3.Hepatic Amoebiasis Year 4 Internal Medicine Notes
Year 4 Internal Medicine study notes: 3.Hepatic Amoebiasis. Full notes on OmpathStudy. Free notes for medical students worldwide.
3.Hepatic Amoebiasis Year 4 · Internal Medicine Collection: 4TH YEAR ALL NOTES / IMED / IMED 4.1 / ALEX -- Slide 1 Hepatic Amoebiasis Dr Alex Mogere. Consultant physician Slide 2 Hepatic Amoebiasis Amoebiasis affects 40-50 million people annually. Majority of infections occur in developing countries \n“poor socioeconomic and sanitation level” High rates of infection occur in India, Africa, Central and South America.\n\nLi et al., 2003 Slide 3 Hepatic Amoebiasis In developed countries amoebiasis is mainly seen in: Migrants from Travelers to Institutionalized patients Active homosexuals Hake et al., 2003 Slide 4 Hepatic amoebiasis cont. In majority of cases,the hepatic complication appears after about 1-3 mths of disappearance of the dysentery attack Generally confined to the postero-superior surface of the right lobe Slide 5 Intestinal amoeba can be one of 3 species Entamoeba histolytica The cause of all symptomatic disease\n\nEntamoeba dispar Entamoeba moshkovski\n\nPetri et al., 2006 Slide 6 E. histolytica exists in 2 forms: A cyst stage: the infective form A trophozoite: causes invasive disease Infection occurs following ingestion of amoebic cysts Via contaminated food or water Venereal transmission through foecal oral contact Cysts can remain viable in the environment for weeks → months\n\nPetri et al., 2006 A single cyst is sufficient to cause disease Slide 7 Other amoebas E.coli E.hartmanni E.polecki Iodamoeba butschlii Endolimax nana Other than E.histolytica, E.polecki, Dientamoeba fragilis, I.butschlii the others are commensal Slide 8 Pathogenesis Cysts pass through the stomach to the small intestine. In the intestine, they excyst to trophozoites The parasite can invade and penetrate the mucous barrier Trophozoites adhere to cells via a specific LECTIN (galactose / N-acetyl galactosamine lectin)\n\nPetri et al., 2006 Slide 9 Pathogenesis The parasite is able to kill cells; epithelial or inflammatory; through: Secretion of proteinases Lysis via contact Killing by apoptosis Formation of ameobopores Small peptides Form pores in lipid bilayers Haque et al., 2003 Cytolysis of infected cells Slide 10 Risk Factors 90% of E. histolytica infections are asymptomatic Extremes of age Pregnancy Corticosteroids and other immunosuppressive drugs Malignancy Malnutrition Alcoholism\n\nPetri et al., 2006 Are the main risk factors Slide 11 Hepatic Amoebiasis The most common extraintestinal manifestation of amoebiasis About 7-10 times more common in adult males despite: Equal gender distribution in infected children Equal sex distribution in colonic amoebic disease\n\nAucott et al., 1993 Stanely et al., 2003 Hormonal effect\n“postmenopausal women have increased rates” \nPossible role of alcohol Slide 12 Hepatic Amoebiasis Pathogenesis Amoebae establish hepatic infection by ascending the portal venous system The amoebae block small portal radicles and release their proteases Acute focal inflammatory lesions are produced Liver abscess results from tissue destruction by contact depending on cytolytic activity of the amoebae Maddrey, 1996 Petri et al., 2006 Slide 13 Clinical Manifestations I. Acute Presentation: One or two weeks of fever Right upper quadrant pain Jaundice is uncommon Concurrent diarrhea in less that 1/3 of patients History of dysentery in the previous few months is not infrequent\n\nKnobloch et al., 1983 Stanely et al., 2003 Amoebic abscess can occur\nafter exposure of only 4 days Slide 14 Cont.clinical manifestations Pain sometimes referred to the right acromial region Dry cough may be associated Occassionally the pain is referred to lower abdomen or the RIF Patient can be emaciated Slide 15 Clinical Manifestations II. Chronic Presentation: Very Occasional Months of fever Weight loss Abdominal pain Hepatomegaly Anaemia\n\nStanely et al., 2003 Important in the differential diagnosis\nof other liver pathologies Slide 16 o/e Tender liver Movt of the right side of chest is diminished Left lobe may undergo a compensatory hypertrophy in a very big abscess Slide 17 Diagnosis Peripheral blood shows leucocytosis without eosinophilia Liver function testing Elevated alkaline phosphatase Transaminases may be raised Foecal microscopy shows amoeba in only 18% of cases Culture for amoeba is positive in 75% of cases Irusen et al., 1992 Slide 18 Imaging Radiological imaging \n“Chest and Abdomen” Ultrasound Computed Tomography Magnetic resonance\n\nKatzenstein et al., 1982 At least one of these studies should be performed in all suspected cases Slide 19 Imaging Chest radiographs may show raised \nimmobile right diaphragm Other imaging modalities show A single abscess in the right or left lobe Multiple lesions can be present\n\nThe diagnosis can usually be presumed while awaiting other test results Katzenstein et al., 1982 None of these modalities can differentiate\namong\namoebic abscess, pyogenic abscess, malignant abscess Slide 20 Serologic Tests Serum antibodies Detectable in 92-97% of cases Negative in the first 7 days