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24 Cards in this Set

  • Front
  • Back
M: osm diuretic, + tubular fluid osmolarity, + urine flow

C: shock, drug OD, - intracranial/intraocular pressure
M: carb anhydrase inhibitor, cause NaHCO3 diuresis, - total body HCO3- stores, prox tubule action

C: glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness
M: sulfonamide loop diuretic, inhibit cotransport system (Na/K/2Cl) of thick asc limb, abolish medullary hypertonicity to prevent concentration of urine, + Ca++ secretion (Loops Lose calcium)

C: edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia
ethacrynic acid
M: phenoxyacetic acid derivative, same action as furosemide

C: diuresis in pts allergic to sulfa drugs
M: thiazide diuretic, inhibit NaCl reabsorption in early distal tubule, reduce diluting capacity of nephron, - Ca++ excretion

C: hypertension, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus
K+ sparing diuretics: spironolactone, triamterene, amiloride, eplereone
M: a) competitive aldosterone receptor antagonist in cortical collecting tubule; b) block Na+ channels in the CCT

C: hyperaldosteronism, K+ depletion, CHF
which diuretics + urine NaCl?
all diuretics increase this urine electrolyte
which diuretics + urine K+?
all but K+ sparing increase this urine electrolyte
which diuretics - blood pH (acidosis)? which + blood pH (alkalosis)?
CA inhibitors, K+ sparing decrease this; loop diuretics, thiazides
which diuretics + urine Ca++? which - urine Ca++?
loop diuretics + this urine electrolyte, while thiazides decrease it
M: + cGMP to relax smooth muscle, vasodilate arterioles more than veins; afterload reduction

C: severe hypertension, CHF
calcium channel blockers: verapamil, diltiazem, nifedipine
M: block voltage-dependent L-type Ca++ channels of cardiac and smooth muscle to reduce contractility

C: hypertension, angina, arrhythmias (NOT nifedipine)
order of CCB's for a) most to least effect on cardiac muscle; b) vascular smooth muscle
a) verapamil>diltiazem>nifedipine

b) nifedipine>diltiazem>verapamil
M: angiotensin II receptor antagonist

T: no cough
ACE inhibitors: captopril, enalapril, lisinopril
C: hypertension, CHF, diabetic renal disease
mechanism of ACE inhibitors: captopril, enalapril, lisinopril
M: inhibit angiotensin-converting enzyme, - angiotensin II levels, prevent inactivation of bradykinin (a potent vasodilator)
toxicity of ACE inhibitors
"CAPTOPRIL": Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, increased Renin, Lower angiotensin II (& hyperkalemia)
nitroglycerine, isosorbide dinitrate
M: vasodilate by releasing NO in smooth muscle, + in cGMP and smooth muscle relaxation, dilates veins >> arteries

C: angina, pulmonary edema, aphrodisiac and erection enhancer
CCB's: nifedipine is similar to xxxx in effect; verapamil is similar to xxxx in effect
a) nitrates; b) beta blockers
antianginal therapy: what are the determinants of myocardial oxygen consumption? (MVO2)
end diastolic volume, blood pressure, contractility, heart rate, ejection time
cardiac glycosides: digoxin
M: 75% bioavailability, 20-40% protein bound, half-life 40hrs, urinary excretion; inhibits Na/K ATPase of cell membrane to + Ca++ inside cells and increases contractility

C: CHF (+ contractility), atrial fibrillation (- AV node conduction)
list the class Ia anti-arrhythmics
quinidine, amiodarone, procainamide, disopyramid
list the class Ib anti-arrhytmics
lidocaine, mexiletine, tocainide
list the class Ic anti-arrhythmics
flecainide, encainide, propafenone