Pharmacology-renal Handling and Nephrotoxity

Question 0

Tubular secretion of weak bases

Answer 0

Cimetidine, quinidine, morphine, ranitidine

Question 1

Renal tubular secretion of weak acids

Answer 1

PAH, salicylate, sulfonamide, penicillin, cephalosporins, thiazides, furosemide, methotrexate, probenecid

Question 2

Alteration of urinary pH may increase excretion of some drugs (what is needed for it)

Answer 2

Primarily eliminated unchanged
Weak electrolyte with appropriate pKA
Minimally protein bound
Small volume of distribution

Question 3

Renal handling of urate

Answer 3

Free plasma urate filtered
98-100% reabsorbed
50-85% secreted
Postsecretory reabsorption leaves 6-12% urate in urine

Question 4

Probenecid

Answer 4

Inhibits post secretory reabsorption

Question 5

P-glycoprotein

Answer 5

Efflux pump in many epithelial cells, excretory function
Found in gut wall renal tubules and BBB
Induced by rifampin
Inhibited by quinidine, verapamil, itraconazole, erythromycin
Digoxin levels are increased when it is inhibited because it is secreted by this pump in the distal nephron

Question 6

Drug that causes acute tubular necrosis

Answer 6

Gentamicin, cisplatin

Question 7

PreRenal ARF

Answer 7

NSAIDS

Question 8

Drug that causes interstitial nephritis

Answer 8

Methicillin

Question 9

Drug that causes obstruction in ARF

Answer 9

Methotrexate

Question 10

Drug related chronic kidney disease

Answer 10

Analgesic, lead

Question 11

Drug related nephrotic syndrome

Answer 11

Gold, penicillamine

Question 12

Drug related hyperkalemia

Answer 12

Ace inhibitors, K-sparing diuretics

Question 13

Drug related hyponatremia

Answer 13

Vincristine, NSAIDs

Question 14

Centrally mediated polyuria

Answer 14

Alcohol-> inhibits ADH

Question 15

Renally mediated polyuria

Answer 15

Lithium-> nephrogenic diabetes insepidus

Question 16

Centrally mediated water retention

Answer 16

CBZ- inappropriate ADH secretion

Question 17

Renally mediated water retention

Answer 17

NSAIDs

Question 18

Anion gap acidosis

Answer 18

Methanol, salicylates, ethylene glycol, par aldehyde, ethanol

Question 19

Nongap acidosis

Answer 19

Acetazolamide, amphotericin B, toluene, analgesic abuse, lithium

Question 20

Chloride dependent metabolic acidosis

Answer 20

Licorice, diuretics

Question 21

Nonchloride dependent metabolic alkalosis

Answer 21

Bicarbonate, carbenicillin

Question 22

Analgesic nephropathy

Answer 22

Chronic interstitial nephritis, papillary necrosis, chronic renal failure, not a smooth contour of the kidney

Question 23

NSAiD induced ARF

Answer 23

Decreased renal flow, prerenal azotemia, sodium retention, associated with CHF, volume depletion, cirrhosis and renal insufficiency

BLOCK compensatory mechanism synthesis of vasodilating prostaglandins

Question 24

Aminoglycoside nephrotoxicity (gentamicin)

Answer 24

Initial excretion of renal brush border enzymes, decrease in renal concentrating ability, mild proteinuria, hyaline and granular casts

Reduction in GFR follows in several more days. Mild rise in serum creatinine is most common significant finding

Accumulate in proximal tubular cells which have capacity to regenerate (toxicity is reversible)

Inhibit various enzymes and alter function of mitochondria and ribosomes

Question 25

Requirements of useful drug removal by dialysis

Answer 25

Small volume of distribution and not highly protein bound to plasma proteins

Question 26

Drugs requiring dosage adjustments in renal function

Answer 26

Aminoglycoside, cephalosporins, sulfonamide, trimethoprim, most penicillin, cimetidine, digoxin