169. Hepatitis: principles of classification, morphological features depending on the etiology, complications, outcomes.

Hepatitis is a liver disease based on its inflammation (dystrophic and necrobiotic changes in the parenchyma and inflammatory infiltration of the stroma).

Classification:

Primary hepatitis: 1. Viral 2. Alcoholic 3. Medicinal 4. Cholestatic.

Secondary hepatitis: 1. Infections (br. Typhus, malaria, tuberculosis, sepsis, etc.) 2. Intoxication (thyrotoxicosis, poisons) 3. Gastrointestinal tract lesions

Acute hepatitis: 1. Exudative (serous, purulent hepatitis) 2. Productive

Chronic hepatitis: 1. Active (aggressive) 2. Persistent 3. Cholestatic

Features:

Acute hepatitis can be exudative and productive. In exudative hepatitis, the exudate may be serous or purulent in nature. For example, with thyrotoxicosis, serous hepatitis is noted, exudate spreads through the stroma of the organ. In purulent cholangitis, the infiltrate has a purulent character and can be diffusely located in the portal tracts or form foci (abscesses), which is more often observed as a complication in purulent appendicitis, amoebiasis, septicopiemia. Acute productive hepatitis is characterized by dystrophy and necrosis of hepatocytes of different parts of the acinus, the reaction of cells of the reticuloendothelial system of the liver. Also, in tuberculosis, sarcoidosis, and PBC, granulomas of different cellular composition may form in different parts of the parenchyma and stroma, which is determined by the etiology of the process. The appearance of the liver in acute hepatitis depends on the nature of the inflammation.

Chronic hepatitis is usually caused by various types of hepatotropic viruses, they have a manifest or asymptomatic course lasting more than 6 months, and are morphologically characterized by diffuse dystrophic and inflammatory liver damage with histiolymphocytic infiltration of portal fields, fibrosis of the interlobular and intralobular stroma, hyperplasia of Kupfer cells with preservation of the lobular structure of the liver. The liver in chronic hepatitis is usually enlarged and compacted. Its capsule is focally or diffusely thickened, whitish. The liver tissue on the incision has a mottled appearance.

Complications:

Cirrhosis, cancer, hepatic coma, hepatic encephalopathy, hemorrhagic syndrome, cholecystitis, cholangitis, massive cirrhosis of the liver, liver failure.

Outcomes:

The outcome of hepatitis depends on the nature and course, on the prevalence of the process, the degree of liver damage and its reparative capabilities. In mild cases, complete restoration of the structure of the liver tissue is possible. With acute massive liver damage, as with chronic hepatitis, cirrhosis may develop.

170. Viral hepatitis b: etiology, pathogenesis, ways of infection, forms, pathological anatomy, outcomes.

Hepatitis B virus is a DNA-containing virus (Dane particle), including three antigenic determinants:

– surface antigen (HBsAg);

– heart-shaped antigen (HBcAg), which is associated with the pathogenicity of the virus;

– HBeAg, which is regarded as a marker of DNA polymerase.

Pathogenesis:

introduction of the pathogen, fixation on the hepatocyte and penetration into the cell

reproduction of the virus and its release onto the surface of the hepatocyte, as well as into the blood

The inclusion of immunological reactions aimed at the elimination of the pathogen

damage to other organs and systems

Further destruction of liver cells occurs under the influence of T-lymphocytes (Killers).

Ways of infection:

Parenteral

Sexual

Transplacental

Infection of a newborn during passage through the birth canal

Morphological forms:

– acute cyclic (jaundice);

– heartless;

– necrotic (malignant, fulminant, lightning-fast);

– cholestatic;

– chronic.

Pathological anatomy:

In the acute cyclic (jaundice) form of viral hepatitis, morphological changes depend on the stage of the disease — the stage of onset and recovery. At the height of the disease (1-2 weeks of the jaundice period), the liver (according to laparoscopy) is enlarged, dense and red, its capsule is tense (large red liver). Microscopic examination (liver biopsies) shows a violation of the hepatic girder structure and pronounced polymorphism of hepatocytes (binuclear and multinucleated cells), often mitosis figures are visible in the cells. Hydropic and balloon dystrophy of hepatocytes prevail, focal (spotted) and drain necrosis of hepatocytes occur in various parts of the lobules, the corpuscles of the Council are in the form of rounded homogeneous eosinophilic formations with or without a pyknotic nucleus — hepatocytes in a state of coagulation necrosis with sharply reduced organelles, or "mummified" hepatocytes. Portal and intracellular stroma are diffusely infiltrated by lymphocytes and macrophages with an admixture of plasma cells, eosinophilic and neutrophilic leukocytes. The number of stellate reticuloendotheliocytes is significantly increased. In the recovery stage (4-5 weeks of the disease), the liver acquires normal dimensions, hyperemia is reduced; the capsule is somewhat thickened, dull, small adhesions occur between the capsule and the peritoneum. Microscopic examination reveals the restoration of the girder structure of the lobules, a decrease in the degree of necrosis and dystrophy. Regeneration of hepatocytes is pronounced, there are many double-core cells in all parts of the lobules. Lymphomacrophagous infiltration in the portal tracts and inside the lobules becomes focal. At the site of discharge necrosis of hepatocytes, a coarser reticular stroma and an overgrowth of collagen fibers are found.

In the acute cyclic form of hepatitis, virus particles and antigens are usually not found in liver tissue. Only with a prolonged course of hepatitis, HBsAg is sometimes detected in single hepatocytes and macrophages.

In the non-jaundiced form of hepatitis, liver changes are less pronounced compared to the acute cyclic form, although a large red liver is found during laparoscopy, only one lobe may be affected. The microscopic picture is different: balloon dystrophy of hepatocytes, foci of their necrosis, and corpuscles are rare; proliferation of stellate reticuloendotheliocytes is significantly pronounced; inflammatory lymphomacrophagal and neutrophil infiltrates, although they capture all parts of the lobules and portal tracts, do not destroy the border plate; cholestasis is absent.

The necrotic (malignant, fulminant or lightning-fast) form of viral hepatitis is characterized by progressive necrosis of the liver parenchyma. The liver is rapidly shrinking, its capsule is wrinkled, the tissue is gray-brown or yellow. Microscopic examination reveals bridged or massive necrosis of the liver. Among the necrotic masses, there are corpuscles of the Councillor, clusters of stellate reticuloendotheliocytes, lymphocytes, macrophages, neutrophils. Bile stasis in the capillaries is pronounced.

The cholestatic form of hepatitis develops mainly in the elderly. It is based on intrahepatic cholestasis and inflammation of the bile ducts. Laparoscopy reveals changes similar to a large red liver, but a liver with foci of yellow-green color and an accentuated lobular pattern. During microscopic examination, the phenomena of cholestasis prevail.

Chronic viral hepatitis is active or persistent hepatitis. Active chronic hepatitis is characterized by cellular infiltration of the portal, periportal and intracellular sclerosed stroma of the liver. Infiltration of lymphocytes, macrophages, and plasma cells through the border plate into the hepatic lobule is especially characteristic, which leads to damage to hepatocytes. Dystrophy (hydropic, balloon) and necrosis of hepatocytes (destructive hepatitis) develop. Destruction of hepatocytes is combined with focal or diffuse proliferation of stellate reticuloendotheliocytes and cholangiol cells. At the same time, the regeneration of the liver parenchyma is imperfect, sclerosis and restructuring of liver tissue develop. Chronic persistent hepatitis is characterized by infiltration by lymphocytes, histiocytes and plasma cells of sclerosed portal fields. Focal histiolymphocytic clusters are rarely found inside the lobules, where hyperplasia of stellate reticuloendotheliocytes and foci of sclerosis of the reticular stroma are noted.

Outcomes: Complete cure, transformation of the acute form into a chronic one, asymptomatic carriage. Death in viral hepatitis occurs from acute (necrotic form) or chronic (active chronic hepatitis with an outcome of cirrhosis) liver failure. Sometimes hepatorenal syndrome develops.