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30 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Common causes of community-acquired AKI |
Volume depletion SE of meds Heart failure Urinary tract obstruction Malignancy |
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Most common clinical settings for hospital acquired AKI |
Sepsis Major surgical procedures Critical illness (heart/liver failure) Nephrotoxic meds |
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Most common form of AKI |
Prerenal azotemia |
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Most common clinical conditions associated with prerenal azotemia |
Hypovolemia Decreased cardiac output NSAIDS, ARBs, ACEIs |
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Definition of prerenal azotemia |
Involves no parenchymal damage to the kidney and is rapidly reversible once parenchymal blood flow and intraglomerular hemodynamics are resolved |
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Normal GFR is maintained by? |
Renal blood flow Relative resistances of the afferent and efferent renal arterioles |
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Definition of AKI |
>2-fold increase in serum crea to >2.5mg/dL within 2 weeks without an alternate cause Rise from baseline of at least 0.3 mg/dL within 2 days or at least 50% higher than baseline within a week Reduced UO to <0.5 mL/kg/h for >6h |
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AKI is a common complication in advanced liver disease and may be triggered by the ff conditions. |
Volume depletion SBP |
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Definition of hepatorenal syndrome |
Prerenal azotemia that wouldn’t improve, often leading to intrinsic AKI, unless a definitive procedure to improve hemodynamics was performed. |
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Most common causes of intrinsic AKI |
Sepsis, ischemia, nephrotoxins |
SIN |
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Major causes of renal AKI involving large vessels |
Renal artery embolus/dissection/vasulitis Renal vein thrombosis Abdominal compartment syndrome |
Think arteries and veins |
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Major causes of renal AKI involving small vessels |
GN Vasculitis TTP/HUS DIC Atheroemboli Malignant HTN Calcineurin inhibitors Sepsis |
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Major causes of renal AKI involving the tubules |
Toxic ATN (d/t rhabdomyolysis, hemolysis, contrast, cisplatin, gentamicin) Ischemic ATN Sepsis |
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Major causes of renal AKI involving interstitium |
Drug allergies Infection Infiltration (lymphoma, leukemia) Inflammatory, sepsis |
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Most hypoxic region in the kidney |
Renal medulla |
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How does hypoalbuminemia increase the risk of nephrotoxin-associated AKI? |
Increases free circulating drug concentrations |
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Clinical course of contrast nephropathy |
Rise in serum crea 1-2 days post exposure Peak within 3-5 days Resolving within 1 week |
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Antibiotics that cause AKI |
Aminoglycosides Amphotericin B Acyclovir Cidofovir Cephalosporin Foscarnet Pentamidine Penicillin Quinolone Rifampin Sulfonamide Tenofovir Vancomycin |
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Clinical features of amphotericin B toxicity |
Polyuria Hypomagnesemia Hypocalcemia NAGMA |
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Adverse effect of ifosfamide |
Hemorrhagic cystitis Tubular toxicity |
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Adverse effect of ifosfamide |
Hemorrhagic cystitis Tubular toxicity |
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Adverse effect if bevacizumab |
Proteinuria Hypertension |
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Tumor lysis syndrome |
Follow initiation of cytotoxic therapy in pts with high-grade lymphoma or ALL Hyperuricemia Hyperphosphatemia Hyperkalemia HYPOCALCEMIA |
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Oliguria |
<400 mL/24h |
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Oliguria |
<400 mL/24h |
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Mild proteinuria |
<1g/day |
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Oliguria |
<400 mL/24h |
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Mild proteinuria |
<1g/day |
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Nephrotic range proteinuria |
>3.5g/day |
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Hallmark of AKI |
Buildup of nitrogenous waste products (increased BUN) |
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