Acute Liver disease and FHF Flashcards

1
Q

can people with cirrhosis have normal LFTs

A

yes, 70% do

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2
Q

what is acute liver disease

A

any insult to the liver causing damage with a duration of less than 6 months

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3
Q

what does acute liver failure

A

when damage causes encephalopathy and prolonged coagulation

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4
Q

what is wilsons disease

A

a rare autosomal recessive inherited disorder of copper metabolism that is characterized by excessive deposition of copper in the liver, brain, and other tissues- can be characterised as an ALD

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5
Q

what are the clinical features of ALD

A
none,
jaundice,
lethargy,
nausea,
anorexia,
pain,
itch,
arthralgia,
abnormal LFTs
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6
Q

what can cause ALD

A
viral; hep A-E, CMV, EBV and toxoplasmosis,
drugs,
shock liver (hypotension),
cholangitis,
alcohol,
malignancy,
paracetamol,

rare:
bidd chiari,
AFLP (acute fatty liver in pregnancy),
cholestasis in pregnancy

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7
Q

how does cholestasis typically present

A

RUQ pain, jaundice

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8
Q

what is seen in alcohol ALD and why

A

high bilirubin due to pro inflammatory cytokine response

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9
Q

what factors can influence ALD

A

direct toxicity (of alcohol, virus, drugs, hyperfusion),
nutrition (NASH, malnutrition),
immunological (PBC, AIH),
genetic; (wilsons haemochromatosis)

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10
Q

what investigations should be done in ALD

A

history; - include sexual health (hep E), Symptoms, durations, drugs (OTC, herbal and food suppliments), Possible toxins, alcohol, food from ‘health food shop’ or corner shop (illegal/legal highs), unusual hobbies (free water swimming)

LFTs, PT time,
ultrasound,
virology, 
chronic liver disease investigations,
rare; liver biospy
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11
Q

what is the treatment foe ALD

A

rest 3-6 months, fluids, no alcohol, increase calories (fatty foods poorly tolerated)
to treat itch: sodium bicarbonate bath, cholestyramine or uresodeoxycholic acid

observation for FHF

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12
Q

what are the metabolic considerations for ALD

A

patients in hypermetabolic state- increased requirements
35-40 kcal/kg/day 1.2-1.5 g protein/kg/day

Higher rate of complications in malnourished patients

Oral suppliments/ NG

monitor K, PO and Mg
Hypoglycaemia a concern

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13
Q

what drugs cause ALD

A

can be any:
common inc
Antibiotics; coamoxiclav, flucloxacillin,
NSAIDs
Euphemisms ‘fat burners’ ‘protein powders’
Imported/ no label drugs
Nurofen/ night nurse: contains paracetamol

rare; statins

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14
Q

how does paracetamol cause ALD

A

when metabolises produces NAPQI which is toxic, produces free radical production

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15
Q

how is NAPQI combated

A

with NAC, replenishes glutathione supply which consumes free radicals

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16
Q

what gene is associated with paracetamol damage and ALD

A

P450

17
Q

what is FHF

A

fulminant hepatic failure; rapid development of jaundice and encephalopathy in a patient with a previously healthy liver

18
Q

what can cause FHF

A
Paracetamol (overdose)
Fulminal viral (hep E- in elderly or pregnant, HBV, non hep A-E)
Drugs
rare;
AFLP
Mushrooms 
Malignancy 
Wilsons 
Bidd chiari
HAV
19
Q

what are the clinical signs and complications of FHF

A

Encephalopathy

Hypoglycaemia- used all glycogen in liver, cant regulate

Coagulatory failure

Circulatory failure- hyperdynamic circulatory out put

Renal failure- complicated by circulatory collapse

20
Q

how is FHF treated

A

Supportive
Inotropes and fluids
Management of raised ICP (intracranial pressure)
Transplant (75% survival, lifelong immunosuppressant, risk of post transplant malignancy)

21
Q

what does the kings college for liver transplant consider

A

split into paracetamol and non paracetamol

Considers: pH after resus, PT time, lactate, wilsons or bidd chiari, encephalopathy