邓昊 病理学硕士 中共党员
1999年至今 病理学与病理生理学教研室 讲师
1999年 毕业于湖北医科大学 获学士学位
2003年 毕业于武汉大学医学院 获硕士学位
2003年至今 就读于华中科技大学同济医学院
攻读博士学位
主要研究方向：
结直肠癌淋巴结转移
病理学教学研究
主要研究成果：
负责及主要参与省市院级在研项目 6项
各等级论文、译文 5篇
校、院级教学奖 3项
办公室, J12-C202
电话,027-84226503
027-51259966
027-82411803（汉口校区）
E-mail,dh100@21cn.com
Disease of
digestive system
Department of Pathology and Pathophysiology,
Medical and Life Science College,Jianghan University
Deng Hao,Liu lijiang
Digestive Tube：
e.g,Esophagus,Stomach,Intestines,et al
Digestive Gland：
e.g,Liver,Pancreas,Mucosal gland,et al
Gastritis
Peptic Ulcer Disease
Viral Hepatitis
Liver Cirrhosis
Carcinoma of Digestive System
Inflammatory bowel disease
Gastritis
Peptic Ulcer Disease
Viral Hepatitis
Liver Cirrhosis
Carcinoma of Digestive System
Inflammatory bowel disease
gastric pit
pyloric gland
lamina propria
muscularis mucosa
Stomach
Gastric fundal gland
parietal cell
surface mucous cell
gastric pit
neck mucous cell
neck mucous cell chief cell
parietal cell
Gastritis
This diagnosis is both overused and
often missed-overused when it is
applied loosely to any transient upper
abdominal complaint in the absence
of validating evidence and missed
because most patients with chronic
gastritis are asymptomatic,
Gastritis is simply defined as
inflammation of the gastric
mucosa,
Gastritis
Chronic Gastritis
Acute Gastritis
Gastritis
Chronic Gastritis
Acute Gastritis
Gastritis
Definition
The presence of chronic mucosal
inflammatory changes leading
eventually to mucosal atrophy and
epithelial metaplasia.
Gastritis
Etiology
Helicobacter pylori
Autoimmune
Chronic irritation
Gastritis
The infection rates in developing
countries are highest.
Puerto Rico >80%
USA >age 50 50%
China 64%
H,pylori is a noninvasive,non-spore-
forming,S-shaped gram-negative rod
meauring approximately 3.5× 0.5μм,
Gastritis
Chronic Atrophic Gastritis
Type A,body and fundus of stomach
autoimmune disease
pernicious anemia
Type B,antrum of stomach
Gastritis
anti-parietal cell antibody
Gastritis
Gross appearance
Pink color Gray color
Thick Thin Blood vessel appear
Granules appearance Mucosa
Gastritis
Chronic Atrophic
Gastritis
Gastritis
Atrophy of gastric gland
Chronic inflammation cells
Intestinal metaplasia
Pathological change in all mucosa
Gastritis
Microscopic appearance
Gastritis
Gastritis
Note
Intestinal metaplasia
Gastrointestinal-type carcinomas
H,pylori-induced proliferation of lymphoid
tissue within the mucosa
Precursor of gastric lymphoma
Gastritis
Clinical Features
Usually causes no symptoms
Upper abdominal discomfort
Nausea Vomiting
Hypochlorhydria Achlorhydria
Hypergastrinemia
Gastric carcinoma H,pylori 5 fold
Autoimmune 2%~4%
Gastritis
Chronic Gastritis
Acute Gastritis
Gastritis
Definition
An acute mucosal inflammatory
process,usually of a transient
nature,It may be accompanied by
hemorrhage into the mucosa and
erosion which is an important
cause of acute gastrointestinal
bleeding.
Gastritis
Etiology
Nonsteroidal anti-inflammatory drugs
(NSAIDs)
Excessibe alcohol consumption
Heavy smoking
Gastritis
Systemic infections
Severe stress(e.g.trauma,burns)
Ischemia and shock
Suicide attempts with acid and alkali
Morphology
Hemorrhage Erosion
Acute irritated gastritis
Acute hemorrhagic gastritis
Corrosive gastritis
Acute infective gastritis
Gastritis
edematous
punctate submucosal hemorrhages
Acute irritated gastritis Gastritis
Gastritis
Clinical Features
Asymptoms
Epigastric pain with Nausea and Vomiting
Hematemesis and melena
Gastritis
Gastritis
Peptic Ulcer Disease
Viral Hepatitis
Liver Cirrhosis
Carcinoma of Digestive System
Inflammatory bowel disease
Definition
A breach in the mucosa of the alimentary
tract that extends through the muscularis
mucosae into the submucosa or deeper.
Ulcer
Erosion
A breach in the epithelium of the mucosa.
Ulceration
Peptic Ulcers
Acute Gastric Ulceration
Ulceration
Peptic Ulcers
Acute Gastric Ulceration
Ulceration
Ulceration
Peptic Ulcers
Any portion of the gastrointestinal tract
Aggressive action of acid-peptic juices
Chronic often Solitary
Stomach Duodenum 98%
Stomach:Duodenum 4:1
Ulceration
Epidemiology
Diagnosed in middle-aged to older YOUNG
Without obvious precipitating influences
Propensity to develop peptic ulcers remain
USA 2.5% Male 1.5% Female
Genetic or racial influences play little role
Ulceration
China?
Pathogenesis
Murky
Gastric acid and pepsin
H,pylori infection
China Stomach 71.9% Duodenum100%
USA Stomach 70% Duodenum70%~90%
The imbalance between defense
and aggressive forces
Ulceration
Prevention
Secretion of Mucus
Secretion of Bicarbonate into mucus
Acid- and Pepsin-containing fluid ―Jets‖
Rapid gastric epithelial Regeneration
Robust mucosal blood flow
Mucosal elaboration of Prostaglandins
Ulceration
Aggressive forces
H.pylori
NSAIDs
Others
Ulceration
Aggressive forces
H.pylori
NSAIDs
Others
Ulceration
Ulceration
Ulceration
H.pylori
Not invade
Mucosal epithelial cells
Neutrophils
Interleukin(IL)-1,6,8 Tumor necrosis factor
An intense inflammatory and immune response
Recruits Activates
Ulceration
Induce
Ulceration
H.pylori
Duodenal biocarbonate production
Areas for H.pylori colonization
Gastric acid secretion
Gastric metaplasia
Reducing luminal PH in the duodenum
Enhance Impair
Ulceration
Ulceration
Aggressive forces
H.pylori
NSAIDs
Others
Ulceration
3% user
The most commonly used medications
Increasing age Higher dose Prolonged usage
Prostaglandin Hydrochloric acid
Bicarbonate Mucin
Glutathione
Impair angiogenesis
Ulceration
Aggressive forces
H.pylori
NSAIDs
Others
Ulceration
Cigarette
Alcohol Alcoholic cirrhosis
Corticosteroids
Psychological stress
Ulceration
Morphology
Lesser curvature of the stomach
The anterior and posterior walls of
the first potion of the duodenum
Ulceration
Round or Ellipse shape
Base appears clean
Surrounding mucosal folds
radiate like wheel spoke
Diameter < 2.5cm (< 1.0cm)
Gross appearance
Ulceration
At least the submucosa
The margins are perpendicular
Mild edema immediately adjacent mucosa
Ulceration
duodenal ulcer
Ulceration
duodenal ulcer
Ulceration
Microscopic appearance
Necrosis layer
Inflammation layer
Granulation tissue layer
Scar layer
Ulceration
repair
mucosae
Necrosis layer
Inflammation layer
granulation tissue layer
Scar layer
damage
Inflammation
accurate
chronic
Ulceration
damage
Ulceration
Ulceration
Thickened vessel
Ulceration
Clinical Features
Epigastric pain
Gnawing,Burning,Boring
More worse night
1 to 3 hours after meals
Relieved by alkalis or food
Nausea,vomiting,bloating,belching
Ulceration
Carcinomatous change(1%or<1%)
Prognosis
Healing
Bleeding(10~35%)
Perforation(5%)
Pyloric stenosis(3%)
Ulceration
Ulceration
Chronic peptic ulcer
Pyloric stenosis
Ulceration
Carcinomatous change
Ulceration
Peptic ulcers are notoriously
chronic,recurrent lesions - they
more often impair the quality of
life than shorten it.
Ulceration
Peptic Ulcers
Acute Gastric Ulceration
Ulceration
Definition
Acutely developing gastric mucosal
defects may appear after severe stress
and are designated stress ulcers.There
are multiple lesions located mainly in
the stomach and occasionally in the
duodenum.
Ulceration
Morphology
Circular and small(D<1cm)
Base is frequently stained a dark brown
Could be find anywhere in the stomach
Often they are multiple
Depth from erosion to ulceration
Ulceration
Acute peptic ulcers
Acute hemorrhagic gastritis
Gastritis
Clinical Features
They may be of limited clinical consequence
or life-threatening.
The gastric mucosa can recover completely
if the patient does not die from the primary
disease.
Ulceration
Gastritis
Peptic Ulcer Disease
Viral Hepatitis
Liver Cirrhosis
Carcinoma of Digestive System
Inflammatory bowel disease
Crohn disease (CD) and ulcerative
colitis (UC) are chronic relapsing
disorders of unknown origin,These
diseases share many common features
and are coectively known as idiopathic
inflammatory bowel disease (IBD),
IBD must be viewed as a systemic
inflammatory disease with predominant
gastrintestinal involvement.
IBD
Genetic predisposition
Immunologic factors
Microbial factor
The normal intestine is in a steady
state of of ―physiologic‖ inflammation.
IBD
Crohn Disease
This disease may affect any level of
the alimentary tract,from mouth to
anus,Active cases of CD are often
accompanied by extraintestinal
complications of immune origin,such
as iritis,uveitis and sacriiliitis,et al,
IBD
cobblestone appearance
IBD
Gross appearance
intestinal wall rubbery and thick
edema,inflammation,fibrosis and hypertrophy
muscularis propria
fissure
mucosal ulcer long,serpentine ulcer fistula or sinus tract
coalesce penetrate
cobblestone appearance
intervening mucosa
skip lesions
sharp demarcation between diseased and uninvolved bowel
IBD
cobblestone appearanceulclear
IBD
IBD
Microscopic appearance
inflammation
lymphoid aggregates scattered through the various
tissue layers.
ulceration
character of ulceration
chronic mucosal damage
distortion atrophy metaplasia
noncaseating granulomas
40% to 60% of cases not be a diagnosis
IBD
Crohn disease
IBD
granuloma
lymphocytes and plasma cells IBD
Ulceration Colitis
UC is an an ulceroinflammatory
disease affecting the colon but limited
to the mucose and submucosa expect
in the most severe cases,UC begins in
the rectum and extends proximally in
a continuous fashion,sometimes
involving the entire colon.
IBD
Feature Crohn Disease (Colon) Ulcerative Colitis
Macroscopic
Owel region Colon or/and ileum Colon only
Distribution Skip lessions Diffuse
Stricture Variable Late/rare
Wall appearance Variable Thin
Dilation Yes Yes
Microscopic
Pseudopolyps Marked Marked
Ulcers Deep,linear Superficial
Lymphoid reaction Marked Mild
Fibrosis Moderate Mild
Serositis Variable Mild to none
Granulomas Yes(40% to 60%) No
Fistulae/sinuses Yes No
Clinical
Malignant potential Yes Yes IBD
mucosal ulceration
pseudopolyp
ulcerative colitis
IBD
mucosal ulceration
pseudopolyploidy
chronic ulcerative colitis
IBD
mucosal ulceration
pseudopolyploidy
chronic ulcerative colitis
IBD
Gastritis
Peptic Ulcer Disease
Viral Hepatitis
Liver Cirrhosis
Carcinoma of Digestive System
Inflammatory bowel disease
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
HBV--DNA HCV– RNA
HDV—RNA HGV--RNA
Infect by intestine
Infect by other ways
HAV– RNA
HEV—RNA
Epidemiology
Viral Hepatitis
Viral Hepatitis
Pathogenesis
HBV Duplication in liver cells
Liver cell membrane
T lymph cell
Liver cell damage
Ab
Enter in blood
sensitization
Viral Hepatitis
The degree of damage
Relationship
The degree of immunity
Viral Hepatitis
Alteration
Exudation
Proliferation
Reversible injury
Necrosis
Inflammatory cells
Hepatocytes
Fibrous tissue
Characteristics
Viral Hepatitis
Cytoplasm rarefaction→Ballooning degeneration
→Lytic necrosis
Acidophilic degeneration →
Acidophilic necrosis (Apoptosis)
Water↑
Water↓
Liver cell
Reversible injury
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Spotty necrosis -- several hepatocytes
Piecemeal necrosis -- liver cells in
limiting plate necrosis
Bridging necrosis -- necrosis band in hepatic
lobule and/or between hepatic lobules
Massive necrosis -- hepatic lobule
Necrosis
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Inflammatory cells,
Exudation
Lymph cell
Monocyt
Viral Hepatitis
Kupffer cell↑
Proliferation
Hepatocytes
Fibrous tissue
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Common viral hepatitis
Accurate hepatitis
Chronic hepatitis
Viral Hepatitis
Common viral hepatitis
Accurate hepatitis
Chronic hepatitis
Viral Hepatitis
Jaundice non-jaundice
Gross appearance
A little bigger
A little softer
Viral Hepatitis
Extensive degeneration
spotty necrosis
Inflammatory infiltration
No obvious proliferation
Light microscopy
Viral Hepatitis
Viral Hepatitis
Liver function
Laboratory examination
No obvious abnormality
Viral Hepatitis
prognosis
Majority recovery
Minority
heavy
chronic
Viral Hepatitis
Common viral hepatitis
Accurate hepatitis
Chronic hepatitis
Viral Hepatitis
Mild
Moderate
Heavy
Light microscopy
Viral Hepatitis
Mild chronic hepatitis
Spotty necrosis
A little piecemeal necrosis
Hepatic lobules
Inflammatory infiltration
Portal
areaFibrous tissue
Complete
Viral Hepatitis
Moderate chronic hepatitis
Spotty necrosis
Bridging necrosis
Moderate piecemeal necrosis
Fibrous septa
Inflammatory infiltration Portal area
Fibrous tissue
CompleteHepatic lobules
Viral Hepatitis
Heavy chronic hepatitis
Bridging necrosis
Piecemeal necrosis
Inflammatory infiltration Portal area
Fibrous tissue
Incomplete
Heavy
Liver Cirrhosis
Hepatocyte irregular regeneration
Fibrous septa
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Gross appearance
More bigger
More and more harder
Micronodular Small
Similar size
Viral Hepatitis
Auto antibody(+)
Liver function
Laboratory examination
Continuous abnormality
Clouded glass liking hepatices
Viral Hepatitis
Primary carcinoma of liver
Prognosis
Clinical situation can be recovered
Recur easily
Micronodular cirrhosis
Viral Hepatitis
Heavy virus hepatitis
Subacute
Accurate
Viral Hepatitis
Heavy virus hepatitis
Subacute
Accurate
Viral Hepatitis
Accurate heavy virus hepatitis
Accurate
Death rate
About 10 days
High
Viral Hepatitis
Chronic inflammatory cells
Massive necrosis
Kupffer cell↑
center edge
Light microscopy
Viral Hepatitis
Viral Hepatitis
Volumev↓↓
Weight↓↓
Soft
Capsule crease
Yellow hepatic atrophy
Red hepatic atrophy
Gross appearance
Viral Hepatitis
Viral Hepatitis
Liver function
Laboratory examination
Obvious abnormality
Viral Hepatitis
Subacute heavy virus hepatitis
Death
Liver function failure
—Hepatic coma
Digestive tract massive hemorrhage
Renal failure
DIC
Prognosis
Viral Hepatitis
Heavy virus hepatitis
Subacute
Accurate
Viral Hepatitis
Subacute heavy virus hepatitis
Majority
Accurate heavy virus hepatitis
Minority
Accurate common virus hepatitis
Viral Hepatitis
Chronic inflammatory cells
Massive necrosis
Light microscopy
Fibrous septaFibrous tissue
wide
Nodular regeneration of hepatocytes
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Gross appearance
More and more harder
Macronodular
Volume of liver↓↓→↓
Viral Hepatitis
Liver function
Laboratory examination
Obvious abnormality
Recovery
Viral Hepatitis
Gastritis
Peptic Ulcer Disease
Viral Hepatitis
Liver Cirrhosis
Carcinoma of Digestive System
Inflammatory bowel disease
DEFORMATION
HARD
Liver
cirrhosis
Concept
Fibrous tissue proliferation
Degeneration and necrosis
Nodular regeneration
Liver Cirrhosis
Liver cirrhosis
Portal cirrhosis
Postnecrotic cirrhosis
Liver Cirrhosis
Liver cirrhosis
Portal cirrhosis
Postnecrotic cirrhosis
Liver Cirrhosis
Portal cirrhosis
Liver Cirrhosis
Virus hepatitis --- China
HBV,HCV
Common virus hepatitis
Excessive drinking
Malnutrition
Poisonous drug
Cause of the disease
Liver Cirrhosis
Fibrosis
Mechanism of the disease
Fat-storing cell
Fibroblast
Nodular regeneration
Liver Cirrhosis
Volume↑
→ Volume↓Weight↓hardness↑
Island-liking
Gross appearance
Micronodular D<1cm
Liver Cirrhosis
Liver Cirrhosis
Ductular proliferation
Nodular
Light microscopy
Fibrous septa Narrow
Liver Cirrhosis
Liver Cirrhosis
Liver Cirrhosis
Portal hypertension
Prognosis
Hepatocellular failure
Liver Cirrhosis
Portal hypertension
Prognosis
Hepatocellular failure
Liver Cirrhosis
Portal hypertension
Congestion gastrointestinal tract
Ascites
Collateral circulation
Splenomegaly
Liver Cirrhosis
splenomegaly
Liver Cirrhosis
Liver Cirrhosis
Liver Cirrhosis
caput medusae
Liver Cirrhosis
Portal hypertension
Prognosis
Hepatocellular failure
Liver Cirrhosis
Hepatocellular failure
Protein
Porphobilin
Hormone
NH4+
Liver Cirrhosis
Postnecrotic cirrhosis
Liver Cirrhosis
Virus hepatitis --- China
Subacute heavy virus hepatitis
Poisonous drug
Cause of the disease
Liver Cirrhosis
Volume↓Weight↓hardness↑
Island-liking
Gross appearance
Macronodular
Liver Cirrhosis
Liver Cirrhosis
Liver Cirrhosis
Liver Cirrhosis
Ductular proliferation
Nodular
Light microscopy
Fibrous septa Wight
Liver Cirrhosis
Carcinomatous change
Prognosis
The course is short
Hepatocellular failure
Liver Cirrhosis
Gastritis
Peptic Ulcer Disease
Viral Hepatitis
Liver Cirrhosis
Carcinoma of Digestive System
Inflammatory bowel disease
Carcinoma of stomach
Carcinoma
40-60 years
Death rate of malignant tumor
Male>Female
First one
Characteristics
Lesser curvature of Antrum of
stomach
Carcinoma
Cause of disease
Diet
HP
Enviroment
Unknown
Carcinoma
Advanced gastric carcinoma
Classification
Early gastric carcinoma
Mucous layer
Under mucous layer
Carcinoma
Funguting type
Ulclerative type
Infiltrating type
Gross appearance
Carcinoma
carcinoma of stomach
funguting type
Carcinoma
carcinoma of stomach
ulclerative type
Carcinoma
carcinoma of stomach
infiltrating type
Carcinoma
leather bottle
Carcinoma
Adenocarcinoma
Tubular adenoma
Papillary adenocarcinoma
Mucinous carcinoma
Signet-ring cell carcinoma
Undifferentiated carcinoma
Inocarcinoma
Squamous carcinoma
Adenosquamous carcinoma
Light microscopy
Medullary carcinoma
Carcinoma
adenocarcinoma
Carcinoma
adenocarcinoma
Carcinoma
signet ring cell
Carcinoma
Carcinoma
undifferentiated carcinoma
Carcinoma
Metastasis and Invasion
Direct spreading
Metastasis
Lymphatic
Hematogenous
Seeding
(Krukenbeng tumour)
Carcinoma
Numbers of metastasis lymph node
--- Prognostic maker
( N1:1-6,N2,7-15,N3:>15,UICC-1998)
Carcinoma
LNM
LNMM
TNM
Carcinoma
Thanks!
1999年至今 病理学与病理生理学教研室 讲师
1999年 毕业于湖北医科大学 获学士学位
2003年 毕业于武汉大学医学院 获硕士学位
2003年至今 就读于华中科技大学同济医学院
攻读博士学位
主要研究方向：
结直肠癌淋巴结转移
病理学教学研究
主要研究成果：
负责及主要参与省市院级在研项目 6项
各等级论文、译文 5篇
校、院级教学奖 3项
办公室, J12-C202
电话,027-84226503
027-51259966
027-82411803（汉口校区）
E-mail,dh100@21cn.com
Disease of
digestive system
Department of Pathology and Pathophysiology,
Medical and Life Science College,Jianghan University
Deng Hao,Liu lijiang
Digestive Tube：
e.g,Esophagus,Stomach,Intestines,et al
Digestive Gland：
e.g,Liver,Pancreas,Mucosal gland,et al
Gastritis
Peptic Ulcer Disease
Viral Hepatitis
Liver Cirrhosis
Carcinoma of Digestive System
Inflammatory bowel disease
Gastritis
Peptic Ulcer Disease
Viral Hepatitis
Liver Cirrhosis
Carcinoma of Digestive System
Inflammatory bowel disease
gastric pit
pyloric gland
lamina propria
muscularis mucosa
Stomach
Gastric fundal gland
parietal cell
surface mucous cell
gastric pit
neck mucous cell
neck mucous cell chief cell
parietal cell
Gastritis
This diagnosis is both overused and
often missed-overused when it is
applied loosely to any transient upper
abdominal complaint in the absence
of validating evidence and missed
because most patients with chronic
gastritis are asymptomatic,
Gastritis is simply defined as
inflammation of the gastric
mucosa,
Gastritis
Chronic Gastritis
Acute Gastritis
Gastritis
Chronic Gastritis
Acute Gastritis
Gastritis
Definition
The presence of chronic mucosal
inflammatory changes leading
eventually to mucosal atrophy and
epithelial metaplasia.
Gastritis
Etiology
Helicobacter pylori
Autoimmune
Chronic irritation
Gastritis
The infection rates in developing
countries are highest.
Puerto Rico >80%
USA >age 50 50%
China 64%
H,pylori is a noninvasive,non-spore-
forming,S-shaped gram-negative rod
meauring approximately 3.5× 0.5μм,
Gastritis
Chronic Atrophic Gastritis
Type A,body and fundus of stomach
autoimmune disease
pernicious anemia
Type B,antrum of stomach
Gastritis
anti-parietal cell antibody
Gastritis
Gross appearance
Pink color Gray color
Thick Thin Blood vessel appear
Granules appearance Mucosa
Gastritis
Chronic Atrophic
Gastritis
Gastritis
Atrophy of gastric gland
Chronic inflammation cells
Intestinal metaplasia
Pathological change in all mucosa
Gastritis
Microscopic appearance
Gastritis
Gastritis
Note
Intestinal metaplasia
Gastrointestinal-type carcinomas
H,pylori-induced proliferation of lymphoid
tissue within the mucosa
Precursor of gastric lymphoma
Gastritis
Clinical Features
Usually causes no symptoms
Upper abdominal discomfort
Nausea Vomiting
Hypochlorhydria Achlorhydria
Hypergastrinemia
Gastric carcinoma H,pylori 5 fold
Autoimmune 2%~4%
Gastritis
Chronic Gastritis
Acute Gastritis
Gastritis
Definition
An acute mucosal inflammatory
process,usually of a transient
nature,It may be accompanied by
hemorrhage into the mucosa and
erosion which is an important
cause of acute gastrointestinal
bleeding.
Gastritis
Etiology
Nonsteroidal anti-inflammatory drugs
(NSAIDs)
Excessibe alcohol consumption
Heavy smoking
Gastritis
Systemic infections
Severe stress(e.g.trauma,burns)
Ischemia and shock
Suicide attempts with acid and alkali
Morphology
Hemorrhage Erosion
Acute irritated gastritis
Acute hemorrhagic gastritis
Corrosive gastritis
Acute infective gastritis
Gastritis
edematous
punctate submucosal hemorrhages
Acute irritated gastritis Gastritis
Gastritis
Clinical Features
Asymptoms
Epigastric pain with Nausea and Vomiting
Hematemesis and melena
Gastritis
Gastritis
Peptic Ulcer Disease
Viral Hepatitis
Liver Cirrhosis
Carcinoma of Digestive System
Inflammatory bowel disease
Definition
A breach in the mucosa of the alimentary
tract that extends through the muscularis
mucosae into the submucosa or deeper.
Ulcer
Erosion
A breach in the epithelium of the mucosa.
Ulceration
Peptic Ulcers
Acute Gastric Ulceration
Ulceration
Peptic Ulcers
Acute Gastric Ulceration
Ulceration
Ulceration
Peptic Ulcers
Any portion of the gastrointestinal tract
Aggressive action of acid-peptic juices
Chronic often Solitary
Stomach Duodenum 98%
Stomach:Duodenum 4:1
Ulceration
Epidemiology
Diagnosed in middle-aged to older YOUNG
Without obvious precipitating influences
Propensity to develop peptic ulcers remain
USA 2.5% Male 1.5% Female
Genetic or racial influences play little role
Ulceration
China?
Pathogenesis
Murky
Gastric acid and pepsin
H,pylori infection
China Stomach 71.9% Duodenum100%
USA Stomach 70% Duodenum70%~90%
The imbalance between defense
and aggressive forces
Ulceration
Prevention
Secretion of Mucus
Secretion of Bicarbonate into mucus
Acid- and Pepsin-containing fluid ―Jets‖
Rapid gastric epithelial Regeneration
Robust mucosal blood flow
Mucosal elaboration of Prostaglandins
Ulceration
Aggressive forces
H.pylori
NSAIDs
Others
Ulceration
Aggressive forces
H.pylori
NSAIDs
Others
Ulceration
Ulceration
Ulceration
H.pylori
Not invade
Mucosal epithelial cells
Neutrophils
Interleukin(IL)-1,6,8 Tumor necrosis factor
An intense inflammatory and immune response
Recruits Activates
Ulceration
Induce
Ulceration
H.pylori
Duodenal biocarbonate production
Areas for H.pylori colonization
Gastric acid secretion
Gastric metaplasia
Reducing luminal PH in the duodenum
Enhance Impair
Ulceration
Ulceration
Aggressive forces
H.pylori
NSAIDs
Others
Ulceration
3% user
The most commonly used medications
Increasing age Higher dose Prolonged usage
Prostaglandin Hydrochloric acid
Bicarbonate Mucin
Glutathione
Impair angiogenesis
Ulceration
Aggressive forces
H.pylori
NSAIDs
Others
Ulceration
Cigarette
Alcohol Alcoholic cirrhosis
Corticosteroids
Psychological stress
Ulceration
Morphology
Lesser curvature of the stomach
The anterior and posterior walls of
the first potion of the duodenum
Ulceration
Round or Ellipse shape
Base appears clean
Surrounding mucosal folds
radiate like wheel spoke
Diameter < 2.5cm (< 1.0cm)
Gross appearance
Ulceration
At least the submucosa
The margins are perpendicular
Mild edema immediately adjacent mucosa
Ulceration
duodenal ulcer
Ulceration
duodenal ulcer
Ulceration
Microscopic appearance
Necrosis layer
Inflammation layer
Granulation tissue layer
Scar layer
Ulceration
repair
mucosae
Necrosis layer
Inflammation layer
granulation tissue layer
Scar layer
damage
Inflammation
accurate
chronic
Ulceration
damage
Ulceration
Ulceration
Thickened vessel
Ulceration
Clinical Features
Epigastric pain
Gnawing,Burning,Boring
More worse night
1 to 3 hours after meals
Relieved by alkalis or food
Nausea,vomiting,bloating,belching
Ulceration
Carcinomatous change(1%or<1%)
Prognosis
Healing
Bleeding(10~35%)
Perforation(5%)
Pyloric stenosis(3%)
Ulceration
Ulceration
Chronic peptic ulcer
Pyloric stenosis
Ulceration
Carcinomatous change
Ulceration
Peptic ulcers are notoriously
chronic,recurrent lesions - they
more often impair the quality of
life than shorten it.
Ulceration
Peptic Ulcers
Acute Gastric Ulceration
Ulceration
Definition
Acutely developing gastric mucosal
defects may appear after severe stress
and are designated stress ulcers.There
are multiple lesions located mainly in
the stomach and occasionally in the
duodenum.
Ulceration
Morphology
Circular and small(D<1cm)
Base is frequently stained a dark brown
Could be find anywhere in the stomach
Often they are multiple
Depth from erosion to ulceration
Ulceration
Acute peptic ulcers
Acute hemorrhagic gastritis
Gastritis
Clinical Features
They may be of limited clinical consequence
or life-threatening.
The gastric mucosa can recover completely
if the patient does not die from the primary
disease.
Ulceration
Gastritis
Peptic Ulcer Disease
Viral Hepatitis
Liver Cirrhosis
Carcinoma of Digestive System
Inflammatory bowel disease
Crohn disease (CD) and ulcerative
colitis (UC) are chronic relapsing
disorders of unknown origin,These
diseases share many common features
and are coectively known as idiopathic
inflammatory bowel disease (IBD),
IBD must be viewed as a systemic
inflammatory disease with predominant
gastrintestinal involvement.
IBD
Genetic predisposition
Immunologic factors
Microbial factor
The normal intestine is in a steady
state of of ―physiologic‖ inflammation.
IBD
Crohn Disease
This disease may affect any level of
the alimentary tract,from mouth to
anus,Active cases of CD are often
accompanied by extraintestinal
complications of immune origin,such
as iritis,uveitis and sacriiliitis,et al,
IBD
cobblestone appearance
IBD
Gross appearance
intestinal wall rubbery and thick
edema,inflammation,fibrosis and hypertrophy
muscularis propria
fissure
mucosal ulcer long,serpentine ulcer fistula or sinus tract
coalesce penetrate
cobblestone appearance
intervening mucosa
skip lesions
sharp demarcation between diseased and uninvolved bowel
IBD
cobblestone appearanceulclear
IBD
IBD
Microscopic appearance
inflammation
lymphoid aggregates scattered through the various
tissue layers.
ulceration
character of ulceration
chronic mucosal damage
distortion atrophy metaplasia
noncaseating granulomas
40% to 60% of cases not be a diagnosis
IBD
Crohn disease
IBD
granuloma
lymphocytes and plasma cells IBD
Ulceration Colitis
UC is an an ulceroinflammatory
disease affecting the colon but limited
to the mucose and submucosa expect
in the most severe cases,UC begins in
the rectum and extends proximally in
a continuous fashion,sometimes
involving the entire colon.
IBD
Feature Crohn Disease (Colon) Ulcerative Colitis
Macroscopic
Owel region Colon or/and ileum Colon only
Distribution Skip lessions Diffuse
Stricture Variable Late/rare
Wall appearance Variable Thin
Dilation Yes Yes
Microscopic
Pseudopolyps Marked Marked
Ulcers Deep,linear Superficial
Lymphoid reaction Marked Mild
Fibrosis Moderate Mild
Serositis Variable Mild to none
Granulomas Yes(40% to 60%) No
Fistulae/sinuses Yes No
Clinical
Malignant potential Yes Yes IBD
mucosal ulceration
pseudopolyp
ulcerative colitis
IBD
mucosal ulceration
pseudopolyploidy
chronic ulcerative colitis
IBD
mucosal ulceration
pseudopolyploidy
chronic ulcerative colitis
IBD
Gastritis
Peptic Ulcer Disease
Viral Hepatitis
Liver Cirrhosis
Carcinoma of Digestive System
Inflammatory bowel disease
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
HBV--DNA HCV– RNA
HDV—RNA HGV--RNA
Infect by intestine
Infect by other ways
HAV– RNA
HEV—RNA
Epidemiology
Viral Hepatitis
Viral Hepatitis
Pathogenesis
HBV Duplication in liver cells
Liver cell membrane
T lymph cell
Liver cell damage
Ab
Enter in blood
sensitization
Viral Hepatitis
The degree of damage
Relationship
The degree of immunity
Viral Hepatitis
Alteration
Exudation
Proliferation
Reversible injury
Necrosis
Inflammatory cells
Hepatocytes
Fibrous tissue
Characteristics
Viral Hepatitis
Cytoplasm rarefaction→Ballooning degeneration
→Lytic necrosis
Acidophilic degeneration →
Acidophilic necrosis (Apoptosis)
Water↑
Water↓
Liver cell
Reversible injury
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Spotty necrosis -- several hepatocytes
Piecemeal necrosis -- liver cells in
limiting plate necrosis
Bridging necrosis -- necrosis band in hepatic
lobule and/or between hepatic lobules
Massive necrosis -- hepatic lobule
Necrosis
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Inflammatory cells,
Exudation
Lymph cell
Monocyt
Viral Hepatitis
Kupffer cell↑
Proliferation
Hepatocytes
Fibrous tissue
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Common viral hepatitis
Accurate hepatitis
Chronic hepatitis
Viral Hepatitis
Common viral hepatitis
Accurate hepatitis
Chronic hepatitis
Viral Hepatitis
Jaundice non-jaundice
Gross appearance
A little bigger
A little softer
Viral Hepatitis
Extensive degeneration
spotty necrosis
Inflammatory infiltration
No obvious proliferation
Light microscopy
Viral Hepatitis
Viral Hepatitis
Liver function
Laboratory examination
No obvious abnormality
Viral Hepatitis
prognosis
Majority recovery
Minority
heavy
chronic
Viral Hepatitis
Common viral hepatitis
Accurate hepatitis
Chronic hepatitis
Viral Hepatitis
Mild
Moderate
Heavy
Light microscopy
Viral Hepatitis
Mild chronic hepatitis
Spotty necrosis
A little piecemeal necrosis
Hepatic lobules
Inflammatory infiltration
Portal
areaFibrous tissue
Complete
Viral Hepatitis
Moderate chronic hepatitis
Spotty necrosis
Bridging necrosis
Moderate piecemeal necrosis
Fibrous septa
Inflammatory infiltration Portal area
Fibrous tissue
CompleteHepatic lobules
Viral Hepatitis
Heavy chronic hepatitis
Bridging necrosis
Piecemeal necrosis
Inflammatory infiltration Portal area
Fibrous tissue
Incomplete
Heavy
Liver Cirrhosis
Hepatocyte irregular regeneration
Fibrous septa
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Gross appearance
More bigger
More and more harder
Micronodular Small
Similar size
Viral Hepatitis
Auto antibody(+)
Liver function
Laboratory examination
Continuous abnormality
Clouded glass liking hepatices
Viral Hepatitis
Primary carcinoma of liver
Prognosis
Clinical situation can be recovered
Recur easily
Micronodular cirrhosis
Viral Hepatitis
Heavy virus hepatitis
Subacute
Accurate
Viral Hepatitis
Heavy virus hepatitis
Subacute
Accurate
Viral Hepatitis
Accurate heavy virus hepatitis
Accurate
Death rate
About 10 days
High
Viral Hepatitis
Chronic inflammatory cells
Massive necrosis
Kupffer cell↑
center edge
Light microscopy
Viral Hepatitis
Viral Hepatitis
Volumev↓↓
Weight↓↓
Soft
Capsule crease
Yellow hepatic atrophy
Red hepatic atrophy
Gross appearance
Viral Hepatitis
Viral Hepatitis
Liver function
Laboratory examination
Obvious abnormality
Viral Hepatitis
Subacute heavy virus hepatitis
Death
Liver function failure
—Hepatic coma
Digestive tract massive hemorrhage
Renal failure
DIC
Prognosis
Viral Hepatitis
Heavy virus hepatitis
Subacute
Accurate
Viral Hepatitis
Subacute heavy virus hepatitis
Majority
Accurate heavy virus hepatitis
Minority
Accurate common virus hepatitis
Viral Hepatitis
Chronic inflammatory cells
Massive necrosis
Light microscopy
Fibrous septaFibrous tissue
wide
Nodular regeneration of hepatocytes
Viral Hepatitis
Viral Hepatitis
Viral Hepatitis
Gross appearance
More and more harder
Macronodular
Volume of liver↓↓→↓
Viral Hepatitis
Liver function
Laboratory examination
Obvious abnormality
Recovery
Viral Hepatitis
Gastritis
Peptic Ulcer Disease
Viral Hepatitis
Liver Cirrhosis
Carcinoma of Digestive System
Inflammatory bowel disease
DEFORMATION
HARD
Liver
cirrhosis
Concept
Fibrous tissue proliferation
Degeneration and necrosis
Nodular regeneration
Liver Cirrhosis
Liver cirrhosis
Portal cirrhosis
Postnecrotic cirrhosis
Liver Cirrhosis
Liver cirrhosis
Portal cirrhosis
Postnecrotic cirrhosis
Liver Cirrhosis
Portal cirrhosis
Liver Cirrhosis
Virus hepatitis --- China
HBV,HCV
Common virus hepatitis
Excessive drinking
Malnutrition
Poisonous drug
Cause of the disease
Liver Cirrhosis
Fibrosis
Mechanism of the disease
Fat-storing cell
Fibroblast
Nodular regeneration
Liver Cirrhosis
Volume↑
→ Volume↓Weight↓hardness↑
Island-liking
Gross appearance
Micronodular D<1cm
Liver Cirrhosis
Liver Cirrhosis
Ductular proliferation
Nodular
Light microscopy
Fibrous septa Narrow
Liver Cirrhosis
Liver Cirrhosis
Liver Cirrhosis
Portal hypertension
Prognosis
Hepatocellular failure
Liver Cirrhosis
Portal hypertension
Prognosis
Hepatocellular failure
Liver Cirrhosis
Portal hypertension
Congestion gastrointestinal tract
Ascites
Collateral circulation
Splenomegaly
Liver Cirrhosis
splenomegaly
Liver Cirrhosis
Liver Cirrhosis
Liver Cirrhosis
caput medusae
Liver Cirrhosis
Portal hypertension
Prognosis
Hepatocellular failure
Liver Cirrhosis
Hepatocellular failure
Protein
Porphobilin
Hormone
NH4+
Liver Cirrhosis
Postnecrotic cirrhosis
Liver Cirrhosis
Virus hepatitis --- China
Subacute heavy virus hepatitis
Poisonous drug
Cause of the disease
Liver Cirrhosis
Volume↓Weight↓hardness↑
Island-liking
Gross appearance
Macronodular
Liver Cirrhosis
Liver Cirrhosis
Liver Cirrhosis
Liver Cirrhosis
Ductular proliferation
Nodular
Light microscopy
Fibrous septa Wight
Liver Cirrhosis
Carcinomatous change
Prognosis
The course is short
Hepatocellular failure
Liver Cirrhosis
Gastritis
Peptic Ulcer Disease
Viral Hepatitis
Liver Cirrhosis
Carcinoma of Digestive System
Inflammatory bowel disease
Carcinoma of stomach
Carcinoma
40-60 years
Death rate of malignant tumor
Male>Female
First one
Characteristics
Lesser curvature of Antrum of
stomach
Carcinoma
Cause of disease
Diet
HP
Enviroment
Unknown
Carcinoma
Advanced gastric carcinoma
Classification
Early gastric carcinoma
Mucous layer
Under mucous layer
Carcinoma
Funguting type
Ulclerative type
Infiltrating type
Gross appearance
Carcinoma
carcinoma of stomach
funguting type
Carcinoma
carcinoma of stomach
ulclerative type
Carcinoma
carcinoma of stomach
infiltrating type
Carcinoma
leather bottle
Carcinoma
Adenocarcinoma
Tubular adenoma
Papillary adenocarcinoma
Mucinous carcinoma
Signet-ring cell carcinoma
Undifferentiated carcinoma
Inocarcinoma
Squamous carcinoma
Adenosquamous carcinoma
Light microscopy
Medullary carcinoma
Carcinoma
adenocarcinoma
Carcinoma
adenocarcinoma
Carcinoma
signet ring cell
Carcinoma
Carcinoma
undifferentiated carcinoma
Carcinoma
Metastasis and Invasion
Direct spreading
Metastasis
Lymphatic
Hematogenous
Seeding
(Krukenbeng tumour)
Carcinoma
Numbers of metastasis lymph node
--- Prognostic maker
( N1:1-6,N2,7-15,N3:>15,UICC-1998)
Carcinoma
LNM
LNMM
TNM
Carcinoma
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