Acute Kidney Injury Flashcards

1
Q

What is the rough definition of AKI and the different stages?

A
  • It is the decline of renal excretory function over hours/days with a rise in serum urea and creatinine.
    Stage 1- Creatinine raised by 50% of baseline.
    Stage 2 - Serum creatinine double the baseline
    Stage 3 - Serum creatine 3x the baseline
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2
Q

What is oliguria?

A

Infants - Less than 1mL/kg/hour
Adults - Less than 0.5mL/kg/hour.
Roughly less than 400-500ml per 24 hours

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3
Q

What is an AKI E-Alert?

A

When the lab identifies a change in serum creatinine, they will notify the doctor. Occurs when the serum creatinine is 50% higher than previous tests

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4
Q

What the categories for the different causes of AKI?

A

Pre-renal - Circulatory failure.
Renal - cells of the kidney.
Post-renal - obstruction

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5
Q

What are some causes of pre-renal AKI?

A
  1. Hypovolaemia and hypotension (could be due to diarrhoea/vomiting, inadequate fluid intake, blood loss)
  2. Reduced effective circulatory volume (cardiac failure or sepsis)
  3. Drugs such as ACEi or NSAIDs.
  4. Renal artery stenosis
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6
Q

What are some renal causes of AKI?

A
  1. Acute tubular Necrosis (often occurs due to untreated pre-renal causes (ischaemia) or toxins).
  2. Untreated obstructive AKI,
  3. Glomerulonephritis,
  4. Acute tubulointerstitial nephritis,
  5. Vasculitis,
  6. Atherothrombolic
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7
Q

What are some causes of post renal AKI?

A

Obstructive things such as calculi, tumours, lymphnodes, prostate. In men THINK PROSTATE, and in women gynae cancers.

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8
Q

What are the causes of acute tubular necrosis?

A
  • ATN is always caused by under perfusion of tubules and/or toxicity. So it can be caused by hypoperfusion, sepsis, toxins or all three
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9
Q

What are some toxins which can cause acute tubular necrosis?

A

Exogenous - Drugs (Gentamicin, NSAIDs or ACEi), contrast or poisons such as metals/antifreeze.
Endogenous - Myoglobin (rhabdomyolysis), haemoglobin, immunoglobins, calcium or urate.

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10
Q

What occurs to the renal arteries when blood pressure falls?

A
  • Prostaglandins trigger vasodilation of the afferent arteriole (increase blood flow into glomeruli)
    -Angiotensin causes vasoconstriction of the efferent arteriole to increase the blood pressure
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11
Q

Explain how NSAIDs and ACE inhibitors can affect the kidneys?

A

NSAIDs - prevent prostaglandin release and therefore stop the dilation of afferent arterioles with hypotension.
ACEi - Stop vasoconstriction of efferent arterioles during hypotension

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12
Q

What is the management of AKI?

A
  • Bloods: Check potassium, if hyperkalaemia then manage asap. Look at urea and creatine.
  • Measure urine output,
  • Clinical assessment of fluid status
  • Remove causes (drugs or sepsis) and exclude obstruction so get an ultrasound. If cause unknown then urinalysis, GN screen, blood films.
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13
Q

What is involved in a glomerulonephritis screen?

A
  • ANA,
  • ANA,
  • Immunoglobulins,
  • Complement,
  • Anti-glomerular basement membrane antibodies,
  • Urine bence jones proteins
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14
Q

What can be seen on a renal ultrasound?

A
  • Obstructions,.
  • Size of kidneys,
  • Loss of corticomedullary differentiation which suggests CKD.
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15
Q

What potassium levels are concerning?

A
  • If K+ is between 6.0-6.4 then ECG needed as there is risk of arrhythmias.
  • If K+ is over 6.5 then it is a medical emergency
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16
Q

What is the treatment of hyperkalaemia?

A
  • Calcium resonium (reduce K+ absorption from gut)
  • Short acting insulin +50ml of 50% dextrose (moves K+ into cells but be careful)
  • Calcium gluconate (stabilises cardiac membrane while you treat hyperkalaemia, should be given first)
17
Q

How can you treat hyperkalaemia and low bicarb?

A

Bicarb supplementation, if bicarb is less than 16 and patient is acidotic

18
Q

What are the absolute and relative indications for dialysis?

A

Absolute - Refractory potassium over 6.5 mmol or refractory (stubborn) pulmonary oedema.
Relative - Acidosis (pH<7.1), Uraemia (esp if >40) and toxins such as lithium.

19
Q

What can occur when recovering from acute tubular necrosis?

A

There is a polyuric phase for 48-72 hours where the kidneys can produce up for 6L of urine per day. It requires careful monitoring of electrolytes.

20
Q

What is the mnemonic for the indications for acute dialysis in patients with severe AKI?

A

AEIOU
- Acidosis (severe and unresponsive to treatment)
- Electrolyte abnormalities (severe and unresponsive hyperkalaemia),
- Intoxication,
- Oedema (severe and unresponsive to treatment)
- Uraemia symptoms such as seziure