AKI Flashcards

1
Q

where in the glomeruli is most of the filtrate reabsorbed?

A
  • 80% is reabsorbed in the proximal tubule
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2
Q

what is a stage 1 AKI

A

<0.5 ml/kh/hr urine output
>6 hrs- 8hrs for children and young people

1.5-2x increase in serum creatinine

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3
Q

what is a stage 2 AKI?

A

<0.5 ml/kh/hr urine output
>12 hrs

2-3x increase in serum creatinine

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4
Q

what is a stage 3 AKI?

A

Less than 0.3 ml/kg/hour for 24 hours or anuria for 12 hours
>3x increase in serum creatinine

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5
Q

what is the normal creatine range?

A

60 - 100 micromoles/Litre

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6
Q

what is oliguria

A

Oliguria
<0.5ml/Kg/Hour urine output
Usually <500ml/24 hours in adults

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7
Q

what is anuria

A

Anuria
Officially would mean no urine output
Softly defined as <100ml/24 hours

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8
Q

what are the 4 phases of an AKI?

A

Onset phase- (hrs -days)

Oliguric/Anuric phase- (8-14 days)

Polyuric/Diuretic phase (7-14 days)

Recovery phase (months -1yr)

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9
Q

what electrolyte disturbance makes AKI a medical emergency?

A

hyperkalaemia
K+ > 6.0 = bad
K+ > 6.5 = medical emergency

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10
Q

what ECG changes can be seen with hyperkalaemia?

A
  • reduced p wave and widened QRS
  • tented T waves
  • sine wave pattern pre cardiac arrest
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11
Q

why do px get fluid overload with AKI?

A

If your patient is oliguric/anuric – they won’t be able to get rid of this excess water

Symptoms:
Breathlessness
Orthopnea
Limb swelling

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12
Q

why can fluid overload in AKI be dangerous?

A

The danger = pulmonary oedema -> severe tissue hypoxia

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13
Q

what are the 4 main indications for dialysis?

A
  1. refractory hyperkalaemia
  2. pulmonary oedema
  3. refractory acid base disturbance
  4. uraemic complications such as coma and pericarditis
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14
Q

what are examples of prerenal causes that are likely to cause AKI?
these are v likely

A
Bleeding
Septic shock
Dehydration
Myocardial Infarction 
Iatrogenic?
Renal artery stenosis
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15
Q

what are renal causes of AKI-?

renal causes are unlikely

A

Direct toxic effects
Drugs
Calcium and other metals

Overproduction leading to blockage of the tubules
Rhabdomyolysis, myeloma,

Inflammation in the kidney
GN, interstitial nephrits, ATN

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16
Q

post renal causes of AKI?

- these are relatively likely

A
Stones
Ureteric/Urethral strictures
BPH
Prostate Cancer 
Urinary Retention e.g. neurogenic, constipation
17
Q

what are chronic background risk factors for AKI?

A
Elderly
CKD
Cardiac Failure
Liver disease
Diabetes
Vascular disease
Background nephrotoxic medications
18
Q

what are acute risks to AKI?

A

S Sepsis and Hypoperfusion
T Toxins
O Obstruction
P Parenchyma

19
Q

what are 4 Ms to predict/prevent AKI?

A

Monitor
Obs/NEWS, regular blood tests, fluid balance charts, pathology alerts

Maintain Circulation
Hydration, resuscitation, oxygenation

Minimise Kidney Insults
Nephrotoxic meds, surgery, contrast, hospital acquired infection

Manage the acute illness
Sepsis, heart failure, liver failure

20
Q

what are red flags in AKI history?

A
Haemoptysis
Rashes
Joint pain/swelling
ENT – crusting of nose/acute hearing impairment
Significant acute limb swelling
Noticable urine frothiness
Jaundice
21
Q

what do you give to stabilise cardiac membrane during hyperkalaemia?

A

Administer intravenous calcium gluconate (10mls of 10% solution) if there are hyperkalaemia associated ECG changes present.

This should help to stabilise the myocardium temporarily for 30-60 minutes and reduce the risk of fatal arrhythmia.

22
Q

what treatment for hyperkalaemia pushes potassium back into the cells?

A

Administer an insulin-glucose intravenous infusion (typically 10 units of soluble insulin are added to 25g of glucose).
Insulin helps to shift potassium from the extracellular to the intracellular compartment, whilst the glucose helps to maintain capillary blood glucose levels.

Salbutamol is often used as adjuvant therapy for hyperkalaemia.
It promotes the movement of potassium into cells and therefore out of the serum.
The onset of action is approximately 15 – 30 minutes
The duration of effect is approximately 2 hours