Hepatitis & Cirrhosis
Dr. Gehan Mohamed
Dr. Abdelaty Shawky
Learning objectives
 Understand the normal Liver Functions so can predict what
is the clinical picture when liver failure occur.
 Recognize definition of hepatitis and discuss its
types(Acute, Chronic, Fulminant).
 List different Causes and Patterns of hepatitis .
 - Understand the differences between different types of viral
hepatitis regarding Transmisson, Carrier state,
Chronicity.
 List the cellular changes in both Acute and chronic
Hepatitis.
Learning objectives
 Understand difference between chronic
hepatitis and fulminant hepatitis.
 Discuss definition ,etiology of cirrhosis and its
variable gross pictures.
discuss the Pathogenesis of Hepatic
Encephalopathy.
Hepatitis
* Definition:
Hepatitis is necro-inflammatory liver disease
characterized by the presence of inflammatory
cells in in the portal tracts then spillover to
neighboring parynchmatous liver cells .
Normal liver
Hepatitis
* Causes of hepatitis:
1. Viral: hepatotropic (A, B, C, D….) and nonhepatotropic (cytomegalovirus and Epstein bar
virus).
2. Alcoholic.
3. immune mediated: autoimmune hepatitis.
4. Drug induced.
5. Metabolic disorders: Hemochromatosis (due to
iron accumulation) and Wilsons disease (copper
accumulation) can cause liver inflammation and
necrosis.
6. Other causes:
 Biliary obstruction by gall stones .
 ischemic hepatitis associating shock.
 giant cell hepatitis ,common in children may
be due to viral infection.
Virus
agent
Transmisson.
Carrier
state
Chronic
Hep-A
Hep-B
RNA
Feco-oral
DNA
Parenteral
Hep-C
RNA
- Parenteral
-maternal to fetal
maternal
to fetal
-sexual
-
Sexual
-drug
abusers
-
drug
abusers
None
0.1-1.0%
0.2-1.0%
None
5-10%
>50%
Patterns of hepatitis
 Carrier state: is an individual who harbor and can transmit
the virus but has no manifest symptoms.
 Acute hepatitis: hepatitis is considered acute if its
manifestation persist for period less than six months.
 Chronic hepatitis: hepatitis is considered chronic if there
is clinical or seriological evidence of liver pathology
persistent for more than six consequent months.
 Fulminant hepatitis: hepatitis is considered fulminant if
massive hepatic cell necrosis happened within few
weeks leading to acute hepatic failure and hepatic
encephalopathy.
Acute Viral Hepatitis
Diagnosis of acute hepatitis
1. Clinical picture.
2. Laboratory investigations.
3. Histopathologic diagnosis of liver biopsy.
1. Clinical picture of acute viral hepatitis (AVH):
 AVH is more likely to be asymptomatic in younger people.
 If AVH is symptomatic, it may be either non specific or
specific symptoms.
 Initial features are of nonspecific flu-like symptoms include
malaise, muscle and joint aches, fever, nausea or vomiting,
diarrhea, loss of appetite, and headache.
 More specific symptoms and signs are: yellow color of
the eyes and skin (i.e., jaundice) and abdominal discomfort
from hepatomegaly (swelling of the liver).
jaundice
2. Laboratory investigations of AVH:
1. Ultrasound examination to detect any biliary stones,
hepatomegaly.
2. Serologic examination to detect :
a- Elevated hepatic enzymes as
- aspartate aminotransferase(AST)
- alanine aminotransferase(ALT).
b- Viral hepatitis markers as HBV sAg, HCV Antigen and
Antibody
c- Autoantibodies as in case of autoimmune hepatitis.
d- Polymerase chain reaction(PCR) to identify the virus.
3. Histopathology of AVH:
 The normal liver architecture is usually preserved.
 Inflammatory cellular infiltrate (plasma cells, lymphocytes and
neutrophils) inside portal tracts and around foci of necrosis.
 The hepatocytes show:
 Apoptosis: the cells appear acidophilic (Councilman
bodies).
 Hydropic degeneration.
 Cholestasis means accumulation of bile in liver cells even
canalicular bile plugs can be formed in cases of hepatitis
caused by biliary obstruction by stones.
 Hepatocyte regeneration.
Acute - Hepatitis - Chronic
Liver Biopsy – Chronic Hepatitis: the inflammatory cells
are present in portal tract and in periportal areas
Councilman bodies are eosinophilic dead apoptotic liver cells
Cholestasis: accumlation of bile inside
hepatocytes
Chronic hepatitis
* Clinical picture of Chronic hepatitis:
 Often no symptoms at all.
 It is commonly identified on blood tests performed
either for screening or to evaluate nonspecific
symptoms.
 nonspecific symptoms such as malaise, tiredness
and weakness.
 The occurrence of jaundice indicates advanced
liver damage.
 On physical examination there may be
enlargement of the liver
* Histopathology for chronic hepatitis:
I. Portal tracts show:
a. Piece meal necrosis: necrosis of the hepatocytes at the
limiting plate.
b. Portal tract inflammation:
 mononuclear inflammatory cells; lymphocytes,
macrophages with occasional plasma cells.
 Lymphoid follicle formation (with HCV).
 Bile duct inflammation (with HCV).
II. The hepatic lobules show:
 Degeneration: Fatty change (with HCV).
 Necrosis:
 Focal (spotty) necrosis surrounded by
inflammatory cells.
 Confluent necrosis and bridging necrosis: with
progressive hepatitis.
 Dysplasia of hepatocytes (precancerous).
 Von Kupffer cell hyperplasia.
 Specific diagnostic lesions:
• Ground glass appearance of hepatocytes
(with HBV).
• Presence of cupper particles inside the
hepatocytes (with Wilson disease).
• Rosseting: occasional arrangement of a group
of hepatocytes around a central bile
canaliculus. Characteristic of auto-immune
hepatitis.
III. Fibrosis & Cirrhosis.
 Grading of chronic hepatitis by assessing
the degree of activity: this is done by
examining 4 parameters; portal inflammation,
piece meal necrosis, focal (spotty) necrosis and
confluent necrosis. The degree of activity is
graded as mild, moderate and marked
according to the score of these parameters.
 Staging of chronic hepatitis by assessment
of the degree of fibrosis
chronic hepatitis with piece
meal necrosis
Histopathology show ground glass hepatocytes, which are seen
in chronic hepatitis B infections represent accumulations of viral
antigen in the endoplasmic reticulum. H&E
Histopathology show lymphoid aggregates and fatty
change of the hepatocytes, which are characteristically
seen in chronic hepatitis C infections
Liver cirrhosis
* Definition:
Chronic Diffuse, irreversible disorder of the liver
characterized by;
1. Liver cell degeneration and necrosis.
2. Replaced by extensive fibrosis .
3. Compensatory hyperplasia of the remaining healthy
liver cells leading to the formation of the
Regenerating parenchymal nodules.
4. Complete loss of normal architecture.
* Etiological classification of Cirrhosis:
A. Congenital cirrhosis:
1. Congenital syphilis.
2. Hemochromatosis.
3. Glycogen storage disease.
4. Wilson disease.
5. α1 antitrypsin deficiency.
B. Acquired cirrhosis:
1. Post-hepatitic (viral).
2. Alcoholic.
3. Biliary cirrhosis.
4. Cirrhosis caused by circulatory disorders e.g.
chronic right sided heart failure.
* Complications of Cirrhosis:
1. Liver cell Failure
2. Portal hypertension
3. Hepatocellular carcinoma.
Normal Liver
Micronodular cirrhosis
Macronodular Cirrhosis
Normal Liver Histology
CV
PT
Liver Biopsy – Cirrhosis
Liver Biopsy – Cirrhosis:
Liver cell failure
* Normal Liver Functions:
 Metabolism – Carbohydrate, Fat & Protein.
 Secretory – bile, Bile acids, salts.
 Excretory – Bilirubin, drugs, toxins.
 Synthesis – Albumin, coagulation factors.
 Storage – Vitamins, carbohydrates etc.
 Detoxification – toxins, ammonia, etc.
* Manifestations of liver cell failure
1. Jaundice: yellow colour of skin ,mucosa due to
hyperbilirubinemia as liver became unable to
conjugate bilirubin so it not secreted in urine and so
it is reabsorbed by blood and precipitate in tissues.
2. Coagulopathy:→ bleeding tendency
3. Hypoproteinemia specially albumin → decrease
osmotic pressure of blood → generalized edema
.
4. Hepatic Encephalopathy: caused by the
inability of the liver to detoxify amonia which
produced by effect of intestinal bacteria on
food so this amonia can affect brain causing
coma.
5. Hyperestrogenemia due to decrease
estrogen degradation by the diseased liver
leading to gynaecomastia and testicular
atrophy in males
Gynaecomastia in cirrhosis i.e. enlargement of male
breast due to failure of degradation of estrogen by the
diseased liver.
Portal hypertension
 Portal hypertension leading to;
1. Varices: esophageal varices, piles.
2. Splenomegaly due to splenic congestion.
3. Ascites which is accumulation of transudate
in the peritoneal cavity.
Ascitis in Cirrhosis
Cirrhosis
Clinical
Features
Thanks