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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