Pharmacology Mnemonics - Flash Cards

Name: Reserpine

Class: Adrenergic Neuron Blocking Agent

Mechanism: Depletes NE, 5-HT, DA from nerve terminals in periph. and CNS. Also depletes some EPI from adrenal medulla. 1° = impairs storage of NE in terminals ® ¯ NE available for release. Cause slow fall in BP, some bradycardia, slight inhib. of cardiovasc reflexes, inhib of catechol. release actions of indirect sympathomimetics, ¯ CO, ¯ TPR.

Absorption: Oral

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Sedation, nightmares, psychic depression (suicide). In GI, parasymp tone predominates (cramps, diarrhea, exacerbated peptic ulcer). Nasal congestion, bradycardia. May potentiate effects of CNS depressants. Adverse interactions w/MAOIs.

Utility: Treat mild-mod. hypertension (concurrent diuretic therapy). Periph. vasc. disease (Raynaud’s Synd.). Antipsychotic (seldom used; higher doses).

Special Features: No longer considered very useful.

Name: Methyldopa (Aldomet)

Class: Centrally Acting Antiadrenergic Agent

Mechanism: Stimulates inhibitory a2 receptors in central cardiovasc pathways involving EPI or NE. a2 are G-protein coupled to inhibit adenylyl cyclase ®
¯ cAMP ® ¯ central symp. activity.

Absorption:

Dist.: Act at medullary and spinal sites.

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Prominent sedation, dry mouth, nightmares, depression, movement disorders, endocrine disturbances (lactation), anemia, rare hypersensitivity of skin and liver. Possible toxic psychosis if given w/levodopa.

Utility: Treat hypertension.

Special Features: Activates a2 via Metabolismolite methylnorepinephrine (false transmitter). Probably the most used hypotensive agent in mgt. of pregnant E.

Name: Guanabenz (Wytensin)

Class: Centrally Acting Antiadrenergic Agent

Mechanism: Stimulates inhibitory a2 receptors in central cardiovasc pathways involving EPI or NE. a2 are G-protein coupled to inhibit adenylyl cyclase ®
¯ cAMP ® ¯ central symp. activity.

Absorption: Oral.

Dist.: Acts at medullary and spinal sites.

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Prominent sedation, dry mouth, depression in those so inclined, constipation. May potentiate actions of other CNS depressants. Rebound hypertension, nervousness, insomnia if w/drawn too quickly.

Utility: Treat hypertension.

Special Features: Direct a2 activation. CV reflexes remain intact; normal homeostatic responses to exercise are maintained.

Name: Clonidine (Catapres)

Class: Centrally Acting Antiadrenergic Agent/Opioid Withdrawal Suppressant

Mechanism: Stimulates inhibitory a2 receptors in central cardiovasc pathways involving EPI or NE. a2 are G-protein coupled to inhibit adenylyl cyclase ®
¯ cAMP ® ¯ central symp. activity.

Absorption: Oral, transdermal.

Dist.: Acts at medullary and spinal sites.

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Prominent sedation, dry mouth, depression in those so inclined, constipation. S.E.s may be reduced by transdermal admin. May potentiate actions of other CNS depressants. Rebound hypertension, nervousness, insomnia if w/drawn too quickly.

Utility: Treat hypertension. DOC for treating opioid w/drawal. No abstinence synd. when withdrawn.

Special Features: Direct a2 activation. Very potent (<0.5 style=""> CV reflexes remain intact; normal homeostatic responses to exercise are maintained.

Name: Spironolactone (Aldactone)

Class: Diuretic (Potassium Sparing Diuretic) (Aldosterone Antagonist)

Mechanism: Competitive inhib. of aldosterone ® block of aldost.-stim. Na⁺ reabsorption and K⁺/H⁺ excretion in late distal tubule and collecting duct. Also reduces aldost.-stim. ammoniagenesis throughout the nephron.

Absorption: Oral. Takes up to 2 days to be effective.

Dist.:

Metabolism.: Hepatic.

Excretion, t½: 20 hr.

Toxicity/S.E.s: Hyperkalemia, gynecomastia, amenorrhea. Absolutely contraindicated w/hyperkalemia.

Utility: Most efficacious in pts. w/high plasma levels of aldosterone (e.g., 1° hyperaldosteronism due to an adrenal tumor or hyperplasia; 2° hyperaldost. due to cirrhosis, etc.).

Special Features: Only diuretic that acts through the blood side of the tubule. Rel. weak diuretic.

Name: Amiloride (Midamor)

Class: Diuretic (Potassium Sparing Diuretic)

Mechanism: Inhib. Na⁺ channel in the apical membrane of the late distal tubule and collecting duct ® block of electrochemical gradient that drives K⁺ & H⁺ secretion ® diuresis & ¯ excretion of K⁺ & H⁺.

Absorption: Oral

Dist.:

Metabolism.:

Excretion, t½: 1° = kidney. 6 hr.

Toxicity/S.E.s: Hyperkalemia (most severe), n/v (most common), Metabolismolic acidosis. Hyponatremia may occur in old folks. Absolutely contraindicated with hyperkalemia.

Utility: Usu. given w/another diuretic (often thiazide or loop). Combination usu. ® normal K⁺ excretion.

Special Features: Rel. weak diuretic.

Name: Triamterene (Dyrenium)

Class: Diuretic (Potassium Sparing Diuretic)

Mechanism: Inhib. Na⁺ channel in the apical membrane of the late distal tubule and collecting duct ® block of electrochemical gradient that drives K⁺ & H⁺ secretion ® diuresis & ¯ excretion of K⁺ & H⁺. Weak anti-HTN activity.

Absorption: Oral

Dist.:

Metabolism.:

Excretion, t½: 1° = kidney. 3 hr.

Toxicity/S.E.s: Hyperkalemia (most severe), n/v (most common), Metabolismolic acidosis. Hyponatremia may occur in old folks. Absolutely contraindicated with hyperkalemia. Adverse rxns w/lithium, ACE inhibitors. Rare renal failure w/NSAIDs.

Utility: Usu. given w/another diuretic (often thiazide or loop). Combination usu. ® normal K⁺ excretion. Used to prevent or correct hypokalemia, and to avoid K⁺ depletion in pts. on digitalis.

Special Features: Rel. weak diuretic.

Name: Furosemide (Lasix)

Class: Diuretic (Loop Diuretic)

Mechanism: Blocks the Na⁺/K⁺/Cl^- co-transporter in the apical membrane of the thick ascending limb of Henle’s loop ® ­ excretion of urinary water, Na⁺, K⁺, Ca²⁺, & Mg²⁺. Also causes venous and renal vasodilation.

Absorption: Oral, IV. Takes effect in 20 min.

Dist.: Metabolism.:

Excretion, t½: 1-1.5 hr. Shorter duration than thiazides.

Toxicity/S.E.s: Hypokalemia (esp. dangerous if pt. is on digitalis), Ca²⁺ & Mg²⁺ depletion, Metabolismolic alkalosis, volume contraction, mild hyperglycemia, thiazide-like lipid changes, sulfonamide allergy cross-rxn, ototoxicity. C/i—pts. susceptible to volume contraction from excessive diuresis (e.g., elderly), and pts. susceptible to problems w/hypokalemia (e.g., cirrhosis, digitalis). Adverse rxn w/lithium, aminoglycosides. Altered doses of anti-diabetic agents required.

Utility: Diuresis for hypertension when a short-acting diuretic is indicated. Treat HTN refractory to thiazides. Very useful in conditions refractory to less potent diuretics (e.g., CHF, renal insufficiency, nephrotic synd.). Treat hypercalcemia.

Special Features: Most potent diuretics available. Can cause excretion of up to 20% of filtered Na⁺.

Name: Chlorthalidone (Hygroton)

Class: Diuretic (Thiazide)

Mechanism: Inhib. Na⁺ & Cl^- transport in the cortical thick ascending limb and the early distal tubule ® ­ NaCl and water excretion & ¯ excretion of Ca²⁺ and uric acid.

Absorption: Oral ® good absorption. Takes effect in 1 hr.

Dist.: Metabolism.: Excretion, t½: Long duration of action.

Toxicity/S.E.s: Hypokalemia, hyponatremia, hyperuricemia, weakness, hypercalcemia, Metabolismolic alkalosis, postural hypotension, hypercholesterolemia, hypertriglyceridemia, hyperglycemia (in patients w/DM), and rare hypersensitivity rxns. C/i—pts susceptible to problems with hypokalemia (cirrhosis, pts on digitalis), hyperuricemia (gout), or hypercalcemia. Adverse rxns w/digitalis, lithium. Altered doses of anti-diabetic agents required. Long-term NSAID use may decrease anti-HTN effects.

Utility: Treat hypertension, CHF, nephrotic synd., other Na⁺-retaining states. Reduce Ca²⁺ excretion (e.g., prevention of kidney stones).

Rel. ineffective in renal insuff.

Name: Hydrochlorothiazide (Hydrodiuril)

Class: Diuretic (Thiazide)

Mechanism: Inhib. Na⁺ & Cl^- transport in the cortical thick ascending limb and the early distal tubule ® ­ NaCl and water excretion & ¯ excretion of Ca²⁺ and uric acid.

Absorption: Oral ® good absorption. Takes effect in 1 hr.

Dist.: Metabolism.: Excretion, t½: Short duration of action.

Toxicity/S.E.s: Hypokalemia, hyponatremia, hyperuricemia, weakness, hypercalcemia, Metabolismolic alkalosis, postural hypotension, hypercholesterolemia, hypertriglyceridemia, hyperglycemia (in patients w/DM), and rare hypersensitivity rxns. C/i—pts susceptible to problems with hypokalemia (cirrhosis, pts on digitalis), hyperuricemia (gout), or hypercalcemia. Adverse rxns w/digitalis, lithium. Altered doses of anti-diabetic agents required. Long-term NSAID use may decrease anti-HTN effects.

Utility: Treat hypertension, CHF, nephrotic synd., other Na⁺-retaining states. Reduce Ca²⁺ excretion (e.g., prevention of kidney stones).

Rel. ineffective in renal insuff

Name: Nimodipine (Nimotop)

Class: Calcium-Entry Blocking Agent (Dihydropyridine)

Mechanism: Binds to L-type Ca²⁺ channels ® ¯ Ca²⁺ in arterial smooth muscle cells ® vasodilation ® ¯ TPR, ­ coronary blood flow, ¯ cardiac afterload. Little/no effect on venous vessels. No direct effect on conduction or automaticity. Vasodilation ® reflex ­ sympathetic response ® ­ HR, ­ contractility. Net = ¯ BP, ­ HR, ­ contractility, ­ CO. May inhib. platelet aggreg.

Absorption: Oral ® nearly complete absorption. 1^st pass Metabolism®¯ bioavail. IV.

Dist.: Significant protein binding.

Metabolism.: Hepatic. Inactive Metabolismolites.

Excretion, t½: 1.5-6 hr. Repeated oral dose ® ­ t½ due to hepatic saturation. Longer t½ in elderly or pts w/hepatic cirrhosis or renal insuff.

Toxicity/S.E.s: 2° to vasodilation—dizziness, hypotension, headache, flushing, edema. Aggravation of myocardial ischemia, angina. C/i w/CHF.

Utility: Rx angina (stable, variant, unstable)[KLW1] . DOC for stable angina w/persistent HTN, sinus bradycardia, or AV node dysfxn.

Name: Bepridil (Vascor)

Class: Calcium-Entry Blocking Agent (Antidysrhythmic Agent Class IV)

Mechanism: Binds to L-type Ca²⁺ channels ® ¯ Ca²⁺ in arterial smooth muscle cells ® vasodilation ® ¯ TPR, ­ coronary blood flow, ¯ cardiac afterload. Little/no effect on venous vessels. ¯ inotropy, chronotropy, & dromotropy. Blocks cardiac Na⁺/K⁺ channel. May inhib. platelet. aggreg.

Absorption: Oral ® nearly complete absorption. 1^st pass Metabolism®¯ bioavail. IV.

Dist.: Significant protein binding.

Metabolism.: Hepatic.

Excretion, t½: Long (24-50 hr.). Repeated oral dose ® ­ t½ due to hepatic saturation. Longer t½ in elderly or pts w/hepatic cirrhosis or renal insuff.

Toxicity/S.E.s: 2° to vasodilation—dizziness, hypotension, headache, flushing, edema. Aggravation of myocardial ischemia. Drug-induced long QT syndrome (DILQT, “torsades de pointes”). C/i w/CHF, b-blockers.

Utility: Rx angina (stable, variant, unstable), supraventricular tachycardia, reentry arrhythmias, hypertension.

Special Features: