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Flashcards in Renal Drugs Deck (42):
1

MOA of mannitol

osmotic diuresis

2

uses of mannitol

drug overdose
increased ICP
increased IOP

3

toxicity of mannitol

pulmonary oedema
dehydration
contraindicated in HF and anuria

4

MOA of acetazolamide

inhibits carbonic anhydrase in the PCT
results in self limited NaHCO3 diuresis and decreased total body HCO3- stores.

5

clinical used of acetazolamide

glaucoma
urinary alkalinisation
metabolic alkalosis
altitude sickness
pseudotumor cerebri (chronic vitamin A use)

6

toxicity of acetazolamide

hyperchloremic metabolic acidosis ACIDazolamide causes Acidosis
paresthesias
NH3 toxicity
sulfa allergy

7

list the sulfa drugs

probenecid
furosemide
thiazides
acetazolamide
sulfa abs
sulfonylureas
sulfasalazine
celecoxib

8

list the loops diuretics

furosemide
bumetanide
torsemide

9

MOA of loops

inhibit the NaK2Cl in the thick ascending loop of henle -- no hypertonicity in the medulla -- no concentration of urine
stimulates PGE release - vasodilation of the afferent arterioles (can inhibit with NSAIDs)
Ca excretion
LOOPS LOSE CALCIUM

10

clinical use of loops

edematous states - HG, irrhosis, nephrotic syndrome, pulmonary yoedema
hypertension
hypercalcemia

11

toxicity of loops

OH DANG
ototoxicity
hyperkalemia
dehydration
allergy (sulfa)
nephritis (interstitial)
glout (hyperuricemia)

12

why would you use ethacrynic acid

for diuress in patients allergic to sulfa drugs (furosemide, acetazolamide, thiazides)

13

MOA of ethacrynic acid please

pheonoxyacetic acid derivative with same MOA of forusemide (NaK2Cl blocker)

14

toxicitiy of ethacrynic acid please

similar to furosemide OH DANG: ototoxicity, hyperkalemia, dehydration, neprhritis, gout`

15

list the thiazide diurectic please

chlorthalidone
hhydrochlorothiazide

16

MOA of thiazides

inhibits NaCl reabsorption in early DCT -- decreases diluting ability
decreased Ca excretion

17

clinical use fo thiazides

hypertenision
HF
idiopathic hypercalciuria
nephrogenic diabtes insipidus
osteoporosis
calcium stones

18

toxicity of thiazides

HyperGLUC
hypokalemic metabolic alkalosis
hyponatremia
hyperglycemia
hyperlipidemia
hyperuricemia
hypercalcemia

19

list the K sparing diuretics

spironolactone, eplerenone
triamterene, amiloride

20

MOA of spironolactone and eplerenone

competitive aldoster recetpro antagos in the cortical collecring tubule

21

MOA of triamterene and amiloride

inhibt ENaC in the cortical collecting tubule

22

cx use of k sparign diuretics

hyperaldosternosim
K depletion
HF

23

toxo of K sparing diuretics

hyperkalaemia - arrhythmias
spironolactone - anti androgenic - gynecomastia

24

which diuretics increased urine NaCl

all but acetazolamide
serum NaCl may decrease as a result

25

which diuretics increased urine K

loops and thiazides
may descreased serum K as a result

26

which diuretics cause acidemia

carbonic anhydrase inhibitos
K sparing

27

which diuretics cause alkalemia

loops
thiazides

28

describe how carbonic anhydrase inhibitors cause acidemia

decreased HCO3 reabsorption

29

describe how K sparers caused acidemia

aldoseterone blockade prevents K secretion and H secrtion
increased K results in H out

30

describe how loops and thiazides cause alkalemia

volume contraction -- increasd AngII -- increased Na/H exchange and icnreasd HCO3 reabsorption CONTRACTION ALKALOSIS
K loss leads to exchange out K out for H in to cells
low K states, H si exchangd for Na in the corical collecting tubules -- paradoxical aciduria

31

what diuretics cause increased urine ca

loops - decreasd paracellular ca reabsorption -- hypocalcemia

32

which diuretcics caus decreasd urine ca

thiazides - enhanced Ca reabsorption in DCT

33

list the ACEi

captopril
enalapril
lisinopril
ramipril

34

MOA of ACEi

inhibit ACE -- decreased ANng II -- decreased GFR by prevention of constriction of efferent arterioles

icnreasd renin due to loss fo negative inhibition

prevents inacativation of bradykinin -- vasodilation

35

cx of ACEi

hypertension
HF
proteinuria
diabetic nephropathy

36

why are ACEi good in chronic hypertension

prevent unfavourable remodelling of heart

37

why are ACEi good in diabetes?

decreased intraglomerular pressure - slows GBM thickenign

38

toxo of ACEi?

Captoprils CATCHH
Cough
Angioedema - don't use with C1 esterase deficiency
Teratogen - fetal kidney abnormalities
Creatinine serum increased - decrease GFR
hyperkalemia
hypotencion

39

list the Ang II receptor blockers/ARBs

losartan
candesartan
valsartan

40

MOA of ARBs

selectively block binding of ant II to AT1 receptor
similar to ACEi but don't prevent breakdown of bradykinine

41

use of ARBs?

hypertension
HF
proteinuria
diabetic nephropathy
when ACEi aren't good (cough angioedema)

42

a/se of ARBS

similar to ACEi (CATCHH)
teratogen
increasd creatinine
hyperkalemia
hypotension