PATHOLOGY OF

DIGESTIVE SYSTEM-
4
LIVER
•25% of the blood in the body flows through the liver.
Functions
•Secretion of bile
•Protein, Carbohydrate and fat metabolism
•Detoxication
•Vitamin metabolism and storage
•Erythropoiesis - In the bird, liver is the site for erythropoiesis. In other
animals, during fetal life, erythropoiesis occurs in the liver. In these
animals in severe anemia, erythropoiesis takes place in the liver even in the
adult as part of extramedullary hemopoiesis
 DEGENERATIONS OF LIVER
Cloudy swelling
Gross pathology
The organ has a dull, parboiled appearance.
The liver is enlarged
The capsule is tense.
Borders are rounded.
Consistency is softer.
Histopathology
Hepatocytes are swollen and have a pale granular cytoplasm due to swelling
of mitochondria. The nuclei may be indistinct.
Hydropic degeneration
Gross pathology
•Gross lesions are more or less similar to that of cloudy
swelling
Histopathology
•The cytoplasm of hepatocyte may contain one, two or more
vacuoles in the cytoplasm.
Fatty change
Aetiology .
.
•Nutritional deficiency: Inadequate choline and apoproteins
•Metabolic diseases– Diabetes mellitus in dogs and cats,
acetonemia/ketosis in cattle
•Bacterial toxins
•Poisons
Pathogenesis
•The liver is too sick to metabolize the dietary as well as the fat
brought to it from the depots. Defect may be anywhere in the process
from metabolism of fatty acids to the formation and release of
lipoproteins.
Gross pathology
•liver is enlarged with round margins
•Fat droplets are seen on the blade.
Histopathology
•hepatic parenchymal cells contain fat droplets
HEPATITIS
•Hepatitis is an alterative inflammation of liver in which the
various degenerative processes like cloudy swelling, fatty
change and necrosis are caused by irritants which also
produce inflammation.
•Hepatitis may be either infectious, non-infectious or toxic.
This may again be acute or chronic. The chronic variety is
usually called Cirrhosis.
Routes of infection of the liver
1. Portal vein : Ingested organisms enter the portal vein and so are
conveyed to the liver.
2. Hepatic artery : Organisms when present in the blood as emboli or
in a bacteremic state reach the liver.
3. Umbilical vein of the new born animals : When the umbilical vein
is contaminated, organisms grow well in the partially coagulated
blood which acts as a good medium and reach the liver.
4. Bile ducts : Infection may ascend from the duodenum. Obstruction of
bile ducts causing biliary stasis may facilitate such infections.
5. By direct extension from neighbouring organs as in traumatic
reticulitis.
ACUTE TOXIC HEPATITIS
•Characterized by necrosis which is usually preceded by
degenerative changes like cloudy swelling and fatty changes.
•Hepatic necrosis is classified as per anatomical distribution into
1. Focal necrosis
2. Centrilobular necrosis
3. Midzonal necrosis
4. Periportal necrosis
5. Diffuse necrosis
6. Paracentral necrosis
1. FOCAL NECROSIS
• numerous small necrotic areas are seen scattered in the liver and may
be found in any part of the lobule.
2. CENTRILOBULAR NECROSIS
• the cells nearest to the central vein are affected.
• Hepatocytes around central vein distrophy, infiltration of inflammatory
cells
3. MID-ZONAL NECROSIS
• lesion is found in mid-way between the central vein and the periphery
of hepatic lobe.
4. PERIPORTAL NECROSIS
•the cells adjoining the portal tract become necrotic
•seen in phosphorus poisoning.
5. MASSIVE NECROSIS / ACUTE YELLOW ATROPHY
•there is necrosis of considerable number of the cells in a lobule.
•Poisons: Carbon tetrachloride, chloroform, phosphorus
•liver is yellow and smaller in size.
•More severe then others.
6. PARACENTRAL NECROSIS
•peculiar type of wedge-shaped necrosis occurring only on one side of
the central vein extending up to the periphery.
•This type is encountered in Rift-valley fever and in uremic conditions.
SAW DUST LIVER/ Diffuse Necrosis
The foci of necrosis may be few or many, and appear to the
naked eye as though saw dust is sprinkled on the liver.
CIRRHOSIS
•Cirrhosis of the liver is chronic hepatitis characterized by
degeneration and hyperplasia of hepatic cells and fibrosis
•The stimulus for the fibroblastic proliferation is some irritant,
chronic and severe enough to produce degeneration and
necrosis of the parenchymatous cells.
•The irritant may reach the liver through (a) The portal vein
(b) hepatic artery and (c) Bile ducts.
Classification
The classification of cirrhosis based on route of
infection
1. Portal or nodular cirrhosis
2. Multinodular or Atrophic or Gindrinker’s or
Laennec’s cirrhosis
3. Biliary cirrhosis (Monolobular or hypertrophic
cirrhosis)
4. Other forms of cirrhosis
1. PORTAL OR NODULAR
CIRRHOSIS
Aetiology
•Toxic plants: Crotalaria saggitalis in horses
•Chemicals: repeated exposure to chloroform, carbon
tetrachloride and phosphorous.
•Long continued intestinal toxaemia
Pathogenesis
1. When the irritant is conveyed via the portal veins, changes are first at
the periphery of the lobules –area next to the portal tract.
•The following changes take place: Proliferation of interlobular connective
tissue, degeneration or necrosis of the hepatic tissue, Infiltration of
lymphocytes and macrophages
2. If irritant enters the liver through the hepatic artery , changes of
damage are first noticed in the tissues of portal canal and inter-lobular
connective tissue. The features here are: lymphocytic infiltration,
proliferation of the connective tissue slowly encroaches into the lobule
which produces changes.
Gross pathology
•liver is hard and firm.
•liver surface is uneven and nodula
•In the early stages the liver may be large. But as the condition
progresses, due to atrophy of the parenchyma, the liver is reduced in size.
Histopathology
•architecture of the liver is lost.
•characteristic picture is the increase in fibrous tissue within and around
the lobules
•Central veins in some lobules are either absent or are placed
eccentrically (Indication of pseudolobulation).
2. MULTINODULAR CIRRHOSIS
•Multinodular Or Atrophic Or Gindrinker's Or Laennec's Cirrhosis
Aetiology
• Deficiency of Vitamin B complex and lipotropic factors, especially in
drunkards produces this condition.
Pathogenesis
•Lack of Vitamin B complex and lipotropic factors will result into a highly
fatty liver and subsequently a severe fibrovascular proliferation.
•Ischemia develop by pressing sinusoids leads to necrosis of parenchyma,
fat globules occupy the cells.
•Cytoplasm pushes nucleus to one side leads to formation of Signet Ring.
Gross pathology
• The gross changes are more or less similar to portal cirrhosis.
Histopathology
• The hepatocytes show severe fatty changes.
• The bulging cells, pressing on the sinusoids produce
ischemia resulting in necrosis of the parenchyma.
• New capillaries form and invade the lobule and connect the
central vein with the portal vessels.
• There is proliferation of the fibrous tissue which is infiltrated
by chronic inflammatory cells.
• The fibrous tissue divides the parenchyma into smaller
lobules.
• Some surviving cells proliferate and form nodules (Hobnail).
• Contracting fibrous tissue makes the liver smaller and hence
“Atrophic cirrhosis” results.
BILIARY CIRRHOSIS
•Biliary cirrhosis or monolobular or hypertrophic cirrhosis
Aetiology
•The causes are :-
•Cholangitis-the inflammatory exudate clogs the bile ducts
•Stone in the common bile duct.
•Obstruction of biliary passages by flukes (Chlonorchis sinesis)
and ascarids.
•Stricture of the bile duct.
•Extramural pressure on the bile ducts from tumour of pancreas
Gross pathology
• The liver is enlarged, greenish and the surface is either smooth or
finely granular.
Histopathology
• Here, the connective tissue encircles individual lobules (hence
monolobular).
• The bile ducts may be dilated and tortuous.
• There is great infiltration of the connective tissue with chronic
inflammatory cells.
• Newly formed non-functional bile ducts are also found.
• Hepatic cells reveal degenerative changes.
OTHER FORMS OF CIRRHOSIS

4. Pericellular cirrhosis
•The fibrous tissue invades the parenchyma and encircles
individual cells.
5. Pigment cirrhosis
•fibrotic condition of the liver that is found in
hemochromatosis
•large amounts of hemosiderin deposited in the hepatic cells
irritate the organ causing cirrhosis.
6. Glissonian cirrhosis
•not true cirrhosis since the liver as a whole is not affected
•Inflammation and thickening of the Glisson’s capsule (layer
of connective tissue surrounding the liver near portal triad)
extends to the adjacent liver parenchyma.
7. Cadiac or central or congestive or stasis cirrhosis
•In chronic venous congestion resulting from cardiac lesions
(right side heart failure), the cells round about the central veins
suffer degeneration and necrosis due to pressure and hypoxia.
8. Parasitic cirrhosis
•chronic obstruction of the bile ducts by flukes or other parasites.
•The changes are localized and are usually restricted in animals to
fibrosis of parenchyma for a short distance around the biliary
passages.
•e.g. Fasciola hepatica causes clay pipe liver or pipe stem liver.
SEQUELAE / EFFECTS OF
CIRRHOSIS
1. Due to disturbance in portal circulation
•Ascites due to:- Increased hydrostatic pressure in portal veins, Decreased
colloid osmotic pressure,
•Varicosity and rupture of esophageal veins may lead to hematemesis.
•Splenomegaly.
•Chronic gastroenteritis
2. Jaundice
3. Anemia – since iron and erythrocyte maturation factor cannot be stored.
4. Vitamin A deficiency since Vitamin A cannot be stored in the liver.
5. Cholengitis (Inflammation of bile duct)
6. Cholecystitis (Inflammation of gall bladder)