Pharmacology Mnemonics - Flash Cards

Name: Diltiazem (Cardizem)

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

Mechanism: Binds 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. Net = ¯ HR, ¯ contractility, ¯ BP. May inhib. platelet aggreg.

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

Dist.: Significant protein binding.

Metabolism.: Hepatic. Inducible Metabolism. Inhib. hepatic enzymes. Active 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: Dizziness, hypotension, headache, flushing, edema, constipation (less than verapamil), bradycardia, gingival hyperplasia. Aggravation of myocardial ischemia (less than w/DHPs). ­ digoxin levels. C/i for pts. w/systolic BP<90 style=""> C/i w/CHF, b-blockers, quinidine.

Utility: Rx angina (stable, variant, unstable). Supraventricular tachycardia, reentry arrhyth..

Name: Nifedipine (Procardia)

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. Inducible Metabolism. 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: Dizziness, hypotension, headache, flushing, peripheral edema, gingival hyperplasia. Aggravation of myocardial ischemia, angina. C/i w/CHF.

Utility: Rx angina (stable, variant, unstable), arrhythmias, hypertension. DOC for stable angina w/persistent HTN, sinus bradycardia, or AV node dysfxn. W/b-blocker & nitrate ® ¯ rest angina, ¯ risk of MI, ¯ risk of emergency revascularization.

Special Features:

Name: Verapamil (Calan)

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

Mechanism: Binds to L-type Ca²⁺ channels ® ¯ Ca²⁺ in arterial smooth muscle cells ® vasodilation ®
¯ cardiac afterload. Little/no effect on venous vessels. ¯ inotropy, chronotropy, & dromotropy.
Net = ¯ HR, ¯ conduction, ¯ contractility, ¯ BP. May inhib. platelet aggreg.

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

Dist.: Significant protein binding.

Metabolism.: Hepatic. Inducible Metabolism. Inhibits hepatic enzymes. Active 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: Dizziness, hypotension, headache, constipation, gingival hyperplasia, flushing, edema. Aggravation of myocardial ischemia (less than w/DHPs). Serious toxicities (bradycardia, transient asystole, exacerbation of heart failure) are rare, but may occur after IV admin; coadmin w/b-blocker (c/i); or in pts. w/ventricular dysfxn, conduction disturbances, or systolic BP < style=""> ­ digoxin levels. C/i w/CHF, quinidine.

Utility: Rx angina (stable, variant, unstable), arrhythmias, hypertension. More effective than propranolol for unstable angina. DOC (IV) for paroxysmal supraventricular tachycardias. Reentry arrhythmias.

Special Features: Blocking action is frequency and voltage dependent. \ more effective in rapidly depolarizing cells. At vasodilatory doses, greater negative chronotropic, dromotropic, and inotropic effects than the dihydropyridines. Greatest effect on heart of channel blockers.

Name: Nitroprusside (Nipride)

Class: Antihypertensive Agent

Mechanism: Stim. membrane-assoc. guanylyl cyclase in vascular smooth muscle cells ® ­ intracellular cGMP ® activation of cGMP-dependent protein ® vasodilation of arterial and venous vessels® reflex tachycardia. Reduces BP in all pts., regardless of etiology. Decreases afterload and preload.

Absorption: Continuous IV infusion. Oral ® cyanide poisoning.

Dist.:

Metabolism.:

Excretion, t½: Minutes

Toxicity/S.E.s: Tachycardia, hypotension, cyanide toxicity (Rx w/sodium thiosulfate).

Utility: Hypertensive emergencies.

Special Features:

Name: Minoxidil (Loniten)

Class: CHF Rx (Vasodilator) (Antihypertensive)

Mechanism: Direct arteriolar vasodilation ® ¯ TPR ® reflex ­ in HR & CO.

Absorption: Oral.

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Severe tachycardia. Serious Na⁺ & H_2­O retention ® volume overload, edema, CHF. Hypertrichosis.

Utility: Treat severe-malignant HTN refractory to other drugs. Male pattern baldness.

Special Features: Reflex tachycardia may be severe, requiring concomitant use of a diuretic and a b-blocker.

Name: Diazoxide (Hyperstat I.V.)

Class: CHF Rx (Vasodilator) (Antihypertensive)

Mechanism: Direct arteriolar vasodilation ® ¯ TPR ® reflex ­ in HR & CO.

Absorption: IV.

Dist.:

Metabolism.:

Excretion, t½: Long duration of action.

Toxicity/S.E.s: Severe tachycardia, prolonged hypotension (possibly resulting in stroke or MI).

Utility: Treat hypertensive emergencies, hypertensive encephalopathy, and eclampsia.

Special Features:

Name: Hydralazine

Class: CHF Rx (Vasodilator)

Mechanism: Acts directly on smooth muscle cells ® vasodilation. Mechanism unknown.
¯ BP ® reflex tachycardia & ­ CO. ­ renin concentration. ­ NE in heart failure.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Reversible lupus-like synd. Headache, nausea, sweating, arrhythmia, angina, tachycardia.

Utility: Treat CHF. Chronic use ® reduction in two year mortality by 34%. Almost always coadmin. w/b-blocker (to oppose tachycardia) and a diuretic (to decrease Na⁺ retention). Treat resistant HTN and hypertensive emergencies.

Special Features:

Name: Amrinone (Inocor)

Class: CHF Rx (PDE Inhibitor)

Mechanism: Inhib. of PDE III® ­ cAMP ® ­ contractility, ­ stroke volume, ­ ejection fraction, ­ heart rate, ­ exercise capacity. In smooth muscle, inhib. ® vasodilation.

Absorption: IV only.

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: ­ mortality from heart failure (possibly due to arrhythmogenesis).

Utility: Treat CHF.

Special Features:

Name: Dopamine

Class: CHF Rx (b-Adrenergic Agonist)

Mechanism: ¯ dose ® D1 stim. ­ dose ® b1 stim. Also releases NE from symp. neur. Causes vasodilation in renal, mesenteric, and coronary beds ® ­ renal blood flow, glomerular filtration, and Na⁺ excretion. Also causes ¯ Na⁺ and H₂0 resorption. High doses ® ­ HR. Usu. increases systolic BP and pulse pressure. Low-mod. doses ® static or decreased vasc. resistance. High conc. ® a1 activation ® vasoconstriction ® ­ BP. ­ cAMP ® ­ contractility.

Absorption: No oral. IV. Onset w/in 5 min.

Dist.:

Metabolism.: Catab. by COMT and MAO, esp. in liver and kidneys. Glucuronidation and sulfconjugation

Excretion, t½: Duration of action 10 min. t½: 2 min.

Toxicity/S.E.s: Nausea, vomiting, tachycardia, anginal pain, arrhythmia, headache, hypertension, vasoconstriction. Usu. due to excessive symp activity. Treat by stopping admin. or w/a blockers. Local ischemic necrosis. Contraind. w/pheochromocytomas, uncorrected tachyarrhythm. or vent. fibrillation, MAO inhibitors, furazolidone. Adjust dose w/tricyclics.

Utility: Some shock (e.g., oliguria and low-normal periph. resist, cardiogenic/septic shock). CHF.

Name: Dobutamine (Dobutrex)

Class: CHF Rx (Mixed (a-b) Agonist (Cardioselective))

Mechanism: Stim. a and b receptors, but not DA. ® ­ CO w/o ­ HR. ­ stroke volume. No/little change in peripheral resistance. ­ cAMP ® ­ contractility.

Absorption: IV ® rapid onset (1-2 min). Peak effect ~ 10 min.

Dist.:

Metabolism.: Methylation by COMT. Conjugation

Excretion, t½: 2 min.

Toxicity/S.E.s: ­ BP, ­ HR, tachycardia, ventricular ectopic activity. ­ myocard. O₂ consump. may cause ­ size MI. Tachyphylaxis to b stim.

Utility: Short-term treatment of cardiac decompensation after cardiac surgery or w/CHF or acute MI. Often DOC after acute MI. Treatment of shock after correction of hypovolemia.

Name: Digitoxin (Crystodigin)

Class: CHF Rx (Cardiac Glycoside)

Mechanism: Inhib. of Na⁺/K⁺ ATPase ® ­ release of Ca²⁺ from SR ® ­ myocardial contractility. Also ­ sensitivity of AV node to vagal stimulation ® ¯ ventricular rate in atrial flutter or fibrillation (i.e., anti-arrhythmic).

Absorption:

Dist.: Strong protein binding.

Metabolism.: Hepatic Metabolism.

Excretion, t½: Feces. Longer t½ than digoxin.

Toxicity/S.E.s: Low therapeutic index. Toxicity enhanced by hypokalemia. Arrhythmias (possibly life-threatening), anorexia, n/v/d, drowsiness, fatigue, visual disturbances. Verapamil or quinidine ® ­ toxicity.

Utility: Treat heart failure.

Special Features: Active Metabolismolites. Longer t½, more GI absorption, and more protein binding than digoxin.

Name: Digoxin (Lanoxin)

Class: CHF Rx (Cardiac Glycoside)

Mechanism: Inhib. of Na⁺/K⁺ ATPase ® ­ release of Ca²⁺ from SR ® ­ myocardial contractility. Also ­ sensitivity of AV node to vagal stimulation ® ¯ ventricular rate in atrial flutter or fibrillation (i.e., anti-arrhythmic).

Absorption:

Dist.:

Metabolism.: Very little.

Excretion, t½: Urine. Short t½.

Toxicity/S.E.s: Low therapeutic index. Toxicity enhanced by hypokalemia. Arrhythmias (possibly life-threatening), anorexia, n/v/d, drowsiness, fatigue, visual disturbances. Verapamil or quinidine ® ­ toxicity.

Utility: Treat heart failure. DOC for atrial fibrillation/flutter.

Special Features: No active Metabolismolites. Shorter t½, less GI absorption, and less protein binding than digitoxin. Only cardiac glycoside routinely used.

Name: Ethanol

Class: Teratogen With Immediate and Delayed Developmental Effects

Mechanism:

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: High risk of fetal alcohol syndrome. Risk present in all trimesters.

Utility:

Special Features:

Name: Diethylstilbestrol (DES)

Class: Teratogen With Delayed Developmental Defects

Mechanism:

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Female fetuses exposed to diethylstilbestrol are at increased risk for vaginal adenosis and clear cell vaginal adenocarcinoma after puberty. Risk present in all trimesters.

Utility:

Special Features: Previously commonly used to treat pregnant women who were threatening spontaneous abortion.

Name: Isotretinoin (Accutane)

Class: Teratogen With Immediate Developmental Effects

Mechanism:

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Extremely high risk of congenital anomalies. Problem for
pimply pregnant people. Risk present in all trimesters.

Utility: Used to treat severe, intractable acne.

Special Features:

Name: Thalidomide

Class: Teratogen With Immediate Developmental Effects

Mechanism:.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Embryonic exposure between weeks 4-7 of gestation ® ­­ risk of birth defects, esp. phocomelia. Paternal use of thalidomide can
also result in serious birth defects. Risk only in first trimester.

Utility: Currently used in treatment of leprosy and AIDS.

Special Features: Previously widely used in Europe as a sedative-hypnotic with the result of ~8,000 babies with phocomelia.

Name: Medroxyprogesterone (Depo-Provera)

Class: Long-Acting Contraceptive (Progestin-Only)

Mechanism: Doesn’t always inhibit ovulation. Produces changes in cervical mucus ® block of sperm penetration.

Absorption: IM

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Irregular menstrual bleeding, headaches, depression. Drug
cannot be removed to alleviate side effects.

Utility: Contraception, esp. in patients c/i for estrogen therapy.

Name: Morning-After Pill (Ovral, The Pill, etc.)

Class: Oral Contraceptive (Estrogen/Progestin Combination)

Mechanism: Blocks nidation by producing an unfavorable endometrium.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Breast fullness, depression, dizziness, edema, headache, n/v, cardiovascular disease (esp. in smokers over age 35). C/i in presence of cerebrovascular and thromboembolic disease,
estrogen-dependent neoplasms, liver disease, and migraine headache.

Utility: Post-coital contraceptive. Usu. ~99% effective if admin. w/in 72 hours.

Special Features:

Name: The Pill (Various)

Class: Oral Contraceptive (Estrogen/Progestin Combination)

Mechanism: Blocks ovulation, suppresses endometrial growth, produces changes in cervical mucus ® block of sperm penetration.

Absorption: Oral.

Dist.: Metabolism.: Excretion, t½:

Toxicity/S.E.s: Breakthrough bleeding, amenorrhea, water retention, headache, breast fullness, depression, dizziness, edema, headache, n/v, weight gain, acne, cardiovascular disease (esp. in smokers over age 35). Absolute C/Is—thromboembolic disorder, CVA, CAD, ¯ liver fxn, hepatic adenoma, estrogen-dependent cancer (e.g., breast, endometrium), pregnancy, undiagnosed vaginal bleeding, tobacco use over age 35. Relative C/Is—migraine headaches, hypertension, leiomyomata, diabetes mellitus or prev. gestational diabetes, elective surgery, seizures or anticonvulsant use, obstructive jaundice in pregnancy, sickle cell disease, gall bladder disease.

Utility: Contraception, dysmenorrhea, prophylaxis against endometriosis.

Special Features: Decreases the risks of endometrial and ovarian cancer and benign breast disease.

Name: Norgestrel (Ovrette)

Class: Oral Contraceptive (Mini-Pill) (Low-Dose Progestin)

Mechanism: Doesn’t always inhibit ovulation. Produces changes in cervical mucus ® block of sperm penetration.

Absorption: Oral

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: High incidence of abnormal bleeding. Headaches, depression.

Utility: Contraception, esp. in patients c/i for estrogen therapy.

Special Features: Less effective than estrogen-progestin combination pills. None of the cardiovascular toxicity of the combination pill.

Name: Levonorgestrel (Norplant)

Class: Long-Acting Contraceptive (Progestin-Only)

Mechanism: Doesn’t always inhibit ovulation. Produces changes in cervical mucus ® block of sperm penetration.

Absorption: Subcutaneous implant

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Irregular menstrual bleeding and headaches.

Utility: Contraception, esp. in patients c/i for estrogen therapy.

Special Features: Cheaper than oral contraceptives, completely reversible, and good for 5 years. Probably the most effective reversible method of contraception available. None of the cardiovascular toxicity of the combination pill.

Name: Norethindrone (Norlutine)

Class: Oral Contraceptive (Progestin-Only) (Mini-Pill)

Mechanism: Doesn’t always inhibit ovulation. Produces changes in cervical mucus ® block of sperm penetration.

Absorption: Oral

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: High incidence of abnormal bleeding. Headache, depression.

Utility: Contraception, esp. in patients c/i for estrogen therapy.

Special Features: Less effective than estrogen-progestin combination pills. None of the cardiovascular toxicity of the combination pill.

Name: Conjugated estrogens (Premarin)

Class: Estrogen

Mechanism: Diffuses across cell membranes and binds to cytoplasmic receptor proteins. Complex enters nucleus and interacts w/DNA to initiate RNA synthesis. Stimulates development of the endometrial lining, maintains normal structure of skin and blood vessels in E, antagonizes PTH effects on bone, reduces motility of the bowel, enhances coagulability of blood, increases HDL, decreases LDL.

Absorption:

Dist.: Metabolism.: Excretion, t½:

Toxicity/S.E.s: Increased risk of breast and endometrial cancer.

Utility: Postmenopausal estrogen replacement therapy to treat hot flashes, atrophic vaginitis, and urethral changes, and to prevent osteoporosis and cardiovascular disease.

Special Features: Usu. combined with a progestin to reduce the risk of endometrial carcinoma. Only useful prophylactically for osteoporosis. Less first-pass Metabolism. than estradiol ® more effective oral administration.

Name: Estradiol (Estrace)

Class: Estrogen

Mechanism: Diffuses across cell membranes and binds to cytoplasmic receptor proteins. Complex enters nucleus and interacts w/DNA to initiate RNA synthesis. Stimulates development of the endometrial lining, maintains normal structure of skin and blood vessels in E, antagonizes PTH effects on bone, reduces motility of the bowel, enhances coagulability of blood, increases HDL, decreases LDL.

Absorption:

Dist.: Metabolism.: Excretion, t½:

Toxicity/S.E.s: May increase risks of breast and endometrial cancer. Nausea/vomiting.

Utility: Postmenopausal estrogen replacement therapy to treat hot flashes, atrophic vaginitis, and urethral changes, and to prevent osteoporosis and cardiovascular disease.

Special Features: Usu. combined with a progestin to reduce the risk of endometrial carcinoma. Only useful prophylactically for osteoporosis,.

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: Metolazone (Mykrox)

Class: Diuretic (Thiazide-Like)

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:

Toxicity/S.E.s: Hypokalemia, hyponatremia, hyperuricemia, hypercalcemia, Metabolismolic alkalosis, postural hypotension, hyperglycemia (in patients w/DM), and rare hypersensitivity rxns. C/i—pts susceptible to problems w/hypokalemia (cirrhosis, pts on digitalis), hyperuricemia (gout), or hypercalcemia.

Utility: The only distal nephron diuretic efficacious in patients w/severe renal insufficiency. Treat hypertension, CHF, nephrotic synd., other Na⁺-retaining states. Reduce Ca²⁺ excretion (e.g., prevention of kidney stones).

Special Features: Strongest inhib. of Na⁺ & water reabsorption of the thiazide and thiazide-like diuretics. Often given in comb. w/a loop diuretic. Milder diuretic action than loop diuretics.

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: 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:

Toxicity/S.E.s: Hypokalemia, hyponatremia, hyperuricemia, hypercalcemia, Metabolismolic alkalosis, postural hypotension, 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.

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

Special Features: Most commonly prescribed class of diuretics. Milder diuretic action than loop diuretics. 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: Ethacrynic Acid (Edecrin)

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.

Toxicity/S.E.s: Hypokalemia (esp. dangerous if pt. is on digitalis), Ca²⁺ & Mg²⁺ depletion, Metabolismolic alkalosis, volume contraction, mild hyperglycemia, ototoxicity. C/i—pts. susceptible to volume contraction from excessive diuresis (e.g., elderly), and pts. susceptible to problems w/hypokalemia (e.g., cirrhosis, pts. taking digitalis).

Utility: Diuresis for hypertension when a short-acting diuretic is indicated. Very useful in conditions refractory to less potent diuretics, including CHF, renal insufficiency, and nephrotic synd. Also used to treat hypercalcemia.

Special Features: More ototoxic than other loop diuretics. Most potent diuretics available. Can cause excretion of up to 20% of filtered Na⁺.

Name: Bumetanide (Bumex)

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.

Toxicity/S.E.s: Hypokalemia (esp. dangerous if pt. is on digitalis), Ca²⁺ & Mg²⁺ depletion, Metabolismolic alkalosis, volume contraction, mild hyperglycemia, 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, pts. taking digitalis).

Utility: Diuresis for hypertension when a short-acting diuretic is indicated. Very useful in conditions refractory to less potent diuretics, including CHF, renal insufficiency, and nephrotic synd. Also used to treat hypercalcemia.

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