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Jaundice and Viral Hepatitis CAITLIN O’NEILL AND ROBYN SMITHJaundice elevated serum bilirubin concentration.clera, and mucus membrane due to Most visible manifestation of liver or biliary disease Causes of Jaundice •3 categories • Prehepatic • Hepatocellular • ObstructivePre-hepatic Haemolysis ◦ Spherocytosis ◦ Pernicious anaemia Congenital enzyme defect ◦ Gilbert’s syndrome Hepatocellular •Acute hepatitis •Chronic hepatitis •Autoimmune hepatitis •Alcoholic hepatitis •End-stage liver disease Obstructive •Gallstones •Benign strictures •Carcinoma pancreas •Cholangiocarcinoma •Pancreatitis •Primary biliary cirrhosis •Pregnancy Liver Function Tests- the basics ALT More liver specific ALP More gallbladder specific Gamma GT Alcoholic liver disease Define terms Hepatitis 🡪 inflammation of the liver Acute viral hepatitis 🡪 symptoms last less than 6 months Fulminant hepatitis 🡪 severe impairment of hepatic functions or severe necrosis of hepatocytes in the absence of pre-existing liver disease Chronic hepatitis 🡪 inflammation of the liver for at least 6 months Cirrhosis 🡪 replacement of liver tissue to scar tissue. This leads to loss of liver functionViral hepatitis heterogenous group of hepatotropic viruses of the liver by any one of the The most common caused are Hepatitis A-E Other causes include Herpes simplex, Cytomegalovirus, and Epstein-Barr virusPathogenesis Immune mediated Viral antigens are recognised by cytotoxic T-cells 🡪 apoptosis Release of chemokines 🡪 antigen non-specific inflammatory cells exacerbate the responsePresentation There is a spectrum depending on age and immune status ◦ Asymptomatic ◦ Mild and non-specific ◦ Fulminant (massive necrosis of hepatocytes and acute liver failure) Signs and symptoms •Abdominal pain (RUQ) •Fatigue •Pruritis •Muscle and joint aches •Nausea and vomiting •Jaundice •Fever •Hepatomegaly •Dark urine/pale stools 42 year old British male Worked in Singapore last year, now returned to the UK Presents with: lethargy Case Scenario On examination- normal Blood tests are taken Results HbA1c = 45 Normal ranges ALT = 60 ALT 3-40 iu/L HbA1c <48 4 weeks later ALT = 64Past Medical History and Social History No significant PMH No injected drugs Drinks 10 units a week, does not binge drink No history of multiple partners Shaved with a traditional razer in Singapore (reused blades) Mode of transmission •Blood-borne/ sexual • HepB • HepC •Faecal-oral • HepA • HepEBlood results HCV RNA positive Active Hep C infection HCV genotype 2 Hepatitis B e antigen (HBeAg) not detected Hepatitis B virus-DNA (HBV DNA) present at low levels IgG antibodyto hepatitis B core antigen (anti-HBc) detected Anti HBe detected Anti HBc detected Anti HBs negative Understanding Hep B serology •HBV envelope antigen 🡪 active viral replication •HBV surface antigen 🡪 active or chronic infection •HBV surface antibody 🡪 shows previous infection or vaccination •HBV core antigen • IgM 🡪 acute infection • IgG 🡪 chronicity or post infection • Anti-HBc 🡪 caughtBack to his results Hepatitis B e antigen (HBeAg) not detected No active replication Hepatitis B virus-DNA (HBV DNA) present at low levels IgG antibodyto hepatitis B core antigen (anti-HBc) detected Acute infection Anti HBe detected Anti HBc detected Previous or current infection Anti HBs negative No vaccination or previous infection. Negative in chronic disease Diagnosis 🡪 Active hepatitis C infection and Chronic inactive Hepatitis B infection Hep C •RNA virus •Spread by blood and body fluids •No vaccine •Curable with direct acting antiviral medications •1 in 4 make a full recovery •3 in 4 becomes chronic •Complications • Liver cirrhosis • Hepatocellular carcinoma Hep B •DNA virus •Blood or bodily fluids • Sexual intercourse • Sharing needles • Sharing toothbrushes • Contact between minor cuts and abrasions •Vertical transmission •Vaccination available Management •Refer for specialist management •Anti-viral treatment with direct acting antivirals – tailored to specific viral genotype •Testing for complications- FibroScan and ultrasound scan •Notify Public Health Cirrhosis •Result of chronic inflammation and damage to the liver cells. •When they are damaged they are replaced with scar tissue –Fibrosis •Fibrosis affects the structure and blood flow to the liver •Portal hypertension •Jaundice •Hepatomegaly (or shrinking of the liver) •Splenomegaly Signs and •Spider naevi symptoms •Palmar erythema •Gynaecomastia •Bruising •Ascites •Caput medusae •Flapping tremor Investigations •Bloods •Ultrasound, CT, FibroScan, MRI •Liver biopsy – Gold standard Management • Supportive care and complication management • Ascites • Varices • Portal hypertension • Nutrition • HCC screening • Removal of etiological factor • Liver transplantationMCQ 1 A 25-year-old pregnant woman attends the emergency department with fever and abdominal pain. She returned from a holiday to Japan 2 weeks ago where she had a short-lived period of food poisoning after eating undercooked pork belly. On examination, she is jaundiced with mild bruising over her extremities. Her abdomen is distended with tender hepatomegaly. Her preliminary laboratory results show deranged liver function tests. 1. Campylobacter jejuni gastroenteritis 2. Escherichia coli gastroenteritis 3. Hepatitis A 4. Hepatitis B 5. Hepatitis E MCQ 2 A 34-year-old male returns to your clinic for review of his blood tests. In particular, his hepatitis screen returns as follows: 1.Acute Hep B infection 2.Susceptible to Hep B infection 3.Immune due to Hep B vaccination 4.Chronically infected 5.Immune due to natural infectionMCQ 3Any questions? (ZERO TO FINALS)URCES- UNDERSTANDING HEPATITIS B SEROLOGY RESULTS HTTPS://WWW.YOUTUBE.COM/WATCH?V=H_9EBVPADNE