Acute Tubular Necrosis/Acute Renal Failure Flashcards

1
Q

Acute interstitial renal inflammation with eosinophils* in the urine?

A

Drug induced interstitial nephritis

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2
Q

Most drugs take _________ to develop Drug induced interstitial nephritis but NSAIDS take __________

A

1-2 weeks

Months

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3
Q

Acute generalized cortical infarction of both kidneys?

A

Diffuse cortical necrosis

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4
Q

MCC of acute injury in hospitalized patients?

A

Acute tubular necrosis (ATN)

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5
Q

With ATN, there will be increased?

A

FENa

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6
Q

What will you see in the urine? Why?

A

granular (“muddy brown”) casts

Tubular cells die and plug the nephron=>intrinsic azotemia=>granular casts

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7
Q

There are 3 stages to ATN; they are?

A
  1. Inciting event
  2. Maintenance phase—oliguric; lasts 1–3 weeks;
  3. Recovery phase—polyuric;
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8
Q

During the maintenance phase you could get?

A

Risk of hyperkalemia, metabolic acidosis,
uremia Why? there is oligouria

Low urine, low urine K+, Low urine H+ and Low urine Urea

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9
Q

During the Recovery phase you could get?

A

BUN and serum creatinine fall; risk of hypokalemia Why? there is polyuria

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10
Q

In ischemic tubular necrosis, what part of the kidney is most susceptible to injury?

A

PCT and thick ascending limb

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11
Q

In Toxic tubular necrosis, what part of the kidney is most susceptible to injury?

A

PCT=>lots to absorb

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12
Q

What are 3 common ways that Toxic tubular necrosis happens?

A
  1. Leukemia=>chemo
  2. Ethylene glycol=>oxalate crystals
  3. Crush Injury
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13
Q

How does a patient with leukemia get toxic tubular necrosis?

A

Leukemia=>chemo=>tumor lysis=>increased uric acid

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14
Q

After 4-6 weeks, ATN cells are able to regenerate. Why?

A

Tubular cells are stable cells (G0=>G1)

Hepatocytes and lymphocytes

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15
Q

Sloughing of necrotic renal papillae with gross hematuria and proteinuria? Dx?

A

Renal papillary necrosis

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16
Q

Renal papillary necrosis causes?

A
SAAD papa with papillary necrosis: 
Sickle cell disease or trait
Acute pyelonephritis
Analgesics (NSAIDs)
Diabetes mellitus
17
Q

What is acute renal failure?

A

Increased creatinine and BUN due to oligouria=>azotemia

18
Q

Prerenal azotemia is due to?

A

=>decreased RBF=>Decreased GFR=>Increased renin=> More BUN is reabsorbed but creatinine is NOT

19
Q

Prerenal azotemia what are the numbers

A

BUN: C=> 20:1

Urine Na+ b/c you are reabsorbing
FENab/c you are reabsorbing
Urine osmolarity= >500

500 20 1

20
Q

Postrenal/Intrinsic azotemia what are the numbers?

A

Decreased tubular function

Urine Na+ >40
FENa >2
Urine osmolarity= 350

350 40 2

21
Q

Postrenal vs Intrinsic Azotemia

A

Intrinisic BUN:C=

22
Q

What is the problem in post renal azotemia?

A

There is backpressure, pushing BUN into the tubular cells but they are damaged

23
Q

Another name for Intrisinic Azotemia?

A

Acute Tubular Necrosis

Tubular cells die=>cannot reabsorb

24
Q

Consequences of Renal Failure?

A

Retention of everything
MAD HUNGER:
ƒ Metabolic Acidosis
ƒ Dyslipidemia (especially 􏰀 triglycerides)
ƒ Hyperkalemia
ƒ Uremia—clinical syndrome marked by
􏰀BUN:
ƒ Nausea and anorexia ƒ Pericarditis
ƒ Asterixis
ƒ Encephalopathy
ƒ Platelet dysfunction
ƒ Na+/H2O retention (HF, pulmonary edema, hypertension)
ƒ Growth retardation and developmental delay
ƒ Erythropoietin failure (anemia)
ƒ Renal osteodystrophy (Hyperphosphatemia)

25
Q

EPO is made by?

A

Renal Peritubular Intersitial cells

26
Q

Patients with chronic renal failure get cysts how?

A

CRF=>Shrunken kidney=>dialysis=>cysts

27
Q

Renal Failing patients have increased risk of?

A

RCC

28
Q

Tumors that secrete EPO?

A
  • Pheochromocytoma
  • Renal cell carcinoma
  • Hepatocellular carcinoma
  • Hemangioblastoma