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Incidence |
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Age |
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Sex |
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Geography |
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Aetiology |
- ethanol is metabolized in the liver by two pathways ->
increased NADH/NAD ratio
-> increased hepatic fatty acid synthesis/reduced fatty acid
oxidation
--> hepatic accumulation of fatty acids -> esterified ->
glygerides
- increased NADH/NAD ratio -> impaired carbohydrate and protein
metabolism -> centrilobular necrosis of acinus
- oxidation of ethanol -> acetaldehyde -> ? factor in hepatic
cell damage
- induces microsomal metabolism -> increases effects of other
toxic metabolites (e.g. paracetamol)
- only 10-20% of those who drink heavily develop cirrosis
- genetic factor
- ? immunological factor
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Presentation |
Fatty liver
- commonly asymptomatic
- may be hepatomegaly with other symptoms of chronic liver disease
Alcoholic hepatitis
- may be well, with hepatitis and fatty change only visible on
liver biopsy
- may be unwell ± jaundice; signs of chronic liver disease;
liver biochemistry deranged, diagnosis on liver histology
- may be ill with jaundice and ascites, abdominal pain, fever
(associated with liver necrosis), jaundice, hepatomegaly ±
splenomegaly, ascites, ankle oedema, signs of chronic liver disease
Alcoholic cirrhosis
- patient usually presents with one of the complications
of cirrhosis
- usually features of alcohol dependancy, involvement of other
systems (e.g. polyneuropathy)
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Investigations |
Fatty liver
FBC - elevated MCV often indicates heavy drinking
LFTs - elevation of AST/ALT; y-GT is a sensitive test
for whether the patient is taking alcohol
USS/CT - fatty infiltration
Liver biopsy - fatty infiltration
Alcoholic hepatitis
LFTs - elevated bilirubinm, AST/ALT, ALP, PT ±
low serum albumin
- prolonged PT makes liver biopsy impossible in severe form
Alcohlic cirrhosis
- as for any cause of cirrhosis
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Macro |
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Micro |
Fatty change
- appearance varies; large alcohol intake -> steatosis ->
swiss-cheese effect on H&E
- no liver cell damage; fat disappears on stopping ethanol
- there may be perivenular fibrosis - directa action of ETOH
on stellate cells
Alcoholic hepatitis
- fatty change with infiltration of PMNs and hepatocyte necrosis
- hepatocytes may show Mallory bodies (dense cytoplasmic inclusions)
and giant mitochondria
Alcoholic cirrhosis
- classically micronodular; may be evidence of pre-existing alcoholic
hepatitis
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Staging |
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Serum markers |
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Management |
Lifestyle
- stop drinking; treat DTs with diazepam or chlormethiazole
- bedrest
- protein and vitamin supplements (but limit protein if there
is encephalopathy)
- most patients continue to drink
- if the patient is suffering from fatty liver, this may
be all the treatment required; patients may drink small amounts
again in the future, as long as they are aware of their problem
- if the patient has alcoholic hepatitis, they should
be advised to be abstinent for life
Medical
Alcoholic hepatitis
- treat encephalopathy
and ascites
- feed via NG tube or TPN
- nitrogen solutions enriched with branched-chain amino acids
may be helpful
- Vitamins B and C by injection
- corticosteroids (little benefit)
Alcoholic cirrhosis
- see management of cirrhosis
- abstinence improves prognosis
Surgical
Alcoholic cirrhosis
- orthoptic liver transplantation improves survival; patients
must show ability to abstain
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Prognosis |
- in severe alcoholic hepatitis, mortality is 50%
- if PT twice normal, with progressive encephalopathy and liver
failure, mortality is up to 90%
- in alcoholic cirrhosis, overall 5-year survival is 90%
- this falls to 60% if the patient continues to drink
- with advanced disease (jaundice, ascites, haematemesis), 5-year
survival is 35%
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Complications |
- HCC
is a complication in men; 10-15% |