Phys Block 6 Question Bank (Review Book, Old Tests, In-Class Questions)

1 Amino acid absorption in the gut is stereospecific, is linked to Na+ movement, and does not require glucose.

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1 Chronic pancreatitis is swelling (inflammation) of the pancreas that leads to scarring and loss of function. The pancreas is an organ located behind the stomach that produces chemicals needed to digest food. It also produces the hormones insulin and glucagon. Chronic pancreatitis can occur due to many reasons, most commonly alcoholism. Most alcoholic patients present with structural and functional damage to the pancreas by the time pancreatitis sets in. Usually, the initial symptoms appear in patients who have been heavy drinkers for a long time. The pain generally is felt in the supraspinal region and it increases during eating. Other symptoms are nausea and vomiting, fatty stools, pale or clay-colored stools and unintentional weight loss. Chronic alcoholism may cause irreversible damage to the pancreas. In anemia, fewer red blood cells than normal are present. In vitamin deficiency anemia, the red blood cells are large and underdeveloped. In advanced deficiencies, white blood cells and platelets also look abnormal. Although in this patient hemoglobin is low, the ESR or sed rate and WBC are high; therefore, the anemia is more likely due to inflammation than a nutritional deficiency. Celiac disease is an inherited, autoimmune disease in which the lining of the small intestine is damaged from eating gluten and other proteins found in wheat, barley, rye, and possibly oats. This patient responded to decreased dietary fat intake and alcohol abstinence. Symptoms of celiac disease would only change with the elimination of gluten. Ulcerative colitis is a type of inflammatory bowel disease (IBD) that affects the large intestine and rectum. In ulcerative colitis, there is gastrointestinal bleeding and joint pain, which this patient does not have. Also, dietary fat restriction does not help these patients. When the bile ducts become blocked, bile builds up in the liver, and jaundice (yellow color of the skin) develops due to a high level of bilirubin in the bloodstream. This patient has a normal bilirubin, so bile duct blockage is unlikely to be present. Also, dietary fat reduction is not likely to improve symptoms.

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1 Distension of the duodenum initiates release of enterogastrone from the mucosal cells of the duodenum. Enterogastrone delays gastric emptying by closing the pyloric sphincter and inhibiting production of gastrin.

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1 Glucagon-like peptide-1 is produced primarily in the distal small intestine and colon by the proglucagon gene in L cells and is cleaved from proglucagon, a prohormone expressed in the gut, pancreas, and brain that is also a precursor of other hormones (glucagon, glucagon-like peptide-2, glicentin, and oxyntomodulin). Secretion of GLP1 is triggered by fat and carbohydrate intake and it inhibits proximal gastrointestinal motility and slows down gastric emptying. Ghrelin is a powerful orexigenic hormone secreted by the stomach and duodenum that increases gastrointestinal motility and insulin secretion. Enterostatin is a polypeptide cleaved in the gut from pancreatic procolipase to facilitate fat digestion. It has also been shown to reduce hunger and food intake in humans. It does not influence gastric motility. Apolipoprotein A-IV is a glycoprotein that packages digested lipids to transit through lymphatics to blood. It is secreted in response to fat absorption and chylomicron formation in the intestine. It does not influence gastric motility. Gastric lipase is a water-soluble enzyme secreted in the stomach to promote hydrolytic action of pancreatic lipase on insoluble triglyceride substrates. It does not influence gastric motility. Diabetic gastroparesis is a disorder of delayed gastric emptying that affects 5-12% of long-term diabetic patients. Other complications are often associated, such as retinopathy, nephropathy, and neuropathy. The vagus nerve is usually dysfunctional and patients usually have a reduction in the number of neurons responsible for motor coordination and pacemaker cells in the stomach. Nausea, vomiting, bloating, and postprandial fullness are common symptoms and treatment is directed towards adequate nutritional support and use of prokinetic drugs (metoclopramide).

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1 Live bile formation is an active process requiring energy. This energy is evident when it is noted that bile can be secreted against a pressure greater than aortic blood pressure. One of the best stimulants for bile secretion is the presentation of small amounts of bile in the blood perfusing the liver. All hepatocytes continually secrete bile into bile canaliculi, running between the cells within each hepatic plate and no special anaerobic process is required for the secretion.

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1 Motility of colon is controlled by a dual system of innervation which contains cholinergic nerves that excite and adrenergic nerves that inhibit the motility of the colon. It is neither inhibited by the vagal nerve nor stimulated by the distention of the ileum.

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1 The active form of lipase is secreted from pancreatic acinar cells in response to a fatty meal. Lipase enters the duodenum along with other secretory enzymes through the pancreatic duct. In the duodenum, lipase acts specifically on triglycerides, hydrolyzing the outer ester bonds to form monoglycerides and fatty acids. The alkaline secretions of the pancreas normally mix with acidic chyme from the stomach resulting in a luminal pH that is normally close to 7.0. The activity of lipase is greatly impaired when duodenal pH falls below neutrality.

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1 The two primary bile acids formed in the liver are cholic acid and chenodeoxycholic acid. In the colon, bacteria convert cholic acid to deoxycholic acid and chenodeoxycholic acid to lithocholic acid. Conjugation of the acids to glycine or taurine occurs in the liver and the conjugates are glycocholic acid and taurocholic acid.

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1 Very large doses of the fat-soluble vitamins are definitely toxic. Acute vitamin A intoxication was first described by Arctic explorers, who developed headache, diarrhea, and dizziness after eating polar bear liver. The liver of this animal is particularly rich in vitamin A. Large doses of water-soluble vitamins (C and B) have been thought to be less likely to cause problems, because they can be rapidly cleared from the body. However, it has been demonstrated that ingestion of large doses of vitamin B6 can produce peripheral neuropathy.

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2 Diminished secretion of saliva is known as xerostomia, and the main problems associated with it are difficulty in chewing and swallowing, inarticulate speech unless frequent sips of water are taken when talking, an increase in the harmful buccal bacterial fauna, a foul taste in the mouth, during prolonged fever or state of prolonged anxiety (when salivation is suppressed), and a rampant increase in dental caries.

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2 Except during swallowing, the gastroesophageal sphincter remains contracted to maintain a barrier between the stomach and esophagus, thus reducing the possibility of reflux of acidic gastric contents into the esophagus. The prevention of the air from entering the esophagus during breathing is the function of the pharyngoesophageal sphincter. The sphincter does not play any active part during either vomiting or the prevention of esophageal secretions (mainly mucus) from leaking into the stomach. The actin of swallowing initiate the closure of the glottis, and this prevents the food from entering the pharynx.

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2 Gastrin increases gastric secretion; secretin inhibits gastric secretion, stimulates pancreatic secretion high in bicarbonate ions, increases the rate of bile secretion, and increases intestinal mucus secretion. GIP also inhibits gastric secretion.

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2 Gastrinomas are small tumors that continually release excessive amounts of gastrin. Hypergastrinemia has a trophic effect on the gastric mucosa and enhances the secretion of hydrochloric acid from gastric parietal cells in both basal and stimulated states. The continued delivery of acid to the upper small intestine exceeds the capacity of acid-neutralizing mechanisms and results in the erosion and ulceration of the intestinal mucosa. In addition to acid secretion, parietal cells release intrinsic factor in response to gastrin. Intrinsic factor is a glycoprotein required for the normal intestinal absorption of vitamin B12. Red blood cell maturation is retarded in the absence of intrinsic factor resulting in pernicious anemia. Intestinal acidosis in hypergastrinemic patients also reduces the activity of pancreatic enzymes, particularly lipases. This inhibits digestion and reabsorption of fat resulting in steatorrhea (fat in the feces) and weight loss.

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2 Monoglycerides, cholesterol, and fatty acids from the micelles enter the mucosal cells by passive diffusion. Thus, the formation of the micellar aggregates by liver bile is crucial for the normal absorption of lipids. Fat digestion requires the presence of pancreatic lipase and may to some extent depend on the lipid solubility of lipase for hydrolysis of triglycerides. However, absorption is a passive phenomenon and as such does not require facilitation by pancreatic enzymes.

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2 Protein digestion begins in the stomach, where pepsins cleave some of the peptide linkages. A gelatinase that liquefies gelatin is also found in the stomach. Chymosin, a milk-clotting gastric enzyme also know as rennin, is found in the stomachs of young animals but is probably absent in humans. Gelatinase has a pH optimum of 1.6 - 3.2, as such its action is terminated when the gastric contents are mixed with the alkaline pancreatic juice in the duodenum, jejunum and ileum (proximal, medial and distal parts of small intestines). Colon (a larger portion of the large intestines) functions primarily in the absorption of electrolytes and fluids.

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2 Secretin inhibits gastric secretion; stimulates pancreatic secretion high in bicarbonate ions; increases the rate of bile secretion; increases intestinal mucous secretion; decreases gastric motility.

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2 Serotonin and substance P (secreted by stomach through colon) as well as motilin (present in small intestines) increase gut motility. Neurotensin (small intestines) inhibits gut motility. Urogastrone (duodenum, Brunner's glands) inhibits gastric HCl secretion and enhances epithelial cell division. Somatostatin (pylorus and duodenum) inhibits nearby enteroendocrine cells, while secretin (small intestine) stimulates bicarbonate secretion by pancreas and biliary tract.

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2 Swallowing (= deglutition) is a reflex response that is triggered by afferent impulses in the trigeminal, glossopharyngeal, and vagus nerves. These impulses are integrated in the nucleus of the tractus solitarius and the nucleus ambiguous of the medulla oblongata. The swallowing reflex is initiated by the voluntary action of collecting the oral contents on the tongue and propelling them backward into the pharynx (and this would involve the cerebrum). Swallowing is difficult, if not impossible, if the mouth is open. Hypothalamus has varied functions (from temperature regulation to sexual behavior) but does not control swallowing. Similarly, the spinal cord controls a number of reflexes, but swallowing is not one of them.

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2 The majority of chloride ions come from potassium chloride. Small amounts of chloride ions are harvested from sodium chloride. Active transport of chloride ions occurs from the cytoplasm to the lumen of the oxyntic cells, while sodium ions are transported into the cells.

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2 The presence of HbsAg antigen, along with elevated levels of IgM antibody, indicates that this disease is in the acute phase. Following exposure, the prodromal phase is accompanied by flu like symptoms and specific identification of the disease is unlikely during this phase, except through sophisticated laboratory tests (e.g. Polymerase Chain Reaction identification of viral antigen). HbsAG will increase to maximal levels in four to six weeks during the Acute phase of the disease, then fall off as body defense mechanisms come into play. IgM antibodies are produced as a result of immune defense mechanisms. In three to four months, recovery phase begins with near complete elimination of HbsAg, and maximal IgM levels. Full recovery phase begins at approximately six months time as anti-HBs and IgG levels increase, and the elimination of any antigen products. Anti-HBs persists throughout the patients lifetime. The persistence of HBsAg and failure to develop anti-HBs usually indicates the presence of chronic hepatitis.

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2 These pangs are associated with low blood glucose levels and pain, but the cause of hunger pangs is unclear, as is their contribution to the control of food intake. However, they do appear 12 to 24 hours after fasting begins and gradually weaken until they disappear after 3 or 4 days.

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2 This patient has right upper quadrant pain, jaundice, and fever, all part of the Charcot triad associated with ascending cholangitis, a complication of choledocholithiasis (common bile duct obstruction). Acute cholangitis is an infection of the common bile duct that typically occurs when the duct becomes obstructed. The patient reports previous episodes of right upper quadrant pain; they were likely caused by gallstones (cholelithiasis). The patient probably has a stone obstructing the bile duct, causing cholangitis. This patient has elevated serum transaminases, but the clinical presentation is not consistent with acute or chronic hepatitis. The pain associated with pancreatitis is usually epigastric, with radiation into the back. If the patient had pancreatitis, lipase would be elevated. Cirrhosis and hepatocellular carcinoma may be associated with jaundice and right upper quadrant pain, but the clinical presentation is not consistent with these diagnoses.

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3 Following their participation in fat digestion and absorption, most bile salts are reabsorbed back into the blood by special active transport mechanisms located in the terminal ileum. From here, they are returned by means of the hepatic portal system to the liver, which re-secretes them into the bile (referred to as enterohepatic circulation). Bile salts are secreted into the duodenum for the emulsification of fats. As such, they cannot be absorbed either into the stomach or duodenal linings.

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3 Food increases the metabolic rate because of specific dynamic action (SDA). The SDA of a food is the obligatory energy expenditure that occurs during its assimilation into the body. An amount of protein sufficient to provide 100 kcal increases the metabolic rate a total of 30 kcal; a similar amount of carbohydrate increases it 6 kcal; and a similar amount of fat increases it 4 kcal.

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3 From 30-80% of ingested Ca+ is absorbed through active transport in the anterior portion of small intestine. A low intestinal pH tends to keep Ca+ in solution and, thus, favors absorption. Ca+ absorption is facilitated by 1,25-dihydroxycholecalciferol, the metabolite of vitamin D produced in the kidney. Neither high fat, low protein diet nor elevated phosphate intake has any influence on the Ca+ absorption.

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3 Secretin and vagal stimulation both can increase the flow of liver bile. However, sympathetic nerve stimulation may have the opposite effect. Gastrin stimulates the secretion of gastric juice, while pancreatic juice has neither a stimulating or antagonistic effect on the bile secretion or flow.

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3 Some amino acids are nutritionally essential (valine, leucine, isoleucine, threonine, methionine, phenylalanine, tryptophan, arginine, lysine, and histidine), which must be obtained in diet, whereas others can be synthesized in vivo at rates sufficient to meet metabolic needs.

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3 The 4 most important factors in the duodenum that influence gastric emptying are fat, acid, hypertonicity, and distention. The presence of a fatty food (fried eggs, bacon, and hash browns) in the duodenum will activate appropriate duodenal receptors, thereby triggering a response that will put brakes on gastric motility by reducing the excitability of the gastric smooth muscles. Other foods (e.g., toast, orange juice, coffee, bowl of cereal with skim milk, and boiled egg) do not have much fat or acid and will leave the stomach within a reasonable time.

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3 The esophageal muscles are innervated primarily by the vagus nerve, which provides somatic motor fibers to the striated smooth muscle, and visceral motor fibers, which connect to the myenteric plexus. The Hypoglossal nerve (12th Cranial nerve) is mainly the motor nerve to the tongue. The Glossopharyngeal nerve (9th Cranial nerve) has afferent function from the tongue and pharynx and efferent function to the stylopharyngeus muscle and the parotid glands. The superior mesenteric plexus provides sympathetic innervation to the stomach and upper intestine, and the inferior mesenteric plexus provides innervation to the colon and pelvic structures.

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3 The pancreatic juice is alkaline, and because of its high NaHCO3 contents (approximately 113 mEq/L versus 24 mEq/L in plasma) has the highest pH (approximately 8.0). Bile and intestinal juices are also neutral or alkaline; the pH of bile ranges between 7.8-8.6 (hepatic duct) and 7.0-7.4 (inside the gallbladder), while that of the secretion of the intestinal glands varies from 7.5-8.3. Saliva has a pH of 6.8 (resting phase) to 8.0 (during active secretion). The gastric juice is acidic, and has the lowest pH, ranging from 3-4.

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3 The two primary bile acids formed in the liver are cholic acid and chenodeoxycholic acid. In the colon, bacteria convert cholic acid to deoxycholic acid and chenodeoxycholic acid to lithocholic acid. Conjugation of the acids to glycine or taurine occurs in the liver and the conjugates are glycocholic acid and taurocholic acid.

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3 There are four chief mechanisms for the production of jaundice. 1. increased destruction of red blood cells. 2. impaired biliary uptake of bilirubin. 3. decreased conjugation of bilirubin. 4. bile outlet obstruction. Jaundice is classified as prehepatic, intrahepatic, and posthepatic. Prehepatic jaundice occurs when there is increased hemolysis of RBCs, releasing bilirubin. This occurs in a number of situations including transfusion reaction, hereditary disease of the red blood cell, and hemolytic diseases. The bilirubin which is present in the blood is unconjugated and measured as indirect bilirubin. Various liver diseases are the cause of intrahepatic jaundice (e.g. hepatitis, cirrhosis, drug toxicity, Gilbert's disease). Due to cellular damage there is decreased conjugation of bilirubin with an accumulation of unconjugated bilirubin in the blood. Post hepatic jaundice occurs with obstruction to the biliary flow as occurs in cholelithiasis, bile duct obstruction, biliary atresia. Both conjugated and unconjugated bilirubin are elevated in these cases. The correct answer, Sickle cell anemia, reflects a congenital defect in RBC in which Hemoglobin S is predominant type, causing malformation of RBC with low oxygen partial pressure in blood, and increased hemolysis of RBC.

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3 This patient most likely has esophageal dysphagia, specifically diffuse esophageal spasm. Diffuse esophageal spasm is a motility disorder defined by simultaneous uncoordinated contraction of several esophageal segments, which can lead to retrosternal pain and is worsened or precipitated by acid reflux, rapid eating, stress, anxiety, and hot or cold food. The dysphagia found in these patients is intermittent and non-progressive, and it does not cause weight loss. These patients have no documented abnormality in the distribution of myenteric neurons, no evidence of obstruction, and normal lower esophageal sphincter relaxation. First-line treatment is oral calcium channel blockers, such as diltiazem, which decreases the pain associated with esophageal spasms. Oral nitrates may be helpful in this disorder, but intravenous nitroglycerin is not indicated in diffuse esophageal spasm. Botulinum toxin is not a first-line treatment for diffuse esophageal spasms; endoscopic administration is considered second-line therapy. Prokinetic agents, such as metoclopramide, are considered treatment options for reflux esophagitis. Oral corticosteroids may be considered in patients with diagnosed eosinophilic esophagitis.

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3 Use of carbonic anhydrase inhibitors, such as acetazolamide, diminish the formation of hydrochloric acid. The hydroxyl ions are formed by the cleaving of water to hydrogen ions and hydroxyl ions. The hydrogen ions are used to form HCl.

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4 Achalasia is a condition in which food accumulates in the esophagus and the organ becomes massively dilated. It is due to increased resting lower esophageal sphincter tension, incomplete relaxation of this sphincter on swallowing, and weak esophageal peristalsis. The number of VIP-containing neurons in the lower esophagus is decreased, and the VIP content is low, suggesting that the condition is caused by VIP deficiency. It can be treated by pneumatic dilation of the sphincter or esophageal myotomy. Aerophagia is the swallowing of air in the process of eating and drinking. Some of this air passes to the colon, where oxygen is absorbed and hydrogen, hydrogen sulfide, carbon dioxide, and methane formed by the colon bacteria from carbohydrates and other substances are added to it. It is then expelled as flatus. In some individuals, gas in the intestines causes cramps, borborygmi (rumbling noises), and abdominal discomfort.

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4 As material enters the stomach, the muscle in the walls will relax, to allow a relatively large change in volume with a small pressure change. Part of this relaxation process is due to the property of plasticity that is inherent in visceral smooth muscles. The decreased peristaltic activity of the stomach (gastric slow wave), plays a major role in the control of gastric emptying, while psychic state has effect on gastric secretion and motility that are mediated principally via the vagi.

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4 Distention of the rectum with feces initiates reflex contractions of its musculature and the desire to defecate. In humans, the sympathetic nerve supply to the internal (involuntary) anal sphincter is excitatory, whereas the parasympathetic supply is inhibitory. This sphincter relaxes when the rectum is distended. The nerve supply to the external (voluntary) sphincter comes from pudendal nerve. The sphincter is maintained in a state of tonic contraction, and moderate distention of the rectum increases the force of its contraction. The urge to defecate first occurs when rectal pressure increases to about 18 mm Hg. When this pressure reaches 55 mm Hg, the external, as well as, the internal sphincter relaxes and the contents of the rectum are expelled. Defecation is therefore a spinal reflex that can be voluntarily inhibited by keeping the external sphincter contracted or facilitated by relaxing the sphincter and contracting the abdominal muscles.

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4 Most vitamins are absorbed in the upper small intestine, but vitamin B12 is absorbed in the ileum. This vitamin binds to intrinsic factor, a protein secreted by the stomach, and complex is absorbed across the ileal mucosa.

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4 No food or water is absorbed into the blood from the stomach mucosa. Carbohydrate and protein digestion are not completed in the stomach, and fat digestion does not even begin in the stomach. The stomach is impermeable to H2O. Even though none of the ingested food is absorbed from the stomach, 2 noteworthy non-nutrient substances, alcohol and aspirin, are absorbed by the stomach. Alcohol is lipid-soluble to a degree, so it can diffuse through the lipid membranes of the epithelial cells that line the stomach. Similarly, weak acids, most notably acetylsalicylic acid, can enter gastric submucosal capillaries from the stomach.

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4 Salivary secretion depends entirely on neural control mechanisms, mainly parasympathetic. The salivatory nuclei (in medulla and pons) are activated by tasting (although it can occur without oral stimulation) and tactile stimulation from the tongue and mouth. There is a considerable variation in the ionic composition of saliva from gland to gland, depending upon the rate of secretion, and the kind of stimulus. Parasympathetic stimulation causes profuse secretion of watery saliva with a relatively low content of organic material. However, stimulation of the sympathetic nerve supply causes secretion of small amount of saliva rich in organic constituents from the submandibular glands.

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4 Secretin and cholecystokinin are hormones produced by enteroendocrine cells in the small intestine. Secretin stimulates bicarbonate secretion in the pancreas and biliary tract. Cholecystokinin stimulates the release of pancreatic enzymes and contraction of the gall bladder. Stomach gastric glands contain diffuse endocrine cells (DES), also called APUD cells (amine precursor uptake and decarboxylation cells), which may secrete glicentin (stomach through colon) and glucagon (stomach and duodenum) (both stimulate hepatic glycogenolysis), as well as a vasoactive intestinal peptide (VIP) (stomach through colon), which increases gut motility and stimulates intestinal ion and water secretion. Paneth cells are present in the crypts of Lieberkühn, and secrete a lysozyme, an antibacterial enzyme. Brunner's glands are contained in the duodenum only, and they secrete an alkaline fluid and urogastrone (a polypeptide hormone that enhances epithelial cell division and inhibits gastric Hcl production).

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4 The bile salts are secreted by the liver and stored inside the gallbladder. It interacts with lipids spontaneously to form micelles. These micelles move down their concentration gradient through the unstirred layer to the brush border of the mucosal cells. The lipids enter the cells by passive diffusion and are rapidly esterified inside the cells, maintaining a favorable concentration gradient from the lumen into the cells. The bile is made up of bile salts, bile pigments, cholesterol, inorganic salts, fatty acids, lecithin, fat, and alkaline phosphatase, dissolved in an alkaline electrolyte solution that resembles pancreatic juice. Bile salts are necessary for the normal digestion of lipids. Complex sugars (carbohydrates) are digested with the aid of enzymes secreted inside the exocrine pancreas, and this secretion is conveyed to the duodenal lumen through the common bile duct.

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4 The correct response is non-formation in the intestine. Patients suffering from jaundice often exhibit yellow color of the skin and conjunctiva along with an excess of bilirubin in the plasma. Excessive bilirubin in the serum can result from hemolytic jaundice, hepatic jaundice, and obstructive jaundice. This patient's findings are suggestive of obstructive jaundice. Extrinsic compression of the common bile duct due to metastatic carcinoma, extension of carcinoma of the gall bladder into the common bile duct, or gallstones may lead to an obstructive type of jaundice. Because of the obstruction to the flow of the bile, there is a rapid increase in pressure in the bile duct. Patients often complain of pain in the upper abdominal region lasting for hours. Chills and fever associated with colic and a history of jaundice are common complaints. Some of the laboratory findings in patients suffering from jaundice are increased serum bilirubin and bilirubinuria. Patients may also bleed excessively due to hypoprothrombinemia, causing prolonged prothrombin time. Failure to notice urobilinogen in the urine is due to the fact that when old RBCs pass through reticula-endothelial cells (mainly spleen), they get destroyed, and haem (part of the hemoglobin molecule) is converted into bilirubin. Plasma proteins carry the bilirubin to the liver and form bilirubin and glucuronides. Bile containing bilirubin is normally released into the intestine by the bile duct. Bacteria in the intestine convert some of the bilirubin in the bile to a colorless derivative called urobilinogen. Urobilinogen is subsequently reabsorbed in the portal circulation where small amounts of urobilinogen enter the general circulation and are excreted in the urine. The absence of urobiinogen in the urine, therefore, suggests bile duct obstruction since it indicates that no bilirubin has reached the intestine to be converted to urobilinogen.

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4 The strong antral peristaltic contractions are responsible for the mixing of food with gastric secretion to produce chyme. The muscular layers in the cardiac portion, fundus, and the body of the stomach are too thin to create strong peristaltic movements required for mixing. Only when these waves reach the antrum, where the muscular layers are thick, they become strong enough to do the mixing.

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4 The two primary bile acids formed in the liver are cholic acid and chenodeoxycholic acid. In the colon, bacteria convert cholic acid to deoxycholic acid and chenodeoxycholic acid to lithocholic acid. Conjugation of the acids to glycine or taurine occurs in the liver and the conjugates are glycocholic acid and taurocholic acid.

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5 Achalasia is the absence of peristalsis in the lower esophagus resulting in the lower esophageal sphincter remaining closed during swallowing, causing dysphagia and regurgitation. Achalasia causes a characteristic "bird's beak" appearance of the esophagus: distal narrowing and proximal dilation. Gastroesophageal reflux disease (GERD) may cause dysphagia, but it would not lead to the narrowing on X-ray. Scleroderma is associated with weakening of the lower esophageal sphincter with dysphagia and regurgitation, but it is not associated with bird's beak appearance on X-ray. Zenker diverticulum is an outpouching in the esophagus associated with regurgitation and dysphagia, but not with bird's beak appearance on X-ray. Esophagitis is associated with dysphagia, but it is not associated with X-ray abnormalities.

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5 Food increases the metabolic rate because of specific dynamic action (SDA). The SDA of a food is the obligatory energy expenditure that occurs during its assimilation into the body. An amount of protein sufficient to provide 100 kcal increases the metabolic rate a total of 30 kcal; a similar amount of carbohydrate increases it 6 kcal; and a similar amount of fat increases it 4 kcal.

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5 Omeprazole is a direct inhibitor of the H+-K+-ATP-ase. The active, inhibitory structure of this drug is formed only at low pH values. This drug is used for rapid treatment of duodenal ulcers and reflux esophagitis. Cimetidine and ranitidine are antagonists on H2-type histamine receptors. These substances are also very effective in reducing of HCl production and are widely used in the treatment of peptic ulcer disease. Atropine, an antagonist of muscarinic acetylcholine receptors, inhibits HCl production. However the efficiency of this inhibition is relatively low, since the stimulatory effect of the vagal nerve on HCl production is only partially mediated by acetylcholine. Acetazolamide is an inhibitor of the enzyme carbonic anhydrase. This enzyme accelerates the formation of H2CO3 from H2O and CO2.

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b Omeprazole is a very effective inhibitor of gastric HCl production. This drug directly inhibits the activity of the H+-K+ ATPase. Ranitidine acts as an antagonist on H2-type histamine receptors. This drug, together with other related substances (cimetidine, famotidine), is widely used in the treatment of peptic ulcer disease. Acetazolamide inhibits the activity of carbonic anhydrase, an enzyme which facilitates the formation of H2CO3 from H2O and CO2. The activity of this enzyme is essential for normal HCl secretion. Ouabain is an inhibitor of the Na+-K+ ATPase.

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A) Although the potassium concentration in saliva is about seven times greater than that of plasma, and the bicarbonate concentration in saliva is only about three times greater than that of plasma, the actual concentration of bicarbonate in saliva is 50 to 70 mEq/L, whereas the concentration of potassium is about 30 mEq/L, under basal conditions.

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A) Basal metabolic rate counts for about 50 percent to 70 percent of the daily energy expenditure in most sedentary persons. Nonexercise activity, such as fidgeting or maintaining posture, accounts for approximately 7 percent of daily energy expenditure, and the thermic effect of food accounts for about 8 percent. Nonshivering thermogenesis can occur in response to cold stress, but the maximal response in adults is less than 15 percent of the total metabolic rate.

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A) CCK is the only gastrointestinal hormone that inhibits gastric emptying under physiological conditions. This inhibition of gastric emptying keeps the stomach full for a prolonged time, which is one reason why a breakfast containing fat and protein "sticks with you" better than breakfast meals containing mostly carbohydrates. CCK also has a direct effect on the feeding centers of the brain to reduce further eating. Although CCK is the only gastrointestinal hormone that inhibits gastric emptying, all the gastrointestinal hormones with the exception of gastrin are released to some extent by the presence of fat in the intestine.

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A) Cholecystokinin is released mainly in response to fats and proteins entering the duodenum and activates sensory receptors in the duodenum, sending messages to the brain stem via vagal afferents that contribute to satiation and meal cessation. All the other changes would tend to increase rather than decrease food intake.

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A) Cholelithiasis is the presence of gallstones (choleliths) in the gallbladder or bile ducts. This patient exhibits typical symptoms caused by gallstones.

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A) Fatty acids are degraded in mitochondria by the progressive release of two-carbon segments in the form of acetyl coenzyme A. This process is known as the beta-oxidation process for degradation of fatty acids.

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A) Gastrin and CCK do not share any effects on gastrointestinal function at normal physiological conditions; however, they have identical actions on gastrointestinal function when pharmacological doses are administered. Gastrin stimulates gastric acid secretion and mucosal growth throughout the stomach and intestines under physiological conditions. CCK stimulates growth of the exocrine pancreas and inhibits gastric emptying under normal conditions. CCK also stimulates gallbladder contraction, relaxation of the sphincter of Oddi, and secretion of bicarbonate and enzymes from the exocrine pancreas.

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A) H. pylori is a bacterium that accounts for 95 percent of patients with a duodenal ulcer and virtually 100 percent of patients with a gastric ulcer when chronic use of aspirin or other NSAIDs are eliminated. H. pylori is characterized by high urease activity, which metabolizes urea to NH3 (ammonia). Ammonia reacts with H+ to become ammonium (NH4+). This reaction allows the bacterium to withstand the acid environment of the stomach. The ammonium production is believed to be the major cause of cytotoxicity because the ammonium directly damages epithelial cells, increasing the permeability of the gastric mucosal barrier. Bile salts and NSAIDs can also damage the gastric mucosal barrier, but these substances are not directly related to H. pylori infection. Pepsin can exacerbate the mucosal lesions cause by H. pylori infection, but pepsin levels are not increased by H. pylori. It should be clear that gastrin does not mediate the mucosal damage caused by H. pylori.

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A) Hemoglobin is metabolized by tissue macrophages (also called the reticuloendothelial system). The hemoglobin is first split into globin and heme, and the heme ring is opened to produce free iron and a straight chain of four pyrrole nuclei, from which bilirubin will eventually be formed. The free bilirubin is taken up by hepatic cells, and most of it is conjugated with glucuronic acid; the conjugated bilirubin passes into the bile canaliculi and then into the intestines.

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A) Hydrogen ions leak into the mucosa when it is damaged. As the hydrogen ions accumulate in the mucosa, the intracellular buffers become saturated, and the pH of the cells decreases, resulting in injury and cell death. The hydrogen ions also damage mast cells, causing them to secrete excess amounts of histamine. The histamine exacerbates the condition by damaging blood capillaries within the mucosa. The result is focal ischemia, hypoxia, and vascular stasis. The mucosal lesion is a forerunner of gastric ulcer. Mucus secretion helps strengthen the gastric mucosal barrier because mucus impedes the leakage of hydrogen ions into the mucosa. Various proton pump inhibitors are used as a treatment modality for gastric ulcers because these inhibitors can decrease the secretion of hydrogen ions (protons). The tight junctions between cells within the mucosa help prevent the back-leak of hydrogen ions. Vagotomy was once used to treat gastric ulcer disease because severing or crushing the vagus nerve decreases gastric acid secretion.

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A) Intestinal absorption of immunoglobulins (present in colostrum) during early infancy occurs by endocytosis. This ability to absorb large molecules by endocytosis occurs during the first several months of life but does not occur thereafter. Facilitated diffusion, passive diffusion, and primary and secondary active transport are all normal transport processes in enterocytes.

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A) Intrinsic factor is a glycoprotein secreted from parietal cells (i.e., acid-secreting cells in the stomach) that is necessary for absorption of vitamin B12. The patient has a diminished capacity to secrete acid because of chronic gastritis. Because acid and intrinsic factor are both secreted by parietal cells, a diminished capacity to secrete acid is usually associated with diminished capacity to secrete intrinsic factor. Ptyalin, also known as salivary amylase, is an enzyme that begins carbohydrate digestion in the mouth. The secretion of ptyalin is not affected by gastritis. Rennin, known also as chymosin, is a proteolytic enzyme synthesized by chief cells in the stomach. Its role in digestion is to curdle or coagulate milk in the stomach, a process of considerable importance in very young animals. It should be clear that saliva secretion is not affected by gastritis. Trypsin is a proteolytic enzyme secreted by the pancreas.

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A) Mass movements force feces into the rectum. When the walls of the rectum are stretched by the feces, the defecation reflex is initiated and a bowel movement follows when this is convenient. Mass movements do not affect gastric motility. Haustrations are bulges in the large intestine caused by contraction of adjacent circular and longitudinal smooth muscle. It should be clear that mass movements in the colon do not affect esophageal contractions or pharyngeal peristalsis.

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A) NPY is an orexigenic neurotransmitter that stimulates feeding and is increased during food deprivation. Leptin, PYY, cholecystokinin, and activation of POMC neurons are all reduced by fasting. Ghrelin is increased, not decreased, by fasting.

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A) One of the basic functions of vitamin A is in the formation of retinal pigments and therefore the prevention of night blindness.

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A) The appearance of mass movements after meals is facilitated by gastrocolic and duodenocolic reflexes. These reflexes result from distention of the stomach and duodenum. They are greatly suppressed when the extrinsic autonomic nerves to the colon have been removed; therefore, the reflexes are likely transmitted by way of the autonomic nervous system. All the gut reflexes are named with the anatomical origin of the reflex as the prefix followed by the name of the gut segment in which the outcome of the reflex is observed. For example, the duodenocolic reflex begins in the duodenum and ends in the colon. When the duodenum is distended, nervous signals are transmitted to the colon, which stimulates mass movements. The enterogastric reflex occurs when signals originating in the intestines inhibit gastric motility and gastric secretion. The intestinointestinal reflex occurs when overdistention or injury to a bowel segment signals the bowel to relax. The rectosphincteric reflex, also called the defecation reflex, is initiated when feces enters the rectum and stimulates the urge to defecate.

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A) The frequency of slow waves is fixed in various parts of the gut. The maximum frequency of smooth muscle contractions cannot exceed the slow-wave frequency. The slow-wave frequency averages about 3 per minute in the stomach, 12 per minute in the duodenum, 10 per minute in the jejunum, and 8 per minute in the ileum. Therefore, the duodenum is most likely to have the highest frequency of smooth muscle contractions.

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A) The transport of glucose through the membranes of most cells is different from that which occurs through the gastrointestinal membrane or through the epithelium of the renal tubules. In both these latter cases, the glucose is transported by the mechanism of secondary active co-transport, in which active transport of sodium provides energy for absorbing glucose against a concentration difference. This sodium co-transport mechanism functions only in certain special epithelial cells that are specifically adapted for active absorption of glucose. At all other cell membranes, glucose is transported only from higher concentrations toward lower concentrations by facilitated diffusion made possible by the special binding properties of membrane glucose carrier protein.

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A) This man has sickle cell disease, which is a hemolytic disease that results in the premature destruction of red blood cells. Release of hemoglobin from damaged red blood cells leads to high levels of bilirubin in the blood plasma. This increase in bilirubin can lead to the development of pigment stones in the gallbladder that are composed primarily of bilirubin. Cholesterol stones are very common, but pigment stones are more likely in this patient because of the decrease in hematocrit, which is indicative of hemolysis. Pigment stones may contain small amounts of calcium carbonate. Kidney stones are often composed of calcium oxalate.

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A) When the body's stores of carbohydrates decrease below normal, moderate quantities of glucose can be formed from amino acids and the glycerol portion of fat. This process is called gluconeogenesis. Glycogenesis is the formation of glycogen. Glycogenolysis means the breakdown of the cell's stored glycogen to re-form glucose in the cells. Glycolysis means splitting of the glucose molecule to form two molecules of pyruvic acid. Hydrolysis is a process in which a molecule is split into two parts by the addition of a water molecule.

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B) Esophageal varices are extremely dilated submucosal veins in the lower third of the esophagus. The submucosal veins have a normal diameter of about 1 millimeter and can enlarge to 1 to 2 centimeters with prolonged portal hypertension, which is common in persons with cirrhosis of the liver. The presence of ascites indicates that the patient has portal hypertension. The dilated esophageal veins often bleed and thus lower the hematocrit. Although colon cancers can also bleed, there is no reason to assume colon cancer in this woman. Pancreatitis can occur in persons with chronic alcoholism, but there is no evidence for this condition, and substantial bleeding is not common in persons with pancreatitis. Jaundice and scleral icterus (i.e., yellowing of the sclera) are common in persons with cirrhosis, but these conditions are unlikely to cause significant bleeding.

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B) Fat entering the small intestine is first emulsified into smaller globules by bile released from the gallbladder. Pancreatic lipase in conjunction with the co-enzyme colipase then digests the fat (which is mostly triglycerides) into monoglycerides and free fatty acids; these substances then become surrounded by bile salts to form water-soluble aggregates called micelles. When a micelle makes contact with an enterocyte of the intestinal wall, the monoglycerides and free fatty acids diffuse directly through the cell membrane into the enterocyte; triglycerides are too large to be absorbed. Once inside the enterocyte, the monoglycerides and free fatty acids form new triglyceride molecules that are subsequently packaged by the Golgi apparatus into chylomicrons. The chylomicrons exocytose at the basolateral membrane of the enterocyte and enter a lymphatic capillary (central lacteal) in the villus.

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B) GLIP is the only gastrointestinal hormone released by all three major foodstuffs (fats, proteins, and carbohydrates). The presence of fat and protein in the small intestine stimulates the release of CCK, but carbohydrates do not stimulate its release. The presence of protein in the antrum of the stomach stimulates the release of gastrin, but fat and carbohydrates do not stimulate its release. Fat has a minor effect to stimulate the release of motilin and secretin, but neither hormone is released by the presence of protein or carbohydrate in the gastrointestinal tract.

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B) Gastrin has a critical role in stimulating mucosal growth throughout the gastrointestinal system.

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B) Gastrin stimulates gastric acid secretion, and secretin and GLIP inhibit gastric acid secretion under normal physiological conditions. It is important to differentiate the physiological effects of the gastrointestinal hormones from their pharmacological actions. For example, gastrin and CCK have identical actions on gastrointestinal function when large, pharmacological doses are administered, but they do not share any actions at normal physiological concentrations. Likewise, GLIP and secretin share multiple actions when pharmacological doses are administered, but only one action is shared at physiological concentrations: inhibition of gastric acid secretion.

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B) Most of the extra energy required for strenuous activity that lasts for more than 5 to 10 seconds but less than 1 to 2 minutes is derived from anaerobic glycolysis. Release of energy by glycolysis occurs much more rapidly than oxidative release of energy, which is much too slow to supply the needs of the muscle in the first few minutes of exercise. ATP and phosphocreatine already present in the cells are rapidly depleted in less than 5 to 10 seconds. After the muscle contraction is over, oxidative metabolism is used to reconvert much of the accumulated lactic acid into glucose; the remainder becomes pyruvic acid, which is degraded and oxidized in the citric acid cycle.

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B) Movement of chloride ions out of cells leads to secretion of fluid by cells. CF is caused by abnormal chloride ion transport on the apical surface of epithelial cells in exocrine gland tissues. The CF transmembrane regulator (CFTR) protein functions both as a cAMP-regulated Cl− channel and, as its name implies, a regulator of other ion channels. The fully processed form of CFTR is found in the plasma membrane of normal epithelia. Absence of CFTR at appropriate cellular sites is often part of the pathophysiology of CF. However, other mutations in the CF gene produce CFTR proteins that are fully processed but are nonfunctional or only partially functional at the appropriate cellular sites.

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B) Neither plasma gastrin levels nor the rate of acid secretion are diagnostic for duodenal ulcer. However, when patients with a duodenal ulcer are pooled together, they exhibit a statistically significant increase in the rate of acid secretion and a statistically significant decrease in plasma gastrin levels. How is this possible? The basal and maximal acid secretion rates of normal subjects range from 1 to 5 mEq/h and from 6 to 40 mEq/h, respectively, which overlaps with the basal (2- 10 mEq/h) and maximal (30-80 mEq/h) acid secretion rates of persons with a duodenal ulcer. The increase in acid secretion of the average person with a duodenal ulcer suppresses the secretion of gastrin from the antrum of the stomach. It should be obvious that endoscopy is diagnostic for duodenal ulcer.

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B) None of the mechanisms of heat loss is effective when a person is placed in water that has a temperature greater than body temperature. Instead, the body will continue to gain heat until the body temperature becomes equal to the water temperature.

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B) Patients with a lactase deficiency cannot digest milk products that contain lactose (milk sugar). The operons of gut bacteria quickly switch over to lactose metabolism, which results in fermentation that produces copious amounts of gas (a mixture of hydrogen, carbon dioxide, and methane). This gas, in turn, may cause a range of abdominal symptoms including stomach cramps, bloating, and flatulence. The gas is absorbed by blood (especially in the colon) and exhaled from the lungs. Blood glucose levels do not increase because lactose is not digested to glucose and galactose in these patients.

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B) Phosphocreatine contains high-energy phosphate bonds and is three to eight times as abundant as ATP or ADP in a cell. Creatine does not contain high-energy phosphate bonds. Creatinine is a breakdown product of creatine phosphate in muscle.

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B) Relaxation of the ileocecal sphincter occurs with or shortly after eating. This reflex has been termed the gastroileal reflex. It is not clear whether the reflex is mediated by gastrointestinal hormones (gastrin and cholecystokinin) or extrinsic autonomic nerves to the intestine. Note that the gastroileal reflex is named with the origin of the reflex first (gastro) and the target of the reflex named second (ileal). This method of naming is characteristic of all the gastrointestinal reflexes. The enterogastric reflex involves signals from the colon and small intestine that inhibit gastric motility and gastric secretion. The gastrocolic reflex causes the colon to evacuate when the stomach is stretched. The intestinointestinal reflex causes a bowel segment to relax when it is overstretched. The rectosphincteric reflex is also called the defecation reflex.

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B) Slow-wave frequency is not affected significantly by either the autonomic nervous system or hormones; it is relatively constant at any given location in the small intestine. When a slow wave reaches a threshold value, a calcium spike potential (action potential) occurs and calcium ions enter the smooth muscle cell, which causes it to contract. Norepinephrine hyperpolarizes smooth muscle cells in the intestine and thereby decreases the likelihood that the membrane potential can reach a threshold value. Therefore, norepinephrine does not affect the basal slow-wave frequency of 10 occurrences per minute but does lower the contraction frequency of the smooth muscle cells to 0 occurrences per minute in this problem.

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B) The degradation of amino acids occurs almost entirely in the liver, and it begins with deamination, which occurs mainly by the following transamination schema: The amino group from the amino acid is transferred to α-ketoglutaric acid, which then becomes glutamic acid. The glutamic acid then transfers the amino group to still other substances or releases it in the form of ammonia. In the process of losing the amino group, the glutamic acid once again becomes α-ketoglutaric acid, so that the cycle can repeat again and again.

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B) The typical series of events that occur during the course of a fever are shown in the below figure. When pyrogens raise the set-point temperature above its normal value, the body activates heat conservation and heat production mechanisms that include cutaneous vasoconstriction, piloerection, epinephrine secretion, and shivering. Within several minutes, the body temperature increases to the elevated set-point value of 103°F in this example. If the factor that is causing the high temperature is removed, the hypothalamic set-point temperature returns to a normal value of about 98.6°F, which leads to activation of heat-loss mechanisms such as sweating and cutaneous vasodilation. The body temperature then returns to its basal level.

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B) The use of NSAIDs may result in NSAID-associated gastritis or peptic ulceration. Chronic gastritis, by definition, is a histopathological entity characterized by chronic inflammation of the stomach mucosa. When inflammation affects the gastric corpus, parietal cells are inhibited, leading to reduced acid secretion. Although diagnosis of chronic gastritis can only be ascertained histologically, the administration of pentagastrin should produce a less than expected increase in gastric acid secretion. Pentagastrin is a synthetic gastrin composed of the terminal four amino acids of natural gastrin plus the amino acid alanine. It has all the same physiological properties of natural gastrin. Although gastrin and pentagastrin can both stimulate growth of the duodenal mucosa, it should be clear that intravenous pentagastrin would not cause substantial growth in the context of a clinical test. In any case, chronic administration of pentagastrin would not lead to a less than expected growth of the duodenal mucosa. Pentagastrin is not expected to increase gastrin secretion, pancreatic enzyme secretion, or pancreatic growth.

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B) Thiamine is needed for the final metabolism of carbohydrates and amino acids. Decreased utilization of these nutrients secondary to thiamine deficiency is responsible for many of the characteristics of beriberi, including peripheral vasodilation and edema, lesions of the central and peripheral nervous system, and gastrointestinal tract disturbances.

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B) This infant has Hirschsprung's disease, which is characterized by a congenital absence of ganglion cells in the distal colon resulting in a functional obstruction. Prolonged fecal stasis can lead to enterocolitis (i.e., inflammation of the colon); full-thickness necrosis and perforation can occur in severe cases. In achalasia, the LES fails to relax during swallowing. Halitosis (bad breath) can occur in persons with Hirschsprung's disease, but this condition is not serious. Peptic ulcer and pancreatitis (inflammation of the pancreas) are not common in persons with Hirschsprung's disease.

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B) This man has cirrhosis of the liver. Fluid accumulates in the abdomen (ascites) for two main reasons: (1) decreased plasma colloid osmotic pressure (COP), and (2) increased capillary hydrostatic pressure in the splanchnic organs. The decrease in plasma COP results from decreased production of albumin by liver hepatocytes; albumin accounts for nearly 80 percent of the plasma COP. The low plasma COP also promotes edema formation in the periphery, especially the feet. Liver parenchymal cells are damaged or destroyed in persons with cirrhosis of the liver; they are replaced with fibrous tissue that eventually contracts around the blood vessels, thereby greatly impeding the flow of portal blood through the liver. This increase in vascular resistance leads to an increase in portal vein pressure, which in turn raises the capillary hydrostatic pressure of the splanchnic organs. There is no reason to assume that capillary hydrostatic pressure is also increased above normal in the feet of this man.

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B) This patient has heatstroke. Patients with heatstroke commonly exhibit tachypnea and hyperventilation caused by direct central nervous system stimulation, acidosis, or hypoxia. The blood vessels in the skin are vasodilated, and the skin is warm. Sweating ceases in patients with true heatstroke, most likely because the high temperature itself causes damage to the anterior hypothalamic-preoptic area. The nerve impulses from this area are transmitted in the autonomic pathways to the spinal cord and then through sympathetic outflow to the skin to cause sweating.

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B) Type 1 diabetes is characterized by a lack of insulin. In the absence of adequate insulin, little carbohydrate can be used by the body's cells, and the respiratory quotient remains near that for fat metabolism (0.70).

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C) About 20 percent of persons older than 65 years have gallstones (cholelithiasis) in the United States, and 1 million newly diagnosed cases of gallstones are reported each year. Gallstones are the most common cause of biliary obstruction. Regardless of the cause of gallstones, serum bilirubin values (especially direct or conjugated) are usually elevated. Indirect or unconjugated bilirubin values are usually normal or only slightly elevated. Only answer C shows a high level of direct bilirubin (conjugated bilirubin) compared with the level of indirect bilirubin (unconjugated bilirubin).

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C) Achalasia is a condition in which the LES fails to relax during swallowing. As a result, food swallowed into the esophagus fails to pass from the esophagus into the stomach. Trace C shows a high, positive pressure that fails to decrease after swallowing, which is indicative of achalasia. Trace A shows a normal pressure tracing at the level of the LES, reflecting typical receptive relaxation in response to the food bolus. Trace E is similar to trace C, but the pressures are subatmospheric. Subatmospheric pressures occur only in the esophagus where it passes through the chest cavity.

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C) Achlorhydria means simply that the stomach fails to secrete hydrochloric acid. This condition is diagnosed when the pH of the gastric secretions fails to decrease below 4 after stimulation by pentagastrin. When acid is not secreted, pepsin also usually is not secreted. Even when it is, the lack of acid prevents it from functioning because pepsin requires an acid medium for activity. Thus, protein digestion is impaired.

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C) Acid acts directly on somatostatin cells to stimulate the release of somatostatin. The somatostatin decreases acid secretion by directly inhibiting the acid-secreting parietal cells and indirectly by inhibiting gastrin secretion from G cells in the antrum. Acid is a weak stimulus for CCK release, but CCK does not inhibit (or stimulate) gastrin release. Acid does not stimulate GLIP release. Fatty acids are a weak stimulus for motilin, but motilin does not affect gastrin release. Fatty acids are not thought to stimulate somatostatin release.

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C) All five gastrointestinal hormones are released from both the duodenum and jejunum. Only gastrin is released from the antrum. Small amounts of cholecystokinin and secretin are also released from the ileum. No gastrointestinal hormones are released from the colon or esophagus.

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C) Before a meal, when the stomach is empty, the pH of the gastric juice is at its lowest point and acid secretion is suppressed. Acid secretion is suppressed in part because (a) the concentrated hydrogen ions in the gastric juice stimulate somatostatin release, which has a direct action to decrease the secretion of both gastrin and acid, and (b) the acid itself has a direct effect to suppress parietal cell secretions. When a meal is taken, the buffering effects of the food cause the gastric pH to increase, which in turn decreases somatostatin release. Cholecystokinin and vasoactive intestinal peptide do not have a role in the regulation of gastric acid secretion.

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C) Gastric emptying is accomplished by coordinated activities of the stomach, pylorus, and small intestine. Conditions that favor gastric emptying include (a) increased tone of the orad stomach, which helps to push chyme toward the pylorus; (b) forceful peristaltic contractions in the stomach that move chyme toward the pylorus; (c) relaxation of the pylorus; which allows chyme to pass into the duodenum; and (d) absence of segmentation contractions in the intestine, which can otherwise impede the entry of chyme into the intestine.

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C) Gastrin, acetylcholine, and histamine can directly stimulate parietal cells to secrete acid. These three secretagogues also have a multiplicative effect on acid secretion such that inhibition of one secretagogue reduces the effectiveness of the remaining two secretagogues. Acetylcholine also has an indirect effect to increase acid secretion by stimulating gastrin secretion from G cells. Somatostatin inhibits acid secretion.

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C) Hepatocytes produce essentially all the albumin normally present in blood. Viable hepatocytes use oxygen and produce carbon dioxide. Glucuronic acid produced by hepatocytes is used to conjugate bilirubin, forming bilirubin glucuronide. Lactate dehydrogenase is an enzyme that converts pyruvic acid to lactic acid under anaerobic conditions.

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C) Lysine is an essential amino acid, which means that it must be included in the diet because the body cannot synthesize it. Alanine, glycine, serine, and tyrosine can be synthesized by the body and are therefore considered nonessential amino acids. This woman has a lysine deficiency, which is common in poorly designed vegetarian diets; symptoms include nausea, fatigue, dizziness, anemia, loss of appetite, and thinning hair. Good dietary sources of lysine include eggs, meat, beans, legumes, soy, dairy products, and certain fish (such as cod and sardines). L-lysine is a building block for all proteins in the body.

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C) MMCs (sometimes called interdigestive myoelectric complexes) are peristaltic waves of contraction that begin in the stomach and slowly migrate in an aboral direction along the entire small intestine to the colon. By sweeping undigested food residue from the stomach, through the small intestine, and into the colon, MMCs function to maintain low bacterial counts in the upper intestine. Bacterial overgrowth syndrome can occur when the normally low bacterial colonization in the upper gastrointestinal tract increases significantly. It should be clear that an absence of MMCs would decrease duodenal motility and gastric emptying. MMCs do not have a direct effect on mass movements and swallowing.

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C) Mutations that produce a nonfunctional melanocortin-4 receptor cause extreme obesity and may account for as much as 5 percent to 6 percent of early onset, morbid obesity in children. All the other changes would tend to reduce food intake and/or increase energy expenditure and thus cause weight loss rather than obesity.

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C) PYY is released from most parts of the intestinal tract, but especially from the ileum and colon, in response to food intake. Increased levels of PYY have been shown to decrease food intake. All the other changes tend to increase food intake.

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C) Pancreatitis is inflammation of the pancreas. The pancreas secretes digestive enzymes into the small intestine that are essential in the digestion of fats, proteins, and carbohydrates. Reduced secretion of fluid into the pancreatic ducts in CF cause these digestive enzymes to accumulate in the ducts. The digestive enzymes then become activated in the pancreatic ducts (which typically would not occur) and can begin to "digest" the pancreas, leading to inflammation and a myriad of other problems (cysts and internal bleeding). Enterokinase is located at the brush border of intestinal enterocytes where it normally activates trypsin from its precursor, trypsinogen. Trypsin inhibitor is normally present in the pancreatic ducts where it prevents trypsin from being activated, and thus prevents autodigestion of the pancreas. When the ducts are blocked in cystic fibrosis, the available trypsin inhibitor is insufficient to prevent trypsin from being activated. Excessive secretion of CCK does not occur in persons with CF. Gallstone obstruction can lead to pancreatitis (by autodigestion) when the obstruction prevents pancreatic juice from entering the intestine, but this is unrelated to CF.

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C) The medical treatment of gastric ulcers is aimed at restoring the balance between acid secretion and mucosal protective factors. Proton pump inhibitors are drugs that covalently bind and irreversibly inhibit the H+/K+ adenosine triphosphatase (ATPase) pump, effectively inhibiting acid release. Therapy can also be directed toward histamine release, that is, H2 blockers, such as cimetidine (Tagamet), ranitidine (Zantac), famotidine (Pepcid), and nizatidine (Axid). These agents selectively block the H2 receptors in the parietal cells. Antibiotic therapy is used to eradicate the H. pylori infection. NSAIDs can cause damage to the gastric mucosal barrier, which is a forerunner of gastric ulcer.

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C) The palatopharyngeal folds located on each side of the pharynx are pulled medially, forming a sagittal slit through which the bolus of food must pass. This slit performs a selective function, allowing food that has been masticated sufficiently to pass by but impeding the passage of larger objects. The soft palate is pulled upward to close the posterior nares, which prevents food from passing into the nasal cavities. The vocal cords of the larynx are strongly approximated during swallowing, and the larynx is pulled upward and anteriorly by the neck muscles. The epiglottis then swings backward over the opening of the larynx. The upper esophageal sphincter relaxes, allowing food to move from the posterior pharynx into the upper esophagus.

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C) The various secretagogues, which include acetylcholine, gastrin, and histamine, have a multiplicative or synergistic effect on gastric acid secretion. This means that histamine potentiates the effects of gastrin and acetylcholine and that H2 blockers attenuate the secretory responses to both acetylcholine and gastrin. Likewise, acetylcholine potentiates the effects of gastrin and histamine and atropine attenuates the secretory effects of histamine and gastrin. Therefore, in the experiment described, the stimulation of acid secretion by pentagastrin is attenuated by the H2 blocker because of this multiplicative effect of the secretagogues.

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C) Themetabolicrateincreasesafteramealbecauseof various chemical reactions associated with digestion, absorption, and storage of food; this phenomenon is known as the thermogenic effect of food. After a meal containing mostly carbohydrates and fats, the metabolic rate usually increases by about 4 percent. However, a high-protein meal often increases the metabolic rate by as much as 30 percent; this effect can last from 3 to 12 hours after the meal and is called the specific dynamic action of proteins. Clearly, assimilation of proteins requires far more energy expenditure compared with fats and carbohydrates.

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C) This child has Hartnup's disease. This condition resembles pellagra (because of the symptoms of diarrhea, dementia, and dermatitis) and may be misdiagnosed as a nutritional deficiency of niacin. Hartnup's disease is an autosomal-recessive trait caused by a defective gene that codes for a sodium-dependent and chloride-independent neutral amino acid transporter expressed mainly in kidney and intestinal epithelium. Poor epithelial transport of neutral amino acids (such as tryptophan) leads to poor absorption of dietary amino acids, as well as excess amino acid excretion in the urine. Tryptophan is a precursor of niacin; it is an essential amino acid that must be included in the diet. Alkaptonuria, also called "black urine disease," is a genetic disorder of phenylalanine and tyrosine metabolism. Beriberi is caused by a nutritional deficit in thiamine. Scurvy results from a deficiency of vitamin C, which is required for collagen synthesis. Stickler's syndrome is a group of genetic disorders that affect connective tissues; it is characterized by eye problems, hearing loss, joint problems, and facial abnormalities.

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C) This woman has celiac disease, also called gluten-sensitive enteropathy, which is a chronic disease of the digestive tract that interferes with the absorption of nutrients from food. Mucosal lesions seen on upper gastrointestinal biopsy specimens are the result of an abnormal, genetically determined, cell-mediated immune response to gliadin, a constituent of the gluten found in wheat; a similar response occurs to comparable proteins found in rye and barley. Gluten is not found in oats, rice, or corn. When persons with celiac disease ingest gluten, the mucosa of their small intestine is damaged by an immunologically mediated inflammatory response, which results in malabsorption and maldigestion at the brush border. Digestion of fat is normal in persons with celiac disease because lipase secreted by the pancreas still functions normally. Malabsorption in celiac disease increases the stool content of carbohydrates, fat, and nitrogen. There is no cure for celiac disease, but a strict gluten-free diet can help manage symptoms and promote intestinal healing.

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C) Trace C shows a basal subatmospheric pressure with a positive pressure wave caused by passage of the food bolus. Trace A does not correspond to any normal event in the esophagus. Trace B could represent the LES in a patient with achalasia. Trace D depicts normal operation of the LES. Trace E show a basal positive pressure trace, which does not occur where the esophagus passes through the chest cavity.

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C) Under basal conditions, saliva contains high concentrations of potassium and bicarbonate ions and low concentrations of sodium and chloride ions. The primary secretion of saliva by acini has an ionic composition similar to that of plasma. As the saliva flows through the ducts, sodium ions are actively reabsorbed and potassium ions are actively secreted in exchange for sodium. Because sodium is absorbed in excess, chloride ions follow the electrical gradient, causing chloride levels in saliva to decrease greatly. Bicarbonate ions are secreted by an active transport process causing an elevation of bicarbonate concentration in saliva. The net result is that, under basal conditions, sodium and chloride concentrations in saliva are about 10 percent to 15 percent of that of plasma, bicarbonate concentration is about threefold greater than that of plasma, and potassium concentration is about seven times greater than that of plasma.

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D) About 94 percent of the bile salts are reabsorbed into the blood from the small intestine, with about half of this by diffusion through the mucosa in the early portions of the small intestine and the remainder by an active transport process through the intestinal mucosa in the distal ileum.

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D) Antagonists of melanocortin-4 receptors have been shown to markedly attenuate anorexia (i.e., reduced food intake due to decreased appetite) and cachexia (i.e., increased energy expenditure as well as decreased food intake) by blocking hypothalamic melanocortin-4 receptors. All the others choices would tend to decrease appetite and/or increase energy expenditure, exacerbating the anorexia/cachexia of a patient with cancer.

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D) Damage to the gastric mucosal barrier allows hydrogen ions to back-leak into the mucosa in exchange for sodium ions. A low pH in the mucosa causes mast cells to leak histamine, which damages the vasculature, causing ischemia. The ischemic mucosa allows a greater leakage of hydrogen ions—leading to more cell injury and death—resulting in a vicious cycle. Factors that normally strengthen the gastric mucosal barrier include mucus (which impedes the influx of hydrogen ions), gastrin (which stimulates mucosal growth), certain prostaglandins (which can stimulate mucus secretion), and various growth factors that can stimulate growth of blood vessels, gastric mucosa, and other tissues. Factors that weaken the gastric mucosal barrier include H. pylori (a bacterium that produces toxic levels of ammonium), as well as aspirin, NSAIDs, ethanol, and bile salts.

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D) Evaporation is the only mechanism of heat loss from the body when the environmental temperature is greater than the body temperature. Each gram of water that evaporates from the surface of the body causes 0.58 kilocalorie of heat to be lost from the body. Even when a person is not sweating, water still evaporates insensibly from the skin and lungs at a rate of 450 to 600 ml/day, which amounts to about 12 to 16 kilocalories of heat loss per hour. Radiation, convection, and conduction are mechanisms of heat loss when the body temperature is greater than the environmental temperature.

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D) GLIP is released by the presence of fat, carbohydrate, or protein in the gastrointestinal tract. GLIP is a strong stimulator of insulin release and is responsible for the observation that an oral glucose load releases more insulin and is metabolized more rapidly than an equal amount of glucose administered intravenously. Intravenously administered glucose does not stimulate the release of GLIP. Neither CCK nor VIP stimulates the release of insulin. GLIP does not stimulate glucagon release, and glucagon has the opposite effect of insulin; that is, it would decrease the rate of glucose clearance from the blood. VIP does not stimulate GLIP release.

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D) Pepsinogen is the precursor of the enzyme pepsin. Pepsinogen is secreted from the peptic or chief cells of the gastric gland (also called the oxyntic gland). To be converted from the precursor form to the active form (pepsin), pepsinogen must come in contact with hydrochloric acid or pepsin itself. Pepsin is a proteolytic enzyme that digests collagen and other types of connective tissue in meats.

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D) Persons with duodenal ulcers have about 2 billion parietal cells and can secrete about 40 mEq H+ per hour. Unaffected individuals have about 50 percent of these values. Plasma gastrin levels are related inversely to acid secretory capacity because of a feedback mechanism by which antral acidification inhibits gastrin release. Thus, plasma gastrin levels are reduced in persons with duodenal ulcers. Maximal acid secretion and plasma gastrin levels are not diagnostic for duodenal ulcer disease because of significant overlap with the normal population among persons in each group.

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D) Primary peristalsis of the esophagus is a continuation of pharyngeal peristalsis; central control originates in the swallowing center located in the medulla and pons. Visceral somatic fibers in the vagus nerves directly innervate smooth muscle fibers of the pharynx and upper esophagus, which coordinate pharyngeal peristalsis and primary peristalsis of the esophagus. Esophageal contractions can occur independently of vagal stimulation by a local stretch reflex initiated by the food bolus itself; this phenomenon is called secondary peristalsis. Although the vagus nerves can stimulate gastric acid secretion, gastrin release, and pancreatic bicarbonate secretion, these processes can be activated by other mechanisms. Thus, elimination of vagal stimulation does not completely eliminate them.

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D) The act of vomiting is preceded by antiperistalsis that may begin as far down in the gastrointestinal tract as the ileum. Distention of the upper portions of the gastrointestinal tract (especially the duodenum) becomes the exciting factor that initiates the actual act of vomiting. At the onset of vomiting, strong contractions occur in the duodenum and stomach along with partial relaxation of the lower esophageal sphincter. From then on, a specific vomiting act ensues that involves (a) a deep breath, (b) relaxation of the upper esophageal sphincter, (c) closure of the glottis, and (d) strong contractions of the abdominal muscles and diaphragm.

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D) The discovery of H. pylori and its association with peptic ulcer disease, adenocarcinoma, gastric lymphoma, and other diseases make it one of the most significant medical discoveries of this century. In the United States about 26 million people will experience ulcer disease in their lifetime, and in up to 90 percent, it will likely be due to H. pylori. H. pylori is a gram-negative bacterium with high urease activity, an enzyme that catalyzes the formation of ammonia from urea. The ammonia (NH3) is converted to ammonium (NH4+) in the acid environment of the stomach. The ammonium damages the gastric mucosal barrier because it damages epithelial cells. H. pylori also increases gastric acid secretion, possibly by increasing parietal cell mass. This combination of increased acid secretion along with damage to the gastric mucosal barrier promotes the development of gastric ulcer. Bile salts can damage the gastric mucosal barrier, but they do not have a clinically significant effect on acid secretion. Epidermal growth factor, gastrin, and mucus strengthen the gastric mucosal barrier.

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D) The fundus of the stomach and lower esophageal sphincter both relax during a swallow while the bolus of food is still higher in the esophagus. This phenomenon is called receptive relaxation. Receptive relaxation is mediated by afferent and efferent pathways in the vagus nerves. Nitric oxide is the neurotransmitter thought to mediate receptive relaxation at the smooth muscle cell. Motilin is a gastrointestinal hormone that mediates migrating motility complexes (also called housekeeping contractions); these contractions occur between meals. Gastrin and histamine do not have significant effects on smooth muscle contraction or relaxation at physiological levels. Norepinephrine can decrease smooth muscle contraction in the small intestine but is not involved in receptive relaxation.

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D) The liver has a high blood flow, low vascular resistance, and low blood pressure. During resting conditions, about 27 percent of the cardiac output flows through the liver, yet the pressure in the portal vein leading into the liver averages only 9 mm Hg. This high flow and low pressure indicate that the resistance to blood flow through the hepatic sinusoids is normally very low.

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D) The rate of protein metabolism can be estimated by measuring the nitrogen in the urine, then adding 10 percent (about 90 percent of the nitrogen in proteins is excreted in the urine) and multiplying by 6.25 (100/16) because the average protein contains about 16 percent nitrogen.

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D) This man has cirrhosis of the liver. In this condition, the rate of bilirubin production is normal, and the free bilirubin still enters the liver cells and becomes conjugated in the usual way. The conjugated bilirubin (direct) is mostly returned to the blood, probably by rupture of congested bile canaliculi, so that only small amounts enter the bile. The result is elevated levels of conjugated (direct) bilirubin in the plasma, with normal or near-normal levels of unconjugated (indirect) bilirubin.

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D) Triglycerides are hydrolyzed to glycerol and fatty acids, which, in turn, are oxidized to provide energy. Almost all cells, with the exception of some brain tissue, can use fatty acids almost interchangeably with glucose for energy.

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D) When feces enters the rectum, distention of the rectal wall initiates signals that spread through the myenteric plexus to initiate peristaltic waves in the descending colon, sigmoid colon, and rectum, all of which force feces toward the anus. At the same time the internal anal sphincter relaxes, allowing the feces to pass. In people with transected spinal cords, the defecation reflexes can cause automatic emptying of the bowel because the external anal sphincter is normally controlled by the conscious brain through signals transmitted in the spinal cord.

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E) A proton pump inhibitor such as omeprazole inhibits all acid secretion by directly inhibiting the H+, K+-ATPase (H+ pump). The parietal cell has receptors for secretagogues such as gastrin, acetylcholine, and histamine. Therefore, antigastrin antibodies, atropine, and histamine H2 blockers can reduce the secretion of acid, but none of these can completely eliminate acid secretion. Antacids neutralize gastric acid once it has entered the stomach, but they cannot inhibit acid secretion from parietal cells.

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E) About 90 percent of the total ATP produced by glucose metabolism is formed during oxidation of the hydrogen atoms released during the early stages of glucose degradation. This process is called oxidative phosphorylation. Only two ATP molecules are formed by glycolysis, and another two are formed in the citric acid cycle. ATP is not formed by glycogenesis or glycogenolysis.

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E) After a meal, the pH of the gastric contents increases because the food buffers the acid in the stomach. This increase in pH suppresses the release of somatostatin from delta cells in the stomach (hydrogen ions stimulate the release of somatostatin). Because somatostatin inhibits secretion of both gastrin and gastric acid, the fall in somatostatin levels leads to an increase in acid secretion. The increase in acid secretion causes the pH of the gastric contents to decrease. As the pH of the gastric contents decreases, the rate of acid secretion also decreases.

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E) All of the gastrointestinal hormones are released after a meal and all have physiological effects.

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E) CCK is the only gastrointestinal hormone that inhibits gastric emptying under normal physiological conditions. CCK inhibits gastric emptying by relaxing the orad stomach, which increases its compliance. When the compliance of the stomach is increased, the stomach can hold a larger volume of food without excess buildup of pressure in the lumen. None of the gastrointestinal hormones increases gastric emptying under physiological conditions; however, gastrin, secretin, and GLIP can inhibit gastric emptying when pharmacological doses are administered experimentally.

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E) Essentially all proteolytic enzymes are secreted in an inactive form, which prevents autodigestion of the secreting organ. Enterokinase is physically attached to the brush border of the enterocytes that line the inner surface of the small intestine. Enterokinase activates trypsinogen to become trypsin in the gut lumen. The trypsin then catalyzes the formation of additional trypsin from trypsinogen, as well as several other proenzymes (e.g., chymotrypsinogen, procarboxypeptidase, proelastase). Pepsin is first secreted as pepsinogen, which has no proteolytic activity. However, as soon as it comes into contact with hydrochloric acid, and especially in contact with previously formed pepsin plus hydrochloride acid, it is activated to form pepsin.

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E) Growth hormone can increase the metabolic rate 15 percent to 20 percent as a result of direct stimulation of cellular metabolism. Fever, regardless of its cause, increases the chemical reactions of the body by an average of about 120 percent for every 10°C rise in temperature. The metabolic rate decreases 10 percent to 15 percent below normal during sleep. Prolonged malnutrition can decrease the metabolic rate 20 percent to 30 percent, presumably because of the paucity of food substances in the cells.

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E) Most of the heat loss from the body occurs by radiation in the form of infrared heat waves, which is a type of electromagnetic wave. Heat waves radiate from all objects toward the body, and the body radiates heat waves to all surrounding objects. The reflective surface of the Mylar blanket prevents heat loss by reflecting infrared heat waves from the body back to the body, which causes the body to warm. At room temperature, 60 percent of the heat loss occurs by radiation, 22 percent by evaporation, 15 percent by conduction to air, and 3 percent by conduction to objects. Convection (i.e., air currents) can increase heat loss by removing the unstirred layer of air close to the skin.

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E) One of the most critical actions of gastrointestinal hormones is their trophic activity. Gastrin can stimulate mucosal growth throughout the gastrointestinal tract as well as growth of the exocrine pancreas. If most of the endogenous gastrin is removed by antrectomy, the gastrointestinal tract atrophies. Exogenous gastrin prevents the atrophy. Partial resection of the small intestine for tumor removal, morbid obesity, or other reasons results in hypertrophy of the remaining mucosa. The mechanism for this adaptive response is poorly understood. Both cholecystokinin and secretin stimulate growth of the exocrine pancreas. GLIP and motilin do not appear to have trophic actions on the gastrointestinal tract.

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E) Oxygen is shunted from the artery of a villus into its venous drainage so that by the time the arterial blood reaches the villus tip, the oxygen tension has been reduced to about 10 mm Hg. Adenosine dilates the villus artery, increasing blood flow to the villus tip. This increase in blood flow decreases the residence time for blood in the artery so that greater amounts of oxygen can reach the villus tip, thus increasing the oxygen tension at the villus tip. Factors that decrease intestinal blood flow (e.g., hemorrhagic shock and a severe degree of exercise) can lead to ischemic death of villi because of their basal low level of oxygenation.

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E) Secretin inhibits gastrin secretion from normal G cells in the antrum and duodenum but actually stimulates gastrin secretion in gastrinoma cells. Any increase in serum gastrin concentration greater than 110 pg/ml above baseline after administration of human secretin is diagnostic of gastrinoma (also called Zollinger-Ellison syndrome). The secretin test is considered the most sensitive and accurate diagnostic method for gastrinoma.

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E) The cephalic phase of gastric secretion occurs before food enters the stomach. Seeing, smelling, chewing, and anticipating food is perceived by the brain, which, in essence, tells the stomach to prepare for a meal. Stimuli for the cephalic phase thus include mechanoreceptors in the mouth, chemoreceptors (smell and taste), thought of food, and hypoglycemia. Because the cephalic phase of gastric secretion is mediated entirely by way of the vagus nerve, vagotomy can abolish the response. Antacids neutralize gastric acid, but they do not inhibit gastric secretion. An antigastrin antibody would attenuate (but not abolish) the cephalic phase because this would have no effect on histamine and acetylcholine stimulation of acid secretion. Atropine would attenuate the cephalic phase by blocking acetylcholine receptors on parietal cells; however, atropine does not abolish acetylcholine stimulation of gastrin secretion. A histamine H2 blocker would attenuate the cephalic phase of gastric secretion but would not abolish it.

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E) The defecation reflex (also called the rectosphincteric reflex) occurs when a mass movement forces feces into the rectum. When the rectum is stretched, the internal anal sphincter relaxes and the rectum contracts pushing the feces toward the anus. The external anal sphincter is controlled voluntarily and can be contracted when defecation is not possible. Therefore, when a person feels the urge to defecate, the internal anal sphincter is relaxed, the rectum contracts, and the external anal sphincter is either contracted or relaxed depending on the circumstances.

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E) The figure below shows the time course of gastric pH, rate of acid secretion, and stomach volume immediately before and for 4 hours after a meal. Note that the pH of the gastric juice is lowest immediately before the meal (not an answer choice) and 4 hours after consuming the meal (the correct answer). It is a common misconception that the pH of the gastric juice is lowest (most acidic) after a meal, when acid secretion is highest.

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E) The presence of acid, fatty acids, and hyperosmotic solutions in the duodenum and jejunum leads to suppression of acid secretion through a variety of mechanisms. Acid stimulates the secretion of secretin from the small intestine, which in turn inhibits acid secretion from parietal cells. Acidification of the antrum and oxyntic gland area of the stomach stimulates the release of somatostatin, which in turn inhibits acid secretion by a direct action on the parietal cells and an indirect action mediated by suppression of gastrin secretion. The presence of fatty acids in the small intestine stimulates the release of GLIP, which inhibits acid secretion both directly (parietal cell inhibition) and indirectly (by decreasing gastrin secretion). Hyperosmotic solutions in the small intestine cause the release of unidentified enterogastrones, which directly inhibit acid secretion from parietal cells. Isotonic solutions have no effect on acid secretion.

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E) This man has heatstroke. When the body temperature rises into the range of 105°F to 108°F, heat-stroke is likely to develop. Heat loss mechanisms are overwhelmed by excessive metabolic production of heat and excessive environmental heat. Heatstroke is usually accompanied by dehydration (poor skin turgor is common), which can produce nausea, vomiting, hypotension, and fainting or dizziness. Interestingly, the skin is frequently dry because the anterior hypo-thalamic-preoptic area of the brain that normally initiates sweating is often compromised by the elevation in body temperature.

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E) This woman has gastroparesis (also called delayed gastric emptying). This disorder slows or at times even stops the movement of chyme from the stomach to the duodenum. Diabetes is the most common known cause of gastroparesis; it occurs in about 20 percent of persons with type 1 diabetes. The high blood glucose is thought to damage the vagus nerve and thereby delay gastric emptying.

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E) Two molecules of ammonia and one molecule of carbon dioxide combine to form one molecule of urea and one molecule of water. Essentially all urea formed in the human body is synthesized in the liver. In the absence of the liver or in serious liver disease, ammonia accumulates in the blood. The ammonia is toxic to the brain, often leading to a state called hepatic coma.

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E) Vitamin B12 is absorbed in the ileum; this absorption requires intrinsic factor, which is a glycoprotein secreted by parietal cells in the stomach. Binding of intrinsic factor to dietary vitamin B12 is necessary for attachment to specific receptors located in the brush border of the ileum. Atrophic gastritis is a type of autoimmune gastritis that is mainly confined to the acid-secreting corpus mucosa. The gastritis is diffuse, and severe atrophy eventually develops. Ileal resection is likely to cause diarrhea but not constipation. A gastric ulcer is possible but relatively unlikely. GERD is caused by gastric acid and bile reflux into the esophagus; mucosal damage and epithelial cell transformation lead to Barrett esophagus, which is a forerunner to adenocarcinoma, a particularly lethal cancer.

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E) Vitamin K is an essential co-factor to a liver enzyme that adds a carboxyl group to factors II (prothrombin), VII (proconvertin), IX, and X, all of which are important to blood coagulation. The other vitamins listed are not directly involved in coagulation.

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F) All these factors can inhibit gastric acid secretion under normal physiological conditions. Gastric acid stimulates the release of somatostatin (a paracrine factor), which has a direct effect on the parietal cell to inhibit acid secretion, as well as an indirect effect mediated by suppression of gastrin secretion. Secretin and GLIP inhibit acid secretion through a direct action on parietal cells as well as indirectly through suppression of gastrin secretion. Enterogastrones are unidentified substances released from the duodenum and jejunum that directly inhibit acid secretion. When acid or hypertonic solutions enter the duodenum, a neurally mediated decrease in gastric acid secretion follows.

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E) When the hypothalamic set-point temperature is greater than the body temperature, the person feels cold and exhibits responses that lead to an elevation of body temperature. These responses include shivering and vasoconstriction, as well as piloerection and epinephrine secretion. Shivering increases heat production. The increase in epinephrine secretion causes an immediate increase in the rate of cellular metabolism, which is an effect called chemical thermogenesis. Vasoconstriction of the skin blood vessels decreases heat loss through the skin.

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A) The toxin from V. cholerae (cholera toxin) causes an irreversible increase in cAMP levels (not cGMP levels) in the enterocytes located in the crypts of Lieberkühn of the small intestine. This increase in cAMP causes an irreversible opening of chloride channels on the luminal membrane. Movement of chloride ions into the gut lumen causes a secondary movement of sodium ions to maintain electrical neutrality. Water follows the osmotic gradient created by sodium and chloride, causing a tremendous increase in fluid loss into the gut lumen. Severe diarrhea follows.

Review Book 19. A toxin from V. cholerae is most likely to stimulate an increase in which of the following in the epithelial cells of the crypts of Lieberkühn in these people ? A) Cyclic adenosine monophosphate (cAMP) B) Cyclic guanosine monophosphate (cGMP) C) Chloride absorption D) Sodium absorption

B) When the hypothalamic set-point temperature is lower than the body temperature, the person feels hot and exhibits responses that cause body temperature to decrease. These responses include sweating and vasodilation. Sweating increases heat loss from the body by evaporation. Vasodilation of skin blood vessels facilitates heat loss from the body by increasing the skin blood flow.

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B) Cholera toxin causes an irreversible opening of chloride channels in the enterocytes located in the crypts of Lieberkühn of the small intestine, as indicated in the explanation for the previous answer. Although sodium ions enter the gut lumen to maintain electrical neutrality after the flux of chloride ions into the gut lumen, the sodium ions move through relatively large paracellular pathways rather than through actual sodium channels. Calcium, potassium, and magnesium do not have a significant role in the course of an infection with V. cholerae.

Review Book 20. Which type of ion channel is most likely to be irreversibly opened in the intestinal epithelial cells of these people? A) Calcium B) Chloride C) Magnesium D) Potassium E) Sodium

A) When the hypothalamic set-point temperature is equal to the body temperature, the body exhibits neither heat loss nor heat conservation mechanisms, even when the body temperature is far above normal. Therefore, the person does not feel hot even when the body temperature is 104°F.

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B) Enterocytes are derived from stem cells located in the crypts of Lieberkühn of the small intestine. They mature as they migrate upward toward the villus tip, where they are extruded into the gut lumen, becoming part of the ingesta. In humans, the entire population of epithelial cells is replaced in 3 to 6 days. Cholera also usually runs its course in 3 to 6 days. Because cholera toxin causes an irreversible opening of chloride channels in the enterocytes, it is thought that the time course of cholera is dictated by the life span of the enterocytes.

Review Book 21. Which range best describes the life span (in days) of an intestinal enterocyte infected with V. cholerae in a person who survives? A) 1 to 3 B) 3 to 6 C) 6 to 9 D) 9 to 12 E) 12 to 15

C) The internal anal sphincter relaxes when the rectum is stretched, as indicated by repeated decreases in pressure after inflation of the rectal balloon. Pressures in the distal and proximal rectum are expected to increase after inflation of the rectal balloon. Inflation of a rectal balloon should not affect pressures at the lower esophageal sphincter or ileocecal valve.

Review Book 37. Which structure best describes the origin of tracing X shown in the figure? A) Distal rectum B) Ileocecal valve C) Internal anal sphincter D) LES E) Proximal rectum

C) Before pelvic floor training, the pressure at the external anal sphincter was unchanged after inflation of the rectal balloon. This failure of the external anal sphincter to contract is expected to result in defecation. After pelvic floor training, the external anal sphincter contracts when the rectal balloon is inflated, which prevents inappropriate defecation.

Review Book 38. Which of the following best describes the condition for which the patient received pelvic floor training? A) Anal fissure (i.e., a tear or superficial laceration) B) Chronic diarrhea C) Fecal incontinence (i.e., no control over defecation) D) Hemorrhoids E) Hirschsprung's disease

B) Continual release of energy from glucose when energy is not needed by the cells would be an extremely wasteful process. Both ATP and ADP control the rate of chemical reactions in the energy metabolism sequence. When ATP is abundant within the cell, it helps control energy metabolism by inhibiting the conversion of fructose-6-phosphate to fructose-1,6-diphosphate. It does so by inhibiting the enzyme phosphofructokinase.

Review Book 8. Abundant amounts of adenosine triphosphate (ATP) in the cytoplasm of the cell inhibit which step in glycolysis? A) Conversion of glucose to glucose-6-phosphate B) Conversion of fructose-6-phosphate to fructose-1,6-diphosphate C) Conversion of 1,3-diphosphoglyceric acid to 3-phosphoglyceric acid D) Conversion of phosphoenolpyruvic acid to pyruvic acid

B) Both ADP and AMP increase the activity of the enzyme phosphofructokinase and increase the conversion of fructose-6-phosphate to fructose-1,6-diphosphate.

Review Book 9. Abundant amounts of adenosine diphosphate (ADP) or adenosine monophosphate (AMP) stimulate which step in glycolysis? A) Conversion of glucose to glucose-6-phosphate B) Conversion of fructose-6-phosphate to fructose-1,6-diphosphate C) Conversion of 1,3-diphosphoglyceric acid to 3-phosphoglyceric acid D) Conversion of phosphoenolpyruvic acid to pyruvic acid