Acute kidney injury Flashcards

(62 cards)

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
What are some causes of renal AKI?
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
Diseases causing inflammation or damage to cells leading to AKI. Which category of AKI does this describe?
Renal
27
How can renal AKI be further subdivided?
Blood vessel Glomerulus Tubular disease Interstitial disease
28
What are the symptoms of AKI?
``` Uraemic - Constitutional (anorexia, fatigue, etc) - Nausea and vomiting - Itch Fluid retention - Fluid overload (oedema, SOB) ```
29
What are the signs of AKI?
Fluid overload (oedema, hypertension, pulmonary oedema, effusion) Uraemic (itch, pericarditis) Oliguria
30
Which points of a history might point towards AKI?
``` Sore throat Rash Joint pain Diarrhoea and vomiting Haemoptysis Drug history Recent contrast (angiogram, etc) ```
31
Which clinical results might point towards AKI?
Urinalysis (blood & protein) Blood results (anaemia, eosinophilia, raised CK) Vascular bruits
32
Why might sore throat point towards AKI?
Post strep glomerulonephritis
33
Why might haemoptysis point towards AKI?
Goodpastures
34
What are the triple whammy drugs?
Diuretics NSAID ACE/ARB
35
Does myeloma cause anaemia?
Yep
36
Haemorrhage can cause anaemia. T/F
True
37
Low calcium and high phosphate points to what?
Vitamin D deficiency perhaps from CKD
38
What might eosinophilia indicated?
Interstitial nephritis (main cause drugs)
39
How can compartment syndrome cause AKI?
Rhabdomyolisis
40
How would you investigate an AKI?
``` U&E FBC & coagulation screening Urinalysis USS Immunology Protein elecrophoresis & bence jones proteinuria (>50 y/o) ```
41
Hyperkalaemia is a medical emergency. T/F
True
42
Haemolytic uraemic syndrome causes which biochemical derangement?
Low platelets
43
What might abnormal clotting indicate in relation to AKI?
Sepsis and disseminated intravascular clotting
44
Blood and protein in the urine indicate which category of AKI?
Renal
45
How is immunology useful in relation to AKI?
ANA (lupus nephritis) ANCA (vasculitis) GBM (goodpastures)
46
What are the urgent and non-urgent indications for renal biopsy?
Urgent - suspected rapidly progressing GN OR positive immunology Non-urgent - unexplained AKI
47
What are the contra-indications to renal biopsy?
Coagulopathy Warfarin or aspirin Hypertension Hydronephrosis (i.e obstruction0
48
Is you've fluid resuscitated but blood pressure is still low then what is the next step?
Inotrope/vasopressor drugs
49
Should nephrotoxic drugs be stopped? What else?
Yes & anti-nephrotics & avoid nephrotoxic/high potassium antibiotics (trimethoprim, gentamicin, co-tramoxazole)
50
What are the complications of AKI?
Hyperkalaemia Pulmonary oedema Severe acidosis (40)
51
What is the pathogenesis of post renal AKI? List the causes
Obstruction causing back pressure & hydronephrosis Stones Malignancy Stricture
52
How is post renal AKI treated?
Catheterisation Nephrostomy Ureteric stenting
53
What is hyperkalaemia associated with?
Cardiac arrhythmia
54
What is the normal range for potassium?
3.5-5 (>5.5 is hyperkalaemia --> 6.5 is life threatening)
55
How should hyperkalaemia be assessed once it has been biochemically noted?
ECG | Muscle weakness & tingling
56
How does hyperkalaemia look on an ECG?
``` Peaked T waves P waves Prolonged PR interval Broad QRS Sine wave pattern Bradycardia ```
57
How is hyperkalaemia managed?
10ml 10% calcium gluconate Insulin (actarapid) and dextrose Salbutamol nebuliser Calcium resonium (NOT in acute setting)
58
What are the indications for haemodialysys?
``` Hyperkalaemia >7 (or >6.5 and non-responsive to treatment) Severe acidosis (40 + pericardial effusion/rub ```
59
How is acidosis treated?
Sodium bicarbonate
60
What is the natural history of AKI?
``` Complete recovery (most) Recover with progressive renal failure (5-10%) No recovery (10-15%) ```
61
Risk factors for developing AKI?
Elderly Diabetes CKD Co-morbidity (heart failure, liver failure, etc)
62
What is the most common cause of AKI?
Pre-renal causes