Renal Pharmacology

Question 1

Mannitol
clinical use
toxicity

Answer 1

used to treat drug overdose
elevated intracranial pressure

toxicity is pulmonary edema
contraindicated in HF

Question 2

Acetazolamide

mechanism

Answer 2

carbonic anhydrase inhibitor

causes self limited NaHCO3 diuresis and decrease in total body HCO3 stores - i.e. metabolic acidosis

Question 3

Acetazolamide

clinical use and toxicity

Answer 3

glaucoma / metabolic alkalosis / alkanilize urine / altitude sicknes / pseudotumor cerebri

toxiticy - metabolic acidosis
sulfa allergy

Question 4

sulfa loop diuretics (3)

Answer 4

furosemid
bumetanide
torsemide

Question 5

mechanism of loop diuretics

Answer 5

inhibit Na/K/2Cl cotransporter in thick ascending abolishing hypertonicity of medulla
also stimulate PGE release which vasodilates affarent arteriole (inhibited by NSAIDS)

Question 6

Why do loops cause potassium wasting

Answer 6

inhibit the NA/K/2CL

Question 7

What effect do loops have on calcium

Answer 7

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

Question 8

toxicity of loops

Answer 8

OH DANG

Ototoxicity
Hypokalemia
Dehydration 
Allergy (sulfa)
Nephritis (interstitial - eosinophils)
Gout - increased urinary calcium - stones

Question 9

alternative loop diuretic for those with sulfa allergy

Answer 9

ethacrynic acid

Question 10

Thiazide diuretics

Answer 10

chlorthalidone

hydrochlorothiazide

Question 11

Thiazide diuretics (chlorthalidone and hctz) work by

Answer 11

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)

Question 12

How do thiazide diuretics cause hypokalemia?

Answer 12

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

Question 13

Calcium and thiazides

Answer 13

increased in blood

Question 14

the following conditions could benefit from what?
hypertension
HF
hypercalcuria
nephrogenic DI
osteoperosis

Answer 14

thiazide diuretic (chlorthalidone/ hctz)

Question 15

thiazide diuretic toxicity

Answer 15

hypokalemia - muscle spasm / weakness?
metabolic alkalosis 
hyponatremia - nausea
hyperGLUC
Glycemia 
Lipid
Uricemia
Calacemia 
Sulfa allergy

Question 16

Potassium sparing diuretics

Answer 16

Spironolactone (eplerenone for gynocomastia)
— competitive androgen receptor antagonists
Triamterene ; Amiloride
—block Na channels in the cortical ct

THE K
Spironolactone
Triamterene
Amiloride
ys

Question 17

potassium sparing diuretic clinical use

Answer 17

hyperaldosteronism
k depletion
HF

Question 18

Toxicity of potassium sparing diuretics

Answer 18

hyperkalemia -

Question 19

ACE inhibitors

Answer 19

captopril
enalopril
lisinopril
ramipril

Question 20

ACE inhibitors effect of GFR

Answer 20

decrease because block at-ii selective efferent constriction - but this is good if you have diabetic nephrophathy

Question 21

bradykinin

Answer 21

potent vasocontrictor

Question 22

ACE inhibitor toxicity

Answer 22

CATCHH

Cough
Angioedema (dont give to C1 esterase deficient)
Teratogenic
Hyperkalemia 
Hypotension

Question 23

Why are ACE inhibitors good for Diabetic nephropathy

Answer 23

lower GFR and slow GBM thickening

Question 24

ARBS

Answer 24

losartan
candesarta
valsartan

Question 25

ARBS difference from ACE-i

Answer 25

not much other than

do not increase bradykinin - cough

Question 26

Aliskiren

Answer 26

Direct renin inhibitor

blocks angiotensinogen –> ang-i

Question 27

erythropoetin - concerns?

Answer 27

thromboembolic events (increase coagulativity)
can cause hypertension via activation of vascular endothelial and smooth muscle receptors