DIGESTIVE SYSTEM
DISEASE
Li shuhua
?The Gastrointestinal Disease
?The Liver and The Biliary Disease
The Gastrointestinal
Disease
?一,gastritis
?二,peptic ulcer
?三,the gastrointestinal carcinoma
一,gastritis
?（一） acute gastritis
?
?（二） chronic gastritis
（一） acute gastritis
? 1,acute irritated gastritis
? 2,acute hemorrhagic gastritis
? 3,acute corrosive gastritis
? 4,acute infective gastritis
（二） chronic gastritis
?Pathologic types
1,chronic superficial gastritis
2,chronic atrophic gastritis
etiology
? 1.chronic irritation
? 2.reflux of the duodenal juice
? 3.autoimmune injury
? 4.helicobacter pylori
chronic superficial gastritis
? Mostly happened,20-40%
? Distributed diffusely,mainly in pylorus
antrum
morphology
⒈ inflammatory changes limit to the upper
1／ 3 of the mucosa；
⒉ a lymphocytic and plasma cell
infiltrate in the upper mucosa；
⒊ swelling, degeneration and necrosis of
the superficial mucosal epithelium
2 chronic atrophic gastritis
? Types;
? type A, autoimmune gastritis leads to
? pernicious anemia
? type B, no association with autoimmune
?
?Morphology,atrophy
（ 1 ）,the color of the mucosa
turn gray and thin,
（ 2 ）,the vessels under the
mucosa is easy to see
microscope
? mucosa,
? like little granular
? gland loss and expendation
?
? lymphocytic and plasma cell infiltrate
in the proper lamina
? decreasing of chief cell and
? parietal cell
intestinal metaplasia
refers to the replacement of
gastric epthelium with columnar
and goblet cells and paneth cell
of intestinal variety；
Clinical
features
Epithelium atrophy
Abdominal discomfort
Nausea
Vomiting
?decreasing of chief cell and
? parietal cell
pepsinogen
Gastric acid
? Hypochlorhydria and pernicious
anemia,severe parietal cell loss
? Risk of gastric carcinoma:2%-4%
peptic ulcer
?peptic ulcers are chronic and
solitary lesions occuring in the
gastrointestinal tract
?At least 98% of peptic ulcers are
either in the first portion of the
duodenum or in the stomach,in a
ratio of about 4:1
etiology
?Main factors(70%-90%):
? HP(infecting)+ pH(gastric acid )
?
others factors:drugs:NSAID
heavy smoking
alcohol
Zollinger-Ellison
syndrome
Mucosal defenses
? Secretion of mucus and bicarbonate into
the surface of mucosa
? Rapid gastric epithelial regeneration
? Robust mucosal blood flow to sweep away
hydrogenions
morphology
? Size,round,2-4cm in diameter
? Depth,may penetrate into the muscularis
propria
? The wall of the ulcer,orderly
? The base,clean and plain
? The margins,edema of adjacent mucosa
and no elevation
Microscopic appearance
?Open ulcer include four zones:
? (from inside to outside）
① necrosis debris
② inflammation
③ granulation
④ scar
chronic
necrosis inflamm
ation
granulatio
n
scar
Ends and complications
?1.healing：
? owing to clearing of the
inflammatory exudate and necrosis，
the ulcer is repaired by the
granulation
Ends and complications
?2.hemorrhage：
? chief complications
? and life-threatening
? ratio,1/3
? cause,erosion of big vessel
Ends and complications
?3.perforation：
Ratio,5%
location,duodenal ulcers
result,peritonitis
Ends and complications
?4.Pyloric stenosis
ratio,3%
?cause,scar withdrawing
?Result,nausea,vomiting、
misnutrition
Ends and complications
?5.malignant transformation：
? ratio,<1%
? location,only gastric ulcer
Gastrointestinal cancers
?（一） carcinoma of esophagus
?（二） gastric carcinoma
?（三） primary carcinoma of
? liver
（一） carcinoma of
esophagus
?1.origin:squamous cell carcinoma
and adenocarcinoma
?2.Location:the middle third >the
lower third >the upper third
?3.Age,>40y especially:60-64y
?4.Sex,male>female
etilogy
?1 Dietary,deficiency of vitamins(A C）
? deficiency of trace metals
? fungal contamination
? high content of nutrosmines,
?2,Environmental factor,lack Mu
?3,Life style, alcohol and tobacco abuse
?4.virus infection:
Pathologenesis
?Pathologic types
?1,early carcinoma of esophagus
?2,middle and late carcinoma of
esophagus
1,early carcinoma of
esophagus
?Limit to the submucosa,no lymp-
hatic metastasis
?5years existence rate:90%
?Prognosis is good
2,middle and late
carcinoma of esophagus
Pathologic types,
?（ 1） medullary type
?（ 2） fungating type
?（ 3） ulcerative type
?（ 4） narrow type
ca
rc
in
om
a
o
f
es
op
ha
gu
s
Pathologic types
?① squamous cell carcinomas
?② adenocarcinomas
?③ undifferentiated carcinomas
squamous cell carcinomas
region:preceded by mucosal epithelial
dysplasia and cancer in situ
ratio:90%
grading:
high differentiation carcinomas
midium differentiation carcinomas
low differentiation carcinomas
Spread of tumor
?1.invasion,adjacent structure
?2.lymphatic metastasis：
? happen extensively and early,
? spread along the lymph network
?3,Hematogenous matastasis:
? happen lately,spread to the liver and
lung
（二） gastric carcinoma
?1.Origin,stem cell in the gland
? and mucosal epithelial
?2.Location:the pylorus antrum,
lesser curvature of stomach and
the front and back wall
?3.Age,40-60y
?4.Sex,male:female=3:1 or 2:1
1,early gastric carcinoma
?Limit to the submucosa,lymphatic
metastasis may occur
?5years existence rate after
operation:>90%
?Micro gastric carcinoma:<0.5cm
?small gastric carcinoma:0.6-1cm
Pathologic types
? Protruded type,beyond the mucosa
? Superficial type,parallel the mucosa
? Excavated type,bellow the mucosa
2,advanced gastric
carcinoma
A neoplasm that has extended
below the submucosa into the
muscular wall
Pathologic types:
? （ 1） fungating type
? （ 2） ulcerative type
? （ 3） infiltrating type
Linitis plastica
Microscopic types
?① papillary ad e no carcinoma；
?② Tubular adenocarcinoma
?③ mucoid adenocarcinoma ；
?④ signet-ring cell cancer
?⑤ undifferentiated carcinoma
spread of tumor
?1,invasion,adjacent structure
?2,lymphatic metastasis：
?3,hematogeneous matastasis:
?4,transcoelomic metastasis
?
1.invasion
?adjacent structure:
? antrum,duodelum,pancrea,the left
leaf of the liver,greater omentum
? cardia and fundus,esophage,
liver,greater omentum
lymphatic metastasis
? Spread like the lymph flow:
? paracoronary venus and subpylorus lymph
node abdominal aorta liver
? thoracic duct the left supraclavicular
lymph nodes
hematogeneous matastasis
? Mostly spread to the liver through portal
vein
? Subsquently spread to the lung, bone and
brain
transcoelomic metastasis
?Type,mucoid adenocarcinoma ；
signet-ring cell cancer
Location,greater omentum
peritoneum
ovary(Krukenberg tumor）
（三） carcinoma of large
intestine
? Happen extensively(only lower than
? gastric cancer in the Gastrointestinal
cancers)
?5years existence rate:90%
?Location:rectum+sigmoid colon>2/3
?caecum+ascending colon+ transverse
colon +decending colon<1/3
etiology
? High fat content disorder of the bacteri
? High protein content transit time increase
? Low fiber content nutrition concetration
? change
?
?carcinoma of oncogene overexpression
large intestine tumor suppressor gene mute
Pathological types
??protruded type
??ulcerative type
??infiltrating type
??colloid type
Microscopic types
??papillary adenocarcinoma；
? ② pipular adenocarcinoma
? ③ mucoid adenocarcinoma
? ④ signet-ring cell cancer
? ⑤ undifferentiated carcinoma
? ⑥ squmous cell carcinomas
? ⑦ adenosqumous carcinomas
Spread of tumor
?1.invasion,adjacent structure
?2.lymphatic metastasis：
?3,hematogeneous matastasis:
?4,transcoelomic metastasis
The Liver and The Biliary
Disease
?一,viral hepatitis
?二,liver cirrhosis
viral hepatitis
?viral hepatitis is an infective disease
which was caused by hepatitis viruses
and characterized by degeneration
and necrosis
?Types:HAV HBV HCV HDV HEV
HGV
Etiology and Mechanism
?Cause:
? heptitis (A,B,C,D,E,G) virus
?Mechanism,remain unknown
Route of transmission
?1.HAV and HEV are spread by
ingestion of contaminated
water and foods and are shed
in the stool,
?Latency:2-3weeks（ HAV） and 2-8
weeks (HEV)
?2.HBV,HCV,HDV:
? blood and body fluids are the primary
vehicles of transmissin
? Vertical transmission from mother to
child during birth
?Body secretions such as semen,
saliva,sweat,tears,breast milk,and
pathologic effusions.
morphology
1.hepatocyte degeneration and
hepatocyte necrosis
2.inflammatory infiltrate;
3.fibrosis hyperplasia and
hepatocyte regeneration
hepatocyte degeneration
and hepatocyte necrosis
?hepatocyte degeneration,
（ 1） diffuse swelling,balloon
ing degeneration
（ 2） acidophilic degeneration
肝细胞疏松化气球样变性
hepatocyte necrosis
（ 1） acidophilic necrosis
（ 2） spotty necrosis
(3)lytic necrosis
(4)piecemeal necrosis
(5)bridging necrosis
Inflammatory infiltrate
?Lymphocyte and monoblast
infiltrate the necrosis and portal
area。
3,fibrosis hyperplasia
and hepatocyte
regeneration
?（ 1） Kupffer cells hypertrophy
and hyperplasia
?（ 2） mesenchymal cell and
fibroblast hypertrophy
?（ 3） hepatocyte regeneration
Kupffer cells hypertrophy
and hyperplasia
?Kupffer cells are often laden
with lipofuscin pigment,they
may protrude into the sinusoid
or may be rushed away
mesenchymal cell and
fibroblast hypertrophy
?They may diffentiate into histiocytes
and inflammatory cells,
?They may also result in cirrhosis if
there is heavy necrosis
hepatocyte regeneration
?Hepatocyte necrosis is repaired by
the regeneration of around normal
hepatocyte
Pathologic types
? Acute hepatitis
Common hepatitis mild
? chronic hepatitis moderate
? severe
? acute Severe hepatitis
? Severe hepatitis
? subacute Severe hepatitis
1,Acute common hepatitis
Mostly happened,
anicteric mild
Pathologic types:
icteric moderate
Cause,HBV
Morphology
?① wide degeneration ＋ diffuse
necrosis
degeneration:;plasma rarefaction
and ballooning degeneration,
necrosis,spotty necrosis ＋
acidophilic necrosis
?② mild inflammatory cells infiltrate
the necrosis and portal area
?③ regeneration,reticular fiber did
not ellapse and the structure and
function of liver can be repaired by
the hepatocyte regeneration
Clinic features
? ① liver enlargement,right upper
quadrant pain：
? ② SGPT
? ③ Jaundice
ends
?Recover in half a year or one
year(HBV)；
?Some cases may advance into
? chronic hepatitis and even
severe hepatitis
Chronic common hepatitis
?Refers to the chronic hepatitis
? last over half a year
（ 1） mild types
Morphology:
1.spotty necrosis and causal
piecemeal necrosis 。
2,mesenchymal cell and fibroblast
hypertrophy in portal area
3.hepatocyte regeneration to keep the
integrity of lobular structure
Moderate types
Morphology:
1.obvious necrosis,moderate piecemeal
necrosis and characteristic bridging
necrosis
2,mesenchymal cell and fibroblast hypertrophy
,linking of fibrous septa between lobules
3.hepatocyte regeneration,integrity of most lobular
structure can be maintained
（ 3） severe types
Morphology:
1.severe massive necrosis and wide
bridging necrosis 。
2,mesenchymal cell and fibroblast
hypertrophy lead to fibrous septa
which devide the lobules
3.hepatocyte irregular regeneration
Ground –glass
hepatocyte
?A finely granular,eosinophilic
cytoplasm contain massive
quantities of HBsAg in the form
of spheres and tubules
? Pseudolobule formation
? become harden and granular-look
? Early cirrhosis
3 Severe viral hepatitis
?This disease is very serious
?Pathologic type
（ 1） acute Severe hepatitis
?（ 2） subacute Severe hepatitis
（ 1） acute Severe hepatitis
?The disease advance acutely and
rapid,with high fatality rate
morphology
Acute yellow or red liver atrophy
?Microscopic view,serious and wide massive
necrosis,migrate from the central to the
portal area,but regeneration was invisible,
?Hepatic cord dissociation
? Hepatic sinusoid extend and hyperemia
and hemorrhage,Kupffer hyperplasia and
? phagocytose debris and pigment
? Lymphocyte and macrophage infiltrate the
portal area
eyesight
?The liver turn small,about 600-800g
in weight,
?the capsule shrink and exhibit yellow
or red in colour
Clinic features
?Serious jaundice
?Hemorrhagic tendency
?Liver failure
?DIC
?Cause of death:hepatic coma
（ 2） subacute Severe hepatitis
It may be natural process or be
an end of acute severe
hepatitis or acute common
hepatitis
morphology
?Microscopic view:
1.wide hepatocyte necrosis;
2.hepatocyte modular regeneration。
?3.reticufiber ellapse and
collagenous fibrosis
?4.inflammatory infiltrate
?5.cholestasis of bilary canaliculi
? around the lobule
Eye-sight
? The liver turn small at diffent degree,,the
capsule shrink and exhibit yellow -green in
colour
二,liver cirrhosis
?Repeative diffuse hepatocyte
necrosis and the subsquent
fibrosis and hepatocyte
regeneration nodules result in
the damage of the constructure
and the blood of lobule
leading to the transformation
and cirrhosis
Pathologic types
?（一） portal cirrhosis
?（二） postnecrosis cirrhosis
?（三） biliary cirrhosis
㈠ portal cirrhosis
?Etilogy:
?1.HBV
?2.chronic alcoholic toxicosis
?3.deficiency of nutrition
?4.toxin toxicosis
Microscopic view
? Pseudolobule formation,the wide fibosis
divide the hepatocyte regenerative nodules and
encompass them into several round hepatocyte
nodules with diffent size
? No central vein or more than ones or disarray
ones in the pseudolobule
? Inflammatory cells infiltrate the hepatocyte
nodules and fiber
? Cholestasis and regeneration of tiny bile
ducts
Eye-sight
? Volume,enlarge lessen
? Weight,enlighten,<1000g
? Surface:similar small nodules,<1.0CM
? Dissection,fibrosis around nodules
? the nodules exhibit yellow-brown or
? yellow –green in colour
假小叶
增生的纤维结缔组织
Clinic features
? Portal hypertension
?cause:
① obstruction of portal vein
② formation of abnormal
circulation
symptoms
?1.Splenomegaly,chronic congestion
?2.gastrointestinal congestion
? 3,hydroperitonia
? 4.collateral circulation:
? varices of the lower esophage vein
? varices of rectum vein
? varices of abdominal wall vein
hepatic insufficiency
?① estrogen↑→A,testis atrophy,male
breast growth,B.spider vascular
nevus
?② hemorrhage tendency
?③ jaundice
?④ hepatic coma:poison accumulation
ends
?1.death,hepatic coma
?2.massive hemorrhage of upper
digestive tract shock
?3.combine hepatic carcinoma and
infection。
㈡ postnecrosis cirrhosis
? Etiology:
? Hepatic viral, migrate from the subacute
severe hepatitis(HBV,HCV)
? Drug and poison
morphology
? Microscopic view:
1,pseudolobules formation with degeneration
and pigment deposition,
2,broad but ununiform fiber septa between
the pseudolobules
3.Inflammatory infiltrate and bile canaliculi
hyperplasia
Eye-sight
? Volume,lessen
? Weight,enlighten,
? Surface:unsimilar large nodules,the largest one
amounts to 6CM
? Dissection,broad fiber septa around nodules,
? the nodules exhibit yellow-brown or
? yellow –green in colour
primary carcinoma of liver
?Origin,liver cell or bile duct
cell
病理变化
morphology：
?1.massive tumor,huge and unifocal
? 〉 15CM,hemorrhage and necrosis
?2.mutinodules,distributed and
variable size
?3.diffuse cancer,small,perrmeating
widely (the entire liver)
巨块型肝癌
结节型肝癌
Microscop types
?1.hepstocellular carcinoma：
? most common
?2.bile duct cancer,less common,
? (clonorchiasis sinensis)
?3.mixture of the two,rare forms
etiology
? 1,HBV
? 2,Chronic liver disease(HCV and alcohol)
? 3.hepatocarcinogens in food(aflatoxin)
临床病理联系
?Development:“hepatosis →
cirrhosis →carcinoma
?Dignosis,AFP is very
important(70-98％ )。
扩散
2.淋巴道播散
肝内静脉播散
卫星小结形成
1.肝内扩散
3,种植性转移
DISEASE
Li shuhua
?The Gastrointestinal Disease
?The Liver and The Biliary Disease
The Gastrointestinal
Disease
?一,gastritis
?二,peptic ulcer
?三,the gastrointestinal carcinoma
一,gastritis
?（一） acute gastritis
?
?（二） chronic gastritis
（一） acute gastritis
? 1,acute irritated gastritis
? 2,acute hemorrhagic gastritis
? 3,acute corrosive gastritis
? 4,acute infective gastritis
（二） chronic gastritis
?Pathologic types
1,chronic superficial gastritis
2,chronic atrophic gastritis
etiology
? 1.chronic irritation
? 2.reflux of the duodenal juice
? 3.autoimmune injury
? 4.helicobacter pylori
chronic superficial gastritis
? Mostly happened,20-40%
? Distributed diffusely,mainly in pylorus
antrum
morphology
⒈ inflammatory changes limit to the upper
1／ 3 of the mucosa；
⒉ a lymphocytic and plasma cell
infiltrate in the upper mucosa；
⒊ swelling, degeneration and necrosis of
the superficial mucosal epithelium
2 chronic atrophic gastritis
? Types;
? type A, autoimmune gastritis leads to
? pernicious anemia
? type B, no association with autoimmune
?
?Morphology,atrophy
（ 1 ）,the color of the mucosa
turn gray and thin,
（ 2 ）,the vessels under the
mucosa is easy to see
microscope
? mucosa,
? like little granular
? gland loss and expendation
?
? lymphocytic and plasma cell infiltrate
in the proper lamina
? decreasing of chief cell and
? parietal cell
intestinal metaplasia
refers to the replacement of
gastric epthelium with columnar
and goblet cells and paneth cell
of intestinal variety；
Clinical
features
Epithelium atrophy
Abdominal discomfort
Nausea
Vomiting
?decreasing of chief cell and
? parietal cell
pepsinogen
Gastric acid
? Hypochlorhydria and pernicious
anemia,severe parietal cell loss
? Risk of gastric carcinoma:2%-4%
peptic ulcer
?peptic ulcers are chronic and
solitary lesions occuring in the
gastrointestinal tract
?At least 98% of peptic ulcers are
either in the first portion of the
duodenum or in the stomach,in a
ratio of about 4:1
etiology
?Main factors(70%-90%):
? HP(infecting)+ pH(gastric acid )
?
others factors:drugs:NSAID
heavy smoking
alcohol
Zollinger-Ellison
syndrome
Mucosal defenses
? Secretion of mucus and bicarbonate into
the surface of mucosa
? Rapid gastric epithelial regeneration
? Robust mucosal blood flow to sweep away
hydrogenions
morphology
? Size,round,2-4cm in diameter
? Depth,may penetrate into the muscularis
propria
? The wall of the ulcer,orderly
? The base,clean and plain
? The margins,edema of adjacent mucosa
and no elevation
Microscopic appearance
?Open ulcer include four zones:
? (from inside to outside）
① necrosis debris
② inflammation
③ granulation
④ scar
chronic
necrosis inflamm
ation
granulatio
n
scar
Ends and complications
?1.healing：
? owing to clearing of the
inflammatory exudate and necrosis，
the ulcer is repaired by the
granulation
Ends and complications
?2.hemorrhage：
? chief complications
? and life-threatening
? ratio,1/3
? cause,erosion of big vessel
Ends and complications
?3.perforation：
Ratio,5%
location,duodenal ulcers
result,peritonitis
Ends and complications
?4.Pyloric stenosis
ratio,3%
?cause,scar withdrawing
?Result,nausea,vomiting、
misnutrition
Ends and complications
?5.malignant transformation：
? ratio,<1%
? location,only gastric ulcer
Gastrointestinal cancers
?（一） carcinoma of esophagus
?（二） gastric carcinoma
?（三） primary carcinoma of
? liver
（一） carcinoma of
esophagus
?1.origin:squamous cell carcinoma
and adenocarcinoma
?2.Location:the middle third >the
lower third >the upper third
?3.Age,>40y especially:60-64y
?4.Sex,male>female
etilogy
?1 Dietary,deficiency of vitamins(A C）
? deficiency of trace metals
? fungal contamination
? high content of nutrosmines,
?2,Environmental factor,lack Mu
?3,Life style, alcohol and tobacco abuse
?4.virus infection:
Pathologenesis
?Pathologic types
?1,early carcinoma of esophagus
?2,middle and late carcinoma of
esophagus
1,early carcinoma of
esophagus
?Limit to the submucosa,no lymp-
hatic metastasis
?5years existence rate:90%
?Prognosis is good
2,middle and late
carcinoma of esophagus
Pathologic types,
?（ 1） medullary type
?（ 2） fungating type
?（ 3） ulcerative type
?（ 4） narrow type
ca
rc
in
om
a
o
f
es
op
ha
gu
s
Pathologic types
?① squamous cell carcinomas
?② adenocarcinomas
?③ undifferentiated carcinomas
squamous cell carcinomas
region:preceded by mucosal epithelial
dysplasia and cancer in situ
ratio:90%
grading:
high differentiation carcinomas
midium differentiation carcinomas
low differentiation carcinomas
Spread of tumor
?1.invasion,adjacent structure
?2.lymphatic metastasis：
? happen extensively and early,
? spread along the lymph network
?3,Hematogenous matastasis:
? happen lately,spread to the liver and
lung
（二） gastric carcinoma
?1.Origin,stem cell in the gland
? and mucosal epithelial
?2.Location:the pylorus antrum,
lesser curvature of stomach and
the front and back wall
?3.Age,40-60y
?4.Sex,male:female=3:1 or 2:1
1,early gastric carcinoma
?Limit to the submucosa,lymphatic
metastasis may occur
?5years existence rate after
operation:>90%
?Micro gastric carcinoma:<0.5cm
?small gastric carcinoma:0.6-1cm
Pathologic types
? Protruded type,beyond the mucosa
? Superficial type,parallel the mucosa
? Excavated type,bellow the mucosa
2,advanced gastric
carcinoma
A neoplasm that has extended
below the submucosa into the
muscular wall
Pathologic types:
? （ 1） fungating type
? （ 2） ulcerative type
? （ 3） infiltrating type
Linitis plastica
Microscopic types
?① papillary ad e no carcinoma；
?② Tubular adenocarcinoma
?③ mucoid adenocarcinoma ；
?④ signet-ring cell cancer
?⑤ undifferentiated carcinoma
spread of tumor
?1,invasion,adjacent structure
?2,lymphatic metastasis：
?3,hematogeneous matastasis:
?4,transcoelomic metastasis
?
1.invasion
?adjacent structure:
? antrum,duodelum,pancrea,the left
leaf of the liver,greater omentum
? cardia and fundus,esophage,
liver,greater omentum
lymphatic metastasis
? Spread like the lymph flow:
? paracoronary venus and subpylorus lymph
node abdominal aorta liver
? thoracic duct the left supraclavicular
lymph nodes
hematogeneous matastasis
? Mostly spread to the liver through portal
vein
? Subsquently spread to the lung, bone and
brain
transcoelomic metastasis
?Type,mucoid adenocarcinoma ；
signet-ring cell cancer
Location,greater omentum
peritoneum
ovary(Krukenberg tumor）
（三） carcinoma of large
intestine
? Happen extensively(only lower than
? gastric cancer in the Gastrointestinal
cancers)
?5years existence rate:90%
?Location:rectum+sigmoid colon>2/3
?caecum+ascending colon+ transverse
colon +decending colon<1/3
etiology
? High fat content disorder of the bacteri
? High protein content transit time increase
? Low fiber content nutrition concetration
? change
?
?carcinoma of oncogene overexpression
large intestine tumor suppressor gene mute
Pathological types
??protruded type
??ulcerative type
??infiltrating type
??colloid type
Microscopic types
??papillary adenocarcinoma；
? ② pipular adenocarcinoma
? ③ mucoid adenocarcinoma
? ④ signet-ring cell cancer
? ⑤ undifferentiated carcinoma
? ⑥ squmous cell carcinomas
? ⑦ adenosqumous carcinomas
Spread of tumor
?1.invasion,adjacent structure
?2.lymphatic metastasis：
?3,hematogeneous matastasis:
?4,transcoelomic metastasis
The Liver and The Biliary
Disease
?一,viral hepatitis
?二,liver cirrhosis
viral hepatitis
?viral hepatitis is an infective disease
which was caused by hepatitis viruses
and characterized by degeneration
and necrosis
?Types:HAV HBV HCV HDV HEV
HGV
Etiology and Mechanism
?Cause:
? heptitis (A,B,C,D,E,G) virus
?Mechanism,remain unknown
Route of transmission
?1.HAV and HEV are spread by
ingestion of contaminated
water and foods and are shed
in the stool,
?Latency:2-3weeks（ HAV） and 2-8
weeks (HEV)
?2.HBV,HCV,HDV:
? blood and body fluids are the primary
vehicles of transmissin
? Vertical transmission from mother to
child during birth
?Body secretions such as semen,
saliva,sweat,tears,breast milk,and
pathologic effusions.
morphology
1.hepatocyte degeneration and
hepatocyte necrosis
2.inflammatory infiltrate;
3.fibrosis hyperplasia and
hepatocyte regeneration
hepatocyte degeneration
and hepatocyte necrosis
?hepatocyte degeneration,
（ 1） diffuse swelling,balloon
ing degeneration
（ 2） acidophilic degeneration
肝细胞疏松化气球样变性
hepatocyte necrosis
（ 1） acidophilic necrosis
（ 2） spotty necrosis
(3)lytic necrosis
(4)piecemeal necrosis
(5)bridging necrosis
Inflammatory infiltrate
?Lymphocyte and monoblast
infiltrate the necrosis and portal
area。
3,fibrosis hyperplasia
and hepatocyte
regeneration
?（ 1） Kupffer cells hypertrophy
and hyperplasia
?（ 2） mesenchymal cell and
fibroblast hypertrophy
?（ 3） hepatocyte regeneration
Kupffer cells hypertrophy
and hyperplasia
?Kupffer cells are often laden
with lipofuscin pigment,they
may protrude into the sinusoid
or may be rushed away
mesenchymal cell and
fibroblast hypertrophy
?They may diffentiate into histiocytes
and inflammatory cells,
?They may also result in cirrhosis if
there is heavy necrosis
hepatocyte regeneration
?Hepatocyte necrosis is repaired by
the regeneration of around normal
hepatocyte
Pathologic types
? Acute hepatitis
Common hepatitis mild
? chronic hepatitis moderate
? severe
? acute Severe hepatitis
? Severe hepatitis
? subacute Severe hepatitis
1,Acute common hepatitis
Mostly happened,
anicteric mild
Pathologic types:
icteric moderate
Cause,HBV
Morphology
?① wide degeneration ＋ diffuse
necrosis
degeneration:;plasma rarefaction
and ballooning degeneration,
necrosis,spotty necrosis ＋
acidophilic necrosis
?② mild inflammatory cells infiltrate
the necrosis and portal area
?③ regeneration,reticular fiber did
not ellapse and the structure and
function of liver can be repaired by
the hepatocyte regeneration
Clinic features
? ① liver enlargement,right upper
quadrant pain：
? ② SGPT
? ③ Jaundice
ends
?Recover in half a year or one
year(HBV)；
?Some cases may advance into
? chronic hepatitis and even
severe hepatitis
Chronic common hepatitis
?Refers to the chronic hepatitis
? last over half a year
（ 1） mild types
Morphology:
1.spotty necrosis and causal
piecemeal necrosis 。
2,mesenchymal cell and fibroblast
hypertrophy in portal area
3.hepatocyte regeneration to keep the
integrity of lobular structure
Moderate types
Morphology:
1.obvious necrosis,moderate piecemeal
necrosis and characteristic bridging
necrosis
2,mesenchymal cell and fibroblast hypertrophy
,linking of fibrous septa between lobules
3.hepatocyte regeneration,integrity of most lobular
structure can be maintained
（ 3） severe types
Morphology:
1.severe massive necrosis and wide
bridging necrosis 。
2,mesenchymal cell and fibroblast
hypertrophy lead to fibrous septa
which devide the lobules
3.hepatocyte irregular regeneration
Ground –glass
hepatocyte
?A finely granular,eosinophilic
cytoplasm contain massive
quantities of HBsAg in the form
of spheres and tubules
? Pseudolobule formation
? become harden and granular-look
? Early cirrhosis
3 Severe viral hepatitis
?This disease is very serious
?Pathologic type
（ 1） acute Severe hepatitis
?（ 2） subacute Severe hepatitis
（ 1） acute Severe hepatitis
?The disease advance acutely and
rapid,with high fatality rate
morphology
Acute yellow or red liver atrophy
?Microscopic view,serious and wide massive
necrosis,migrate from the central to the
portal area,but regeneration was invisible,
?Hepatic cord dissociation
? Hepatic sinusoid extend and hyperemia
and hemorrhage,Kupffer hyperplasia and
? phagocytose debris and pigment
? Lymphocyte and macrophage infiltrate the
portal area
eyesight
?The liver turn small,about 600-800g
in weight,
?the capsule shrink and exhibit yellow
or red in colour
Clinic features
?Serious jaundice
?Hemorrhagic tendency
?Liver failure
?DIC
?Cause of death:hepatic coma
（ 2） subacute Severe hepatitis
It may be natural process or be
an end of acute severe
hepatitis or acute common
hepatitis
morphology
?Microscopic view:
1.wide hepatocyte necrosis;
2.hepatocyte modular regeneration。
?3.reticufiber ellapse and
collagenous fibrosis
?4.inflammatory infiltrate
?5.cholestasis of bilary canaliculi
? around the lobule
Eye-sight
? The liver turn small at diffent degree,,the
capsule shrink and exhibit yellow -green in
colour
二,liver cirrhosis
?Repeative diffuse hepatocyte
necrosis and the subsquent
fibrosis and hepatocyte
regeneration nodules result in
the damage of the constructure
and the blood of lobule
leading to the transformation
and cirrhosis
Pathologic types
?（一） portal cirrhosis
?（二） postnecrosis cirrhosis
?（三） biliary cirrhosis
㈠ portal cirrhosis
?Etilogy:
?1.HBV
?2.chronic alcoholic toxicosis
?3.deficiency of nutrition
?4.toxin toxicosis
Microscopic view
? Pseudolobule formation,the wide fibosis
divide the hepatocyte regenerative nodules and
encompass them into several round hepatocyte
nodules with diffent size
? No central vein or more than ones or disarray
ones in the pseudolobule
? Inflammatory cells infiltrate the hepatocyte
nodules and fiber
? Cholestasis and regeneration of tiny bile
ducts
Eye-sight
? Volume,enlarge lessen
? Weight,enlighten,<1000g
? Surface:similar small nodules,<1.0CM
? Dissection,fibrosis around nodules
? the nodules exhibit yellow-brown or
? yellow –green in colour
假小叶
增生的纤维结缔组织
Clinic features
? Portal hypertension
?cause:
① obstruction of portal vein
② formation of abnormal
circulation
symptoms
?1.Splenomegaly,chronic congestion
?2.gastrointestinal congestion
? 3,hydroperitonia
? 4.collateral circulation:
? varices of the lower esophage vein
? varices of rectum vein
? varices of abdominal wall vein
hepatic insufficiency
?① estrogen↑→A,testis atrophy,male
breast growth,B.spider vascular
nevus
?② hemorrhage tendency
?③ jaundice
?④ hepatic coma:poison accumulation
ends
?1.death,hepatic coma
?2.massive hemorrhage of upper
digestive tract shock
?3.combine hepatic carcinoma and
infection。
㈡ postnecrosis cirrhosis
? Etiology:
? Hepatic viral, migrate from the subacute
severe hepatitis(HBV,HCV)
? Drug and poison
morphology
? Microscopic view:
1,pseudolobules formation with degeneration
and pigment deposition,
2,broad but ununiform fiber septa between
the pseudolobules
3.Inflammatory infiltrate and bile canaliculi
hyperplasia
Eye-sight
? Volume,lessen
? Weight,enlighten,
? Surface:unsimilar large nodules,the largest one
amounts to 6CM
? Dissection,broad fiber septa around nodules,
? the nodules exhibit yellow-brown or
? yellow –green in colour
primary carcinoma of liver
?Origin,liver cell or bile duct
cell
病理变化
morphology：
?1.massive tumor,huge and unifocal
? 〉 15CM,hemorrhage and necrosis
?2.mutinodules,distributed and
variable size
?3.diffuse cancer,small,perrmeating
widely (the entire liver)
巨块型肝癌
结节型肝癌
Microscop types
?1.hepstocellular carcinoma：
? most common
?2.bile duct cancer,less common,
? (clonorchiasis sinensis)
?3.mixture of the two,rare forms
etiology
? 1,HBV
? 2,Chronic liver disease(HCV and alcohol)
? 3.hepatocarcinogens in food(aflatoxin)
临床病理联系
?Development:“hepatosis →
cirrhosis →carcinoma
?Dignosis,AFP is very
important(70-98％ )。
扩散
2.淋巴道播散
肝内静脉播散
卫星小结形成
1.肝内扩散
3,种植性转移
