Term
| What bacterial infections commonly secondarily involve the liver? |
|
Definition
| sepsis, typhoid fever, miliary TB, secondary or tertiary syphilis |
|
|
Term
| What parasitic infections commonly damage the liver? |
|
Definition
| malaria, trematodes (opisthorchiasis, chlonorchiasis, fascioliasis), echinococcosis, amebiasis |
|
|
Term
| What are the causes of abscesses in developing coutneries versus developed countries? |
|
Definition
developing= amebic
developed= pyogenic/bacterial |
|
|
Term
| By what routes can organisms get to the liver to cause liver abscesses? |
|
Definition
| biliary tract (ascending cholangitis) is the most common, arterial (sepsis), portal vein (pylephlebitis), direct extension, penetrating injuries |
|
|
Term
| What routes are used to cause multiple, small liver abscesses? |
|
Definition
| biliary, arterial, portal |
|
|
Term
| What routes are use to cause solitary abscesses? |
|
Definition
|
|
Term
| The contents of an amebic abscess are often described as.. |
|
Definition
|
|
Term
| What is the route for amebic absceses? Are they multiple or solitary? |
|
Definition
|
|
Term
| T/F Liver abscesses have a high mortality. |
|
Definition
| true: they can rupture into the abdominal cavity causes peritonitis and peritoneal abscesses, OR rupture into the thoracic cavity causes empyema or lung abscesses |
|
|
Term
| Which nonhepatotropic viruses cause viral hepatitis? |
|
Definition
| mononucleosis (epstein barr virus), yellow fever in children and immunosuppressed: CMV, herpesvirus, adenovirus, etc. |
|
|
Term
| Name the hepatotrophic viruses. |
|
Definition
| hepatitis A, B, C, D, and E |
|
|
Term
| Which hepatotropic viruses are unenveloped? |
|
Definition
|
|
Term
| What are the transmission characteristics of unenveloped viruses? |
|
Definition
| survive exposure to bile (emulsification) and shed in feces. Waterborne-fecal-oral transmission. Rare bloodborne transmission |
|
|
Term
| Are the unenveloped hepatitis viruses (A and E) linked to long term problems such as chronic hepatitis and hepatocellular carcinoma? |
|
Definition
| no linked to chronic hepatitis, no carrier state, not linke to hepatocellular carcinoma |
|
|
Term
| What is the genome of hep A? |
|
Definition
|
|
Term
| What is the incubation period of hep A? |
|
Definition
|
|
Term
| What are the symptoms of hepA? |
|
Definition
prodromal state (malaise, anorexia, nausea, vomiting, fever) and icteric state (jaundice, improvement of symptoms).
May be anicteric, subclinical esp in children or could be fulminant |
|
|
Term
| When in the course of illness is HepA shed? |
|
Definition
| shed in feces 2-3 weeks before to 1 week after jaundice |
|
|
Term
| What can cause epidemics of hepatitis A? |
|
Definition
| contaminated agricultural products |
|
|
Term
| How do you diagnose HepA? |
|
Definition
| acute hepatitis with IgM anti-HAV in the blood and HAV RNA in the feces. |
|
|
Term
| How can you tell if a patient has had HepA in the past? |
|
Definition
| IgG anti-HAV and protective immunity |
|
|
Term
| Do we vaccinate against Hep A? |
|
Definition
|
|
Term
| What is the genome of Hep E? |
|
Definition
|
|
Term
| What is the incubation period of hep E? |
|
Definition
|
|
Term
| T/F HepE is enzootic/zoonotic. |
|
Definition
|
|
Term
| What population is mostly affected by hep E in developing countries? |
|
Definition
| young and middle age adults |
|
|
Term
| T/F Hep E can be subclinical in children. |
|
Definition
|
|
Term
| What population has a high mortality rate from hep E? |
|
Definition
| pregnant women. mortality is 20-30% in the third trimester |
|
|
Term
| What is the geographic distribution of hep E? |
|
Definition
| mexico, india, china, nepal, northern africa |
|
|
Term
| Hep E cases in developed countries are associated with.. |
|
Definition
| older individuals (severity increases with age), pet ownership, and occupational exposure to pigs |
|
|
Term
| How do you diagnose acute Hep E? |
|
Definition
| igM anti-HEV in the blood and HEV RNA in the feces |
|
|
Term
| T/F Reinfections can occur with both hep A and hep E. |
|
Definition
| false, reinfections can only occur in hep E because of loss of IgG anti-HEV over time |
|
|
Term
| Is there a hep E vaccine? |
|
Definition
| vaccine is in phase III trials |
|
|
Term
| Which hep viruses are enveloped? |
|
Definition
|
|
Term
| How are the enveloped hep viruses shed? |
|
Definition
| dirsupted by bile so not shed in feces. transmission by contact with body fluids (percutaneous, mucosal/sexual, vertical) |
|
|
Term
| Which hepatits viruses have long incubation periods, cause persistent viremia and chronic infection? |
|
Definition
|
|
Term
| What is defined as a chronic hepatis? |
|
Definition
| one that causes disease for more than 6th months |
|
|
Term
| Which hep viruses are linked to carrier states, hepatocellular carcinoma, and immune complex deposition? |
|
Definition
|
|
Term
| What are the three classic problems with immune complex deposition? |
|
Definition
| arthralgia, vasculitis, glomerulonephritis |
|
|
Term
| What is the genome of hep B? |
|
Definition
|
|
Term
| What is the incubation of hep B? |
|
Definition
|
|
Term
| What is the course of hep B? |
|
Definition
| acute illness similar to hep A (jaundice occurs less often). May be fulminant or resolve completely. May become chronic (asympomatic-carrier state or symptomatic) |
|
|
Term
| What percent of patients with hep B make a full recovery? |
|
Definition
|
|
Term
| What is the most commonly reported hep viruses? |
|
Definition
|
|
Term
| What risk factors are reported in pts with hep B infection? |
|
Definition
one third have at least 1 sexual risk factor. 6% sex with person known to have hep B. 38% have multiple sex partners. 11% are MSM.
15% are IVDU.
53% report no risk factor |
|
|
Term
| What is the risk of vertical transmission of hep B? |
|
Definition
|
|
Term
| What's the risk of chronicity with hep B for immunocompetent versus immunocompromised adults? |
|
Definition
<5% of immunocompetent
>50% of immunocompromised |
|
|
Term
| Do we have a hep B vaccine? |
|
Definition
|
|
Term
| What is the dane particle? |
|
Definition
| HBV virion. Has HBsAG, HBcAg, HBeAg, HBx protein (replication, trans-acivate host genes), DNA polymerase, and HVB DNA |
|
|
Term
| What are the antigens of the HBV virion? |
|
Definition
surface antigen (HBsAg)
nucleocapsid "core" antigen (HBcAg)
non-structural "e" antigen (HBeAg) |
|
|
Term
| What are the phases of hep B? |
|
Definition
| proliferative (episomal) and integrated |
|
|
Term
| What happens in the proliferative phase of hep B? |
|
Definition
| formation of complete virions, hepatocyte destruction |
|
|
Term
| What happens in the integrated phase of hep B? |
|
Definition
| virus integrated into the host's genome, cessation of viral replication, hepatocyte destruction subsides, continuous production of HBsAg |
|
|
Term
| What is the pathogenesis of Hep B? How does this explain the different disease course found in immunosuppressed individuals? |
|
Definition
| expression of HBsAg and HBcAg on hepatocytes activates cytotoxic T lymphocytes, responsible for the cell damage. This is why immunosuppressed patients suffer less cell damage but are more likely to develop chronicity |
|
|
Term
| T/F HepB can cause cancer. |
|
Definition
|
|
Term
| How do you diagnose an acute hep B infection? |
|
Definition
|
|
Term
| How do you determine if a pt with Hep B is having active viral replication/infectivity? |
|
Definition
|
|
Term
| How do you determine if patient is having a chronic hep B infection? |
|
Definition
| symptoms for more than 6 months. Has HBsAg, HBeAg, and HBV DNA |
|
|
Term
| How do you tell if a patient has had a resolution of prior infection with hep B? |
|
Definition
HBsAg, HBV DNA, and HBeAg disappear
anti-HBsAg and anti-HBcAg appear and persist |
|
|
Term
| What is the effect of hep B vaccination on patient labs? |
|
Definition
| anti-HBsAg WITHOUT anti-HBcAg because vaccine is made of recombinant HBsAg |
|
|
Term
| What histological finding is classical for HBV? |
|
Definition
| ground class hepatocytes, sanded nuclei, HBV core antigen seen with immunoperoxidase |
|
|
Term
| What is the genome of hep D? |
|
Definition
|
|
Term
| Hep D has defective replication and therefore requires ___. |
|
Definition
|
|
Term
| What are the two types of diseases caused by hep D? |
|
Definition
coinfection with Hep B: fulminant disease more likely. Chronicity <5%
superinfection of HBV carrier: fulminant less likely. Chronicity 80% |
|
|
Term
| In the US, the population that gets Hep D is mostly restricted to... |
|
Definition
| drug addicts, hemophiliacs, their sexual contacts |
|
|
Term
| How do you prevent hep D? |
|
Definition
|
|
Term
| What is the genome of hep C? |
|
Definition
| ssRNA; classified into 6 major genotypes |
|
|
Term
| Which genotypes of hep C cause most infections? |
|
Definition
| 1a and 1b cause 70% of all infections in the US |
|
|
Term
| What is the incubation period of hep C? |
|
Definition
|
|
Term
| What is the disase course of hep C? |
|
Definition
| acute infection commonly subclinical; no fulminant presentation. High rate of chronicity 55-85% and high rate of progression to cirrhosis or HCC |
|
|
Term
| What percent of people with HCV go on to experienc chronic problems? |
|
Definition
|
|
Term
| What are the risk factors for hep C? |
|
Definition
| IVDU (60%, highly efficient), sexual (less than 20%, rare b/t long term sex partners), needle stick (1.8 to 10%), no recognized source of infection for 10% |
|
|
Term
| T/F Perinatal transmission of hep C is low. |
|
Definition
|
|
Term
| Why is it difficult to develope hep C vaccine? |
|
Definition
| HCV genome is unstable and variable. IgG anti-HCV does not confer protection. Emergence of mutated strains (quasispecies) causes recurrences |
|
|
Term
| How do you diagnose hep C? |
|
Definition
anti-HCV (EIA- enzyme immunoassay, RIBA-Recombinant immunoblot assay)
HCV RNA: qualitative and quantitative |
|
|
Term
| What's another name for hep G? |
|
Definition
|
|
Term
| What is the viral family of hep G? |
|
Definition
| RNA virus, flavivirus (same family as hep C, yellow fever, and west nile) |
|
|
Term
| How is Hep G transmitted? |
|
Definition
| parenteral, sexual, verticle transmission. Transmission by transfusion has been documented. |
|
|
Term
| Coinfection with HIV and GBV-C causes.... |
|
Definition
| possible improvement of prognosis of HIV infection |
|
|
Term
| What are some causes of non-infectious hepatitis? |
|
Definition
| autoimmune hepatitis, drug toxicity, alcoholic and non-alcoholic steatohepatitis, inborn errors of metabolism (wilson's and alpha-1 antitrypsin deficiency) and primary biliary cirrhosis |
|
|
Term
| What disease is morphologically similar to viral hepatitis? |
|
Definition
|
|
Term
| What characterizes AI hepatitis? |
|
Definition
| prominent plasma cell infiltrate, more severe than viral, high frequency of cirrhosis, female predominence (>70%), concurrent AI diseases, responds to immunosuppressive therapy |
|
|
Term
| What antibodies are associated with AI hepatitis? |
|
Definition
| anti-nuclear antibodies, anti-smooth muscle, anti-liver/kidney microsome 1 (LKM1), anti-soluble liver antigen |
|
|
Term
| What are the two types of drug and toxic liver injury? |
|
Definition
predictable or intrinsic= occurs in anyone at sufficient dose (acetaminophen)
unpredictable (idiosyncratic)= immune response (halothane) or slow metabolism (isoniazid) |
|
|
Term
| List toxins that cause macrovesicular steatosis. |
|
Definition
| methotrexate, ethanol, amiodarone |
|
|
Term
| What toxins cause microvesicular steatosis? |
|
Definition
| salicylates (reyes), tetracycline |
|
|
Term
| What toxins cause centrilobular necrosis? |
|
Definition
| carbon tetrachloride and acetominophen |
|
|
Term
| What toxins cause massive necrosis? |
|
Definition
| isoniazid, acetaminophen, halothane, and amanita phalloides |
|
|
Term
| What toxins causes chronic hepatitis? |
|
Definition
| nitrofurantoin, methyldopa, isoniazid, phenytoin, oxyphenisatin |
|
|
Term
| What toxins cause granulomatous hepatitis? |
|
Definition
| phenylbutazone, sulfonamides, hydralazine, allopurinol, quinidine |
|
|
Term
| What toxins cause cholestasis? |
|
Definition
| erythromycin estolate, chlorpromazine, anabolic steroids, and contraceptives |
|
|
Term
| How is acetominophen toxic? |
|
Definition
| small amount of acetominophen is metabolized by cytochrome P450 to form toxic oxidative metabolites that are then inactivated by glutathione. Alcohol potentiation b/c alcohol induces cytochrome p-450 and depletes glutathione |
|
|
Term
| What causes Reye's syndrome? |
|
Definition
| children given aspirin for virus induced fever (resp or varicella). Defect in mitochondrial fatty acid oxidation. Fatty acids accumulate in the SER causing extensive microvesicular steatosis. |
|
|
Term
| What causes death in Reye's syndrome? |
|
Definition
| liver failure and hepatic encephalopathy |
|
|
Term
| What percent of hospitalized patients are there fore alcoholic liver disease? how does alcoholic liver disease rate as death causing disease? |
|
Definition
| 25-30%; 5th leading cause of death |
|
|
Term
| Who is more susceptible to alcoholic steatohepatitis? |
|
Definition
| women > men, asians (slow aldehyde dehydrogenase) and african americans |
|
|
Term
| What percent of alcoholics develop cirrhosis? |
|
Definition
|
|
Term
| What causes alcoholic steatohepatitis? |
|
Definition
| induction of cytochrome P-450 (increase in toxic metabolites), generation of free radicals, depletion of glutathione, acetaldehyde, lipid peroxidation and protein adduct formation, malnutrition |
|
|
Term
| How is alcohol metabolized? |
|
Definition
Alcohol dehydrogenase and NAD to NADH + H ----> acetaldehyde
aldehyde dehydrogenase and NAD to NADH + H-----> acetate |
|
|
Term
| What is the etiology of alcoholic fatty accumulation in liver? |
|
Definition
| shunt metabolism toward lipid biosynthesis (alcohol dehydrogenase, aldehyde dehydrogenase generate excess NADH), impaired assembly and secretion of lipoproteins, increased peripheral catabolism of fat |
|
|
Term
| What are the histological features of alcoholic steatohepatitis? |
|
Definition
| steatosis (centrilobular), cell injury (ballooning, mallory bodies, necrosis, apoptosis), fibrosis (centrilobular), and cirrhosis (Laennec) |
|
|
Term
| What's another name for mallory body formation? |
|
Definition
|
|
Term
|
Definition
| non-alcoholic fatty liver disease. continuum of steatosis, inflammation, cell injury (ballooning), fibrosis, and cirrhosis. NAFLD is a generic designation that includes non-alcoholic steatohepatitis (NASH) |
|
|
Term
| What is the major risk factor for NAFLD? other risk factors? |
|
Definition
| visceral adiposity insulin resistance (glucose intolerance)/type 2 diabetes and hypertriglyceridemia |
|
|
Term
| T/F Prevalence and severity of NAFLD increase with age. |
|
Definition
|
|
Term
| What percent of americans are affected by NAFLD? |
|
Definition
|
|
Term
|
Definition
| when you have NAFLD and also have significant inflammation and hepatocellular injury. Likelihood of progression to cirrhosis |
|
|
Term
| How do alcoholic steatohepaitis and NASH compare morphologically? |
|
Definition
| similar but NASH is less severe |
|
|
Term
| What labs could you run to determine if a patient has NASH? |
|
Definition
| asymptomatic elevation of aminotransferases |
|
|
