Term
| Acute/chronic Temporal aspect of liver disease |
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Definition
o Acute (days/weeks/months): injury to hepatocytes or bile duct cells
o Chronic (months/years): injury/repair/fibrosis, cirrhosis, etiology may be obscure |
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Term
| inflammation histopath findings in hep |
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Definition
| portal tract (triad) with excess lymphocytes and lymphocytes infiltrating into parenchyma |
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Term
| Variables that determine AST/ALT level are |
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Definition
| rate of death of hepatocyte, rate of enzyme clearance |
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Term
| • Assessing liver dysfunction |
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Definition
function is affected by hepatocyte dysfunction, hepatocyte death rate, duration of disease, regeneration rate
o Protein synthetic function (bili, albumin), organic anion transport (bilirubin - less specific), glucose production (hypoglycemia – late finding), urea synthesis (hyperammonia – hepatic encephalopathy) |
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Term
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Definition
| asymptomatic (abnormal LFTs only), nonspecific constitutional symptoms (fever, N/V, fatigue), physical findings (jaundice, tender liver, altered mental status/coma, bleeding), uncommon (headaches, myalgias, arthritis, rash, urticaria, arthritis) |
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Term
• Release of inflammatory mediators, cytokines, TNF: fever, myalgias, fatigue, nausea
• Liver dysfunction: bleeding, jaundice, coma
• Immune-complex-mediated disease (e.g. from viral hepatitis): rash, urticaria, arthritis |
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Definition
| Origins of symptoms in acute hepatocellular disease |
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Term
| Definition of Fulminant hepatic failure: |
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Definition
onset of failure within 8 weeks after onset of new liver disease
• Defined by: evidence of impaired liver function
o Any of the following - increased PT, hypoglycemia, encephalopathy
• Caused by >80% loss of hepatocytes
• Mortality rate: 40-80%
• Approach: hospitalize and consider liver transplant |
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Term
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Definition
persistent liver disease >6 months, may evolve through fibrosis to cirrhosis, complications of cirrhosis, HCC
Low grade daily injury - accumulation of injury
• Liver function fine until enough injury accumulated (years down the road)
Daily liver injury tests (AST/ALT) tend to be low to moderate
Daily symptoms often mild or even absent
Hepatic regeneration occurs but may or may not equal injury
Long-term: new symptoms may arise due to liver dysfunction and/or as consequences of cirrhosis |
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Term
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Definition
| • IgM anti-HA Ab for acute disease (Ab against capsid protein), IgG anti-HA Ab for past disease (lifetime protection – now immune) |
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Term
| What's unique about HBV surface antigen? |
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Definition
Hep B surface antigen (sAg)
• Hepatitis B produces excess coat protein (surface antigen sAg) as long as virus is present in liver
• Excess sAg is released from the liver as small spheres/rods – there is so much excess sAg that it is the one virus where you can measure viral protein in blood
• If present, demonstrates that the virus is in liver and making new virus |
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Term
| unique about HBV replication |
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Definition
| replicates through RNA intermediate like HIV so many of drugs are similar |
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Term
| T/F: Dx of HBV can be made by either cAg/eAg measured in blood or antibodies to it |
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Definition
Hep B core antigen (cAg)
• Principal component of the virus nucleocapsid
• Released from liver only in intact virions
• cAg cannot be readily measured in blood (inside viral particles)
• Ab made to cAg early in infection and it can be measured (IgM and IgG)
o Determines if it is chronic or acute HBV
• eAg, a product of cAg is released free into blood where it can be measured
o Ab made to eAg
o e antigen is an alternatively spliced version of the core protein gene (no DNA binding region, so just secreted in liver) |
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Term
| How to differentiate between someone who was infected and someone who just got vaccinated against HBV? |
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Definition
• In long-term, can detect
o anti-HBs (surface) protective against the virus
o anti-HBe (e antigen)
o anti-HBc (core)
• Levels of these will fall over many years, so years later all three may not be at detectable levels (however, life-long protection against refinfction remains)
• Note: HBV vaccine is anti-HBs, so this is how you can differentiate between someone who was infected and someone who just got vaccinated
• While virus is in the body, viral proteins, DNA etc. are around, but after resolution only the 3 Ab are left |
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Term
| How to tell if acute HBV becomes chronic? |
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Definition
Acute Hep B that becomes chronic
• Surface antigen persists – reliable marker that virus is present in liver
• Eventually, eAg is not produced as much as virus slows down
o Tells whether there is high replication or low replication of the virus
• Anti-HBc IgG is also reliable marker for chronic infection |
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Term
| HBV with high replication rate or low (resolving)...how to differentiate? |
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Definition
Hep B infection (acute or chronic) with high replication rate: Hep B DNA, HBsAg, HBeAg, anti-HBc
Hep B infection (resolving acute or chronic) with low replication rate: HBsAg, anti-HBe, anti-HBc |
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Term
| Why can't you have HDV on its own? |
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Definition
Cannot make its own coat protein – uses surface antigen of Hep B
• Cannot have Hep D infection without Hep B |
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Term
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Definition
• Hep C IgG antibody: appears weeks after onset of new infection, signifies past resolved or chronic hep C, occasional false positives, no IgM Ab available for acute infection (since it is almost never caught anyway because its asymptomatic)
• Hep C RNA (by PCR): signifies virus is present in liver/blood, found in acute or chronic hep C
• Interpretation
o When first infected, RNA present and Ab shows up later
o If becomes chronic, RNA and Ab both present
o If virus resolves, Ab only |
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Term
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Definition
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Term
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Definition
| Injury to normal hepatocytes by infiltrating lymphocytes (T cells) and PLASMA CELLS leading to fibrosis/cirrhosis |
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Term
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Definition
o Characteristic Ab: anti-nuclear Ab, anti-smooth muscle (actin) Ab
o High level of polyclonal immunoglobulin (IgG) |
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Term
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Definition
| • Chronic disease, but usually highly responsive to suppression by prednisone and azathioprine |
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Term
| T/F: Pathophys of AFLD and NAFLD is quite different |
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Definition
o Many similarities between alcoholic and non-alcoholic
o Both start with large globules of triglyceride in hepatocytes
o Both can, in some patients, lead to inflammation, hepatocyte necrosis, fibrosis and cirrhosis
o Development of fatty liver
• Fatty liver to steatohepatitis
o Further insults must occur to cause continued and progressive damage to hepatocytes and promote inflammation/fibrosis (e.g. oxidative stress, polymorphisms etc.) |
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