Pathoma12.2 Acute Renal Failure (ARF) Flashcards

1
Q

What are the 2 hallmarks of acute renal failure (ARF)?

A

Azotemia

oliguria

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2
Q

What is azotemia

A

increased BUN and Creatinine (Cr)

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3
Q

What causes prerenal azotemia

A

decreased BF to kidneys

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4
Q

what is a normal BUN:Cr ratio?

A

15

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5
Q

when the tubule is intact, what is the fractional excretion of Sodium [FENa] and urine osmolality [osm]

A

FENa <1%

[osm] > 500mOsm/kg

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6
Q

What happens to BUN:Cr ratio in prerenal azotemia?

A

it increases >15

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7
Q

What is Mechnism of BUN:Cr increase in prerenal azotemia?

A

decreased GFR –> decreased Na–> renin–> Aldo–> Na and water reabsorbed–> BUN reabsorbed–> increased BUN:Cr ratio

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8
Q

what happens to FENa and urine osm in prerenal azotemia and why

A

nothing

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9
Q

what happens to FENa and urine osm in early stages of postrenal azotemia and why

A

nothing= normal

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10
Q

what happens to FENa and urine osm in late stage postrenal azotemia and why

A

FENa increases (>2%) because tubule can’t reabsorb sodium and [osm] decreases (<500) bc can’t concentrate urine

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11
Q

what is cause of Postrenal azotemia (MOA)

A

obstruction of urinary tract (ureter) downstream from kidney–> decreased outflow–> decreased GFR (backpressure), azotemia, oliguria

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12
Q

BUN:Cr in early postrenal azotemia and why?

A

> 15 because increased tubular pressure forces BUN into blood

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13
Q

BUN:Cr in late postrenal azotemia and why?

A

<15 because tubular damage makes reabsorbing BUN impossible–> decreased BUN:Cr

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14
Q

What are the 2 forms of intrarenal azotemia?

A

Acute tubular necrosis

Acute interstitial nephritis

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15
Q

What happens to GFR in Acute tubular necrosis and why

A

decreases becuase necrotic tubular cells plug the tubule

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16
Q

What is seen in the urine in Acute tubular necrosis

A

brown, granular casts (made of necrotic tubular cells)

17
Q

What happens to BUN:Cr in Acute tubular necrosis

18
Q

What does BUN reabsorption depend on ***

A

normal/intact tubular cells

19
Q

What happens to FENa and urine osm in Acute tubular necrosis

A
FENa increases (>2%) because can't reabsorb sodium
[osm] decreases (<500) because can't concentrate urine
20
Q

2 etiologies of Acute Tubular necrosis

A

Ischemia

Nephrotoxic

21
Q

Ischemic Acute Tubular necrosis affects what parts of the tubule?

A

PCT, medullary segment of TAL

22
Q

Nepphrotoxic Acute Tubular necrosis affects what parts of the tubule?

23
Q

6 common causes of Nephrotoxic Acute Tubular necrosis

A
  1. Aminoglycosides
  2. Urate (tumor lysis syndrome)
  3. Lead
  4. Myoglobinuria (crush injury)
  5. ethylene glycol (oxalate crystals in urine)
  6. radiocontrast dye
24
Q

What is tumor lysis syndrom eand why does it cause nephrotoxic Acute Tubular necrosis?

A

chemothx kills large amounts of cells which leads to release of nuclear contents including uric acid–>tubular damage

25
What 2 things are used to prevent urate-induced Acute Tubular necrosis
Hydration (increased GFR) | Allopurinol
26
what electrolytes are changed in ATN?
hyperkalemia | metabolic acidosis
27
WHat happens to BUN and Cr levels in ATN and why?
both increase due to decreased GFR
28
What happens to urine output in ATN?
it decreases
29
Prognosis of ATN
reversible but requires dialysis
30
how long does oliguria persist in ATN and why?
2-3 weeks because tubular cells are STABLE and take time to reenter the cell cycle and regenerate
31
What is the cuase of Acute Interstitial Nephritis (AIN)?
drug-induced HSR
32
3 drug types that cause AIN
penicillin, diuretics, NSAIDs
33
how does AIN present? 4 things?
oliguria, rash, fever, eosinophils in urine
34
What does AIN progress to?
Renal Papillary Necrosis
35
How does Renal Papillary Necrosis present (2)
gross hematuria, flank pain
36
4 causes of Renal Papillary Necrosis
1. Chronic analgesic abuse (phenacetin or aspirin) 2. Diabetes Mellitus 3. Sickle cell trait or disease 4. Acute pyelonephritis