2 MAJOR GROUPS :1. ULCERATIVE COLITIS – colon involved2. CROHN’S DIDEASE – the hole GI tract

EPIDEMIOLOGY most common in whites than in blacks and Orientals , with increased

incidence in Jews compared to non-Jews both sexes are equally afected UC is most common than CD 2,5% of persons with IBD will have ≥ 1 relatives affected hereditary basis ± strong environmental componentA. GENETIC FACTOR : monozygotic twins, NO single markerB. INFECTIONS : Pseudomonas, Yersinia enterocolitica (self limited ,

acute ileitis)C. IMMUNOLOGIC: humoral antibodies to colon cells, bacterial antigens

(E.coli, lipopolysacharides, foreign proteins), immune complexes –extraintestinal manifestations of IBD

D.PHYHOLOGICAL FACTORS: loss of a family member, anger, anxiety, depression are important in modifying the course of these disease and the response to therapy

CDCD-often discontinuous : severely involved segments of bowel are separated from each other with segments of apparently normal bowel producing “skip areas”; in the ~ 50% of CD of the colon , the rectum may be separated. The transmural inflammatory process affects serosa , mezentery , fistula and abcess formation.

UC – the involvement is contigous and the rectum is almost always involved

CD - As a result of serosal inflamation, adiacent loops of small intestine may become adherent and matted together by a fibrinous peritoneal reaction leading to palpable mass , most often in the right lower quadrant

Microscopically, granulomas ≠ UC (in rectal or colonoscopic biopsies). Chronic inflamation involving all layers of the intestinal wall most caracteristic

30% small intestine (terminal ileum) 30% colonic involvement 40% ileocolonic (ileum + right colon)

Major symptoms: bloody diarrhea abdominal pain fever (in severe forms) weight loss (in severe forms) frequent liquid stools with

blood and pus severe cramps (signs of dehidratation , anemia) Physical findings in UC are usually nonspecific (abdominal

distension, tenderness along the course of the colon) Mild cases – general examination is normal.

EXTRACOLONIC MANIFESTATIONS:1.Arthritis ~25 % (knees, ankles, wrists ) ( FR,ANB,LE – for

specific artritis)2.Skin changes 15%3.Liver disease

reflect the degree and severity of bleeding and inflamation :

iron deficiency anemia leukocytosis, ↑VSH hypokalemia hypoalbuminemia- luminal protein loss from ulcerated mucosa

1. Peripheral arthritis in patients with colonic than small bowell involvement alone. Central artritis (ankylosing spondylitis )+ IBD is unrelated to the activity of the underlying bowel disease; HLA-B27 + ankylosing spondylitis whether or not IBD

2. Erythema nodosum, pyoderma gangrenosum , aphthous ulcers (in active disease and than resolved), ocular manifestations (5%) ( episcleritis , recurrent iritis, uveitis )

3. Liver function ALT, AST, AF ↑ = non specific focal hepatitis or

fatty infiltration; non-progressive, remision Pericholangitis – lesions of intrahepatic form of sclerosing colangitis; non progressive and

requires no therapy Colangiocarcinoma in the extrahepatic biliary tree Chronic active hepatitis cirrhosis

The clinical course of UC is variable. Most of the patients will suffer a relapse within 1 year of

the first attack recurrent nature of the disease periods of remission with only minimal symptoms in general, the severity of symptoms reflects the extend of

colonic involvement and the intensity of the inflammation limited colonic involvement (proctosigmoiditis mild

disease) with minimal systemic manifestation ( non extensive disease)

MAJOR SYMPTOMS: rectal bleeding + tenesmus 85 % mild and moderate of intermittent nature that can

be managed without hospitalisation 15 % - fulminant course – entire colon- with systemic signs

and symptoms risc to develop toxic dilatation and perforation of the colon

medical emergency

CROHN’S DISEASE ULCERATIVE COLITIS