Acute Kidney Injury Flashcards

1
Q

def

A

AKA acute renal failure

is an acute decline in the GFR from baseline, with or without oligouria/anuria

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2
Q

what might cause AKI

A
pre-renal:
-impaired renal perfusion
intrinsic
-exposure to nephrotoxins
-intrinsic renal disease
post-renal:
-outflow obstruction
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3
Q

what is the most common AKI

A

acute tubular necrosis (often caused by sepsis)

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4
Q

why are patients with CAD at risk of AKI

A

CAD patients undergoining PCI, contrast is used which causes contrast nephropathy

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5
Q

epi

A

associated with elderly

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6
Q

how are AKI causes classified

A

pre-renal azotaemia
intrinsic
post-renal

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7
Q

what results in damage in pre-renal causes of AKI

A

pre-renal azotaemia (high levels of nitrogen rich compounds (urea, creatinine) in the blood

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8
Q

what are causes of pre-renal azotaemia

A
1 reduced renal perfusion
-hypovolaemia
-haemorrhage
-HF
2 hepatorenal syndrome
-this is seen is severe liver disease and is not reponsive to fluid administration (see above)
3 renovascular disease
-ACE inhibitors in those with renal artery stenosis can lead to acute tubular necrosis
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9
Q

what is acute tubular necrosis

A

death of tubular epithelial cells in the renal tubules of the kidney

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10
Q

what are common causes of acute tubular necrosis

A

low BP

use of nephrotoxic drugs

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11
Q

what are causes of intrinsic AKI

A

most commonly:

  • acute tubular necrosis (nephrotoxins)
  • glomerulonephritis
  • interstitial nephritis
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12
Q

what category does haemolytic uraemic syndrome fall into

A

intrinsic AKI

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13
Q

what are causes of post-renal injury

A

these are due to mechanical obstruction of the urinary outflow tract:

  • prostate hyperplasia or tumour
  • ascending urinary infection (pyelonephritis)
  • urinary retention
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14
Q

glomerulonephritis and pyelonephritis are what kind of AKI causes

A

glomerulonephritis intrinsic

pyelonephritis post-renal

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15
Q

risk factors

A
age
underlying renal disease
malignant HTN
DM
Na retaining states such as CHF, cirrhosis, nephrotic syndrome
nephrotoxins
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16
Q

name some nephrotoxins

A

aminoglycosides (streptomycin)
NSAIDs
ACE inhibitors

17
Q

history

A

reduced urine production
nausea + vomiting
dizziness
SOB, orthopnoea, PND (fluid overload in HF)

18
Q

if vomiting or dizziness is seen in the history what does it suggest

A

a pre-renal cause (azotaemia)

19
Q

what does muscle tenderness, limb ischaemia, seizures in AKI suggest

A

rhabdomyolysis

20
Q

if fever, rash or joint pain is seen in the history what does it suggest

A

interstitial nephritis

21
Q

examination

A

hypotension + tachycardia (pre-renal azotaemia which may progress to acute tubular necrosis)
pulmonary or peripheral oedema (HF + fluid overload is a risk factor for AKI)

22
Q

what are signs of uraemia

A

asterixis

23
Q

a 65y/o male smoker with HTN, dyslipidaemia, DM presents with chest pain. ECG suggests MI. He is taken for an urgent coronary angiogram. 3/7 later he has developed elevated serum creatinine, oliguria, hyperkalaemia

A

AKI

24
Q

a 35y.o man with a history of congenital valvular heart disease undergoes a dental procedure without antibiotic prophylaxis. Several weeks later he presents with fever and respiratory distress. laboratory tests reveal a high serum creatinine and low urine output. Urine analysis reveals more than 20 WBCs, more than 20 RBCs, and red cell casts. Serum ESR is elevated.

A

AKI

25
Q

investigations

A

1 bloods
-high serum creatinine, high serum potassium, metabolic acidosis indicates impaired renal function
-serum urea:creatinine of 20:1 indicates pre-renal azotaemia
2 urine
-infection
-high urine osmolality, low urine Na

26
Q

what might be seen on an ECG in AKI

A

signs of hyperkalaemia

tented T waves (earliest sign)
absent p waves + PR lengthens
sinus bradycardia or slow AF
VF (severe hyperkalaemia)

27
Q

what does glomerular disease typically present with

A

proteinuria, microscopic haematuria with HTN + oedema

28
Q

management for pre-renal azotaemia

A

1 volume expansion +/ transfusion is first line
-reduced renal perfusion must be treated
2 if pt hypotensive give dopamine, adrenaline, noradrenaline
3 if pt fluid overloaded give diuretic such as furosemide

29
Q

when is crystalloid used and when is colloid used

A

crystalloid (normal saline) is used most commonly

colloid is used in states of hypoalbuminaemia

30
Q

management for intrinsic

A

1 treat underlying condition is first line

if pt is fluid overloaded give diuretic (furosemide) if pt is fluid depleted give crystalloids or colloids

31
Q

management for post-renal injury

A

1 bladder catheterisation is first line

2 relieve bladder neck obstruction

32
Q

complications

A

hyperphosphataemia
uraemia (lethargy, confusion)
hyperkalaemia which may result in cardiac arrest caused by VF
CKD

33
Q

prognosis

A

significant mortality