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Renal Final > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

bioavailability

A

AUCx/AUCiv

IV drugs bioavailability=1

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2
Q

volume of distribution

A

Q (dose)/ Cp (plasma concentration)

constant value for a given drug, depends on which compartments

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3
Q

clearance

A

CL= UV/Cp

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4
Q

Ke (equilibrium of clearance)

A

CL/Vd

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5
Q

half life equation

A
  1. 7 Vd/ CL or

0. 7/Ke

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6
Q

maintenance dose

A

MD= (Cp *CL *t)/ F

t= dosing interval

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7
Q

loading dose

A

LD= (Cp*Vd)/ F

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8
Q

acetazolamide moa

A

carbonic anhydrase inhibition, blocks generation of H+ in cell which lowers Na reabsorption

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9
Q

acetazolamide toxicity

A

met acidosis (also blocks bicarb reabsorption)

hypokalemia- high Na and water delivery to distal segments

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10
Q

loop diuretic examples and moa

A

furosemide. torsemide, bumetanide, etharcrynic acid

inhibit NKCC on loop of henle- reduce Na reabsorption

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11
Q

loop toxicities (4)

A

hypokalemia- more Na and water delivery, RAAS activation from volume loss (more potent w/ loop)

met alkalosis- aldo promotes H+ secretion along w/ K+

hypocalcemia/hypercalciuria- less Na thru NKCC means less K is secreted thru ROMK, loss of the lumen positivity that normally drives Ca reabsorption paracellularly
-can drive formation of kidney stones, nephrolithiasis

hyperuricemia/gout- compete w/ same proteins for secretion as urea (OAT1, 2, 4, 10)

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12
Q

thiazide examples

A

HTCZ, chlortalidone, metolazone

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13
Q

thiazide moa

A

NCC block at the DCT, less potent than loop diuretics

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14
Q

thiazide toxicity (5)

A

hypokalemia

hypercalcemia- reduciton in intracellular Na causes more activity at basolateral Na/Ca exchanger (moving Ca into interstitium) which stimulates Ca uptake from urine

met alkalosis- RAAS activation, less so than loops

hyperuricemia and gout- competition w/ urate secretion

hyperglycemia/DM- volume reduction causes sympathetic stim, less glucose uptake and a higher serum glucose
-loss of K reduces insulin stimulus, raising glucose

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15
Q

distinguish 2 moas of K sparing drugs

A

aldo receptor inhibs- sprionolactone and eplerenone

ENaC inhibs- amiloride, tramterene

both cause lack of ENaC fn

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16
Q

K sparing toxicities

A

met acidosis- inhibition of H secretion (positive lumen w/o Na reabsorption)

  • from spironolactone- sex side effects from effects on testosterone (conversion to estradiol, loss of production, displaced from binding, competition at site of action)
  • things like gynecomastia, impotence
17
Q

mannitol moa

A

IV administration, not reabsorbed or secreted

osmotic force to retain water in urine

18
Q

mannitol toxicities

A

hypokalemia and met alkalosis- increasing water content in urine lowers concentration of K and H, creating a gradient for them to be lost in urine

19
Q

drugs causing T4 RTA (6)

A

ACEi, ARBs, cyclosporin, tacrolimus

also trimethoprim and NSAIDs (w/ AIN too)

20
Q

drugs causing AIN (7)

A
  • penicillin
  • cephalosporin
  • cipro
  • vanc
  • rifampin
  • omeprazole (PPIs)
  • lansoprazole

also trimethoprim and NSAIDs

21
Q

ATN drugs (3)

A
  • aminoglycosides
  • ampB
  • RC dyes (iohexol)
22
Q

3 mechanisms for AIN reaction

A

neoantigen
antigen mimicry

haptenization- drug binds to immunogenic structure, new hapten is also immunogenic

all 3 are recognized by kidney dendritic cells and stimulate inflammation

23
Q

3 clinical manifestations of AIN beside AKI

A

rash, fever, eosinophilia

24
Q

reason for aminoglycoside toxicity

A

accumulate in renal tubular cells b/c have pKa above 9- positively charged at phys pH and bind to neg lipids in cell membranes

kill cells and result in ATN, can take weeks

25
Q

gradations of aminoglycoside toxicity

A

higher affinity for phospholipids= more toxic

worst is neomycin, best is streptomycin

26
Q

ampB mech for ATN

A

interacts w/ cholesterol in tubular membranes, makes them more permeable

27
Q

overall cause of T4 RTA

A

impaired aldo signaling to kidney- causes hyperkalemia and acidosis

28
Q

NSAID mech for RTA

A

block secretion of renin

29
Q

TMP and CNI mech for RTA

A

reduce aldo sensitivity- TMP blocks ENac

CNIs reduce amount of aldoR

30
Q

aldo independent effects of NSAIDs and ACEi on kidney fn

A

NSAIDs- cause efferent vasoconstriction (block PGs which normally dilate)

ACEi- block angII, dilating efferent (exacerbate loss of GFR w/ renal artery stenosis)

both serve to reduce GFR, urine output

Renal Final (13 decks)

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