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COMMON HEPATIC DISORDERS: points for health education DR. Ahmed Zeid HPBU. Alexandria university.

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Presentation on theme: "COMMON HEPATIC DISORDERS: points for health education DR. Ahmed Zeid HPBU. Alexandria university."— Presentation transcript:

1 COMMON HEPATIC DISORDERS: points for health education DR. Ahmed Zeid HPBU. Alexandria university

2 Acute and chronic hepatitis

3 DEFINITION Acute hepatitis: Acute inflammation of the liver with significant elevation of serum transaminases usually 10 folds than normal or more with preservation of synthetic hepatic functions. Chronic hepatitis: P ersistent inflammation of the liver lasting for 6 months or more after the initial exposure and or initial detection of liver disease.

4 Viral infection is the primary cause of acute and chronic hepatitis. Hepatitis (A and E) are self limited but sometimes cause severe hepatitis and liver failure but not chronic hepatitis. Hepatitis (B and C) represent the major agents currently known to cause chronic hepatitis which if not properly treated, it might be complicated by cirrhosis, portal hypertension and hepatocellular carcinoma.

5 Treatment of acute hepatitis: 1.Bed rest. 2.Dietary advise. 3.Supportive treatment. 4.Suspect and early detect complications. 5.Treatment of the cause if possible.

6 Egypt is a hyperendemic area of HCV

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8 Treatment of HCV: Who to treat? 1.chronic hepatitis. 2.acute hepatitis if no viral clearance within 2-3 m. 3.Early and compensated cirrhosis. What is the course of treatment? pegylated interferon alpha ( subcutaneous injection once/w) + ribavirin ( oral 800-1200 mg/d)

9 What is the duration of treatment ? ( From 6-12 m according to the genotype). a) Genotypes 2 and 3 usually need 6 m treatment b) Genotypes 1 and 4 (common in Egypt) usually need 12 m treatment. What are the success rate, side effects and contraindications of treatment ? ----------------------------------- How do you follow up your patients during and after treatment ? -----------------------------------

10 Treatment of indicated HBV infection: Whether compensated or decompensated by suitable drugs which may be sometimes life long treatment. Prophylaxis from HBV infection by administration of HBV vaccine for all persons susceptible for infection (health work staff, family members of infected patient) and booster doses of vaccine for previously vaccinated subjects.

11 Points for health education about acute and chronic hepatitis: How to prevent hepatitis A virus ? contacts of patient,...food handlers,..hygiene... How to prevent new cases of hepatitis B and C viruses ? contacts of patient,..health care providers ( doctors, dentists, nurses, workers),..barbers

12 Liver Cirrhosis

13 Cirrhosis is defined histologically as a diffuse hepatic process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules.

14 Cirrhosis

15 Cirrhosis represents the final common histologic pathway for a wide variety of chronic liver diseases.

16 Etiology of cirrhosis : – Viral hepatitis ( B,C,D ). – Autoimmune chronic hepatitis. – Alcohol. – Metabolic ( Non-alcoholic steatohepatitis, hemochromatosis, Wilson's disease, alpha1- antitrypsin deficiency, type IV glycogenosis ). – Cholestatic ( Primary biliary cirrhosis, Primary sclerosing cholangitis). – Hepatic venous outflow obstruction ( veno-occlusive disease, Budd-Chiari syndrome ). – Drug-induced ( methotrexate, amiodarone ) – Cryptogenic.

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20 All cirrhotic patients should be screened regularly for early development of HCC.

21 Points for health education about cirrhosis: Screening for early detection and prevention of serious complications. Any patient with GIT bleeding should be hospitalized even if mild attack of bleeding till proper diagnosis and management. Early cases of HCC can be cured and late cases might be palliated.

22 HPATIC ENCEPHALOPATHY

23 A wide spectrum of neuropsychiatric abnormalities (potentially reversible) occurring in patients with significant liver dysfunction and/or porto- systemic shunts due to an as yet uncertain mechanism.

24 Sheila Sherlock - Concept of portal- systemic encephalopathy Eine kurze Geschichte der Ammoniak-Hypothese... S.Sherlock, Lancet 1954 The mechanism of portal-systemic encephalopathy Hypovolemia Hyponatremia Infection Drugs Surgery Toxic substances Neurochemical changes

25 West Haven criteria Grade0: Lack of clinically detectable changes Grade1: Trivial lack of awareness Shortened attention span Impaired performance of addition Euphoria or anxiety Grade2: Lethargy or apathy Minimum disorientation for time or place Subtle personality change Inappropriate behaviour Impaired performance of substraction Grade3: Somnolence to semistupor, Confusion, Gross disorientation, bizarre behaviour Grade4: Coma Conn et al MHE

26 “MHE….....occurs in epidemic proportion of cirrhotic patients estimated as high as (30-84%) of the population tested“. World J Gastroenterology 2008

27 MHE may have an adverse impact on the ability to perform daily activities. It is important for subjects whose occupations demand attentional and motor abilities such as driving a motor vehicle.

28 60-85% of cirrhotic patients are unfit to drive Dig Dis Sci 1986

29 MHE has a profound negative impact on the ability to drive a car and may be a significant factor behind motor vehicle accidents World J Gastroenterology 2008

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31 Management of HE Identify and correct the precipitating factor. 1.Hypovolemia. 2.Hyponatremia. 3.Sepsis. Decrease ammonia formation and increase ammonia clearance.

32 Points for health education about HE: Early recognition of mild manifestations of HE. Avoid possible precipitating factors of HE. Home treatment till searching for a specialist. Avoid risky jobs and car driving particularly for patients with MHE.

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