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Pathoma LAH > Renal: 12.2: Acute Renal Failure > Flashcards

Renal: 12.2: Acute Renal Failure Flashcards

1
Q

BUN:Cr ratio is greater than 15:1. Dx?

A

prerenal azotemia

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2
Q

How does acute interstitial nephritis present?

A
  • Days to week after starting a drug:
    • oliguria
    • fever
    • rash
    • hematuria
    • CVA tenderness
    • Eos in the urine
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3
Q

What are the clinical features of acute tubular necrosis?

A
  • oliguria with brown, granular casts
  • elevated BUN and Cr
  • Hyperkalemia
  • Metabolic acidosis
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4
Q

Why does acute tubular necrosis cause hyperkalemia?

A

decreased renal excretion of K+

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5
Q

What are the consequences of renal failure?

A

MAD HUNGER

  • Metabolic Acidosis
  • ƒƒDyslipidemia (esp. triglycerides) ƒƒ
  • Hyperkalemia ƒƒ
  • Uremia ƒƒ
  • Na+/H2O retention (HF, pulmonary edema, HTN) ƒƒ
  • Growth retardation and developmental delay
  • ƒƒErythropoietin failure (anemia) ƒƒ
  • Renal osteodystrophy
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6
Q

What do all of the following have in common?:

  • Chronic analgesic use (ie phenacetin, aspirin, NSAIDs)
  • Diabetes mellitus
  • Sickle cell trait or disease
  • Severe acute pyelonephritis
A

they can cause renal papillary necrosis

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7
Q

What is the most common cause of acute renal failure?

A

acute tubular necrosis

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8
Q

What are the 2 major causes of acute tubular necrosis?

A
  1. ischemia
  2. nephrotoxic
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9
Q

What is allopurinol used for?

A
  • to prevent uremia/tumor lysis syndrome kidney damage
  • tx for gout
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10
Q

Which parts of the kidney are particularly susceptible to toxins?

A

proximal tubule

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11
Q

What is the ratio of BUN:Cr in acute tubular necrosis?

A

less than 15

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12
Q

What items are very nephrotoxic?

A
  • aminoglycosides
  • heavy metals (ie lead)
  • myoglobinuria (ie crush injury)
  • ethylene glycol (antifreeze)
  • radiocontrast dye
  • urate/uric acid (ie tumor lysis syndrome)
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13
Q

What is azotemia? How is it measured?

A
  • an increase of nitrogenous waste products in the blood
  • increased BUN and Cr
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14
Q

What is post-renal azotemia?

A

obstruction of the urinary tract downstream from the kidney

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15
Q

Which parts of the kidney are particularly susceptible to ischemia?

A
  • proximal tubule
  • medullary segment of the thick ascending limb
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16
Q

What happens to the tubular function in acute tubular necrosis? What will the tests of tubular function show?

A
  • decreased
  • FENa greater than 2%
  • urine osm less than 500
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17
Q

What does post-renal azotemia do to the GFR?

A

decreases it

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18
Q

What is prerenal azotemia?

A

decreased blood flow to the kidney

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19
Q

What does pre-renal azotemia do to the GFR?

A

decreases it

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20
Q

What happens to the tubular function in prerenal azotemia? What will the tests of tubular function show?

A
  • it’s normal
  • FENa = less than 1%
  • urine osm = greater than 500
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21
Q

What is renal papillary necrosis?

A

necrosis of the renal papillae –> sloughing –> gross hematuria and proteinuria

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22
Q

What happens to the tubular function in post-renal azotemia? What will the tests of tubular function show?

A
  • early: remains intact
    • FENa = less than 1%
    • urine osm = greater than 500
  • late: decreased resorption of Na
    • FENa greater than 2%
    • urine osm less than 500
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23
Q

How can acute tubular necrosis be reversed?

A
  • tubular cells can regenerate (although slowly)
  • often req’s supportive dialysis
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24
Q

What is oliguria?

A

low urine production

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25
Q

How does renal papillary necrosis present?

A
  • gross hematuria
  • flank pain
  • proteinuria
26
Q

What kind of casts are seen in acute tubular necrosis?

A

brown, granular

27
Q

How is acute interstitial nephritis treated?

A

cessation of the drug

28
Q

What is found in the urine in acute interstitial nephritis?

A

Eosinophils

29
Q

What happens to the GFR in acute tubular necrosis?

A

it decreases

30
Q

What is the hallmark of acute renal failure?

A

azotemia

31
Q

This is a drug-induced hypersensitivity rxn of the interstitium and tubules (inflammation).

A

acute interstitial nephritis

32
Q

Dx?

  • Days to week after starting a drug:
    • oliguria
    • fever
    • rash
    • hematuria
    • CVA tenderness
    • Eos in the urine
A

acute interstitial nephritis

33
Q

What is the ratio of BUN:Cr in post-renal azotemia?

A
  • early: BUN:Cr greater than 15
  • late: BUN:Cr less than 15
  • *** Late = LESS than
34
Q

This is an increase of nitrogenous waste products in the blood.

A

azotemia

35
Q

What is acute interstitial nephritis?

A

a drug-induced hypersensitivity rxn of the interstitium and tubules (inflammation)

36
Q

What are the s/s of uremia?

A
  • increased BUN ƒƒ
  • Nausea and anorexia ƒƒ
  • Pericarditis ƒƒ
  • Asterixis ƒƒ
  • Encephalopathy
  • ƒƒPlatelet dysfunction
37
Q

This is necrosis of the renal papillae –> sloughing –> gross hematuria and proteinuria.

A

renal papillary necrosis

38
Q

What causes renal papillary necrosis?

A
  • Chronic analgesic use (ie phenacetin, aspirin, NSAIDs)
  • Diabetes mellitus
  • Sickle cell trait or disease
  • Severe acute pyelonephritis
39
Q

What category of azotemia is acute tubular necrosis?

A

intrarenal azotemia

40
Q

Dx?

  • injury of tubular epi cells –> necrosis –> plug tubules with brown, granular casts –> decreased GFR
A

acute tubular necrosis

41
Q

What does acute interstitial nephritis cause?

A

intrarenal acute renal failure

42
Q

Is acute tubular necrosis fatal? Why/why not?

A
  • it can be
  • electrolyte imbalances
43
Q

Dx?

  • oxalate crystals in the urine
A

ethylene glycol poisoning

44
Q

What is acute tubular necrosis?

A

injury of tubular epi cells –> necrosis –> plug tubules with brown, granular casts –> decreased GFR

45
Q

What is the ratio of BUN:Cr in prerenal azotemia?

A

greater than 15:1

46
Q

What is Fomepizole? What is it used to treat?

A
  • an alcohol dehydrogenase inhibitor
  • tx for methanol or ethylene glycol poisoning
47
Q

What is the tx for ethylene glycol poisoning?

A

Fomepizole

48
Q

Pts that have ingested ethylene glycol often have _____ in their urine.

A

oxalate crystals

49
Q

What do the following drugs have in common?:

  • NSAIDs
  • penicillin
  • diuretics
  • PPIs
  • sulfonamides
  • rifampin
A

they all can cause acute interstitial nephritis

50
Q

Are BUN and Cr reabsorbed?

A

only BUN is

51
Q

What is asterixis?

A

a recurrent flapping tremor of the arms, like the action of a bird’s wings

52
Q

This is a recurrent flapping tremor of the arms, like the action of a bird’s wings. When is it seen?

A
  • asterixis
  • hyperammonemia (liver or kidney dysfunction)
53
Q

What is the normal ratio of BUN:Cr?

A

15:1

54
Q

How is tumor lysis syndrome prevented?

A
  • hydration
  • allopurinol
55
Q

How is tubular function measured? What are the normal values?

A
  • FENa = less than 1%
  • urine osm = greater than 500
56
Q

What do all these items have in common?:

  • aminoglycosides
  • heavy metals (ie lead)
  • myoglobinuria (ie crush injury)
  • ethylene glycol
  • radiocontrast dye
  • urate (ie tumor lysis syndrome)
A

they’re all nephrotoxic

57
Q

Is acute tubular necrosis reversible?

A

yes

58
Q

What causes acute interstitial nephritis?

A
  • drugs, including:
    • NSAIDs
    • penicillin
    • diuretics
    • PPIs
    • sulfonamides
    • rifampin
59
Q

Why does acute tubular necrosis cause metabolic acidosis? What kind of metabolic acidosis is it?

A
  • decreased excretion of organic acids
  • anion gap metabolic acidosis
60
Q

What can acute interstitial nephritis progress to?

A

renal papillary necrosis

Pathoma LAH (77 decks)

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