This document discusses gastrointestinal tract lesions, focusing on peptic ulcer disease and inflammatory bowel diseases (IBD) such as Crohn's disease and ulcerative colitis. It highlights the characteristics, epidemiology, pathogenesis, morphology, clinical features, and complications of these conditions. Detailed descriptions of ulcer types, histological findings, and treatment options are provided, emphasizing the chronic nature and potential for complications in IBD.

1. LESIONS OF
GASTROINTESTINAL TRACT
Dr. Ina Shah

2. PEPTIC ULCER DISEASE

3. 
Ulcer- breach in the mucosa of GIT that extends
through muscularis mucosa into the submucosa
or deeper

Erosion – epithelial disruption wiyhin the
mucosa not extending into muscularis mucosa.

Peptic ulcer- Chronic , usually solitary (<4cm in
diam) lesions that occur in any portion of the GIT
,exposed to aggressive action of acid/peptic juice.

4. 
Common site-

Duodenum-1st portion -90%}

Stomach- antrum –

At the gastro-oeso junction or barrete’s oeso
In patients with Zollinger – Ellison syndrome.

Within or adjacent to an ilial meckel’s
diverticulum.

Epidemiology
Middle aged or older adults
recurrent infection with H. Pylori.

Without any obvious ppting condition.

5. 
Pathogenesis
o Due to imbalance between gastroduodenal mucosal surface
defence & damaging force like gastric acid &pepsin.
o H.Pylori infection.
o Chronic use of NSAIDs.
o Cigarrete smoking & alcohol
o Corticosteroids
Morphology
Ant. Wall of duodenum is affected more often than post.
Wall.
Gastric ulcers are located mostly along the lesser curvature,
in or around the border zone betweeen oxyntic mucosa &
antral mucosa.
10%-20% of patients with gastric ulcer may have co-existent
duodenal ulcer.

6. 
Gross findings-
 Round to oval , sharply punched out defect with
relatively straight walls. The mucosal margins may
overhang the base slightly. The margins are usually
in level with surr. Mucosa or only slightly elevated.
Base – smooth &clean
Depth of ulcer- variable. Supe. lesions only involving
mucosa &musc. Mucosa to deeply excavated ulcers
with base on musc. mucosa.
Puckering of surr. mucosa due to scarring
Mucosal folds radiate from crater in spoke like
fashion.
Surr. gastric mucosa- oedematous & reddened due to
gastritis.

7. HISTOLOGY OF CHRONIC PEPTIC
ULCER

8. Duodenal ulcer Gastric ulcer
Pathological changes
Site First part of duodenum Along the lesser
curvature & pyloric
antrum
size Solitary,1-2.5 cm in
size, round to oval ,
punch out defect
Grossly similar
histology 4 layers-
necrotic,superficial
exudative,granulation
tissue, cicatrisation
similar
Complication Hemorrhage,
perforationis
common.sometimes
obstruction.
perforation.,hemorrhag
e &at times obstruction.
Malignant
transformation in <1%
cases.

9. Duodenal ulcer Gastric ulcer
Clinical features Pain-food-relief
pattern
Food-pain pattern
Night pain common No
vomitting ab common
Malena More common
hemetemesis More common
Loss of weight no significant
diet No particular choice Bland diet devoid of
fried foods, curries etc.
tenderness Rt hypochondrium Midline in
epigastrium
Seasonal variation marked ab

10. CHRONIC DUODENAL ULCER- 1ST
PART OF DUODENUM

11. CHRONIC PEPTIC ULCER WITH
MUCOPURULENT BED

12. IDIOPATHIC INFLAMMATORY
BOWEL DISEASE

Definition- a set of chronic infla. Conditions
resulting from inappropriate and persistant
activation of the mucosal immune system, driven
by the presence of normal intraluminal flora.

Two disorders- Crohn’s Disease (CD)
- Ulcerative Colitis(UC)

Both are chronic , relapsing ,infla. disorders of
unknown origin.

CD is an autoimmune disease that may affect
any portion of GIT ,but most often involvesthe
distal small intestine and colon.
UC is a chronic infla. disease limited to the colon
& rectum.

13. CHROHN’S DISEASE

An autoimmune disease affecting any part of GIT
,but most commonly affects distal small inte &
colon. There may be asso. systemic
manifestations.

3 main features-
1.Sharply delimited & transmural involvement of
bowel by infla. Process with mucosal damage.
2. presence of non caseating granuloma
3.Fissuring with formation of fistula.

14. Epidemiology

Western countries- 3 per 1,00,000 population.

Age- 20-30 yrs –peak
females> males
whites>blacks- 5:1
In U.S.- Jews >nonjews

Strong exogenous risk factor- smoking
Morphology

Site- small inte. – 40%
-colon- 30%
- both- 30%

15. MACROSCOPIC EXAMINATION-
Serosa - granular & dull gray.
Creeping fat- mesentric fat wraps around the bowel surface.
Mesentry is thickened,oedematous , fibrotic.
Inte. wall is rubbery & thick due to edema, infla. , fibrosis &
hypertrophy of muscularis propria. So, lumen is narrowed.
String Sign- due to narrowing of lumen of small inte. , on x-ray ,
thin stream of barium passes through the diseased segment.
Skip lesion- classic feature of CD. The sharp demarcation of
diseased bowel segments from adjacent normal bowel. when
multiple bowel segments are involved , the intervenning bowel is
essentially normal.
Ulcers- Initially focal mucosal ulcer, same as canker sores, edema
& loss of normal mucosal texture.
With progression, these ulcers coalease into long
serpentine linear ulcers , which are oriented along the long axis of
bowel.

16. CROHN’S DISEASE- APHTHOID
ULCER

17. COBBLE STONE APPEARANCE

18. 
Intervening mucosa is relatively normal. So
mucosa acquires Cobblestone appearance.

Narrow fissures develop between the fold of
mucosa which may penetrate through bowel wall
& leads to peritoneal adhesion & serositis.

Extension of fissures may lead to fistula or sinus
tract formation or free perforation or localised
abscesses.

19. MICROSCOPIC EXAMINATION
Mucosal inflammation-

Initially focal neutrophilic infilteration into the
epi. Layer.

Crypt abscess- neutrophils infilterate isolated
crypts & complete destruction of crypt occurs.

Chronic mucosal damage-

Hallmark of IBD
Villous blunting or irregularity & branching of
crypts with crypt destruction.

Progresssive atrophy in the colon.
Pyloric metaplasia or paneth cell metaplasia.

20. COMPLICATIONS
1. Malabsorption due to impaired absorption of
fat, vit-B12 ,proteins and electrolytes from the
diseased small bowel.
2. Fistula formation- occur in longstanding cases.
These may be internal fistulae bet’n the loops of
the intestine or external fistulae such as
enterocutaneous ,rectal and anal fistulae.
3. Stricture formation- due to extensive fibrosis.
4. Carcinoma- very rare.

21. ULCERATIVE COLITIS

Age grp- 20-30yrs
- 70-80yrs 2nd peak

M:F - equal

Clinical course is very long with many remissions
& exacerbations.
Accompaning features- nutritional defi. &
anemia.

Site- Rectosigmoid area(left sided disorder)
- Only rectum- ulcerative proctitis
- entire colon- pancolitis

22. GROSS FEATURES-

depends on stages of disease-
* Acute stage- surface of bowel is wet, covered with
blood & mucus.
-petechial hemorrhage is also seen.
-Pseudopolyp- elevated sessile reddish nodules, usually
multiple.
• Quiscent stage- ulceration is absent,mucosa is atrophic
with extensive submucosal fat deposition
* Advancedstage- the entire bowel becomes fibrotic &
narrowed.

23. MICROSCOPIC FEATURES
-primarily a mucosal & submucosal disease.
- Crypt abscess- collection of neutrophils in glandular
lumen
Progressive destruction of glands with marked
decrease in cytoplasmic mucus.
Regenerative changes- increase mitotic activity &
nuclear enlargement.
Paneth cell metaplasia.
Stromal infla. Infilterate composed of
neutrophils,lymphocytes,plasma cells,few histiocytes
and mast cells.
- Mast cells are said to accumulate at the line of
demarcation.

24. 
Blood vesels are dilated &mucosal capillary
thrombi may be seen.

The pseudopolyps are largely composed of
granulation tissue mixed with inflamed &
hyperemic mucosa.

Submucosa may shaw non specific granulation
tissue.

Appendix is involved in 10-20% cases.

Local complications-

Perforation with peritonitis & abscess

Toxic megacolon

Venous thrombosis

Dysplasia & carcinoma

Treatment- depends on extent, duration & severity
-local and systemic steroids
- total colectomy