Renal I Flashcards
mannitol MOA
osmotic diuretic
adverse mannitol
pulmonary edema
dehydration
CI in heart failure
mannitol clinical use
drug overdose
elevated intracranial/intraocular pressure
acetazolamide MOA
carbonic anhydrase inhibitor
decrease total body HCO3 stores
acetazolamide clinical use
glaucoma urinary alkalinization metabolic alkalosis altitude sickness pseudotumor cerebri - high pressure in skull
acetazolamide adverse
hyperchloremic metabolic acidosis
paresthesia
NH3 toxicity
sulfa allergy
furosemide
loop diuretic
bemetanide
loop diuretic
torsemide
loop diuretic
loop diuretic MOA
inhibit cotransport Na/K/2Cl thick ascending limb
prevent concentration of urine
stimulate PGE release - vasodilatory effect
-inhibited by NSAIDs
incrased Ca excretion - hypoCa
clinical use loop diuretics
edematous state - HF, cirrhosis, nephrotic syndrome, pulmonary edema
HTN
hyperCa
adverse loop diuretics
ototoxicity hypoK ehydration sulfa allergy nephritis - interstitial gout
ethacrynic acid
non - sulfonamide loop diuretic
clinical use ethacrynic acid
sulfa allergy - diuresis tx
chlorthalidone
thiazide diuretic
thiazide diuretic MOA
inhibit NaCl reabsorption - early DCT
-decreased diluting capacity of nephron
decrease Ca excretion
thiazide clinical use
HTN heart failure idiopathic hyperCa nephrogenic DI osteoporosis
adverse thiazide
hypoK metabolic alkalosis hypoNa hyperglycemia hyperlipidemia hyperuricemia hyperCa
sulfa allergy
spironolactone
aldosterone antagonist - K sparing
eplerenone
aldosterone antagonist - K sparing
triamterene
Na channel blocker - K sparing
amiloride
Na channel blocker - K sparing
K sparing MOA
aldosterone antagonist in collecting tubule
or as Na channel blocker collecting tubule
K sparing clinical use
hyperaldosteronism
K depletion
heart failure
adverse K sparing
hyperK - arrhythmia
endocrine effect - spironolactone - gynecomastia, antiandrogen effects
diuretics
acetazolaminde mannitol loops thiazides K sparing
acid base with CAIs
acidemia
-decreased bicarb reabsorption
acid base with K sparing
acidemia
-aldosteorne block - prevent K secretion and H secretion
also - hyperK leads to K entering all cells in exchange for H
acid base with loops
alkalemia - volume contraction
-increased angiotensin II - more Na/H exchange PCT > more bicarb reabsorption (contraction alkalosis)
K loss - leads to K exiting cells exchange for H entering cell
low K state - H exchanged for Na in cortical collecting tubule
acid base with thiazides
alkalemia - volume contraction
-increased angiotensin II - more Na/H exchange PCT > more bicarb reabsorption (contraction alkalosis)
K loss - leads to K exiting cells exchange for H entering cell
low K state - H exchanged for Na in cortical collecting tubule
urine Ca with loops
decreased paracellular Ca reabsorption
increased urine Ca
urine Ca with thiazides
enhanced Ca reabsorption - DCT
decreased urine Ca
urine potassium
increased with loops
captopril
ACE inhibitor
ramipril
ACE inhibitor
ACE inhibitor mechanism
inhibit ACE
- decreased ANG II > decreased GFR
- decreased constriction efferent arterioles
renin increase - loss of feedback
also prevent inactivation of bradykinin
ACE inhibitor clinical use
HTN, HF, proteinuria
diabetic nephropathy
prevent unfavorable heart remodeling
adverse ACE inhibitor
cough angioedema - lots of bradykinin teratogen creatinine increase hyperKa hypotension
avoid in B/L renal artery stenosis
ACE inhibitor - because will further decrease GFR > renal failure
losartan
ANG II blocker
candesartan
ANG II blocker
valsartan
ANG II blocker
ANG II blocker MOA
block ANG II binding AT1 receptor
clinical use ANG II blocker
HTN
HF
proteinuria
diabetic nephropathy
adverse ANG II blocker
hyperK
decreased renal function
hypotension
teratogen
aliskiren
direct renin inhibitor
block conversion angiotensinogen to ANG I
clincal use aliskiren
HTN
adverse aliskiren
hyperK
decreased renal f unction
hypotension
CI - diabetic taking ACE I or ARBs