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Semester 3 - Urinary > Session 10 - Acute Kidney Injury > Flashcards

Session 10 - Acute Kidney Injury Flashcards

1
Q

What is Oliguria?

A
  • Little urine

* Less than 500ml of urine/day or less than 20ml/hour

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2
Q

What is anuria?

A
  • No urine
    • Less than 100ml of urine/day
    • Indicates blockage of urine flow
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3
Q

Give three causes of acute kidney injury

A 
• Pre-renal disease
		○ Decreased perfusion
	• Post-renal failure
		○ Obstruction 
	• Intrinsic Renal Failure
		○ Dame to kidney
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4
Q

What is pre-renal acute kidney injury caused by?

A
  • A reduction in renal perfusion

* If not treated promptly acute tublar necrosis will develop

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5
Q

Give two over arching causes of pre-renal AKI

A

• Reduced effect ECF volume

Impaired renal autoregulation

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6
Q

Give three overarching causes of reduced effective ECF volume

A
  • Hypovolaemia
    • Systemic vasodilation
    • Cardiac failue
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7
Q

Give two causes of hypovolaemia

A
  • Blood loss

* Fluid loss

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8
Q

Give three causes of systemic vasodilation

A
  • Sepsis
    • Cirrhosis
    • Anaphylaxis
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9
Q

Give three causes of cardiac failure

A
  • LV dysfunction
    • Valve disease

Tamponade

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10
Q

Give two causes of impaired renal autoregulation

A
  • Preglomerular vasoconstriction

* Postglomerular vasodilation

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11
Q

Give four causes of preglomerular vasoconstriction

A
  • Sepsis
    • Hypercalcaemia
    • Hepatorenal syndrome
    • Drugs - NSAIDS
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12
Q

Give two causes of post glomerular vasodilation

A
  • ACE inhibitors

* Angiotensin 2 antagonists

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13
Q

What is post renal AKI?

A

• Injury as a result urine flow obstruction

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14
Q

What are the three sites at which urine flow can be blocked, causing post renal AKI?

A
  • Ureters
    • Bladder
    • Urethra
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15
Q

What are three places obstructions can be at each particular site in post renal AKI?

A
  • Within the lumen
    • Within the wall
    • Pressure from outside
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16
Q

Give four causes of blockage within the wall of the ureter, bladder or urethra

A
  • Calculi
    • Blood clot
    • Papillary necrosis
    • Tumour of renal pelvis, ureter or bladder
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17
Q

How large must a calculi be to stop it passing?

A

> 10mm

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18
Q

Give two causes of obstruction within the wall of the ureter, bladder or urethra

A
  • Congenital

* Ureteric stricture

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19
Q

What does obstruction with the wall of the ureter, bladder or urethra usually cause other than acute post renal AKI?

A

Chronic kidney injury

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20
Q

Give three congenital causes of obstruction within the wall of the ureter, bladder or urethra

A
  • Pelviureterteric neuromuscular dysfunction
    • Megaureter
    • Neurogenic bladder
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21
Q

Give five causes of pressure from outside causng post-renal AKI

A
  • Prostatic hypertrophy
    • Malignancy
    • Aortic aneurysm
    • Diverticulitis
    • Accidental ligation of ureter
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22
Q

Give three causes of intrinsic AKI

A
  • Acute tubular necrosis
    • Glomerular and arteriolar disease
    • Acute tubule-interstitial
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23
Q

What are the two main causes of acute tubular necrosis?

A
  • Severe acute ischaemia

* Toxic acute tubular necrosis

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24
Q

What is severe acute ischaemia caused by?

A

• Pre-renal fall in perfusion, causing tubular necrosis

25
Q

What is toxic acute tubular necrosis?

A
  • Nephrotoxins damage the epithelial cells lining the tubules and cause cell death
    • Nephrotoxins can be endogenous or exogenous
26
Q

What is the most common cause of acute tubular necrosis?

A

• Where there is toxic acute tubular necrosis AND severe acute iscaemia

27
Q

Name three endogenous nephrotoxins

A

BUM
• Bilirubin
• Urate
• Myoglobin

28
Q

Give four exogenous causes of ATN

A
  • Endotoxin
    • X-ray contrast
    • Drugs
    • Other poisons
29
Q

Give three main drugs which are exogenous nephrotoxins

A
  • ACE inhibitors
    • NSAIDs
    • Aminoglycosides
30
Q

How are NSAIDs toxic to the kidney?

A
  • Prostaglandins usually causes vasodilation of afferent arterioles in renal autoregulation
    • NSAIDs inhibit prostaglandin production by inhibition of COX
    • Unopposed vasoconstriction of afferent arteriole occurs -> Reduced glomerular perfusion pressure -> AKI
31
Q

Why are ACE inhibitors exogenous nephrotoxins?

A
  • Angiotensin II has a key role in homeostatic control of kidney blood flow
    • Efferent arteriole constriction
    • ACE inhibtors remove this effect, decreasing GFR
32
Q

What will you see in Acute Tubular Necrosis?

A
  • Muddy brown casts in urine

* Fractional excretion of Na+ >3%

33
Q

How do you calculate fractional excretion of Na?

A

• (Na (urine) x Cr (plasma)/Cr (urine) x Na (plasma) ) x 100

34
Q

Give two types of glomerular and arteriolar disease

A
  • Primary acute glomerulonephritis

* Secondary acute glomeurlonephritis

35
Q

What is acute glomerulonephritis?

A

• Immune disease affecting glomerulus (See session 9)

36
Q

Give two causes of secondary acute glomerulonephritis?

A

• Systemic lupus erthyrematosus

Vasculitis

37
Q

What is acute tubulo-interstitial nephritis? Give two causes

A
  • Inflammation of the kidney intersitium

* Acute pyelonephritis and drugs

38
Q

What are the three questions that should be asked when treating a patient with AKI?

A
  • Are the kidneys underperfused? Pre-renal injury
    • Are nephrotoxins implicated? Direct renal injury
    • Is there a renal tract obstruction? Post-renal injury
39
Q

If kidneys are underperfused, what are two main causes?

A
  • Shock

* Severe vascular disease

40
Q

What are the three main types of shock?

A
  • Hypovoleamic
    • Septic
    • Cardiac
41
Q

What is the main cause of severe vascular disease causing AKI?

A

Emboli

42
Q

What are three main possible nephrotoxins in direct renal injury?

A
  • Drugs
    • Sepsis (endotoxins)
    • Myoglobin
43
Q

What is one disease you can NEVER forget which also causes direct renal injury?

A

• UTI progressing to pyelonephritis

44
Q

Give five signs of cardiac failure

A
  • Gallop rhythm
    • Raised BP
    • Raised JVP
    • Pulmonary oedema – Basal crackles and dyspnoea
    • Peripheral oedema (Sacral/ankle)
45
Q

Give five signs of sepsis

A
  • Pyrexia and rigors
    • Vasodilation, warm peripheries
    • Bounding pulse
    • Rapid capillary refill

Hypotension

46
Q

Give six signs of a urinary tract obstruction

A
  • Anuria
    • Single functioning kidney
    • History of renal stones, prostatism or previous pelvic/abdominal surgery
    • Palpable bladder
    • Pelvic/abdominal masses
    • Enlarged prostate (DRE)
47
Q

What signs will you see in ALL AKI?

A
  • Increased serum urea and creatinine
    • Hyperkalaemia
    • Hyponatraemia
    • Hypocalcaemia
    • Hypophosphataemia
48
Q

What investigations are peformed in AKI?

A
  • ECG
    • Urine tests - Dipstick and microscopy
    • Soluble immunological tests
    • Imaging
    • Biopsy
49
Q

What ECG changes will you see in hyperkalaemia?

A
  • Tall T waves
    • Small/Absent P waves
    • Increase P-R interval
    • Wide QRS complex
    • ‘sine wave’ pattern

Asystole

50
Q

What do you look for in dipstick tests?

A
  • Blood
    • Protein
    • Leucocytes
51
Q

Will there be proteinuria/haematuria/any abnormal microscopy in the urine of someone with PRE-RENAL AKI?

A
  • No proteinuria
    • No haematuria
    • Hyaline cast in urine - Aggregations of protein seen in concentrated urine (normal sign, but will be present on every urination)
52
Q

Will there be proteinuria/haematuria/any abnormal microscopy in the urine of someone with ACUTE TUBULAR NECROSIS

A
  • No proteinuria
    • No haematuria
    • Muddy brown casts in urine
53
Q

Will there be proteinuria/haematuria/any abnormal microscopy in the urine of someone with

GLOMERULONEPHRITIS?

A
  • Heavy proteinuria
    • Heavy haematuria
    • RBC casts
54
Q

What soluble immunological tests can you do in AKI?

A

• Look for ANA (anti-nuclear antibody)
○ Indication for SLE
• Look for ANCA (anti-neutrophil cytoplasmic antibody (ANCA)
○ Systemic vasculitis
• Look for anti-glomerular basement membrane antibodies

Goodpasture’s disease

55
Q

What are two imagine techniques used in AKI?

A 
• Ultrasound 
		○ Renal size
		○ Hydronephrosis 
		○ Presence of obstruction
	• Chest X-ray
		○ Pulmonary oedema
56
Q

What is the treatment for pre-renal AKI

A

• Volume correction
○ Hypovolaemia -> Fluids
○ Heart failure -> Diuretic

57
Q

What is the treatment for post-renal failure?

A

• Urological intervention to re-establish urine flow

58
Q

What is the treatment for acute tubular necrosis

A

• Maintain good kidney perfusion

Avoid nephrotoxins

59
Q

When is dialysis indicated?

A

When kidneys can no longer adequately excrete salt, water and potassium

Semester 3 - Urinary (33 decks)

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