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home - Liver - Alcohol - Haematology Written by Dr Sebastian Zeki

Recognises the rising incidence of acute and chronic liver disease in
the UK related alcohol abuse and in particular the increasing alcohol
consumption in adole nts young adults women and growth in

Recognises alcoholic hepatitis and understands the prognostic
scores determined by Maddrey’s discriminant function the Glasgow
alcoholic hepatitis score and their role in identifying which patients
may benefit from corticosteroids Can treat alcohol withdrawal

Aware of appropriate use of benzodiazepines in alcohol withdrawal
and can recognise the early signs of delirium tremens

Is able to take a relevant history and perform appropriate examination
Recognises those patients who would benefit from corticosteroids
instituting treatment and has awareness of indications for withdrawing
their use
Aware of the potential complications of alcoholic hepatitis chronic
liver disease and able to prevent or intervene where appropriate

Appreciates the role of other specialists nurse specialists
intensivists radiologists dieticians psychiatrists and addiction

Communicates effectively with patients their relatives in the context
of their disease its severity prognosis and substance abuse

Identifies the abstinent alcoholic who would benefit from

Considers all therapeutic modalities and preparedness to refer to
specialist centre where diagnosis remains in doubt or appropriate
management cannot be performed as per national guidelines


Written by Dr Sebastian Zeki Rebound thrombocytosisPatients can get a rebound platelet count after abstinence and a normal diet.No intervention is needed and it usually resolves in 7-10 days. Mechanism of Alcohol ToxicityAcetaldehyde from EtOH metabolism can produce RBC protein-acetaldehyde adducts, which may generate immune responses against these modi-fied proteins. Macrocytosis90 % of alcoholics have a macrocytosis (MCV 100-110) in absence of folate or B12 deficiency or liver disease- the cause is unknown.Macrocytosis often resolves in 2-4 months.Be suspicious for other causes if the MCV >110. Haemolysis —This is usually a production defect.Haemolysis can co-exist due to splenic sequestration (enlarged spleen).Spur cell haemolysis can occur in severe alcoholic cirrhosis. Causes of decreased red cell production:Direct toxic effect of alcohol.Iron deficiency due to GI bleeding.Nutritional folate deficiency.Anemia of chronic disease. Anaemia 25% have ringed sideroblasts in erythroid precursors.Very heavy alcohol intake is associated with vacuoles in proerythroblasts and granu-locytic precursors.Alcoholics can also get hypoplastic or aplastic anaemia with pancytopoe-nia.Abstinence results in reversal of the hypoplasia. LeukopoeniaNeutropenia occurs in 8%.Neutrophil dysfunction can occurs.Splenomegaly contributes to the leukopoenia. Thrombocytopoenia80 % of hospitalized alcoholics have a platelet count <150,000/µL due to the direct toxic effect on megakaryocytes and splenomegaly.In some patients, platelet function may also be abnormal. Alcohol abuse and hematologic disorders

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