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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
