Jan16 M1-Drugs in renal failure Flashcards

1
Q

limitation for drug to be filtered at the glomerulus

A

free from protein carriers

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2
Q

drugs handling in the tubule

A

some reabso by transporters in the distal tubule (active) but most by nonionic diffusion

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3
Q

week acids and bases in tubules

A

in proximal and distal tubule, their nonionized forms pass through passive reabso

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4
Q

effect of urine pH on clearance of weak acids and bases

A

low pH: bases reabsorbed more easily

high pH: acids reabsorbed more easily

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5
Q

single dose medication: does GFR matter

A

no. med will reach same peak conc as in patient with normal kidney fct but will take longer to be eliminated

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6
Q

5 nephrotoxins

A
NSAIDs
acetaminophens
IV contrast dyes
chemo
antibiotics
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7
Q

why kidneys exposed to high conc of drugs

A

are 0.4% of body weight but receive 25% of resting CO

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8
Q

why NSAIDs can cause renal failure and in what patients does it happen (how much are PGs important)

A

PGs responsible for dilating AA (but are a small thing in the balance)
happens only in reduced GFR

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9
Q

why contrast dyes are toxic to the kidneys

A

toxicity to the tubular cells and renal medullary ischemia

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10
Q

2 most used chemo drugs and reason they are dose limited by their nephrotoxicity

A

cisplastin and carboplatin

reduce GFR by 50%

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11
Q

antibiotic type that are nephrotoxic and otoxotic

A

aminoglycosides

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12
Q

use of aminoglycosides

A

antibacterial properties for gram negative infections in clinically unstable patients

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13
Q

aminoglycosides: pathophgy of renal toxicity

A

upake by PCT cells where more conc than in the blood. sequester in lysosomes and then get lysosomal phospholipidosis and then cell necrosis

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14
Q

multiple doses of a drug: what’s the effect of giving higher dose less often + what mode of administration is like that

A

higher swings in plasma conc. this happens in IV.

p.o. : smaller swings

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15
Q

multiple dosing in kidney failure: principle

A

reduce the dose and give less often

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16
Q

how to manage hyperK in kidney failure

A

diuretics and kayexalate (K exchange resin)

17
Q

kayexelate mode of action

A

removes K and replaces it with Na in the large intestine

18
Q

treating hyperPO4 and associated hypoCa in renal failure

A

Ca carbonate
lanathum carbonate
sevelemer

19
Q

treating hyperPTH in CKD

A
give rocaltrol (active vit D)
cinacalcet
20
Q

sevelamer mode of action

A

binds PO4 in your food to stop it from going in your blood and it stays in the GI tract

21
Q

actual treatment of hypoPO4 (what do they really use)

A

500 mg CaCO3 with each meal + sevelamer or lanthanum as 2nd agent if needed

22
Q

hyperPTH and sequence of disease that leads to it in CKD (2ndary hyperPTH) (2 things)

A

CKD-hyperPO4-hypoCa-hyperPTH

Also CKD = low calcitriol

23
Q

treatment of hyperPTH

A

vit D

cinacalcet

24
Q

cinacalcet mode of action for hyperPTH

A

acts as a ‘‘pharmacological’’ parathryoidectomy. increases sensitivity of CaSR on PT gland so thinks Ca is there so doesn’t release PTH

25
Q

where cinacalcet binds

A

allosteric site on CaSR (other site. not the site for Ca binding)