INFLAMMATORY BOWEL DISEASE IBD INFLAMMATORY BOWEL DISEASE IBD
INFLAMMATORY BOWEL DISEASE (IBD)
INFLAMMATORY BOWEL DISEASE (IBD) �IS A CHRONIC CONDITION RESULTING FROM INAPPROPRIATE MUCOSAL IMMUNE ACTIVATION. THE TWO DISORDERS � CROHN DISEASE ULCERATIVE COLITIS � SEVERE ULCERATING INFLAMMATORY DISEASE THAT IS LIMITED TO THE COLON AND RECTUM � EXTENDS ONLY INTO THE MUCOSA AND SUBMUCOSA. CROHN DISEASE, (REGIONAL ENTERITIS) � ILEAL INVOLVEMENT) TRANSMURAL
PATHOGENESIS ETIOLOGIC FACTORS: � IN A GENETICALLY PREDISPOSED INDIVIDUAL � THE EFFECTS OF EXOGENOUS AND ENDOGENOUS HOST FACTORS � DYSREGULATION OF MUCOSAL IMMUNE FUNCTION, � MODIFIED BY CERTAIN ENVIRONMENTAL FACTORS.
ETIOPATHOGENESIS. 1. GENETIC FACTORS. � OCCURRENCE OF IBD IN FIRST-DEGREE RELATIVES. � GENETIC DEFECT CAUSING DIMINISHED EPITHELIAL BARRIER FUNCTION. MONOZYGOTIC TWINS. q DISEASE-PREDISPOSING LOCI ARE PRESENT IN CHROMOSOMES 16 Q, 12 P, 6 P, 14 Q AND 5 Q. HLA-DRB 1 ALLELES
�DEFECTIVE REGULATION OF IMMUNE SUPPRESSION. � IN A NORMAL INDIVIDUAL, THERE IS LACK OF IMMUNE RESPONSIVENESS TO DIETARY ANTIGEN � CD 4+ T CELLS (IL-10, TGF-Β-------- SECRETING CYTOKINES INHIBITORY TO INFLAMMATION) � IN IBD ----- SUPPRESSION OF INFLAMMATION IS DEFECTIVE ---------- UNCONTROLLED INFLAMMATION.
. Type of inflammatory cells. , activated CD 4+ T cells are present in the lamina propria activate other inflammatory cells (e. g. macrophages and B cells) or recruit more inflammatory cells : TH 1 cells secrete proinflammatory cytokines IFN-γ and TNF ------ transmural granulomatous inflammation TH 2 cells ---- IL-4, IL-5 and IL-13 ------superficial mucosal inflammation.
3. EXOGENOUS FACTOR I) MICROBIAL FACTORS: � MYCOBACTERIUM PARATUBERCULOSIS, � SALMONELLA, � SHIGELLA, � HELICOBACTER � CLOSTRIDIA � BACTEROIDES, ESCHERICHIA, MEASLES VIRUS ETC.
II) PSYCHOSOCIAL FACTORS: �WHO ARE UNDULY SENSITIVE, DEPENDENT ON OTHERS AND UNABLE TO EXPRESS THEMSELVES, OR � SOME MAJOR LIFE EVENTS SUCH AS ILLNESS OR DEATH �III) SMOKING �IV) ORAL CONTRACEPTIVES: LONG-TERM USE
CROHN DISEASE, • AN EPONYM BASED ON THE 1932 DESCRIPTION BY CROHN • LOUIS XIII OF FRANCE (1601– 1643) SUFFERED RELAPSING BLOODY DIARRHEA, FEVER, RECTAL ABSCESS, SMALL INTESTINAL AND COLONIC ULCERS.
CROHN DISEASE MOST COMMON SITES INVOLVED ARE TERMINAL ILEUM ILEOCECAL VALVE CECUM. MORPHOLOGY MULTIPLE SEPARATE SHARPLY DELINEATED SKIP LESIONS STRICTURES ARE COMMON
THE EARLIEST CROHN DISEASE LESION, q APHTHOUS ULCER------- COALESCE INTO ELONGATED, SERPENTINE ULCERS ORIENTED ALONG THE AXIS OF THE BOWEL q EDEMA AND LOSS OF THE NORMAL MUCOSAL TEXTURE q SPARING OF INTERSPERSED MUCOSA q RESULTS IN A COARSELY TEXTURED, COBBLE STONE APPEARANCE q DISEASED TISSUE IS DEPRESSED BELOW THE LEVEL OF NORMAL MUCOSA q MAY EXTEND DEEPLY TO BECOME FISTULA TRACTS OR
q THE INTESTINAL WALL IS q THICKENED AND RUBBERY q TRANSMURAL EDEMA, q INFLAMMATION q SUBMUCOSAL FIBROSIS HYPERTROPHY OF THE MUSCULARIS PROPRIA q CONTRIBUTE TO STRICTURE FORMATION q EXTENSIVE TRANSMURAL DISEASE-------MESENTERIC FAT FREQUENTLY EXTENDS AROUND THE SEROSAL SURFACE (CREEPING FAT)
Gross pathology of Crohn disease. A, Small-intestinal stricture. B, Linear mucosal ulcers and thickened intestinal wall. C, Perforation and associated serositis . D, Creeping fat.
MICROSCOPICALY � NEUTROPHILS THAT INFILTRATE AND DAMAGE CRYPT EPITHELIUM � CRYPT ABSCESSES ASSOCIATED WITH CRYPT DESTRUCTION. ULCERATION COMMON � AN ABRUPT TRANSITION BETWEEN ULCERATED AND ADJACENT NORMAL MUCOSA. � REPEATED CYCLES OF CRYPT DESTRUCTION AND REGENERATION LEAD TO DISTORTION OF MUCOSAL ARCHITECTURE � MUCOSAL ATROPHY, WITH LOSS OF CRYPTS � NONCASEATING GRANULOMAS A HALLMARK OF CROHN DISEASE EPITHELIAL METAPLASIA ------- PSEUDOPYLORIC METAPLASIA.
Microscopic pathology of Crohn disease A Haphazard crypt organization results from repeated injury and regeneration B Noncaseating granuloma. C Transmural Crohn disease with submucosal and serosal granulomas (arrows).
�PANETH CELL METAPLASIA (PANETH CELLS ARE NORMALLY ABSENT IN COLON) �GRANULOMAS MAY ALSO BE PRESENT IN MESENTERIC LYMPH NODES � CUTANEOUS GRANULOMAS FORM NODULES ( METASTATIC CROHN DISEASE).
CLINICAL FEATURES INTERMITTENT ATTACKS OF � MILD DIARRHEA, �FEVER, AND � ABDOMINAL PAIN. MIMIC ACUTE APPENDICITIS OR BOWEL PERFORATION. � PERIODS OF ACTIVE DISEASE INTERRUPTED BY ASYMPTOMATIC PERIODS THAT LAST FOR WEEKS,
COMPLICATION � IRON-DEFICIENCY ANEMIA HYPOALBUMINEMIA, MALABSORPTION OF VITAMIN B 12 AND BILE SALT � FIBROSING STRICTURES � FISTULAE DEVELOP BETWEEN LOOPS OF BOWEL � PERFORATIONS AND PERITONEAL ABSCESSES EXTRA-INTESTINAL MANIFESTATIONS OF CROHN DISEASE � UVEITIS, � MIGRATORY POLYARTHRITIS, � SACROILIITIS, ANKYLOSING SPONDYLITIS, � ERYTHEMA NODOSUM, PRIMARY SCLEROSING CHOLANGITIS
MORPHOLOGY. OF ULCERATIVE COLITIS ALWAYS INVOLVES THE RECTUM AND EXTENDS PROXIMALLY IN A CONTINUOUS FASHION TO INVOLVE PART OR ALL OF THE COLON. �SKIP LESIONS ARE NOT SEEN � DISEASE OF THE ENTIRE COLON IS TERMED PANCOLITIS � LIMITED DISTAL DISEASE ------- ULCERATIVE PROCTITIS � SMALL INTESTINE IS NORMAL, � MILD MUCOSAL INFLAMMATION OF THE DISTAL ILEUM, BACKWASH ILEITIS
GROSSLY � COLONIC MUCOSA MAY BE SLIGHTLY RED AND GRANULAR � HAVE EXTENSIVE, BROAD-BASED ULCERS � ULCERS ARE ALIGNED ALONG THE LONG AXIS OF THE COLON � ISOLATED ISLANDS OF REGENERATING MUCOSA OFTEN BULGE INTO THE LUMEN TO CREATE PSEUDOPOLYPS
pancolitis showing active disease, with red, granular mucosa in the cecum (left) and smooth, atrophic mucosa distally (right). B, Sharp demarcation between active ulcerative colitis (right) and normal (left). C, Inflammatory polyps. D, Mucosal bridges
CHRONIC DISEASE � MUCOSAL ATROPHY WITH A FLAT AND SMOOTH MUCOSAL SURFACE THAT LACKS NORMAL FOLDS. UNLIKE CROHN DISEASE, � MURAL THICKENING IS NOT PRESENT, � SEROSAL SURFACE IS NORMAL, � STRICTURES DO NOT OCCUR. � INFLAMMATION AND INFLAMMATORY MEDIATORS CAN DAMAGE THE MUSCULARIS PROPRIA � DISTURB NEUROMUSCULAR FUNCTION
HISTOLOGIC FEATURES MUCOSAL DISEASE � INFLAMMATORY INFILTRATES, CRYPT ABSCESSES, CRYPT DISTORTION, � EPITHELIAL METAPLASIA �INFLAMMATORY PROCESS IS DIFFUSE LIMITED TO THE MUCOSA AND SUPERFICIAL SUBMUCOSA � BUT THE MUSCULARIS PROPRIA IS RARELY INVOLVED. �SUBMUCOSAL FIBROSIS, MUCOSAL ATROPHY, AND DISTORTED MUCOSAL ARCHITECTURE IN HEALED DISEASE � GRANULOMAS ARE NOT PRESENT IN
MICROSCOPIC PATHOLOGY OF ULCERATIVE COLITIS. A, CRYPT ABSCESS. B, PSEUDOPYLORI C METAPLASIA (BOTTOM) . C, DISEASE IS LIMITED TO THE MUCOSA.
CLINICAL FEATURES q ULCERATIVE COLITIS IS A RELAPSING DISORDER CLINICAL FEATURES q ATTACKS OF BLOODY DIARRHEA WITH STRINGY MUCOID MATERIAL, q LOWER ABDOMINAL PAIN, q CRAMPS THAT ARE TEMPORARILY RELIEVED BY DEFECATION
Feature MACROSCOPIC Bowel region Distribution Stricture Wall appearance MICROSCOPIC Inflammation Pseudopolyps Ulcers Crohn Disease Ulcerative Colitis Ileum ± colon Skip lesions Yes Thick Colon only Diffuse Rare Thin Transmural Moderate Deep, knife-like Limited to mucosa Marked Superficial, broad-based Lymphoid reaction Marked Moderate Marked Yes (∼ 35%) Yes Mild to none No No Yes (in colonic disease) No Fat/vitamin malabsorption Yes No Malignant potential With colonic involvement Yes Recurrence after surgery Common No Toxic megacolon No Yes . Fibrosis Serositis Granulomas Fistulae/sinuses CLINICAL Perianal fistula
IMPORTANT QUESTIONS • Q. DEFINE INFLAMMATORY BOWEL DISEASE (IBD). WRITE BRIEFLY ON ITS AETIOPATHOGENESIS • Q. OUTLINE THE CLINICAL FEATURES AND MORPHOLOGY OF CROHN DISEASE • Q. DESCRIBE THE CLINICAL FEATURES, MORPHOLOGY AND COMPLICATIONS OF ULCERATIVE COLITIS. • Q. DIFFERENTIATE BETWEEN CROHN DISEASE AND ULCERATIVE COLITIS. • Q. WRITE BRIEFLY ON AMOEBIC COLITIS. DIFFERENTIATE BETWEEN AMOEBIC AND ULCERATIVE COLITIS
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