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8. Urology (Medical Knowledge) > acute kidney injury > Flashcards

acute kidney injury Flashcards

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USMLE® Step 1 flashcards
1
Q

what does AKI stand for?

A

acute kidney injury

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2
Q

what is the definition of acute kidney injury?

A

increase in serum creatinine:

  • by 26.5umol/L or more within 48 hours or
  • to >1.5x baseline, which is known or presumed to have occurred within the prior 7 days or
  • urine volume <0.5ml/kg/h for 6 hours
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3
Q

how many stages of acute kidney injury are there?

A

3

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4
Q

what does the immediately dangerous consequences of AKI depend on?

A

causes

  • acidosis
  • electrolyte imbalance
  • intoxication toxins
  • overload
  • uraemic complications
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5
Q

what can the causes of AKI be classified into?

A

pre-renal

intrinsic (renal)

post-renal

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6
Q

what are the normal functions of the kidneys?

A
  • body fluid homeostasis
  • electrolyte homeostasis
  • acid/base homeostasis
  • regulation of vascular tone
  • excretory function
  • endocrine function
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7
Q

what are possible bad short term and intermediate/long term complications of AKI?

A

short term (in hospital): death, dialysis, length of stay

intermediate/long term (post-discharge): death, CKD, dialysis, CKD related CV elements

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8
Q

how does mortality change with the stage of AKI?

A

mortality increases with stage

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9
Q

What does renal hypoperfusion cause

A

Ischemia of renal parenchyma → prolonged ischemia → intrinsic damage → Acute tubular necrosis (ATN)

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10
Q

what are pre-renal causes of AKI?

A

Renal hypoperfusion:

cardiac failure( reduced CO)

haemorrhage (hypovolaemia)

sepsis (systemic vasodilatation)

vomiting and diarrhoea

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11
Q

How are causes of intrinsic renal causes of AKI categorised?

A

Location of pathology:

  • Vasculature
  • Glomerular
  • Tubulointerstitial
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12
Q

what are renal causes of AKI?

A
  • Vasculature
    • Large vessel disease:
      • Atherosclerosis (Renal artery stenosis)
      • Thromboembolic disease (renal artery thrombosis)
      • Dissections (aortic)
    • Small vessel disease
      • Vasculitidies
      • Thromboembolic disease
      • Microangioplastic haemolytic anaemias
      • Malignant hypertension
  • Glomerular
    • Primary (no systemic disease association)
      • glomerulonephritis
    • Secondary (systemic disease association)
  • Tubulointerstitial

radiocontrast

myeloma

rhabdomyolysis

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13
Q

what are post renal causes of AKI?

A

Caused by obstructions:

tumours

prostate disease

stones

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14
Q

how is AKI prevented?

A

by identifying patients who are at risk

(presence of risk event or risk factor)

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15
Q

what are examples of AKI risk events?

A

sepsis (pneumonia, cellulitis, UTI)

toxins (x-ray contrast, NSAIDs, gentamicin, herbal medicine)

hypotension

hypovolaemia (haemorrhage, vomiting, diarrhoea)

major surgery

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16
Q

what are some risk factors for AKI?

A
  • age > 75
  • previous AKI
  • ♡ failure
  • liver disease
  • chronic kidney disease
  • DM
  • vascular disease
  • cognitive impairment
17
Q

What is the protocol when identifying patients at risk of AKI?

A

In presence of risk event or factor consider:

  • treat sepsis if present
  • avoid toxins
  • optimise BP and volume status
  • prevent harm
18
Q

Much of AKI is avoidable, how can it be prevented?

A
  • Avoid dehydration
  • Avoid nephrotoxic drugs
  • Review clinical status in those at risk and act on findings
19
Q

What are medicine “sick day rules”?

A

When you have vomiting or diarrhoea (unless only minor) or fever, sweats and shaking you stop taking certain medications

Restart medications when well (24-48 hours after eating and drinking normally)

20
Q

When should medicines be restarted after “sick day” rules?

A
  • Restart medications when are well (after 24-48 hours of eating and drinking normally)
21
Q

What are exampls of medications that should be stopped on “sick days”?

A
  • ACE inhibitors
  • ARBs
  • NSAIDs
  • Diuretics
  • Metformin
22
Q

What investigations should be done for AKI?

A
  • Renal function
  • Urine dipstick
  • FBC
  • USS
  • Blood gas
  • Specific blood tests if indicated
23
Q

What parts of the history are important for AKI?

A
24
Q

What parts of the examination are important for AKI?

A
25
Q

What does RRT stand for?

A

Renal replacement therapy

26
Q

What are potential indications for renal replacement therapy (RRT)?

A
  • Dependant on cause to an extend of at least in the first few hours
    • Acidosis
    • Electrolyte imbalance
    • Intoxication toxins
    • Overload
    • Uraemic complications
27
Q

What electrolyte imbalance can occur in AKI that can have serious consequences?

A

Hyperkalaemia

28
Q

What are ECG changes present in hyperkalaemia?

A
  • Peaked T waves (usually earliest sign of hyperkalaemia)
  • P wave widens and flattens
  • PR segment lengthens
  • P waves eventually disappear
  • Prolonged QRS interval with bizarre QRS morphology
  • High-grade AV block with slow junctional and ventricular escape rhythms
  • Any kind of conduction block (bundle branch blocks, fascicular blocks)
  • Sinus bradycardia or slow AF
  • Development of sine wave appearance
  • Can cause cardiac arrest
    • Asystole
    • Ventricular fibrillation
    • PEA with bizarre, wide complex rhythm
29
Q

What is usually the earliest sign of hyperkalaemia?

A

Peaked T-waves

30
Q

What is the treatment of hyperkalaemia?

A
  • Stabilise (myocardium)
    • Calcium gluconate
  • Shift (K+ intracellularly)
    • Salbutamol
    • Insulin-dextrose
  • Remove
    • Diuresis
    • Dialysis
    • Anion exchange resins
31
Q

What medicine can be used to stabilise the myocardium in hyperkalaemia?

A

Calcium gluconate

32
Q

What medication can be used to shift K intracellular in hyperkalaemia?

A
  • Salbutamol
  • Insulin-dextrose
33
Q

What can be done to remove K from the body in hyperkalaemia?

A
  • Diuresis
  • Dialysis
  • Anion exchange resins
34
Q

What kind of cardiac arrest can hyperkalaemia cause?

A
  • Can cause cardiac arrest
    • Asystole
    • Ventricular fibrillation
    • PEA with bizarre, wide complex rhythm
35
Q

How does the T wave change in hyperkalaemia?

A

Peaked T waves

36
Q

How does the P wave change in hyperkalaemia?

A

Widens and flattens at first

Eventually completely disapears

37
Q

How does the PR segment change in hyperkalaemia?

A

Lengthens

38
Q

How does the QRS complex change in hyperkalaemia?

A

8. Urology (Medical Knowledge) (17 decks)

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