Session 10 Flashcards

1
Q

What is AKI?

A

A decline in GFR that occurs over a period of <2 weeks. Usually measured by an increase in serum creatinine

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2
Q

What is oliguria and Anuria?

A

Oliguria: <500ml of urine per day
Anuria: <100ml urine per day

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3
Q

What is pre renal AKI and what can it progress to if not treated?

A

Decreased renal perfusion if BP falls below a threshold level for autoregulation. Can be reversible as there is no kidney injury (volume responsive).
Can progress to acute tubular necrosis (ATN).

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4
Q

What are the causes of pre renal AKI?

A

Reduced BP - Hypovolaemia, systemic vasodilation (anaphylaxis, sepsis) or cardiac failure
Impaired renal autoregulation - preglomerular vasoconstriction (NSAIDs/sepsis) or postglomerular vasodilation (ACEi/ang II antagonists)

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5
Q

What is post renal AKI and what can cause it?

A

Indicates an obstruction to urine flow after it has left the kidneys - in BOTH ureters, bladder or urethra. Obstructions are either in the lumen (stones/tumour), in the wall, or from pressure from the outside (enlarge prostate, tumour, aneurysm)

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6
Q

What is intrinsic AKI and what can cause it?

A

Results from direct damage to the kidney:
ATN can be due to ischaemic damage (pre renal) or nephrotoxins or both. Nephrotoxins can be endogenous (myoglobin/bilirubin) or exogenous (ACEi, NSAIDs, endotoxin)
Immune diseases
Intra tubular obstruction
Inflammation of kidney interstitium (infection/toxin)

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7
Q

What is the prevalence of different causes of AKI?

A

Pre renal + ATN = 85%
Post renal = 10%

ATN counts for 90% of intrinsic AKI

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8
Q

Describe the dipstick (proteinuria and haematuria) and microscopy findings for the different causes of AKI

A

Pre renal - all normal
Glomerulonephritis - protein, blood and RBC on microscopy
ATN - no protein or blood, mouldy brown cast on microscopy

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9
Q

When is ultrasound preformed for AKI?

A

If obstruction suspected or cause unclear.

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10
Q

When is a kidney biopsy preformed for AKI?

A

When pre&post renal ruled out and/or systemic inflammatory signs present

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11
Q

How is pre renal AKI treated?

A

Restoring renal perfusion by restoring volume (fluids) or treating pump failure (diuretics)

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12
Q

How is post renal AKI treated?

A

Urological intervention to re establish flow

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13
Q

How is ATN treated?

A

Supportive - maintaining good kidney perfusion, avoiding nephrotoxins and nutritional support

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14
Q

What is rhabdomyolysis?

A

When damaged skeletal muscle breaks down rapidly (trauma/drug users). The myoglobin that is released in an endogenous nephrotoxin

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15
Q

What are the risk factors for AKI?

A

Increasing age, CKD, DM, heart/liver disease, cancer, previous AKI

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16
Q

Why is the osmolality of urine in pre renal disease lower (less Na and H2O) than in ATN?

A

The kidneys hold on to as much plasma volume as possible as in ATN they lose their concentrating ability