Fa Pharm Renal

Front 1

mannitol

Back 1

osmotic diuretic, increases tubular fluid osmoarlity producing increased urine flow.

use: shock, drug overdose, to decrease intracrnial/intraocular pressure.

toxicity: pulmonary edema, dehydration.

CI in anuria and CHF

Front 2

acetazolamide

Back 2

carbonic anhydrase inhibitor. causes self-limited NaHCO3 diurecis and reduction in total body HCO3 stores.

use: glaucoma, urinary alkalinzation, metabolic alkalosis, altitude sickness.

toxicity: hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allery.

Front 3

furosemide

Back 3

sulfonamide loop diuretic. inhibits cotransport system (Na/K/Cl) of thick ascending limb of loop of henle. abolishes hyperttonicity of medulla, preventing concentration of urine. increased Ca excretion. Loops Lose Calcium.

use; edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, hypecalcemia.

toxicity: ototoxicity, hypokalemia, dehydration , allergy (sulfa), nephritis (interstitial), gout.

OH DANG!

Front 4

ethacrynic acid

Back 4

phenoxyacetic acid derivative (not sulfonamide). essentially same action as furosemide.

use: diuresis in patients allergic to sulfa drugs.

toxicity: similar to fuosemide; can be used in hyperuricemia, acute gout 9never used to treat gout).

drug interactions:
aminoglycosides (ototoxicity)
digoxin (increased toxicity due to electrolyte changes)
lithium (decreased clearnance of loops)

Front 5

hydrochlorothiazide

Back 5

thiazide diuretic. inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity of the nephron. decreases Ca excretion.

use: hypertension, CHF, idiopathic hypecalciuria, nephrogenic DI.

toxicity: hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia. sulfa allergy.

hyperGLUC

Front 6

potassium sparing diuretics:

spironolactones, triamterene, amiloride, eplerenone.

the K+ STAys.

Back 6

spironolactone is a competitive aldosterone receptor antagonist in teh cortical collecting tubule.
triamterene and amiloride act at the same part of hte tubule by blocking Na channels in the CCT

use: hyperaldosteronism, K depletion, CHF.

toxicity: hyperkalemia (can lead to arrhythmias), endocrine effects with aldosterone antagnoist (eg spironolactone causes gynecomastia, antiandrogen effects).

Front 7

Electrolyte changes with diuretic use:

urine NaCl

Back 7

increased with all diuretics. serum NaCl decreased.

Front 8

Electrolyte changes with diuretic use:

urine K

Back 8

increased in all except K sparing diuretics. decreased serum K may result.

Front 9

Electrolyte changes with diuretic use:

decreased blood pH

Back 9

decreased (acidemia): carbonic anhydrase inhibitors: decreases HCO3 reabsorption. K sparing: aldosterone blockade prevents K and H secretion. Hyperkalemia leads to K entering all cells (via H/K exchanger) with H exicting cell.

Front 10

Electrolyte changes with diuretic use:

increased blood pH

Back 10

increased (alkalemia): loop diuretics and thiazide cause alkalemlia through several mechanisms:
1. volume contraction: increased AT II: increased Na/H exchange in proximal tuble: increased HCO3 (contraction alkalosis).
2. K loss leads to K exiting all cells (via H/K exchanger) with H entering cell.
3. in low K state, H, rather than K is exchanged for Na in cortical collecting tubule, leading to alkalosis and paradoxical aciduria.

Front 11

Electrolyte changes with diuretic use:

urine Ca

Back 11

increased with loop diuretics: abolish lumen-positive potential in thick ascending limb of loop of Henle: decrease paracellular Ca reabsorption: hypocalcemia, increased urinary Ca.

decreased with thiazides: volume depletion: upregulation of sodium reabsorption: enhanced paracellular Ca reabsorption in proximal tubule and loop of Henle. Thiazides also block luminal Na/Cl cotransport in distal convoluted tubule: increase Na gradient: increased interstitial Na/Ca exchange: hypercalcemia.

Front 12

ACE inhibitors
captopril, enalapril, lisinopril

Back 12

inhibit ACE, reducing ATII and preventing inactivation of bradykinin, a potent vasodilator. Renin release is increased due to loss of feedback inhibition.

use: hypertension, CHF, diabetic renal disease.

toxicity:
Cough
Angioedema
Proteinuria
Taste changes
O - hypOtension
Pregnancy problems (fetal renal damage)
Rash
Increased renin
Lower angiotensin II
+ hyperkalemia.

avoid with bilateral renal artery stenosis b/c ACE inhibitors significantly decrease GFR by preventing constriction of efferent arterioles.

Front 13

Losartan

Back 13

AT II receptor antagonist. not an ACE-I and does not produce cough