This document discusses various ulcerative lesions of the intestine. It begins by describing the normal histology of the small and large intestine. It then lists and describes the major types of ulcerative lesions including duodenal and amoebic ulcers, typhoid ulcers, tuberculous ulcers, bacillary dysentery, inflammatory bowel disease (ulcerative colitis and Crohn's disease), carcinoma, and others such as GVHD and Behcet's syndrome. For each type of ulcer, it discusses causative agents, pathogenesis, gross and microscopic morphology, clinical features, and complications.

1. ULCERATIVE LESIONS OF
INTESTINE
Dr. Roopa Urs
Assistant professor

4. Histology of duodenum

5. Histology of jejunum

6. Histology of ileum

7. Payer’s patches

8. Electron microscopy- villi

10. Colonic mucosa

11. What are the ulcerative lesions?
• Duodenal Ulcer
• Amoebic ulcer
• Typhoid ulcer
• Tuberculous ulcer
• Bacillary dysentry
• Viral
-CMV
-AIDS

12. • IBD
-Ulcerative colitis
-Crohns disease
• Carcinoma
• Others
GVHD- Graft Verses Host Disease
Hyperplastic tuberculosis
Behcet’s syndrome

13. Duodenal Peptic Ulcers
• Young men
• Causes- H.pylori
Stress, spicy food
NSAID- aspirin
Cigarette smoking
Heavy drinking
Chemotherapy/Radiation therapy
• Symptoms- Burning sensation, bloating, hunger,

14. • Pathogenesis
Alteration in the balance b/w acid production
and mucosal defence barrier resulting in
damage to the lining epithelium.

15. GROSS
Chronic duodenal ulcer
Proximal duodenum
 few centimeters of
pyloric valve n involve
anterior duodenal valve
Solitary
<0.3cm
Shallow
0.6cm- deeper ulcers
Round, oval, sharply
punched out defect
Mucosal margin may
overhang the base slightly
Base is smooth and
clean as a result of peptic
digestion of exudate
Blood vessels+

16. MICROSCOPY
• Active ulcers the base may have thin layer of
fibrinoid debris underlaid by neutrophilic
inflammatory infiltrate.
• Beneath this active granulation tissue infiltrated
with mononuclear leucocyte and a fibrous or
collagenous scar forms the ulcer base
• Vessel wall thickened, occasionally thrombosed
• Scarring – entire thickness, pucker surrounding
mucosa

17. MICROSCOPY
Low-power cross-section view of a duodenal
ulcer crater with an acute inflammatory
exudate in the base

18. Complications
Bleeding
Perforation
Cancer

19. AMOEBIC ULCER
• Amoebiasis is caused by Entamoeba histolytica
(ameba)
• Dysentery-causing protozoan parasite spread by fecal-
oral transmission.
• Pathogenesis.
-E. histolytica cysts, which have a chitin wall and
four nuclei, are the infectious form because they are
resistant to gastric acid.
-Cysts release trophozoites, the ameboid forms,
which reproduce under anaerobic conditions without
harming the host.

21. Morphology of amoebic ulcer
• Cecum and ascending colon, followed by the
sigmoid colon, rectum, and appendix.

22. Discrete areas of ulceration
covered by exudate, with
normal intervening mucosa

23. • MICROSCOPY- Ulcer shows inflammatory infiltrates and
granulation tissues.
• Trophozoites of amoebae can mimic the appearance of
macrophages because of their comparable size and large
number of vacuoles.
• Amoebic ulcer-fan out laterally to create a flask-shaped ulcer
with a narrow neck and broad base.
• Erythrophagocytosis.
• Special stains:
- PAS- positive.
- Iron Hematoxylin -positive.

24. Entamoeba histolytica

25. COMPLICATIONS:
• Parasites may penetrate splanchnic vessels and
embolize to the liver to produce amoebic liver
abcesses.
• Amebic liver abscesses, which can exceed 10 cm
in diameter, have a scant inflammatory reaction
at their margins and a shaggy fibrin lining.
• Amebae may also spread via the bloodstream
into the kidneys and brain.

26. SALMONELLOSIS- Typhoid ulcer
Causative agent- S. typhimureum.
S. paratyphi.

27. • PATHOGENESIS:
Salmonella possess virulence genes that
encode a type III secretion system capable of
transferring bacterial proteins into enterocytes.
The transferred proteins activate host cell
Rho GTPases, bacterial uptake that allow bacterial
growth within phagosomes.
In addition, flagellin, the core protein of
bacterial flagellae, activates TLR5 on host cells and
increases the local inflammatory response

29. GROSS
• Usually affects ileum and colon.
• It present as longitudinal ulcer over the peyers
patches.
Typhoid ulcer

30. MICROSCOPY
- Neutrophils accumulate within the superficial
LP & macrophages containing bacteria, RBCs,
nuclear debris mix with lymphocytes n plasma
cells in LP.
- Mucosal shedding create oval longitudinal
ulcers
- Blunting of villi
- Mucosal congestion and edema

31. CLINICAL FEATURES
Anorexia, abdominal pain, bloating, nausea,
vomiting, and bloody diarrhea.
Blood cultures are positive in >90% of affected
individuals during the febrile phase.
In chronic phase- Rose spots, small
erythematous maculopapular lesions, are seen
on the chest and abdomen.

32. • Extra-intestinal complications including
encephalopathy, meningitis, seizures,
endocarditis, myocarditis, pneumonia,
cholecystitis and Salmonella osteomyelitis.

33. TUBERCULAR ULCER
• Causative agent- Mycobacterium tuberculosis
• Mostly affects the ileum or ileocaecal junction
• May or may not be associated with TB elsewhere
• Intestinal tuberculosis contracted by the drinking
of contaminated milk.
• In countries where milk is pasteurized, intestinal
TB is caused by the swallowing of coughed-up
infective material in patients with advanced
pulmonary disease

34. MORPHOLOGY OF TUBERCULAR
ULCER
GROSS
-Transverse ulcer in the direction of lymphatics
-muliple and circumferential
- Ulcer leads to fibrosis which cause stenosis and
obstruction

36. MICROSCOPY
• CASEATING GRANULOMA
- Shows central caseous necrosis
surrounded by granuloma
- Granuloma composed of epitheloid cells,
langhans giant cells and lymphocytes.
- AFB/ ZN Stain positivity.

37. TB- microscopy

38. BACILLARY DYSENTRY-
Clostridium toxin
• It affects colon
• CAP LESION- Small yellow white plaque like
lesions
• PSUEDOMEMBRANE FORMATION- fibrino
purulent necrotic debris

39. GROSS

40. MICROSCOPY
Epithelium- denuded
Superficial LP- dense
neutrophilic infiltrate,
occasional fibrin thrombi
within capillaries
Damaged crypts are
distended by mucopurulent
exudate forming
Mushroom/ Volcano
fibrinous exudates.

41. BACILLARY DYSENTRY-
Campylobacter jejuni
• It affects jejunum to ileum.
• Muiltiple superficial ulcer over the mucosa
• Microscopy -Cryptitis
-Crypt abscess
-Congestion
-Ulceration

42. BACILLARY DYSENTRY-
Campylobacter jejuni
Crypt abscess

43. ULCERATIVE COLITIS
• It is a inflammatory bowel disease.
• It usually affects the rectosigmoid junction.
• Gross:
- Irregular multiple ulcer
-Multiple pseudopolyp
-Continuos lesion with retrograde
progression

44. UC- Inflammatory polyp

45. • Microscopy :
-Mucosal edema and hyperemia.
-Crypt distortion
-Crypt abscess
-Mucosal depletion

46. UC- crypt abscess

47. CROHN’S DISEASE
• It is another inflammatory bowel disease.
• Affects ileum and proximal colon.
• Gross:
-Long serpentine linear ulcer.
-Cobblestone appearance.
-Skip lesions.
-Fissure and fistula.
• Microscopy shows non-caseating granuloma.

48. CROHNS DISEASE- Non caseating
granuloma

51. CARCINOMATOUS ULCER
• Commonly affects the rectosigmoid area and
affects any part of colon.
• Gross:
- Single, firm, everted, large cauliflower
shaped ulcer.
• Microscopy:
-Shows malignant glands infiltrating to
deep muscle area.

52. Carcinoma- gross

53. Carcinoma- microscopy

54. GRAFT VERSUS HOST DISEASE
• Usually occurs after bone marrow
transplantation and rarely occurs following
blood transfusion
• Symptoms include fever, skin rash, hepatitis,
bone marrow suppression and the outcome is
fatal.
• Pre-transfusion irradiation of all blood
components containing lymphocytes will
prevent GVHD

55. GVHD-Graft Verses Host Disease
• Any where in gastrointestinal tract.
• Features :
-Crypt abscesses.
-Inflammatory polyp.
-Fibrosis.
-Chronic inflammation.

56. BEHCET’S SYNDROME
• Affects large bowel.
• Shows multiple ulcers of various sizes, shape and
depth.
• Microscopy shows lymphocytic vasculitis of
submucosal veins.