Renal Pharmacology Flashcards
mannitol–mechanism
- osmotic diuretic
- increase tubuar fluid osmolarity –> increase urine flow, decrease intracranial/intraocular pressure
mannitol–use
- drug overdose
- elevated intracranial/intraocular pressure
mannitol–toxicity
- pulmonary edema
- dehydration
what are contraindications for mannitol?
- anuria
- HF
acetazolamide–mechanism
- carbonic anhydrase inhibitor
- causes self limited NaHCO3 diuresis and decrease in total body HCO3- stores
acetazolamide–use
- glaucoma
- urinary alkalinization
- metabolic alkalosis
- altitude sickness
- pseudotumor cerebri
acetazolamide–toxicity
- proximal renal tubular acidosis
- paresthesias
- NH3 toxicity
- sulfa allergy
- “ACIDazolamide causes ACIDosis”
name the 4 loop diuretics
- furosemide
- bumetanide
- torsemide
- ethacrynic acid
furosemide, bumetanide, torsemide–mechanism
- inhabit contransport system (Na/K/2Cl) of thick ascending limb of loop of Henle
- abolishes hypertonicity of medulla which prevents concentration of urine
- increase Ca2+ excretion
- Loops Lose Ca2+
furosemide, bumetanide, torsemide–what type of loop diuretic?
- sulfonamide loop diuretic
what does furosemide, bumetanide, torsemide stimulate and what is the effect?
- stimulates the release of PGE
- vasodilatory effect on afferent arteriole
what is furosemide, bumetanide, torsemide inhibited by?
NSAIDs
furosemide, bumetanide, torsemide–use
- edematous states
- HF
- cirrhosis
- nephrotic syndrome
- pulmonary edema
- hypertension
- hypercalcemia
furosemide, bumetanide, torsemide–toxicity
-
OH DANG
- Ototoxicity
- Hypokalemia
- Dehydration
- Allergy (sulfa) and Metabolic Alkalosis
- Nephritis (interstitial)
- Gout
ethacrynic acid–mechanism
- nonsulfonamide inhibitor of cotransport system (Na/K/2Cl) of thinck ascending limb of loop of Henle
ethacrynic acid–use
- diuresis in patients allergic to sulfa drugs
ethacrynic acid–toxicity
- similar to furosemide
- more ototoxic
- “Loop earrings hurt your ears”
- more ototoxic
- hyperuricemia
- never use to treat gout
name the diuretics that work at the PCT:
- mannitol
- acetazolamide
name the diuretics that work at the loop of Henle:
- furosemide
- bumetanide
- torsemide
- ethacrynic acid
name the diuretics that work at the DCT:
- hydrochlorothiazide
- chlorthalidone
- metolazone
name the diuretics that work at the collecting duct:
- K+ sparing diuretics
- spironolactone
- eplerenon
- triamterene
- amiloride
name the thiazide diuretics:
- hydrochlorothiazide
- chlorthalidone
- metolazone
hydrochlorothiazide, chlorthalidone, metolazone–mechanism
- inhibit NaCl reabsorption in early DCT –> decrease diluting capacity of nephron
- decrease Ca2+ excretion
hydrochlorothiazide, chlorthalidone, metolazone–use
- hypertension
- HF
- idiopathic hypercalciuria
- nephrongenic diabetes insipidus
- osteoporosis
hydrochlorothiazide, chlorthalidone, metolazone–toxicity
- hypokalemic metabolic alkalosis
- hyponatremia
- hyperGlycemia
- hyperLipidemia
- hyperUricemia
- hyperCalcemia
- HyperGLUC
- sulfa allergy
name the potassium sparing diuretics
- Spirinolactone and eplerenone
- Triamterene
-
Amiloride
- “the K+ STAys”
spironolactone and eplerenone–mechanism
- (K+ sparing)
- spironolactONE and eplerenONE are competitive aldosterONE receptor antagonists in cortical collecting tubule
triamterene and amiloride–mechanism
- (K+ sparing)
- act at the same part of the tubule by blocking Na+ channels in the cortical collecting tubule
K+ sparing diuretics–use
- hyperaldosteronism
- K+ depletion
- HF
- hepatic ascites (spironolactone)
- nephrongenic DI (amiloride)
K+ sparing diuretics–toxicity
- hyperkalemia–can lead to arrhythmias
- endocrine effects with spironolactone
- gynecomastia
- antiandrogen effects
diuretic induced electrolyte change: urine NaCl
- inc with all diuretics
- strength varies on potency of diuretic effect
- serum NaCl may decrease as a result
diuretic induced electrolyte change: urine K+
- inc especially with loop and thiazide diuretics
- serum K+ may dec as a result
diuretic induced electrolyte change: decreased blood pH (acidemia)
- carbonic anhydrase inhibitors
- decrease HCO3- reabsorption
- K+ sparing:
- aldosterone blockade prevents K+ secretion adn H+ secretion
- hyperkalemia –> K+ entering all cells via H/K exchanger in exchange for H exiting cells
diuretic induced electrolyte change: increase in blood pH (alkalemia)
- loop diuretics and thiazides cause alkalemia through severeal mechanisms:
- volume contraction –> increase AT II –> increase Na/K exchange in PCT –> inc HCO3- reabsorption
- “contraction alkalosis”
- K+ loss leads to K+ exiting all cells (via H+/K+ exchanger) in exchange for H+ entering cells
- in low K+ state, H+ (rather than K+_ is exchanged for Na+ in cortical collecting tubule –> alkalosis and “paradoxical aciduria”
- volume contraction –> increase AT II –> increase Na/K exchange in PCT –> inc HCO3- reabsorption
diuretic induced electrolyte change: urine Ca2+
- increase with loop diuretics:
- decrease paracellular Ca2+ reabsorption –> hypocalcemia
- decrease with thiazides:
- enhanced Ca2+ reabsorption
name the angiotensin converting enzyme inhibitors
- captopril
- enalapril
- lisinopril
- ramipril
ACE inhibitors–mechanism
- inhibit ACE –> decrease AT II –> decrease GFR by preventing constriciton of efferent arterioles
- increase renin due to loss of negative feedback
- inhibition of ACE also prevent inactivation of bradykinin, a potent vasodilator
ACE inhibitors–use
- HTN
- HF (dec mortality)
- proteinuria
- diabetic neuropathy
what are 2 things that ACE inhibitors can prevent?
- unfavorable heart remodeling
- diabetic neuropathy
- increase intraglomerular pressure, slows GBM thickening
ACE inhibitors–toxicity
- “Captopril’s CATCHH”
- Cough
-
Angiodema
- due to increased bradykinin
-
Teratogen
- fetal renal malformation
- increased Creatinine
- decrease GFR
- Hyperkalemia
- Hypotension
what are contraindications for ACE inhibitors?
- CI esterase inhibitor deficiency
- bilateral renal artery stenosis
why are ACE inhibitors contraindicated in bilateral renal artry stenosis?
- b/c ACE inhibitors further decrease GFR –> renal failure
name the 3 Angiotensin II receptor blockers (ARBs)
- losartan
- candesartan
- valsartan
Angiotensin II Receptor Blockers–mechanism
- selectively block binding of angiotensin II to AT1 receptor
- effects similar to ACE inhibitors
- but ARBs do not increase bradykinin
Angiotensin II Receptor Blockers–use
- HTN
- HF
- proteinuria
- diabetic neuropathy with intolerance to ACE inhibitors
- ie. cough, angioedema
Angiotensin II Receptor Blockers–toxicity
- hyperkalemia
- decrease GFR
- hypotension
- teratogen
Aliskiren–mechanism
- direct renin inhibitor
- blocks conversion of angiotensinogen to angiotensin I
Aliskiren–use
- hypertension
Aliskiren–toxicity
- hyperkalemia
- decrease GFR
- hypotension
what is a contraindication for aliskiren?
- patients already taking ACE inhibitors or ARBs
