Pharm Renal

Question 1

What is the mechanism of mannitol in the kidney? Clinical use? Toxicity? CIs?

Answer 1

Osmotic diuretic

Incr. tubular fluid osmolarity leads to incr. urine flow leads to decr. ICP/IOP

Drug overdose
elevated ICP/IOP

Pulmonary edema, dehydration
CI: Anuria, HF

Question 2

What is the mechanism of acetazolamide? Clnical uses? Toxicity?

Answer 2

CA inhibitor.
Self limited NaHCO3 diuresis and decr. total body HCO3 stores

Glaucoma
urinary alkalinization
metabolic alkalosis
altitude sickness
pseudotumor cerebri

Hyperchloremic metabolic acidosis
Paresthesias
NH3 toxicity
sulfa allergy

Question 3

What type of drugs are furosemide, bumetanide, and torsemide, and ethacrynic acid (1)? What inhibits them? Derivation? Of 1? Mechanism? Clinical use? Of 1? Toxicity?

Answer 3

Sulfonamide loop diuretics.
1=phenoxyacetic acid derivative (not sulfa)

Inhibit cotransport (Na/K/2Cl) of thick ascending limb of loop of henle.
Abolish hypertonicity of medulla, preventing concentration of urine.
Stimulate PGE release (vasodilatory effect on afferent arteriole)
Incr. Ca excretion

Inhibited by NSAIDS

Edematous states (HF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia
1=same but if they are allergic to sulfa drugs

Ototoxicity
Hypokalemia
Dehydration
Allergy (sulfa)
Nephritis (interstitial)
Gout

OH DANG!

Question 4

What type of drugs are chlorthalidone and hydrochlorothiazide? Mechanism? Clinical use? Toxicity?

Answer 4

Thiazides

Inhibit NaCl reaab in early DCT leads to decr. diluting capacity of nephron
Decr. Ca excretion

Hypertension, HF, idiopathic hypercalciuria, NDI, osteoporosis

Hypokalemic metabolic alkalosis
Hyponatremia
Hyperglycemia
hyperlipidemia
hyperuricemia
hypercalcemia
Sulfa allergy

Question 5

What kind of drugs are spironolactone (1) and eplerenone? mechanism? Clinical use? Toxicity? Of just 1?

Answer 5

potassium sparing diuretic

Competitive aldo receptor antag in cortical collecting tubule

Hyperaldosteronism, K+ depletion, HF

Hyperkalemia (arrythmias)
1=endocrine effects (gynecomastia, antiandrogen effects)

Question 6

What kind of drugs are amiloride and triamterene? mechanism? Clinical use? Toxicity?

Answer 6

potassium sparing diuretic

Blocking ENAC channels in Cort. collecting tubule

Hyperaldosteronism, K+ depletion, HF

Hyperkalemia (arrythmias)

Question 7

Which diuretics affect urine NaCl? In which way? Results? Which diuretics affect urine K+? IN which way? Results? Which diuretics lead to acidemia? How? Which diuretics lead to alkalemia? How? What diuretics have an effect on urine Ca? In which way? Results?

Answer 7

Incr in allAll except acetazolamide
Serum NaCl may decrease

Incr. in loop and thiazide
Serum K may decrease as a result

Acidemia: CA inhib (decr. HCO3 reab)
K sparing: aldo blockade prevents K+ secretion and H+ secretion; hyperkalemia leads to K entering all cells in exchange for H+.

Alkalemia: Loop and thiazides
volume contraction leads to ATII leads to Na/H exchange in PCT leading to incr. HCO3 reab (contraction alk)
H/K exchanger
Low K state, H is exchanged for Na is cort. collecting tubule (principal cells)=alkalosis and paradoxical aciduria

Incr. Ca in urine with loop diuretics due to decr. paracellular Ca reab leading to hypocalcemia
Decr. urine Ca with thiazides due to enchanced Ca reab in DCT.

Question 8

What type of drugs are captopril, enalapril, lisinopril, ramipril? Mechanism? Clinical use? Toxicity? CI?

Answer 8

ACE inhibitors

Inhibit ACE which decreases ATII which decreases GFR by preventing constriction of efferent arterioles.
Levels of renin incr as a result.
Also prevents inactivation of bradykinin, a potent vasodilator

Hypertension, HF, proteinuria, diabetic nephropathy
Prevent unfavorable remodeling as a result of chronic hypertension

Cough, angioedema (CI in C1 esterase inhib defic), teratogen (renal malformations), Incr. creatinine (decr. GFR), hyperkalemia, hypotension

Avoid in bilateral renal artery stenosis, because ACE inhib will further decr. GFR leading to renal failure

Question 9

What type of drugs are losartan, candesartan, and valsartan? Mechanism? Clinical use? Toxicity?

Answer 9

Angiotensin II receptor blockers

Selectively block binding of ATII to AT1 receptor. Effects similar to ARBs but do not decrease bradykinin.

Hypertension, HF, proteinuria, or diabetic nephropathy with intolerance to ACEIs (cough, angioedema)

Hyperkalemia, decr. renal function, hypotension, teratogen

Question 10

What is the mechanism of aliskiren? Clinical use? Toxcity? CI?

Answer 10

Direct renin inh, blocks conversion of angiotensinogen to AT-I

Hypertension

Hyperkalemia, decr. renal function, hypotension

CI in diabetics taking ACEIs or ARBs