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Urinary > Week 9 - Acute Kidney injury > Flashcards

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
Q

Name some endogenous nephrotoxins

A

-Myoglobin, bilirubin, urate

26
Q

NAme some exogenous nephrotoxins?

A
  • Endotoxin
  • X-ray contrast
  • drugs eg gentamycin, NSAIDs
  • Poisons
27
Q

What is rhabdomyolysis and why can it cause AKI?

A
  • 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
Q

What is characteristic of rhabdomyolysis?

A

-Produces black urine

29
Q

What is acute glomerulonephritis?

A
  • Immune diseases which affect the kidney

- Can by primary and only affect the kidneys or secondary as part of a systemic process

30
Q

Name some secondary glomerulonephritis

A
  • Systemic lupus erythema

- Vasculitis

31
Q

What is wegners granulomatosis?

A

-Rapid progressive glomerulonephritis with granulomatosis and polyangitis

32
Q

Name a primary glomeruonephritis

A

-IgA nephropathy

33
Q

Name 2 causes of acute tubulo-interstitial nephritis

A
  • Infection eg acute pyelonephritis

- Toxin-induced eg NSAIDs

34
Q

Describe the pathophysiology of post-renal AKI

A
  • 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
Q

What 3 groups can cause obstruction AKI?

A
  • Within the lumen eg stones, tumours
  • Within the wall, stricture post TB, congenital megaureter
  • Pressure from outside eg enlarged prostate, tumour, aortic aneurysm
36
Q

What criteria must stones meet to cause AKI?

A

-Must be in neck of bladder, urethra or both ureters

37
Q

What are the common signs of renal stones?

A
  • Loin to groin pain
  • Haematuria
  • Cannot lie still
38
Q

What U+E results would indicate AKI?

A
  • Hyponatraemia
  • Hyperkalaemia
  • High urea
  • High creatinine
  • Hypocalcaemia and hyperphosphataemia
39
Q

What ECG changes signify hyperkalaemia?

A
  • Tall, tented T waves
  • Small/absent P waves
  • Increased PR interval
  • Widened QRS
40
Q

Describe signs which would point towards the patient being volume depleted

A

-Cool peripheries, increased pulse, low bp, dry axillae

41
Q

Describe signs which would point towards the patient being fluid overloaded

A

-Gallop rhythm, pulmonary oedema, peripheral oedema

42
Q

What is mandatory in every patient with AKI?

A

-Urinalysis using dipstick for blood, protein and leukocytes

43
Q

Describe how AKI is investigated

A
  • Urine dipstick, culture and chemitry
  • USS, CXR
  • Biopsy if appropriate
44
Q

When do you use USS in AKI?

A

-Post-renal or pre-renal/ATN not improving

45
Q

When do you biopsy in AKI?

A
  • Pre and Post-renal ruled out
  • Confident ATN diagnosis cannot be made
  • SIRS present
46
Q

What is the main priority in AKI?

A

-BP and blood vol followed by pH and hyperkalaemia then watse and drug metabolism

47
Q

How do you prevent AKI?

A
  • Identify risk factors and monitor at-risk patients
  • Ensure adequate hydration
  • Avoid nephrotoxins
48
Q

Describe some risk factors for developing AKI

A
  • Advanced age
  • CKD
  • Heart/liver disease
  • Sepsis/critical illness
  • Burns/trauma
49
Q

How do you manage patients in volume overload?

A

-Restrict dietary Na and water intake

50
Q

How do you manage hyperkalaemia?

A
  • Calcium gluconate
  • IV insulin + dextrose
  • Restrict dietary K
  • Stop K sparing diuretics and ACEI
51
Q

What are indications of AKI for dialysis?

A
  • High K+ non-responsive to treatment
  • Fluid overload despite diuretics
  • Metabolic acidosis where NaHCO3 not appropriate
  • Presence of dialysable nephrooxin
  • Signs of uraemia
52
Q

Describe some signs of uraemia

A
  • Pericarditis
  • Reduced consciousness
  • Intactable N&V
53
Q

Describe the prognosis of uncomplicated ATN

A
  • Expect recovery in 2-3 weeks

- Mortality varies from 30-80%

54
Q

Patients who experience AKI are at risk of what in later life?

A
  • Higher risk of death for 1 year

- Higher risk of developing CKD

55
Q

What is acute kidney injury?

A

-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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