L53 Flashcards

1
Q

Creatinine is a metabolic product from (what) and (what)? Why do you care?

A

From arginine & creatine
Formed at constant rate
Plasma Cr used to monitor GFR (P Cr = 1/GFR)
- Everything that is filtered gets excreted in urine
Formation = filtration = elimination rate

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2
Q

Describe the 4 stages of change to Cr in the unsteady state of AKI

A

P Cr does NOT reflect GFR

  1. Generation = excretion (can’t see damage effects yet)
  2. G > E
  3. G = E as damage plateaus
  4. G
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3
Q

What is the cause of AKI if there are WBC casts + eosinophils in the urine?

A

Acute intersitital nephritis

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4
Q

What is the cause of AKI if there is protein, RBC casts and WBCs in the urine?

A

Acute glomerulonephritis

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5
Q

What is the cause of AKI if there are granular casts in the urine?

A

Acute tubular necrosis

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6
Q

Causes of pre-renalAKI

A
Volume loss: hemm, diarrhea/vomiting, diuretics
Look intravasc depleted:
- CHF
- Nephrotic syndrome
- Cirrhosis
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7
Q

Describe changes with pre-renal cause of AKI

  • GFR
  • BUN/Cr
  • FE Na
A

↓RBF -> ↓GFR -> ↑Cr

↑BUN + ↓FE Na as trying to ↑ECF

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8
Q

4 big causes of intra-renal AKI

A

ATN
Acute interstitial nephritis
Acute glomerulonephritis
TTP, HUS

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9
Q

Give some examples of things that would cause ischemia leading to ATN

A

Hypotension
Cardiac bypass
Aortic crossclamp during aneurysm repair

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10
Q

Histo for ATN

A

Flattened epithelia
Debris in tubular lumen
+/- mitotic figures (if recovering)

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11
Q

Treat ATN

A

Supportive

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12
Q

Most common drugs that cause acute interstitial nephritis

A

Antibiotics

NSAIDs

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13
Q

What is the classic triad of acute interstitial nephritis (that may not be seen together)

A

**Fever + CVA tenderness
Rash
Eosinophilia

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14
Q

Urinalysis of acute interstitial nephritis

A

WBCs +/- casts

Eosinophils

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15
Q

Treat acute interstitial nephritis

A

Supportive

Remove the insult (but might not need to do this since presentation is delayed, drug may have already stopped)

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16
Q

5 big causes of rapidly progressive glomerulonephritis

A
  1. Goodpastures
  2. Granulomatous polyangitis
  3. Mircoscopic polyarteritis
  4. SLE
  5. Post-infectious (strep)
17
Q

What is rapidly progressive GN?

A

Renal fxn deteriorates fast (days/wks), poor prognosis
Nephritic syndrome = inflam process = glomerular basement membrane disrupted
- ↑BUN
- HTN
- ↓Urine output

18
Q

Urinalysis for RPGN

A

RBC casts indicates effects glomerulus

19
Q

What is granulmoatosis polyangitis? What is the key histo finding

A
= Wegner's syndrome
AI inflam of BVs
**+ c ANCA**
Symptoms:
- Nephritis
- Pulm infiltrates // hemoptysis
20
Q

What is ANCA?

A

Anti-neutrophil cytoplasmic Abs
c = cytoplasmic
p = perinuclear

21
Q

Treat Wegner’s

A

Steroids

Cyclophosphamide - immune suppression, cross links DNA

22
Q

What do you see on renal biopsy for Wegner’s

A

Crescents
Segmental necrotizing lesions
Pauci-immune

23
Q

What is Goodpasture’s disease?

A

Abs vs glomerular & alveolar basement membrane (T2 HST)

Pulm hemm + RPGN

24
Q

Renal biopsy of Goodpasture’s

A

Crescent

LINEAR IgG deposits

25
Q

Treat Goodpasture’s

A

Plasma exchange
Steroids (methylpredniolone)
Cyclophosphomide

26
Q

What is the immuno-fluorescence + electron microscopy for RPGN after strep?

A

Lumpy bumpy on IF

Subepithelial humps on EM (immune deposits)

27
Q

Treat TTP/HUS as cause of RPGN

A

Plasma exchange ASAP

28
Q

What are causes of post-renal AKI

A

BLOCKAGE
@ ureter
@ bladder outlet obstruction

29
Q

Dx post-renal cause of AKI

A

Palpable bladder
Large prostate
Hydronephrosis on imaging (enlarged renal pelvis)