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
What is toxic acute tubular necrosis?
* Nephrotoxins damage the epithelial cells lining the tubules and cause cell death * Nephrotoxins can be endogenous or exogenous
26
What is the most common cause of acute tubular necrosis?
• Where there is toxic acute tubular necrosis AND severe acute iscaemia
27
Name three endogenous nephrotoxins
BUM • Bilirubin • Urate • Myoglobin
28
Give four exogenous causes of ATN
* Endotoxin * X-ray contrast * Drugs * Other poisons
29
Give three main drugs which are exogenous nephrotoxins
* ACE inhibitors * NSAIDs * Aminoglycosides
30
How are NSAIDs toxic to the kidney?
* 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
Why are ACE inhibitors exogenous nephrotoxins?
* Angiotensin II has a key role in homeostatic control of kidney blood flow * Efferent arteriole constriction * ACE inhibtors remove this effect, decreasing GFR
32
What will you see in Acute Tubular Necrosis?
* Muddy brown casts in urine | * Fractional excretion of Na+ >3%
33
How do you calculate fractional excretion of Na?
• (Na (urine) x Cr (plasma)/Cr (urine) x Na (plasma) ) x 100
34
Give two types of glomerular and arteriolar disease
* Primary acute glomerulonephritis | * Secondary acute glomeurlonephritis
35
What is acute glomerulonephritis?
• Immune disease affecting glomerulus (See session 9)
36
Give two causes of secondary acute glomerulonephritis?
• Systemic lupus erthyrematosus Vasculitis
37
What is acute tubulo-interstitial nephritis? Give two causes
* Inflammation of the kidney intersitium | * Acute pyelonephritis and drugs
38
What are the three questions that should be asked when treating a patient with AKI?
* Are the kidneys underperfused? Pre-renal injury * Are nephrotoxins implicated? Direct renal injury * Is there a renal tract obstruction? Post-renal injury
39
If kidneys are underperfused, what are two main causes?
* Shock | * Severe vascular disease
40
What are the three main types of shock?
* Hypovoleamic * Septic * Cardiac
41
What is the main cause of severe vascular disease causing AKI?
Emboli
42
What are three main possible nephrotoxins in direct renal injury?
* Drugs * Sepsis (endotoxins) * Myoglobin
43
What is one disease you can NEVER forget which also causes direct renal injury?
• UTI progressing to pyelonephritis
44
Give five signs of cardiac failure
* Gallop rhythm * Raised BP * Raised JVP * Pulmonary oedema – Basal crackles and dyspnoea * Peripheral oedema (Sacral/ankle)
45
Give five signs of sepsis
* Pyrexia and rigors * Vasodilation, warm peripheries * Bounding pulse * Rapid capillary refill Hypotension
46
Give six signs of a urinary tract obstruction
* Anuria * Single functioning kidney * History of renal stones, prostatism or previous pelvic/abdominal surgery * Palpable bladder * Pelvic/abdominal masses * Enlarged prostate (DRE)
47
What signs will you see in ALL AKI?
* Increased serum urea and creatinine * Hyperkalaemia * Hyponatraemia * Hypocalcaemia * Hypophosphataemia
48
What investigations are peformed in AKI?
* ECG * Urine tests - Dipstick and microscopy * Soluble immunological tests * Imaging * Biopsy
49
What ECG changes will you see in hyperkalaemia?
* Tall T waves * Small/Absent P waves * Increase P-R interval * Wide QRS complex * ‘sine wave’ pattern Asystole
50
What do you look for in dipstick tests?
* Blood * Protein * Leucocytes
51
Will there be proteinuria/haematuria/any abnormal microscopy in the urine of someone with PRE-RENAL AKI?
* 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
Will there be proteinuria/haematuria/any abnormal microscopy in the urine of someone with ACUTE TUBULAR NECROSIS
* No proteinuria * No haematuria * Muddy brown casts in urine
53
Will there be proteinuria/haematuria/any abnormal microscopy in the urine of someone with GLOMERULONEPHRITIS?
* Heavy proteinuria * Heavy haematuria * RBC casts
54
What soluble immunological tests can you do in AKI?
• 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
What are two imagine techniques used in AKI?
``` • Ultrasound ○ Renal size ○ Hydronephrosis ○ Presence of obstruction • Chest X-ray ○ Pulmonary oedema ```
56
What is the treatment for pre-renal AKI
• Volume correction ○ Hypovolaemia -> Fluids ○ Heart failure -> Diuretic
57
What is the treatment for post-renal failure?
• Urological intervention to re-establish urine flow
58
What is the treatment for acute tubular necrosis
• Maintain good kidney perfusion Avoid nephrotoxins
59
When is dialysis indicated?
When kidneys can no longer adequately excrete salt, water and potassium