29 terms

14. Renal Pharm

STUDY
PLAY
Drugs/Exposures that cause transitional cell carcinoma
phenacetin (aspirin derivative)
smoking
aniline dyes
cyclophosphamide
Mannitol--Mechanism
PCT

osmotic diuretic, inc tubular fluid osmolarity = inc urine flow

gets filtered but can't be absorbed, leads to dec Na+ and H20 reabsorbtion
Mannitol--Use
shock
drug overdose
inc intracranial/intraocular pressure
Mannitol--Toxicity
pulmonary edema
dehydration
contraindicated in anuria, CHF
Acetazolamide--Mechanism
PCT

carbonic anydrase inhibitor = self-limited NaHCO3 diuresis and dec in HCO3- stores
Acetazolamide--Use
glaucoma
urinary alkalinization
metabolic alkalosis
altitude sickness
Acetazolamide--Toxicity
hyperchloremic metabolic acidosis
neuropathy
NH3 toxicity
sulfa allergy
Furosemide--Mechanism
sulfonamide loop diuretic
inhibits Na+, K+, Cl- cotransport of thick ascending limb
stops hypertonicity of medulla preventing concentration of urine
inc Ca2+ excretion
Furosemide--Use
edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema)
HTN
hyperCa2+
Furosemide--Toxicity
"OH DANG"

ototoxicity
hypoK+
deH20
Allergy (sulfa)
Nephritis (interstitial)
Gout
Ethacrynic acid--Mechanism and Use
same action as furosemide (NOT sulfa)
phenoxyacetic acid derivative

diuresis in patients with sulfa allergy
Ethacrynic acid--Toxicity
same as furosemide BUT can be used in hyperuricemia/acute gout
Hydrochlorothiazide--Mechanism
thiazide diuretic
inhibits NaCL reabsorption in DCT
dec Ca2+ excretion
Hydrochlorothiazide--Use
HTN
CHF
idiopathic hypercalciuria
nephrogenic diabetes insipidus
Hydrochlorothiazide--Toxicity
hypoK+metabolic alkalosis
hypoNa+
hyperglycemia
hyperlipidemia
hyperuricemia
hyperCa2+
sulfa allergy
K+ sparing diuretics--List
spironolactone
triamterene
amiloride
eplerenone
K+ sparing diuretics--Mechanism
spironolactone = competitive aldosterone receptor antagonist in collecting tubule

triamterene and amiloride = block Na+ channels on CCT
K+ sparing diuretics--Use
hyperaldosteronism
K+ depletion
CHF
K+ sparing diuretics--Toxicity
hyperK+
endocrine effects with aldosterone antagonists
(ex: spironolactone causes gynecomastia, antiandrogen effects)
Diuretic Effects on Urine NaCL
Increased

serum NaCL may dec
Diuretic Effects on Urine K+
Increased in all except K+ sparing

serum K+ may dec
Diuretics that cause dec pH (acidemia)
Carbonic anhydrase inhibitors
K+ sparing (aldosterone block prevents K+ and H+ secretion)

also..hyperK+ causes K+ to enter and H+ to leave (K+/H+ transporter)
Diuretics that cause inc pH (alkalosis)
Loop diuretics and thiazides
1) Volume contraction: inc ATII = inc Na+/H+ exchange in proximal tubule = inc HCO3-

2) K+ loss leads to K+ exiting cells and H+ entering cells

3) In low K+ state, H+ is exchanged for Na+ leading to "paradoxical aciduria)
Effect of loop diuretics on urine Ca2+
Increased

abolish lumen-positive potential in thick ascending limb = dec paracellular Ca2+ reabsorption = hypoCa2+ = inc urinary Ca2+
Effects of thiazides on urine Ca2+
Decreased

volume depletion = upregulation of Na+ reabsorption = enhanced paracellular Ca2+ reabsorption in PCT and loop of Henle

also block luminal Na+/Cl- cotransport in DCT = inc Na+ gradient = increased Na+/Ca2+ exchange
ACE Inhibitors--List
captopril
enalapril
lisinopril
ACE Inhibitors--Mechanism
inhibit angiotensin converting enzyme and prevent inactivation of bradykinin (vasodilator)

renin release is increased d/t loss of feedback inhibition
ACE Inhibitors--Use
HTN
CHF
diabetic renal disease
ACE Inhibitors--Toxicity
"CAPTOPRIL"

cough
angioedema
proteinuria
taste changes
hypOtn
pregnancy problems (fetal renal damage)
rash
increased renin
lower angiotensin II
AND hyperK+

avoid with bilateral renal artery stenosis because ACE inhibitors dec GFR by preventing constriction of efferent arterioles