Pharmacology of Renal Failure Flashcards Preview

CVPR: Renal > Pharmacology of Renal Failure > Flashcards

Flashcards in Pharmacology of Renal Failure Deck (16)
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1

Impact of CKD on pharmacologic tx

  • decreasing fxn (decreased ability to eliminate drugs/regulate solutes) & increasing complications ==> complicated/coordinated pharmacologic tx
  • altered bodily response to meds via pharmacokinetic and pharmacodynamic

2

Impact of CKD on absorption/bioavailability of drugs

  • limited impact except for GI alterations may affect bioavailability 
  • drug-drug interactions:
    • posphate binders & bile acid sequestrants ==> reduce availability of drugs given concomitantly

3

Impact of CKD on drug distribution

  • both decreases & increases ==> increased unbound drug & Cp
  • e.g. any given dose of digoxin will result in a higher Cp due to the smaller Vd
  • e.g. CKD pts taking phenytoin have increased Vd ==> greater levels of free phenytoin and greater ability to distribute outside of the plasma and greater potential for toxicity

4

CKD impact on drug metabolism

  • insulin = metabolism decreased in CKD ==> dosage reduction necessary
  • active hepatic metabolities accumulate in CKD ==> drug toxicity
    • e.g. meperidine (aka "Demerol" = opoid/sedation) metabolites
    • e.g. acetominophen metabolites

5

Dosing adjustments neccesary in CKD (general)

  • stage 1 & 2 = no dosage adjustment neccessary
  • stage 3 & 4 = renally eliminated drugs require dosage reduction

6

Arteriolar resistance (@ glomerulus) impact on GFR and drugs that affect resistance

  • Dilate Afferent
    • increased GFR
    • <== Dopamine; Caffeine (=Adenosine antagonist)
  • Constrict Afferent
    • decrease GFR
    • <== NSAIDs via decreased PGs
  • Constrict Efferent
    • increase GFR
    • <== AgII
  • Dilate efferent
    • decrease GFR
    • <== ACE-Is, ARBs via decreased AgII

7

Diuretics adjustment in CKD

  • thiazide = first-line HTN
    • decreased efficacy as GFR falls b/c less drug reaches site of action
    • ==> addition of more potent loop diuretic
  • Diuretic resistance develops @ later stages ==> use synergistic combos of diuretics

8

Dosage considerations in CKD for diabetes medications

  • oral hypoglycemics
    • glyburide: half-life prolonged
    • metformin: NOT recommended if Cr > 1.5
  • insulin = half-life prolonged

9

Dosage considerations in CKD for HTN medications

  • Diuretics
    • Thiazides lose effectiveness as renal fxn declines ==> add loop diuretics
    • avoid potassium-sparing diuretics
  • ACE-Is
    • used through all stages ==> moniter for hyperkalemia/Cr elevations
    • may cause ARF in hypovolemic pts
  • Beta-blockers
    • atenolol: half-life prolonged
  • No adjustments neccesary in other meds

10

Dosage considerations in CKD for hyperlipidemia medications

  • Fibrates
    • Gemfibrozil recommended fibrate @ CKD stage 5
  • No other adjustments needed

11

Pharm tx of Anemia in CKD

  • Epoetin Afla & Darpepoetin Alfa
    • MOA: glycoproteins w/bio activity=EPO
    • Pharm: parenterally (SC) weekly
    • AE: HTN
  • Iron supplements/tx
    • MOA: aid in hemoglobin/RBC production
    • Pharm: oral w/poor absorption; IV often required
    • AE: oral=GI complaints; IV=allergy, hypotension, headaches

12

Pathophys/Pharm tx of Renal Osteodystrophy in CKD

  • decreased renal fxn => elevated serum phosphate => decreased Ca2+ => increased PTH
  • PTH initially normalizes Ca2+/PO4 ==> long term = osteodystrophy
  • Compounded by kidney inability to activate Vit D => further reduction of Ca2+
  • Tx:
  • Phosphate binding agents
  • Vit D agents
  • Calcimimetics

13

Pharmacologic properties of phosphate binding agents

  • e.g. Calcium acetate (PhosLo); Sevelamer (Renagel)
  • MOA:  Bind dietary phosphate in GI tract to form insoluble compounds excreted in the feces ==> decreasing phosphate
  • Pharmacokinetics:  Given orally, best taken with meals.
  • Side effects:  Primarily GI side effects – Hypercalcemia possible with Ca++ salts; CNS toxicity with Al+++ salts limits use.

14

Pharmacologic properties of Vit D compounds

  • e.g. Calcitriol/1,25-dihydroxy vit D3
  • MOASuppresses PTH secretion indirectly by stimulating intestinal calcium absorption + decreasing PTH synthesis in parathyroid gland.
  • Pharmacokinetics:  Available in oral (Stage 1-4) and intravenous (Stage 5) dosage forms
  • Side effectsHypercalcemia and hyperphosphatemia possible.

15

Pharmacotherapy for acute hyperkalemia

  • hemodialysis
  • temporary tx:
    • IV calcium gluconate
    • insulin + glucose
    • sodium bicarbonate
    • nebulized albuterol
  • MOA: 
    • insulin/glucose, albuterol, sodium bicarb: shift K into cells
    • calcium: antagonizes cardiac conduction abnormalities

16

Pharmacotherapy in chronic hyperkalemia

MOA:  Cation exchange resin that binds (exchanges) potassium for sodium in intestine.

Pharmacokinetics:  Oral (more effective) and rectal.

Side effects:  Constipation, fecal compaction, nausea, vomiting.