Gastrointestinal Drugs Quiz

Gastrointestinal Drugs

• Gastroesophageal Reflux Disease (GERD) occurs when stomach acid and pepsin flow back into the esophagus, often called heartburn.
• Causes of GERD include overproduction of acid/pepsin and over-relaxation of the lower esophageal sphincter (LES).
• Peptic Ulcer Disease is a benign lesion of the gastric or duodenal mucosa.
• Causes of PUD include excess acid production and an intrinsic defect in the mucosal defense barrier.
• Helicobacter pylori (H. pylori) infection is a significant cause of peptic ulcers.
• Not all individuals infected with H. pylori develop ulcers.
• H. pylori can weaken the mucosal defense system, leading to ulcer development.
• Nonsteroidal anti-inflammatory drugs (NSAIDs) can contribute to PUD by blocking COX enzymes and decreasing prostaglandins.
• Gastrinoma (Zollinger-Ellison Syndrome) involves tumors in the duodenum or pancreas, secreting excessive gastrin, which stimulates gastric acid.
• Stress ulcers result from physical trauma like severe burns.

Strategies for Protecting Gastric Mucosa from Acid Exposure

• Mechanisms to protect the gastric mucosa from acid exposure include inhibiting acid secretion, preventing direct contact with acid, and neutralizing the acid.
• Medications like cimetidine, omeprazole, prostaglandin antagonists, and muscarinic antagonists target acid secretion.
• Sucralfate forms a protective barrier by adhering to the gastric mucosa. Antacids neutralize the acid.
• Multiple mechanisms, including hormonal (gastrin), paracrine (histamine), and neural (acetylcholine), regulate gastric acid production.
• Gastrin, histamine, and acetylcholine stimulate gastric acid secretion, utilizing specific pathways.

Strategies for Inhibiting Parietal Cell Acid Secretion

• Gastrin antagonists, histamine antagonists, and muscarinic antagonists inhibit acid secretion mediated by different pathways.
• These drugs decrease the stimulation for Parietal cells to produce acid.
• Proton pump inhibitors (PPIs) like omeprazole irreversibly inhibit the H+, K+-ATPase, the enzyme responsible for transporting hydrogen ions into the stomach.
• Omeprazole needs a low pH to be active.
• It leads to profound acid suppression, significantly raising gastric pH.
• Omeprazole is highly protein-bound and metabolized by specific enzymes (CYP2C & CYP3A).
• Esomeprazole, a derivative of omeprazole, is an effective H+, K+-ATPase inhibitor.
• Different forms of H+, K+-ATPase inhibitors exist (e.g., rabeprazole, lansoprazole, pantoprazole).
• Pantoprazole is acid-stable and can be administered intravenously.
• PPIs are well-tolerated, although potential side effects include hypergastrinemia and, rarely, nausea, headaches, or skin rashes.

Histamine H₂ Antagonists

• Cimetidine, ranitidine, famotidine, and nizatidine are examples of histamine H₂ antagonists.
• These drugs reduce acid secretion.

Antacids

• Antacids are weak bases that neutralize stomach acid (HCl).
• Common antacids include magnesium hydroxide, magnesium trisilicate, magnesium-aluminum mixtures, calcium carbonate, and sodium bicarbonate.
• Antacids differ in their onset and duration of action.
• Some may cause systemic alkalosis.

Sucralfate

• Sucralfate is an aluminum salt of sucrose octasulfate.
• In acidic environments, it forms a protective layer on the gastric and duodenal mucosa.
• This黏附黏稠物質 helps protect against further damage, especially to damaged areas of the GI tract.

Role of H. pylori in Peptic Ulcer Disease

• If H. pylori infection is identified, treatment focuses on eradicating the bacteria and inhibiting acid production.
• A common treatment approach includes combining Omeprazole with Amoxicillin.

Functional Disorders of the GI Tract

• Primary functional disorders are due to infection, inflammation, or congenital issues in neuronal/muscular activity.
• Secondary disorders are associated with metabolism issues (e.g., hypo-hyperparathyroidism, hypercalcemia), neurologic disorders (e.g., diabetes mellitus), nerve damage, or other factors (e.g., MS, heavy metal toxicity, or carcinoma).

Prokinetic Drugs

• Used to improve GI motility, assisting materials through the GI tract.
• They boost neuro-muscular signaling and promote transit.
• Common indications include GERD, gastroparesis, nighttime heartburn, and severe refractory constipation.
• Drugs like Metoclopramide and Domperidone are often used.
• Metoclopramide is an antiemetic that enhances gastric emptying but has a potential for side effects.
• Metoclopramide can increase nervous activity and potentially cross the blood–brain barrier.
• Domperidone also enhances gastric emptying, but it lacks efficacy in specific situations like GERD and may have side effects.
• Domperidone largely stays in the digestive tract, minimizing crossing to the brain.

Anti-emetics

• Address nausea and vomiting.
• These medications work at specific receptor sites to reduce nausea and vomiting signals.
• Classified as prokinetics, 5-HT3 antagonists, antimuscarinics, H1 antihistamines, or neuroleptics.
• Specific drugs for motion sickness, cancer-related vomiting, and post-operative conditions.

Laxatives

• Used for constipation relief.
• Types include osmotic, stimulant, and bulk-forming laxatives or cathartics.
• Bulk-forming laxatives add bulk to stools, promoting easier passage.
• Other types act on bowel muscles to increase contractions.

Diarrhea

• Characterized by three or more loose stools per day.
• Often caused by infection with viruses, bacteria, or parasites (gastroenteritis).
• Can be caused from food or water contaminated with fecal material.
• Treatment often involves replacing lost fluids and electrolytes, using oral rehydration salts (ORS).
• Antidiarrheal medications reduce bowel movements.
• These can include antimotility drugs (e.g., codeine, diphenoxylate, loperamide) or agents targeting certain specific receptors and mechanisms (e.g., bismuth subsalicylate, cholestyramine).