Ulcerative colitis is a chronic inflammatory bowel disease that affects the colon. It involves diffuse inflammation and ulceration of the colonic mucosa. The cause is unknown but likely related to genetic and immune factors. Symptoms include bloody diarrhea. Diagnosis involves colonoscopy and biopsy. Treatment involves medications to induce and maintain remission such as mesalamine, corticosteroids, immunomodulators, and biologics. Surgery may be required for severe cases or cancer prevention. Long-term monitoring is needed due to cancer risk.

1. ULCERATIVE COLITIS
BY
AHMED FAWZY SELIM
Assistant lecturer of Internal Medicine
Faculty of medicine – Tanta university

2. Definition of UC
• Ulcerative colitis is a diffuse non-
specific inflammatory disease of
the large intestine of unknown
cause, primarily affecting the
mucosa, characterized by
erosions and/or ulcerations. The
disease is characterized by
repeated cycles of relapses and
remissions, occasionally
accompanied by extra-intestinal
manifestations.

3. Epidemiology of UC
• Ulcerative colitis is more common in the
Western and Northern hemispheres with
highest incidence in USA and UK.
• In the Past 2 decades , its incidence
increased in Middle east and Asia and may be
due to westernization of diet .
• Ulcerative colitis is slightly more common in
women than in men. Age of onset around 15-
25 years, although the disease can occur in
people of any age. Ulcerative colitis is
uncommon in persons younger than 10 years.

4. Etiology of UC
• the exact etiology of ulcerative colitis is
unknown, but certain factors have been
found to be associated with the disease,
include genetic factors, immune system
reactions, environmental factors,
nonsteroidal anti-inflammatory drug (NSAID)
use, low levels of antioxidants, psychological
stress factors, and consumption of milk
products.
• The incidence of UC is lower in smokers than
in nonsmokers.
• Ingestion of animal fat can increase the
occurrence of UC.
• A history of appendectomy is correlated
negatively with the occurrence of UC.

5. Pathophysiology
• A variety of immunologic changes have been
documented in UC. T cells accumulate in the
lamina propria of the diseased colonic
segment. these T cells are cytotoxic to colonic
epithelium. This change is accompanied by an
increase in the population of B cells and
plasma cells, with increased production of
immunoglobulin G (IgG) and immunoglobulin
E (IgE).[9]
• Anticolonic antibodies have been detected in
patients with UC. A small proportion of
patients with ulcerative colitis have smooth
muscle and anticytoskeletal antibodies.

6. • Microscopically, acute and chronic
inflammatory infiltrate of the lamina propria,
crypt branching, and villous atrophy are
present in ulcerative colitis. Microscopic
changes also include inflammation of the
crypts of Lieberkühn and abscesses. These
findings are accompanied by a discharge of
mucus from the goblet cells, the number of
which is reduced as the disease progresses.
The ulcerated areas are soon covered by
granulation tissue. Excessive fibrosis is not a
feature of the disease. The undermining of
mucosa and an excess of granulation tissue
lead to the formation of pseudopolyps.

8. Clinical presentation
• A major symptom of UC is bloody diarrhea,
occasionally accompanied by abdominal
pain
• UC should be suspected in cases with a
history of persistent or repetitive mucous
bloody stool/bloody feces.
• Patients with UC often have no abnormal
findings on physical examination, but
anemia, weight loss, abdominal tenderness
and fresh bleeding on digital rectal
examination are occasionally seen.

9. Classification of ulcerative colitis by severity

10. Classification by the extent of the lesions

11. Extra-intestinal manifestations of UC
• Extraintestinal IBD-related immune disease
can be classified into two major groups:
• The first one includes reactive
manifestations often associated with
intestinal inflammatory activity and therefore
reflecting a pathogenic mechanism common
with intestinal disease (arthritis, erythema
nodosum, pyoderma gangrenosum,
aphthous stomatitis, iritis/
uveitis)
• The second one includes many autoimmune
diseases independent of the bowel disease
that reflect only a major susceptibility to
autoimmunity.

12. Major extraintestinal immune-related
manifestations of IBD
• Arthritis
• Erythema nodosum
• Pyoderma gangrenosum
• Aphthous stomatitis
• Iritis/uveitis

13. Autoimmune disorders associated to IBD
• Alopecia areata
• Ankylosing spondylitis
• Cold urticaria
• Hemolytic anemia
• Henoch-Schoenlein purpura
• Insulin-dependent diabetes mellitus
• Pancreatitis
• Primary biliary cirrhosis
• Primary sclerosing cholangitis
• Polymyositis
• Raynaud phenomenon
• Seropositive rheumatoid arthritis
• Sjogren syndrome
• Thyroid disease
• Vitiligo
• Wegener’s granulomatosis

14. Extra – intestinal complication of IBD
• Anemia due to Iron deficiency, inflammation
• Thromboembolic events from Hypercoagulopathies,
platelet activation
• Osteopathy due to Steroid therapy, vitamin D deficiency
inflammation
• Growth failure and Malnutrition
• Urinary stones from Dehydration, hyperoxaluria, low
urinary PH
• Gall bladder stones from Intestinal loss of bile acids
• Amyloidosis Acute phase reaction, chronic inflammation
• Fatty liver from Malnutrition

15. Diagnostic criteria of UC
(A) Symptoms: continuous or repeated bloody diarrhea;
(B) endoscopy: diffuse inflammation, loss of vascular pattern, friability
(bleeding at contact), abundant mucus and (i) granular appearance;
(ii) multiple erosions, ulcers; and (iii) pseudopolyps, loss of haustration
(lead-pipe pattern), lumen narrowing, and colonic shortening.
(C) Histology: active: inflammatory cells infiltration, crypt
abscess, goblet cell depletion. Remission: crypt architectural
abnormalities (distortion branching), atrophic crypts.
These changes usually begin in the rectum and extend proxi-mally in
continuity.
Definite diagnosis: A+one item of B and C.

16. Investigations
1- Colonoscopy is the basic tool for diagnosis of UC
Typically, UC shows endoscopic findings such as loss of
vascular pattern, granular mucosa, easy
bleeding, and ulceration in a continuous manner.
The mucosa is involved diffusely, the vascular pattern
cannot be observed, and a coarse or microgranular
appearance is noted. Furthermore, the mucosa is fragile
and easy to bleed by contact. Mucous/bloody/
puriform secretions, multiple erosions, ulcers and/or
pseudopolyposis are observed

19. 2-Serological markers
- ANCA is most commonly associated with ulcerative colitis
while ASCA is more highly associated with Crohn
disease and is present in 60% of cases
3- Markers of activity
a) Acute phase reactants ESR , CRP , TLC
b) Fecal calprotectin can reflect the severity of the
disease

20. 4- Radiological assessment
• Double-contrast barium enema examination is a
valuable technique for diagnosing ulcerative colitis even
in patients with early disease.
• Cross-sectional imaging studies (eg, US, MRI, CT
scanning) are useful for showing the effects of these
conditions on the wall of the bowel.
• Radionuclide studies are useful in cases of acute
fulminant colitis when colonoscopy or barium enema
examination is contraindicated

21. Comparison between UC and Crohns disease

22. I-Remission induction therapy for active distal
colitis
• The basic drugs that are used in the treatment of mild to
moderate distal colitis are oral ASA preparations,
topical 5-ASA preparations and topical steroids.
• The optimal dose level of 5-ASA enema for mild to
moderate distal colitis is 1 g/day.
• When used for the treatment of active distal colitis, 5-
ASA enema is superior to steroid enema in terms of
improvement of the clinical symptoms, endoscopic
findings and histological findings.
• It is not uncommon to find that 5-ASA enema is effective
even in patients with active distal colitis who do not
respond to steroid enema.

23. • The efficacy of a combination of oral and topical 5-ASA
therapy is superior to that of either drug alone.
• Treatment of active distal colitis resistant to 5-ASA
preparations
In cases who do not respond to oral 5-ASA therapy at an
optimal dose combined with topical 5-ASA or steroid
therapy, oral PSL (prednisolone) should be started at a
daily dose of 30-40 mg.

25. • In January 2013, the US Food and Drug Administration
(FDA) approved an extended-release oral formulation of
budesonide for the treatment of active mild-to-moderate
ulcerative colitis in adults patients.Because budesonide
is a potent corticosteroid that exerts only minimal
systemic activity, this formulation provides the benefit of
a potent anti-inflammatory drug delivered locally while
avoiding many of the systemic side effects associated
with systemic steroids.
• Budesonide rectal foam was approved in October 2014
and is indicated for the induction of remission in adults
with active mild-to-moderate distal ulcerative colitis
extending up to 40 cm from the anal verge

26. II- Remission induction therapy for mild to
moderate total colitis and left sided colitis
• Treatment is started with oral ASA preparations. SASP (2-6 g/day)
can induce remission in 50-80% of all cases
• In patients who do not respond to ASA preparations or require rapid
alleviation of symptoms, PSL is administered orally at the dose of
30-40 mg/day.
• It has been shown in a meta-analysis of multiple RCTs that in
patients with active left-sided colitis, remission can often be induced
by topical 5-ASA therapy alone and this therapy is superior to oral
systemic drug therapy. “Comparing the efficacy between 5-ASA
enema and steroid enema, many studies demonstrated superiority
of 5-ASA.

27. III-Treatment of severe ulcerative colitis
• Patients failing to respond to maximum oral/topical
treatment or those satisfying the criteria of severe
disease are generally required to be hospitalized and to
receive intravenous steroid therapy and intravenous
alimentation.
• The optimal steroid dose level for intravenous
administration is 1-1.5 mg/k/day
• In patients who does not respond to 7-10 days of
intensive steroid therapy, continuation of steroid is not
expected to improve the efficacy, and surgical treatment
or cyclosporine is indicated the optimal cyclosporine
dose is 2 mg/kg

28. • Combined use of antimicrobial agents such as
ciprofloxacin with steroid therapy for severe UC does not
improve the responses.
• Antimicrobial agents are used only in cases possibly
complicated by infection and patients immediately
before surgery.
• Anticholinergics, antidiarrheal agents, NSAIDs,
narcotics, etc., should be discontinued.
• Infection with C. difficile or CMV needs to be checked
during treatment.

29. • According to a recent large-scale multicenter study
conducted overseas, infliximab was useful for both
inducing and maintaining remission in patients with
therapy-resistant moderate to severe UC. In the USA,
the use of infliximab in UC patients has been approved
by the FDA.

30. IV- maintenance therapy
• None of commonly employed dietary restriction has been
shown to reduce the risk of relapse
• All ASA preparations are effective for maintaining
remission.
• Steroids are ineffective for maintenance of remission.
• Immunosuppressants (AZA/6-MP, etc.) are used in
steroid-dependent patients or patients who are difficult
to wean from steroids.

31. INDICATION OF SURGERY
• Indications for urgent surgery in patients with ulcerative
colitis include (1) toxic megacolon refractory to medical
management, (2) fulminant attack refractory to medical
management, and (3) uncontrolled colonic bleeding.
• Indications for elective surgery in ulcerative colitis
include (1) long-term steroid dependence, (2) dysplasia
or adenocarcinoma found on screening biopsy,

32. LONG TERM MONITORING
• Patients with extensive colitis or left-sided colitis with negative
findings on screening colonoscopy should begin surveillance
colonoscopy in 1-2 years. For patients with ulcerative colitis and
primary sclerosing cholangitis, screening and subsequent
surveillance colonoscopy should begin on an annual basis at the
time of onset of primary sclerosing cholangitis.
• Patients with proctosigmoiditis have no increased risk for colorectal
cancer compared with the general population. However, these
patients should be managed according to the current guidelines on
colorectal cancer screening. If high-grade dysplasia or cancer is
found, colectomy is performed. The management of low-grade
dysplasia is controversial[79] ; however, most experts would
recommend colectomy.

33. PROGNOSIS
• The most common cause of death of patients with
ulcerative colitis is toxic megacolon. Colonic
adenocarcinoma develops in 3-5% of patients with
ulcerative colitis, and the risk increases as the duration
of disease increases. The risk of colonic malignancy is
higher in cases of pancolitis and in cases in which onset
of the disease occurs before the age of 15 years. Benign
stricture rarely causes intestinal obstruction.