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home - Liver - Alcohol - Metabolism Written by Dr Sebastian Zeki
Knowledge


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
obesity

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

Skills
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

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

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
transplantation

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

Metabolism

Polymorphisms of ADH do not predict the susceptibility to alcoholic liver disease, but could explain variations in blood alcohol levels among individuals ingesting the same amount of ethanol. ALCOHOL METABOLISM3 Routes Induction of microsomal enzyme oxidation system (MEOS)= intracellular membrane compartments, such as smooth endoplasmic reticulum) due to spillover from the ADH pathway. Polymorphisms of P4502E1 may correlate with differences in susceptibility to alcoholic liver disease.Both ADH and P4502E1 are more concentrated in the centrizonal region of the hepatic lobule, the area in which alcoholic liver injury is most prominent. Gastric metabolism of ethanol —Stomach can metabolize alcohol via ADH.More gastric ADH in men than womenStomach pathology can reduce gastric ADH (gastritis etc) Occurs in the mitochondriaALDH has multiple isoforms with differing activities.The flushing reaction in Asians is due to relative deficiency of the ALDH2 isozyme, which results in the accumulation of acetaldehyde.Disulfiram inhibits this and, after alcohol ingestion, results in plasma acetaldehyde levels 5 to 10 times that seen in the absence of disulfiram.The accumulation of acetaldehyde leads to facial flushing, tachycardia, hypotension, dyspnea, nausea, vomiting, headache, blurred vision, vertigo, and anxiety within 15 to 30 minutes of alcohol ingestion.The syndrome lasts for several hours and the inhibitory activity lasts for several days. Acetaldehyde Pathway Microsomal enzyme oxidation system (MEOS) Catalase Enzymes Minor pathways of ethanol metabolism (ie microscomal) Diversion of ethanol to minor pathways of oxidation in heavy drinkers may be a critical determinant of liver injury, because these pathways are more likely to generate injurious reactive oxygen intermediates than ADH. Oxygen radicals Hydroxyethyl Radicals Ethanol Cytochrome P4502E1 Acetaldehyde NADPH NADP+ Alcohol Alcohol dehydrogenase Acetaldehyde Acetaldehyde dehydrogenase Acetate Acetyl CoA Citric Acid Cycle Cross link complexes Imino derivatives Thial intermediate Cross linking Detoxific-tion Carcino-genicity Written by Dr Sebastian Zeki

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