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Year 2 > Acute kidney injury > Flashcards

Acute kidney injury Flashcards

1
Q

Is acute kidney injury common?

A

Yes

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2
Q

Mortality increases with increasing severity of AKI. T/F

A

True

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3
Q

Define acute kidney injury (AKI)

A

Rapid decrease in kidney function characterised by >26.4mmol rise in serum creatinine OR 50% increase creatinine from baseline OR reduction in urine output

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4
Q

When is AKI defined?

A

After fluid resuscitation

After obstruction is excluded

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5
Q

Define the stages of AKI

A

Stage 1 - creatinine rise >26 OR increase 1.5-1.9 reference creatinine
2-2.9 reference creatinine
3 reference creatinine OR increase to >354 OR need for renal replacement therapy

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6
Q

Is AKI usually based on urine production or creatinine? Why?

A

Creatinine

Because urine output is usually poorly measured on wards

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7
Q

AKI is a diagnosis. T/F

A

False - it’s a description for which there will be an underlying cause

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8
Q

How can you categorise the causes of AKI?

A

Pre-renal (functional)
Renal (structural)
Post-renal (obstruction)

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9
Q

What are some pre-renal causes of AKI?

A

Hypovolaemia

  • haemorrhage
  • diarrhoea & vomiting
  • burns

Hypotension

  • cardiogenic shock
  • sepsis
  • anaphylaxis

Renal hypoperfusion

  • NSAIDs
  • ACE/ARB
  • hepatorenal syndrome
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10
Q

What is hepatorenal syndrome?

A

Kidney failure as a result of liver failure

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11
Q

Define oliguria

A
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12
Q

Is pre-renal AKI reversible?

A

Volume depletion can be reversed and AKI can recover

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13
Q

How does angiotensin II affect the kidney?

A

Efferent arteriolar vasoconstriction and thus increased kidney BP (hydrostatic capillary pressure) and thus increased GFR

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14
Q

How does an ACE inhibitor affect the kidney?

A

Loss of angiotensin II vasoconstriction and thus no arteriolar constriction (i.e vasodilation) and thus reduced GFR

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15
Q

Why might a patient with diarrhoea and vomiting (i.e volume depletion) who is on an ACE inhibitor present with AKI? How is this prevented?

A

Reduced volume combined with vasodilation from effects of ACEi causes reduced GFR and hence AKI

Tell patients on ACEi/NSAID/Diuretic to stop drugs during periods of diarrhoea and vomiting

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16
Q

Explain the pathphysiology of AKI

A 
Volume depletion -->
Decreased intravascular volume -->
RAAS system & ADH increase -->
Salt & water retention -->
Oliguria -->
AKI
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17
Q

What happens if pre-renal AKI is missed?

A

It can lead to acute tubular necrosis

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18
Q

What is acute tubular necrosis? What are the common causes?

A 
Histological diagnosis of a type of AKI (commonest form)
Volume depletion
Sepsis
Rhabdomyolisis
Drug toxicity
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19
Q

How is pre-renal AKI treated?

A

Reversal/removal of precipitating factors

  • Assess hydration
  • Fluid challenge for hypovolaemia
  • Supportive
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20
Q

How can you assess the hydration status of a patient?

A 
Heart rate
Blood pressure
Urine output 
JVP 
Cap refill
Peripheral oedema
Pulmonary oedema
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21
Q

What types of fluid challenge are indicated in AKI?

A

Crystalloid (NaCL)

Colloid (gelofusin)

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22
Q

Over which level of fluids given, with no clinical improvement, should you seek help?

A

1000ml

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23
Q

How are fluid challenges given?

A

Give fluid bolus, reassess, repeat as needed

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24
Q

Why should dextrose not be given in AKI? Why not hartmans?

A

It does not go into the intravascular volume

It contains potassium which is not ideal in AKI

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25
Q

What are some causes of renal AKI?

A

Vasculitis
- ANCA associated small vessel - Wegner’s, GPA

Glomerulonephritis

  • lupus nephritis
  • goodpastures
  • post infective
  • infective endocarditis

Acute tubular necrosis

  • rhabdomyelitis
  • contrast
  • ischaemia
  • gentamicin

Acute interstitial nephritis

  • antibiotics
  • PPI
  • NSAIDs
  • TB infection
  • sarcoidosis
26
Q

Diseases causing inflammation or damage to cells leading to AKI. Which category of AKI does this describe?

A

Renal

27
Q

How can renal AKI be further subdivided?

A

Blood vessel
Glomerulus
Tubular disease
Interstitial disease

28
Q

What are the symptoms of AKI?

A 
Uraemic 
- Constitutional (anorexia, fatigue, etc)
- Nausea and vomiting
- Itch
Fluid retention
- Fluid overload (oedema, SOB)
29
Q

What are the signs of AKI?

A

Fluid overload (oedema, hypertension, pulmonary oedema, effusion)
Uraemic (itch, pericarditis)
Oliguria

30
Q

Which points of a history might point towards AKI?

A 
Sore throat 
Rash
Joint pain
Diarrhoea and vomiting
Haemoptysis 
Drug history
Recent contrast (angiogram, etc)
31
Q

Which clinical results might point towards AKI?

A

Urinalysis (blood & protein)
Blood results (anaemia, eosinophilia, raised CK)
Vascular bruits

32
Q

Why might sore throat point towards AKI?

A

Post strep glomerulonephritis

33
Q

Why might haemoptysis point towards AKI?

A

Goodpastures

34
Q

What are the triple whammy drugs?

A

Diuretics
NSAID
ACE/ARB

35
Q

Does myeloma cause anaemia?

A

Yep

36
Q

Haemorrhage can cause anaemia. T/F

A

True

37
Q

Low calcium and high phosphate points to what?

A

Vitamin D deficiency perhaps from CKD

38
Q

What might eosinophilia indicated?

A

Interstitial nephritis (main cause drugs)

39
Q

How can compartment syndrome cause AKI?

A

Rhabdomyolisis

40
Q

How would you investigate an AKI?

A 
U&E
FBC & coagulation screening
Urinalysis 
USS
Immunology
Protein elecrophoresis & bence jones proteinuria (>50 y/o)
41
Q

Hyperkalaemia is a medical emergency. T/F

A

True

42
Q

Haemolytic uraemic syndrome causes which biochemical derangement?

A

Low platelets

43
Q

What might abnormal clotting indicate in relation to AKI?

A

Sepsis and disseminated intravascular clotting

44
Q

Blood and protein in the urine indicate which category of AKI?

A

Renal

45
Q

How is immunology useful in relation to AKI?

A

ANA (lupus nephritis)
ANCA (vasculitis)
GBM (goodpastures)

46
Q

What are the urgent and non-urgent indications for renal biopsy?

A

Urgent - suspected rapidly progressing GN OR positive immunology
Non-urgent - unexplained AKI

47
Q

What are the contra-indications to renal biopsy?

A

Coagulopathy
Warfarin or aspirin
Hypertension
Hydronephrosis (i.e obstruction0

48
Q

Is you’ve fluid resuscitated but blood pressure is still low then what is the next step?

A

Inotrope/vasopressor drugs

49
Q

Should nephrotoxic drugs be stopped? What else?

A

Yes & anti-nephrotics & avoid nephrotoxic/high potassium antibiotics (trimethoprim, gentamicin, co-tramoxazole)

50
Q

What are the complications of AKI?

A

Hyperkalaemia
Pulmonary oedema
Severe acidosis (40)

51
Q

What is the pathogenesis of post renal AKI? List the causes

A

Obstruction causing back pressure & hydronephrosis
Stones
Malignancy
Stricture

52
Q

How is post renal AKI treated?

A

Catheterisation
Nephrostomy
Ureteric stenting

53
Q

What is hyperkalaemia associated with?

A

Cardiac arrhythmia

54
Q

What is the normal range for potassium?

A

3.5-5 (>5.5 is hyperkalaemia –> 6.5 is life threatening)

55
Q

How should hyperkalaemia be assessed once it has been biochemically noted?

A

ECG

Muscle weakness & tingling

56
Q

How does hyperkalaemia look on an ECG?

A 
Peaked T waves 
P waves 
Prolonged PR interval 
Broad QRS
Sine wave pattern 
Bradycardia
57
Q

How is hyperkalaemia managed?

A

10ml 10% calcium gluconate
Insulin (actarapid) and dextrose
Salbutamol nebuliser
Calcium resonium (NOT in acute setting)

58
Q

What are the indications for haemodialysys?

A 
Hyperkalaemia >7 (or >6.5 and non-responsive to treatment)
Severe acidosis (40 + pericardial effusion/rub
59
Q

How is acidosis treated?

A

Sodium bicarbonate

60
Q

What is the natural history of AKI?

A 
Complete recovery (most)
Recover with progressive renal failure (5-10%)
No recovery (10-15%)
61
Q

Risk factors for developing AKI?

A

Elderly
Diabetes
CKD
Co-morbidity (heart failure, liver failure, etc)

62
Q

What is the most common cause of AKI?

A

Pre-renal causes

Year 2 (72 decks)

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