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RENAL PATHOLOGY > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

Definition of Acute Renal failure?

A

Rapid loss of GFR and tubular function - hours to days
Urea/creatinine retention
Oliguric/non-oliguric

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2
Q

What is the biochemical definition of acute renal failure?

A 
Serum creatinine ↑:
>26.5umol within 48hrs
or
>1.5x baseline within 7 days
and
Urine volume <0.5ml/kg/h for 6hrs
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3
Q

How is AKI stage 1 defined?

A 
Serum creatinine ↑:
>26.5umol within 48hrs
or
>1.5x baseline within 7 days
and
Urine volume <0.5ml/kg/h for 6hrs
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4
Q

How is AKI stage 2 defined?

A

Serum creatinine ↑:
2-3x baseline
and
Urine volume <0.5ml/kg/h for 12hrs

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5
Q

How is AKI stage 3 defined?

A 
3x baseline
or 
Increase to >354umol
or
Initiation of RRT
and 
<0.3ml/kg for 24hrs
or
Anuria for 12hrs
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6
Q

How common is AKI?

A

1 in 7

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7
Q

What factors can increase the risk of AKI?

A

Comorbidities

Old Age

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8
Q

How does AKI present?

A 
AEIOU
A - acidosis
E - electrolyte disturbance
I - intoxication
O - overload
U - Uraemia
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9
Q

What is the mortality in dialysis-requiring AKI?

A

45-70%

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10
Q

What is the mortality in non-dialysis requiring AKI?

A

AKI 1 - 8%
AKI 2 - 25%
AKI 3 - 33%

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11
Q

What are the long term outcomes of AKI?

A

Death
CKD
Dialysis
CV events

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12
Q

What are the main types of AKI?

A

Pre-renal (blood flow to kidney)
Renal (intrinsic)
Post-renal (obstruction of urine)

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13
Q

What are the causes of pre-renal AKI?

A 
Volume depletion
Hypotension
Shock
Congestive HF
Liver failure
Arterial occlusion
Vasomotor
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14
Q

What drugs can cause vasomotor pre-renal AKI?

A

NSAIDs

ACEi

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15
Q

What are the causes of intrinsic renal AKI?

A 
Acute Tubular Necrosis
Toxins
Acute interstitial nephritis
Acute glomerulonephritis
Myeloma
Intra-renal vascular obstruction
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16
Q

Which toxins are commonly associated with intrinsic AKI?

A 
Amphotericin, aminoglycosides, NSAIDs
Radiocontrast (iodinated)
Rhabdomyolysis 
Snake venom
Heavy metals
Mushrooms
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17
Q

What are the causes of post-renal AKI?

A

Obstruction
Intraluminal
Intramural
Extramural

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18
Q

What are the intralumal causes of post-renal AKI?

A

Calculus
Clout
Sloughed papilla

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19
Q

What are the intramural causes of post-renal AKI?

A

Malignancy
Ureteric stricture
Radiation fibrosis
Prostate disease

20
Q

What are the extramural causes of post-renal AKI?

A

RPF

Malignancy

21
Q

What is the course of acute ischaemic renal injury?

A

Initiation
Maintenance (established parenchymal damage, maximally oliguric, 1-2 wks)
Recovery

22
Q

What is the cause of excessive recovery diuresis?

A

GFR recovering faster than tubule resorptive capacity

23
Q

How does radiocontrast nephropathy present?

A

AKI following iodinated contrast administration
Transient renal dysfunction
72hr resolution
May be permanent

24
Q

What are the risk factors for radiocontrast nephropathy?

A 
DM
Renovascular disease
Impaired renal function
Paraprotein
Large volume of contrast
25
Q

What is multiple myeloma?

A

Monoclonal proliferation of plasma cells producing excess Ig, light chains

26
Q

How does myeloma typically present?

A 
Anaemia
Back pain
Weight loss
Fractures
Infections
Cord compression
Marked elevated ESR
Hypercalcaemia
27
Q

Myeloma is common in who?

A

the elderly

28
Q

How is myeloma diagnosed?

A

Bone marrow aspirate
Serum paraprotein
Urinary Bence-Jones protein
Skeletal survey

29
Q

How does renal failure present in myeloma?

A 
Cast nephropathy
Light chain nephropathy 
Amyloidosis
Hypercalcaemia
Hyperuricaemia
30
Q

What blood tests should be performed in suspected AKI?

A 
FBC
U&amp;E
Bicarb
LFTs
Clotting
Blood gas
(ANCA/Ig/C3,C4)
31
Q

What urine tests should be performed in suspected AKI?

A

Urine dip
Urine PCR
Urine bence jones protein

32
Q

What are the risk factors for AKI?

A 
Age >75
Previous AKI
HF
Liver disease
CKD
DM
Vascular disease
33
Q

What are the AKI risk events?

A 
Sepsis
Toxins
Hypotension
Hypovolaemia 
Major surgery
34
Q

What should you consider in patients with one or more risk event/factor?

A 
STOP
S - sepsis
T - Toxins
O - Optimise BP/volum
P - prevent harm
35
Q

What steps should be taken to prevent AKI?

A 
Avoid dehydration
Avoid nephrotoxins 
Review clinical status, U&amp;E, fluid balance
Hold medications
Treat sepsis
36
Q

What should the next step be in sepsis?

A 
Sepsis 6
Blood cultures
Urine output monitoring, U&amp;E
Fluids 
Antibiotics
Lactate 
O2 saturation
37
Q

What should be considered in hypotensive patients?

A

Withdraw:
- Antihypertensives
- Diuretics
Vasopressors

38
Q

What are the insensible losses of water in the body?

A

Skin

Lungs

39
Q

What ECG changes are seen in hyperkalemia?

A 
Peaked, tented T waves
P-wave widens then disappears 
PR lengthens 
Prolonged QRS 
Bradycardia 
High grade AV block
40
Q

How is Hyperkalemia treated?

A 
Stabilise Myocardium
- Calcium Gluconate
Shift K+ intracellularly
- Insulin-dextrose
- Salbutamol
Remove
- Diuresis
- Dialysis
- Anion exchange resins
41
Q

What is the antidote to morphine?

A

Naloxone

42
Q

What is the antidote to digoxin?

A

Digibind

43
Q

What are the indications for dialysis in AKI?

A 
Acidosis (↓HCO3-)
Electrolytes (↑K+)
Intoxication
Overload (Pulmonary oedema)
Uraemia (pericarditis)
44
Q

What are the advantages of haemodialysis?

A

Fast solute/volume removal
Fast correction of electrolytes
Efficient for hypercatabolic patients

45
Q

What are the disadvantages of haemodialysis?

A

Haemodynamic instability
Concern with hypotension
Fluid removal only during short treatment time

46
Q

What are the advantages of continuous therapy?

A

Slow removal = greater haemodynamic stability

Less fluctuation in volume/solute control

47
Q

What are the disadvantages of continuous therapy?

A

Continuous anticoagulation
Delay weaning
Hypercatabolic Pt - less clearance

RENAL PATHOLOGY (16 decks)

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