Liver II pathology
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| these disorders dominate the clinical practice of hepatology. Any insult to the liver can killhepatocytes and recruit inflammatory cells. | infectious disorders
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| what are some frequent causes of infectious disorders? | viruses, bacterial, helminthic, parasitic
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| this is the term applied for hepatic infections caused by hepatotropic viruses (ABCDE) unless otherwise specified. | viral hepatitis
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| can systemic viral infections affect the liver? | yes
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| give some examples of systemic viral infections which can affect the liver | infectious mononucleosis (EBV), CMV in newborns and immunosuppressed, yellow fever (yellow fever virus) in topical countries.
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| these studies are essential for the diagnosis of viral hepatitis | serologic and molecular studies
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| this virus causes a benign, self limited disease with an incubation period of 3-6 weeks. it is endemic in countries with poor hygiene and sanitation, does not cause chronic hepatitis or a chronic carrier state; negligible fatality. | Hepatitis A virus
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| give some symptoms of Hepatitis A virus | fatigue, loss of appetitie and often jaundice, virus is shed in stool 2-3 weeks before and one week after the onset of jaundice. can be detected in serum and saliva, viremia is transient
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| in the serology of Hepatitis A, when do you see IgG HAV start to elevate? | when IgM HAV starts to decline
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| to check for immunity for Hepatitis A, what do you look for in the blood? | total anti HAV.
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| in hepatitis A, what is your marker to indicate active disesae? | IgM
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| describe the Hepatitis B virus genome | partially double stranded circular DNA molecule
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| this antigen has a nucleocapsid core protein, and remains in the hepatocyte for assembly of virion | HBcAg
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| this antigen of the hepatitis B vaccine has a core and a pre-core, which directs secretion of virion into the blood. it's how you know a person is infected. | HbeAg
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| this antigen is an envelope glycoprotein; noninfective sAg infected hepatocytes synthesize and secrete this protein (mainly small) | HbsAg
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| this is a polymerase thet exhibits DNA polymerase and reverse transcriptase activity DNA to RNA to DNA | Pol
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| in the Hepatitis B vaccine, this is necessary for virus replication; acts as transcriptional activator of genes implicated in pathogenesis of liver cancer. | HBx
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| if you were to make a vaccine for Hepatitis B, which protein would you purify and use as a target for AB production? why? | HbSAg, because it is the non-infective component.
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| once a diagnosis of Hepatitis B is established, it is used to do what? | define the phase of the infection, degree of infectivity, prognosis, immune status,
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| describe the mutated strains of HBV | they do not produce HBeAGg but has HBcAg and are replication competent and yet have HBV viral load. this allows them to escape vaccines.
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| how are vaccines for the mutated HBV produced? | from the HBsAg and this induces an antibody response
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| this describes an individual without HbeAg, but with presence of anti-Hbe. they have normal aminotransferase, low or undetectable serum HBV DNA, liver biopsy without significant inflammation and necrosis | the HBV carrier state
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| list some goals of treatment for chronic hepatitis B? | slow disease progression, reduce liver damage, prevent liver cirrhosis or liver cancer
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| what are some major problems with current treatment of Hep B? | viral resistance, side effects
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| this virus is the major cause of liver diseaes worldwide. It is the most common blood borne infection, and most common cause of chronic viral hepatitis | heaptitis C virus
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| what is a characteristic feature of hepatitis C virus? | repeated bouts of hepatic damage.
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| majority of the cases of hepatitis C progress to what? | chronic liver disease, and cirrhosis eventually develops over 5 to 20 years in about thirty percent of individuals.
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| describe the genomic structure of the hepatitis C virus | there is a core protein, with the same sequence from one species to another. at the end, you have nonstruc proteins and in the middle you have an E2 protein, which is the highest variable region (also the region ofABtarget), cuasing antigen variability.
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| explain why ou have repeated bouts of hepatitis C infection | because the NS5B RNA polymerase has poor fidelity, making the virus inherently unstable (it doesn't copy correctly or exactly as it should), giving rise to multiple genotypes and subtypes creating a quasispecies.
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| this describes a population of divurgent but closely relatd variants | quasispecies
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| in acute infection with HCV, you develop these symptoms... | jaundice
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| what is the difference in recovery with acute and chronic HCV infection/ | with recovery from acute HCV infection, you get Anti-HCV antibodies and the HCV RNA doesnt last that long. you don't get antibodies with chronic disease. the HCV RNA persists.
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| what is the clinical utility of HCV RNA detection and quantificaiton important for? | confirming the diagnosis of HCV, distinguishing active from resolved infection, assessing virologic response to therapy, screening the blood supplly.
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| in HCV, what gives antigenic variability? | the envelope 2 protein.
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| this virus has unique RNA virus that is dependent for its life cycle on HBV | Hepatitis D virus
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| does vaccination for HBV also prevent HDV infection? | yes
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| what is the only protein produced by hepatitis D virus? | the external coat antigen of HBsAg surrounds a internal polypeptide assembly, designating delta antigen.
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| when is HDV RNA detectible in the blood and liver of the patient? | just before and in the early days of acute symptomatic disease.
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| what is the most reliable indicator of recent HDV exposure, although it is short lived and appears late? | IgM.
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| replication of hepatitis D virus is through what? | RNA directed RNA synthesis by host RNA polymerase, mainly pol II.
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| in this setting for Hepatitis D infection, you get the disease following infection of both hepatitis B and D viruses. HBV must be established first to provide HBs Ag. it is usually transient and self limited, clinically similar to acute hep B | acute coinfection
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| how do you diagnose acute coinfection for hepatitis D infection? | IgM against both HDAg and HBcAg
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| this setting of HDV infeciton when a chronic carrier of HBV is exposed to a new inoculum of HDV and results in disease 30-50 days later. may represent as acute or severe hap in unrecognized HBV carrier or as exacerbation of HBV | superinfection
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| the acute phase of superinfection is characterized by... | active HDV replication; suppression of HBV, high ALT
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| the chronic phase of HDV superinfection is characterized by.... | HDV replication decrease, HBV increase, ALT fluctuates
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| how do you diagnose HDV superinfection | HBsAg and anti-HDV (IgG and IgM)
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| this setting for infection with HDV is seen in patients withliver transplants. HDV is seen in the nuclei of the transplanted liver without evidence of HBV or HDV reinfection. it is due to the infeciton of the donor HDV alone | helper independen latent infection
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| this virus is an enterically transmitted water borne infection, virions are shed in stool during acute illness. occurs primarily in young to middle aged adults. in india, it surpasses the frequency of HAV | hepatitis E virus
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| HEV has a high mortality rate among which population? | pregnant women. the virus is self limiting, not associated with chronicity or persistent viremia.
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| this describes clinicopathologic syndrome of viral hepatitis where incidentally discovered on the basis of elevated transaminase presence of anti viral Ab (anti-HAV or anti-HBV) | acute asymptomatic infection with recovery
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| this describes clinicopathologic syndrome of viral hepatitis where peak infectivity occurs during hte last asymptomatic days of the incubation period and early days of the acute symptoms | acute symptomatic infection with recovery
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| this describes clinicopathologic syndrome of viral hepatitis: symptomatic, biochemical, or serologic evidence of continuing or relapsing hepatitis diseaes for more than six months. incidence in HCV>>HBV. | chronic hepatitis...mostly with HCV
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| how do people with HIV get chronic viral hepatitis? | when they are co-infected with HBV and HCV.
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| why is it common for HIV patient to be infected with both HCV and HBV? | due to similar transmission mode, similar high risk patient population.
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| does HIV significantly exacerbate the severity of viral hepatitis? | yes
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| why do anti-HIV agents cause hepatotoxicity in some patients with viral hepatitis? | because their liver is already compromised.
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| which is the only hepatitis virus has DNA? | hepatitis B
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| which hepatitis viruses have the potential to cause chronic hepatitis? this makes the patient more likely to develop what? | hepatitis B and C. because of this, patients are more likely to develop cirrhosis, and cirrhosis is a risk factor for hepatocellular carcinoma.
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| list some morphological features of acute hepatitis | inflammatory infiltrate, ballooning degeneration, macrophage aggregates, apoptosis.
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| what is the histological hallmark of chronic liver damage? | fibrosis
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| in this hepatitis virus, the histological change you see is diffuse glanular cytoplasm with "ground glass hepatocyte" due to cytoplasmic inclusions of HBsAg | chronic hepatitis B
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| in this type of hepatitis virus, on histological appearance you see lymphoid aggregates, bile duct reactive changes and steatosis | chronic hepatitis C
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| besides viruses, what are some other infectious hepatic disorders? | bacterial and nonbacterial
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| in hepatitis due to this, you see sepsis and extrahepatic infection, cholestasis due to effects of proinflammatory cytokines, released by kupfer cells and endothelial cells, in response to endotoxins, ascending cholangitis, severe acute inflammatory resp | bacterial infections
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| hepatic lobatum is caused by what? | tertiary syphillis: but you don't really see cases of these because we have ABX
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| in tertiary syphillis, this is a white, gray, rubbery, occur singly or as multiple lesions resembling tubercles to large tumor like masses | syphilitic gumma
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| in tertiary syphillis, this is described by scarring in the liver as a result of gumma | Hepar lobatum
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| these are common in devleoping countries and usually caused by: echinococccal and amoenbic infecitons | liver abscesses. routes of infection: blood, ascending cholangitis, direct invasion, penetrating injury.
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