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					Nem’s Notes…                                                                       Phase 2 Year 2


GASTROENTEROLOGY 11 (page 1 of 4)
Liver 3

Acute             Acute hepatitis can be caused by a number of things including:
Hepatitis                 (a) Viral (Hep A, B, C, E, (D), EBV, CMV, Yellow Fever)
                          (b) Non-viral (toxoplasma gondii, leptospira icterohaemorrhagiae)
                          (c) Drugs (paracetamol, halothane)
                          (d) Alcohol
                          (e) Poison (mushroom, aflatoxin, carbon tetrachloride)
                          (f) Other (pregnancy, circulatory insufficiency)


Viral Hepatitis

                             HAV              HBV             HCV              HDV             HEV
              Group       Enterovirus       Hepadna         Flavivirus     Incomplete       Calcivirus
  Virus     Genetics         RNA              DNA             RNA              RNA             RNA
               Size         27nm              42nm          30-38nm           35nm            27nm
             Faecal                                                                         
              Blood       Uncommon                                                           
 Spread       Saliva                                                         ?               ?
             Sexual       Uncommon                        Uncommon                            ?
            Vertical                                     Uncommon                            
      Incubation          2-4 weeks        4-20 weeks      2-26 weeks       6-9 weeks       3-8 weeks
  Chronic Infection           No             5-10%             50%                             



Hepatitis A       Most common viral hepatitis worldwide. Poor sanitation and hygiene cause epidemics.

                  Clinical Features: (a) Fever
                                     (b) Lethargy
                                     (c) Jaundice

                  Diagnosis:         (a) IgM anti-HAV
                                     (b) Alkaline phosphatase increased
                                     (c) Alanine transferase increased
                                     (d) Bilirubin increased

                  Prevention:        (a) Immunisation by inactivated vaccine

                  Treatment:         (a) No specific treatment


Hepatitis B       2000 million people affected with 300 million carriers worldwide. UK and USA have
                  lower prevalence of carriers than Africa, Far and Middle East. Risk factors include
                  multiple sexual partners and IV drug use.

                  Clinical Features: (a) Same as HAV
                                     (b) Chronic (asymptomatic) hepatitis
                                     (c) Cirrhosis (also ascites, variceal haemorrhage, encephalopathy)

                  Natural History:   (a) 30% die of cirrhosis
                                     (b) Hepatocellular carcinoma
                                     (c) HBe antigen negative virus may emerge

                  Diagnosis:         (a) Markers for HBV
                                     (b) ALT increased

                  Prevention:        (a) Passive and active immunisation

                  Treatment:         (a) No specific treatment




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 1 of 4
Nem’s Notes…                                                                       Phase 2 Year 2


GASTROENTEROLOGY 11 (page 2 of 4)
Liver 3

Hepatitis C   Rates of infection in healthy blood donors is 0.02% in Europe, 6% in Africa, 19% in
              Egypt. Transfusion before the screening of donor’s blood is a major risk factor.

              Clinical Features: (a) Mild flu-like symptoms
                                 (b) Jaundice
                                 (c) May present with chronic liver disease years after infection
                                 (d) Extrahepatic manifestations (arthritis, aplastic anaemia)

              Natural History:   (a) Progresses over 15-50 years to cirrhosis in 20-30% of cases
                                 (b) 2-3% die of hepatocellular carcinoma per year

              Diagnosis:         (a) Anti-HCV
                                 (b) HCV-RNA positive

              Prevention:        None

              Treatment:         (a) Interferon-α plus ribavarin for 6-12 months



Hepatitis D   Can only be acquired by patients with pre-existing HBV infection

              Clinical Features: (a) Severe hepatitis if HBV and HDV infect together
                                 (b) Progressive disease if HDV superimposed on HBV

              Diagnosis:         (a) IgM anti-HDV
                                 (b) IgM anti-HBc antigen

              Prevention:        (a) None

              Treatment:         (a) None



Hepatitis E   Epidemics seen in developing countries

              Clinical Features: (a) Mild hepatitis (more severe in pregnancy)
                                 (b) Frequently cholestatic
                                 (c) Mortality from fulminant hepatic failure

              Diagnosis:         (a) ELISA for IgG and IgM anti-HEV (unreliable)

              Prevention:        (a) Good sanitation and hygiene

              Treatment:         (a) Conservative



Hepatitis G   Hepatitis G is a parenterally transmitted flavivirus (also GBV-C). It replicates to a
              minor degree in the liver, but the main site is unknown. It rarely causes mild hepatitis
              but usually causes chronic disease. No treatment is needed.




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 2 of 4
Nem’s Notes…                                                                       Phase 2 Year 2


GASTROENTEROLOGY 11 (page 3 of 4)
Liver 3

Alcoholic Liver Epidemiology     (a) Causes 12% of male and 3% of female deaths.
Disease                          (b) Causes 27% of medical and 20% of psychiatric admissions.
                                 (c) There is strong evidence for a genetic component to the disease
                                 and its aetiology.

               Pathology         (a) Fatty change in liver cells (especially zone 3).
                                 (b) Acute hepatitis (with Mallory’s hyalin)
                                 (c) Architectural damage (eg portal fibrosis, cirrhosis)

               Clinical Features (a) Can have few or mild symptoms (diagnosed histologically)
                                 (b) Jaundice
                                 (c) Ascites
                                 (d) Abdominal Pain
                                 (e) Fever
                                 (f) Hepatomegaly

               Diagnosis         (a) Elevated MCV
                                 (b) High serum gamma-glutamyl transferase
                                 (c) Fat in liver histology
                                 (d) High serum bilirubin
                                 (e) High serum AST and ALT
                                 (f) High ALP
                                 (g) Increased PT

               Treatment         (a) Encourage patient to stop drinking
                                 (b) Diazepam or chlormethiazole for delirium tremens
                                 (c) Bed rest
                                 (d) Protein and vitamin supplements



Cirrhosis      Liver cirrhosis is a condition in which the liver responds to injury or death of some of
               its cells by producing interlacing strands of fibrous tissue between which are nodules
               of regenerating cells.

               Causes            (a) Hepatitis B, C or D
                                 (b) Alcohol
                                 (c) Biliary cirrhosis
                                 (d) Primary sclerosing cholangitis
                                 (e) Haemochromatosis
                                 (f) Wilson’s Disease
                                 (g) α-antitrypsin deficiency

               Complications     (a) Portal hypertension
                                 (b) GI haemorrhage
                                 (c) Ascites
                                 (d) Encephalopathy
                                 (e) Renal failure
                                 (f) Hepatocellular carcinoma

               Investigation     (a) Liver function tests
                                 (b) Liver biochemistry
                                 (c) Serum electrolytes
                                 (d) Imaging
                                 (e) Liver biopsy (if PT is not too long)

               Management        (a) US scan and α-fetoprotein every 6 months to check for HCC




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 3 of 4
Nem’s Notes…                                                                    Phase 2 Year 2


GASTROENTEROLOGY 11 (page 4 of 4)
Liver 3

Chronic Biliary Causes Common (a) Gallstones
Disease                       (b) Infections
                              (c) Strictures (benign or malignant)
                       Rare   (a) Primary biliary cirrhosis
                              (b) Sclerosing cholangitis
                              (c) Drugs
                              (d) Congenital (biliary atresia, fibropolycystic disease)

                 Clincal Features (a) Abdominal Pain
                                  (b) Jaundice
                                  (c) Dark urine, pale stools
                                  (d) Itching
                                  (e) Nausea and vomiting
                                  (f) Fevers and rigors
                                  (g) Hepatomegaly
                                  (h) Weight loss
                                  (i) Skin pigmentation
                                  (j) Xanthomas, xanthalasmas

                 Biochemistry      (a) Increased bilirubin
                                   (b) Increased alk phosp
                                   (c) Increased transaminases
                                   (d) Increased cholesterol
                                   (e) Increased prothrombin time
                                   (f) Normal albumin

                 Imaging           (a) Abdo X-Ray
                                   (b) USS
                                   (c) CT
                                   (d) MRI
                                   (e) ERCP
                                   (f) Percutaneous transhepatic cholangiography (PTC)




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 4 of 4