Inflammatory bowel diseases
diseases
Dr Nishat Afroz
Professor D/O Pathology
• Crohn’s disease
• Ulcerative Colitis
• Ulcerative Colitis
CROHN’S DISEASE
When fully developed, it is characterised pathologically by
1)Sharply delineated and typically transmural involvement of the bowel by an inflammatory involvement of the bowel by an inflammatory process with mucosal damage.
2)The presence of non-caseating granulomas.
3)Fissuring with formation of fistulae.
Skip Lesions (segmental)
CROHN’S DISEASE Characterized by
sharply delineated and typically
transmural
involvement of the bowel by an
inflammatory process with mucosal
damage, non- caseating
granulomas, and
AKA terminal ileitis, regional enteritis, & granulomatous colitis
Skip Lesions
Transmural Inflammation Ulcerations, Fissures,
50% Granulomas
GRIPE
granulomas, and fissuring with fistula formation.
Crohn’s Disease
• Any region of bowel; sm. intestine (40%), small
& large intestine (30%), colon (30%)
• Epidemiology
– World-wide, but most prevalant in developed Western countries
Western countries
– Any age; peak incidence in 2nd & 3rd decades; and minor peak in 6th & 7th decades
– F>M; whites 2-5X >non-whites – US: Jews 3-5X > non-Jews
– Smoking is a strong risk factor
• It can occur at any age but is more common in 2nd and 3rd decade
• Females are affected slightly more often than males
• It affects commonly the segment of terminal ileum and/or colon, although any part of the
and/or colon, although any part of the gastrointestinal tract maybe involved
• There is gross involvement of the small intestine alone in 40% cases, of small intestine and colon in 30% cases and of the colon alone in 30% cases.
Crohn’s Disease - Morphology
Granular serosa with
“creeping fat” and thick wall; mesentery also
thickened and edematous
GRIPE
Crohn’s Disease - Morphology
Skip lesions
Bowel wall thick due to inflammation, edema, fibrosis, and hypertrophy narrow lumen
GRIPE
ETIOPATHOGENESIS 1) Infectious mechanism
2) Immunological mechanism a) Humoral factors
- specific anti-colon antibodies to bacterial antigens - increased synthesis of IgG
- circulating immune complexes - circulating immune complexes
- Ig E mediated hypersenstivity reaction b)Cell-mediated immunologic factors
- decreased no. of peripheral T cells & cutaneous anergy
- T cells sensitised to various bowel antigens - Antibody dependent cellular cytotoxicity
c) Immunodeficiency of Ig A d) Other mechanisms
a) Psychological factors b) Genetic factors
c) Racial factors d) Food allergies e) Trauma
On Gross examination
• Multiple well demarcated segmental bowel
involvement with intervening uninvolved ‘skip areas’.
• Wall of the affected bowel is segment is thick and hard resembling a ‘hose pipe’.
• Serosa maybe studded with minute granulomas.
• Serosa maybe studded with minute granulomas.
• Lumen of affected segment is markedly narrowed.
• Mucosa shows ‘serpiginous ulcers’ while
intervening surviving mucosa is swollen giving
‘cobblestone appearance’
Crohn’s Disease - skip lesions
Chrohn’s Disease - skip lesions
On Microscopy
• Transmural inflammatory cell infiltrate consisting of chronic inflammatory cells (lymphocytes, plasma
cells and macrophages)
• Non-caseating discrete sarcoid like granulomas
• Patchy ulceration of the mucosa which take the form of deep fissures, accompanied by inflammatory
of deep fissures, accompanied by inflammatory infiltrate of lymphocytes and plasma cells
• In more chronic cases, fibrosis becomes increasingly prominent in all the layers disrupting muscular
layer.
COMPLICATIONS
• Malabsorption
• Fistula formation
• Stricture formation
• Carcinoma (very rare)
• Carcinoma (very rare)
Ulcerative Colitis : Presentation
• Mild attack:
– Most common form, mainly left sided colitis, <4 BM/day with no blood
• Moderate attack:
• Moderate attack:
– 25% of all patients, 4-6 BM/day with blood.
• Severe or fulminant colitis:
– ~ 15% of cases, >6BM/day, bloody, fever, weight loss, diffuse abd tenderness, elevated WBC, most refractory to medical therapy
Ulcerative Colitis: Presentation
• Must exclude infectious cause before making Dx.
• Rectal Bleeding
• Diarrhea:
– frequent passage of loose or liquid stool, often associated with passing large quantities of mucus.
with passing large quantities of mucus.
• Abdominal Pain:
– it is not a prominent symptom.
• Anorexia, nausea, fever…
PATHOLOGY
• The inflammation is predominantly confined to the mucosa.
• Non-specific (can be seen with any acute inflammation)
– The lamina propria becomes edematous.
– Inflammatory infiltrate of neutrophils – Inflammatory infiltrate of neutrophils
– Neutrophils invade crypts, causing cryptitis &
ultimately crypt abscesses.
• Specific (suggest chronicity):
– Distorted crypt architecture, crypt atrophy and a chronic inflammatory infiltrate.
Continuous inflammation beginning in rectum and extending to the terminal ileum in some cases
Pseudopolyps Ulcers
Robbin’s 6th Edition
Ulcerative Colitis
UC
Ulcerative Colitis
Crypt Abscess
Diagnosis
• Exclude other possibilities (need good history, physical exam, labs, imaging and endoscopy with biopsy)
• There are many distinguishing features of CD and UC.
• In about 5% it is classified as indeterminate because of
• In about 5% it is classified as indeterminate because of overlapping features.
Distinguishing characteristics of CD and UC
UC CD
Features
Only colon (rarely
“backwash ileitis”
Small intestine or colon
Location
Continuous, Skip lesions
Anatomic Continuous,
begins distally Skip lesions
Anatomic distribution
Involved in >90%
Rectal spare Rectal involvement
Universal Only 25%
Gross bleeding
Rare 75%
Peri-anal disease
No Yes
Fistulization
No 50-75%
Granulomas
Endoscopic features of CD and UC
UC CD
Feature
Continuous Discontinuous
Mucosal involvement
Rare Common
Aphthous ulcers
Abnormal Relatively
Surrounding Relatively Abnormal normal
Surrounding mucosa
Rare Common
Longitudinal ulcer
No In severe cases
Cobble stoning
Common Uncommon
Mucosal friability
distorted Normal
Vascular pattern
Pathologic features of CD and UC
UC CD
Feature
Uncommon Yes
Transmural inflammation
No 50-75%
Granulomas 50-75% No
Granulomas
Rare Common
Fissures
No Common
Fibrosis
Uncommon Common
Submucosal inflammation
Idiopathic inflammatory bowel disease
Crohn’s disease
• Small bowel and colon (mostly right side)
• Patchy involvement
• Transmural inflammation, fistulas, strictures, serositis
• Non-caseating granulomas
Ulcerative colitis
• Colon only
• Continuous involvement
• Superficial inflammation
• No granulomas
• Good response to surgery Non-caseating granulomas
• Poor response to surgery • Good response to surgery
• Increased risk for cancer
Treatment
• Goals of therapy
– Induce and maintain remission.
– Ameliorate symptoms
– Improve pts quality of life – Improve pts quality of life – Adequate nutrition
– Prevent complication of both the disease and medications
Treatment
• Topical corticosteroids/oral prednisolone in doses ranging up to 60 mg per day.
• IV steroids is warranted for patients who are sufficiently ill to require hospitalization.
• 5-aminosalicylic acid :For patients with distal colonic disease, a suppository or enema form will be most disease, a suppository or enema form will be most appropriate.
• Azathioprine & 6-Mercaptopurine, Methotrexate ,Cyclosporine.
• Surgery
INTESTINAL TUBERCULOSIS
It can occur in 3 forms-
Primary intestinal tuberculosis
-the affected lymph nodes are enlarged, matted and caseous (tabes mesenterica).
-on M/E, there is primary complex or Ghon’s focus in the intestinal mucosa and the affected lymph nodes
show typical tuberculous granulomatous inflammatory reaction with caseation necrosis.
Secondary intestinal tuberculosis
-swallowing of sputum in patients with active
pulmonary tuberculosis. Most commonly seen in
terminal ileum .The lesions begin in Payer’s patches or the lymphoid follicles with formation of
small ulcers that spread through the lymphatics to form
large ulcers which are transverse to the long axis of the bowel
axis of the bowel
-in advanced cases, transverse fibrous strictures and intestinal obstruction may be seen.
-on M/E, the tuberculous lesions in the intestine are similar to those observed elsewhere i.e. presence of tubercles
Hyperplastic ileocaecal tuberculosis
-
a variant of secondary tuberculosis secondary to
pulmonay tuberculosis. Clinically the lesion is palpable.
-the caecum and/or ascending colon are thick walled with mucosal ulceration
-on M/E, the presence of caseating tubercles
distinguishes the condition from Crohn’s disease
in which the granulomas are non-caseating.
ENTERIC FEVER
• Acute infection caused by Salmonella typhi (typhoid fever) and Salmonella paratyphi (paratyphoid fever)
PATHOGENESIS
Typhoid bacilli ingested through contaminated food/water
↓
Asymptomatic incubation period (2 weeks)
↓
Bacilli invade lymphoid follicles & Payer’s patches
↓↓
Bacilli invade the blood stream
↓
Eventually bacilli are localised in the intestinal lymphoid tissue (typhoid intestinal lesion), mesenteric lymph nodes,
liver, gall bladder, spleen
INTESTINAL LESIONS
• Terminal ileum is affected most often, but jejunum and colon may also be affected
• Payer’s patches show oval typhoid ulcers with their long axis along the length of the bowel
• Regional lymph nodes are invariably enlarged
• On M/E, there is hyperemia, edema, phagocytic histiocytes (showing characteristic
erythrophagocytosis), lymphocytes and plasma cells
