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ABIM Nep Drugs
ABIM NEP Drugs in Renal Failure
| Question | Answer |
|---|---|
| FDA requires use of ___ for drug dosing. | Creat clearance. GFR not validated! |
| ______ determines loading dose of medication. | Volume of distribution |
| ______ determines maintenance dose of medication. | creatinine clearance, half life. |
| T/F uremia decreases plasma protein binding of mycophenolic acid, thereby increasing free drug concentration. | TRUE. Those patients with poor CrCl more likely to have diarrhea |
| Rx acute dabigatran ingestion? | Activated charcoal. Hemodialysis is effective, removing 50-60% of dabigatran over a 2- to 4-hour dialysis session. However, lg vol of distribution (50-70 L) results in "rebound" levels after HD. May consider CVVH. |
| Renal effects of dasatinib, a protein-tyrosine kinase inhibitors? | nephrotic-range proteinuria from dasatinib but not imatinib (Gleevec) or nilotinib (Tasigna). Poss mech of action? disruption of the VEGF signaling pathway. dasatinib also assoc w pulm HTN, pleural effusions, myelosuppression. |
| Acidosis from NSAIDS caused by? | blockade of prostaglandins and is usually hyperchloremic w/o anion gap. |
| nucleoside reverse transcriptase inhibitors (NRTI) adjustments for dialysis? | give after dialysis, may cause of lactic acidosis. |
| Non-nucleoside reverse transcriptase inhibitors (NNRRTI) adjustments for dialysis? | no adjustments needed for renal failure. have P450 3A4 interactions |
| T/F Venlafaxine (Effexor) overdose has been associated with seizures, serotonin syndrome, neuroleptic malignant syndrome, and rhabdomyolysis. | TRUE |
| Sodium thiosulfate is used for? | calcific uremic arteriolopathy. The drug is a strong acid, & causes +AGMA. In rare circumstances, the metabolic acidosis can be severe, requiring a dosage reduction. |
| How does acetaminophen toxicity causes AG? | when there’s depletion of glutathione, pyroglutamic acid is overproduced in the presence of large amounts of acetaminophen |
| Renal effects of tenofovir? | AKI and proximal tubular injury (fanconi syn) via mitochondrial toxicity. |
| Renal effects of indinavir? | no adjustment needed. May cause Stones and interstitial nephritis |
| Renal effects of ritonavir? | no adjustments needed. May cause AKI. |
| Renal effects of gentamicin? | AKI, Fanconi syndrome, and Bartter-like syndrome. |
| Renal effects of Rosiglitazone (thiazolidinedione) | increased renal salt retention and the development of edema. |
| Renal effects of Cisplatin? | causes AKI, tubulopathies, Fanconi syndrome, salt wasting, and magnesium wasting, NDI, CKD |
| Renal effects of Amphotericin B? | AKI and a distal renal tubular acidosis (RTA). |
| Renal effects of Mitomycin C? | causes a thrombotic microangiopathy. |
| Renal effects of bevacizumab | Anti-VGEF: anti-angiogenic agents that inhibit vascular endothelial growth factor (VEGF) signaling pathways regularly produce a rise in arterial pressure, often associated with HTN, proteinuria and renal dysfunction |
| Renal effects of IVIG | AKI, hypoNa, pseudohypnatremia, + osm gap from maltose accumulation |
| Renal effects of Ifosfamide? | Fanconi syndrome, proximal phosphate wasting, AKI, and nephrogenic diabetes insipidus. Renal tubular dysfunction can develop months after completing chemotherapy. |
| Renal effects of Paclitaxel? | NONE! Not associated with any significant renal toxicity. |
| Renal effects of ciprofloxacin? | - crystalline nephropathy d/t crystal precipitation in the renal tubules. Risk factors: excessive dose, alkaline urine, underlying kidney injury, and old age. |
| Renal effects of HES ? | AKI, sometimes requiring dialysis, is more common when this drug is used in critically ill patients with sepsis and acute lung injury/acute respiratory distress syndrome (ARDS) |
| Renal effects of NSAIDS? | HTN, edema, AKI (esp w/ vol depletion, lower renal blood flow or hyperCa), nephropathy (MCD or MGN), hyperK, hypoNa, AIN. |
| Mechanism of action of NSAIDs in kidney? | Lower renin production through inh of PGs. Cause HYPORENIN/HYPOALDO (RTAIV)+ hyperK. Also, enhance [urine] ability via PGE2 that usu attenuates ADH effect—>counteract diuretic effect via lower RBF, inc UNa reabsorption in PCT, |
| Renal effects of Pentamidine? | like amiloride, triamterene, and trimethoprim, pentam is associated with hyperkalemia by blocking the epithelial sodium channel in the principal cell in the cortical collecting duct. |
| Renal effects of linezolid therapy? | lactic acidosis by disrupting mitochondrial function. |
| Renal effects of Acetaminophen? | oxoproline acidosis in alcoholics and patients with poor nutrition due to the underlying glutathione and deficiencies these patient maintain. |
| Renal effects of Interferon? | nephrotic syndrome (usu MCD) and AKI from AIN. Other glomerular lesions include FSGS and MGN. |
| The drugs most often noted in the published literature as causing AIN? | antimicrobial agent. PPIs are likely the overall leading cause of drug-induced AIN, based on their massive use. |
| pts with HIV starting cART can develop ___. | IRIS: restoring protective immune responses —> pathological inflammatory response (AIN) |
| Describe Acute phosphate nephropathy. | Intense ppt of CaPhos in medulla>>cortex. The serum phosphate levels likely >7, resulting in phosphaturia. Recall crystals are needle-like. CaPhos stained using von Kossa stain, which will not stain calcium oxalate. |
| Hormonal effects of ACEIs ? | raise plasma renin activity and renin levels, but lower AII and aldosterone |
| Hormonal effects of ARBs ? | raise plasma renin activity, renin levels and AII levels, but lower aldosterone. |
| Hormonal effects of Aldosterone antagonists ? | raise the levels of all of the hormones, but antagonize the mineral corticoid receptor. |
| Metformin requires adjustment and what stage of renal function? | CKD4. Usual dosing acceptable in CKD 3/4 w/o increased incidence of lactic acidosis |
| Lithium nephrotoxicity may be prevented or treated by the use of ___. | Amiloride is Rx of choice for NDI. (no hypoK & no need Na restrict thus less vol depletion). Also reduce Li uptake into cells. NOTE Li dosage may be affected by amiloride. |
| T/F Administration of activated charcoal is useful for lithium OD. | FALSE because charcoal does not bind lithium ions. Consider polyethylene glycol |
| Preferred agent to bind lithium in G.I. tract? | polyethylene glycol. especially important for patients who ingest a sustained-release lithium. Charcoal does not work. |
| Conventional hemodialysis can reduce plasma lithium by ___. | 1 mEq/L per 4 h of treatment. High flux likely more effective, but unproven. HD does not clear intracellular lithium effectively, expect rebound. |
| Hemodialysis should be performed for lithium OD for what scenarios? | coma, convulsions, respiratory failure, deteriorating mental status, or renal failure… or if lithium level fails to fall. Also strongly consider HD if level > 4 mEq/L, or levels 2.5-4 w CV or CNS symptoms. Seldom needed if lvl<2.5 |
Created by:
ka1usg
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