone:  Feedback 3. What key aspect distinguishes positive and negative feedback? a. Positive feed back is rare in biology because it can easily lead to derangement of the process i. ­hormone amplifies the physiological process  b. Majority of hormones are in negative feedback 4. Describe the functions of the cell types of the anterior pituitary. a. Thyrotrophs: produce thyrotropin, also called thyroid stimulating hormone (TSH) b. Corticotrophs: produce corticotrophin, also called adrenocorticotropic hormone (ACTH) c. Gonadotrophs: produce the gonadotropins, luteinizing hormone (LH), and follicle­stimulating  hormone (FSH) d. Somatotrophs: produce growth hormone (GH) e. Lactotrophs: produce prolactin 5. Describe the mechanisms of regulation of the pituitary gland, and how would the functions of the  pituitary be affected if the routes of regulation were disrupted? a. Hypothalamus communicates with anterior pituitary via protal veins i. ­communicates via supraoptic and para ventricular nerve fibers  ii. ­secretes growth hormone, releasing hormone, somatastatin, dopamine, TRH, CRH,  GNRH iii. ­releasing hormones regulate the excretion growth hormone, thyroid stimulating  hormone, ACTH, melanocytes stimulating hormone, lactin, LH,  FSH b. ADH is primary product of psterior pituitary Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. Chapter 49  1. Describe the mechanisms that cause endocrine disorders? a. Primary i. Originate in the target gland responsible for producing the hormone b. Secondary i. The target gland is normal, but function is altered by defective levels of stimulating or  releasing hormones c. Tertiary i. Result from hypothalamic dysfunction  ii. Pituitary and target organ understimulation 2. Describe the mechanism(s) of action of pituitary tumors. Page 1279 a. Primary tumors i. Pituitary gland b. Secondary tumors i. Metastatic lesions c. Functional tumors i. Secrete pituitary hormones d. Nonfunctional tumors i. Don’t secrete hormones 3. Hypopituitarism : Under production of pituitary hormone creating a cascade of pathology in other  endocrine systems a. Risk factors/cause i. Tumors and mass lesions­ pituitary adenomas, cysts, metastatic cancer, other lesions ii. Pituitary surgery or radiation iii. Infiltrative lesions and infections­ hemochromatosis, lymphocytic hypophysitis iv. Pituitary infarction­ infarction of the pituitary gland after substantial blood loss during  childbirth (Sheehan syndrome) v. Pituitary apoplexy­ sudden hemorrhage into the pituitary gland vi. Genetic diseases­ rare congenital defects of one or more pituitary hormones Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. vii. Empty sella syndrome­ an enlarged sella turcica that isn’t entirely filled with pituitary  tissue viii. Hypothalamic disorders­ tumors and mass less (ex­ craniopharyngiomas and metastatic  malignancies), hypothalamic radiation, infiltrative lesions (ex­ sarcoidosis), trauma,  infections b. Signs/symptoms i. Being chronically unfit ii. Weakness and fatigue iii. Loss of appetite iv. Impairment of sexual function v. Cold intolerance ****Sequence of loss of pituitary reserve Go Look For The Adenoma GLFTA­ GH (typically the first to be lost), LH(sex hormone deficiency), FSH (infertility),  TSH(leads to secondary hypothyroidism) , ACTH (usually the last to become deficient,  results in secondary adrenal insufficiency) c. Complications i. Decline is slow 4. Hyperpituitarism pg 1291 a. Risk factors/cause b. Signs/symptoms c. Complications 5. Juvenile growth hormone deficiency pg. 1281 a. Risk factors/cause i. LBW, endocrine disorders, chronic illness, malnutrition, chromosomal disorders, skeletal  abnormalities b. Signs/symptoms i. Short stature ii. Idiopathic­ occur when individual has sufficient somatotrophs but insufficient growth  hormone releasing hormone iii. Tumors or agenesis 1. Compromises the number of somatotrophs available for hormone synthesis iv. Panhypopituitarism 1. Insufficiency in all pituitary hormones Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. v. Laron­Type Dwarfism vi. Hereditary defect in Igf function with adequate GH production vii. Congenital­ maybe idiopathic 1. Turner Syndrome a. Congenital syndrome  2. Renal Failure a. Supplementation for developmental stature c. Complications i. Interferes with linear bone growth ii. Results in short stature or dwarfism 6. Juvenile growth hormone excess a. Risk factors/cause i. Fusion of the epiphyses of the long bones results in gigantism b. Signs/symptoms i. Tall stature c. Complications i. Results in increased linear bone growth ii. Gigantism  7. Adult growth hormone deficiency pg 1283 a. Risk factors/cause i. Growth hormone insufficiency from childhood ii. Growth hormone deficiency developed in adulthood 1. Hypopituitarism 2. Pituitary tumor/treatment 3. Aging b. Signs/symptoms i. Stimulation tests c. Complications i. Arthrosclerosis  ii. Increased cardiovascular risk Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. 8. Adult growth hormone excess a. Risk factors/cause i. Acromegaly ii. Continued growth of soft tissues  b. Signs/symptoms i. Increased size of hands and feet ii. Thickened skin iii. Degenerative arthritis  iv. Cardiomegaly (HTN) 9. Marfan syndrome a. Marfan syndrome is a genetic condition that results in rapid bone growth and late/absence of  epiphyseal capping. b. Mutation of TGF­β i. Results in connective tissue disorders, enlarged aorta, very tall and thin stature 10.Acromegaly a. Risk factors/cause i. Somatotrope adenoma  ii. Excess secretion of GHRH by hypothalamic tumors iii. Ectopic GHRH secretion by nonendocrine tumors such as carcinoid tumors or small cell  lung cancers iv. Ectopic secretion of GH by nonendocrine tumors 11.Gigantism a. Risk factors/cause i. Somatotrope adenoma 1. Excess before puberty and epiphyseal fusion ii. High IGF­1 stimulates excessive skeletal growth b. Signs/symptoms i. Increased stature c. Complications i. Treatment of adenoma halts excessive growth 12.Precocious puberty pg. 1285 a. Risk factors/cause i. Can be idiopathic, but be caused by gonadal, adrenal, or hypothalamic disease ii. Benign and malignant tumors of the CNS  b. Signs/symptoms Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. i. Physical finding of early thelarche ii. Breast and testicular development iii. menarche c. Complications i. Tall as kids, short as adults ii. Can result in decreased levels of GH, thyroid hormones, adrenal corticosteroid hormones, and testosterone in the male and estrogens and progesterone in the female 13.How is thyroid function assessed to determine treatment options? a. Measures of T ,3T 4 and TSH  b. Resin uptake test  c. Assessment of thyroid autoantibodies  123 d. Radioiodine ( I) upt123 99mt  e. Thyroid scans (i.e.,  I,  Tc­pertechnetate)  f. Ultrasonography  g. CT and MRI scans  h. Fine­needle aspiration (FNA) biopsy of a thyroid nodule 14.Hypothyroidism: pg 1289 a. Primary, most common i. Glandular dysfunction b. Secondary i. Pituitary dysfunction c. Tertiary i. Hypothalamic dysfunction d. Risk factors/cause i. Decreased metabolic rate ii. Accumulation of hydrophilic mucopolysaccharide substance (myxedema) in the  connective tissues iii. Elevated serum cholesterol e. Signs/symptoms i. Mental retardation, impairment of physical growth 1. Cretinism (congenital) ii. Weight gain iii. Deep voice iv. Dry skin f. Complications i. Cardiovascular function ii. Respiratory function iii. Muscle tone Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. 15.Hyperthyroidism a. Risk factors/cause i. Increased metabolic rate and oxygen consumption ii. Increased use of metabolic fuels iii. Increased sympathetic nervous system responsiveness b. Signs/symptoms i. c/o nervousness, irritability, fatigability ii. weight loss iii. tachycardia, palpitations, SOB, excessive sweating, muscle cramps, hat intolerance c. Complications i. Drugs and surgery to help as treatment options 16. Graves Disease a. Risk factors/cause i. Familial tendency ii. Is associated with human leukocyte antigen (HLA)­DR3 and HLA­B8 b. Signs/symptoms i. abnormal stimulation of the thyroid gland by thyroid­stimulating antibodies (thyroid­ stimulating immunoglobulins [TSI]) that act through the normal TSH receptors ii. ophthalmopathy  17. Cushing syndrome page 1299 a. Risk factors/cause i. Glucocorticoid Hormone Excess b. Signs/symptoms i. Altered fat metabolism, muscle weakness, muscle wasting, purple striae, mild acne,  menstrual abnormalities c. Complications i. osteoporosis 18. Adrenal cortical insufficiency pg. 1297 a. Primary adrenal cortical insufficiency (Addison disease) i. ACTH levels are elevated because of lack of feedback inhibition. b. Secondary adrenal cortical insufficiency i. Occurs as a result of hypopituitarism or because pituitary gland has been surgically  removed c. Acute adrenal crisis i. Life­threatening situation occurs 19. Congenital adrenal hyperplasia: pg. 1296 Exam 4 Study Guide HCR 240 Spring 2016 Helpful hint – Identify the slides and pages that help you address the following study prompts. a. Increased levels of ACTH i. Over stimulation of adrenal androgens and mineral corticoids ii. Virilization of genitals in female infants  b. 21­hydroxylase (accounting for >90% of cases) c. 11­β­hydroxylase deficiency 20. Addison Disease pg. 1299 a. Glucocorticoid insufficiency – Primary insufficiency i. Destruction of adrenal glands b. Treatment i. Lifetime management ii. Oral replacement therapy iii. Hydrocoritsone with or without fludrocortisone iv. DHEAS in female patients v. Regular meals and exercise vi. Medical alert bracelet or lanyard


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