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29 Cards in this Set
- Front
- Back
Mannitol
mechanism |
osmotic diuretic - totally excreted so water follows
no cross BBB - pulls fluid from brain |
|
Mannitol
uses |
shock
drug overdose high intracranial/intraocular pressure |
|
Mannitol
SE |
pulmonary edema, dehydration
contraindicated in anuria and CHF |
|
Acetazolamide mechanism
|
carbonic anhydrase inhibitor
excrete bicarb as NaHCO3 |
|
Acetazolamide
use |
glaucoma
urinary alkalinization metabolic alkalosis altitude sickness (acidotic state stimulates ventilation increasing O in blood) |
|
Acetazolamide
SE |
hyperchloremic metabolic acidosis (H backs up entering cell w/ Cl symport)
neuropathy NH3 toxicity sulfa allergy |
|
Furosemide
mechanism |
loop diuretic (thick ascending limb)
inhibits NaK2Cl cotransport medulla becomes hypotonic so water flows into urine (pee no concentrated) loops lose calcium (no paracellular transport) |
|
Furosemide
use |
edema states
hypertension hypercalcemia |
|
Furosemide
SE |
OH DANG
ototoxicity hypokalemia dehydration allergy - sulfa nephritis - interstitial gout |
|
Ethacrynic acid
mechanism |
like furosemide but no sulfa
block NaK2Cl symport decrease Ca paracellular reabsorption |
|
Ethacrynic acid
use |
edema
hypertension hypercalcemia |
|
Ethacrynic acid
use |
ototoxic
hypokalemia dehydration nephritis (interstiital) * can be used in hyperuricemia/acute gout, no sulfa allergy |
|
Hydrochlorothiazide
mechanism |
inhibit NaCl reabsorption in early distal tubule
increase Ca reabsorption |
|
Hydrochlorothiazide
use |
hypertension
CHF idiopathic hypercalciuria nephrogenic diabetes insipidus |
|
Hydrochlorothiazide
SE |
hypokalemic metabolic alkalosis
hyponatremia hyperGLUC (glycemia,lipidemia,uricemia,calcemia) sulfa allergy |
|
Spirinolactone
mechanism |
competitive aldosterone receptor agonist in collecting duct
block Na channel |
|
Spirinolactone
use |
hyperaldosteronism
hypokalemia (Na absorption drives K excretion so cut off Na increase K) CHF |
|
Spirinolactone
SE |
hyperkalemia
arrythmia endocrine effect like gynecomastia and antiandrogen effects (blocking aldosterone) |
|
Triamterene and Amiloride
mechanism |
block Na channel in collecting duct (like spirinolactone)
|
|
Triamterene and Amiloride
use |
hyperaldosteronism
hypokalemia CHF |
|
Triamterene and Amiloride
SE |
hyperkalemia - arrythmia
endocrine effect (gynecomastia and antiandrogen effects) |
|
Captopril, enalapril, LIsinorpril
mechanism |
ACE inhibitor
reduce Ang II and prevent inactivation of bradykinin (vasodilator) increase renin (lose Ang II feedback) |
|
Captopril, Enalapril, Lisinopril
use |
hypertension
CHF diabetic renal disease |
|
Captopril, Enalapril, Lisinopril
SE |
* CAPTOPRIL and hyperkalemia
Cough (increase bradykinin) Angioedema Proteinuria Taste change hypOtension Preggers prob (fetal renal damage) Rash Increased renin Low Ang II * Contraindicated in renal bilateral artery stenosis b/c ACE-I decrease GFR by preventing constriction of efferent arteroles |
|
Diuretics
increasing urine K |
all e/c spirinolactone, triamterene, amiloride
|
|
Diuretics
decrease blood pH |
acetazolamide by decreasing bicarb reabsorption
spirinolactone, triamterene, amiloride by preventing K and H secretion |
|
Diuretics
increasing blood pH |
loops and thiazides
1. volume contract increase Ang2 increase Na/H antiport 2. K loss so K leaves cell and H enters cell 3. in hypokalemia state, H exchanged for Na so H excreted instead |
|
Diuretics
increase urine Ca |
loop diuretic
no more lumen+ potential in TAL of loop --> paracellular Ca reabsorp decrease |
|
Diuretic
decrease urine Ca |
hydrochlorothiazide
volume depleted Na reabsorption increase more paracellular ca reabsorption in PT and loop block Na/Cl transport so less Na coming in thus increasing Na/Cl antiport on blood side |