Jan16 M1-Drugs in renal failure Flashcards
limitation for drug to be filtered at the glomerulus
free from protein carriers
drugs handling in the tubule
some reabso by transporters in the distal tubule (active) but most by nonionic diffusion
week acids and bases in tubules
in proximal and distal tubule, their nonionized forms pass through passive reabso
effect of urine pH on clearance of weak acids and bases
low pH: bases reabsorbed more easily
high pH: acids reabsorbed more easily
single dose medication: does GFR matter
no. med will reach same peak conc as in patient with normal kidney fct but will take longer to be eliminated
5 nephrotoxins
NSAIDs acetaminophens IV contrast dyes chemo antibiotics
why kidneys exposed to high conc of drugs
are 0.4% of body weight but receive 25% of resting CO
why NSAIDs can cause renal failure and in what patients does it happen (how much are PGs important)
PGs responsible for dilating AA (but are a small thing in the balance)
happens only in reduced GFR
why contrast dyes are toxic to the kidneys
toxicity to the tubular cells and renal medullary ischemia
2 most used chemo drugs and reason they are dose limited by their nephrotoxicity
cisplastin and carboplatin
reduce GFR by 50%
antibiotic type that are nephrotoxic and otoxotic
aminoglycosides
use of aminoglycosides
antibacterial properties for gram negative infections in clinically unstable patients
aminoglycosides: pathophgy of renal toxicity
upake by PCT cells where more conc than in the blood. sequester in lysosomes and then get lysosomal phospholipidosis and then cell necrosis
multiple doses of a drug: what’s the effect of giving higher dose less often + what mode of administration is like that
higher swings in plasma conc. this happens in IV.
p.o. : smaller swings
multiple dosing in kidney failure: principle
reduce the dose and give less often
how to manage hyperK in kidney failure
diuretics and kayexalate (K exchange resin)
kayexelate mode of action
removes K and replaces it with Na in the large intestine
treating hyperPO4 and associated hypoCa in renal failure
Ca carbonate
lanathum carbonate
sevelemer
treating hyperPTH in CKD
give rocaltrol (active vit D) cinacalcet
sevelamer mode of action
binds PO4 in your food to stop it from going in your blood and it stays in the GI tract
actual treatment of hypoPO4 (what do they really use)
500 mg CaCO3 with each meal + sevelamer or lanthanum as 2nd agent if needed
hyperPTH and sequence of disease that leads to it in CKD (2ndary hyperPTH) (2 things)
CKD-hyperPO4-hypoCa-hyperPTH
Also CKD = low calcitriol
treatment of hyperPTH
vit D
cinacalcet
cinacalcet mode of action for hyperPTH
acts as a ‘‘pharmacological’’ parathryoidectomy. increases sensitivity of CaSR on PT gland so thinks Ca is there so doesn’t release PTH
where cinacalcet binds
allosteric site on CaSR (other site. not the site for Ca binding)
