Acute Kidney Injury Flashcards

1
Q

What is acute kidney injury?

A

sudden kidney failure meaning that blood volume and electrolytes cannot be managed properly and urea and nitrogenous waste are retained

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2
Q

What 3 things classify acute kidney injury?

A
  • anuria/oliguria (<0.5ml/kg/hr) for >8 hours
  • rapid rise in plasma creatinine
  • hypertension with fluid overload
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3
Q

By how much does the creatinine have to increase to be worried about AKI?

A

1.5x age specific reference creatinine or previous baseline if known

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4
Q

What are the 3 levels of the AKI warning score and what is it based on?

A
  • AKI 1-3

- based on increasing creatinine levels on relation to the upper limit of reference interval

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5
Q

AKI 1.

A

measured creatinine>1.5-2 times ULRI

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6
Q

AKI 2.

A

measured creatinine 2-3 times ULRI

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7
Q

AKI 3.

A

serum creatinine >3 times ULRI

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8
Q

How is acute kidney injury managed?

A
  • prevention!!
  • Monitor: urine output, PEWS, BP, weight
  • Maintain: good hydration
  • Minimise: Drugs
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9
Q

What are the 3 different ways be can split up thinking of causes of acute kidney injury?

A
  • pre-renal
  • intra-renal
  • post-renal
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10
Q

Generally speaking, what causes pre-renal AKI?

A

a perfusion problem e.g. volume depletion, hypotension, renal artery stenosis

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11
Q

What are intra-renal causes of AKI?

A
  • glomerular disease such as haemolytic uraemic syndrome*** and glomerulonephritis
  • tubular injury e.g. acute tubular necrosis because of hypo perfusion or drugs
  • interstitial nephritis as a result of NSAIDs, penicillin or diuretics
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12
Q

What is haemolytic uralic syndrome?

A
  • a condition caused by bacterial toxins from eating contaminated food
  • results in acute haemolytic anaemia and thrombocytopenia
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13
Q

What bacteria are normally involved in HUS?

A
  • shiga toxin producing e.coli

- shigella species

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14
Q

What toxin do the bacteria produce that causes the problems?

A

shiga toxin

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15
Q

What is the pathophysiology behind HUS?

A
  • the shiga-toxin binds to endothelial cells in the glomerular arteriole
  • this results in clots forming with platelets to try to plug the gap
  • RBCs get damaged travelling through the arterioles and so get removed from blood by spleen resulting in haemolytic anaemia
  • platelets being used up for clots results in thrombocytopenia
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16
Q

What are the presenting symptoms in HUS?

A
3 days after eating dodgy meat:
-diarrhoea
-abdominal pain
-fever
-vomiting
after a couple of days:
-bloody diarrhoea
17
Q

What is the triad of HUS?

A
  • microangiopathic haemolytic anaemia
  • thrombocytopenia
  • acute renal failure
18
Q

How is HUS managed?

A

3Ms:
Monitor:
fluid balance, electrolytes, acidosis, hypertension and other organs

Maintain:
IV normal saline and fluid
renal replacement therapy

Minimise:
no antibiotics

19
Q

What can cause post-renal AKI?

A

obstruction

20
Q

What are long term consequences of AKI?

A
  • blood pressure
  • proteinuria monitoring
  • evolution to CKD