Acute Liver disease and FHF Flashcards
can people with cirrhosis have normal LFTs
yes, 70% do
what is acute liver disease
any insult to the liver causing damage with a duration of less than 6 months
what does acute liver failure
when damage causes encephalopathy and prolonged coagulation
what is wilsons disease
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
what are the clinical features of ALD
none, jaundice, lethargy, nausea, anorexia, pain, itch, arthralgia, abnormal LFTs
what can cause ALD
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
how does cholestasis typically present
RUQ pain, jaundice
what is seen in alcohol ALD and why
high bilirubin due to pro inflammatory cytokine response
what factors can influence ALD
direct toxicity (of alcohol, virus, drugs, hyperfusion),
nutrition (NASH, malnutrition),
immunological (PBC, AIH),
genetic; (wilsons haemochromatosis)
what investigations should be done in ALD
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
what is the treatment foe ALD
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
what are the metabolic considerations for ALD
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
what drugs cause ALD
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
how does paracetamol cause ALD
when metabolises produces NAPQI which is toxic, produces free radical production
how is NAPQI combated
with NAC, replenishes glutathione supply which consumes free radicals
what gene is associated with paracetamol damage and ALD
P450
what is FHF
fulminant hepatic failure; rapid development of jaundice and encephalopathy in a patient with a previously healthy liver
what can cause FHF
Paracetamol (overdose) Fulminal viral (hep E- in elderly or pregnant, HBV, non hep A-E) Drugs
rare; AFLP Mushrooms Malignancy Wilsons Bidd chiari HAV
what are the clinical signs and complications of FHF
Encephalopathy
Hypoglycaemia- used all glycogen in liver, cant regulate
Coagulatory failure
Circulatory failure- hyperdynamic circulatory out put
Renal failure- complicated by circulatory collapse
how is FHF treated
Supportive
Inotropes and fluids
Management of raised ICP (intracranial pressure)
Transplant (75% survival, lifelong immunosuppressant, risk of post transplant malignancy)
what does the kings college for liver transplant consider
split into paracetamol and non paracetamol
Considers: pH after resus, PT time, lactate, wilsons or bidd chiari, encephalopathy