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Renal > 1: AKI > Flashcards

1: AKI Flashcards

1
Q

What is the KIGO definition of AKI

A
  1. Increase in serum creatinine of >26 in 48h
  2. Or, increase in serum creatinine 1.5-times baseline in 7-days
  3. Urine output <0.5ml/Kg/h for 6 hours
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2
Q

How is AKI categorised

A

Stage 1, Stage 2, Stage 3

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3
Q

What is creatinine in stage I AKI

A

Increase 1.5 - 2 times baseline

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4
Q

What is urine output in stage 1 one AKI

A

<0.5ml/Kg/h for 6-12h

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5
Q

What is serum creatinine in stage 2 AKI

A

Increase 2-2.9 times baseline

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6
Q

What is urine output in stage 2 AKI

A

<0.5ml/Kg/h for more-than 12h

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7
Q

What is creatinine in stage 3 AKI

A

3-times baseline

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8
Q

What is urine output in stage 3 AKI

A

<0.3ml/Kg/h for >24h

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9
Q

How can aetiology of AKI be divided

A

Pre-renal
Renal
Post-renal

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10
Q

What are 5 causes of pre-renal AKI

A

Hypovolaemia due to: sepsis, haemorrhage, D+V, pancreatitis, burns, NSAIDs, ACEi, Renal-artery stenosis, Hepatorenal syndrome

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11
Q

What are 5 causes of intrinsic renal AKI

A 
ATN
Interstitial nephritis 
Glomerulonephritis 
Infiltration (sarcoid) 
MAHA: TTP, DIC, HUS
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12
Q

What causes post-renal AKI

A

Obstruction due to: stricture, malignancy, BPH

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13
Q

What are risk factors for AKI

A
  • Age
  • Male
  • DM
  • CKD
  • Malignancy
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14
Q

How can AKI be divided clinically

A

Into 4 phases of presentation

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15
Q

What is phase I of AKI

A

(Hours-Days):

- Underlying symptoms of AKI

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16
Q

What is phase 2 AKI

A

(Weeks): Anuric/Oliguric phase

  • Reduce urine output
  • Increase urea and creatinine
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17
Q

How long does AKI last

A

Less than 2-weeks

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18
Q

What happens in phase 2 AKI

A

Decrease urine output

Increase urea and creatinine

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19
Q

What are 4 complications of phase 2 AKI

A
  • Hyperkalaemia
  • Acidosis
  • Uraemia
  • Fluid retention
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20
Q

What is phase 3 AKI

A

Polyuric phase (3-Weeks)

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21
Q

What can phase 3 AKI lead to

A

The kidney can produce more urine meaning urine output increases. However, reabsorption in tubules is still impaired causing electrolyte deficiencies

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22
Q

What is phase 4 AKI

A

Recovery: kidney function and urine production normalise

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23
Q

What can uraemia cause

A

Pericarditis

Encephalitis

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24
Q

Explain reabsorption of urea and creatinine in the kidney

A

Urea is reabsorbed in the kidney. However, very little creatinine is reabsorbed

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25
Q

What is the normal ratio of blood urea nitrogen (BUN) to creatinine

A

5-20:1

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26
Q

What causes pre-renal AKI

A

Decrease renal perfusion

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27
Q

Give 3 broad aetiological categories for AKI

A
  1. Actual decrease blood volume (haemorrhage)
  2. Relative decrease blood volume = distributive shock
  3. Renal artery disease - renal artery stenosis
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28
Q

Explain pathophysiology of pre-renal AKI

A
  • Reduced blood flow through glomerulus decreasing
    GFR
  • Reduction in GFR activates the RAAS system
  • RAAS increases sodium and hence water reabsorption
  • With water comes urea - causing BUN: Cr >20:1
  • Increased sodium reabsorption decreases urinary sodium concentration causing <20
  • Increase water reabsorption increases urine concentration - increasing urinary osmolality
29
Q

What is BUN:Creatinine ratio in pre-renal AKI and why

A

20: 1

- Due to urea being reabsorbed with water

30
Q

What is urinary sodium in pre-renal AKI and why

A

<20 - due to increase reabsorption stimulated by RAAS

31
Q

What is urine osmolality in pre-renal AKI and why

A

> 200 - increase water reabsorption stimulated by RAAS

32
Q

What causes intra-renal AKI

A

Damage to:

  • Tubules (ATN)
  • Glomerulus (Glomerulonephritis)
  • Interstitial (Acute interstitial nephritis)
33
Q

What is the most common cause of tubule damage

A

Acute Tubular Necrosis

34
Q

What usually causes acute tubular necrosis (ATN)

A

Most commonly occurs due to ischaemia - often following pre-renal AKI

35
Q

What are other causes of ATN

A
  • Toxins: ethylene glycol, aminoglycosides, contrast
  • Uric acid (eg. TLS)
  • Myoglobin (Rhabdomyolysis)
36
Q

Explain what ATN leads to

A

ATN causes ischaemia and hence death of cells which appear as muddy brown casts in the urine. Death of cells leads to increase pressure in the tubules. This reduces the pressure gradient with the glomerulus - decreasing GFR causing oliguria

37
Q

What is characteristic of ATN

A

Muddy brown casts

38
Q

Explain urea and creatinine in in ATN

A

Due to decrease filtration - urea and creatinine are increased

39
Q

What is a cause of glomerular AKI

A

Glomerular nephritis

40
Q

Explain pathophysiology of glomerular damage causing AKI

A
  • Formation antibody-antigen complexes
  • Activate complement
  • Complement damages podocytes
  • This leads to large molecules (RBC) to filter through
  • Damage reduces filtration capabilities - hence decreasing GFR
  • Decrease in GFR leads to oliguria, oedema and HTN
41
Q

What causes interstitial AKI

A

Acute interstitial nephritis

42
Q

What causes interstitial nephritis

A

Usually medications cause infiltration of immune cells that result in inflammation

43
Q

What 3 medications cause interstitial nephritis

A
  • NSAID
  • Diuretics
  • Penicillin
44
Q

What medication causes acute tubular necrosis

A

Aminoglycosides

45
Q

In acute interstitial nephritis, if the medication is not stopped what can it lead to

A

Renal papillary necrosis.

Presents as haematuria and flank pain

46
Q

Explain BUN:Cr in intra-renal AKI and why

A

BUN: Cr <15:1

Damage to kidney cells impairs reabsorption of urea leading to a low BUN: Cr ration.

47
Q

Explain urinary sodium in intra-renal AKI and why

A

Urinary sodium is high (>40) as impaired re-absorption at the kidneys

48
Q

Explain urine osmolality in intra-renal AKI and why

A

Urine osmolality is low - as water is not reabsorbed

49
Q

What may cause post-renal AKI

A

Obstruction ureter: stone, malignancy

50
Q

Explain when post-renal AKI occurs

A

If one ureter is obstructed, kidney function is usually preserved. If both are obstructed it leads to AKI

51
Q

Explain pathophysiology of post-renal AKI

A

Obstruction causes increase in pressure in the kidney. This reduces pressure gradient and hence GFR, leading to oliguria. Reduced filtration of urea and creatinine results in higher circulating concentration. Increase urea to creatinine causes BUN 15:1. Urine sodium <20 and urine osmolality >500

52
Q

What happens over-time in post-renal AKI

A

Pressure causes destruction renal epithelial cells - reduces reabsorption BUN and urine sodium

53
Q

What is first-step in investigation for AKI

A

Determine if any life-threatening complications (eg. pulmonary oedema) and treat accordingly

54
Q

What investigations are usually first performed in AKI

A

ABG (VBG) and ECG to assess for hyperkalaemia

55
Q

When is hyperkalaemia managed

A

> 6.5 or any ECG changes

56
Q

How is hyperkalaemia managed

A
  • Calcium glutinate

- Insulin and 5% Dextrose

57
Q

How is hypovolaemia in AKI managed

A

500ml Saline Fluid Challenge

58
Q

What is monitored in AKI

A
  • Observations
  • VBG (for K+)
  • Fluid balance
  • Creatinine
59
Q

What is the problem with creatinine

A

Lags by 24h

60
Q

How is cause of AKI identified

A
  • Urinalysis

- USS

61
Q

When should USS be performed

A

If suspect pyelonephritis - perform in 6 hours.

If suspect obstruction or cannot find cause of AKI - perform in 24h

62
Q

Why may FBC and coagulation studies be ordered in AKI

A

Look for MAHAs (HUS, TTP, DUS)

63
Q

Why may ANA, anti-GBM be ordered in AKI

A

Look for intrinsic renal causes

64
Q

Describe management of AKI

A
  • Treat cause
  • Ensure fluid
  • Stop nephrotoxic medications
65
Q

What is a mnemonic of medications to stop in AKI as they worsen renal function

A

NADA

NSAIDS
ACEi
Diuretics
ARB

66
Q

What 3 medications are stopped in AKI - as it can lead to toxicity of the medication

A

Metformin
Lithium
Digoxin

67
Q

What are 5 criteria to refer AKI to nephrologist

A
  • Stage 3
  • Fluid Overload
  • Difficult fluid balance (low albumin, pregnant)
  • Caused by intrinsic renal disease
  • HTN
68
Q

Give 4 complications of AKI

A
  • High Uric Acid
  • Metabolic acidosis
  • Hyperkalaemia
  • Pulmonary oedema
69
Q

How may uraemia present

A

Pericarditis

Encephalitis

Renal (15 decks)

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