MEDICAL BIOLOGY, HUMAN ANATOMY, PHYSIOLOGY AND PATHOLOGY - Ya.I. Fedoniuk 2010

ANATOMY, PHYSIOLOGY, PATHOLOGY

CHAPTER 7. NUTRITION AND ITS PATHOLOGY

PATHOLOGY OF THE DIGESTIVE SYSTEM

LIVER PATHOLOGY

3. HEPATITIS

3.1. Viral Hepatitis

Viral hepatitis is a group of diseases characterized by a fecal-oral or Blood-borne transmission mechanism, accompanied by intoxication and primary Liver damage, frequently presenting with jaundice.

Viral hepatitis types A, B, C, D, and E are distinguished, each caused by a specific pathogen.

Viral hepatitis A is a typical intestinal infection transmitted primarily from an infected person, mostly during the initial stage of the disease. Patients with subclinical and anicteric forms pose the greatest epidemiological threat. Transmission occurs via the fecal-oral route. Recovery confers lasting Immunity.

In hepatitis B, sources of infection include patients with various Clinical forms of acute and chronic viral hepatitis, cirrhosis of the liver, as well as healthy carriers. The primary route of transmission is parenteral, most commonly associated with blood transfusions and blood products, surgical Procedures, drug injections, sharing razors, or manicure sets. Sexual transmission is possible, and in tropical countries, transmission can occur via vectors.

Viral hepatitis C is transmitted parenterally and, less frequently, sexually. The primary vehicle of transmission is donor Blood and Its components.

Viral hepatitis D is caused by the delta virus, which is defective. To form its envelope, it utilizes the surface antigen of the hepatitis B virus, thereby infecting individuals already infected with hepatitis B. The pathogen is transmitted primarily through blood; consequently, the highest infection rates are found among intravenous drug users. Immunity to hepatitis B also protects against delta virus infection.

Viral hepatitis E features a fecal-oral transmission mechanism. It is characterized by high morbidity rates and epidemic outbreaks in regions with inadequate Water supply.

The following clinical and morphological forms of viral hepatitis are distinguished:

- cyclic icteric;

- anicteric;

- malignant or fulminant (viral hepatitis with massive hepatic necrosis);

- chronic;

- cholestatic and cholangiolytic.

The cyclic icteric form of epidemic hepatitis includes pre-icteric and icteric periods. During the pre-icteric period, the liver is enlarged and red due to vascular hyperemia and interstitial edema. In the icteric period, protein dystrophy develops, followed by hepatocyte necrosis, Bile stasis in the bile capillaries, and the onset of jaundice.

In the anicteric form of viral hepatitis, Changes in the liver are analogous to those observed during the pre-icteric period of the cyclic icteric form.

The malignant, or fulminant, form of viral hepatitis is characterized by massive hepatic necrosis, with the liver rapidly decreasing in size, its capsule wrinkling, and the tissue turning a bright yellow color.

The chronic active form of viral hepatitis develops against a Background of sclerotic changes in the liver that outweigh regenerative processes, which is why this form frequently progresses to cirrhosis.

In the chronic persistent form of viral hepatitis, only protein dystrophy is observed in hepatocytes, alongside signs of regeneration.

In the last two forms of the disease, the liver is initially enlarged, dense, with a sharp edge, and subsequently shrinks and becomes nodular, indicating The Development of sclerotic changes within it.

The cholestatic and cholangiolitic forms are dominated by cholestasis. These are manifested by the dilation of bile capillaries, The formation of "bile thrombi" within their lumens, and the accumulation of bile pigments in hepatic Cells.

Extrahepatic manifestations of viral hepatitis include jaundice, multiple hemorrhages in the Skin, serous and mucous membranes, as well as enlargement of the Lymph Nodes—particularly the mesenteric ones—and the Spleen.