acute renal failure Flashcards

1
Q

definition of acute renal failure

A

acute, severe decrease in renal occurring over days

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2
Q

what is the hallmark of ARF

A

azotemia, increase in BUN and creatinine often with oliguria

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3
Q

prerenal azotemia causes

A

this occurs due to decreased blood flow to the kidneys and is a common cause of prerenal KF. the decrease blood flow results in decreased GFR, azotemia, and oliguria

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4
Q

characteristics of prerenal

A

since there is decreased GFR there will be a decreased feNa and the urine osmolarity will be high (greater than 500). because BUN is reabsorbed, the BUN/Cr will be greater than 15.

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5
Q

postrenal azotemia

A

this is caused by obstruction of the kidney out flow AKA the ureters. the decreased out flow causes decreased GFR, azotemia, and oliguria.

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6
Q

characteristics of short-term postrenal azotemia

A

the BUN/Cr will be greater than 15 due to the BUN being forced into the serum. tubular function remains intact and causes the FeNa to be less than 1% and the urine osmolarity to be greater then 500.

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7
Q

characteristics of long-term postrenal azotemia

A

tubular damage ensues resulting in decreased reabsorption of BUN thus the BUN/Cr <15. there will also be decreased reabsorption of Na and thus FENa will be greater than 2%.

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8
Q

acute tubular necrosis

A

injury and necrosis of tubular epithelial cells. this is the most common cause of intrarenal azotemia.

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9
Q

characteristics of acute tubular necrosis

A

the necrotic epithelial cells slough off of the tubular lumen and clog the tubular lumen. this obstruction causes decreased GFR and forms brown, granular casts in the urine.

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10
Q

labs of acute tubular necrosis

A

the dysfunctional tubules result in decreased reabsorption of BUN and thus BUN/Cr 2%. and there will be an inability to concentrate urine oSm >500.

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11
Q

etiology of acute tubular necrosis

A

can be nephrotoxic or ischemic

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12
Q

ischemic acute tubular necrosis

A

decreased blood supply results in the necrosis of the tubules. this is often preceded by prerenal azotemia.

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13
Q

what are the most sensitive segments to ischemic acute tubular necrosis

A

proximal tubule and medullary segment of the thick ascending limb.

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14
Q

nephrotoxic acute tubular necrosis

A

toxic agents result in the necrosis of tubules.

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15
Q

causes of nephrotoxic acute tubular necrosis

A

aminoglycosides, heavy metals, myoglobinuria, ethylene glycol, radio contrast dye and urate.

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16
Q

most susceptible regions of the kidney to acute tubular necrosis

A

proximal tubule.

17
Q

how do we stop rate induced acute tubular necrosis

A

allopuranol and hydration. this happens before giving chemotherapy.

18
Q

clinical features of acute tubular necrosis

A

oliguria with brown granular casts. there will be elevated BUN and Cr. hyperkalemia due to decreased renal excretion with metabolic acidosis. the things you are supposed to get rid of you can’t, so they accumulate. hyperkalemia, acidosis, BUN all elevated. tubular plugging by casts

19
Q

is acute tubular necrosis reversible?

A

yes, but usually requires therapeutic dialysis.

20
Q

how long does the oliguria persist in acute tubular necrosis

A

usually 2-3 weeks because it takes time for the tubular cells to reenter the cycle and regenerate.

21
Q

acute interstitial nephritis description

A

drug-induced hypersensitivity involving the interstitium and tubules. results in acute renal failure. intrarenal azotemia.

22
Q

common causes of acute interstitial nephritis

A

NSAIDs, penicillin, diuretics.

23
Q

how does acute interstitial nephritis present?

A

oliguria, fever, and rash days after starting the drug. eosinophils seen in the urine. resolves with cessation of the drug

24
Q

what can acute interstitial nephritis progress too?

A

renal papillary necrosis.

25
Q

renal papillary necrosis description

A

necrosis of the renal papilla. presents as gross hematuria

26
Q

causes of renal papillary necrosis?

A

chronic anagesic abuse (tylenol, aspirin), DM, sickle cell trait or disease. severe, acute pyelonephritis.