1. Chapter 8 The diseases of digestive system

2. 8.1.1 ESOPHAGITIS reflux esophagitis
Definition: esophageal irritation and inflammation due to reflux of gastric secretions into the esophagus
Pathologic changes:
Eosinophiles, with or without neutrophils, in the epithelial layer
Basal zone hyperplasia
Elongation of lamina propria papillae
Intraepithelial neutrophils are markers of more severe injury
Presentation: heartburn and reguritation
Complications: bleeding, stricture, bronchospasm and asthma,
barrett esophagus

3. 2.Barret esophagus
Definition: metaplasia of the squamous eosphageal mucosa to a more protective columnar type because of chronic exposure to gastric secretions
Cause: gastroesophageal reflux disease
Gross: irregular gastroesophageal junction with tongues of red granular mucosa extending up into the esophagus
Increased risk of dysplasia and esophageal adenocarcinoma

4. Esophageal carcinoma Squamous cell carcinoma Adenocarcinoma
Epidemiology
The most common type of esophageal cancer
Males>females; age usually>50
Risk factors
Heavy smoking and alchol use
Achalasia
Plummer-vinson syndrome
Tylosis
Prior lye ingestion
Presentation
Often asymptomatic until late in the course
Progressive dysphagia
Weight loss and anorexia
Bleeding
Hoarseness or cough (advanced cancers)
Diagnosis: endoscopy and biopsy
Treatment: surgery
Prognosis: poor
Adenocarcinoma
Arises in the distal esophagus
Associated with Barrett esophagus and dysplasia
Prognosis: poor

7. GASTRITIS

8. inflammation of gastric mucosa
acute gastritis
pathogens clear
acute inflammation (neutrophils )
chronic gastritis
autoimmune
bilious duodenal secretion reflex
HP infection

9. acute gastritis
Definition: acute inflammation, erosion, and hemorrhage of the gastric mucosa due to a breakdown of the mucosal barrier and acid-induced injury
Etiology: chronic aspirin or NSAID use/ Alcohol use/ Smoking/ Postsurgery/ Burns/ Ischemia/ Stress/ Uremia/ Chemotherapy
Presentation
　　Epigastric abdominal pain
　　Gastric hemorrhage, hematemesis, and melena

10. (1) acute irritated gastritis
1）pathogens：diet
2）lesions：edema, hyperemia, hypersection of mucus, erosion

11. (2) acute hemorrhagic gastritis
1）pathogens: medicines ( aspirin )/alcoholism
2）lesion: usually in fundus and body

12. (3) acute corrosive gastritis
1）pathogen：engulf acid/ base
2）lesion：stomach wall necrosis →perforation

13. (4) acute infective gastritis
1）pathogens: purulent bacterium
2）lesions: acute phlegmonous inflammation

14. 2. chronic gastritis—chronic mucosal inflammatory changes leading eventually to mucosal atrophy and epithelial metaplasia.
Pathogenesis
HP chronic infection
chronic irritation
autoimmune
reflex of bilious duodenal secretion

17. (1) chronic superficial gastritis (CSG) common
glands in lamina propria intact,
lymphocyte/plasma infiltrate in shallow mucosa

18. (2) chronic atrophic gastritis (CAG)
gross：mucosa thin, folds flatten LM
within mucosa: lymphocyte, plasma cells infiltrate, aggregate, lymph follicle form
mucosal proper glands (gastric glands,cardiac glands, pyloric glands）atrophy or disappear, dilate
intestinal metaplasia (replacement of gastric epithelium with columnar and goblet cells of intestinal-type), pseudopyloric metaplasia

19. chronic atrophic gastritis (CAG)
loss of rugal folds in the body and fundus

21. chronic atrophic gastritis

22. Persisting glands frequently undergo cystic dilation

23. Intestinal metaplasia
replacement of gastric epithelium with absorptive and goblet cells of intestinal-type
Variable gland loss and mucosal atrophy, lymphocyte and plasma cell infiltration in the lamina propria.

25. Fundic type (type A) Antral type （type B)
Autoimmune atrophic gastritis
rare
Involve the body and fundus
Autoantibodies to parietal cells / intrinsic factor
Loss of parietal cells
Decreased acid secretion
Increased serum secretion ( G cell hyperplasia)
Pernicious anemia (megaloblastic anemia due to lack of intrinsic factor and B12 malabsorption)
Helicobactor pylori gastritis
Common
Helicobactor pylori
Curved, gram negative rods
Urease producing
Risk of infection increase with age
Associated with chronic gastritis (type B)
Associated with duodenal / gastric peptic ulcers
Associated with gastric carcinoma
Gross: loss of rugal folds in the body and fundus
Micro:
mucosal atrophy with loss of glands and parietal
cells
Chronic lymphoplasmacytic inflammation
Intestinal metaplasia
foci of acute inflammation
Chronic inflammation with lymphoid follicules
Increased risk of gastric carcinoma

26. 8.1.3 peptic ulcer
Ulcer: defects in the mucosa that penetrate at least into the submucosa, and often into the muscularis propria or deeper
Definition: ulcers of the distal stomach and proximal duodenum caused by gastric secretion (hydrochloric acid and pepsin) and impaired mucosal defenses
Diagnosis: endoscopy ±biopsy
Treatment:
acid suppression (H2 blocker, proton pump inhibitor)
eradication of H. pylori
Complications:
hemorrhage: 1/3，common, hematemesis, melena, shock
iron deficiency anemia
penetration into adjacent organs: 5%, acute diffuse peritonitis , local peritonitis
perforation (X-ray: free air under the diaphragm)
pyloric obstruction : 2- 3%
gastric ulcer: 1%; duodenal ulcer: no

27. 2)Pathogenesis of peptic ulcer
Increased damage
Damaging factors HP
NSAIDs
smoking
alcohol
gas. acidity
Duo-gast.reflux
Peptic acid
pepsin
hemorrhage
p.stenosis
Normal mucosa
Peptic ulcer
healing
Impaired defenses
Defensive factors
ischeria
shock
Delayed
gastric empty
Malignant t.
Surface mucus secr.
HCO- into mucus
Mucosal blood flow
Epithelia regenera PG
Epithelial barrier
perforation
2)Pathogenesis of peptic ulcer
NSAIDs：非类固醇类抗炎药

31. gastric ulcer Associated with H. pylori (75%)
Location: lesser curvature of the antrum
Gross:
small (<2cm), solitary ulcers
round or oval shape
sharply demarcated, punched-out ulcers
overhanging margins
radiating mucosal folds, wheel spokelike fashion
base clean, flat, smooth

33. gastric ulcer

34. exudate layer：WBC+fibrin necrosis layer granulation tissue scar tissueLM
exudate layer：WBC+fibrin
necrosis layer
granulation tissue
scar tissue
Proliferative endocarteritis: inhibit regeneration/ prevent hemorrhage
Nodular regeneration of NF: pain
Classic presentation: burning epigastric pain, which worsens with eating

38. A渗出层 B:坏死层C:肉芽组织层 D:瘢痕层E:增生性动脉内膜炎 血栓机化再通F:创伤性神经瘤

39. Duodenal ulcer common Location: anterior wall of the proximal duodenum
Classic presentation: burning epigastric pain 1-3 hours after eating, which is relived by food
Peptic ulcer of the dudenum. The ulcer is small with a sharply punched-out appearance. Unlike cancerous ulcers, the margins are not elevated. The ulcer base shows a small amount of blood but is otherwise clean.

41. 8.2 tumor of digestive system

42. 8.2.1 Gastric carcinoma Epidemiology: Japan/ Chile/ Columbia
Risk factors:
dietary factors: smoked fish and meats/ pickled vegetables
HP infection
chronic atrophic gastritis
smoking
prior subtotal gastrectomy
presentation
often asymptomatic until late in the course
weight loss and anorexia
epigastric abdominal pain mimicking a peptic ulcer
early satiety
occult bleeding and iron deficiency anemia
Location: lesser curvature of the antrum

44. Gross
Large (>2cm), irregular ulcer
Heaped-up margins and a necrotic ulcer base
May also occur as a flat or polypoid mass
Metastasis
Virchow (sentinel) node: left supraclavicular lymph node
Krukenberg tumor: spread to the ovary
Diagnosis: endoscopy and biopsy
Treatment: gastrectomy
Prognosis: poor; over all 5-year survival 20%

45. Intestinal type
micro: gland-forming adenocarcinoma
Diffuse type
diffuse infiltration of stomach by poorly differentiated tumor cells
signet-ring cells: nucleus is displaced to the periphery by intracellular mucin
linitis plastica: thickened “leather bottle”-like stomach

47. pathologic change (1) early gastric car. (shallow spread car.） concept
confined to the mucosa and submucosa, regardless of the size of area, or absence of perigastric lymph node metastasis

48. protruded type (typeⅠ) >2 times thickness gastric mucosa, polypoid
图9-10 早期胃癌各型模式图
2）gross types
protruded type (typeⅠ)
>2 times thickness gastric
mucosa, polypoid
superficial type (type Ⅱ)
superficial elevated type（Ⅱa）
< 2 times thickness
superficial flat type （Ⅱb）
superficial depressed （ Ⅱc）
depth within mucosa
excavated type (type Ⅲ)
common, ulcer
早期胃癌各型模式图

53. 3）histologic types
tubular adenocarcinoma>papillary adenocarcinoma>undifferentiated carcinoma

54. (2) advanced gastric carcinoma
concept：extended below the submucosa into the muscular wall and has perhaps spread more widely
gross
① polypoid or fungating type
② ulceration type：
erosive crater, D>2.5cm
③ infiltrating type:（Linitis plastica）

56. 3）histologic types：
papillary adeno.，tubular adeno., mucous adeno., signal cell car., undifferentiated car.
Lauren：intestine type, diffuse type

59. fungating type

64. ulceration type (the ulcer is large with irregular, heaped-up margins
ulceration type (the ulcer is large with irregular, heaped-up margins. There is extensive excavation of the gastric mucosa with a necrotic gray area in the ddepest portion.

65. ulceration type

66. infiltrating type (a broad region of the gastric wall, or the entire stomach, is extensively infiltrated by maglinancy. The rigid and thickened stomach is termed a leather bottle stomach, or linitis plastica.)

67. Gastric adenocarcinoma (gland formation by malignant cells, which are invading the muscular wall of the stomach.)

68. Gastric mucous adenocarcinoma

69. Gastric signet cell carcinoma (permeate the mucosa and wall as scattered individual “signet-ring” cells or in small clusters.)

70. Gastric undifferentiated carcinoma

71. 4）spread pathways
① direct spread：liver, pancreas
② lymphatic metastasis：main pathways
Virchow lymph nodes
③ hematogenous metastasis：
liver/ lung/ bone/ brain
④ seeding： abdominal cavity, peritonaeum,
ovary—Krukenberg tumor