Accesory Gland of Git Pathology

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Accesory Gland of Git Pathology

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Disease of the liver

JaundiceIt is a yellow discoloration of skin, sclerae, and tissues caused by hyperbilirubinemia. It is most often associated with hepatocellular disease, biliary obstruction, or hemolytic anemia.i

Ai. Physiologic jaundice of the newborn: iis commonly noted during the first week of life, but is not usually clinically important. It is characterized chemically by unconjugated hyperbilirubinemia.iThis form of jaundice results from both increased bilirubin production and a relative deficiency of glucuronyl transferase in the immature liver; these phenomena are exaggerated in premature infants.i

Bi. Congenital hyperbilirubinemias:i1i. Gilbert syndrome:i

Is extremely common, occurring in almost 5% of the population. This familial disorder is characterized by a modest elevation of serum unconjugated bilirubin. The cause is a combination of decreased bilirubin uptake by liver cells and reduced activity of glucuronyl transferase.i2i. Crigler-Najjar syndrome:i

Is a severe familial disorder characterized by unconjugated hyperbilirubinemia caused by a deficiency of glucuronyl transferase.iThere are 2 forms of this disease:i

Ii. One form leads to early death from kernicterus; damage to the basal ganglia and other parts of the central nervous system are caused by unconjugated bilirubin.i

IIi. A less severe form responds to phenobarbital therapy.i3i. Dubin-Johnson syndrome:iIs an autosomal recessive form of conjugated hyperbilirubinemia characterized by defective bilirubin transport. It is characterized by a striking brown-to-black discoloration of the liver.i

Viral hepatitisWe have 5 RNA viruses are:ii1. Hepatitis A virus (HAV).ii2. Hepatitis C virus (HCV).ii3. Hepatitis D virus (HDV).ii4. Hepatitis E virus (HEV).ii5. Hepatitis G virus.iAnd one DNA virus:iHepatitis B virus (HBV).iHepatitis A and E are both transmitted via the fecal-oral route, while the rest are transmitted via blood-to-blood (parenteral) contact.iMnemonics: Just as A and E are at both ends of ABCDE, so they are transmitted by elements of both ends of GIT !!!iAcute viral hepatitis is characterized by jaundice and extremely high elevations of serum aspartate [AST] and alanine aminotransferases [ALT].ii1.Hepatitis A virus [HAV]:i1i. Spread occurs by fecal-oral transmission.ii2. The incubation period is 1545 days.ii3. HAV does not cause a chronic carrier state or lead to chronic hepatitis; complete recovery almost always occurs. There is no relation to hepatocellular carcinoma.ii2. Hepatitis B virus [HBV]:i

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As figures above HBV is composed of central core containing the viral DNA genome, DNA polymerase, hepatitis B core antigen (HBcAg), and hepatitis B e antigen (HBeAg), and an outer lipoprotein coat containing the hepatitis B surface antigen(HBsAg) .iPrincipal considerations:iAsymptomatic carrier: the carrier patient never develops antibodies against HBsAg (anti-HBsAg) and harbors the virus without liver injury.iChronic persistent hepatitis: the patient has a low-grade hepatitis.iChronic active hepatitis: the patient has an acute hepatitis state that continues without the normal recovery (last longer than 6-12 months).iFulminant hepatitis: severe acute hepatitis with rapid destruction of the liver.ii>>>Transmission is via parenteral, sexual, and vertical (mother to neonate) routes. There is an increased incidence of HBV infection in male homosexuals.ii>>>The incubation period averages 6090 days.ii>>>HBV has a major association with hepatocellular carcinoma.ii>>>Disease can result in a carrier state or in chronic liver disease.i i>>>The sequence in which the various antigens or antibodies to these antigens appear in the serum is of clinical significance.iSerology:ii1. HBsAg: the presence of HBsAg always means there is LIVE virus and infection, either acute, chronic, or carrier. When anti-HBsAg develops, HBsAg disappears and the patient is protected and immune. ii2.HBcAg: antibodies to HBcAg are not protective but we can use them to understand how long the infection has been ongoing.iWith acute illness we will see IgM anti-HBcAg.iWith chronic illness we will see IgG anti-HBcAg.ii.e.i :IgM anti-HBcAg = NEW INFECTION (acute infection)i IgG anti-HBcAg = OLD INFECTION ( chronic infection)i i3. HBeAg: it is the soluble component of the core, this soluble component (HBeAg) is released during active infection.iThe presence of HBeAg indicates a high infectivity and active disease, i Presence of anti-HBeAg suggests lower infectivity.ii.e.i :HBeAg = HIGH INFECTIVITY Anti-HBeAg = LOW INFECTIVITYNotes:i i>>> When HBsAg is still persistent as detectable serum antigen for more than 6 months this denotes the carrier state.ii>>> Both Anti-HBcAg and Anti-HBeAg are markers used to diagnose hepatitis during the "window phase"ii>>> Window phase: it is a period of time in which there is neither detectable HBsAg nor Anti-HBsAg (HBsAb) in the serum of infected person.ii>>> During window phase: i :In the window phaseHBsAg number = Anti-HBsAg numberFor this reason we cannot detect neither HBsAg nor Anti-HBsAg (HBsAb) in the serum of infected person in this period.i

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i>>> HBV DNA can also be detected in serum and is an index of infectivity.iThe outcome of hepatitis B in adult:i

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In acute hepatitis B the serum analysis become as follow:i

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While in chronic state of hepatitis it become as follow:ii

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i3. Hepatitis C virus [HCV]:iTransmission is parenteral. HCV is a frequent cause of transfusion-mediated hepatitis and often leads to a carrier state and chronic hepatitis.iHCV is frequently associated with hepatocellular carcinoma.iThe outcome of hepatitis C in adult:i

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i4. Hepatitis D virus [HDV]:iHDV is replicatively defective, requiring simultaneous infection with HBV for viral replication. It usually causes illness more severe than HBV infection alone.iTransmission is via sexual or parenteral routes.iIncidence is especially high in intravenous drug users.ii5. Hepatitis E virus [HEV]:i

causes an enterically transmitted form of viral hepatitis similar to HAV infection that occurs in water-borne epidemic form in underdeveloped countries.iIt has a high incidence of mortality (about 20%) when occurring in pregnancy.iChronic hepatitisChronic hepatitis is defined by the persistence of abnormalities for more than 6 months. It may result from any of the viral hepatitides except HAV or HEV infection and also from liver damage induced by nonviral agents.iAutoimmune hepatitis is morphologically indistinguishable from other forms of chronic hepatitis. It is secondary to various immunologic abnormalities. It is clinically marked by hypergammaglobulinemia and antismooth muscle antibodies.iMicrovesicular fatty liver

This group of serious disorders is associated with the presence of small fat vacuoles in parenchymal liver cells, which differ from the large fat-containing vacuoles characteristic of fatty change.i

i1. Reye syndrome:i Ai. This acute disorder of young children is characterized by encephalopathy, coma, and microvesicular fatty liver.iBi. Reye syndrome is associated with aspirin administration to children with acute viral infections.i

2i. Fatty liver of pregnancy:iIs acute hepatic failure during the third trimester of pregnancy associated with microvesicular fatty liver. This condition has a high mortality rate.i

3i. Tetracycline toxicity:iResults in an unpredictable hypersensitivity-like reaction with microvesicular fatty change.i

Alcoholic liver disease

is the summation of hepatic changes associated with excessive alcohol consumption; it varies from fatty change to alcoholic hepatitis and cirrhosis.i

it may be asymptomatic or may be associated with mild-to-severe hepatic inflammation, cirrhosis, or encephalopathy.i

1i. Fatty change (steatosis): is the most frequent morphologic abnormality caused by alcohol and is reversible. Nonalcoholic fatty liver disease, or NAFLD, is a related condition unrelated to alcohol consumption.i

i2. Alcoholic hepatitis: is often associated with irreversible fibrosis that characteristically surrounds central veins and has been referred to as perivenular fibrosis, sclerosing hyaline necrosis, or central hyaline sclerosis. This fibrosis can lead to cent