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Questions and Answers
What primarily causes the formation of peptic ulcers?
Which type of drug is primarily used to suppress gastric acid production?
Which of the following is NOT considered a defensive factor in the stomach lining?
What is the main goal of drug therapy for peptic ulcers?
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How do mucosal protectants function in the treatment of peptic ulcers?
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Which of the following statements about prostaglandins is true?
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Which category of drugs includes agents that neutralize existing stomach acid?
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What major imbalance leads to the formation of peptic ulcers?
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What is a common side effect of both Metronidazole and Tinidazole?
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Which antibiotic combination includes a Proton Pump Inhibitor (PPI)?
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What is the main mechanism of action (MOA) of H2 Receptor Antagonists (H2RAs)?
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Which drug is NOT a common H2 Receptor Antagonist?
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Which of the following statements about Cimetidine is true?
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What type of reaction occurs when Tinidazole is combined with alcohol?
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What effect does food have on the absorption of Cimetidine?
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Which of the following is a risk associated with Cimetidine's use?
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Which drug is primarily used to block neurokinin-1 (NK1) receptors?
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What is the primary mechanism of action of proton pump inhibitors (PPIs)?
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What is a common side effect of serotonin receptor antagonists?
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In which scenario is Ondansetron particularly cautioned against due to its formulation?
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Which condition is NOT an indication for the use of PPIs?
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Which of the following correctly pairs a receptor type with its corresponding blocker?
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What is a potential adverse effect associated with long-term use of PPIs?
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What is the primary therapeutic use of Aprepitant (Emend)?
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What adverse effect is specifically associated with sudden discontinuation of PPIs?
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Which common side effect is associated with dopamine antagonists like Prochlorperazine?
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Which of the following drugs may have its absorption reduced when taken with sucralfate?
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What is the mechanism of action of misoprostol?
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What is the mechanism of action of serotonin receptor antagonists?
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Which drug causes anticholinergic effects and should be used cautiously in certain populations?
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What is one of the serious risks associated with long-term PPI therapy?
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Why should antacids be administered at least 30 minutes apart from sucralfate?
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What is a significant risk associated with the use of promethazine in children under 2?
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What is the primary mechanism of action of scopolamine?
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Which of the following is NOT a common side effect of scopolamine?
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Which of the following antihistamines is primarily used for motion sickness?
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What is a rare but serious risk associated with loperamide use?
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How does loperamide primarily exert its effect in treating diarrhea?
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Which condition is directly caused by H.pylori infection?
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Nonsteroidal anti-inflammatory drugs (NSAIDs) can lead to ulcers primarily due to their effect on:
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Study Notes
Peptic Ulcer Disease (PUD) Overview
- Peptic ulcers are open sores in the esophagus, stomach, or small intestine.
- They develop when the protective mucus lining is compromised, allowing stomach acid to damage tissue.
- Most ulcers occur in the stomach's lesser curvature and the duodenum.
- Most ulcers are caused by Helicobacter pylori (H. pylori) infection, which weakens the mucus layer.
Goals of Drug Therapy
- Alleviate symptoms such as pain and discomfort.
- Promote ulcer healing by reducing acid production and strengthening protective mechanisms.
- Prevent complications like bleeding or perforation.
- Reduce ulcer recurrence by eradicating H. pylori and maintaining adequate protection.
Categories of Drugs for PUD
- Antibiotics: Target and eradicate H. pylori.
-
Antisecretory Agents:
- Proton Pump Inhibitors (PPIs): Suppress gastric acid production.
- Histamine-2 Receptor Blockers (H2 blockers): Reduce stomach acid secretion.
- Mucosal Protectants: Form a protective barrier over the ulcer.
- Antisecretory Agents Enhancing Mucosal Defenses: Boost the body's natural defenses.
- Antacids: Neutralize existing stomach acid for immediate relief.
Development of Peptic Ulcers: Defensive vs. Aggressive Factors
- Peptic ulcers form when defensive factors (protecting the stomach lining) are overwhelmed by aggressive factors (damaging the stomach lining).
- Defensive factors include mucus, bicarbonate, and prostaglandins.
- Mucus: Forms a protective barrier.
- Bicarbonate: Neutralizes stomach acid.
- Prostaglandins: Stimulate mucus and bicarbonate production, promote blood flow to the stomach.
Prostaglandins: Side Effects
- Side Effects: Headache, nausea, and a disulfiram-like reaction with alcohol (not safe in pregnancy).
Antibiotic Combinations
-
Clarithromycin-Based Triple Therapy (PAC)/PMC if allergic to A:
- P: PPI (e.g., omeprazole)
- A: Amoxicillin
- C: Clarithromycin
-
Bismuth-Based Quadruple Therapy (BMPT):
- B: Bismuth
- M: Metronidazole
- P: PPI
- T: Tetracycline
-
Sequential Therapy (5+5):
- First 5 days: PPI + Amoxicillin
- Next 5 days: PPI + Clarithromycin + Tinidazole
H2 Receptor Antagonists (H2RAs)
- MOA: H2RAs promote ulcer healing by suppressing gastric acid secretion.
- Common Drugs: Cimetidine, ranitidine, famotidine, nizatidine.
Cimetidine Key Points
- Routes: Oral, intramuscular (IM), or intravenous (IV).
- Absorption: Food slows absorption but prolongs effects.
- Crosses the blood-brain barrier (BBB): Can cause central nervous system (CNS) side effects.
- Elimination: Mostly excreted intact in urine. Dosage should be reduced in patients with renal impairment.
Cimetidine Safety Points
- CNS Effects: Confusion, hallucinations, CNS depression/excitation, especially in older adults or those with renal/hepatic impairment.
- Antiandrogenic Effects: Gynecomastia, reduced libido, and impotence.
- Pneumonia Risk: Increased risk of pneumonia due to reduced gastric acidity.
- Drug Interactions: Inhibits liver enzymes, increasing levels of drugs like warfarin, phenytoin, theophylline, and lidocaine.
- Antacids: Decrease absorption of cimetidine---administer at least 1 hour apart.
Proton Pump Inhibitors (PPIs)
- Most effective drugs for suppressing gastric acid secretion.
- Indications: Gastric/duodenal ulcers, GERD, Zollinger-Ellison syndrome.
- Mechanism of Action: Irreversibly inhibits the proton pump (H+/K+-ATPase) in stomach parietal cells, blocking acid production.
- Common Drugs: Omeprazole (prototype).
- Administration: Short-term use (4-8 weeks) for ulcers and GERD; long-term use for hypersecretory conditions.
Adverse Effects of PPIs
- Pneumonia: Increased risk during the first few days of therapy.
- Fractures: Long-term use can reduce calcium absorption, increasing fracture risk.
- Rebound Acid Hypersecretion: Sudden discontinuation can cause excessive acid production.
- Hypomagnesemia: Long-term use may reduce magnesium levels.
- C.difficile Infection: Increased risk of severe diarrhea due to Clostridium difficile infection.
"PPIs Have Real Danger" Summary
- P: Pneumonia (increased risk)
- P: Poor bone health (fractures and osteoporosis)
- H: Hypomagnesemia (low magnesium)
- R: Rebound acid hypersecretion
- D: Diarrhea (C.difficile infection risk)
Drug Interactions with PPIs
- Reduces absorption of some HIV drugs (atazanavir, nelfinavir) and antifungals (ketoconazole, itraconazole).
- May reduce the beneficial antiplatelet effects of clopidogrel.
Sucralfate Key Points
- Mechanism of Action (MOA): Sucralfate forms a sticky gel in acidic conditions (pH < 4) that adheres to the ulcer crater, creating a protective barrier against acid, pepsin, and bile salts.
- Drug-Drug Interactions:
- Antacids: Can interfere with sucralfate's action---administer at least 30 minutes apart.
- Other drugs: May reduce absorption of drugs like phenytoin, digoxin, warfarin, theophylline, and fluoroquinolones---administer at least 2 hours apart.
Misoprostol Key Points
- Mechanism of Action (MOA): Misoprostol is a prostaglandin analog that replaces the protective prostaglandins inhibited by NSAIDs.
Anti-Emetic Drugs
- Glucocorticoid receptors: Blocked by dexamethasone.
- Neurokinin-1 (NK1) receptors: Blocked by aprepitant (Emend).
- Dopamine receptors: Blocked by prochlorperazine.
- Histamine (H1) receptors: Blocked by dimenhydrinate.
- Acetylcholine (muscarinic) receptors: Blocked by scopolamine.
Serotonin Receptor Antagonists
- Mechanism of Action: Blocks 5-HT3 (serotonin) receptors in the CTZ and on vagal neurons in the GI tract.
- Uses: Chemotherapy-induced nausea and vomiting (CINV), nausea from radiation, anesthesia, viral gastritis, and pregnancy.
- Common Drugs: Ondansetron (Zofran), granisetron, dolasetron, palonosetron.
Key Side Effects of Serotonin Receptor Antagonists
- Most common: Headache, diarrhea, and dizziness.
- Serious: Prolongs the QT interval (risk of torsades de pointes). Use cautiously in patients with electrolyte imbalances, heart failure, or those on other QT-prolonging drugs.
- Avoid ondansetron ODT in patients with phenylketonuria (PKU) due to the presence of aspartame.
Aprepitant (Emend) Key Points
- Mechanism of Action: Blocks neurokinin-1 (NK1) receptors in the CTZ, preventing substance P from triggering nausea and vomiting
- Uses: Primarily for preventing chemotherapy-induced nausea and vomiting (CINV) and postoperative nausea.
- Duration: Long-acting; useful for both acute and delayed CINV
- Adverse Effects: Fatigue, hiccups, dizziness, and diarrhea.
Dopamine Antagonists (Phenothiazines) Key Points
- Mechanism of Action: Block dopamine-2 receptors in the CTZ to suppress nausea and vomiting.
- Uses: Surgery, chemotherapy, and toxins.
- Common Drugs: Prochlorperazine, promethazine (Phenergan).
Key Side Effects of Dopamine Antagonists
- Extrapyramidal reactions (EPS), anticholinergic effects, hypotension, and sedation.
- Contraindications:
- Avoid in patients with Parkinson's disease (worsens motor symptoms).
- Caution with lithium due to increased risk of EPS.
Promethazine Black Box Warning
- Risk of respiratory depression (contraindicated in children under 2).
- Risk of tissue injury with IV use, including necrosis and gangrene.
Scopolamine Key Points
- Class: Muscarinic antagonist.
- Mechanism of Action: Suppresses nerve traffic between the vestibular apparatus and the vomiting center, preventing motion sickness.
- Uses: Prevention and treatment of motion sickness (best when used prophylactically)
- Common Side Effects: Dry mouth, blurred vision, and drowsiness.
- More Severe Side Effects: Urinary retention, constipation, and disorientation.
- Administration: Oral, subcutaneous, and transdermal patches (transdermal has less intense anticholinergic effects).
Antihistamines for Motion Sickness Key Points
- Common Drugs: Dimenhydrinate (Dramamine), meclizine (Antivert), cyclizine (Cyclivert).
- Mechanism of Action: Block H1 (histamine) receptors and muscarinic cholinergic receptors in the pathway between the inner ear and the vomiting center.
- Side Effects:
- Sedation (from H1 receptor blockade).
- Dry mouth, blurred vision, urinary retention, and constipation (from muscarinic receptor blockade).
- Effectiveness: Less effective than scopolamine for motion sickness.
Loperamide (Imodium) - Anti-Diarrheal Key Points
- Class: Structural analog of meperidine.
- Mechanism of Action: Suppresses bowel motility and reduces fluid secretion into the intestines.
- Uses: Treats diarrhea and reduces discharge from ileostomies.
- Safety: Poorly absorbed, does not cross the blood-brain barrier, and has no potential for abuse.
- Rare Risks: May cause toxic megacolon or colon dilation, especially in patients with inflammatory bowel disease (IBD).
Notable Terms
- H.pylori: A bacterium that causes ulcers.
- NSAIDs: Nonsteroidal anti-inflammatory drugs that can cause ulcers.
- Prostaglandins: Compounds that protect the stomach lining.
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Description
Explore the fundamentals of Peptic Ulcer Disease (PUD), including its causes, symptoms, and the therapeutic goals for drug treatment. This quiz covers the various categories of medications used to alleviate ulcer-related pain, promote healing, and prevent complications. Test your knowledge on the role of medications like antibiotics and antisecretory agents in managing PUD.
