GIT Part 1: Acid Peptic Disease and Acid Suppressants

Vocabulary practice cards covering GIT pharmacology notes: acid peptic diseases, proton pump inhibitors, H2 receptor blockers, mechanisms of action, adverse effects, and drug interactions.

Hyperacidity

A condition in which gastric parietal cells produce excess $HCl$, leading to pain, heartburn, and dyspepsia.

Peptic Ulcers

Lesions resulting from elevated $HCl$ secretion that damages stomach and duodenal cells, producing mucosal ulcers.

Gastroesophageal Reflux Disease (GERD)

A condition where $HCl$ refluxes into the esophagus, causing mucosal cell damage.

Acid Suppressants

Drugs that decrease $HCl$ production from parietal cells; prescribed on a long-term basis to provide 'round the clock protection.'

Acid Neutralizers (Antacids)

Basic drugs that directly neutralize $HCl$ within the gastric lumen.

Ulcer Protectives

Mucosa-shielding agents used in acid peptic diseases, exemplified by sucralfate and bismuth compounds.

Alginic Acid

A miscellaneous antifoaming agent used in the management of GERD.

Simethicone

A miscellaneous gastrointestinal agent utilized for its antiflatulence properties.

Histaminocytes

Histamine-producing cells whose $M_1$ receptors are activated by acetylcholine ($Ach$) released from the vagus nerve, triggering histamine release to stimulate parietal $H_2$ receptors.

Pirenzepine and Telenzepine

Rarely used anticholinergic drugs that block $M_1$ receptors, reducing meal-induced acid secretion by $40\text{--}60\%$ while exerting no effect on nocturnal or basal acid production.

Proton Pump Inhibitors (PPIs)

Irreversible inhibitors of the parietal cell $H^+/K^+$ ATPase pump that provide $80\text{--}95\%$ acid suppression, making them the most effective acid-suppressing agents.

Hit and Run Drug (Suicide Inhibitor)

A pharmacokinetic/pharmacodynamic description applied to PPIs because they bind irreversibly to the proton pump for $2\text{--}5\,\text{days}$ despite having a brief plasma half-life of $30\,\text{mins}\text{ to }3\,\text{hours}$.

Sulfenamide Moiety

The active form of proton pump inhibitors, generated after the inactive prodrug undergoes conversion in the acidic environment of gastric parietal cells.

Dexrabeprazole

The most potent drug among the proton pump inhibitors.

Pantoprazole

The least potent PPI requiring the highest therapeutic dose; available in both oral and injectable (IV/IM) preparations.

Omeprazole

The fastest-acting PPI, but also the most unsafe PPI in pregnancy and the strongest inhibitor of the CYP2C19 enzyme.

Lansoprazole

The safest proton pump inhibitor to administer during pregnancy.

Acid-Resistant / Enteric-Coated PPI Formulations

Special delayed-release coatings engineered to protect acid-labile PPI prodrugs from gastric degradation so they can reach the intestine intact for systemic absorption.

CYP2C19 Clopidogrel Interaction

Drug interaction occurring when omeprazole inhibits CYP2C19, blocking metabolic activation of clopidogrel and lowering antiplatelet efficacy, which elevates the risk of recurrent myocardial infarction and stroke.

Aspiration Pneumonia Prophylaxis Regimen

Combination therapy of a PPI plus a prokinetic agent (such as domperidone or mosapride) to close the lower esophageal sphincter in unconscious surgical patients who have lost protective reflexes.

Octreotide (in Zollinger-Ellison Syndrome)

A somatostatin hormone analogue co-administered with PPIs to decrease gastrin secretion from gastrinomas.

Tenatoprazole

A novel PPI characterized by reversible proton pump inhibition and lack of metabolism by the CYP2C19 enzyme pathway.

Potassium-Competitive Acid Blockers (P-CABs)

New acid-suppressing agents, including vonoprazan, revaprazan, and tegoprazan, that act as $K^+$ antagonists on the $H^+/K^+$ ATPase enzyme to produce faster and more effective inhibition.

$H_2$ Receptor Blockers

Competitive inhibitors of histamine $H_2$ receptors on gastric parietal cells that reduce $HCl$ production by $60\text{--}80\%$ and serve as the drug of choice for stress ulcers.

Famotidine

The most potent $H_2$ receptor antagonist, acting as a non-competitive blocker of $H_2$ receptors.

Cimetidine

The least potent $H_2$ blocker (no longer in use) that produces maximum CYP enzyme inhibition, blocks dopamine $D_2$ receptors to cause galactorrhea, and induces gynecomastia and menstrual irregularities.

Nizatidine

An $H_2$ blocker possessing maximum oral bioavailability and no inhibitory action on CYP enzymes.

Lafutidine

An $H_2$ receptor antagonist that elevates endogenous somatostatin levels, subsequently suppressing gastrin production and downstream $HCl$ secretion.

Rebound Acid Secretion

A sudden surge in gastric $HCl$ production following abrupt cessation of prolonged PPI or $H_2$ blocker therapy, caused by persistent hypergastrinemia stimulating CCK-2 receptors on parietal cells.

Netazepide

A CCK-2 receptor blocker that serves as the drug of choice for treating rebound $HCl$ hypersecretion.