Pharmacology Mnemonics - Flash Cards

Name: Metronidazole (Flagyl)

Class: Nitroimidazole derivative

Mechanism: Inhib. DNA synth, degrades DNA, e- acceptor for reduced substrates.

Absorption: Complete, quick oral absorption.

Dist.: Well distrib to all tissues and fluids (including CSF)

Metabolism.: Hepatic Metabolism.

Excretion, t½:

Toxicity/S.E.s: GI, metallic taste, neurotox (vertigo), disulfiram-like effect w/alcohol, neutropenia. Not for first trimester preg (mutagenic). Not for patients w/active CNS disease or hist. of blood dyscrasias.

Utility: IV treatment of anaerobic infects. Oral for amebiasis, giardiasis, and genital infects of Trichomonas vaginalis. H. pylori (PUD).

Special Features: Antiparasitic and antibacterial activity. All anaerobic cocci and anaerobic gram- bacilli, including Bacterioides. Trichomoniasis, amebiasis, giardiasis.

Name: Sucralfate (Carafate)

Class: Cytoprotective Agent

Mechanism: Complex of aluminum hydroxide and sulfated sucrose. Forms complex gels w/mucus ® physical barrier than impairs diffusion of HCl and prevents peptic mucus degradation. Stim. prostaglandin release and secretion of mucus and bicarbonate. Inhib. acid secretion by ~50%.

Absorption: Not absorbed.

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Well tolerated.

Utility: PUD

Special Features: Largely supplanted by H2RAs and PPIs. Requires acidic pH for activation. \ should not be admin. w/antacids, PPIs, or H2RAs.

Name: Bismuth-Subsalicylate (Pepto-Bismol)

Class: Cytoprotective Agent/Hydrophilic Agent/Absorbent/Antimicrobial.

Mechanism: Inhib. pepsin activity, ­ mucus secretion, coats & protects ulcer. Antimicrobial action. May have antiinflammatory action.

Absorption:

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Toxicity/S.E.s: Binds tetracyclines. Turns stools and tongue black. Contains salicylate ® additive effects w/aspirin, tinnitus. Don’t use w/salicylate allergy. May cause GI impaction in debilitated patients.

Utility: PUD. Traveler’s Diarrhea (at least in Mexico)—8 doses (1-2 tablets every eight hours). Prophylaxis for Traveler’s Diarrhea. General diarrhea (usu. controls diarrhea w/in 24 hr).

Special Features:

Name: Calcium Carbonate (Tums, Rolaids)

Class: Antacid

Mechanism: Weak base ® ¯ gastric acidity. ­ pH ® ¯ peptic activity.

Absorption:

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Excretion, t½:

Toxicity/S.E.s:

Utility: PUD

Special Features: Counterproductive—Ca²⁺ stimulates gastrin release.

Name: Misoprostol (Cytotec)

Class: Prostaglandin Analogue (PGE₁)

Mechanism: Stim. mucus and bicarbonate secretion, mucosal blood flow, cell turnover. Inhib. acid secretion.

Absorption:

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Excretion, t½: Longer t½ than natural prostaglandins.

Toxicity/S.E.s: ­ intest. secretion ® diarrhea. Nausea. Uterine contractions. \ c/i during pregnancy.

Utility: PUD, prevention of NSAID injury.

Special Features:

Name: Magnesium Hydroxide (Milk of Magnesia)

Class: Antacid

Mechanism: Weak base ® ¯ gastric acidity. ­ pH ® ¯ peptic activity.

Absorption:

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Excretion, t½:

Toxicity/S.E.s: Diarrhea.

Utility: PUD

Special Features:

Name: Al-Mg Hydroxides

Class: Antacid

Mechanism: Weak base ® ¯ gastric acidity. ­ pH ® ¯ peptic activity.

Absorption:

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Excretion, t½:

Toxicity/S.E.s: Al³⁺ can form insoluble complexes w/other drugs ® ¯ absorption (e.g., tetracycline).

Utility: PUD

Special Features: Comb. of constipation (Al) and laxative (Mg) effects may cancel ® rel. normal bowel function.

Name: Omeprazole (Prilosec)

Class: Proton Pump Inhibitor

Mechanism: Irreversible inhib. of H⁺/K⁺ ATPase ® > 95% inhib. of acid secretion.

Absorption: Oral ® 30-40% bioavail. Peak plasma levels at 0.5-3.5 hr. Give prior to meals, preferably in the morning. Additional dose, if necessary, should be given later in the day.

Dist.:

Metabolism.:

Excretion, t½: 0.5-1 hr.

Toxicity/S.E.s: Rare headache, diarrhea, rash. Inhib. of cyt. P-450 requires altered doses of warfarin, phenytoin, diazepam, and cyclosporin. Inhib. of vitamin. B12 absorption.

Utility: PUD, erosive esophagitis, Zollinger-Ellison synd., GERD.

Special Features: Mismatch between pharmacokinetics & pharmacodynamics. Short t½, but actions last > 24 hr (irreversible binding). Acid inhib. ® ­ gastrin.

Name: Aluminum Hydroxide (Maalox)

Class: Antacid

Mechanism: Weak base ® ¯ gastric acidity. ­ pH ® ¯ peptic activity.

Absorption:

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Excretion, t½:

Toxicity/S.E.s: Constipation. Al³⁺ can form insoluble complexes w/other drugs ® ¯ absorption (e.g., tetracycline).

Utility: PUD

Special Features:

Name: Famotidine (Pepcid)

Class: H2 Receptor Antagonist

Mechanism: Competitive inhib. of the histamine H2 receptor, but not of the H1 receptor ® inhib. of fasting and stim. acid secretion. No disruption of circadian rhythm of acid secretion. Inhib. of 80-90% of gastrin and vagal-stim. acid secretion.

Absorption: Oral ® rapid, good absorption. Single nighttime dose.

Dist.:

Metabolism.: Partial hepatic Metabolism.

Excretion, t½: Excreted intact in urine. 1.5-3 hr.

Toxicity/S.E.s: Uncommon. Diarrhea, headaches, myalgias, skin rashes. Occasional cardiac arrhythmias (more common than in other H2RAs).

Utility: PUD, Zollinger-Ellison synd., acute stress ulcers, GERD

Special Features: Potency—famotidine > ranitidine/nizatidine > cimetidine. Tachyphylaxis—50% less effective after 6 months. Rebound hypersecretion 2° to receptor upregulation and inhib. of ATPase recycling.

Name: Nizatidine (Axid)

Class: H2 Receptor Antagonist

Mechanism: Competitive inhib. of the histamine H2 receptor, but not of the H1 receptor ® inhib. of fasting and stim. acid secretion. No disruption of circadian rhythm of acid secretion. Inhib. of 80-90% of gastrin and vagal-stim. acid secretion.

Absorption: Oral ® rapid, good absorption. Single nighttime dose.

Dist.:

Metabolism.: Partial hepatic Metabolism.

Excretion, t½: Excreted intact in urine. 1.5-3 hr.

Toxicity/S.E.s: Uncommon. Diarrhea, headaches, myalgias, skin rashes. Occasional cardiac arrhythmias.

Utility: PUD, Zollinger-Ellison synd., acute stress ulcers, GERD

Special Features: Potency—famotidine > ranitidine/nizatidine > cimetidine. Tachyphylaxis—50% less effective after 6 months. Rebound hypersecretion 2° to receptor upregulation and inhib. of ATPase recycling.

Name: Cimetidine (Tagamet)

Class: H2 Receptor Antagonist

Mechanism: Competitive inhib. of the histamine H2 receptor, but not of the H1 receptor ® inhib. of fasting and stim. acid secretion. No disruption of circadian rhythm of acid secretion. Inhib. of 80-90% of gastrin and vagal-stim. acid secretion.

Absorption: Oral ® rapid, good absorption. Single nighttime dose.

Dist.:

Metabolism.: Partial hepatic Metabolism.

Excretion, t½: Excreted intact in urine. 1.5-3 hr.

Toxicity/S.E.s: Uncommon. Diarrhea, headaches, myalgias, skin rashes. Large doses over prolonged periods assoc. w/impotence & gynecomastia. Inhib. cyt. P-450 ® dose adjustment with phenytoin, warfarin, & theophylline. Occasional cardiac arrhythmias.

Utility: PUD, Zollinger-Ellison synd., acute stress ulcers, GERD

Special Features: Potency—famotidine > ranitidine/nizatidine > cimetidine. Tachyphylaxis—50% less effective after 6 months. Rebound hypersecretion 2° to receptor upregulation and inhib. of ATPase recycling.

Name: Ranitidine (Zantac)

Class: H2 Receptor Antagonist

Mechanism: Competitive inhib. of the histamine H2 receptor, but not of the H1 receptor ® inhib. of fasting and stim. acid secretion. No disruption of circadian rhythm of acid secretion. Inhib. of 80-90% of gastrin and vagal-stim. acid secretion.

Absorption: Oral ® rapid, good absorption. Single nighttime dose.

Dist.:

Metabolism.: Partial hepatic Metabolism.

Excretion, t½: Excreted intact in urine. 1.5-3 hr.

Toxicity/S.E.s: Uncommon. Diarrhea, headaches, myalgias, skin rashes. Inhib. cyt. P-450 (less than cimetidine) ® dose adjustment with phenytoin, warfarin, & theophylline. Occasional cardiac arrhythmias.

Utility: PUD, Zollinger-Ellison synd., acute stress ulcers, GERD

Special Features: Potency—famotidine > ranitidine/nizatidine > cimetidine. Tachyphylaxis—50% less effective after 6 months. Rebound hypersecretion 2° to receptor upregulation and inhib. of ATPase recycling.

Name: Magnesium

Class: Antidysrhythmic Agent

Mechanism:

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Excretion, t½:

Toxicity/S.E.s:

Utility: DOC for torsades de pointes (DILQT synd). Treat pts w/digitalis-induced arrhythmia if hypomagnesemia is present.

Special Features:

Name: Adenosine (Adrenocard)

Class: Antidysrhythmic Agent

Mechanism: High doses ® ¯ conduction velocity, ­ refractory period, ¯ automaticity in the AV node.

Absorption: IV

Dist.:

Metabolism.:

Excretion, t½: Extremely short duration of action (15 sec.).

Toxicity/S.E.s: Low toxicity. Flushing, chest pain, hypotension, transient dyspnea, non-myocardial chest discomfort, metallic taste.

Utility: DOC for acute supraventricular tachycardia. Treat AV nodal reentry, orthodromic tachycardia.

Special Features:

Name: Amiodarone (Cordarone)

Class: Antidysrhythmic Agent (Class III)

Mechanism: Structurally related to thyroxine. 1° effect is prolongation of action potential and refractory period. Antiarrhythmic activity and antianginal activity.

Absorption: Oral.

Dist.:

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Excretion, t½: 25-110 days.

Toxicity/S.E.s: Common (>75% of pts). Interstitial pulmonary fibrosis, GI intolerance, tremor, ataxia, dizziness, depression, nightmares, hallucinations, hyper/hypothyroidism, liver toxicity, photosensitivity, periph. neuropathy, muscle weakness, blue skin (I₂), possibly irreversible hepatic dysfxn. DILQT synd., sinus bradycardia. Asympt. corneal deposits in all pts. Substantial ­ in LDL. Phospholipidosis. Enhances effect of warfarin. ­ conc. of digoxin, quinidine, procainamide, et. al.

Utility: Treat severe refractory supraventricular and ventricular tachyarrhythmia.

Special Features: Usefulness limited by toxicity. Full effects may take up to 6 weeks to manifest.

Name: Sotalol (Betapace)

Class: Antidysrhythmic Agent (Class III)

Mechanism: Blocks rapid outward K⁺ current (delayed rectifier) ® prolonged repolarization and action potential ® ­ effective refractory period. Little effect on rate of depolarization. L-isomer is a potent b-blocker.

Absorption:

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Toxicity/S.E.s: Rel. low rate of adverse effects. DILQT synd., sinus bradycardia.

Utility: Long-term therapy to decrease the rate of sudden death following acute MI. Modest ability to suppress ectopic beats and ¯ O₂ demand. Strong antifibrillary effect. Prevents arrhythmia and decreases mortality in pts. w/sustained ventricular tachycardia.

Name: Flecainide (Tambocor)

Class: Antidysrhythmic Agent (Class IC)

Mechanism: Slow dissociation from Na⁺ channels ® marked suppression of phase 0 upstroke ® marked slowing of conduction. ­ threshold potential ® ¯ automaticity.

Absorption: Oral.

Dist.:

Metabolism.: Minimal.

Excretion, t½: 16-20 hr.

Toxicity/S.E.s: Long-term Rx ® ­ mortality. Dizziness, blurred vision, tremor, agitation, headache, nausea. Aggravation of preexisting arrhythmias, negative inotropy, induction of life-threatening ventricular tachycardia (CAST proarrhythmia), aggravation of CHF, infranodal conduction block.

Utility: Treat refractory ventricular arrhythmias. Suppress premature ventricular contraction. Treat AV nodal reentry, WPW-related arrhythmia.

Special Features: Class IC drugs have the highest potency as Na⁺ channel blockers

Name: Mexiletine (Mexitil)

Class: Antidysrhythmic Agent (Class IB)

Mechanism: Shortens phase 3 repolarization. Decreases action potential duration. Inhibits arrhythmias caused by abnormal automaticity. Rapid speed of dissociation from Na⁺ channels.

Absorption: Oral

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Excretion, t½:

Toxicity/S.E.s: Proarrhythmic effects, negative inotropy, infranodal conduction block. N/v, dizziness, disorientation, tremor.

Utility: Chronic treatment of ventricular arrhythmias assoc. w/previous myocardial infarction.

Special Features: Concurrent use w/quinidine may be effective at lower doses than either alone ® ¯ adverse effects of each.

Name: Tocainide (Tonocard)

Class: Antidysrhythmic Agent (Class IB)

Mechanism: Shortens phase 3 repolarization. Little change in action potential duration. Inhibits arrhythmias caused by abnormal automaticity. Rapid speed of dissociation from Na⁺ channels.

Absorption: Oral

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Excretion, t½:

Toxicity/S.E.s: Proarrhythmic effects, negative inotropy, infranodal conduction block. N/v, dizziness, disorientation, tremor. Hematologic effects (agranulocytosis, bone marrow suppression, thrombocytopenia) can be fatal.

Utility: Treat ventricular tachyarrhythmias (only as a last resort).

Special Features: Concurrent use w/quinidine may be effective at lower doses than either alone ® ¯ adverse effects of each.

Name: Lidocaine (Zylocaine)

Class: Antidysrhythmic Agent (Class IB)

Mechanism: Shortens phase 3 repolarization. Little change in action potential duration. Inhibits arrhythmias caused by abnormal automaticity. Rapid speed of dissociation from Na⁺ channels.

Absorption: IV

Dist.:

Metabolism.: Hepatic.

Excretion, t½:

Toxicity/S.E.s: Fairly wide therapeutic index. Proarrhythmic effects, negative inotropy, infranodal conduction block. Drowsiness, slurred speech, paresthesia, agitation, confusion, convulsions, resp. depression, tinnitus, muscle twitching, psychosis, seizures. ­ CNS toxicity if used w/tocainide or mexiletine (e.g., seizures).

Utility: DOC for sustained ventricular tachycardia. Treat ventricular arrhythmias arising during myocardial ischemia or digitalis-induced VA.

Special Features: Class IB drugs have the lowest potency as Na⁺ channel blockers.

Name: Disopyramide (Norpace)

Class: Antidysrhythmic Agent (Class IA)

Mechanism: Binds to open and inactivated Na⁺ channels and prevents Na⁺ influx ® slowing of the rapid upstroke during phase 0. Also decreases the slope of phase 4 spontaneous depolarization. Prolongs repolarization. Inhibits arrhythmias due to ­ normal automaticity. Intermed. speed of dissociation from Na⁺ channels. Peripheral vasoconstriction. The stereoisomers have opposite effects on repolarization.

Absorption:

Dist.:

Metabolism.: Hepatic.

Excretion, t½: Urine.

Toxicity/S.E.s: Proarrhythmic effects, negative inotropy, infranodal conduction block, DILQT. Anticholinergic effects—dry mouth, urinary retention, blurred vision, constipation. N/v/d, abd. pain. Less GI intolerance than quinidine.

Utility: Alt. to procainamide or quinidine for treatment of ventricular arrhythmia.

Special Features:

Name: Procainamide (Pronestyl)

Class: Antidysrhythmic Agent (Class IA)

Mechanism: Binds to open and inactivated Na⁺ channels and prevents Na⁺ influx ® slowing of the rapid upstroke during phase 0. Also decreases the slope of phase 4 spontaneous depolarization. Prolongs repolarization. Inhibits arrhythmias due to ­ normal automaticity. Intermed. speed of dissociation from Na⁺ channels.

Absorption: Oral. IV rarely used, as hypotension occurs w/too rapid infusion.

Dist.: Excretion, t½: Urine. 2-3 hr.

Metabolism.: Hepatic ® active Metabolismolite NAPA (­ duration of action potential).

Toxicity/S.E.s: Proarrhythmic effects, negative inotropy, infranodal conduction block, DILQT. Hypotension (ganglion-blocking activity). Chronic use ® reversible SLE-like synd. Depression, hallucination, psychosis, giddiness. Less GI intolerance than quinidine. Hypersensitivity rxns—fever, agranulocytosis, Raynaud’s synd., myalgias, rashes, digital vasculitis.

Utility: Treat atrial, AV junctional, & ventricular tachyarrhythmias. Maintain sinus rhythm after direct current cardioversion of atrial flutter or fibrillation. Prevent frequent ventricular tachycardia.