Drugs And Ckd Flashcards

0
Q

Equation to determine drug dosing in Aki on crrt

A
Crrt clearance (ie what clearance u assume patient to have to figure out appropriate drug dosing). =
Unbound fraction of drug x effluent rate
Effluent rate= dialysis the plus UF
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1
Q

Haart meds

A

NRTI- may produce lactic acidosis, give after dialysis: zidovudine, didanosine, zalcitabine, stavudine, lamivudine
NNRTI- nevirapine, delavirdine, efavirenz: potent p450 interaction: cyclosporine, tacrolimus, diltaizem, verapamil– levels go up. Don’t need to dose adjust in renal failure.
PI: no dose adjustment necessary
Eg ritonovir: Aki
Nelfinavir: stones tubular dysfunction
Saquinavir: lactic acidosis and hypocalcemia
Indinavir: stones interstitial nephritis

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2
Q

Activated charcoal works for

A

Drugs w Small VD or Low protein binding
Not for Tca
Digoxin, salicylate, phenobarbital, carbamazepine, theophylline

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3
Q

Antidote for methanol

A

Fomepizole or 4 methylpyrazole
Or ethanol
HD if level >50mg/dL
Visual abnormalities renal failure electrolyte imbalance not responsive to conventional therapy
Cofactors folate, increases metabolism of formate to CO2 and water

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4
Q

Antidote for cyanide

A

Sodium thiosulfate

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5
Q

Antidote for ethylene glycol

A

Ethanol
Fomepizole
Give cofactors pyridoxine and thiamine, which increase metabolism of glyoxylate to hippuric acid and alpha OH B ketoadipic acid, respectively
If no fomepizole start HD level>50mg/dL continue until <20.

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6
Q

Antidote for benzos

A

Flumazenil

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7
Q

When do u dialyze for lithium

A

Level 4-6mmol/L
Or 2.5-4 w severe sx
Or <2.5 in ESRD pt or rising Li level
Need to check levels again 2 and 4hr later to look for rebound

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8
Q

Antidote for salicylate

A

Activate charcoal in ED
If level <100 can do urinary alkali cation
Supplement glucose bc CNS levels drop
Aim for urine ph 7.5 and blood ph 7.5-7.59 bc acidemic increases CNS salicylate toxicity

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9
Q

Antidepressants that need dose adjustment in ESRD

A

Paxil and venlafaxine

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10
Q

Drug classes that decrease CNI levels

A

Anti TB: rifampin rifabutin INH
Anti seizure: barbiturates phenytoin carbamazepine
St. John’s worry

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11
Q

Drug classes that increase CNI levels

A

Macrolides
CCB diltaizem and verapamil
Mtor inhibitors
Antifungals keto and fluconaxole

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12
Q

CSA blocks entering empathic circulation of what drug

A

Mmf. So some mmf ends up in stool and there is no second plasma peak. Contrast to tac and mmf.

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13
Q

Pentamidine

A

ATN most likely. Reversible.
Hyperkalemia
Use for Pcp

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14
Q

Foscarnet

A
Directly toxic to tubular cells
Rise in cr 6-15 days after
UA bland
Freq poly iris and polydipsia by ADH interference and sometimes DI
Reduced Aki by giving saline
Hypocalcemia and mag
High phos
Used for cmv, hsv, vzv
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15
Q

Cidofovir

A

Dose dependent nephrotocicity
Fanconi
Usually reversible
Should get saline prior and probenecid which blocks the active renal tubular secretion. Prevents uptake of cidofovir into proximal tubular cells

16
Q

Vincristine

A

Siadh

17
Q

Alpha interferon

A

Proteinuria- can be massive
Looks like minimal change dz on bx
Tma is rare

18
Q

Interferon gamma

A

ATN

19
Q

Tmp smx

A

Hyperkalemia due to blockade of collecting tubule sodium channel by trimethoprim (similar to amiloride)
TMP also decreases tubular secretion of Cr

20
Q

Sirolimus

A

Increases total cholesterol and TG- LDL VLDL HDL
Dose dependent
Moa: decreased catabolism of apoB containing lipoproteins
Reversible generally
Respond to lips reducing agents. Not interaction w atorvastatin
Inhibits erythropoiesis at level of EPO receptor

21
Q

Ace and arb associated with what hematologic change

A

Post transplant anemia

Used to rx erythrocytosis

22
Q

Drug Causes of low mag

A

Aminoglycosides ?bind to calcium mag receptor
Cisplatin inhibits distal nephron mag
Pentamidine
cNI reduce expression of Claudin 16 and also inhibit distal nephron mg transport

23
Q

Familial hypomagnesemia and hypercalciuria and nephrocalcinosis FHHNC

A

Mutation in Claudin 16/19 genes
Loss of cation selectivity in the para cellular pathway
Decreased reabsorption of ca mag with increased urinary loss
Presents in childhood or adolescence with hypocalcemia, recurrent nephrolithiasis and nephrocalcinosis and progresses to CKD

24
Q

Methanol is converted to

A

Formic acid

25
Q

Ethylene glycol is converted to

A

Glycolic acid

26
Q

Osmolal gap is produced by

A

Ethylene glycol not its metabolite glycolic acid
Therefore acidosis may not be present until ethylene glycol is metabolized
Started with OG
Then closes and becomes AG

27
Q

Propylene glycol toxicity seen with what drugs

A

Prolonged infusion of lorazepam digoxin phenytoin trimethoprim and diazepam
PG is the carrier for th drug and has higher concentrations in lorazepam than in other meds
PG is metabolically active, Renault cleared and metabolized to lactate

Accumulation results in OG AG acidosis and osmotic diuresis w AKI
Can be dialyzed

28
Q
Confusion 
Cardiac toxicity
Pancreatitis
Rhabdo
Lactic acidosis
Aki
Risk factors is rapid infusion or longer than 48h

Txp is supportive

A

Propofol toxicity

29
Q

Visual impairment

Loss of pupillary light reflex or papillaedema

A

Methanol

30
Q

Inebriation without fetor
Hypocalcemia
Calcium oral are crystalluria
Fluorescing urine under woods lamp

A

Ethylene glycol

31
Q

Effect of imatinib on electrolytes

A

Hypophos by decreasing bone turnover

Relative or absolute hypocalcemia

32
Q

Heavy metal presenting as gout HTN CKD

A

Lead

33
Q

Insulin replacement in dka or hyperosmolar

A

0.1u/kg/hr

34
Q

Rx for central DI

Or pregnancy associated DI

A

Ddavp 10 ug intranasal