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Session 3 CM- GI-5
CM- GI-5- Viral Hepatitis
| Question | Answer |
|---|---|
| What are the five recognized hepatitis viruses | A, B, C D, E&G |
| Does acute hepatitis only occur because of hepatitis virus infections | no, CMV, EBV, HSV, Yellow Fever virus, Rubella all can cause acute hepatitis |
| What s/sx can help you differentiate cause of acute viral hepatitis between hepatitis viruses and other viral causes | actually they present clinically in similar ways and the only way to differentiate them is Lab results |
| What clinicla features will patient with hepatitis present with | anorexia, nausea, vomiting, right upper quadrant pain, elevated liver enzymes AST and ALT, headache, malaise, fever, Jaundice, dark urine, pale stool |
| What two hepatitis viruses are from fecal source | A and E |
| what is the source of the majority of hep viruses | Blood or body fluids |
| What hep viruses cause chronic infection | those that are of blood or body fluid source B, C, and D |
| What are the best ways to avoid hep infection | immunization and avoiding high risk behaviours |
| What will you likely see on lab eval of pt w/ viral hep | WBC normal to low, Lymphocytes (large atypical), Mild protienuria, bilirubinuria (precedes jaundice), elecated AST/ALT early, then ALT/AST, acholic stool |
| What is the hallmark s/sx of viral hep | Jaundice, usually develops late in infection |
| Hep called infectious hepatitis, incubation period 2-5 weeks, milder disease than hep B, asymptomatic infections are common especially in kids | Hep A |
| What groupd is more likely to develop severe infectious hepatits from Hep A | Adults especially pregnant women, |
| Is there a chronic form of Hep A | no |
| What is the pathogenesis of HEP A | viruses eneter via gut (fecal oral transmission), replicates in alimentary tract then spreads to infect liver hepatocytes, viremia is transient, virus is excreted in stools for 2 weeks preceding onset of s/sx |
| How do you dx Hep A | culture of virus from in vitro material or HAV IgM in patients blood |
| How can you prevent Hep A infections | passive immunization or active immunization(not in general use) |
| This hepatits has incubation period of 30-40 days acute self limiting hepatits no chronic carrier state and predominantly found in young adults 15-40yrs of age. (not hep A) | Hep E |
| What is a major complication associated w/ Hep E | Fulminant Hep in preganat women w/ high mortality rate up to 40% |
| What is the pathogenesis of Hep E | replicates in gut then invades liver shed in stool prior to s/sx viremia is transient requires large inoculum to establish infection (very similar to Hep A) |
| How can you dx Hep E | Specific IgM in serum though no routine lab tests are available |
| This Hepatitis has a incubation period of 1-6 months, insidious onset of s/sx, tend to cause more severe disease than Hep A asymptomatic infections occur frequently | Hep B |
| How is Hep B transmitted | sexually, parenterally, mucus membrane exposure, |
| What hep is associated with polyarteriitis nodosa (PAN) | Hep B and C |
| Patient has an Ab against the surface (coat) protein of Hep B what antigen does it target | HBsAG- produced as small spheres and tubules |
| What are HBcAg and HBeAg | antigens of Hep B inner core protein (HBcAg) and secreted protein (HBeAg) |
| What is the first marker present in a pt w/ viral Hep B | HBsAg |
| Will you find Hep B antigen HBcAg in the pts serum | no it does not circulate |
| What is the HBV window period | period during which HBsAg is not detectable and Anti HBs is not present but Anti HBc appears. Can last several weeks during this time a pt is likely to test negative but still be able to infect others |
| What is the pathogenesis of HBV | infection from blood or body fluid exposure, virus replicates in liver, virus is shed into blood viremia is prolonged, blood is highly infectious of conatminated individual |
| What is the likely course of a HBV infection | 90% self limited, 1-2% fulminant and 5-7% chronic carriers |
| What group is most likely to become a chronic carrier of HBV | infants that get infected, immunocompromised pt, male>female |
| Can HBV be transmitted across the placenta | yes 5-10% transmission rate |
| pt has failed to eliminate HBV and have a chronic infection what two ways could this chronic infection go | Chronic Persistent- minimal liver damage or Chronic Active- aggressive destruction of liver tissue and rapid progression to cirrhosis or liver failure |
| What are chronic HBV patients at increased risk of developing | Hepatocellular Carcinoma (HCC), 80% of pt w/ HCC are HBV carriers, have virus DNA in HCC cells |
| the following are high risk activities for what disease blood transfussions, serum product transfussion, sharing needles, razors, tattooing, acupuncture, renal dialysis, organ donation | HBV, Hep C, HIV |
| What 2 hep antigens when found in the blood or serum indicate viral replication is taking place in the liver | HBsAg and HGeAg |
| What ab indicates immunity following a hep infection it is detectable for life and is not found in chronic carriers | Anti-HBs |
| When does the anti-HBe antibody become detectable | when viral replication falls |
| What indicates pt has been exposed to HBV | core IgM and core IgG antibodies against core protein |
| How can you prevent HBV infection | active immunization with 3 doses of either serum derived or recombinant HBsAg vaccines both are eqully safe and effective |
| What liver condition can chronic viral hepatits B lead to | macronodular cirrhosis |
| Your pt was working at a laundry and has never been vaccinated for HBV they got stuck by a needle left in someones clothes what should you order for them as a precaution (assume HIV isn't a problem) | Hep B immune Globulin + vaccine if HBsAg negative. Newborns of Hep B mothers should get HBIG as well |
| Your patient is a chronic carrier of Hep B and just gave birth to a baby what should be done for the baby | Give baby Hep B immune Globulin |
| This viral hep has an incubation period of 4-8 weeks cases are milder but more people infected develop chronic infection (50%) | Hep C |
| What are major complications of Hep C | Chronic liver disease and hepatocellular carcinoma |
| How is Hep C transmitted | exposure to blood or body fluids of infected individual especially blood transfusion/products, organ donation, IV drug use, sex |
| How can you dx Hep C | serology- HCV specific IgG indicates exposure not infectivity, PCR detects viral genome in pt serum, HCV RNA |
| What is chronic viral hepatitis | >6months infection with either B,C, or D |
| What tx can you give for chronic HBV carrier | interferon alpha 30% long term remission, or Lamivudine reduces HBV-DNA reduces ALT levels and 15-20% seroconvert |
| What tx can you give for chronic HCV | Interferon alfa, 15% remit, Interferon/Ribavirin |
| If pt has inflammation extending beyond the portal areas into surrounding hepatic structures w/ extensive necrosis and fibrosis what are they suffering from | chronic active hepatitis CAH |
| If pt has chronic inflammatory infiltration of portal areas with little or no fibrosis what are they suffering from | chronic persistent hepatitis CPH |
| This hep virus requires comorbid infection with HBV | Hep D uses the Hep B capsule so Hep D has HBsAg |
| What are the consequences of Hep D infection in pt | increased severity of liver disease in hep B carriers. |
| pt is infected w/ a flavivirus, they present w/ glomerulonephritis, cryoglobulins, porphyria cutanea tarda (PCT), thrombocytopenia, neuropathy, thyroiditis sjorgren's syndrome or inflammatory arthritis name cause | Hep G |
| What are the non viral causes of acute hepatitis | Drugs, Alcohol, toxins, metabolic and autoimmune |
| What is the leading cuase of Acute Liver Failure in the US | drug related hepatotoxicity |
| Pt has liver disease and is taking cascara, chaparral, comfrey, kava and ma-huang (they really like herbal meds) why could this be a problem | compound liver disease |
| What drug is most common implication in alcoholic liver | acetaminophen it has a syngergistic effect w/ alcohol |
| What are s/sx of alcoholic liver w/ acetaminophen | nausea, vomiting, diarrhea abdominal pain and shock alt/ast |
| exposure to this drug can cause a Type I mild hepatitis which is typically benign or self limiting 20-30%, or can causea type II rxn w/ fever, jaundice and increased transaminases mortality of 50% | Halothane and the fluranes |
| What effect can INH (isoniazid) have on the liver | This drug causes a mild hepatitis toxicity in 20% of patients more men then female more in adults and cannot be distinguished clinically from viral heptatitis |
| This drug accumulate in hepatocytes and rarely causes clinical iver disease liver injury once done may continue for months you will see a transaminase elevation | Amiodarone |
| Why do you see liver damage in HIV patients | Anti-retroviral therapy has liver toxicity especially in HAART- highly active retroviral therapy |
| what is steatosis | fatty liver |
| what is cirrhosis | scarring and fibrosis of liver tissue |
| pt test positive for smooth mucle antibody they also have clinical signs of hepatitis what is the likely cause of their hepatitis | autoimmune hepatitis AIH |
| What is Gilbert's sndrome | glucoronyl transferase deficiency which is a benign chronic disorder w/ asymptomatic hereditary jaundice. |
Created by:
smaxsmith
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