PATHOLOGY OF LIVER & BILIARY TRACTامراض الجهاز الهظمي الكبد والمرارة البروفسيور علي التميمي

PATHOLOGY OF LIVER & BILIARY TRACT

امراض الجهاز الهظمي الكبد والمرارة البروفسيور د.علي التميمي/

محاضرات الامراض للاقسام الطبية لطلبة كلية الرافدين الجامعة

The liver is the largest visceral organ in the body and receives about 25% of cardiac output through the portal vein

(2/3) and the hepatic artery (1/3). Blood from the stomach, intestines, spleen, and pancreas drains into the liver via the portal vein. Therefore, oxygen is carried to the liver by both the portal vein and the hepatic artery. The liv er is the central organ for the metabolism of carbohydrates, proteins, lipids, vitamins and hormones as well as for detoxification, excretion, storage and digestion. Its size and location expose it to a myriad of injurious agents but it has are markable functional reserve and regenerative capacity. Consequently, an injury must be severe or strategically located to result in clinical signs or altered laboratory tests. Hepatic failure is associated with retention of ammonia, bile salts and pigments and failure of synthetic functions.
Clinical signs of liver disease are often variable and nonspecific but most commonly include
jaundice, ascites and  hepatomegaly

HEPATOBILIARY INJURY AND RESPONSES

PATTERNS OF HEPATOCELLULAR DEGENERATION & NECROSIS
Cellular degeneration and/or necrosis in the liver occurs in one of two morphologic patterns

-random and zonal

Random hepatocellular degeneration & necrosis
The change occurs in one of three forms:

Single cell necrosis or apoptosis throughout the liver, not visible grossly.
Multifocal necrosis (scattered randomly throughout the liver). There is no predictable location within liver lobules. It is typical of many infectious agents (viruses, bacteria, certain protozoa). Grossly the lesions appear as discrete, pale or dark-red foci, sharply delineated
from normal parenchyma. The size varies from less than 1 mm to several mm.
Microscopically, affected cells are degenerate or necrotic and there may be inflammation.
Zonal hepatocellular degeneration & necrosis
Zonal change affects hepatocytes within defined areas of the hepatic lobule and leads to enhanced lobular pattern on the capsular and cut surfaces

Centrilobular degeneration and necrosis.

Midzonal degeneration and necrosis.

Periportal degeneration and necrosis.

PATTERNS OF HEPATIC INFLAMMATION

Acute hepatitis  as seen in several bacterial, protozoal and viral infections. Neutrophils

predominate in bacterial and protozoal hepatitis whereas in viral hepatitis, it is mostly

necrosis with or without lymphocytes Chronic hepatitis when there is persistence of the injury. It is characterized by fibrosis accumulation of mononuclear cells (lymphocytes, plasma cells and macrophages) with or without neutrophils, and frequently, regeneration. Lesions may be focal/multifocal in the form of abscesses or granulomas, or they may be diffuse with loss of hepatic parenchyma fibrosis and nodular regeneration. It can lead to end-stage liver

GENERAL RESPONSES OF THE LIVER TO INJURY
Responses of the liver to different noxious insults that cause destruction of hepatic parenchyma include (1) regeneration of parenchyma, (2) replacement by fibrosis, and (3) biliary hyperplasia.

The outcome of any given hepatic insult reflects the nature and duration of the insult.

  1. . Regeneration.
  2. Fibrosi.
  3. Biliary hyperplasia.

END-STAGE LIVER (Cirrhosis). Cirrhosis has been defined as “a diffuse process
characterized by fibrosis and the conversion of the normal liver architecture into structurallyabnormal lobules” but a better term is “end-stage liver”. It is the final, irreversible result of different hepatic diseases and it usually involves severe nodular regeneration, fibrosis and bile duct hyperplasia
MANIFESTATIONS OF LIVER FAILURE

  1. Hepatic encephalopathy
  2. Disturbances of bile flow and hyperbilirubinemia (icterus, jaundice)

Elevated levels (> 2 mg/dl) of bilirubin in blood (hyperbilirubinemia) can produce icterus which is yellow discoloration of tissues and body fluids caused by accumulation of bilirubin.

  1. Prehepatic – Overproduction of bilirubin
  2. Hepatic – Decreased uptake, conjugation or secretion of bilirubin

iii. Posthepatic – Reduced outflow of bile ( cholestasis)

METABOLIC DISTURBANCES & NUTRITIONAL DISEASES

FATTY LIVER (HEPATOCELLULAR LIPIDOSIS, STEATOSIS)

GLYCOGEN ACCUMULATION

AMYLOIDOSIS

PIGMENT ACCUMULATION

Bile: Excess bile (cholestasis)

Hemosiderin

 Hemosiderosis

 Hemochromatosis

INFECTIOUS DISEASES OF THE LIVER (HEPATITIS)

Viral Hepatitis

Hepatotropic:

–HepatitisA Virus

–HepatitisB Virus

–HepatitisC Virus

–HepatitisD Virus

–HepatitisE Virus

Alcohol (Toxic) Related Injury

Drug Induced Injury

Obstructive Biliary Disease