Chronic gastritis is defined as chronic inflammatory changes in the gastric mucosa leading to mucosal atrophy and epithelial metaplasia. The most important cause is chronic Helicobacter pylori infection, which causes type B gastritis affecting mainly the antrum. Autoimmune mechanisms can cause type A gastritis affecting the body and fundus. Chronic gastritis is usually asymptomatic but long term risks include gastric atrophy, intestinal metaplasia, and increased risk of gastric adenocarcinoma.

1. Diseases of the
gastrointestinal tract
Pathology,

2. Anatomy of the digestive system

3. •
•
•
•
•
•
•
•
CONTENTS
Esophagitis
Esophageal carcinoma
Gastritis (acute, chronic )
Peptic ulcer
Gastric tumors
Appendicitis
Inflammatory bowel disease
Tumors of the small and large
intestines

4. Esophagitis
Inflammation of the esophagus occurs most commonly from reflux,
although a number of other clinical conditions and infections may
also cause esophagitis as under:
Reflux esophagitis
Reflux of the gastric juice is the commonest cause of esophagitis.
PATHOGENESIS. Gastro-esophageal reflux may occur in normal
healthy individuals after meals and in early pregnancy. However,
in some clinical conditions, the gastro-esophageal reflux is
excessive, resulting in inflammation of the lower esophagus.

5. MORPHOLOGIC FEATURES.
Endoscopically, the demarcation between normal
squamous and columnar epithelium at the junctional
mucosa is lost. The affected distal esophageal mucosa is
red, friable and bleeds on touch.

6. Microscopically, the reflux changes in the distal
esophagus include basal cell hyperplasia and deep
elongation of the lamina propria papillae. In early stage,
mucosa and submucosa are infiltrated by some
eosinophils with or without neutrophils; in chronic
stage, there is lymphocytic infiltration and fibrosis of
all the layers of the esophageal wall.

7. Reflux esophagitis
Numerous eosinophils (arrows) are present within the mucosa,
and the stratified squamous epithelium has not undergone
complete maturation because of ongoing inflammatory damage.

8. Clinical Features
The dominant manifestation of reflux disease is
heartburn, sometimes accompanied by regurgitation
of a sour brash. The severity of symptoms is not
closely related to the presence and degree of
anatomic esophagitis. The potential consequences of
severe reflux esophagitis are bleeding, development
of stricture, and Barrett esophagus, with its
predisposition to malignancy.

9. Barrett esophagus



Barrett esophagus is defined as the replacement of the normal
distal stratified squamous mucosa by metaplastic columnar
epithelium containing goblet cells.
It is a complication of long-standing gastroesophageal reflux;
Barrett esophagus affects males more often than
females(ratio of 4:1) and is much more common in whites than in
other races;
Persons with Barrett esophagus have a 30- to 100-fold greater
risk of developing esophageal adenocarcinoma than do normal
populations, the greatest risk being associated with high-grade
dysplasia.

10. Barrett esophagus


Barrett esophagus is apparent as a salmon-pink,
velvety mucosa between the esophageal squamous
mucosa and the gastric mucosa；
It may exist as “tongues” extending up from the
gastroesophageal junction, as an irregular
circumferential ban displacing the squamocolumnar
junction cephalad.
Morphology

11. Barrett esophagus
A. Normal gastroesophageal junction；B. The granular zone of
Barrett esophagus(arrow); C. Endoscopic view showing red
velvety gastrointestinal-type mucosa extending from the
gastroesophageal orifice

12. Barrett esophagus



Microscopically, the esophageal squamous
epithelium is replaced by metaplastic comumar
epithelium;
Barrett mucosa may be quite focal and variable
from one site to the next;
Critical to the pathologic evaluation is the
recognition of dysplastic changes in the mucosa
that may be precursors of cancer.

13. Microscopic view showing squamous mucosa (left) and
intestinal-type columnar epithelial cells in glandular mucosa。
Barrett esophagus

14. Part of the esophagus undergoes metaplastic change to
columnar epithelium of intestinal type。
Barrett esophagus

15. Esophageal carcinoma
Carcinoma of the esophagus is diagnosed late, after
symptomatic esophageal obstruction (dysphagia) has
developed and the tumour has transgressed（侵犯）
the anatomical limits of the organ. The tumour occurs
more commonly in men over 50 years of age. Prognosis
is dismal: with standard methods of therapy (surgical
resection and/or irradiation), 70% of the patients die
within one year of diagnosis.

16. Esophageal carcinoma
ETIOLOGY
Although exact etiology of carcinoma of the esophagus is not
known, a number of factors have been implicated as under:
1. Diet and personal habits:
i) Heavy smoking
ii) Alcohol consumption
iii) Intake of foods contaminated with fungus
2. Esophageal disorders: Esophagitis (especially Barrett’s
esophagus in adenocarcinoma)
3. Other factors: Race; Family history; Genetic factors and HPV
infection.

17. MORPHOLOGIC FEATURES
Carcinoma of the esophagus is mainly of 2 types—squamous cell
(epidermoid) carcinoma and adenocarcinoma.
SQUAMOUS CELL CARCINOMA.
Squamous cell or epidermoid carcinoma
comprises 90% of primary esophageal
cancers. The disease occurs in 6th to 7th
decades of life and is more common in
men than women. Half of the squamous
cell carcinomas of esophagus occur in
the middle third, followed by lower third.

18. i)
Grossly, 3 types of patterns are recognized :
Polypoid fungating type—is the most common form. It appears as
a cauliflower-like friable mass protruding into the lumen.
ii) Ulcerating type—is the next common form. It looks grossly like
a necrotic ulcer with everted edges (边缘外翻)
iii) Diffuse infiltrating type—appears as an annular（环形）,
stenosing narrowing of the lumen due to infiltration into the wall
of esophagus.
Gross patterns of
squamous cell carcinoma
of the esophagus

19. Polypoid fungating
type
Ulcerating type Diffuse infiltrating type

20. Microscopically, majority of the squamous cell carcinomas of the
esophagus are well-differentiated or moderately differentiated
Prickle cells, keratin formation and epithelial pearls(角化珠) are
commonly seen.
Low power view of cancer invasion of the submucosa

21. ADENOCARCINOMA
Adenocarcinoma of the esophagus constitutes less than 10% of
primary esophageal cancer. It occurs predominantly in men in
their 4th to 5th decades. The common locations are lower and
middle third of the esophagus. These tumours have a strong and
definite association with Barrett’s esophagus in which there are
foci of gastric or intestinal type of epithelium.
Grossly, esophageal adenocarcinoma appears as nodular, elevated
mass in the lower esophagus.

22. ADENOCARCINOMA
Microscopically, adenocarcinoma of the esophagus can have 3
patterns:
i) Intestinal type—is similar to that seen in adenocarcinoma of
intestine or stomach.
ii) Adenosquamous type—is an irregular admixture of
adenocarcinoma and squamous cell carcinoma.
iii) Adenoid cystic type—is an uncommon variety.

23. SPREAD
The esophageal cancer spreads locally as well as to distant sites.
i) Local spread. This is the most important mode of spread and is
of great importance for surgical treatment. The local spread may
occur in the transverse(横向) as well as longitudinal direction（纵
向）.
ii) Lymphatic spread. Submucosal lymphatic permeation may lead to
multiple satellite nodules away from the main tumour. Besides,
the lymphatic spread may result in metastases to the cervical,
paraesophageal, and tracheobronchial lymph nodes.
iii) Haematogenous spread. Blood-borne metastases from the
esophageal cancer are rare.

24. Gastritis
Gastritis is simply defined as inflammation of the
gastric mucosa. By far the majority of cases are
chronic gastritis, but occasionally, distinct forms of
acute gastritis are encountered.
Acute gastritis
Chronic gastritis

25. Acute gastritis
•
•
•
Acute gastritis is an acute mucosal inflammatory
process.
Accompanied by hemorrhage and by sloughing of the
superficial mucosal epithelium (erosion糜烂).
The severe erosive form is an important cause of
acute gastrointestinal bleeding.

26. 



Pathogenesis
A variety of etiologic agents have been implicated in
the causation of acute gastritis.
1.Diet and personal habits:
Highly spiced food
Excessive alcohol consumption
Malnutrition
Heavy smoking

27. 

2. Infection
Bacterial infections e.g. Helicobacter pylori
Viral infections e.g. viral hepatitis, influenza
Helicobacter pylori gastritis. A Steiner silver stain demonstrates
the numerous darkly stained Helicobacter organisms along the
luminal surface of the gastric epithelial cells.

28. 

3.Drugs
Intake of drugs like nonsteroidal anti-inflammatory
drugs(NSAIDs), aspirin, cortisone, chemotherapeutic agents.
4. Chemical and physical agents
Intake of corrosive chemicals such as caustic soda(烧碱)
Gastric irradiation
Corrosive gastritis

29. 


5.Severe stress
Emotional factors like shock, resentment etc.
Trauma(创伤)
Surgery
Acute hemorrhagic gastritis

30. MORPHOLOGIC FEATURES
Grossly, the gastric mucosa is edematous with
abundant mucus and haemorrhagic spots.
Microscopically, depending upon the stage, there is
variable amount of edema and infiltration by
neutrophils in the lamina propria（固有层）. In acute
haemorrhagic and erosive gastritis, the mucosa is
sloughed off and there are haemorrhages on the
surface.

31. Clinical features
Depending on the severity of the anatomic changes,
acute gastritis may be entirely asymptomatic, may
cause variable epigastric（上腹部） pain with nausea
and vomiting , or may present as overt
hematemesis（吐血）, melena（黑粪）, and potentially
fatal blood loss.

32. Chronic gastritis


Chronic gastritis is defined as the presence of
chronic inflammatory changes in the mucosa leading
eventually to mucosal atrophy and epithelial
metaplasia.
Chronic gastritis is the commonest histological
change observed in biopsies（活检） from the stomach
The condition occurs more frequently with
advancing age, average age for symptomatic chronic
gastritis is 45 years.

33. Etiology and pathogenesis
1.Helicobacter pylori
The most important etiology association is chronic infection by
the H. pylori. Most individuals with the infection have the
associated gastritis but are asymptomatic.
2.Autoimmune damage
Autoimmune damage appears to be a major causal factor in
type A gastritis, which results from the production of
autoantibodies to the gastric gland parietal cells.
3.A variety of mucosal irritants（刺激物）
Tobacco, alcohol and reflux of biliary secretions. It may be
closely correlated with type B gastritis.

34. Clinicopathologic classification
Based on the type of mucosa affected, a clinicopathologic
classification has been proposed:
1.Type A gastritis(Autoimmune gastritis)
Type A gastritis involves mainly the body-fundic（胃底） mucosa.
It is also called autoimmune gastritis due to the presence of
circulating antibodies;
2.Type B gastritis(H. pylori-related)
Type B gastritis mainly involves the region of antral mucosa and
is more common. It is also called hypersecretory gastritis due to
excessive secretion of acid, commonly due to infection with H.
pylori.

35. 3.Type AB gastritis(Mixed gastritis)
Type AB gastritis affects the mucosal region of A as well as B
types(body-fundic and antral mucosa). This is the most common
type of gastritis in all age groups. It is also called environmental
gastritis because a number of unidentified environmental
factors have been implicated in its etiopathogenesis.
Clinicopathologic classification

36. Morphologic classification
Histologically, criteria for categorisation are based on the followin
i)Extent of inflammatory changes in the mucosa(i.e. superficial or
ii)Activity of inflammation(i.e. quiescent or active; acute or chroni
iii)Presence of and type of metaplasia(i.e. intestinal or pseudopylo
Base on above, morphologic classification has been proposed:
1.Chronic superficial gastritis
2.Chronic atrophic gastritis
3.Chronic hypertrophic gastritis
4.Uncommon forms of chronic gastritis

37. •
•
•
•
1. Chronic superficial gastritis, CSG:
Mucosal congestion and edema.
Chronic inflammatory cell infiltration (mainly lymphocytes and
plasmacytes浆细胞) in superficial mucosa.
Glands keep intact.
May resolve completely or may progress to chronic gastric
atrophy.

38. 2. Chronic atrophic gastritis, CAG:



Glandular atrophy, decrease or loss of specialized
secretory cell ( parietal cells, chief cells)
Chronic inflammatory cell infiltration and H.pylori-
induced proliferation of lymphoid tissue within the
gastric mucosa.
Intestinal and pseudopyloric metaplasia are commonly
associated with atrophic gastritis.

39. 2. Chronic atrophic gastritis, CAG:
A.
B.
There is marked gastric atrophy with disappearance of gastric
glands and appearance of goblet cells (intestinal metaplasia).
Photomicrograph showing chronic atrophic gastritis with
intestinal metaplasia.

40. Intestinal metaplasia
•
•
Refers to the replacement of gastric epithelium with columnar
and goblet cells of intestinal variety; Paneth cells and
endocrine cells may also be present.
Gastric intestinal type carcinomas appear to arise from
dysplasia of this metaplastic epithelium.

41. The difference between Type A and Type B
Type A Type B
Location mainly in the corpus in the antrum
Gastric secretion severe impair moderate
imparir
Parietal cell Antibody + -
Intrinsic antibody + -
Serum gastrin higher lower
Autoimmune + -
endocrine disorders frequent none
Malignant change none about 8%

42. 


3. Chronic hypertrophic gastritis
The gastric pits are elongated and are tortuous;
The mucosa is markedly thickened and parts of muscularis
mucosae (粘膜肌层)may extend into the thickened folds;
Epithelium-lined cysts are commonly seen in the glandular
layer
4.Uncommon forms of chronic gastritis
A few other types of gastritis are as: Eosinophilic gastritis;
Chronic follicular gastritis; Haemorrhagic gastritis;

43. Clinicopathological correlation
1. Usually causes few or no symptoms; upper abdominal
discomfort and nausea and vomiting can occur;
2. When severe parietal cell loss, hypochlorhydria（胃酸
过少） or achlorhydria（胃酸缺乏） and
hypergastrinemia are characteristically present;
3. The long-term risk of gastric carcinoma for persons
with H. pylori –associated chronic gastritis is increased
about 5-fold relative to the normal population.

44. Peptic ulcers


Definition: Peptic ulcers are chronic, most often
solitary, lesions that occur in any portion of
gastrointestinal tract exposed to the aggressive
action of acidic peptic juices(酸性消化液).
At least 98% of peptic ulcers are either in the first
portion of the duodenum or in the stomach;
The male/female ratio for duodenal ulcers is about 3:
1;

45. Etiology and pathogenesis


Peptic ulcers are created by an imbalance between the
gastroduodenal mucosal defenses and the damaging forces that
overcome such defenses.
The following conditions are key for the development of peptic
ulcers:
(1)H. pylori infection, which has a strong causal relationship with
peptic ulcer development:
H. pylori infection is present in virtually all patients with
duodenal ulcers and about 70% of those with gastric ulcers.
Antibiotic treatment of H.pylori infection promotes healing of
ulcers and tends to prevent their recurrence.

46. 

(2)NSAIDs-induced mucosal injury:
NSAIDs are the major cause of peptic ulcer disease in persons
who do not have H. pylori infection;
NSAIDs are responsible for direct toxicity, endothelial damage
and epithelial injury to both gastric as well as duodenal mucosa.
(3)Acid-pepsin secretions:
Peptic ulcers never occur in association with pernicious
anaemia(恶性贫血) in which there are no acid and pepsin-
secreting parietal and chief cells respectively

47. 

(4)Genetic factors;
People with blood group O appear to be more prone to
develop peptic ulcers than those with other blood
groups;
Genetic influences appear to have greater role in
duodenal ulcers

48. Morphology
Gross appearance:
1. Shape: round, sharply, punched-out holes in the mucosa.
2. Size: usually less than 2 cm in diameter.
3. Base: remarkably clean and flat.
4. Location: the lesser curvature of the stomach; the first
portion of the duodenum.
5. The mucosal folds radiating from the crater.

49. Peptic ulcer of the duodenum
The ulcer is small(2cm) with a sharply punched-out
appearance. Unlike cancerous ulcers, the margins are not
elevated. The ulcer base is clean.

50. Microscopic appearance
1. Microscopically, chronic peptic ulcers have four
histological zones :
(1)Necrotic zone—lies in the floor of the ulcer and is
composed of fibrinous exudate containing necrotic
debris(坏死碎片) and a few leucocytes;
(2)Superficial exudative zone—lies underneath the
necrotic zone. The tissue elements show coagulative
necrosis(凝固性坏死) giving eosinophilic, smudgy
appearance with nuclear debris;

51. Microscopic appearance
(3) Granulation tissue zone—is seen merging into the
necrotic zone. It is composed of nonspecific
inflammatory infiltrate and proliferating capillaries;
(4)Zone of cicatrisation—is seen merging into thick
layer of granulation tissue. It is composed of dense
fibrocollagenic scar tissue(致密的纤维结缔组织).

52. The panel shows the basis of a nonperforated ulcer,
demonstrating necrosis(N), inflammation(I), granulation
tissue(G) and fibrosis(F).

53. The layers of necrosis(N),
inflammation(I), granulation
tissue(G), and scar(S)
moving from the luminal
surface at the top to the
muscle wall at the bottom.

54. Clinical features
1.
Peptic ulcers are remitting（缓解） and relapsing lesions.
Age: The peak incidence of duodenal ulcer is in 5th decade while
that for gastric ulcer is a decade later
2.People at risk: Duodenal ulcer occurs more commonly in people
faced with more stress and strain of life(e.g. executives, leaders),
while gastric ulcer is seen more often in labouring groups.
3.Pain: In gastric ulcer, epigastric pain occurs immediately or
within 2 hours after food and never occurs at night. In duodenal
ulcer, pain is severe, occurs late at night(hunger pain) and is
usually relieved by food.

55. 5. Vomiting: Vomiting which relieves the pain is a
conspicuous feature in patients of gastric ulcer.
Duodenal ulcer patients rarely have vomiting but instead
get heart-burn(retrosternal pain) and “water brash”
(burning fluid into the mouth)
6.Heamatemesis（吐血） and melaena: Heamatemesis
and melaena occur in gastric ulcers in the ratio of 60:40,
while in duodenal ulcers in the ratio of 40:60

56. Complication
1. Haemorrhage:
Chronic blood loss may result in iron deficiency anemia. Severe
bleeding may cause “coffee ground” vomitus or melaena. A
penetrating chronic ulcer may erode a major artery and
cause a massive and severe hematemesis and sometimes
death
2. Perforation:
A perforated peptic ulcer is an acute abdominal emergency.
Perforation occurs more commonly in chronic duodenal ulcers
than chronic gastric ulcers.

57. Complication
3. Obstruction
Development of fibrous scar at or near the pylorus results in
pyloric stenosis（幽门狭窄）. Healed ulcers along the lesser
curvatures may produce “hourglass” deformity（沙漏畸形） due
to fibrosis and contraction.
4. Malignant transformation
A chronic duodenal ulcer never turns malignant, while less than
1% of chronic gastric ulcers may transform into carcinoma.

58. Gastric carcinoma
Gastric carcinoma is the most common cause of death
in malignant tumors of alimentary system in China. It
usually appears in fifth and sixth decade of life. The
male-female ratio is approximately 2~3:1.

59. Etiology
A number of etiologic factors have been implicated in causation
of gastric cancer. These are as under:
1.H. pylori infection: Epidemiologic studies throughout world
have shown that a seropositive with H. pylori is associated with
3 to 6 times higher risk of development of gastric cancer.
2.Dietary factors
3.Geographical factors: There are geographic variations in the
incidence of gastric cancer. Japan, Chile and Italy have the
highest recorded death rate from gastric cancer.
4.Racial factors 5.Genetic factors

60. Histologic classification
Histologic appearances of gastric cancer are classified
into the intestinal type and diffuse type.
i)Intestinal variant: is composed of malignant cells
forming neoplastic intestinal glands resembling those of
colonic adenocarcinoma.
ii)Diffuse variant: is composed of gastric-type mucous
cells that generally do not form glands but rather
permeate the mucosa and wall as scattered individual
“signet-ring” cells or small clusters in an “infiltrative”
growth pattern.

61. Gastric cancer
A. Demonstrating intestinal type of
gastric carcinoma with gland
formation by malignant cells that
are invading the muscular wall of
the stomach
B. Diffuse type of gastric carcinoma
with signet-ring tumor cells

62. Clinical classification
Based on the depth of invasion, macroscopic growth
pattern and histologic subtype, gastric carcinoma are
classified into Early gastric carcinoma and Advanced
gastric carcinoma.
I) Early gastric carcinoma
Early gastric carcinoma is defined as a lesion confined
to the mucosa and submucosa , regardless of the
presence or absence of perigastric lymph node
metastases.

63. I) Early gastric carcinoma
Grossly, the lesion of EGC may have 3 patterns-
polypoid(protruded), superficial and ulcerated:
Type I : Polypoid type
Type IIa: Superficial elevated
Type IIb: Superficial flat
Type IIc: Superficial depressed
Type III: Ulcerated type
Diagrammatic representation of gross pattern of early
gastric carcinoma

64. Histologically, EGC is a typical glandular adenocarcinoma,
usually well-differentiated type. Prognosis of EGC
after surgical resection is quite good, 5-year survival
rate being 93-99%.
II)Advanced gastric carcinoma
Advanced gastric carcinoma is a neoplasm that has
extended below the submucosa into the muscular wall
and has perhaps spread more widely. It has following 4
patterns:

65. i)Ulcerative carcinoma: This is the most common pattern.
Histologically, ulcerative carcinoma are poorly-differentiated
adenocarcinomas, which invade deeply into the stomach wall.
Tubular and acinar patterns are seen more commonly.
A. The luminal surface shows an elevated irregular growth with ulcerated
surface. B. Malignant cells forming irregular glands are seen invading the
layers of the stomach wall.

66. ii)Fungating (polypoid) carcinoma:
The second common pattern is a cauliflower growth
projecting into the lumen. It is seen more often in the
fundus.

67. iii)Scirrhous carcinoma(Linitis plastica)(革囊胃):
The stomach wall is thickened due to extensive desmoplasia(结缔
组织形成) giving the appearance as “leather bottle stomach” or
“linitis plastica”. The lumen of the stomach is reduced..
C. The wall of the stomach is markedly thickened and fibrotic while the mucosal
folds are lost D. Microscopy shows characteristic signet ring tumour cells
having abundant mucinous（粘液）

68. iv)Colloid (Mucoid) carcinoma
The tumour grows like masses
having gelatinous（凝胶状）
appearance due to secretion of
large quantities of mucus.
Histologically, mucoid carcinoma
contains abundant pools of
mucin in which are seen a small
number of tumour cells,
sometimes having signet-ring
appearance.

69. Spread
Carcinoma of the stomach may spread by the following routes:
1: Direct spread
Direct spread by local extension is the most common feature of
gastric carcinoma. After the peritoneal covering of the stomach
has been invaded, transcoelomic dissemination may occur in any
other part of the peritoneal cavity but ovarian masses occur more
commonly, referred to as Krekenberg tumours
2.Lymphatic spread
Metastases to regional lymph nodes occur early, especially in the
scirrhous carcinoma. Involvement of left supraclavicular lymph
node, Virchow sign, is sometimes the presenting feature of
gastric carcinoma.
3.Haematogenous spread
Blood spread of gastric carcinoma may occur to the liver, lungs,
brain, bones, kidneys and adrenals. It occurs more commonly with
the poorly differentiated carcinoma.

70. Clinical features





The usual clinical features are as under:
Persistent abdominal pain
Gastric distension（胃胀） and vomiting
Loss of weight
Loss of appetite
Anaemia（贫血）, weakness , malaise（全身乏力）

71. Appendicitis
Acute appendicitis is the most common acute
abdominal condition confronting the surgeon. The
condition is seen more commonly in older children and
young adults.
The inflamed appendix(bottom)
is red, swollen, and covered
with a fibrinous exudate. For
comparison, a normal
appendix is shown(top).

72. Appendicitis
Etiopathogenesis
The most common mechanism is obstruction of the lumen from
various etiologic factors that leads to increased intraluminal
pressure. This presses upon the blood vessels to produce
ischemic injury which in turn favours the bacterial proliferation
and hence acute appendicitis.

73. Morphologic features
Grossly, In early acute appendicitis, the organ is swollen and
serosa shows hyperaemia. In well-develop acute inflammation
called acute suppurative appendicitis, the serosa is coated with
fibrinopurulent exudate and engorged vessels on the surface. In
further advanced cases called acute gangrenous appendicitis,
there is necrosis and ulcerations of mucosa which extend through
the wall and the surface is coated with greenish-black
gangrenous necrosis.

74. Microscopically, the most important diagnostic histological
criterion is the neutrophilic infiltration of the muscularis. In
early stage, the other changes are congestion and edema of the
appendiceal wall. In late stage, the mucosa is sloughed off, the
wall becomes necrotic, the blood vessels may get thrombosed and
there may be neutrophilic abscesses in the wall.
Acute phlegmonous
appendicitis/ acute
suppurative appendicitis:
Microscopic appearance
showing neutrophilic
infiltration into the

75. Inflammatory Bowel Disease (IBD)
1.
Definition: The term “inflammatory bowel disease(IBD)” is
commonly used to include 2 idiopathic bowel diseases having many
similarities but the conditions usually have distinctive
morphological appearance. These 2 conditions are Crohn’s
disease(regional enteritis) and ulcerative colitis.
Crohn’s disease or Regional enteritis is an idiopathic chronic
ulcerative IBD, characterised by transmural（透壁性的）,
noncaseating（非干酪样） granulomatous inflammation,
affecting most commonly the segment of terminal ileum and/or
colon,

76. 2. Ulcerative colitis is an idiopathic form of acute and
chronic ulcero-inflammatory colitis affecting chiefly the
mucosa and submucosa of the rectum and descending
colon.
Both diseases can occur at any age but are more
frequent in 2nd and 3rd decades of life. Female are
affected slightly more often.

77. Etiology and Pathogenesis
The normal intestine is in a steady state of
“physiologic” inflammation, representing a dynamic
balance between factors that activate the host immune
system and host defense that down-regulate
inflammation and maintain the integrity of the mucosa.
The exact etiology of IBD remains unknown. However,
the pathogenesis involves genetic susceptibility, failure
of immune regulation, and triggering by microbial flora.

78. Crohn’s disease
This disease may affect any level of the alimentary tract, from
mouth to anus, but most commonly located at the terminal ileum.
Grossly, characteristic feature is the multiple, well-
demarcated segmental bowel. The wall of the affected
bowel segment is thick and hard, resembling a “hose pipe”
. The lumen of the affected segment is markedly
narrowed. The mucosa shows “serpiginous ulcers”. While
intervening surviving mucosa is swollen giving “cobble
stone appearance”. There may be deep fissuring into the

79. 1.
2.
3.
4.
Histologically, the characteristic features are as follows:
Transmural inflammatory cell infiltrate consisting of
chronic inflammatory cells(lymphocytes, plasma cells and
macrophages) is the classical microscopic feature.
Non-caseating, sarcoid-like granulomas are present in
all the layers of the affected bowel wall in 60% of cases.
There is patchy ulceration of the mucosa which may
take the form of deep fissures.
There is widening of the submucosa due to edema and
foci of lymphoid aggregates.

80. Crohn’s disease showing a
deep fissure extending into
the muscle wall, shallow ulcer
(upper right) and relative
preservation of the
intervening mucosa.
Abundant lymphocyte
aggregates are present.

81. Ulcerative colitis
Ulcerative colitis is an ulceroinflammatory diseases
affecting the colon, which is limited to the mucosa and
submucosa, except in the most severe cases. Ulcerative
colitis begins in the rectum and extends proximally in a
continuous fashion, sometimes involving the entire
colon.

82. Ulcerative colitis
Grossly, the characteristic feature is the continuous
involvement of the rectum and colon without any
uninvolved skip areas. Mucosa shows linear and
superficial ulcers, usually not penetrating the
muscular layer. The intervening intact mucosa may
form inflammatory “pseudopolyps”. The muscle layer is
thickened due to contraction.

83. Histologically, the changes in the “active disease process”
are as under:
1.Crypt distortion, cryptitis and focal accumulations of
neutrophils forming crypt abscesses.
2. Marked congestion, dilatation and haemorrhages from
mucosal capillaries.
3. Superficial mucosal ulceration, usually not
penetrating into the muscle coat, and is accompanied by
nonspecific inflammatory cell infiltrate.

84. 4. Goblet cells are markedly diminished in cases of active
disease.
5.In long-standing cases, epithelial cytologic atypia
ranging from mild to marked dysplasia and sometimes
developing into carcinoma in situ and frank
adenocarcinoma.

85. Ulcerative colitis. Low-power micrograph showing marked chronic
inflammation of the mucosa with atrophy of colonic glands,
moderate submucosal fibrosis, and a normal muscle wall.

86. Distinguishing features of Crohn’s Disease and Ulcerative Colitis
Macroscopic
Feature
Crohn’s Disease Ulcerative Colitis
Distribution Segmental with skip
areas
Continuous without skip
areas
Location Commonly terminal ileum
and/or ascending colon
Commonly rectum,
sigmoid colon and
extending upwards
Extent Usually involves the
entire thickness of the
affected segment
Usually superficial,
confined to mucosal
layers
Ulcers Serpiginous ulcers, may
develop into deep
fissures
Superficial mucosal
ulcers without fissures
Pseudopolyps Rarely seen Commonly present
Fibrosis Common Rare

87. Distinguishing features of Crohn’s Disease and Ulcerative Colitis
Microscopic
Feature
Crohn’s Disease Ulcerative Colitis
Depth of
inflammation
Typically transmural Mucosal and submucosal
Type of
inflammation
Non-caseating
granulomas and
infiltrate of
mononuclear
cells(lymphocytes,
plasma cells and
macrophages)
Crypt abscess and non-
specific acute and
chronic inflammatory
cells(lymphocytes,
plasma cells, neutrophils,
eosinophils, mast cells)
Mucosa Patchy ulceration Haemorrhagic mucosa
with ulceration
Submucosa Widened due to edema
and lymphoid
aggregates
Normal or reduced in
width

88. Colorectal carcinoma
Colorectal cancer comprises 98% of all malignant
tumours of the large intestine. The incidence of
carcinoma of the large intestine rises with age; average
age of patients is about 60 years. Cancer in the rectum
is more common in males than females in the ratio of 2:1.

89. Etiology
Etiology of colorectal carcinoma is not clear but a few
etiological factors have been implicated:
1.Geographic variations. It is much more common in
North America, Northern Europe than in South America,
Africa and Asia.
2.Dietary factors. i)A low intake of vegetable fibre-diet
leading is associated with higher risk of colorectal
cancer. ii)Consumption of large amounts of fatty foods
results in excessive cholesterol(胆固醇) which may be

90. 3. Adenoma-carcinoma sequence. There is strong
evidence to suggest that colonic adenocarcinoma
evolves from pre-existing adenomas, referred to as
adenoma-carcinoma sequence.
4.Other factors. Presence of certain pre-existing
diseases such as inflammatory bowel disease(especially
ulcerative colitis) increase the risk of developing
colorectal cancer subsequently.

91. Morphologic features


Grossly, there are distinct differences between the
growth on the right and left half of the colon.
Right-sided colonic growths tend to be large,
cauliflower-like, soft and friable masses projecting into
the lumen. Obstruction is uncommon.
Left-sided colonic growths have napkin-ring
configuration i.e. they encircle the bowel wall
circumferentially with increased fibrous tissue forming
annular ring, and have central ulceration on the
surface.

92. Microscopically, the appearance of right and left-sided
growths is similar. Almost all are adenocarcinomas that
range from well-differentiated to undifferentiated,
frankly anaplastic masses. Many tumours produce mucin,
which is secreted into the gland lumina or into the
interstitium of the gut wall. Cancers of the anal zone
are predominantly squamous cell in origin.

93. Spread
Carcinoma of the large intestine may spread by the following
routes:
1.Direct spread. The tumour spreads most commonly by direct
extension in both ways- circumferentially into the bowel wall as
well as directly into the depth of the bowel wall to the serosa.
2. Lymphatic spread. Spread via lymphatics occurs rather
commonly and involves the regional lymph nodes in the vicinity of
the tumour.
3. Haematogenous spread. Blood spread of large bowel cancer
occurs relatively late and involves the liver, lungs, brain and

94. Clinical Features
Clinical symptoms in colorectal cancer are as follows:
1.Occlut bleeding(melaena)
2.Change in bowel habits, more often in left-sided
growth
3.Loss of weight
4.Loss of appetite
5.Anaemia, weakness, malaise
The most common complications are obstruction and
haemorrhage; less often perforation and secondary

95. THE END