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Pharmocology - step > Renal Drugs > Flashcards

Renal Drugs Flashcards

1
Q

MOA of mannitol

A

osmotic diuresis

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2
Q

uses of mannitol

A

drug overdose
increased ICP
increased IOP

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3
Q

toxicity of mannitol

A

pulmonary oedema
dehydration
contraindicated in HF and anuria

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4
Q

MOA of acetazolamide

A

inhibits carbonic anhydrase in the PCT

results in self limited NaHCO3 diuresis and decreased total body HCO3- stores.

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5
Q

clinical used of acetazolamide

A 
glaucoma
urinary alkalinisation
metabolic alkalosis
altitude sickness
pseudotumor cerebri (chronic vitamin A use)
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6
Q

toxicity of acetazolamide

A

hyperchloremic metabolic acidosis ACIDazolamide causes Acidosis
paresthesias
NH3 toxicity
sulfa allergy

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7
Q

list the sulfa drugs

A 
probenecid
furosemide
thiazides
acetazolamide
sulfa abs
sulfonylureas
sulfasalazine
celecoxib
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8
Q

list the loops diuretics

A

furosemide
bumetanide
torsemide

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9
Q

MOA of loops

A

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

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10
Q

clinical use of loops

A

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

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11
Q

toxicity of loops

A 
OH DANG
ototoxicity
hyperkalemia
dehydration
allergy (sulfa)
nephritis (interstitial)
glout (hyperuricemia)
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12
Q

why would you use ethacrynic acid

A

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

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13
Q

MOA of ethacrynic acid please

A

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

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14
Q

toxicitiy of ethacrynic acid please

A

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

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15
Q

list the thiazide diurectic please

A

chlorthalidone

hhydrochlorothiazide

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16
Q

MOA of thiazides

A

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

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17
Q

clinical use fo thiazides

A 
hypertenision
HF
idiopathic hypercalciuria
nephrogenic diabtes insipidus
osteoporosis
calcium stones
18
Q

toxicity of thiazides

A 
HyperGLUC
hypokalemic metabolic alkalosis
hyponatremia
hyperglycemia
hyperlipidemia
hyperuricemia
hypercalcemia
19
Q

list the K sparing diuretics

A

spironolactone, eplerenone

triamterene, amiloride

20
Q

MOA of spironolactone and eplerenone

A

competitive aldoster recetpro antagos in the cortical collecring tubule

21
Q

MOA of triamterene and amiloride

A

inhibt ENaC in the cortical collecting tubule

22
Q

cx use of k sparign diuretics

A

hyperaldosternosim
K depletion
HF

23
Q

toxo of K sparing diuretics

A

hyperkalaemia - arrhythmias

spironolactone - anti androgenic - gynecomastia

24
Q

which diuretics increased urine NaCl

A

all but acetazolamide

serum NaCl may decrease as a result

25
Q

which diuretics increased urine K

A

loops and thiazides

may descreased serum K as a result

26
Q

which diuretics cause acidemia

A

carbonic anhydrase inhibitos

K sparing

27
Q

which diuretics cause alkalemia

A

loops

thiazides

28
Q

describe how carbonic anhydrase inhibitors cause acidemia

A

decreased HCO3 reabsorption

29
Q

describe how K sparers caused acidemia

A

aldoseterone blockade prevents K secretion and H secrtion

increased K results in H out

30
Q

describe how loops and thiazides cause alkalemia

A

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
Q

what diuretics cause increased urine ca

A

loops - decreasd paracellular ca reabsorption – hypocalcemia

32
Q

which diuretcics caus decreasd urine ca

A

thiazides - enhanced Ca reabsorption in DCT

33
Q

list the ACEi

A

captopril
enalapril
lisinopril
ramipril

34
Q

MOA of ACEi

A

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
Q

cx of ACEi

A

hypertension
HF
proteinuria
diabetic nephropathy

36
Q

why are ACEi good in chronic hypertension

A

prevent unfavourable remodelling of heart

37
Q

why are ACEi good in diabetes?

A

decreased intraglomerular pressure - slows GBM thickenign

38
Q

toxo of ACEi?

A

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

39
Q

list the Ang II receptor blockers/ARBs

A

losartan
candesartan
valsartan

40
Q

MOA of ARBs

A

selectively block binding of ant II to AT1 receptor

similar to ACEi but don’t prevent breakdown of bradykinine

41
Q

use of ARBs?

A 
hypertension
HF
proteinuria
diabetic nephropathy
when ACEi aren't good (cough angioedema)
42
Q

a/se of ARBS

A 
similar to ACEi (CATCHH)
teratogen
increasd creatinine
hyperkalemia
hypotension

Pharmocology - step (16 decks)

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