Gastrointestinal Drugs Overview

<p>Neutralizing hydrochloric acid (B)</p> Signup and view all the answers

<p>Inhibiting acetylcholine's action on parietal cells (A)</p> Signup and view all the answers

<p>Increasing neuromuscular transmission (A)</p> Signup and view all the answers

<p>Sedation (D)</p> Signup and view all the answers

<p>Does not cross the blood-brain barrier (C)</p> Signup and view all the answers

<p>Omeprazole and Amoxycillin (D)</p> Signup and view all the answers

<p>Direct alkaline buffering (D)</p> Signup and view all the answers

<p>Prokinetic drugs (B)</p> Signup and view all the answers

<p>5-HT3 antagonists (A)</p> Signup and view all the answers

<p>Increased motility (A)</p> Signup and view all the answers

<p>Inhibition of H+, K+-ATPase (C)</p> Signup and view all the answers

<p>Diarrhea (B)</p> Signup and view all the answers

<p>Inhibits basal and nocturnal acid secretion (D)</p> Signup and view all the answers

<p>Lower risk of drug interactions (C)</p> Signup and view all the answers

<p>Stimulate bicarbonate secretion (D)</p> Signup and view all the answers

<p>Rapid (B)</p> Signup and view all the answers

<p>Mydriasis (D)</p> Signup and view all the answers

<p>Less frequent dosing (B)</p> Signup and view all the answers

<p>Cyclazine (B)</p> Signup and view all the answers

<p>Alter motility of the intestines (D)</p> Signup and view all the answers

<p>They neutralize HCl by raising gastric pH (B)</p> Signup and view all the answers

<p>Ibuprofen use (A)</p> Signup and view all the answers

<p>Immediate inhibition of proton pumps (B)</p> Signup and view all the answers

<p>Sodium chloride (C)</p> Signup and view all the answers

<p>Enhance retention of intraluminal fluid (B)</p> Signup and view all the answers

<p>Lactulose (B)</p> Signup and view all the answers

<p>Motion sickness (A)</p> Signup and view all the answers

<p>Bacterial gastroenteritis (D)</p> Signup and view all the answers

<p>Anticholinergic drugs (D)</p> Signup and view all the answers

<p>Diarrhea (B)</p> Signup and view all the answers

<p>Decrease in cAMP levels (A)</p> Signup and view all the answers

<p>Activation of EP3 receptors (D)</p> Signup and view all the answers

<p>Stimulation of histamine release from enterochromaffin-like cells (B)</p> Signup and view all the answers

<p>Inhibition of acetylcholine at muscarinic receptors (B)</p> Signup and view all the answers

<p>By directly inhibiting the proton-potassium ATPase enzyme (D)</p> Signup and view all the answers

<p>Neutralization of gastric acid (D)</p> Signup and view all the answers

<p>Gastrin increases intracellular cAMP levels in parietal cells (B)</p> Signup and view all the answers

<p>Decreases acid secretion (C)</p> Signup and view all the answers

<p>Histamine (A)</p> Signup and view all the answers

<p>Prostaglandin-mediated mucosal defense (B)</p> Signup and view all the answers

<p>It weakens the mucosal defense systems. (A)</p> Signup and view all the answers

<p>Chronic use of antacids (C)</p> Signup and view all the answers

<p>Gastrinoma (Zollinger-Ellison Syndrome) (D)</p> Signup and view all the answers

<p>Sucralfate (B)</p> Signup and view all the answers

<p>Decreased mucosal defense barrier effectiveness (B)</p> Signup and view all the answers

<p>Regulates the backflow of stomach contents to the esophagus (B)</p> Signup and view all the answers

<p>Decreased mucosal defense response (A)</p> Signup and view all the answers

<p>Antagonizes dopamine D2 receptors (A)</p> Signup and view all the answers

<p>Low oral bioavailability and does not cross the blood-brain barrier (A)</p> Signup and view all the answers

<p>It must be eradicated to promote healing of ulcers (B)</p> Signup and view all the answers

<p>Stimulation of cholinergic neurons (D)</p> Signup and view all the answers

<p>Sedation (D)</p> Signup and view all the answers

<p>Decrease of cAMP levels (A)</p> Signup and view all the answers

<p>It activates muscarinic receptors to promote acid secretion (B)</p> Signup and view all the answers

<p>Decrease in cAMP levels (D)</p> Signup and view all the answers

<p>Prostaglandins inhibit acid secretion by activating protein kinases (B)</p> Signup and view all the answers

<p>Stimulation of protein kinase A (D)</p> Signup and view all the answers

<p>Increased gastric motility (A)</p> Signup and view all the answers

<p>Prostaglandin E2 (PGE2) (C)</p> Signup and view all the answers

<p>Enhanced gastric acid secretion (D)</p> Signup and view all the answers

<p>They decrease cAMP production (B)</p> Signup and view all the answers

<p>It forms a covalent bond with the proton pump. (C)</p> Signup and view all the answers

<p>It requires ATP for the initiation of acid secretion. (C)</p> Signup and view all the answers

<p>It is the S-isomer of omeprazole. (A)</p> Signup and view all the answers

<p>It elevates gastric pH significantly. (C)</p> Signup and view all the answers

<p>Short half-life but long duration due to irreversible binding. (D)</p> Signup and view all the answers

<p>Using with other acid-suppressing agents. (C)</p> Signup and view all the answers

<p>Lower pH is required for its activation. (A)</p> Signup and view all the answers

<p>Acetylcholine. (B)</p> Signup and view all the answers

<p>It is found in the apical membrane of parietal cells. (D)</p> Signup and view all the answers

<p>Hypergastrinemia leading to tumor growth (B)</p> Signup and view all the answers

<p>Longer duration of action (A)</p> Signup and view all the answers

<p>It is a synthetic analog of Prostaglandin E1 (D)</p> Signup and view all the answers

<p>Gynecomastia (D)</p> Signup and view all the answers

<p>Blockade of acetylcholine at muscarinic receptors (C)</p> Signup and view all the answers

<p>They inhibit acid secretion while promoting mucus and bicarbonate secretion (B)</p> Signup and view all the answers

<p>By raising the gastric pH with weak bases (C)</p> Signup and view all the answers

<p>Misoprostol (D)</p> Signup and view all the answers

<p>Moderate duration of action (A)</p> Signup and view all the answers

<p>Significant central nervous system side effects (C)</p> Signup and view all the answers

Sucralfate adheres to ulcerated stomach/duodenum lining, forming a protective layer.

Eliminating H. pylori bacteria and reducing stomach acid to treat peptic ulcers.

Enhance gastrointestinal motility, speeding up movement through the GI tract.

Used for GERD, gastroparesis, nighttime heartburn, and severe constipation.

Metoclopramide blocks dopamine receptors, increasing acetylcholine and gastric emptying.

Blocks dopamine receptors, improves gastric emptying, and is less effective for GERD compared to Metoclopramide.

Primary causes involve infections, inflammation, birth defects, and nervous system issues. Secondary causes include metabolic and neurological problems.

Drugs are classified by mechanism of action. The provided text briefly mentions prokinetics, 5-HT3 antagonists, and antimuscarinics among several others.

Drugs like cyclazine and promethazine used to treat nausea and vomiting, often due to motion sickness.

Medications like chlorpromazine and haloperidol used to treat severe vomiting, sometimes in combination with other therapies.

Drugs that promote bowel movements, including more powerful cathartics and milder laxatives.

A condition characterized by difficulty in bowel movements, often with hardened feces.

Drugs that stimulate bowel movements in a gentler manner.

A condition involving frequent loose stool, often caused by infection or other factors.

Infection of the intestines, often causing diarrhea, vomiting, and abdominal cramps.

Solutions containing essential salts and sugars to replenish lost fluids and electrolytes during diarrhea.

Drugs, like adsorbents (e.g., kaolin, pectin, charcoal), used to reduce diarrhea frequency or treat its symptoms.

Laxatives work by either increasing fluid retention in the bowel, decreasing water absorption, or altering the bowel movements's contractions to induce defecation.

The process by which parietal cells in the stomach release hydrogen ions (H+) into the gastric lumen, resulting in the production of gastric acid.

Drugs that block the histamine (H2) receptor on parietal cells, preventing histamine from stimulating acid secretion.

Drugs that block the M3 muscarinic receptors on parietal cells, preventing acetylcholine from stimulating acid secretion.

Drugs that block the gastrin receptor on parietal cells, preventing gastrin from stimulating acid secretion.

A signaling pathway in parietal cells that is activated by histamine, acetylcholine, and gastrin, leading to increased acid secretion.

Drugs that block the hydrogen-potassium ATPase (proton pump) in parietal cells, preventing the final step of acid secretion.

Lipid molecules that act as signaling molecules in the body, including inhibiting acid secretion by parietal cells.

A receptor on parietal cells that, when activated by prostaglandins, inhibits acid secretion.

A protective layer lining the stomach and duodenum, preventing damage from acid.

A cell in the stomach lining, involved in the production of gastric acid, which is stimulated by histamine, acetylcholine, and gastrin.

Common PPIs include Rabeprazole, Lansoprazole, and Pantoprazole.

PPIs can be given intravenously or orally, and the effects of PPIs last longer than H2 receptor antagonists.

Common H2 receptor antagonists include Cimetidine, Ranitidine, Famotidine, and Nizatidine.

Drugs that block acetylcholine from binding to muscarinic receptors, which also results in reduced acid secretion.

Pirenzepine and Telenzepine are commonly used anticholinergics.

Prostaglandins like Misoprostol are effective in treating acid-related disorders by both reducing acid secretion and increasing protective mechanisms in the stomach.

Weak bases that neutralize stomach acid by raising its pH.

Common antacids include Magnesium hydroxide, Magnesium trisilicate, Calcium carbonate, and Sodium bicarbonate.

GERD (Gastroesophageal Reflux Disease) occurs when stomach acid and pepsin flow back into the esophagus. This can be caused by:

1. Overproduction of acid/pepsin: The stomach produces too much acid.

2. Relaxation of the Lower Esophageal Sphincter (LES): The LES, a muscle that prevents acid reflux, doesn't close tightly enough.

Peptic Ulcer Disease is a sore or lesion that forms in the lining of the stomach or duodenum (first part of the small intestine). It is often caused by excess acid production or a weakened mucosal defense barrier.

Helicobacter pylori (H. pylori) is a bacteria that can infect the stomach and is a major cause of peptic ulcers. It weakens the mucosal defense system, allowing acid to damage the lining.

Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or naproxen, can increase the risk of developing peptic ulcers. NSAIDs block COX enzymes, which reduces the production of prostaglandins that protect the stomach lining.

Gastrinoma is a tumor in the duodenum or pancreas that secretes abnormally high levels of gastrin, a hormone that stimulates stomach acid production. This leads to excessive acid production, which can cause ulcers.

Gastroesophageal Reflux Disease (GERD) is when stomach acid and pepsin back up into the esophagus, causing heartburn.

The most common cause of Peptic Ulcer Disease is infection with Helicobacter pylori (H. pylori).

NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) are pain relievers that can cause ulcers by reducing prostaglandins, which protect the stomach lining.

Gastrinoma is a tumor that produces excessive gastrin, a hormone that stimulates acid production leading to ulcers.

Strategies include things like protecting the stomach lining (e.g., sucralfate) or neutralizing the acid (e.g., antacids)

Parietal cells, responsible for stomach acid production, are stimulated by histamine, acetylcholine, and gastrin.

These drugs block acetylcholine from binding to its receptor on parietal cells, decreasing acid production.

Sucralfate is a medication that forms a thick, protective layer over ulcers in the stomach and duodenum, shielding them from damaging acid.

Prokinetic drugs speed up the movement of food through the digestive tract by increasing muscle contractions in the stomach and intestines.

The final transport pathway for hydrogen ions (H+) in parietal cells, responsible for acid secretion. It is located in the apical membrane of the parietal cell. The pump requires energy from ATP.

Prototype H+, K+-ATPase inhibitor; a prodrug that needs a low pH to be active. It irreversibly binds to the proton pump, inhibiting acid production for a long duration, greatly reducing gastric acidity.

The S-isomer of omeprazole, also an H+, K+-ATPase inhibitor, administered orally.

A network of channels within the parietal cell that increase the surface area for acid secretion. The H+, K+-ATPase pump resides in the apical membrane of these canaliculi.

Parietal cells secrete acid through a multi-step process involving H+, K+-ATPase, ATP, and a complex interplay of signaling pathways involving histamine, acetylcholine, and gastrin.

ATP provides energy for the H+, K+-ATPase pump, allowing it to transport hydrogen ions against their concentration gradient, driving acid secretion by parietal cells.

These cells can produce H+, K+-ATPase in massive quantities, thus allowing rapid and substantial acid secretion. They are specialized for their function.

Blocking the H+, K+-ATPase pump disrupts the final step of acid secretion, effectively reducing both basal and stimulated acid production.

Omeprazole is inactive in its original form and requires conversion to its active form within the acidic environment of the stomach. This ensures targeted action at the site of acid production.

Omeprazole forms a strong covalent bond with the proton pump, making the inhibition long-lasting, effectively blocking acid production for extended periods.

Prostaglandins (PGE2 & PGI2) are involved in both inhibiting acid secretion and enhancing defense mechanisms in the stomach. They act on EP3 receptors on parietal cells and epithelial cells, reducing acid production and increasing mucus and bicarbonate secretion.

Antacids are weak bases that neutralize hydrochloric acid (HCl) in the stomach, raising the gastric pH.

Common side effects include headache, nausea, constipation, and diarrhea. Cimetidine may interact with other medications due to effects on the P450 enzyme system.

Common side effects include headache, nausea, diarrhea, and abdominal pain.

H2 receptor antagonists block the histamine receptor, while PPIs block the proton pump. PPIs have a longer duration of action than H2 receptor antagonists.

Common PPIs include Rabeprazole, Lansoprazole, and Pantoprazole.

Common H2 receptor antagonists include Cimetidine, Ranitidine, Famotidine, and Nizatidine.

Common antacids include Magnesium hydroxide, Magnesium trisilicate, Calcium carbonate, and Sodium bicarbonate.