Urinary 12 - AKI Flashcards

1
Q

List the 3 possible findings in AKI:

A

1) Increased serum Creatinine by > 26.5uM in 48hrs
2) Increased serum Creatinine by > 1.5x baseline within 7 days
3) Urine volume < 0.5 ml/kg/hr for 6 hrs

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2
Q

Define AKI:

A

Decline in GFR over days/weeks, upsetting ECF volume, electrolyte and acid-base homeostasis, and causing accumulation of nitrogenous waste products

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3
Q

The causes of AKI are split into which 3 categories?

A

1) Pre-Renal
2) Intrinsic Renal
3) Post-Renal

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4
Q

How do heart failure, sepsis, cirrhosis and anaphylaxis all cause AKI?

A

Decreased ECF volume = Decreased renal perfusion

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5
Q

How do NSAIDs, ACEi and AIIR antagonists cause AKI?

A

Impair renal autoregulation pathways = cannot increase renal perfusion

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6
Q

If pre-renal AKI is not rapidly treated, what will it develop into? Why?

A

ATN - Acute Tubular Necrosis
Inadequate perfusion = ischaemic cell damage
Drug OD = nephrotoxic cell damage

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7
Q

What are the 2 types of Acute Tubular Necrosis (ATN)?

A

1) Ischaemic

2) Nephrotoxic

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8
Q

What parts of the kidney is most susceptible to ischaemia?

A
Proximal tubule (part. S3 segment)
Thick Ascending Limb of LoH (TAL)
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9
Q

Give 5 causes of nephrotoxic ATN (acute nephrotoxic necrosis):

A

1) Myoglobin
2) Poisons
3) Drugs
4) Bilirubin
5) Urate

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10
Q

Why may an elderly person develop nephrotoxic ATN after prolonged immobilisation?

A

Prolonged immobilisation causes rhabdomyolysis

Myoglobin is toxic to tubular cells, and may obstruct tubule = necrosis

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11
Q

Name 5 intrinsic renal diseases leading to AKI:

A

1) Acute Tubular Necrosis (ATN)
2) Glomerulonephritis - IgA nephropathy, SLE
3) Small vessel disease - Haemolytic anaemia
4) Acute Tubulo-Interstitial Nephritis - Infection/toxin-induced
5) Renal artery/vein occlusion

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12
Q

Describe post-renal causes of AKI:

A

1) Obstruction within lumen
2) Obstruction within wall
3) External compression
Must affect both kidneys

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13
Q

What serum findings are ALWAYS found in AKI?

A

Raised Creatinine

Raised Urea

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14
Q

What ECG changes are associated with raised serum K+?

A
  • Tall T waves
  • Small/absent P waves
  • Increased P-R interval
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15
Q

What changes to ECF [K+] typically occurs in AKI?

A

Raised ECF [K+]

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16
Q

What signs of underperfusion can you check for externally?

A
  • Cool peripheries
  • Increased pulse
  • Decreased BP/postural hypotension
  • Decreased skin turgor
17
Q

If dipstick test shows ^ proteinuria and ^ haematuria, what is the most likely cause of the AKI?

A

Glomerulonephritis (intrinsic renal)

18
Q

Which investigations would be carried out if suspected glomerulonephritis, and what would the findings be?

A

Urinalysis: Proteinuria + Haematuria
Urine microscopy: RBC casts
Biopsy

19
Q

List some risk factors for AKI:

A
  • Increasing age
  • Diabetes mellitus
  • Cancer
  • Trauma
  • Sepsis
  • Dehydration
20
Q

Why is it important to restrict Na+ and water intake in AKI?

A

To reduce fluid retention and overload, as kidneys cannot adequately excrete fluid/toxins

21
Q

Give some treatments for high [K+] in AKI:

A
  • Restrict dietary K+
  • Calcium gluconate
  • IV Insulin + Dextrose
  • Stop K+ sparing diuretics +/- ACEi / ARBs
22
Q

What is the treatment of acidosis caused by AKI?

A

Sodium bicarbonate

23
Q

In which situations may you perform dialysis on a patient with AKI?

A
  • Presence of dialysable nephrotoxin
  • Hyperkalaemia not responding to treatment
  • Severe metabolic acidosis
  • Fluid overload not responding to diuretics
  • Signs of uraemia (^thirst, muscle cramps, confusion, anorexia, fatigue, nausea/vomiting, pruritis)
24
Q

If hyperkalaemia or fluid overload in AKI is not responding to treatment, what could be considered?

A

Dialysis

25
Q

If patient with AKI has the following symptoms:
Increased thirst, pruritus, confusion, anorexia, fatigue, muscle cramps…
What do you suspect and how will you treat it?

A

Uraemia

Dialysis