Anozie chukwuebuka chibueze, Hepatitis in adults.

ANOZIE CHUKWUEBUKA CHIBUEZE.ROLL NO:0630

MD5

ALCOHOLIC LIVER DISEASE

• OUTLINE IN APPROXIMATE SEQUENCE• DEFINITION• PATHOLOGICAL MECHANISM• ASSOCIATED SYMPTOMS• DIAGNOSIS• MANAGEMENT

DEFINITION

• Alcoholic liver disease is simply defined as alcohol induced liver changes, that change the structure, function and will eventually lead to deterioration of liver functions.

• Enhanced measures aimed at early detection and management of the patient should be employed.

THE LIVER

• Anatomically, the liver is divided into four un-equal lobes.

• blood flows to the liver through the hepatic artery from the Aorta and to from the Gastrointestinal tract through the portal vein.

• 80 percent of the liver cells are parenchymal cells called hepatocytes, the rest of the liver cells are non-parenchymal.

Pathologic mechanism

• ALCHOLIC LIVER DISEASE HAS THREE STAGES

• Fatty liver

• Hepatitis

• cirrhosis



• FATTY LIVER• This occurs acutely in people using alcohol. This

occurs in about 90 percent of the people using Alcohol.

• It is characterized by an acute inflammation and fatty distortion of the liver

• Most people who stop using alcohol in time experience reversal of the fatty liver.

pathologic mechanism

• Hepatic steatosis actually called microvesicular fatty change, causes displacement of the nucleus towards the periphery.

• Chronic intake of alcohol eventually leads to a macrovesicular change in the long term.

• The liver enlarges in size up to 4 to 6 kilograms and turns out to be yellow and greasy in colour.

Pathologic mecganism

• Shunting of normal substrates of catabolism towards lipid synthesis is the primary cause of hepatic steatosis.

• Impaired secretion of lipoproteins• Increased peripherial catabolism of fat.


• Alcohol induced impaired metabolism of gluthathione leads to gsh levels, sensitizing the liver to oxidative injury.

• Cyp450 enzymes induces the catabolism of alcohol and other metabolites.

• reactive oxygen species react with celluler proteins, damages membranes and alter hepatocellular function.

• alcohol also causes release of endothelins that are potent vasoconstrictors in the body.


• Single or scattered foci of cells undergoing swelling(balloning) and necrosis.

• There might be cholestasis and mild deposition of hemosiderin in hepatocytes and kupffer cells.

• Mallory bodies are hepatocye accumulation of cyto-keratin intermediate filament and other proteins visible as eosinophilic inclusions.



• Other causes of fatty liver partially related to alcohol includes:

• Hepatitis c• Iron overload• Obesity• diet

Alcoholc hepatitis

Alcoholic hepatitis is a reversible form of liver injury secondary to alcoholic steatosis.

patients tend to have jaundice, poor apetite and malaise.

This disease might lead to liver cirrhosis in the long run.

cirrhosis

• Over time cirrhosis tends to be the last stage of alcoholic liver disease.

• This usually results from excessive proliferative activity of the fatty cells of ito or stellate cells. This eventually leads to excessive collagen deposition in the liver cells.

• Cirrhosis of the liver is an irrversible process and signifies end stage alcoholic liver disease.

Associated symptoms

• Hepatic steatosis clinically presents with signs of hepatomegaly, mild elevation of serum bilirubin and alkaline phosphatase.

• Alcohol withdrawal with adequate provision of diet might be helpful.

• Alcoholic hepatitis appears acutely, usually after a bout of alcohol, between two extremes non-specific symptoms like malaise anorexia and weight loss might occur.

Associated symptoms

• Fulminant hepatic failure is evident in alcoholic hepatitis, leukocytosis.

• hepatitis can be superimposed on cirrhosis of the liver.

• Alcoholic cirrhosis causes variceal hemorrhage and extreme portal hypertension.

• Alternatively, malaise, weight loss and loss of appetite precede the jaundice, ascites and peripherial edema.

Associated symptoms

• Hypoproteinemia basically leads to the peripherial edema prominent.

• Cirrhosis in some cases might be clinically silent and detected only at autopsy

• Patients with cirrhosis also tend to have anemia

Diagnosis

• Gold standard diagnosis of cirrhosis can be made by liver biopsy which tends to show excess fibrogenic growth pattern

• Ast and alt liver function tests are good in diagnosing alcoholic hepatitis, usually ast is twice higher than alt.

• Albumin levels help to determine cirrhosis of the liver

• Summary cbc, liver function tests and biopsy.

Diagnosis

• Albumin levels help to determine, decreased activity of the liver in protein synthesis.

• Prothrombin time might also be helpful in liver disease

Five year survival rates could be up to 90 percent inabstainers who are free of jaundice, ascites or hematemesis. Cause of death includes massive bleeding, hepatic coma, hepatorenal syndrome, hepatocellular carcinoma.

Management

• Alcohol withdrawal would be efficient in this patients.

• Dietary changes might prove some beneficial effect in these patients

• The most effective in this case would be liver transplant, if there is severe damage of the liver

• Replacement with multivitamins might be very effective in this patients.

Wilson’s disease

• Wilson’s disease is simply a metabolic liver disease that leads to excessive accumulation of copper in the human body.

• Patients usually affected come down with brain and liver problems in the long run after being affected with the disease.



• 40 to 60 percent of copper in the body is absorbed in the stomach and duodenum and transported to the liver complexed with albumin.

• Free copper is to form ceruloplasmin, ceruloplasmin accounts for 90 to 95 percent of plasma copper.

• Estimated total body copper is only 50 to 150 mg


• Wilson’s disease is an autosomal recessive disorder that affects atp 7b on chromosome 13, and encodes a transmemebrane copper transporting atpase

• Defective biliary secretion leads to excessive copper accumulation in the liver, causing toxic injury through the generation of reactive oxygen species.


• Copper accumulation could go on to cause pathologic changes in:

• Brain• Cornea• Kidneys• Bones• Joints and parathyroids


• Morpholgic changes might be prominent in the affected liver of the individual.

• Fatty change may be mild to moderate, vacuolization and focal hepatocyte necrosis might be present.

• Massive liver necrosis in wilson’s disease can’t be differentiated from that caused by drugs.

Associated symptoms

Kayser fleischer rings in the eye which are green to brown pigments are suggestive of wilson’s disease.

Hepatitis which can cause jaundice, vomiting and abdominal pain might be present in these patients

Liver scarring or cirrhosis might be a late complication of the disease

Associated symptoms

• Neurologic symptoms can be prominent in patients with wilson disease,

• Signs of tremor in arms, difficulty in movement and swallowing, headache, seizures and an unsteady walk might be prominent in these patients.

• If left untreated muscular rigidity and dementia might develop in these patients.

Associated symptoms

Associated symptoms

diagnosis

• Liver function tests might aid in diagnosis• Blood ceruloplasmin levels tend to be generally low.• Brain mri can be very efficient in detecting

abnormalities.• Liver biopsy helps to examine histologic

composition of the liver.• Urine levels of copper can be significant.

management

• Liver transplant might be helpful in severe organ damage

• Diet would be helpful to prevent excessive copper accumulation

• physiotherapy helps patient’s neurologic symptoms.

• drugs like penicillamine and dimercaprol would be useful.

• References• Patient.co.uk wilson’s disease, alcoholic liver

disease• Nhs choices, journal of wilson’s disease• Robbins pathology seventh edition• Medline plus wilson’s disease, alcoholic liver diseaseMayo clinic .com journal of wilson’s disease.

Anozie chukwuebuka chibueze, Hepatitis in adults.

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