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Questions and Answers
What is the primary mechanism of action for sucralfate in treating peptic ulcer disease?
What is the primary mechanism of action for sucralfate in treating peptic ulcer disease?
- Enhances mucosal barrier through prostaglandin synthesis (correct)
- Inhibits gastric acid secretion
- Stimulates gastric emptying
- Directly neutralizes stomach acid
Which side effect is commonly associated with sucralfate?
Which side effect is commonly associated with sucralfate?
- Constipation (correct)
- Hypercalcemia
- Flatulence
- Diarrhea
Bismuth subsalicylate has several roles in treatment. Which of the following is NOT one of them?
Bismuth subsalicylate has several roles in treatment. Which of the following is NOT one of them?
- Binding intestinal toxins
- Inhibiting intestinal motility
- Being part of quadruple therapy for H. pylori
- Stimulating gastric mucosal barrier (correct)
Why should sucralfate not be taken with antacids, H2 blockers, or proton pump inhibitors?
Why should sucralfate not be taken with antacids, H2 blockers, or proton pump inhibitors?
In patients taking sucralfate, when should other medications be administered to avoid interference?
In patients taking sucralfate, when should other medications be administered to avoid interference?
What is the likely reason for the patient's elevated PT levels?
What is the likely reason for the patient's elevated PT levels?
Which of the following medications can lead to gynecomastia?
Which of the following medications can lead to gynecomastia?
What is the mechanism of action of H2 receptor blockers?
What is the mechanism of action of H2 receptor blockers?
Which clinical condition is NOT typically treated with H2 receptor blockers?
Which clinical condition is NOT typically treated with H2 receptor blockers?
What symptom did the 59-year-old man present with that is suggestive of a gastric ulcer?
What symptom did the 59-year-old man present with that is suggestive of a gastric ulcer?
Which of the following side effects is specifically associated with cimetidine?
Which of the following side effects is specifically associated with cimetidine?
What lifestyle factors are relevant in assessing the 59-year-old man's condition?
What lifestyle factors are relevant in assessing the 59-year-old man's condition?
What is one of the primary effects of prochlorperazine when used as an anti-emetic agent?
What is one of the primary effects of prochlorperazine when used as an anti-emetic agent?
Which of the following is a common side effect associated with prochlorperazine and metoclopramide?
Which of the following is a common side effect associated with prochlorperazine and metoclopramide?
What is the mechanism of action for bulking laxatives?
What is the mechanism of action for bulking laxatives?
Lactulose is indicated for which of the following clinical uses?
Lactulose is indicated for which of the following clinical uses?
Which of these medications is considered a stimulant laxative?
Which of these medications is considered a stimulant laxative?
What is a common side effect of laxatives?
What is a common side effect of laxatives?
Which clinical scenario best describes the use of stool softeners?
Which clinical scenario best describes the use of stool softeners?
What activity does prochlorperazine inhibit that leads to its anti-emetic effect?
What activity does prochlorperazine inhibit that leads to its anti-emetic effect?
What is one reason an 82-year-old woman may experience constipation?
What is one reason an 82-year-old woman may experience constipation?
What is the primary mechanism by which lactulose improves encephalopathy associated with hyperammonemia?
What is the primary mechanism by which lactulose improves encephalopathy associated with hyperammonemia?
What side effect is commonly associated with the use of lactulose?
What side effect is commonly associated with the use of lactulose?
What is the action of rifaximin in treating hepatic encephalopathy?
What is the action of rifaximin in treating hepatic encephalopathy?
Which of the following is NOT a clinical use of lactulose?
Which of the following is NOT a clinical use of lactulose?
What condition is a 54-year-old man with a history of alcoholic cirrhosis AT RISK for, as suggested by his symptoms?
What condition is a 54-year-old man with a history of alcoholic cirrhosis AT RISK for, as suggested by his symptoms?
Which of the following drugs is effective for treating simple traveler's diarrhea?
Which of the following drugs is effective for treating simple traveler's diarrhea?
What are the common side effects of rifaximin?
What are the common side effects of rifaximin?
What indicates a significant change in a patient when using lactulose?
What indicates a significant change in a patient when using lactulose?
Which physical exam finding is indicative of hepatic encephalopathy?
Which physical exam finding is indicative of hepatic encephalopathy?
Flashcards
What are gastric mucosal protective agents?
What are gastric mucosal protective agents?
Gastric mucosal protective agents are drugs that help protect the stomach lining from damage, often by promoting prostaglandin synthesis.
How does sucralfate work and what to avoid when taking it?
How does sucralfate work and what to avoid when taking it?
Sucralfate acts as a barrier against stomach acid, but requires an acidic environment to work. It can be taken with PPIs, but should not be taken with antacids or H2 blockers.
What are the actions of bismuth subsalicylate?
What are the actions of bismuth subsalicylate?
Bismuth subsalicylate has multiple actions, including reducing intestinal motility, binding intestinal toxins, and stimulating fluid absorption. It can also be used as an anti-diarrheal medication and in quadruple therapy for H. pylori infections.
What are the common side effects of bismuth subsalicylate?
What are the common side effects of bismuth subsalicylate?
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What are the clinical uses of gastric mucosal protective agents?
What are the clinical uses of gastric mucosal protective agents?
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What is the mechanism of action for H2 receptor blockers?
What is the mechanism of action for H2 receptor blockers?
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List four examples of H2 receptor blockers.
List four examples of H2 receptor blockers.
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What are the clinical uses of H2 receptor blockers?
What are the clinical uses of H2 receptor blockers?
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What are some side effects of H2 receptor blockers?
What are some side effects of H2 receptor blockers?
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How can H2 receptor blockers affect drug interactions?
How can H2 receptor blockers affect drug interactions?
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What is peptic ulcer disease?
What is peptic ulcer disease?
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Describe a patient with potential peptic ulcer disease.
Describe a patient with potential peptic ulcer disease.
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What is the mechanism of action of prochlorperazine and what are its other actions?
What is the mechanism of action of prochlorperazine and what are its other actions?
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What are the common side effects of prochlorperazine?
What are the common side effects of prochlorperazine?
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What are laxatives and how do they work?
What are laxatives and how do they work?
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How do irritant or stimulant laxatives work?
How do irritant or stimulant laxatives work?
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How do bulking laxatives work?
How do bulking laxatives work?
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How do stool softeners work?
How do stool softeners work?
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What are the clinical uses of laxatives?
What are the clinical uses of laxatives?
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What are the common side effects of laxatives?
What are the common side effects of laxatives?
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What is another clinical use of lactulose?
What is another clinical use of lactulose?
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Hepatic Encephalopathy
Hepatic Encephalopathy
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Lactulose
Lactulose
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How does Lactulose work?
How does Lactulose work?
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Rifaximin
Rifaximin
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How does Rifaximin work?
How does Rifaximin work?
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Cirrhosis
Cirrhosis
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Asterixis
Asterixis
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Jaundice
Jaundice
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Hyperammonemia
Hyperammonemia
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Study Notes
Gastrointestinal Agents
- Agents used to treat peptic ulcer disease include antacids, mucosal protective agents, H₂ receptor blockers, and proton pump inhibitors
- Anti-emetics include ondansetron and metoclopramide
- Other gastrointestinal agents include laxatives, anti-diarrheal agents, and others
Mechanism of Gastric Acid Secretion
- Gastric parietal cells contain carbonic anhydrase, which converts CO2 and H2O into H⁺ and HCO3⁻
- Bicarbonate (HCO3⁻) is exchanged for chloride (Cl⁻) into the bloodstream
- Hydrogen (H⁺) is pumped out of the parietal cell by H⁺/K⁺ ATPase, and chloride follows
- H⁺ and Cl⁻ form hydrochloric acid (HCl) in the stomach lumen
Regulation of Gastric Acid Secretion
- Gastrin stimulates H⁺ secretion by interacting with an uncharacterized receptor
- Histamine stimulates acid secretion by activating H₂ receptors, leading to increased cyclic AMP
- The vagus nerve stimulates acid secretion via M3 receptors on parietal cells and G cells
- Chyme and low pH inhibit gastrin secretion and acid secretion
Antacids
- Antacids are weak bases that react with gastric hydrochloric acid to increase pH and reduce acidity
- Antacids inactivate pepsin, decreasing protein breakdown
- Some antacids may stimulate prostaglandin synthesis, increasing the mucosal barrier
Mucosal Protective Agents
- Sucralfate is believed to enhance the mucosal barrier by either stimulating prostaglandin synthesis or acting as a physical barrier
- Bismuth subsalicylate inhibits intestinal motility, binds toxins, and stimulates fluid absorption
H₂ Receptor Blockers
- H₂ receptor blockers (ranitidine, cimetidine, famotidine, nizatidine) reversibly block histamine binding to H₂ receptors on parietal cells
- This inhibits cyclic AMP and decreases the activity of the H⁺/K⁺ proton pump, reducing gastric acid secretion
Proton Pump Inhibitors
- Proton pump inhibitors (omeprazole, lansoprazole, pantoprazole, esomeprazole, rabeprazole, dexlansoprazole) irreversibly inhibit the H⁺/K⁺ ATPase pump
- This suppresses gastric acid secretion
Ondansetron
- Ondansetron blocks 5-HT3 receptors in the chemoreceptor trigger zone and GI tract, inhibiting activation of the vomiting reflex pathway
- Treatment for nausea and vomiting
Metoclopramide
- Metoclopramide is a dopamine receptor antagonist, stimulating gastric and small intestinal motility
- It treats diabetic gastroparesis and is an anti-emetic
Laxatives
- Bulking laxatives (lactulose, sorbitol, polyethylene glycol, magnesium salts) increase intestinal motility by drawing water into the intestine
- Irritants or stimulants (Castor oil, senna, bisacodyl) increase intestinal peristalsis through mucosal irritation or stimulation
Lactulose
- Lactulose is degraded by bacteria into lactic acid and acetic acid, which increase gut pH and promote nitrogen excretion, improving hepatic encephalopathy
- Treatment for hepatic encephalopathy
Anti-diarrheal Agents
- Diphenoxylate and loperamide bind to opioid receptors in the intestine, inhibiting acetylcholine release and decreasing gut peristalsis
- Treatment of diarrhea
Sulfasalazine
- Bacteria in the colon metabolize sulfasalazine into sulfapyridine and 5-ASA
- 5-ASA is an anti-inflammatory, inhibiting prostaglandin and leukotriene production, preventing further mucosal damage
Ursodiol
- Ursodiol decreases cholesterol gallstones by inhibiting cholesterol synthesis, decreasing intestinal reabsorption of cholesterol, and inhibiting cholesterol secretion into bile
- Treatment for primary biliary cirrhosis and cholesterol gallstones
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