Renal Drugs Flashcards
MOA of mannitol
osmotic diuresis
uses of mannitol
drug overdose
increased ICP
increased IOP
toxicity of mannitol
pulmonary oedema
dehydration
contraindicated in HF and anuria
MOA of acetazolamide
inhibits carbonic anhydrase in the PCT
results in self limited NaHCO3 diuresis and decreased total body HCO3- stores.
clinical used of acetazolamide
glaucoma urinary alkalinisation metabolic alkalosis altitude sickness pseudotumor cerebri (chronic vitamin A use)
toxicity of acetazolamide
hyperchloremic metabolic acidosis ACIDazolamide causes Acidosis
paresthesias
NH3 toxicity
sulfa allergy
list the sulfa drugs
probenecid furosemide thiazides acetazolamide sulfa abs sulfonylureas sulfasalazine celecoxib
list the loops diuretics
furosemide
bumetanide
torsemide
MOA of loops
inhibit the NaK2Cl in the thick ascending loop of henle – no hypertonicity in the medulla – no concentration of urine
stimulates PGE release - vasodilation of the afferent arterioles (can inhibit with NSAIDs)
Ca excretion
LOOPS LOSE CALCIUM
clinical use of loops
edematous states - HG, irrhosis, nephrotic syndrome, pulmonary yoedema
hypertension
hypercalcemia
toxicity of loops
OH DANG ototoxicity hyperkalemia dehydration allergy (sulfa) nephritis (interstitial) glout (hyperuricemia)
why would you use ethacrynic acid
for diuress in patients allergic to sulfa drugs (furosemide, acetazolamide, thiazides)
MOA of ethacrynic acid please
pheonoxyacetic acid derivative with same MOA of forusemide (NaK2Cl blocker)
toxicitiy of ethacrynic acid please
similar to furosemide OH DANG: ototoxicity, hyperkalemia, dehydration, neprhritis, gout`
list the thiazide diurectic please
chlorthalidone
hhydrochlorothiazide
MOA of thiazides
inhibits NaCl reabsorption in early DCT – decreases diluting ability
decreased Ca excretion
clinical use fo thiazides
hypertenision HF idiopathic hypercalciuria nephrogenic diabtes insipidus osteoporosis calcium stones
toxicity of thiazides
HyperGLUC hypokalemic metabolic alkalosis hyponatremia hyperglycemia hyperlipidemia hyperuricemia hypercalcemia
list the K sparing diuretics
spironolactone, eplerenone
triamterene, amiloride
MOA of spironolactone and eplerenone
competitive aldoster recetpro antagos in the cortical collecring tubule
MOA of triamterene and amiloride
inhibt ENaC in the cortical collecting tubule
cx use of k sparign diuretics
hyperaldosternosim
K depletion
HF
toxo of K sparing diuretics
hyperkalaemia - arrhythmias
spironolactone - anti androgenic - gynecomastia
which diuretics increased urine NaCl
all but acetazolamide
serum NaCl may decrease as a result
which diuretics increased urine K
loops and thiazides
may descreased serum K as a result
which diuretics cause acidemia
carbonic anhydrase inhibitos
K sparing
which diuretics cause alkalemia
loops
thiazides
describe how carbonic anhydrase inhibitors cause acidemia
decreased HCO3 reabsorption
describe how K sparers caused acidemia
aldoseterone blockade prevents K secretion and H secrtion
increased K results in H out
describe how loops and thiazides cause alkalemia
volume contraction – increasd AngII – increased Na/H exchange and icnreasd HCO3 reabsorption CONTRACTION ALKALOSIS
K loss leads to exchange out K out for H in to cells
low K states, H si exchangd for Na in the corical collecting tubules – paradoxical aciduria
what diuretics cause increased urine ca
loops - decreasd paracellular ca reabsorption – hypocalcemia
which diuretcics caus decreasd urine ca
thiazides - enhanced Ca reabsorption in DCT
list the ACEi
captopril
enalapril
lisinopril
ramipril
MOA of ACEi
inhibit ACE – decreased ANng II – decreased GFR by prevention of constriction of efferent arterioles
icnreasd renin due to loss fo negative inhibition
prevents inacativation of bradykinin – vasodilation
cx of ACEi
hypertension
HF
proteinuria
diabetic nephropathy
why are ACEi good in chronic hypertension
prevent unfavourable remodelling of heart
why are ACEi good in diabetes?
decreased intraglomerular pressure - slows GBM thickenign
toxo of ACEi?
Captoprils CATCHH
Cough
Angioedema - don’t use with C1 esterase deficiency
Teratogen - fetal kidney abnormalities
Creatinine serum increased - decrease GFR
hyperkalemia
hypotencion
list the Ang II receptor blockers/ARBs
losartan
candesartan
valsartan
MOA of ARBs
selectively block binding of ant II to AT1 receptor
similar to ACEi but don’t prevent breakdown of bradykinine
use of ARBs?
hypertension HF proteinuria diabetic nephropathy when ACEi aren't good (cough angioedema)
a/se of ARBS
similar to ACEi (CATCHH) teratogen increasd creatinine hyperkalemia hypotension
