Pharm lecture 3 Flashcards
osmotic diuretic
mannitol
MOA osmotic
filter at the glomerulus, water is held in the lumen by the osmotic effect producing diuresis
where does osmotic diuretic occurs
proximal convoluted tubule
main use of mannitol
rapid treatment of increased intracranial pressure
carbonic anhydrase inhibitor
-Acetazolamide
-Dorzolamide
-Brinzolamide
-Methozolamide
MOA of carbonic anhydrase inhibitor
inhibit the reabsorption of sodium and bicarb
Where is the carbonic anhydrase inhibitor
proximal convoluted tubule
therapeutic use of carbonic anhydrase inhibitor
metabolic alkalosis and glaucoma
Loop diuretics
-furosemide
-bumetanide
-torsemide
-ethacrynic acid
therapeutic use of loop diuretic
CHF, edema and kidney disease
which diuretic is the most potent
loop diuretic
- inhibit the reabsorption of sodium up to 25%
MOA of loop diuretics
inhibits sodium, potassium, chloride transporter and reduce sodium reabsorption in the ascending loop of hence
what ions are loss in the loop diuretics
sodium, chloride, water, potassium, magnesium, calcium
_____ is about 40 times more potent than ______
- bumetanide
2.furosemide
which loop diuretic can be used if pt has allergy to other loop diuretics
ethacrynic acid
concern with ethacrynic acid
greater ototoxic than other loop diuretics
SE of loop diuretics
tinnitus (ototoxicity), limit the rate of infusion of furosemide to 4mg/min
electrolyte disturbance in loop diuretic
hypokalemia, hypochloremia, hypomagnesemia, alkalosis
adverse effect associated with hypokalemia
arrhythmia, potential for digoxin toxicity
which diuretic cause increase risk of gout
loop diuretic
thiazide diuretics
-chlorothiazide
-HCTZ
-metolazone
-chlorthalidone
-indapamide
MOA of thiazide diuretic
inhibit the reabsorption of sodium and chloride ions in the distal convoluted tubules by blocking NA-Cl transporter
therapeutic use of thiazide diuretics
HTN, edema, preventative treatment for hypercalcemia kidney stones
SE of thiazide diuretics
hypokalemia, hypochloremia, hypomagnesemia, hyperuricemia
Loop and thiazide
used together to optimize the diuretic efficacy by interfering with sodium reabsorption at the thick ascending loop and distal convoluted tubules
* used for diuretic resistance
Potassium sparing diuretics
spironolactone and eplerenone
-amiloride, triamterene
MOA of potassium sparing diuretics
competes with aldosterone in the collecting duct to reduce the synthesis of sodium channel resulting in loss of sodium and retention of potassium
SE of spironolactone
gynecomastia
Calcium channel MOA
blocks the influx of calcium in vascular smooth muscle and cardiac muscle resulting in decrease intracellular calcium
CCB meds
Dihydropyridine
-amlodipine
-nifedipine
nondihydropyridines
-diltiazem
-verapamil
therapeutic use of CCB
HTN, angina, arrhythmia
which diuretic increase the risk of gout?
Loop diuretics
which CCB cause bradycardia
Nondihydropyridines
-diltiazem, verapamil
MOA BB
reduce HR and contractility by blocking the release of norepinephrine and epinephrine at b1
mixed a and b blockers
block the action of norepinephrine at a-1 receptors and BB action
therapeutic use of BB
HTN, angina, CHF, arrhythmia, cirrhosis
What happens with chronic use of BB
increase in beta receptors, super sensitive to beta agonist action and possibly lead to MI if suddenly stop
Meds of mixed a and B
carvedilol, labetalol
Beta-blocker with ISA vs Beta blocker without ISA
BB with ISA doesn’t reduce the resting CO and HR as effectively as BB without ISA
BB with ISA
Acebutolol, Sotalol, Pinodolol
SE of BB
bradycardia, hypotension, mask signs of hypoglycemia, bronchoconstriction
