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Usmle Rx Qbank 2017 Step 1 Renal Item: 1 of 24 ~ 1 • M k -<:J 1>- Jil ~· !:';-~ QIO: 4749 ..L a r Previous Next Labfli!llues Not es Calculat o r • 1 & & A 67-year-old man admitted for postoperative recovery is found to be oliguric. Laboratory studies show a blood urea nitrogen level of 200 • 2 mg/dl and a serum creatinine level of 6 mg/dl. Urinalysis shows: • 3 Specific gravity: 1.050 · 4 Urine osmolality: 670 mOsm/kg • 5 Sodium: 14 mEq/L BUN/Creatinine ratio: 56 • 6 Fractional excretion of Na: 0.54% • 7 Protein: negative Casts: negative · 8 . 9 • 10 Which of the following is the most likely cause of this patient's oliguria? • 11 : • 12 A. Acute interstitial nephritis • 13 B. Acute tubular necrosis • 14 C. Bladder calculus • 15 • 16 D. Heart failure • 17 E. Nephrotic syndrome • 18 • 19 • 20 • 21 • a s 8 Lock Suspend End Block Item: 1of24 ~ . , . M k <:] t> al ~· ~ QIO: 4749 .l. ar Previous Next Lab'lifllues Notes Calculator 1 • The correct a nswer is 0. 4 80/o c hose t his. • 2 This patient's laboratory tests confirm the classic criteria for d iagnosing prerenal azotemia. Prerenal azotemia is caused by a reduction of the • 3 g lomerular filtration rate (GFR} provoked by an insult to the vascular supply to the kidney. Causes of prerenal azotemia include heart failure, sepsis, and renal artery stenosis. The reduction in GFR increases the accumulation of both blood urea nitrogen (BUN} and creatinine (Cr} in the • 4 blood, but because the BUN concentration in blood is determined by both g lomerular filtration and reabsorption (in contrast to Cr, which is • 5 limited to filtration and not reabsorbed}, the BUN level rises out of proportion to the Cr leveL This therefore elevates the BUN :Cr ratio. In • 6 addition, this patient's fractional excretion of sodium (FeNa) is less than 1%, ind icative of a prerenalI cause. f the FeNa is g reater than 2%, an intrinsic renal orig in, such as acute tubular necrosis, is the cause. Of the causes listed here, heart failure is the most likely option for a prerenal • 7 cause. • 8 Renal artery stenosis Blood urea nitrogen Azotemia Renal function Acute tubular necrosis Urea Creatinine Sepsis Fractional sodium excretion Kidney Renal artery Glomerulus Sodium Glomerulus (kidney) Stenosis Necrosis Blood vessel Nitrogen Heart failure Excretion • 9 A is not correct. 1 50/o c hose t his . • 10 Acute interstitial nephritis (AIN} is an intrarenal cause of azotemia caused by inflammation due to a number of factors, includ ing toxins and · 11 d rugs. AIN usually manifests with eosinophilic casts in the urine and with findings similar to acute tubular necrosis (ATN}, includ ing an elevated • 12 fractional excretion of sodium . Interstitial nephritis Acute tubular necrosis Nephritis Azotemia Fractional sodium excretion Urine Interstitial fluid Sodium Necrosis Inflammation Excretion • 13 B is not correct. 200/o c hose t his . • 14 Acute tubular necrosis (ATN} can mimic prerenal azotemia in many ways, although it is essentially an intrarenal azotemia. However, the maj or • 15 d istinguishing features that make this patient unlikely to have ATN are the absence of casts in the urine, the high urine-specific g ravity (ATN • 16 usually causes nonoliguric azotemia), and the very high BUN :Cr ratio. In addition, in ATN the fractional excretion of sodium is usually >2%, which is not the case in this patient. • 17 Acute tubular necrosis Azotemia Fractional sodium excretion Necrosis Sodium Urine Excretion • 18 C is not correct. 130/o c hose t his . • 19 Bladder calculi are a maj or cause of postrenal azotemia, which is d istinguished from prerenal azotemia by the relatively normal BUN :Cr ratio and, • 20 more importantly, the lack of highly concentrated urine. This patient's BUN :Cr ratio, urine specific g ravity, and fractional excretion of sodium suggest the presence of prerenal azotemia . • 21 • Specific gravity Azotemia Fractional sodium excretion Urine Urinary bladder Sodium Excretion 6 s 0 lock Suspend End Block Item: 1of24 ~ . , . M k <:] t> al ~· ~ QIO: 4749 .l. ar Previous Next Lab'lifllues Notes Calculator 1 A is not correct. 1 50/o c hose t his. 2 Acute interstitial nephritis (AIN} is an intrarenal cause of azotemia caused by inflammation due to a number of factors, includ ing toxins and d rugs. AIN usually manifests with eosinophilic casts in the urine and with findings similar to acute tubular necrosis (ATN}, includ ing an elevated • 3 fractional excretion of sodium. 4 Interstitial nephritis Acute tubular necrosis Nephritis Azotemia Fractional sodium excretion Urine Interstitial fluid Sodium Necrosis Inflammation Excretion • 5 B is not correct. 20 0/o c hose t his. • 6 Acute tubular necrosis (ATN} can mimic prerenal azotemia in many ways, although it is essentially an intrarenal azotemia. However, the maj or d istinguishing features that make this patient unlikely to have ATN are the absence of casts in the urine, the high urine-specific g ravity (ATN . 7 usually causes nonoliguric azotemia), and the very high BUN :Cr ratio. In addition, in ATN the fractional excretion of sodium is usually >2%, • 8 which is not the case in this patient. Acute tubular necrosis Azotemia Fractional sodium excretion Necrosis Sodium Urine Excretion • 9 • 10 C is not correct. 130/o c hose t his . Bladder calculi are a maj or cause of postrenal azotemia, which is d istinguished from prerenal azotemia by the relatively normal BUN :Cr ratio and, · 11 more importantly, the lack of highly concentrated urine. This patient's BUN :Cr ratio, urine specific g ravity, and fractional excretion of sodium • 12 suggest the presence of prerenal azotemia . Specific gravity Azotemia Fractional sodium excretion Urine Urinary bladder Sodium Excretion • 13 E 4 0/o • 14 is not correct. c hose t his . Nephrotic syndrome is caused by excessive g lomerular filtration of protein due to loss of the g lomerular filtration barrier. The characteristic • 15 clinical feature of nephrotic syndrome is the presence of proteinuria, which is not seen in this patient. Patients with nephrotic syndrome also • 16 commonly have hypertension, edema, and hypercholesterolemia . Nephrotic syndrome Proteinuria Hypercholesterolemia Hypertension Protein Glomerulus Edema Glomerulus (kidney) Renal function • 17 • 18 • 19 Bottom Line : • 20 Prerenal azotemia is caused by a reduction of the g lomerular filtration rate (heart failure, sepsis, and renal artery stenosis) . Renal artery stenosis Azotemia Renal function Sepsis Renal artery Glomerulus Stenosis Glomerulus (kidney) Heart failure • 21 6 s 0 lock Suspend End Block Item: 1 of 24 ~ 1 • M k -<:J 1>- Jil ~· !:';-~ QIO: 4749 ..L a r Previous Next Labfli!llues Not es Calculat o r 1 & & FA17 p 571 .2 • 2 Acute kidney injury • 3 Acute kidney injury is de fin ed as an abrupt decline in renal functi on as measured by t creatinine (acute renal failure) and t BU! or by oliguria/anuria. · 4 Prerenal azotemia Due to l RBF (eg, hypotemion) - l CFR. la•/ 11 0 and BUt retained by kidn ey in an attempt to • 5 1 consen e volume - t BU '/creatinine ratio (BUN is reabsorbed, crea ti nine is not) and l F'E'Ia· • 6 Intrinsic renal failure Cenerallr due to acute tubular necrosis or ischemia/toxins; less commonly due to acute • 7 glomerulonephritis (eg, RPCN, hcmol) Lie uremic S) nd rome) or ac ute interstitial nephritis. · 8 In ATN, patchy necrosis - debr is obstructing tubule and Auid backAow across necrotic tubule . 9 - l C FR. Urine has epithel ial/granular c~1 s t s. BU!': reabsorption is impaired - l BUI':/crcatininc • 10 rati o and t FENa· • 11 Postrenal azot emia Due to outfl ow obstructi on (stones, BPI I, neoplasia, congenital anomalies). De,·elops onl y with • 12 bilateral obstruction . • 13 Pre renal Intrinsic renal Postrenal • 14 Urine osmolality > 500 < 350 < 350 • 15 (mOsm/kg) • 16 Urine Na+ (mEq/l) <20 > 40 > 40 • 17 FENa < I% >2% < 1% (mild) • 18 > 2% (se,·ere) • 19 Serum BUN/Cr > 20 < 15 Varies • 20 • 21 • FA17 o 562.2 a s 8 Lock Suspend End Block Item: 1 of 24 ~ 1 • M k -<:J 1>- Jil ~· !:';-~ QIO: 4749 ..L a r Previous Next Labfli!llues Not es Calculat o r 1 & & • 2 FA17 p 562.2 • 3 Casts in urine Presence of casts indicates that hematuria/pyuria is of glomerular or renal tubular origin. · 4 Bladder cancer, kidney stones - hematuria, no casls. • 5 Acute cystitis - pyuria, no casts. • 6 RBC casts Glomerulonephritis, malignant hypertension. • 7 WBC casts Tubulointerstitial inAammation, acute pyelonephritis, transplant rejection. · 8 Fatty casts ("oval fat 'ephrotic syndrome. Associated with ·· i\ laltese cross" sign. 9 bodies") • 10 Granular ("muddy Acute tubular necrosis. • 11 brown") casts • 12 Waxy casts I!] End-stage renal disease/chronic renal failure. • 13 Hyaline casts 0 1'\onspecific, can be a normal finding, often seen in concentrated urine samples. • 14 • 15 • 16 ' • 17 • 18 • 19 • 20 • 21 • a s 8 Lock Suspend End Block Item: 2 of 24 ~ 1 • M k -<:J 1>- Jil ~· !:';-~ QIO: 4162 ..L a r Previous Next Labfli!l tues Not es Calculat o r 1 & & On a routine physical examination, a previously healthy 26-year-old woman has a blood pressure of 150/85 mm Hg . She has had no other • 2 physical symptoms. She begins following a diet and exercise program, but on her next visit, her blood pressure is 170/95 mm Hg. A blood • 3 test demonstrates elevated plasma renin. · 4 Which is the most likely explanation for this patient's condition? • 5 • 6 A. A thromboembolus lodged in the renal artery • 7 of the renal artery · 8 B. Atherosclerosis . 9 C. Conn syndrome • 10 D. Fibromuscular dysplasia • 11 E.
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