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Hepatitis Jane E. Binetti DNP MSN RN Objectives • Describe the pathophysiological principles that occur wit liver disease • Compare normal structure and function • • • • • Identify clinical decision making and pharmacological management Discuss Collaborative interventions identified by the physician Describe diagnostic tests and therapeutic interventions Identify appropriate teaching/learning strategies Utilize holism to assess, plan, implement and evaluate care Liver • • • • Largest internal organ Built on a framework of lobes Right and left lobes are predominant 100,000 lobules made of hepatocytes • Each have capillaries (sinusoids) in rows of hepatocytes • Lined with Kupffer cells • Hepatic cells secrete bile to canaliculi and bile ducts Liver Vascularity • Hepatic Artery • Carries blood from the heart to the liver to provide nourishment • Portal Vein • Carries blood that has circulated through the abdominal organs and processes it to take both nutrients and toxins • Hepatic Vein • Carries blood away from the liver and connects to the inferior vena cava to go back to the heart Liver Functions • Metabolic Functions • Carbohydrate metabolism • Glycogenesis, glycogenolysis, gluconeogenesis • Protein metabolism • • • • Synthesis of non essential amino acids Synthesis of plasma proteins Formation of urea from ammonia Synthesis of clotting factors • Vitamins • A,D,E,K; B1, B2, B9 and B12, Iron Liver Functions • Bile synthesis • Production • Excretion • Storage • Mononuclear Phagocyte System • Kupffer cells • Clotting Factors • Synthesizes fibrinogen, prothrombin, vitamin K dependent clotting factors Hepatitis • General term for inflammation of the entire liver • Causes: • • • • • Viruses Drugs Chemicals Auto immune disease Metabolic abnormalities Viral Hepatitis – What Happens? • With infection, cytotoxic cytokines and killer cells lyse infected liver cells • Inflammation interferes with bile flow • Chronic hepatitis causes chronic inflammation and fibrosis that over time leads to cirrhosis • Antigen-antibody complexes activate the compliment system: • Antigen is foreign, antibody tries to neutralize it. • Rash, angioedema, arthritis, fever, malaise, • Cryoglobinemia leads to glomerulonephritis and vasculitis Viral Hepatitis • Types of viral hepatitis differ by: • Mode of transmission • Clinical manifestation • All types can cause: • Acute or chronic liver disease • We will review one at a time Hepatitis A (HAV) • What is it? • RNA virus • How is it transmitted? • Fecal-oral route • Poor food handling or contaminated drinking water • Poor hygiene, crowded living, institutions, day care • Incubation period • 2 weeks prior to symptoms found in stool; 1-2 weeks after More on HAV • Symptoms: • Range from flu-like illness to acute hepatitis with jaundice • Diagnostics: • Anti HAV IgM acute hepatitis; • Anti HAV IgG means history of infection, lifelong immunity • Treatment: • No specific treatment for acute cases, usually managed at home with rest • No drug therapies • Prognosis: • Can relapse in 2-3 months, most recover completely Nursing • What do you do? • Focus on prevention and control • HAV vaccines are dead viruses • Havrix, Vaqta, Avraxim: IM dose with booster 6-12 months later • IgG can be given after suspected exposure • Teaching • Vaccination and handwashing are important Hepatitis B Virus (HBV) • What is it? • DNA virus • “Serum” hepatitis • How is it transmitted? • Infected blood/body fluids in someone not vaccinated • Prenatal mothers, IV drug users, needles, tattoos, piercings, sex – infected semen and saliva, GI Bleeds • Risk to hemodialysis pts, living with Hep B pts, healthcare workers • HBV can live on dry surfaces up to seven days! More on HBV • Incubation period • Before and after symptoms appear • Infectious 4-6 months after start of symptoms • Carriers are infectious for life • Symptoms • Anorexia, nausea, vomiting • Abdominal pain, malaise, fever • Arthralgia, dark urine, clay stools HBV Diagnostics • Diagnostics – 3 distinct antigens • HBV surface antigen (HBsAG) • Acute and presence 6 mo or more means chronic infection • HBV core antigen (HBcAG) • Made by IgM in active stages • HBV e antigen (HBeAG) • Reflects replication and infectivity • HBV DNA • Viral replication and effectiveness of therapy for chronic HBV • Genotype testing is done for patients during drug therapy • 8 different genotypes that are great predictor of tx and prognosis HBV Antibody Testing • Indicative of past infections • • • • AntiHBs – means immunity AntiHBe AntiHBc IgG AntiHBC IgM • IgG and IgM do not appear in the person who has been vaccinated HBV Treatment • Acute and is only treated for severe hepatitis and failure • Chronic tx is to decrease viral load, reduce transaminitis, and slow progression disease • Interferon: blocks viral entry to cell, blocks protein synthesis and assembly • Standard: Intron A – short half life means 3 doses/ week, subcu • Pegylated Interferon: PegIntron, Pegasys – long half life, weekly doses, subcuc • 1/3 of patients will have reduced HBV DNA and decreased ALT and HBeAg loss • Nucleoside and Nucleotide analogs: decrease viral replication • Lamivudine (Epivir), adefovir (Hepsera), entevacir (Baraclude) • Oral meds, treatment is long, non-compliance causes exacerbation Nursing – What do you do? • Identify at risk populations, screen and vaccinate • HBV vaccine (Recombivax HB or Energix B) series of 3 injections are highly effective • Children are vaccinated but high risk populations should be too • Dialysis patients should be vaccinated • Post exposure, Vaccine and HBIG (Hep B immunoglobin) are given within 24 hrs • Teach • Handwashing, don’t share personal items, safe sex • Prognosis • In healthy adults the infection resolves • 15-25% of chronically infected pts die from chronic liver disease Hepatitis C Virus (HCV) • What is it? • RNA virus • How is it transmitted? • • • • • • • • Sex with infected partners Blood and blood products, needles and syringes 10% is occupational, dialysis or perinatal Transfusions before 1992 place people at higher risk Many will not know their source Can be 15-20 years between infection and symptoms Chronic HBV and HCV are 80% of HCC cases 30-40% of HIV pts also have HCV More on HCV • Incubation period • 1-2 weeks before symptoms appear • 75-85% develop chronic HCV and remain infectious • Symptoms • • • • • • Initially asymptomatic Mild but persistent Most are unaware; the majority will be chronic May have hepatomegaly, splenomegaly and hepatic tenderness 20-30% lead to Cirrhosis Most common cause of liver transplantation in US HCV Diagnostics • RIBA: HCV recombinant immunoblot assay (RIBA) • Confirms an Anti-HCV is a true positive • Enzyme Linked Immunosorbent Assay (ELISA) - confirms anti-HCV • Anti-HCV • Marker of acute or chronic infection • HCV RNA quantitation • Active ongoing viral replication • HCV genotyping • 6 genotypes with 50 subtypes • Helps with treatment and prognosis • Liver Biopsy can be done if patient is a candidate • Non-invasive: Fibroscan, and FibroSure HCV Treatment • Drug therapy aims at killing virus and preventing complications • Treatment is dictated by : • • • • Genotyping of Hep C Co-morbitidies of the patient Possible side effects Patient willingness to comply • Pegylated Interferon (Pegasys, PegIntron) with Ribavirin (Rebetol, Copegus) • Pegylated interferon is taken once a week, sc • Ribavirin is taken orally twice a day More HCV Treatment • Protease Inhibitors for specific genotypes: • • • • Telaprevir (Incivek), Boceprevir (Victrelis) Protease inhibitors are taken every 8 hours – compliance! Treatment will depend on ability of liver to compensate Depression and mood swings are common for patients with HCV treatment • Screening prior to and during treatment is important Nursing • • • • No vaccine is available Screening is essential for blood, organ and tissue donation Infection control precautions Identify at risk groups: • CDC recommends all people born between 1945-1965 be tested • No post exposure prophylaxis • If exposed, anti-HCV and ALT levels should be drawn and repeated in 4-6 weeks Hepatitis D (HDV) • What is it? • RNA virus – single stranded so it cannot exist on its own • Needs HBV to replicate • How is it transmitted? • Transmitted transcutaneously like HBV • Often contracted along with HBV, needs HBV to exist • Incubation period • 2-26 weeks, constantly infectious Diagnostics • Anti-HDV • Present in in past or current infection with HDV • HDV Ag • Present a few days after infection • Treatment • No vaccination but Hep B vaccination reduces risk of co-infection • No pharmacologic treatment for HDV has been approved • Prognosis • HBV infected patients always at risk for Delta • HDV can be an acute, short-term, infection or a long-term, chronic infection Hepatitis E (HEV) • What is it? • RNA virus • How is it transmitted? • Fecal-oral route • Usually from contaminated drinking water • Common in developing countries, epidemics noted in India, Mexico, Africa and Asia • Cases in US usually people who have traveled to the above countries More on HEV • Incubation period • 2 weeks-3 months; infective time frame not known • 15-60 days after innoculation • Symptoms • • • • Fever, fatigue, loss of appetite Nausea, vomiting, abdominal pain Jaundice, dark urine, clay-colored stool Joint pain Diagnostics and Treatment • Diagnostics • Cases of Hepatitis E are not clinically distinguishable from other types of acute virus • No serologic tests to diagnose HEV infection have been approved by FDA in the US. • Anti HEV IgG and IgM • Present 1 week to 2 months after onset • HEV RNA quantitation • Indicative of active ongoing viral replication • Blood tests are most definitive for the antigen or antibody • Treatment • HEV usually resolves on its own without treatment. No specific antiviral therapy for HEV • Rest, get adequate nutrition and fluids, avoid alcohol Other Viral Sources of Hepatitis • • • • • Cytomegalovirus (CMV) Epstein-Barr Virus (EBV) Herpesvirus Coxsackievirus Rubella virus What can happen? • Most cases of acute viral hepatitis recover completely • Mortality for acute viral hepatitis is less than1% • Complications: • Acute liver failure, chronic Hepatitis, Cirrhosis and Hepatocellular Ca (HCC) • Fading jaundice is not indicative of resolution • HBV and HCV can cause chronic viral infection Drug and Chemical Causes • Alcohol is a common cause of acute and chronic Liver Disease and can cause • • • • Elevated liver enzymes (AST, ALT) Acute hepatitis Advanced fibrosis Cirrhosis • Acute Alcoholic Hepatitis • Hepatomegaly • Jaundice, elevated ALT, AST, low grade fever, ascites and prolonged PT • Cessation of ETOH, may improve symptoms Chemical • Chemical Hepatotoxicity • Caused by systemic poisons • Carbon tetrocholoride or gold compounds • Not see much anymore since restrictions • Drug Induced Liver Injury (DILI) • Caused by Prescription, OTC drugs and herbal remedies • Acetaminophen is most common cause of DILI • Safe at recommended doses Autoimmune and Metabolic Causes • Autoimmune Hepatitis • • • • • Chronic inflammatory condition with unknown etiology Autoantibodies work against normal hepatocytes Increased serum immunoglobulins Often seen with other auto immune disorders Lab tests differentiate from other forms of hepatitis • ANA’s and anti-DNA antibodies Autoimmune continued • Often cause chronic hepatitis or acute liver failure • Treatment is prednisone with azathioprine (Immuran) for active hepatitis • If no response • • • • Cyclosporine (Gengraf) Tacrolimus (Prograf) Methotrexate Mycophenolate(Cellcept) • All are hepatotoxic! Metabolic Causes of Hepatitis • Wilsons’s Disease – genetic – copper transport • Hemochromocytosis – iron overload • Primary Biliary Cirrhosis • Primary Sclerosing Cholangitis • NAFLD or NASH Collaborative Care • No specific treatment; rest allows liver to regenerate • • • • • • • Adequate nutrition; increased calories in acute phase Rest to reduce metabolic demands Parameters of care depend on severity of symptoms Counseling for alcohol avoidance Diversional activities Compliance with follow up care Education about treatment What do you do? • Assess your patient!!! • History • • • • Onset of symptoms Exposure to infected individuals Medications Chemical exposure • Teach risks • Support the patient • Standard Precautions Nursing Diagnoses • Imbalanced Nutrition: Less than body requirements related to anorexia and nausea • Activity Intolerance related to fatigue and weakness • Risk for impaired liver function related to viral infection • Goals of Care: • Relief of discomfort • Resumption of normal activities • Normal liver functions Liver Transplantation • Option for patients with • End Stage Liver Disease (ESLD) • Localized Hepatocellular Carcinoma (HCC) • • • • Chronic viral Hepatitis is primary indicator in US About 6,000 are done annually in US Intense screening for co-morbidities Contraindications • Metastatic disease • Non compliance • Ongoing ETOH/Drug use Cadaver vs Split Liver Transplants • Cadaver transplants are most common • Split liver transplants are live donations • • • • Biliary disease Hepatic artery thrombosis Pneumo, wound infections, ileus Success rate lower than cadavers • Complications • Bleeding, infection, rejection • Survival is best within 5 year window • Depends on need for transplant Anti-rejection Therapy • Prednisone • Calcineurin inhibitor • Cyclosporine • Tacrolimus • Azathioprine • Two months following transplant are critical • Infection – any kind • Emotionally • Reinfection of virus Nursing Care • • • • • • • ICU until extubated and stable Neuro status Watch for bleeding IV fluids Prevent respiratory complications I&O and electrolytes Drains • JP, NG,T-tubes • UOP