Renal Pharmacology Flashcards
(27 cards)
Mannitol
clinical use
toxicity
used to treat drug overdose
elevated intracranial pressure
toxicity is pulmonary edema
contraindicated in HF
Acetazolamide
mechanism
carbonic anhydrase inhibitor
causes self limited NaHCO3 diuresis and decrease in total body HCO3 stores - i.e. metabolic acidosis
Acetazolamide
clinical use and toxicity
glaucoma / metabolic alkalosis / alkanilize urine / altitude sicknes / pseudotumor cerebri
toxiticy - metabolic acidosis
sulfa allergy
sulfa loop diuretics (3)
furosemid
bumetanide
torsemide
mechanism of loop diuretics
inhibit Na/K/2Cl cotransporter in thick ascending abolishing hypertonicity of medulla
also stimulate PGE release which vasodilates affarent arteriole (inhibited by NSAIDS)
Why do loops cause potassium wasting
inhibit the NA/K/2CL
What effect do loops have on calcium
increase calcium excretion by fucking with the lumenal negativity - which normally drives Ca and Mg back into blood - so we could give to someone with hypercalcemia but we would not give loops to someone with kidney stones as this would exacerbate the problem
toxicity of loops
OH DANG
Ototoxicity Hypokalemia Dehydration Allergy (sulfa) Nephritis (interstitial - eosinophils) Gout - increased urinary calcium - stones
alternative loop diuretic for those with sulfa allergy
ethacrynic acid
Thiazide diuretics
chlorthalidone
hydrochlorothiazide
Thiazide diuretics (chlorthalidone and hctz) work by
inhibit the NaCl reabsorption in early DCT leading to a decreased medulla concentration / ability to concentrate urine
Also via decreased Na reabsorption - decrease Na/Ca exchanger and thus increase Calcium in blood (via decreased sodium blood exchange)
How do thiazide diuretics cause hypokalemia?
because the diuresis induced leads to renin release which leads to aldosterone which leads to blocking of k reabsorption in the collecting duct - also leads to blocking of H+ in the collecting duct - alkalosis
Calcium and thiazides
increased in blood
the following conditions could benefit from what? hypertension HF hypercalcuria nephrogenic DI osteoperosis
thiazide diuretic (chlorthalidone/ hctz)
thiazide diuretic toxicity
hypokalemia - muscle spasm / weakness? metabolic alkalosis hyponatremia - nausea hyperGLUC Glycemia Lipid Uricemia Calacemia Sulfa allergy
Potassium sparing diuretics
Spironolactone (eplerenone for gynocomastia)
— competitive androgen receptor antagonists
Triamterene ; Amiloride
—block Na channels in the cortical ct
THE K Spironolactone Triamterene Amiloride ys
potassium sparing diuretic clinical use
hyperaldosteronism
k depletion
HF
Toxicity of potassium sparing diuretics
hyperkalemia -
ACE inhibitors
captopril
enalopril
lisinopril
ramipril
ACE inhibitors effect of GFR
decrease because block at-ii selective efferent constriction - but this is good if you have diabetic nephrophathy
bradykinin
potent vasocontrictor
ACE inhibitor toxicity
CATCHH
Cough Angioedema (dont give to C1 esterase deficient) Teratogenic Hyperkalemia Hypotension
Why are ACE inhibitors good for Diabetic nephropathy
lower GFR and slow GBM thickening
ARBS
losartan
candesarta
valsartan
