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Year 2 - Renal > Acute kidney injury > Flashcards

Acute kidney injury Flashcards

1
Q

Define acute kidney injury (used to be called acute renal failure)

A

Acute decline in renal function (decreased GFR), leading to a rise in serum creatinine (≥26.5 micromol/L) and/or a fall in urine output

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2
Q

Acute kidney injury can be staged into 3 stages (AKI 1/2/3)

How much has the serum creatinine rised by compared to baseline in each stage

A

AKI 1 - 1.5-2.99 times (rise of 50–99% from baseline within 7 days)

AKI 2 - 2-2.99 times (100–199% creatinine rise from baseline within 7 days)

AKI 3 - >3 times (200% or more creatinine rise from baseline within 7 days) - NEED RRT

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3
Q

Immediate dangerous consequences of AKI (hint: AEIOU)

A 
Acidosis
Electrolyte imbalance
Intoxication - from toxins
Overload - from fluid
Uraemia complications
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4
Q

3 types of AKI

A

Pre-renal
Intra-renal
Post-renal

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5
Q

Pre-renal AKI refers to damage due to

A

Kidney hypoperfusion –> decreased GFR –> accumulation of toxins in blood

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6
Q

Blood urea nitrogen to creatinine ratio

A

5-20 : 1 (much more urea than creatinine in blood because a lot of urea reabsorbed whereas most creatinine excreted)

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7
Q

Causes of pre-renal AKI (4)

A

Absolute fluid loss

  • dehydration
  • haemorrhage
  • vomiting/diarhhoea

Relative fluid loss

  • hypotension/septic shock
  • congestive cardiac failure

Renal artery stenosis/embolus

Liver failure

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8
Q

Renal (intrinsic) AKI refers to damage …

A

within the renal parenchyma

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9
Q

Post-renal AKI refers to damage …

A

due to obstruction of urine outflow tract (i.e. ureter)

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10
Q

All types of AKI exhibit decreased GFR which stimulates what system

A

RAAS to increase Na+ and water retention and therefore urea follows which increases the blood urea nitrogen ratio to creatinine

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11
Q

Causes of renal (intrinsic) AKI (5)

A

Glomerulonephritis, e.g. crescentic (rapidly progressive) GN

Tubular injury, e.g. acute tubular necrosis (usually from ischaemia)

Nephrotoxins - e.g. drugs (NSAIDs, aminoglycosides), radiocontrast

Interstitial injury, e.g. acute interstitial nephritis (due to allergic reaction to drugs)

Multiple myeloma (blood cancer)

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12
Q

Causes of post-renal AKI (3)

A

Compression

  • of ureter, e.g. intra-abdo tumours
  • of urethra - e.g. BPH

Obstruction within lumen
-calculi within ureter, bladder or urethra

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13
Q

Most common type of AKI is

A

pre-renal, i.e. hypoperfusion of kidneys

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14
Q

If pre-renal AKI sustains, it will go on to cause what

A

renal AKI - as persistent hypoperfusion will result in ischaemia of the tubules –> acute tubular necrosis because not enough oxygen and nutrients

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15
Q

What is azotaemia

A

High nitrogen containing compounds in urine

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16
Q

Acute tubular necrosis is a cause of renal (intrinsic) AKI - what is usually the cause of this

A

Sustained hypoperfusion (in pr-renal AKI) leading to ischaemia of tubules

17
Q

Aminoglycosides (a type of antibiotic) are nephrotoxic - give an example

A

gentamicin

18
Q

Investigations of AKI (6; 1 is radiological)

A 
Serum creatinine
U+Es
Urine dipstick/other urinalysis
FBC - may show anaemia
Venous blood gas - indicates metabolic acidosis from anion gap

Renal USS

19
Q

Questions to ask to confirm AKI history (4)

A

PMH of diabetes, hypertension, liver disease, congestive heart failure

Family history of congenital/systemic diseases like DM

Any nephrotoxic medication

Symptoms of uraemia

20
Q

Symptoms (7) /signs (3) of AKI (most common is pre-renal AKI)

A

Symptoms

  • oliguria
  • symptoms of azotaemia (high nitrogenous compounds in blood) - confusion, lethargy, fatigue, anorexia, nausea/vomiting
  • orthopnoea

Signs

  • tachycardia
  • hypotension (suggests pre-renal AKI)
  • dry mucous membranes, skin turgor loss
21
Q

Risk factors of AKI (6)

A 
Age >65
CKD
DM
Malignant hypertension
Congestive heart failure
Nephrotoxins - aminoglycosides, NSAIDs, radiocontrast
22
Q

Principles of management of AKI (STOP ACRONYM)

A

Suspect sepsis and treat

Toxins - stop/avoid nephrotoxic drugs

Optimise BP - IV fluids if dehydrated, diuretics if overhdyrated, stop antihypertensives if on them

Prevent harm - treat complications, review U+Es daily, review medication

23
Q

Supportive management of AKI (3)

A

Fluid balance

  • IV fluids if hypovolaemic
  • restrict fluids if hypervolaemic

Optimise BP

  • IV fluids or vasopressors
  • stop antihypertensives

Stop nephrotoxic drugs - NSAIDs, aminoglycosides

24
Q

1st line treatment of renal (intrinsic) AKI

A

Treat the underlying condition with SPECIFIC THERAPY, e.g. glomerulonephritis (often steroids, other immunosuppressants), acute tubular necrosis, interstitial injury

+ supportive measures (in other flashcard)

25
Q

1st line treatment of post-renal AKI

+ then

A

Catheterisation - to relieve urinary retention

Relief of obstruction
-e.g. if stone then ureteral stent or lithotripsy

26
Q

Dialysis is indicated in AKI if patient has… (think AEIOU complications of AKI)

A

severe metabolic Acidosis

hyperkalaemia (Electrolyte) refractory to medication

volume Overload unresponsive to diuretics - i.e. pull oedema

Uraemia (severe) –> pericarditis

27
Q

Severe electrolyte imbalance of what cation occurs in AKI

A

K+ –> hyperkalaemia

28
Q

ECG changes of hyperkalaemia (3)

A

Tall tented T waves
Broad QRS
Flat p waves

29
Q

Hyperkalaemia has a high risk of going on to cause

A

arrhythmias - ventricular fibrillation –> cardiac arrest

30
Q

Acute treatment of hyperkalaemia secondary to AKI (2)

A

Stabilise myocardium with IV calcium gluconate

Shift K+ back into cells with

  • insulin + glucose infusion
  • or salbutamol
31
Q

Biochemical investigations of renal disorders (5)

A 
U+Es - high K+, high urea
Serum creatinine - increased
FBC: +/- low RBCs, +/- leukocytes (infection) 
Urine dipstick
Urine culture
32
Q

1st line treatment of pre-renal AKI

+ then

A

Volume expansion and/or blood transfusion

Vasopressor if severe hypotension

33
Q

COMMONEST CAUSE OF ACUTE KIDNEY INJURY

A

ACUTE TUBULAR NECROSIS (due to sustained hypoperfusion of kidneys)

Year 2 - Renal (21 decks)

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