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Renal > AKI > Flashcards

AKI Flashcards

1
Q

What is AKI

A

Acute kidney injury- defined as an acute drop in renal function characterised by a rise in serum creatinine levels

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2
Q

NICE CRITERIA FOR AKI

A

-Rise in creatinine of ≥ 25 micromol/L in 48 hours
-Rise in creatinine of ≥ 50% in 7 days
-Urine output of < 0.5ml/kg/hour for > 6 hours

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3
Q

List some of the functions of the kidneys

A
  • waste excretion
  • acid base balance
  • blood pressure ( renin)
  • water hormone/ homeostasis
  • Vit D
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4
Q

Risk factors for AKI

A

hronic kidney disease
Heart failure
Diabetes
Liver disease
Older age (above 65 years)
Cognitive impairment
Nephrotoxic medications such as NSAIDS and ACE inhibitors
Hypovolemia
Nephrotoxic drugs
Trauma

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5
Q

What medications are deemed nephrotoxic

A

Ibuprofen- NSAID
Naproxen
Aminiglycosides
ACE inhibitors

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6
Q

Aetiology of AKI

A

Split into pre renal, renal and post renal

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7
Q

What are the pre renal causes of AKI

A
  • Dehydration
  • Hypotension
  • Heart Failure
  • Low blood volume
  • liver failure
  • renal artery stenosis
  • Drugs NSAIDs or ACEi
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8
Q

What causes pre renal issues

A

HYPOVOLAEMIA

Due to inadequate blood supply to kidneys reducing filtration of blood

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9
Q

What can cause renal AKI

A

Split into 4

Glomerular- glomerular nephritis
Tubular - acute tubular necrosis due to prolonged ischaemia
Interstitial - acute interstitial nephritis
Vascular - vasculatis

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10
Q

Renal causes may be ..?

A

Glomerulonephritis
Interstitial Nephritis
Acute tubular necrosis
Rhabdomyolysis

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11
Q

What causes post renal AKI

A

Obstruction of the outflow of urine from the kidney causing back pressure into the kidney and reduced kidney function

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12
Q

Post renal causes include …?

A
  • Kidney stones
  • Masses such as cancer in the abdomen
  • Ureter or uretral structures
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13
Q

T2DM, HTN, low urine osmolality , high urine Na+ K+ would suggest

A

Intrinsic causes

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14
Q

Investigations for AKI

A
  • Bloods
    • FBC: anaemia and very high ESR suggests myeloma or vasculitis as underlying cause
    • U&E
    • Blood gas: check for metabolic acidosis
    • Creatine kinase
  • Urinalysis: dipstick and microscopy
    • Urine osmolality and electrolytes checked
    • Leucocytesandnitritessuggest infection
    • Proteinandbloodsuggestacute nephritis(but can be positive in infection)
    • Glucosesuggests diabetes

Renal biopsy - for intrarenal cause
Renal USS - for post renal causes

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15
Q

Why would an US be used

A

to look for obstruction

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16
Q

Management of AKI

A
  • Fluid rehydration with IV fluids in pre-renal AKI
  • Stop nephrotoxic medications such as NSAIDS and antihypertensives that reduce the filtration pressure (i.e. ACE inhibitors)
  • Relieve obstruction in a post-renal AKI, for example insert a catheter for a patient in retention from an enlarged prostate
  • treat underlying cause - hypotension, infection, stones
  • if severe: Dialysis
17
Q

Complications for AKI

A
  • Hyperkalaemia
  • Fluid overload,
  • heart failure
  • pulmonary oedema
  • Metabolic acidosis
  • Uraemia (high urea) can lead to encephalopathy or pericarditis
18
Q

Key diagnostic factors for AKI

A
  • Hypotension
  • Risk Factors
  • Kidney insults
  • Reduced urine production
19
Q

What would bloods show for aki

A

Anaemia , high esr
High creatinine kinase

20
Q

What is RIFLE

A

Three levels of renal dysfunction

RISK
INJURY
FAILURE
LOSS
END STAGE- RENAL DISEASE

21
Q

3 stages of acute tubular necrosis

A

-Initiation: acute decrease in renal perfusion causing a reduced GFR
-Maintenance: GFR remains low for days or weeks
-Recovery: GFR recovers, regeneration of tubulointerstitial cells, polyuric phase may occur

22
Q

ongoing ischaemia causes …..?

A
  • pro inflammatory response with the release of cytokines , oxygen, free radicals and activation of leukocytes
  • at this point if renal perfusion is not restored the ongoing ischaemia
23
Q

why are tubular cells susceptible to ischaemia

A

they have a limited blood supply and a high metabolic demand

24
Q

Pre - renal clinical manifestations of AKI

A
  • Due to hypovolaemia
  • reduced capillary refill time
  • dry mucus membrane
  • thirst
25
Q

Intrinsic renal clinical manifestations of AKI

A

Vascular- arterial hypertension
Nephrotic syndrome- heavy proteinuria

26
Q

Presentation of AKI

A

Substance accumulation
Hyperkalaemia - arrhythmias, muscle weakness
Hyperuraemia - NV,weakness, pericarditis
Fluid overload - oedema, hypovolemic shock, decreased urine
Acid build up - metabolic acidosis

27
Q

What do we use to treat hyperkaleamia?

A

Calcium gluconate

28
Q

presentation of AKI

A

Hyperkalemia
Hyperuraemia
Fluid overload
acid build up

Renal (15 decks)

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