Lecture 25 diseases of liver and pancreas

Prof.Dr.
Khalil Hassan Zenad
Aljeboori
Copyrights©2017lAliraqiaUniversitylDentistrylPathologylProf.Dr.KhalilHassanZenadAljeboori.
Lecture 25
DISEASES OF LIVER AND
PANCREAS

Chronic venous congestion:
Is common findings in liver occur in circulatory deficiency, grossly contrasted
red areas due to congestion of blood vessels and yellow brown areas
(degeneration) produce nutmeg appearance.
Infarction:
Occur when block in portal vein or hepatic artery branch, associated with
tumor in liver.
Degenerations:
Cloudy swelling, fatty changes, amyloid, glycogen disorders (D.M) glycogen
storage disease, lipid storage disease.
Circulatory disturbances:

Caused by a variety of poisons, infections, metabolic disorders:-
1. Diffuse necrosis: (acute yellow atrophy)
It Caused by a variety of chemical poisons, viral affections, metabolic disturbances,
complicated pregnancy and hyperthryroidism.
The liver is shrunken and wrinkled capsule, mottled patchy yellowish and red color,
microscopically, necrosis of nuclei, fatty degeneration in chronic form, regeneration of
liver cells, fibrosis and cirrhosis.
2. Focal necrosis:
Occur in a variety of infections such as thypoid fever, pneumonia…
3. Zonal necrosis:
A.Central (nutmeg liver, carbon tetrachloride ,and chloroform poisoning.
B.Mid-zonal ( yellow fever)
C.Peripheral Eclampsia, phosphorus poisoning.
Necrosis:

toxic complication of later months of pregnancy in which
hypertension albuminuria, edema, convulsion.
The lesion in liver are areas of necrosis confluent with
patchy distributed hemorrhage under the capsule give the
liver mottled appearance.
Eclampsia

Caused by:
1.Bacterial infection, pyogenic abscesses T.B.
2.Protozoal infection amebic abscess.
3.Spirochetal infection weil's disease , syphilis.
4.Viral infection such as viral hepatitis.
5.Helminthic infection, hydatid cyst, bilharziasis.
6.Fungal infection, such as actionomycosis.
Infections of liver:

May result from:
a) Spread of organisms to liver.
b)Extension of organism to liver from bile duct (cholangitis).
c) Spread to liver from contagious disease.
d)Infection carried to liver by hepatic arteries in septicemia.
e) Penetrating traumatic injuries. Staph, streptococcus, E.Coli are common
bacteria.
Pyogenic abscesses:

Multiple hepatic abscesses most frequently as an
extension of appendicitis, the abscess more abundant on
right lobe it’s size from microscopical size to few
centimeters and coalesce to form large cavities so
extensive necrosis, cellular disintegration and leukocytes
accumulation found.
Pylephlebitis:

Tuberculosis:
Mainly miliary T.B, associated with caseating granuloma.
Visceral leishmaniasis (kala-azar):
Infection of reticuloendothelial cells by leishmania donavani, liver enlarged
fatty, narrowed sinusoids, swelling of kupffer cells contain the parasites.
Amebic abscess:
Spread of E.histolytica from intestine by portal vein so lysis if liver tissue
accompanied by inflammatory and multiple abscesses coalesce to form
considerable size.

Due infection by leptospira icterohemorragiae and affect
kidney, liver so enlarged and bile stained, microscopically
degeneration, necrosis, inflammation focal or diffuse,
biliary stasis.
Weil’s disease:

Syphilis:
 Congenital syphilis-diffuse pericellular fibrosis around
each cell with mononuclear cells infiltration.
 Acquired syphilis:
Acquired gumma, single or multiple in the tertiary stage,
there is necrotic mass with thick fibrous capsule healing
induce scars dividing the liver into coarse nodules.
Diffuse liver necrosis=acute yellow atrophy.

Viral hepatitis:
Both virus A and B and C affecting liver A has 20-40 days of incubation period, B,C have
longer 60 days and more incubation period, the infection occur through blood or infected
materials containing human serum or plasma but A affection through food and water
contaminated. Liver, spleen, lymph node may be enlarged and jaundice.
Yellow fever:
it caused by virus and transmitted to man by mosquito, the liver, pale yellow, greasy
with multiple areas of hemorrhage so there is mid-zonal necrosis, with area of fatty
change and hemorrhage. There is no inflammatory cells reaction.

Hydatid cyts:
It is space occupying lesion due to larval stage of Echinococcus granulosus,
the cyst wall composed of germinal cells layer from which grow daughter
cyst, broad capsule and scolices , surrounded by hyalinized layer and fibrous
layer outside.
Schistosomiasis (bilharziasis):
Portal fibrosis and cellular infiltration (mononuclear cells) auto immune
response with auto antibodies against liver and lung homogenate, correlate
with bilharzial hepatic fibrosis or cirrhosis.

Actionomycosis abscesses:
Also occurred as a result of spread infection by portal
blood, so multiple ragged abscess cavities are produced in
which actionmycotic colonies are found the ragged abscess
are purulent granulomas with radiating clubs of fungal
reaction (Ag-Ab) complexes.

a) Anatomical definition:
1. All part of liver are involved
2. Cellular necrosis
3. Nodular parenchymal regeneration
4. Diffuse fibrosis
5. Disorganization of the lobular architecture with connective tissue bands uniting
centrolobular zone with portal tract.
b) Clinical concepts include:
1. Chronic disease.
2. Liver cells failure with portal hypertension.
Cirrhosis of liver:

a) Morphological:
Portal, postnecrotic and biliary
b) Etiological:
Malnutrition, viral hepatits, cardiac failure, syphilis, Bilharzia , toxic
agents, disturbances in copper metabolism, hematochromatosis.
c) Functional:
1. Liver cells failure associated with jaundice, icterus, ascites.
2. Portal hypertension, is shown splenomegaly, esophageal varices
3. Activity of the disease whether progressive, regressive, stationary.
For classification:

Distinctive patterns of cirrhosis:
Of cases in central pathology institute and medical city.
1. Portal cirrhosis: 79% of cases Laennec, diffuse nodular, atrophic, hobnail,
alcoholic , nutritional and fatty cirrhosis.
Grossly: outer surface uniform nodules 2-3 mm, red brown ,hard.
Microscopically: fine fibrosis, micronodulation, and
pseudolobules,intracellular fat.
2. Post necrotic cirrhosis: toxic, chronic yellow atrophy, coarse nodular.
Grossly: large nodules 1cm or more in diameter, are not uniformly or
diffusely distributed.
Microscopically, fatty change is not usually present.

3. Cardiac cirrhosis, 14% congestive cirrhosis.
Grossly:Liver firm, reddish brown, granular
Microscopically: Fibrosis in portal zones as well as centrally proliferation
of portal C.T and bile duct. Similar in portal cirrhosis.
4. Biliary cirrhosis: 4% dark green liver, fine nodular surface grossly.
Microscopically: inspissated masses of bile distend the canaliculi fibrosis
and chronic inflammatory cells infiltration.

5. Bilharzial cirrhosis:
Grossly.Liver firm, brown red, thick capsule, dense scar like tissue around dilated portal
vein branch (pipestem fibrosis)
Microscopically:Fibrosis and granuloma involving the portal tract, cellular infiltration,
bilharzial pigment, two main type recognized:
1. Coarse periportal fibrosis ( clay pipe fibrosis).
2. Fine periportal fibrosis (diffuse bilharzial fibrosis) depending on large or small
portal tract are involved, bilharzial hepatic fibrosis of either type is occasionally associated
with portal or postnecrotic cirrhosis. Bilharzial hepatic lesions are met in 45% of patient
with urinary bilharziasis in Iraq.
6. Hematochromatosis: 1% similar features to mild portal cirrhosis with addition of large
amount of hemosiderin pigment.

1. Neonatal cirrhosis: short course of disease it's differentiation from neonatal hepatitis is emphasized.
2. Infantile cirrhosis: it begin in first 2 years follow some condition such as:
1) Atresia of bile duct
2) Galactosemia, liver large, fatty changes, bile stasis, liver become cirrhotic.
3) Congenital syphilis
4) Neonatal hepatitis, may lead to fibrosis.
5) Neimann-pick disease- may occur with it cirrhosis as a complication.
6) May follow viral hepatitis
7) Biliary atresia
8) Posthepatitic and post necrotic cirrhosis.
9) Cirrhosis accompanying the fibrocystic disease of pancreas and polycystic diseases of liver.
3. In India. Both, children and adult have ingested (bush tea) made from boiling leaves Crotolaria fulva and
Senecio discolor may close central and sublobular vein so hepatomegally, ascites and jaundice- similar in
Egyptian children(chiari’s disease) in which closing hepatic vein.
Cirrhosis in infancy and childhood

1) Post hepatitic cirrhosis.
2) Laennec’s cirrhosis in born errors of metabolism responsible for cirrhosis.
3) Glycogen storage disease-in which periportal fibrosis and cirrhosis develop.
4) Wilson’s disease also cirrhosis develop
5) Gaucher’s disease, also scaring, nodular liver.
6) Lignac-Detoni-Fanconi-Syndrome: also nodular, cirrhosis develop in liver
7) Hurler’s syndrome- liver also enlarged and cirrhotic.
Term: juvenile cirrhosis: in patient between 2-16 years, it is:

1. Benign:
1)adenoma.
2)Hemangioma.
2. Malignant:
1)Hepatocellular carcinoma.
2)secondary metastatic carcinoma from intestine,stomach.
3)cholangio carcinoma.
Liver Neoplasms

Lecture 25 diseases of liver and pancreas

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Lecture 25 diseases of liver and pancreas

Similar to Lecture 25 diseases of liver and pancreas (20)

More from Green-book

More from Green-book (20)

Recently uploaded

Recently uploaded (20)

Lecture 25 diseases of liver and pancreas