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Week 9 - Acute Kidney injury Flashcards

1
Q

How is GFR measured?

A

-Measure in serum creatinine

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2
Q

Why is AKI treated as a medical emergency?

A

-Delayed treatment leads to irreversible renal failure

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3
Q

What are the three groups of causes of AKI?

A
  • Pre-renal
  • Intrinsic renal
  • Post-renal
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4
Q

What type of injury cause pre-renal failure?

A

-Anything which causes volume depletion to the kidney eg heart failure, cirrhosis

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5
Q

What type of diseases cause intrinsic renal AKI?

A

-Any kind of necrosis or ischaemia which affects the parenchyma eg glomerulonephritis, Acute Tubular Necrosis

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6
Q

What type of injury causes post-renal AKI?

A

-Anything which obstructs the urinary tract eg stones, prostate hyperplasia

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7
Q

What is the major cause of AKI?

A

-Acute tubular necrosis

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8
Q

Describe the pathophysiology of pre-renal AKI

A
  • Reduced renal blood flow reduces GFR

- There is no cellular damage so kidneys work hard to restors bloodflow and avidly resorb salt and water

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9
Q

Does pre-renal AKI respond to fluid resuscitation?

A

Yes

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10
Q

Describe urine production in pre-renal AKI

A

-Little and concentrated because reabsorbing fluid

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11
Q

Why is hypertension significant in pre-renal AKI?

A

-Blood pressure may seem adequate however the patient may normally have high BP so their current BP is low and the person is at risk of pre-renal AKI

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12
Q

Describe autoregulation in pre-renal AKI

A
  • Reduced renal perfusion causes vasodilation of afferent arteriole to increase renal blood flow
  • Vasoconstriction of efferent arteriole to increase renal blood pressure
  • Attempts to maintain GFR
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13
Q

Why does AKI occur in pre-renal states?

A

-Autoregulation becomes overwhelmed and cannot maintain GFR

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14
Q

At what pressures is autoregulation able to work?

A

-80-180mmHg

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15
Q

Name 2 drugs which can override autoregulation and explain why?

A
  • NSAIDs -> inhibit prostaglandin production -> inadequate vasodilation of afferent arteriole
  • ACE inhibitor -> inhibits angiotensin II which acts as a vasoconstrictor of efferent arteriole
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16
Q

What develops from pre-renal AKI if the underlying cause is not treated?

A

-Acute tubular necrosis

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17
Q

What are the major causes of acute tubular necrosis?

A
  • Ischaemia
  • Necrosis
  • Sepsis
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18
Q

What is acute tubular necrosis?

A

-Injury to proximal tubular cells which results in inability to resorb salts and water efficiently or expel excess water

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19
Q

Does ATN respond to fluid resuscitation?

A

-Sometimes but high risk of fluid overload

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20
Q

Is AKI reversible?

A

-Potentially yes

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21
Q

When does mortality significantly increase in AKI?

A

-If dialysis is required

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22
Q

Describe the pathophysiology of ischaemic necrosis

A
  • The PCT is the most susceptible area to hypoxia as it has the higest O2 demand
  • Any cause of hypoxia to the cells results in injury and the cells can no longer function
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23
Q

Describe the urine produced in ATN

A

-Often copious and dilute

24
Q

Describe the pathophysiology of toxin ATN

A
  • Nephrotoxins damage epithelial cells lining tubules and cause shedding into lumen
  • ATN is much more likely to occur if there is reduced perfusion and presence of a nephrotoxin
25
Name some endogenous nephrotoxins
-Myoglobin, bilirubin, urate
26
NAme some exogenous nephrotoxins?
- Endotoxin - X-ray contrast - drugs eg gentamycin, NSAIDs - Poisons
27
What is rhabdomyolysis and why can it cause AKI?
- Muscle necrosis, often due to crush injuries, causes release of myoglobin - Myoglobin is filtered at the glomerulus and is toxic to tubule and may cause obstruction -> causes AKI
28
What is characteristic of rhabdomyolysis?
-Produces black urine
29
What is acute glomerulonephritis?
- Immune diseases which affect the kidney | - Can by primary and only affect the kidneys or secondary as part of a systemic process
30
Name some secondary glomerulonephritis
- Systemic lupus erythema | - Vasculitis
31
What is wegners granulomatosis?
-Rapid progressive glomerulonephritis with granulomatosis and polyangitis
32
Name a primary glomeruonephritis
-IgA nephropathy
33
Name 2 causes of acute tubulo-interstitial nephritis
- Infection eg acute pyelonephritis | - Toxin-induced eg NSAIDs
34
Describe the pathophysiology of post-renal AKI
- Obstruction which blocks both kidneys causes an increase in intraluminal pressure as urine is continually being produced - This causes dilation of renal pelvis (hydronephrosis) - Decreased renal function
35
What 3 groups can cause obstruction AKI?
- Within the lumen eg stones, tumours - Within the wall, stricture post TB, congenital megaureter - Pressure from outside eg enlarged prostate, tumour, aortic aneurysm
36
What criteria must stones meet to cause AKI?
-Must be in neck of bladder, urethra or both ureters
37
What are the common signs of renal stones?
- Loin to groin pain - Haematuria - Cannot lie still
38
What U+E results would indicate AKI?
- Hyponatraemia - Hyperkalaemia - High urea - High creatinine - Hypocalcaemia and hyperphosphataemia
39
What ECG changes signify hyperkalaemia?
- Tall, tented T waves - Small/absent P waves - Increased PR interval - Widened QRS
40
Describe signs which would point towards the patient being volume depleted
-Cool peripheries, increased pulse, low bp, dry axillae
41
Describe signs which would point towards the patient being fluid overloaded
-Gallop rhythm, pulmonary oedema, peripheral oedema
42
What is mandatory in every patient with AKI?
-Urinalysis using dipstick for blood, protein and leukocytes
43
Describe how AKI is investigated
- Urine dipstick, culture and chemitry - USS, CXR - Biopsy if appropriate
44
When do you use USS in AKI?
-Post-renal or pre-renal/ATN not improving
45
When do you biopsy in AKI?
- Pre and Post-renal ruled out - Confident ATN diagnosis cannot be made - SIRS present
46
What is the main priority in AKI?
-BP and blood vol followed by pH and hyperkalaemia then watse and drug metabolism
47
How do you prevent AKI?
- Identify risk factors and monitor at-risk patients - Ensure adequate hydration - Avoid nephrotoxins
48
Describe some risk factors for developing AKI
- Advanced age - CKD - Heart/liver disease - Sepsis/critical illness - Burns/trauma
49
How do you manage patients in volume overload?
-Restrict dietary Na and water intake
50
How do you manage hyperkalaemia?
- Calcium gluconate - IV insulin + dextrose - Restrict dietary K - Stop K sparing diuretics and ACEI
51
What are indications of AKI for dialysis?
- High K+ non-responsive to treatment - Fluid overload despite diuretics - Metabolic acidosis where NaHCO3 not appropriate - Presence of dialysable nephrooxin - Signs of uraemia
52
Describe some signs of uraemia
- Pericarditis - Reduced consciousness - Intactable N&V
53
Describe the prognosis of uncomplicated ATN
- Expect recovery in 2-3 weeks | - Mortality varies from 30-80%
54
Patients who experience AKI are at risk of what in later life?
- Higher risk of death for 1 year | - Higher risk of developing CKD
55
What is acute kidney injury?
-Clinical syndrome characterised by an abrupt decline in GFR, upset of ECF volume, electrolyte and acid-base homeostasis and accumulation of nitrogen waste products

Urinary (21 decks)

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