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BCPS study guide


formula for fractional excretion of sodium [urine Na/urine Cr]/[serum Na/serum creatinine]x100
definition of anuric vs oliguric vs non-oliguric urine output anuric is anything less than 50 ml in 24 hours. oliguric is between 50 and 500 ml in 24 hours. non-oliguric is greater than 500 ml in 24 hours.
what is pseudonephrotoxicity drug induced inhibition of creatinine secretion, examples trimethoprim and cimetidine. increases in BUN due to drugs such as steroids and tetracyclines. drugs that interfere with creatinine assay such as cefoxitin/cephalosporins
three classifications of AKI interstitial/intrinsic (AIN/ATN), prerenal and postrenal
examples of causes of prerenal AKI volume depletion, CHF, renal artery stenosis, high calcium, NSAIDS/ACEi/ARBs, cyclosporine
examples of causes of postrenal AKI kidney stones, BPH, cancers
examples of causes of intrinsic AKI or acute tubular necrosis or acute interstitial nephritis nephrotoxins, vasculitis, glomerulonephritis, long standing renal hypoperfusion
urinalysis indications of prerenal AKI BUN:Scr >20:1, urinalysis shows concentrated urine, urine sodium <20, FeNa<1%,
urinalysis indications of intrinsic AKI BUN:Scr <15:1, urine not concentrated, muddy casts, FeNa>2%, urine sodium >40. WBCs/RBCs positive, protein positive,
urinalysis indications of postrenal AKI BUN Scr <15:1, urine not concentrated, FeNa>2%, urine sodium >40. protein negative, blood positive,
causes of acute tubular necrosis aminoglycosides, iodinated contrast, cisplatin/carboplatin, amphotericin B
causes of acute allergic interstitial nephritis, timing of presentation and treatment beta lactams and NSAIDS - for beta lactams usually presents 1-2 weeks into treatment. for NSAIDs presents after 6 months. treat with withdrawal of the offending drug and give steroids
causes of chronic interstitial nephritis, timing of presentation lithium (>10 years of treatment), cyclosporin and tacrolimus (6-12 months of therapy for both.
how do you prevent ATN due to radiocontrast give fluids for volume expansion with NS or bicarb 6-12 hours prior to procedure. maintain a urine output of >150 ml/hr.
treatments for prerenal AKI correct the primary hemodynamics with NS, pressure management and blood products
treatments for intrinsic AKI remove causative agent, manage fluids and electrolytes, loops to deal with hypervolemia.
treatments for post renal AKI relieve obstructions
indications for renal replacement therapy in AKI BUN>100, volume overload not responding to diuretics, uremia or encephalopathy, life threatening electrolyte imbalances such as K or Mg, refractory metabolic acidosis
Created by: mjuhlin