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50 Cards in this Set
- Front
- Back
when is coronary artery calcium score indicated?
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asymptomatic patients with intermediate risk of CAD (10%-20% 10-year risk) --> high score (>400) is an indication for more intensive preventive treatment
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what is Fanconi syndrome?
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disease of proximal renal tubules; where BAGUP (bicarbonate, amino acids, glucose, uric acid, phosphate) are passed into the urine, instead of being reabsorbed
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findings in minimal change disease
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normal light and immunofluorescence microscopies; effacement of podocyte foot processes on electron microscopy.
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biopsy findings in primary membranous glomerulopathy
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diffuse glomerular membrane thickening without cellular infiltration, and coarsely granular deposits of IgG and C3 along the capillary loops by immunofluorescence microscopy. Electron microscopy shows moderate podocyte foot process effacement
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clinical clue to diagnosis of multiple myeloma
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elevated total urine protein, (quantifies both albumin and non-albumin protein (paraprotein)) with small amounts of protein on urine dipstick (measures only albumin)
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when to change HCTZ to furosemide
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GFR <30, HCTZ becomes ineffective as a diuretic
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kidney biopsy, what is an acceptable BP?
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<160/95
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contraindications to kidney biopsy (7)
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uncontrolled HTN, coagulopathy, thrombocytopenia, hydronephrosis, atrophic kidney, numerous kidney cysts, and acute pyelonephritis
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describe FENA in urinary obstruction
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in early obstruction, urine sodium and FENa may be low; in late obstruction, urine sodium and FENa may be high (tubular damage)
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lab findings in gentamicin toxicity
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hypokalemic metabolic alkalosis
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describe pathophysiology of gentamicin nephrotoxicity
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Aminoglycosides are divalent cations that activate calcium-sensing receptor in TALOH; this inhibits Na-K-Cl cotransporter, mimicking effect of loop diuretics and leading to hypokalemic metabolic alkalosis
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fibrosing skin disease caused by an inflammatory reaction to gadolinium that accumulates in the body due to kidney failure
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nephrogenic systemic fibrosis
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in DM, when to test for microalbuminuria?
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annual testing to assess urine albumin excretion in patients with type 1 diabetes of 5 years' duration and in all patients with type 2 diabetes starting at the time of diagnosis by measuring the albumin–creatinine ratio
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how is microalbuminuria diagnosed?
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albumin–creatinine ratio of 30 to 300 mg/g; diagnosis requires an elevated albumin–creatinine ratio on two of three random samples obtained over 6 months
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how do NSAIDs cause hyperkalemia?
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inhibit renin synthesis, resulting in hyporeninemic hypoaldosteronism, decreased potassium excretion, and hyperkalemia
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formula for TTKG
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TTKG = [Urine Potassium ÷ (Urine Osmolality/Plasma Osmolality)] ÷ Serum Potassium OR Uffine K / serum K all div by Uosm/Posm
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how to interpret TTKG?
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TTKG in patient on normal diet is 8 to 9; >10 in hyperkalemic states, reflecting excretion of excess potassium; if not then prob hypoaldosterone state
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fevers and leukopenia post kidney transplant
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CMV infection
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mechanism of kidney injury due to tenofovir
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drug-related damage to mitochondrial DNA (most significantly in renal tubules causing tubular dysfunction)
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mechanism of kidney injury due to Bactrim?
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Trimethoprim, particularly in acid urine, blocks the epithelial sodium channel in the cortical collecting duct, leading to increased lumen positive potential, impaired potassium and proton secretion, hyperkalemia, and metabolic acidosis
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X-linked disease affecting basement membranes due to a collagen protein synthesis defect. Clinical disease is characterized by sensorineural hearing loss, ocular abnormalities, and a family history of kidney disease and deafness
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Alport syndrome
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differential diagnosis of combined increased anion gap metabolic acidosis and respiratory alkalosis
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salicylate toxicity, liver disease, and sepsis
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ferritin levels that exclude or diagnose iron deficiency
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>100ng/mL excludes and <15 diagnoses iron def
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formula for urine potassium–creatinine ratio
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Urine Potassium (meq/L) × 100 [(mg × L)/(dL × g)] ÷ Urine Creatinine (mg/dL)
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interpretation of urine K-crea ratio
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> 20 meq/g c/w kidney potassium wasting, << 15 meq/g suggests extrarenal potassium loss, cellular redistribution, or decreased intake
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metabolic alkalosis, urine cl levels low, differentials?
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vomiting or decreased effective arterial blood volume (prior diuretics)
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metabolic alkalosis, urine Cl levels high, differentials?
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on diuretics, Bartter or Gitelman syndrome
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define hypercalciuria
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urine calcium >300
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treatment of calcium stones with hypercalciuria
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thiazide diuretic, promotes distal reabsorption of calcium
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kidney injury which results when a patient with vascular risk factors and hypertension attains a blood pressure lower than usual measurements
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normotensive ischemic AKI
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time frame for AIN to occur
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1 week of exposure
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JNC 7 definition of prehypertension
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average blood pressure reading of 120 to 139 mm Hg systolic or 80 to 89 mm Hg diastolic
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blood pressure that is higher at home than in the office setting
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Masked hypertension
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White coat hypertension
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3 office BP >140/90 mm Hg, 2 home BP <140/90 mm Hg and no target organ damage.
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Resistant hypertension
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BP above goal despitee 3 antihypertensives, including 1 diuretic
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pathophysiology of Gitelman syndrome
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defect is due to inactivating mutations in the gene for the thiazide-sensitive sodium chloride cotransporter in the distal convoluted tubule, and the electrolyte profile is analogous to that induced by thiazide diuretics
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electrolyte and acid base abnormality in diuretic abuse and surreptitious vomiting
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hypokalemic metabolic alkalosis
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define gestational hypertension
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refers to hypertension that develops after 20 weeks' gestation in the absence of proteinuria or other maternal end-organ damage
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what is preeclampsia?
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new-onset hypertension accompanied by the development of proteinuria, develops any time after 20 weeks of pregnancy but usually occurs close to term.
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classic presentation of AIN
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fever, rash, and eosinophilia with elevated crea (only in 10%)
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how to interpret fractional excretion of urea
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<35% prerenal (less influenced by diuretics)
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propofol-related infusion syndrome is characterized by
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type B lactic acidosis, hypertriglyceridemia, rhabdomyolysis, and J-point elevation or a Brugada-like pattern on EKG
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treatment of primary membranous glomerulopathy
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control risk factors - ACEi for HTN and statin if HL
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differentiate type A and type B lactic acidosis
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Type A due to tissue hypoperfusion / hypoxia. Type B due to medication / toxin; or in advanced malignancy, liver disease, or G6PD def
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drugs that cause type B lactic acidosis
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linezolid, acetaminophen overdose, metformin, the NRTis stavudine and didanosine, propofol, and salicylates
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kidney stones that will pass and will not pass?
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5mm or less will pass, 10mm or more will not
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at what levels of creatine kinase should one suspect rhabdo?
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>5000
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abnormal ARR
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>25 considered abnormal
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when to start bicarbonate therapy in CKD?
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Stage 4-5 with bicarb 15-20 (delays progression of CKD)
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treatment of hyperoxaluria
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calcium carbonate supplements
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