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* GI and ENdo

#128668nishi - 10/15/06 19:34

GI,ENDORelease of which of the following peptides leads to an increasein the secretion of pancreatic enzymes into thesmall intestine?

A. Cholecystokinin

B. Gastrin

C. Motilin

D. Secretin

E. Somatostatin

Explanation:

The correct answer A. Release of cholecystokinin is stimulatedby the presence of peptides, amino acids, orfatty acids in the small intestine. Cholecystokinin acts on thepancreas to stimulate secretion of pancreaticenzymes that aid in the digestion of these compounds.

Gastrin (choice B) secretion is stimulated by the presence ofpeptides or amino acids in the lumen of thestomach, and produces an increase in gastric H+ secretion.

Motilin (choice C) is a hormone that regulates the migratingmyoelectric complex, a series of contractions thatoccur during fasting, clearing the stomach and small intestineof any residual food.

Secretin (choice D) secretion is stimulated by the presence ofH+ and fatty acids in the duodenum, and causesan increase in pancreatic and biliary HCO3 release and adecrease in gastric H+ release.

Somatostatin (choice E) secretion is stimulated by thepresence of H+ in the lumen, and results in decreasedrelease of all gastrointestinal hormones and decreased H+secretion in the stomach.

A 42-year-old obese woman experiences episodic abdominalpain. She notes that the pain increases after theingestion of a fatty meal. The action of which of the followinghormones is responsible for the postprandialintensification of her symptoms?

A. Cholecystokinin

B. Gastrin

C. Pepsin

d ENdo - USMLE Forum Archives http://www.usmleforum.com/archives/2006/1/12

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D. Secretin

E. Somatostatin

Explanation:

The correct answer is A. This woman has a risk profile (female,fat, forties) and symptomatology consistent withgallstones (cholelithiasis). As would be expected, contraction

of the gallbladder following a fatty meal oftenexacerbates the pain caused by gallstones. Cholecystokinin(CCK), the release of which is stimulated by dietaryfat, is the hormone responsible for stimulation of gallbladdercontraction. It is produced in I cells of theduodenum and jejunum. In addition to gallbladdercontraction, CCK also stimulates pancreatic enzyme secretionand decreases the rate of gastric emptying.

Gastrin (choice B) is produced by the G cells of the antrumand duodenum. Gastrin stimulates the secretion ofHCl from the parietal cells and pepsinogen from the chief cellsof the stomach. Gastrin secretion is stimulated bygastric distention, digestive products (e.g., amino acids), andvagal discharge.

Pepsin (choice C) is a protease produced by the chief cells ofthe stomach (as pepsinogen). It is involved in thedigestion of proteins. Pepsinogen release is stimulated byvagal stimulation, gastrin, local acid production,secretin, CCK, and histamine.

Secretin (choice D) is produced by the S cells of theduodenum. It is secreted primarily in response toacidification of the duodenal mucosa. Secretin stimulates thesecretion of bicarbonate-containing fluid from thepancreas and biliary ducts. This neutralization allowspancreatic enzymes to function. Secretin also inhibitsgastric acid production and gastric emptying.

Somatostatin (choice E) is produced by the D cells of thepancreatic islets and in the gastric and intestinalmucosa. Somatostatin is an inhibitory hormoneit inhibitsmost gastrointestinal hormones, gallbladdercontraction, gastric acid and pepsinogen secretion, pancreaticand small intestinal fluid secretion, and bothglucagon and insulin release.

A young boy presents with failure to thrive. Biochemicalanalysis of a duodenal aspirate after a meal reveals adeficiency of enteropeptidase (enterokinase). The levels ofwhich of the following digestive enzymes would beaffected?

A. Amylase

B. Colipase

C. Lactase

D. Pepsin

E. Trypsin

Explanation:


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The correct answer is E. Enteropeptidase, formerly calledenterokinase, activates trypsinogen by limitedproteolytic digestion to give trypsin. Trypsin is itself capableof activating trypsinogen, which produces a positivefeedback effect. Trypsin also activates chymotrypsinogen (andseveral other proteolytic enzymes), sodeficiency of enteropeptidase results in a severe deficiency ofenzymes that digest protein.

Amylase (choice A) aids in the breakdown of starches tooligosaccharides, maltose, and maltotriose.

Colipase (choice B), along with other lipases, functions todigest fats.

Lactase (choice C) is a brush-border disaccharidase thathydrolyzes the bond between galactose and glucosein lactose.

Pepsin (choice D) is a proteolytic enzyme secreted in aninactive form (pepsinogen) by the chief cells of thestomach. Pepsinogen is activated by stomach acid, and so isnot dependent on enteropeptidase. Pepsin alonewill not replace the activities of other proteolytic enzymes,partly because food does not remain in the stomachfor an extended period of time.

A 70-year-old woman undergoes a gastrectomy for Zollinger-Ellison syndrome. Her doctor informs her that shewill need to take intramuscular vitamin B12 shots for the restof her life. Absence of which of the following celltypes is responsible for this vitamin replacement requirement?

A. Chief cells

B. G cells

C. Goblet cells

D. Mucous neck cells

E. Parietal cells

Explanation:

The correct answer is E. The parietal cells of the stomachproduce intrinsic factor, a glycoprotein that bindsvitamin B12 in the lumen of the stomach and facilitates itsabsorption in the terminal ileum. Patients without astomach and those with pernicious anemia (autoimmunedestruction of parietal cells) will require B12replacement therapy. Recall that B12 deficiency will lead tomegaloblastic anemia and the USMLE-favorite

picture of a blood smear with hypersegmented neutrophils.Note that parietal cells also synthesize and secreteHCl.

Chief cells (choice A) are responsible for secretingpepsinogen, the precursor to pepsin.

G cells (choice B) are gastrin-secreting cells. Gastrinstimulates secretion of acid by the parietal cells found inthe body and fundus of the stomach. Zollinger-Ellisonsyndrome is caused by a pancreatic or duodenal tumorthat secretes gastrin (a gastrinoma). It is characterized by thedevelopment of severe peptic ulcer disease.


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Goblet cells (choice C) are part of the mucosa of the smallintestine, not the stomach. They produceglycoproteins (mucins) that protect and lubricate the lining ofthe intestine.

Mucous neck cells (choice D) are mucus-secreting cellslocated in the necks of the gastric glands.

During a fast, a brief phase of intense sequential contractions

begins in the stomach and gradually migrates tothe ileum. Release of which of the following intest inalhormones is most likely responsible for this observedeffect?

A. Cholecystokinin

B. Gastrin

C. Gastrin-releasing peptide

D. Motilin

E. Secretin

F. Somatostatin

Explanation:

The correct answer is D. Motilin is a hormone released by thesmall intestine during the fasting state. Its waxingand waning blood levels correlate with the initiation andending of migrating motor complexes (MMC).Furthermore, injection of motilin has been shown to evokeMMC activity. The MMC typically begins in thestomach, and over a 90-120 minute period, migrates to theileum, where it dies out. As one complex dies out inthe ileum, another complex begins in the stomach providedthe fasting state continues. Eating a meal interruptsthe MMC activity.

Cholecystokinin (choice A) is released during the intestinalphase of the digestive period (not during a fast). Itssecretion is evoked by the presence of fat and proteindigestion products in the duodenum. It inducescontraction of the gall bladder and relaxation of the sphincterof Oddi.

Gastrin (choice B) is released from G cells in the antrum,mostly during the gastric phase of the digestive period(not during a fast). It tends to increase stomach motility,although the rate of emptying is decreased becausegastrin also causes the pyloric sphincter to contract. It alsomay contribute to the increase in ileal and colonic

motility as part of the gastroileal and gastrocolic reflexes,respectively.

Gastrin-releasing peptide (choice C) mediates the neuralrelease of gastrin. Antral enteric neurons that areactivated by vagal efferents or by local reflexes releasegastrin-releasing peptide, which stimulates the G cellsto secrete gastrin.

Secretin (choice E) is a duodenal hormone that is releasedduring the intestinal phase of the digestive period(not during a fast). Its secretion is evoked by a duodenal pHless than 4.5. Secretin tends to decrease the rateof stomach emptying.


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F. Somatostatin

Explanation:

The correct answer is D. Motilin is a hormone released by thesmall intestine during the fasting state. Its waxingand waning blood levels correlate with the initiation andending of migrating motor complexes (MMC).Furthermore, injection of motilin has been shown to evokeMMC activity. The MMC typically begins in the

stomach, and over a 90-120 minute period, migrates to theileum, where it dies out. As one complex dies out inthe ileum, another complex begins in the stomach providedthe fasting state continues. Eating a meal interruptsthe MMC activity.

Cholecystokinin (choice A) is released during the intestinalphase of the digestive period (not during a fast). Itssecretion is evoked by the presence of fat and proteindigestion products in the duodenum. It inducescontraction of the gall bladder and relaxation of the sphincterof Oddi.

Gastrin (choice B) is released from G cells in the antrum,mostly during the gastric phase of the digestive period

(not during a fast). It tends to increase stomach motility,although the rate of emptying is decreased becausegastrin also causes the pyloric sphincter to contract. It alsomay contribute to the increase in ileal and colonicmotility as part of the gastroileal and gastrocolic reflexes,respectively.

Gastrin-releasing peptide (choice C) mediates the neuralrelease of gastrin. Antral enteric neurons that areactivated by vagal efferents or by local reflexes releasegastrin-releasing peptide, which stimulates the G cellsto secrete gastrin.

Secretin (choice E) is a duodenal hormone that is releasedduring the intestinal phase of the digestive period(not during a fast). Its secretion is evoked by a duodenal pHless than 4.5. Secretin tends to decrease the rateof stomach emptying.

Somatostatin (choice F) is released by delta cells in thestomach mucosa. It mediates the inhibition of gastrinsecretion that occurs when the pH of the gastric juice fallsbelow 3. It also acts directly on the parietal cell todecrease acid secretion.A 70-year-old woman undergoes a gastrectomy for Zollinger-Ellison syndrome. Her doctor informs her that shewill need to take intramuscular vitamin B12 shots for the restof her life. Absence of which of the following celltypes is responsible for this vitamin replacement requirement?

A. Chief cells

B. G cells

C. Goblet cells

D. Mucous neck cells

E. Parietal cells

Explanation:

The correct answer is E. The parietal cells of the stomach


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produce intrinsic factor, a glycoprotein that bindsvitamin B12 in the lumen of the stomach and facilitates itsabsorption in the terminal ileum. Patients without astomach and those with pernicious anemia (autoimmunedestruction of parietal cells) will require B12replacement therapy. Recall that B12 deficiency will lead tomegaloblastic anemia and the USMLE-favoritepicture of a blood smear with hypersegmented neutrophils.Note that parietal cells also synthesize and secreteHCl.

Chief cells (choice A) are responsible for secretingpepsinogen, the precursor to pepsin.

G cells (choice B) are gastrin-secreting cells. Gastrinstimulates secretion of acid by the parietal cells found inthe body and fundus of the stomach. Zollinger-Ellisonsyndrome is caused by a pancreatic or duodenal tumorthat secretes gastrin (a gastrinoma). It is characterized by thedevelopment of severe peptic ulcer disease.

Goblet cells (choice C) are part of the mucosa of the smallintestine, not the stomach. They produceglycoproteins (mucins) that protect and lubricate the lining ofthe intestine.

Mucous neck cells (choice D) are mucus-secreting cellslocated in the necks of the gastric glands.

A patient undergoes a total gastrectomy because of aproximally located gastric cancer. After the surgery, whichof the following digestive enzymes will be produced ininadequate amounts?

A. Amylase

B. Chymotrypsin

C. Lipase

D. Pepsin

E. Trypsin

Explanation:

The correct answer is D. Pepsin is secreted (in an inactive orzymogen form as pepsinogen) by the chief cells ofthe stomach. Pepsinogen is activated by contact with stomachacid. Although protein digestion usually beginswith the actions of hydrochloric acid and pepsin, pancreaticenzymes complete the job as the food passes intothe small intestine.

Amylases (choice A) hydrolyze 1->4 glycosidic linkages ofstarches to produce oligosaccharides, maltose,maltotriose, and limit dextrins. These enzymes are producedby the pancreas and salivary glands.

Chymotrypsin (choice B) is a proteolytic enzyme released bythe pancreas as the inactive proenzyme,chymotrypsinogen.

Lipases (choice C) are mostly released by the pancreas, andserve to digest various lipids, includingtriacylglycerols.

Trypsin (choice E) is a proteolytic enzyme released by the


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pancreas as the inactive proenzyme, trypsinogen.

A 42-year-old obese woman experiences episodic abdominalpain. She notes that the pain increases after theingestion of a fatty meal. The action of which of the followinghormones is responsible for the postprandialintensification of her symptoms?

A. Cholecystokinin

B. Gastrin

C. Pepsin

D. Secretin

E. Somatostatin

Explanation:

The correct answer is A. This woman has a risk profile (female,fat, forties) and symptomatology consistent withgallstones (cholelithiasis). As would be expected, contractionof the gallbladder following a fatty meal oftenexacerbates the pain caused by gallstones. Cholecystokinin(CCK), the release of which is stimulated by dietaryfat, is the hormone responsible for stimulation of gallbladdercontraction. It is produced in I cells of theduodenum and jejunum. In addition to gallbladdercontraction, CCK also stimulates pancreatic enzyme secretionand decreases the rate of gastric emptying.

Gastrin (choice B) is produced by the G cells of the antrumand duodenum. Gastrin stimulates the secretion ofHCl from the parietal cells and pepsinogen from the chief cellsof the stomach. Gastrin secretion is stimulated bygastric distention, digestive products (e.g., amino acids), andvagal discharge.

Pepsin (choice C) is a protease produced by the chief cells ofthe stomach (as pepsinogen). It is involved in thedigestion of proteins. Pepsinogen release is stimulated byvagal stimulation, gastrin, local acid production,secretin, CCK, and histamine.

Secretin (choice D) is produced by the S cells of theduodenum. It is secreted primarily in response toacidification of the duodenal mucosa. Secretin stimulates thesecretion of bicarbonate-containing fluid from thepancreas and biliary ducts. This neutralization allowspancreatic enzymes to function. Secretin also inhibits

gastric acid production and gastric emptying.

Somatostatin (choice E) is produced by the D cells of thepancreatic islets and in the gastric and intestinalmucosa. Somatostatin is an inhibitory hormoneit inhibitsmost gastrointestinal hormones, gallbladdercontraction, gastric acid and pepsinogen secretion, pancreaticand small intestinal fluid secretion, and bothglucagon and insulin release.

Release of which of the following peptides leads to an increase


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in the secretion of pancreatic enzymes into thesmall intestine?

A. Cholecystokinin

B. Gastrin

C. Motilin

D. Secretin

E. Somatostatin

Explanation:

The correct answer A. Release of cholecystokinin is stimulatedby the presence of peptides, amino acids, orfatty acids in the small intestine. Cholecystokinin acts on thepancreas to stimulate secretion of pancreaticenzymes that aid in the digestion of these compounds.

Gastrin (choice B) secretion is stimulated by the presence ofpeptides or amino acids in the lumen of thestomach, and produces an increase in gastric H+ secretion.

Motilin (choice C) is a hormone that regulates the migratingmyoelectric complex, a series of contractions thatoccur during fasting, clearing the stomach and small intestineof any residual food.

Secretin (choice D) secretion is stimulated by the presence ofH+ and fatty acids in the duodenum, and causesan increase in pancreatic and biliary HCO3 release and adecrease in gastric H+ release.

Somatostatin (choice E) secretion is stimulated by thepresence of H+ in the lumen, and results in decreasedrelease of all gastrointestinal hormones and decreased H+secretion in the stomach.

A young boy presents with failure to thrive. Biochemicalanalysis of a duodenal aspirate after a meal reveals adeficiency of enteropeptidase (enterokinase). The levels ofwhich of the following digestive enzymes would beaffected?

A. Amylase

B. Colipase

C. Lactase

D. Pepsin

E. Trypsin

Explanation:

The correct answer is E. Enteropeptidase, formerly calledenterokinase, activates trypsinogen by limitedproteolytic digestion to give trypsin. Trypsin is itself capableof activating trypsinogen, which produces a positivefeedback effect. Trypsin also activates chymotrypsinogen (andseveral other proteolytic enzymes), sodeficiency of enteropeptidase results in a severe deficiency of


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enzymes that digest protein.

Amylase (choice A) aids in the breakdown of starches tooligosaccharides, maltose, and maltotriose.

Colipase (choice B), along with other lipases, functions todigest fats.

Lactase (choice C) is a brush-border disaccharidase thathydrolyzes the bond between galactose and glucosein lactose.

Pepsin (choice D) is a proteolytic enzyme secreted in aninactive form (pepsinogen) by the chief cells of thestomach. Pepsinogen is activated by stomach acid, and so isnot dependent on enteropeptidase. Pepsin alonewill not replace the activities of other proteolytic enzymes,partly because food does not remain in the stomachfor an extended period of time.

A pregnant woman in her second trimester complains of heatintolerance and palpitations. Physical examinationreveals a slightly enlarged, non-tender thyroid gland, and anormal cardiac exam. The serum thyroxine (T4) levelis increased; however, the serum thyroid-stimulating hormone

(TSH) is normal. Which of the following bestexplains the laboratory findings in this patient?

A. Decreased estrogen

B. Increased free thyroxine (T4)

C. Increased progesterone

D. Increased serum triiodothyronine (T3)

E. Increased thyroid-binding globulin (TBG)

Explanation:

The correct answer is E. The total serum thyroxine (T4)represents the sum of the T4 bound to thyroid-bindingglobulin (TBG) and the free T4. An increased total T4 may bedue to an increase in TBG or an increase in freeT4, the latter leading to signs of thyrotoxicosis. A decreasedtotal T4 may be secondary to a reduction in TBGor in free T4, the latter leading to signs of hypothyroidism.

In a euthyroid state, one-third of the binding sites on TBG areoccupied by T4. An increase in estrogen(pregnancy, birth control pills) increases the synthesis of TBG.Since one-third of the binding sites on TBG willbe occupied, the T4 bound to the additional TBG increases thetotal serum T4. The addition of extra TBG does

not alter the free T4 level because of the equilibrium betweenthe serum concentration of T4 and thyroid glandT4 production. Since the free T4 level is normal, there is nostimulus to release thyroid-stimulating hormone(TSH) from the pituitary gland. Regarding the patient'senlarged thyroid gland, heat intolerance, andpalpitations, these are normal findings in pregnancy and donot indicate an overactive thyroid gland.

Estrogen is increased (not decreased) in pregnancy (choiceA).

The serum free T4 (choice B) is normal in pregnancy. Thisexplains why the serum TSH is normal in the


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presence of an elevated serum T4, which reflects the increasein TBG normally occurring in pregnancy.

The increase in progesterone (choice C) during pregnancy hasno effect on TBG levels.

Although the serum T3 (choice D) concentration is increasedin pregnancy for the same reason as serum T4(more T3 is bound to TBG), it is not responsible for theincrease in synthesis of TBG that leads to the increasein serum T4.

An asymptomatic, 24-year-old African-American woman in hersecond trimester of pregnancy has the followinglaboratory findings:

Based on the laboratory data,which of the following tests is necessary for further evaluationof this patient?LAB VALUES

A. Creatinine clearance

B. Oral glucose tolerance test

C. Serum ferritin

D. Sickle cell preparation

E. No further study is necessary

Explanation:

The correct answer is E. All of the laboratory data in thispregnant woman are normal, hence no further study isnecessary. In a normal pregnancy, both the plasma volumeand RBC mass are increased with a greater increase inthe plasma volume than RBC mass (2:1 ratio). This has adilutional effect on many laboratory tests.

Increasing plasma volume in pregnancy increases thecreatinine clearance (choice A) due to the expected elevationin the glomerular filtration rate (GFR). The reference intervalsfor serum blood urea nitrogen and creatinine are lowerthan normal, due to the dilutional effect of increased plasmavolume and increased clearance of both analytes in theurine caused by the rise in the GFR.

The threshold for glucose is reduced in pregnancy, so patientscan have a positive dipstick test for glucose in thepresence of a normal serum glucose. Therefore, an oralglucose tolerance test (choice B) is not indicated.

The hemoglobin (Hb) concentration in pregnancy is normally

decreased because of the dilutional effect of increasedplasma volume. Since the Hb is normal (for a pregnantwoman) in this patient, a serum ferritin (choice C) to rule outiron deficiency is unnecessary. Furthermore, iron deficiency isusually associated with a low MCV (microcytic anemia),and her MCV is normal.

Although sickle disease is the most common genetichemoglobinopathy among African Americans, the patient isnotanemic, so there is no reason to order a sickle cell preparation(choice D).


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Two normal, healthy subjects volunteer for a study on insulinsecretion. In Patient 1, blood glucose is increasedto 150 mg/dL by direct intravenous infusion. In Patient 2,blood glucose is increased to 150 mg/dL by ingestion oforal glucose. The peak plasma insulin concentration producedin Patient 1 is 70 U/mL while in Patient 2, it is 95U/mL. Which of the following best explains the higherinsulin concentration in Patient 2?

A. Ingested glucose activates a sympathetic reflex thatincreases cell release of insulin

B. Ingested glucose increases duodenal secretion of gastricinhibitory peptide (GIP),increasing cell release of insulin

C. Intravenous glucose increases islet cell secretion ofsomatostatin, inhibiting cell release ofinsulin

D. Intravenous glucose increases islet cell secretion ofglucagon, inhibiting cell release of insulin

Explanation:

The correct answer is B. Ingestion of glucose results insecretion of a "gut factor" into the blood thatsubsequently increases insulin secretion by cells. The mostlikely candidate for this action is theintestinal peptide known as gastric inhibitory peptide (GIP),which obviously was named for its effects on thestomach. GIP secretion is increased during ingestion ofglucose and the blood level produced is sufficient tostimulate insul in secretion. Because of this effect on insulinsecretion, GIP is sometimes referred to asglucose-dependent insulinotropic peptide.

Activation of the sympathetic innervation to the pancreasinhibits insulin secretion via an 2-adrenergicmechanism. Hence, any sympathetic reflexes activated duringingestion of glucose would decrease (notincrease, choice A) insulin secretion.

While paracrine release of somatostatin (choice C) by cellsin the islets does inhibit insulin secretion bycells, there is no reason to suspect that intravenous versusingested glucose would have a differentialeffect on somatostatin release. The same holds true forglucagon secretion by cells. Furthermore,glucagon has a paracrine effect to increase (not decrease,choice D) insulin secretion.

An XX genotypic infant is born with ambiguous genitalia.Laboratory examination reveals hypoglycemia,hyperkalemia, and salt wasting. Serum 17-OH progesterone ismarkedly increased. Which of the following is themost likely diagnosis?

A. 5-alpha-reductase deficiency

B. 11-beta-hydroxylase deficiency

C. 17-alpha-hydroxylase deficiency


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D. 21-hydroxylase deficiency

E. Complete androgen resistance

Explanation:

The correct answer is D. 21-hydroxylase deficiency is the mostcommon form of congenital adrenal hyperplasia.The simple virilizing variant (without salt wasting) is most

common, but with severe 21-hydroxylase deficiency,virilization and salt wasting occur. The infant described aboveexhibits salt wasting and hyperkalemia becausealdosterone secretion is diminished by the enzyme deficiency.The hypoglycemia is due to cortisol deficiency.Because cortisol secretion is diminished in congenital adrenalhyperplasia, ACTH secretion from the anteriorpituitary is increased due to loss of negative feedbackinhibition. The high levels of ACTH are responsible forthe adrenal hyperplasia and the increased secretion of theadrenal androgens, dehydroepiandrosterone andandrostenedione, which are responsible for the virilization ofthe external genitalia. 17-OH progesterone is thesteroid precursor just proximal to 21-hydroxylase and is alsoincreased because of the excessive drive to the

adrenal cortex by ACTH.5-alpha-reductase deficiency (choice A) in male fetuses willproduce normal differentiation of the internalreproductive tracts, but the external genitalia will befeminized. This is because testosterone needs to beconverted to dihydrotestosterone (by 5-alpha-reductase) inthe external genitalia and the prostate for normaldifferentiation into the male phenotype.

11-beta-hydroxylase deficiency (choice B) is another form ofcongenital adrenal hyperplasia. It is characterizedby salt retention due to excessive secretion by the inner zonesof the adrenal cortex of the weakmineralocorticoid, deoxycorticosterone. Again, the excessivedrive to the adrenal cortex is due to increasedACTH resulting from diminished negative feedbacksuppression by cortisol. The adrenal also secretes excessiveandrogens and virilization occurs in female fetuses.

17-alpha-hydroxylase deficiency (choice C) is another from ofcongenital adrenal hyperplasia that isaccompanied by salt retention. The high levels of ACTH drivethe adrenal cortex to secrete increased amountsof deoxycorticosterone and corticosterone, both of which haveweak mineralocorticoid activity. Without the abilityto 17-alpha-hydroxylate progesterone or pregnenolone,steroid-secreting cells cannot produce sex steroids.When 17-alpha-hydroxylase deficiency is present in theadrenal cortex, it is also present in the gonads. Hence,whether it occurs in a male or female fetus, sex steroid

production will be diminished. Female fetuses willdevelop normal reproductive tracts and genitalia since thesestructures are programmed in utero to"automatically" become female. Male fetuses, however, willhave their reproductive tracts and genitaliafeminized.

Complete androgen resistance (choice E) results infeminization of affected male fetuses. It is characterized byan XY genotypic male with phenotypically female externalgenitalia and a vagina that ends as a blind sac.


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Most of the testosterone secreted by the testes exists in theplasma in the form of

A. dihydrotestosterone bound to gonadal steroid-bindinghormone

B. free dihydrotestosterone

C. free testosterone

D. testosterone bound to albumin

E. testosterone bound to sex-steroid-binding globulin

Explanation:

The correct answer is E. The majority of circulatingtestosterone is bound to plasma protein (around 98%),rather than existing in free form (choice C). Of this, a majorityis bound to a specific sex (or gonadal)steroid-binding protein (choice E), and a minority is bound toalbumin (choice D). Dihydrotestosterone isproduced from testosterone in the tissues by a specificenzyme, 5-alpha-reductase, rather than circulating in

bound (choice A) or free (choice B) form.

Which of the following directly inhibits insulin secretion?

A. Alpha2-adrenergic agonist

B. Beta2-adrenergic agonist

C. Cholecystokinin

D. Glucagon

E. Ingestion of a high-sugar meal

F. Muscarinic agonists

Explanation:

The correct answer is A. Alpha2-receptor agonists directlyinhibit pancreatic insulin secretion.

Beta2-adrenergic agonists (choice B) stimulate insulinsecretion.

Cholecystokinin (choice C) is a hormone that not only causesgallbladder contraction, but also causes insulinsecretion from the pancreas.

Pancreatic glucagon (choice D) release acts as a paracrinestimulus for insulin secretion.

Ingestion of high-sugar meals (choice E) is a stimulus for thesecretion of insulin from the pancreas.

Muscarinic activity (choice F) in the GI tract enhancessecretion of insulin from the pancreas.

Endometrial biopsy demonstrates a thick endometrium withlong, coiled glands lined by a columnar epitheliumwith prominent cytoplasmic vacuoles adjacent to the gland


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lumen. Earlier in the menstrual cycle, the glands weremuch smaller and were lined with cells that did not havevacuoles. Which of the following hormones is primarilyresponsible for inducing this change in appearance?

A. Aldosterone

B. Cortisol

C. Estrogen

D. Progesterone

E. Thyroxine

Explanation:

The correct answer is D. The endometrial phase with smallglands is the proliferative phase; the one with largeglands with secretory cells is the secretory phase. Estrogen(choice C) is necessary for both phases, but it isthe addition of progesterone (choice D), secreted by thecorpus luteum after the Graafian follicle ruptures, thattriggers the switch from proliferative to secretory

endometrium.Glucocorticoids (choice B) and the mineralocorticoidaldosterone (choice A) are secreted by the adrenalglands. They do not produce the endometrial changesdescribed.

Thyroxine (choice E) is secreted by the thyroid gland, and isunrelated to the observed morphologic changes inthe endometrium.

A 55-year-old woman stopped menstruating approximately 3months ago. Worried that she may be pregnant, shedecided to have a pregnancy test. The test came backnegative. Which of the following series of tests resultswould confirm that the woman is postmenopausal?

A. Decreased LH, decreased FSH, increased estrogen

B. Decreased LH, increased FSH, decreased estrogen

C. Increased LH, decreased FSH, decreased estrogen

D. Increased LH, increased FSH, decreased estrogen

E. Increased LH, increased FSH, increased estrogen

Explanation:

The correct answer is D. During menopause, there is a loss offunctioning follicles in the ovaries such thatGnRH-stimulated LH and FSH secretion do not result innormal estrogen secretion. The low estrogen levelscannot inhibit gonadotropin secretion in a negative-feedbackfashion, resulting in very high levels of LH andFSH.

Choices A, B, C, and E do not accurately describe normalhormonal levels in menopause.


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Which of the following hormones is most important ininitiating gall bladder contraction?

A. Cholecystokinin (CCK)

B. Gastric inhibitory peptide (GIP)

C. Gastrin

D. Secretin

E. Vasoactive intestinal polypeptide (VIP)

Explanation:

The correct answer is A. Cholecystokinin, or CCK, issynthesized in the duodenal and jejunal mucosa andstimulates gall bladder contraction and pancreatic enzymesecretion. Other functions include slowing of gastricemptying, an atrophic effect on the pancreas, and secretion ofantral somatostatin, which in turn, decreasesgastric acid secretion.

Gastric inhibitory peptide, or GIP (choice B), stimulatespancreatic insulin secretion at physiologic doses andinhibits gastric acid secretion and gastric motility atpharmacologic doses.

Gastrin (choice C) prepares the stomach and small intestinefor food processing, including stimulating secretionof HCl, histamine, and pepsinogen. It also increases gastricblood flow, lower esophageal sphincter tone, andgastric contractions.

Secretin (choice D) stimulates secretion of bicarbonate-containing fluid from the pancreas and biliary ducts.

Vasoactive intestinal polypept ide, or VIP (choice E), relaxesintestinal smooth muscle and stimulates gutsecretion of water and electrolytes.

Maintenance of the corpus luteum during the first trimester ofpregnancy is accomplished principally by thesecretion of

A. antidiuretic hormone (ADH)

B. follicle stimulating hormone (FSH)

C. human chorionic gonadotropin (hCG)

D. luteinizing hormone (LH)

E. progesterone

Explanation:

The correct answer is C. The corpus luteum secretesestrogens, progesterone, and relaxin. hCG, secreted bythe syncytiotrophoblast lining the placental villi, maintains thecorpus luteum during the first trimester ofpregnancy.


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Antidiuretic hormone (vasopressin; choice A) does not play asignificant role during pregnancy.

FSH (choice B) acts on granulosa cells to promote theconversion of androstenedione to estradiol.

LH (choice D) acts on theca cells to promote androstenedionesecretion.

Progesterone (choice E) is important for maintaining thepregnancy, however, it does not act to maintain the

corpus luteum.

In the transition from a Graafian follicle to a functional corpusluteum, which of the following cellular eventsoccurs?

A. Granulosa cells begin to express aromatase

B. Granulosa cells begin to express FSH receptors

C. Granulosa cells begin to express LH receptors

D. Theca cells begin to express LH receptors

E. Theca cells begin to express side-chain cleavage enzyme

Explanation:

The correct answer is C. The secretion of estrogen by thedeveloping follicle can best be explained using the"two cell" hypothesis. Theca cells are stimulated by LH (thecacells express LH receptors prior to formation ofthe corpus luteum, choice D) to secrete the androgensandrostenedione and testosterone. The androgens thendiffuse into the granulosa cells, where they are aromatized toestrogens. Hence, theca cells express side-chaincleavage enzyme (first step in steroidogenesis) prior to theformation of the corpus luteum (choice E). FSHstimulates aromatase activity in the granulosa cells (receptorsfor FSH and aromatase enzyme are present priorto the formation of the corpus luteum, choices A and B). Thegranulosa cells apparently have the ability toproduce steroids (progesterone), but lack 17-hydroxylaseactivity and cannot synthesize estrogenthemselves. Only as the follicle approaches ovulation do LHreceptors begin to be expressed by the granulosacells. Estrogen and FSH probably are responsible for thechange. After ovulation, the scar of the follicleundergoes luteinization. The theca cells decrease17-hydroxylase activity and secrete moreprogesterone. The granulosa cells decrease aromatase activityand also secrete more progesterone.

Which of the following areas of the adrenal gland would youexpect to increase in activity in a patient subjected tosalt restriction?

A. Adrenal medulla

B. Zona fasciculata of the adrenal cortex

C. Zona glomerulosa of the adrenal cortex

D. Zona reticularis of the adrenal cortex


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Explanation:

The correct answer is C. This question requires you to equatesalt restriction with an increased synthesis ofaldosterone (aldosterone promotes sodium reabsorption) andthen to remember that aldosterone is produced inthe zona glomerulosa of the adrenal cortex. The zonaglomerulosa is the outermost layer of the adrenal cortex.

The adrenal medulla (choice A) secretes catecholamines.

The zona fasciculata (choice B) is the middle layer of theadrenal cortex. It primarily secretes glucocorticoids.

The zona reticularis (choice D) is the innermost layer of theadrenal cortex. It primarily secretes androgens suchas dehydroepiandrosterone (DHEA).

A series of photographs taken of a middle-aged man over aperiod of two decades demonstrates gradualcoarsening of facial features and progressive protrusion of the

brows. Upon questioning, the patient reportshaving to wear larger shoes than he did as a young man.Which of the following pair of hormones regulates thehormone responsible for these changes?

A. Dopamine and norepinephrine

B. LH and hCG

C. Prolactin and FSH

D. Somatostatin and GHRH

E. TSH and ACTH

Explanation:

The correct answer is D. The disease is acromegaly, which istypically produced by a growth hormone-secretingpituitary adenoma. Growth hormone synthesis ispredominately regulated by hypothalamic GHRH (growthhormone releasing hormone), and its pulsatile secretion ispredominately regulated by hypothalamicsomatostatin.

Dopamine and norepinephrine (choice A) are catecholaminesthat regulate smooth muscle tone and cardiacfunction.

Choice B is incorrect because luteinizing hormone (LH)regulates sex steroid hormone production by bothtestes and ovaries; human chorionic gonadotropin (hCG) isproduced by the placenta and has actions similar toLH.

Choice C is incorrect because prolactin regulates menstruationand lactation, while follicle stimulating hormone(FSH) regulates ovarian and testicular function.

Choice E is incorrect because thyroid stimulating hormone(TSH) regulates secretion of thyroid hormones andadrenocorticotropin (ACTH) regulates glucocorticoid secretion.


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A normal, healthy, 24-year-old woman has regular menstrualcycles, each lasting about 28 days. Daily serumsamples from the woman reveal decreasing progesterone and17--estradiol levels. Serum LH and FSHlevels are low, and begin rising. Basal body temperaturebegins falling. Within three days, which of the followingevents would be expected to occur?

A. Markedly increased inhibin levels

B. Menstruation

C. Ovulation

D. Rapidly decreased LH levels

E. Significantly increased basal body temperature

Explanation:

The correct answer is B. A typical menstrual cycle lasts around26-30 days. The luteal phase (post-ovulation)

generally lasts fourteen days; the length of the follicularphase (pre-ovulation) is far more variable, andaccounts for most of the variability observed in the length ofthe menstrual cycle. Just before menstruation, sexsteroid levels are low, but gonadotropin levels (especiallyFSH) begin rising slightly. Basal body temperatureremains high during the luteal phase of the menstrual cycle,but falls precipitously a few days before the onsetof menstruation.

Markedly increased inhibin levels (choice A) are seen in themiddle of the luteal phase, dropping to low levels

just before menstruation.

LH levels peak approximately 36 hours before ovulation(choice C), then decrease rapidly (choice D) within afew days to a low level during the mid-luteal phase, graduallydecreasing until menstruation.

The basal body temperature significantly increases (choice E)shortly after ovulation, due to the metaboliceffects of progesterone produced by the corpus luteum.

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* Re:GI and ENdo

#508543 surgeon1982 - 10/15/06 19:35

Thanks nishi very nice review of subjects

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