Question#13 Which of the following statements is FAlSE? A.2rec or antagonists can diminish gastric acid secretion in response to acetylcholine,gastrin or histamine B.The effects of omeprazole on gastric acid secretion are more long lasting than the effects of H2 receptor antagonists. C.The rate of HCl secretion during the cephalic phase can be quite high.but the anount of bCl secreted isa small fraction of the total secreted in response toa meal D.Distention of the body and fundus elicit reflexes that inhibit HCl secretion. E.Low pH in the antrum dramatically inhibits HCI secretion in response to all stimuli. Question 14 Which of the following statements is NOT true? A Secretion of both and bicarb e is vital for the function of the gastric mcosal barrie B.Some of the stimuli that enhance HCI secretion by parietal cells also stimlate chief cells to releas pepsinogens. C.12 histamine receptor antagonists and blockers of the Kt,H-ATPase are equally effective in suppressing gastric HCl secretion. D.An acid-loving bacteriu my play an imortant role in gastric ulcer disease in mny cases E.Patientswith duodenal ulcers tend tobe less sensitive to secretin and other horones that are release by the duodenum and inhibit HCI secretion. Question #15 Which of the following statements is FALSE? tion of duodenal ulcers B.H pylori is responsible for st pepticers that are not caused by edication C.H.pylori damages the gastric mucosa by invading the gastric epithelial cells. D.Aspirin and other nonsteroidal anti-inflanmatory drugs diminish the effectiveness of the gastric wcosal barrier. ELong ter therapyith antagonistil not peranently cureulcers due to H.pylor Answer: 1.B2.B3.A4.A5.A6.B7.A8.A9.E10.C 11.C12.E13.D14.C15.C Pancreatic Secretions Question#1 During the cephalie phase,pancreatic secretion is stimulated by CCK released from the duodenal mcosaQuestion # 13 Which of the following statements is FALSE? A. H2 receptor antagonists can diminish gastric acid secretion in response to acetylcholine, gastrin, or histamine. B. The effects of omeprazole on gastric acid secretion are more long lasting than the effects of H2 receptor antagonists. C. The rate of HCl secretion during the cephalic phase can be quite high, but the amount of HCl secreted is a small fraction of the total secreted in response to a meal. D. Distention of the body and fundus elicit reflexes that inhibit HCl secretion. E. Low pH in the antrum dramatically inhibits HCl secretion in response to all stimuli. -------------------------------------------------------------------------------- Question # 14 Which of the following statements is NOT true? A. Secretion of both mucus and bicarbonate is vital for the function of the gastric mucosal barrier. B. Some of the stimuli that enhance HCl secretion by parietal cells also stimulate chief cells to release pepsinogens. C. H2 histamine receptor antagonists and blockers of the K+,H+-ATPase are equally effective in suppressing gastric HCl secretion. D. An acid-loving bacterium may play an important role in gastric ulcer disease in many cases. E. Patients with duodenal ulcers tend to be less sensitive to secretin and other hormones that are released by the duodenum and inhibit HCl secretion. -------------------------------------------------------------------------------- Question # 15 Which of the following statements is FALSE? A. Hypersecretion of HCl conduces to formation of duodenal ulcers. B. H. pylori is responsible for most peptic ulcers that are not caused by medication. C. H. pylori damages the gastric mucosa by invading the gastric epithelial cells. D. Aspirin and other nonsteroidal anti-inflammatory drugs diminish the effectiveness of the gastric mucosal barrier. E. Long term therapy with omeprazole or an H2 receptor antagonist will not permanently cure ulcers due to H. pylori. ----------------------------------------------------------------------------------- Answer： 1.B 2.B 3.A 4.A 5.A 6.B 7.A 8.A 9.E 10.C 11.C 12.E 13.D 14.C 15.C Pancreatic Secretions Question # 1 During the cephalic phase, pancreatic secretion is stimulated by CCK released from the duodenal mucosa