ABIM NEP Drugs, AIN & CIN
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| Explain DRESS Syndrome | Life threatening drug reaction with fever, rash, eosinophilia, LAD, atypical lymphocytes, and and organ damage (granulomatous AIN, hepatitis, pneumonitis). Fever develops 1st then rash.
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| Explain Aristolochic acid nephropathy. | aka Chinese herb slimming regimen associated with GU malignancy. Tends to progress rapidly, assoc w/ fanconi syn, enzymuria, LMW proteinuria, small kidneys with extensive fibrosis and tubular atrophy. Rx-stop drug, steroids may slow progression
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| Cause of Balkan nephropathy? | Aristolochic acid! Seeds of Aristolochia clematitis co-mingled with wheat grain during annual harvest.
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| What is main concern long term for pts w Aristolochic acid nephropathy | lifelong risk of transitional cell carcinoma esp after transplantation, where it may occur in >30% of patients
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| Gold causes ___________. | Nephrotic syndrome from membranous disease and not minimal change lesions
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| Platinum compounds cause ___________. | acute tubular necrosis (ATN) through both apoptosis and necrosis, especially of the proximal tubule
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| Noni juice can cause ______ | hyperK
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| Ephedra (Ma Huang) can cause ______ | HTN and stones
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| Star fruit (carambola) can cause ______ | oxalate nephropathy & neurotoxin accumulates in renal disease
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| Glycerrhizic acid (used as a sweetener) can cause_______. - | “apparent” mineralocorticoid excess (AME)
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| Cadmium exposure can cause? | HTN +CKD from chronic tubulointerstitial nephritis w non-nephritic proteinuria and a bland urine sediment, but not associated with gout. Associations inc working in battery plant, bone disease and stones.
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| Cadmium affects the_____? | proximal tubule
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| Chronic lead toxicity can cause? | triad of gout, HTN, and CKD. Lead is similar to cadmium in causing a chronic tubulointerstitial nephritis with non-nephritic proteinuria and a bland urine sediment
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| Which cancer drugs cause AIN/CIN? | ifosfamide, TKI (tyrosine kinase inh), platins, ipilimumab
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| What AIN associated with urothelial cancers? | Aristolochic acid nephropathy
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| Ascorbic acid (vit C) can cause what type of kidney disease? | oxalate nephropathy
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| Three main causes of AIN? | antibiotics, NSAIDs, PPIs (can develop after yrs)
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| T/F urine eosinophils are specific for AIN. | FALSE. 1/3 of AKI cases have + eos. very nonspecific. Also + eos with UTI, pyelo, etc.
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| T/F WBC casts are common with AIN. | FALSE. 50% of pos have no WBC or RBC casts. many pos have casts, but seldom WBC casts. Can see RBC casts. Think pyelonephritis if see WBC casts.
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| Gallium scan usefulness in AKI? | (based on binding of lactoferrin on WBCs). Gallium scan measures uptake 48-72 hrs after injection. + in normal kidneys, ATN, cancer, pyelo, CIN, atheroembolic dz, GNs, IgAN, MCD, and AIN!!! Not very sensitive or specific.
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| Diagnosis of AIN made using ________. | kidney biopsy.
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| Drug induced AIN associated with what microscopy findings? | >10 eos/20x field + granulomas
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| T/F steroid therapy within a week of AIN diagnosis is associated with improved kidney function. | TRUE. Stop offending agent + SM 1gram pulse + pred 1 mg/kg for ?time.
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| Most common renal manifestation of sarcoidosis? | hypercalciuria 50%. Hypercalcemia seen in 10%. Glomeruli normal. T-cell interstitial infiltrate, sometimes with granulomas or giant cells
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| Renal manifestations of Sjogren Syndrome? | AIN, CIN. Assoc w/ + serologies, bland sediment, ,1 g proteinuria, AKI with tubulopathies (Fanconi, dRTA, NDI, fibrosis).
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| Explain renal manifestations of TINU. | uveitis, AIN, sterile pyuria, tubulopathies (Fanconi, dRTA, NDI, fibrosis). +/- granulomas.
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| What is IgG4 disease? | lymphoplasmacytic (T&B). infiltrate with reactive changes, plasma + for IgG4.. Rx- steroids. 60% have high IgG4 levels. + nodular masses on imaging suspicious for malignancy.
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| “Whorled” or storiform pattern of interstitial fibrosis is seen with ________. | IgG4 disease. Immunoperoxidase stain + IgG4 in plasma cells.
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| Microcystic dilatation of tubules is seen in _____. | lithium induced CIN. Rx CKD care, amiloride, adequate hydration if have NDI.
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| Lead nephropathy findings? | AKI, Fanconi's syndrome, CKD (CIN), HTN
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| Sickle cell nephropathy? | hematuria, AKI, CKD (CIN), FSGS, papillary necrosis.
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| Presentation of papillary necrosis? | asymptomatic hematuria, , Gross hematuria, Pain, UTI. + renal tissue and sediment, imaging shows partial or complete necrosis of papilla (“claw”)
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| Medullary sponge kidney is caused by _____. | Ectasia collecting ducts. Urine stasis, lo citrate, dRTA—> ca containing stones. Asymptomatic hematuria and flank pain. Dx made on CT urogram. Rx citrate.
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| Name immune mediated causes of CIN. | Sjogrens, sarcoidosis, IgG4 disase.
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| Xanthogranulomatous CIN distinguished by _______. | lipid laden macrophages. Usually infected with gram negative bacteria. Form staghorn calculi.
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| Michaels Guttman bodies seen in _______. | renal malacoplakia.
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| Nl physiologic fcns of prostaglandins? | maintain renal blood flow& GFR: inc Na reabsorption, inc aldo secretion (results in inc K secretion), lowers water reabsorption, causes vasodilation
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| List NSAID induced renal problems/diseases. | edema, exa HTN, CHF, hyperK, RTA IV, hypoNa, pre renal AKI, ischemic ATN, AIN, NS (MCD, membranous), analgesic nephropathy, papillary necrosis, renal cancer.
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| Describe drug induced small vessel vasculitis | classic leukocytoclastic skin lesion & necrotizing and prolif GN with 2+ IgG stain in mesangium . Often Low complements +MPO & PR3 & human neutrophil elastase. Assoc w levamisole used to cut cocaine (potentiates euphoria)
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| Gemcytabine causes ____. | AKI from TMA. low plt, low haptoglobin, , hi LDH,
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| Drugs reported to cause TMA | bevacizumab, CNI, gemcitobine, mitomycinC, clopidrogel, ticlopidine, opana (oxy morphone), quinine
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| Drugs reported to cause vasculitis | cocaine, PTU, infliximab
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| Interferon reported to cause? | NS from min change dz MCD
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| Anabolic steroids reported to cause? | FSGS
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| Zolendronate reported to cause? | ATN
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| Tenofivir reported to cause? | AKI/ATI/ATN, CKD, fanconi like tubulopathy (RTAII) , rarely NDI (mitochondrial toxin)
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| Aminoglycosides reported to cause? | tubular injury starts 3+days, AKI seen after 7-10 days, usually recovers. EM—> abnl mitochondria, myelin bodies d/t liposomal injury. Causes Bartter like (Na, K, Mg, Ca wasting +, met alk), fanconi syn
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| Polymyxin B or E reported to cause? | ATI/ATN, most common w high dose and long duration of rx + other nephrotoxin
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| Vancomycin reported to cause? | ATI/ATN. AIN. NOT metabolized & excreted by kidney. Dose related. Suspected mech: mitochondrial inj, complement activation & inflammation, oxidative stress.
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| Amphotericin B reported to cause? | ATI/ATN, dRTAI, NDI, hypoK, hypoMg. Constricts off arteriole, creates pores—> permeability cause K & Mg leak out of cells and H+ to leak back in (hypoMg, hypoK, RTAI distal)
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| Hydroxymethyl starch (Hextend) reported to cause? | osmotic nephropathy
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| Atazanavir reported to cause? | crystal nephropathy (rod like crystals) w granulomas + (radioopaque) stones
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| Indinavir reported to cause? | crystal nephropathy (rod like crystals) + (radioopaque) stones
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| Quinolones reported to cause? | AIN (+/-granulomatous), necrotizing vasculitis, ATN, crystal nephropathy (rod like crystals). AIN is most commonly seen on biopsy. No stones.
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| Methotrexate reported to cause? | crystalline nephropathy, most common ppt in acid urine pH <7. Avoid with IVF + alkalinization.
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| Rx methotrexate nephrotoxicity? | leucovorin, hi flux dialysis but see rebound, glucarbidase (cleaves MTX to nontoxic metabolite)
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| Acyclovir reported to cause? | crystalline nephropathy, no stones. Note usu IV high dose, not oral.
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| Sulfadiazine reported to cause? | crystalline nephropathy, +/- (radioluscent) stones. Rx alkalinize urine.
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| Ascorbic acid reported to cause? | crystalline nephropathy
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| Orlistat reported to cause? | crystalline (oxalate) nephropathy
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| Topiramate reported to cause? | (weak CA inh) met acidosis + CaPhos stones, RTAIII
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| Lithium reported to cause? | NDI (hyperNa w dilute urine), ATI/ATN, CIN, renal cysts, FSGS
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| ARBs and ACEIs reported to cause? | hemodynamic AKI, ATI/ATN, hyperK, NAGMA (hi renin, low aldo)
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| Alendronate reported to cause? | no renal effects
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| Pamidronate reported to cause? | NS, AKI from collapsing FSGS or MCD
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| Zolendronic acid reported to cause? | AKI from toxic ATI/ATN
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| PPIs to cause? | AIN, rarely hypoNa, hypoMg or CKD
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| reported to cause? |
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| Medication causes of crystal nephropathy | atazanavir/indinavir, quinolones, acyclovir, sulfonamides, MTX, ascorbic acid, orlistat, triamterene,
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| Medication causes of nephrolithiasis | atazanavir/indinavir (radioopaque), topiramate, carbonic anhydrase inh, sulfadiazine, triamterene,ephedrine
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| Explain osmotic nephropathy & list causes. | Cause AKI/ATI. IVIG/sucrose, hydroxyethyl starch, dextran, mannitol, radiocontrast. drug taken into cell by pinocytosis and cannot be metabolized—> swell
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| Tyrosine kinase inhibitors (sunitinib and sorafenib) reported to cause? | TMA & preeclampsia-like state. Also, acute & chronic interstitial nephritis, CKD, hypophosphatemia. Have anti-VGEF effect
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| Anti-VEGF agents like bevacizumab reported to cause? | preeclampsia-like state w/ HTN and proteinuria. Dose dependent denovo HTN or worsened preexisting HTN..
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| SGLT2 inhibitors (canagliflozin) renal effects? | cause the kidneys to remove sugar from the body through the urine—>UTIs + euglycemic diabetic ketoacidosis
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