Generally present with bloody diarrhea with rectal urgency, discomfort& cramps.
They have profound tenesmus (feelings of urgency& incomplete evacuation), secondary to proctitis, this can cause constipation to be a more common manifestation than diarrhea; in such patients, determining the activity of the disease& treating it can be challenging.
UC extends proximally from the anal verge&can progress to pancolitis involving the cecum.
Fever is infrequent, but weight loss secondary to the inflammatory disease itself or to the chronic diarrhea is common.
Physical examination findings can range from mild lower abdominal tenderness to abdominal distention with rebound tenderness& hypoactive bowel sounds, suggestive of toxic megacolon.
More protean in its manifestations than ulcerative colitis, as the disease can affect any portion of the GIT& frequently has so-called “skip lesions” with areas of normal mucosa juxtaposed with severe inflammation.
The transmural nature of the disease results in three distinct manifestations: inflammatory, fistulizing& fibrostenotic.
Large-volume diarrhea can occur; diarrhea is associated with both small& large-bowel Crohn disease, whereas hematochezia is almost always a sign of colonic disease.
The inflamed tissue causes a secretory diarrhea& a protein-losing enteropathy, steatorrhea from fat malabsorption (with patients who have ileal or ilealocolic disease frequently being vitamin B12- & vitamin D-deficient)& other types of malabsorption.
Patients who have had their terminal ileum resected are also at risk for a choleretic diarrhea secondary to bile salt wasting.
Fistulae are abnormal connections between the bowel& adjacent organs.
Abscesses may form& the fistula acts as a natural drainage mechanism, causing pus to emerge from the fistulae.
The fistulae become symptomatic with drainage of fecal material around the anus (perianal fistulae), seepage of bowel contents through the skin (enterocutaneous fistulae), passage of feces through the vagina (rectovaginal fistulae)& pneumaturia or recurrent urinary tract infections (enterovesical fistulae).
The intestinal inflammation may extend to adjacent musculature &result in neuromuscular sequelae; for example, a patient with Crohn disease&a new limp likely has a psoas muscle abscess.
Distinguishing characteristics of CD and UC UC CD Feature Only colon (rarely “ backwash ileitis ” SB or colon Location 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 10-30% Granulomas
Endoscopic features of CD and UC UC CD Feature Continuous Discontinuous Mucosal involvement Rare Common Aphthous ulcers Abnormal Relatively 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 Rare Common Fissures No Common Fibrosis Uncommon Common Submucosal inflammation
Radiologic features of CD and UC UC CD Feature Collar button ulcers Nodularity granularity cobble stoning string sign of SB
Comparison of Features in Ulcerative Colitis and Crohn's Disease Crohn's Disease Ulcerative Colitis Feature Transmural Mucosal Depth of inflammation Skip areas Contiguous Pattern of disease Mouth to anus Colorectum Location Less common Usual Rectal involvement Common Backwash ileitis (15%–20% of patients ) Ileal disease Common Rare Fistulas Common Rare Perianal disease 10%–30% of patients Unlikely Granulomas Less common Usual Overt bleeding More common Unlikely Malnutrition Colorectal cancer, small bowel cancer (depending on disease location ) Colorectal cancer, cholangiocarcinoma (if primary sclerosing cholangitis is present ) Cancer risk Harmful Protective Tobacco use
Occur in 10-20% at some time in the course of their disease.
Arthritis, the most common, can either be related to the intestinal inflammation itself or be part of an overlap syndrome with rheumatoid arthritis.
Sacroiliitis &ankylosing spondylitis, in association with HLA B27, occur in 5-10%.
Uveitis & episcleritis may also occur.
Erythema nodosum, which manifests as small exquisitely tender nodules on the anterior tibial surface, occurs more commonly in Crohn disease, whereas pyoderma gangrenosum is more common in ulcerative colitis& can range from small lesions to large ulcers. Even small amounts of trauma to the skin can activate this inflammatory process.
Increased risk for CRC; the risk is associated with the age of onset; duration, extent, severity of disease& whether the patient has a family history of CRC.
Annual CRC rate in extensive colitis is at least 0.5% /year after the first decade of colitis.
Screening recommendations include colonoscopy every 1 to 2 years beginning 8 years after diagnosis.
Unlike sporadic colorectal cancer that develops primarily from colon polyps, inflammatory bowel disease-associated colon cancer can arise from flat dysplastic mucosa which is not readily detectable from underlying inflammatory tissue.
50% with IBD have osteopenia, with a substantially increased risk of osteoporosis & fracture.
The risk is present in patients with ulcerative colitis / Crohn disease, in both sexes&in patients who are taking corticosteroids & those who have never taken them.
Patients with prolonged IBD, malabsorption, a history of using corticosteroids for >3 months, cigarette smoking, older age, history of fractures, or a family history of osteoporosis should be evaluated for the presence of metabolic bone disease.
Kidney stones / gallstones are other extraintestinal manifestations of inflammatory bowel disease.
Cancer: Patients with either UC or CD have an increased risk of intestinal dysplasia & CRC that is related to the duration, extent& severity of the inflammation,so those with extensive/longstanding disease should undergo regular colonoscopic examinations with mucosal biopsies to detect these complications.
2/3 with ulcerative colitis, but only 15- 20% with Crohn disease &< 5% of persons without IBD have p-ANCA , a serum antibody directed against a particular histone H1 antigen& detectable by immunofluorescence or specific enzyme immunoassay.
Approximately 50% with Crohn disease have anti- Saccharomyces cerevisiae antibodies (ASCA), as opposed to < 5% of patients with ulcerative colitis &control subjects.
So measuring both serum p-ANCA & ASCA is reasonably reliable for the diagnosis of Crohn disease or ulcerative colitis.
Newer antibody tests, directed against the outer membrane porin of Escherichia coli (Omp-C)& against the flagellum of pathogenic polyflagellated organisms (Cbir1), are also predictive of classic Crohn disease,but not differentiating atypical presentations or diagnosing indeterminate colitis.
MOA: anti-inflammatory effects secondary to inhibition of arachidonic acid in the bowel mucosa by cyclooxygenase.
5 oral formulations developed from sulphaslazine.
2 mesalamines are released in the small bowel in a pH- time-dependent manner used to treat both CD &ulcerative colitis.
Mesalamine is available in suppository & enema formulations, which are effective alone in patients who have inflammation limited to the rectosigmoid & may also be used in combination with an oral 5-ASA.
Ileal-release preparations of budesonide are indicated for the treatment of patients with mild ileal & right-sided colonic Crohn disease.
Budesonide is a topically active corticosteroid with a very high affinity for the glucocorticoid receptor (*15 that of prednisolone *195 that of hydrocortisone).
Only 10-15% of the drug reaches the systemic circulation; the rest is converted in the liver to inactive metabolites.
Conventional corticosteroids are effective in the short-term induction of remission in patients with Crohn disease but are generally used in patients with moderate disease at any location or in patients with ileal disease who have failed to respond to the 5-ASAs or budesonide.
Because of the toxic effects of long-term corticosteroid therapy (for example, osteoporosis, avascular necrosis, psychosis), it is important to devise a strategy for tapering the dosage& discontinuing corticosteroid therapy before the therapy is started.
Their onset of full activity is slow, may take up to 3 months.
These drugs are effective for the maintenance of remission in patients with Crohn disease regardless of disease distribution.
Adverse side effects include leukopenia, hepatotoxicity.
Before being treated with these agents, patients should be tested for thiopurine methyltransferase, the enzyme involved in the conversion of 6-mercaptopurine to inactive metabolites; patients who have low enzyme activity (or who are homozygous deficient in thiopurine methyltransferase) should not be treated with these agents.
Methotrexate is an immunomodulator induce / maintain remission in Crohn disease but not in ulcerative colitis.
There is a risk for hepatotoxicity& patients with persistently elevated liver tests may need to undergo liver biopsy.
Methotrexate is both a teratogen&abortifacient contraindicated in pregnant patients & breastfeeding.
In patients not responsive to the 5-ASAs or in those with more severe disease, corticosteroids may induce remission.
In hospitalized patients IV therapy is usually administered, whereas in the outpatient setting oral & rectal corticosteroids are used.
No dose effect above the equivalent of prednisone 60 mg/d has been found.
Corticosteroid therapy does not maintain remission & is appropriate only as short-term therapy.
Although some patients may be put back successfully to 5-ASA as maintenance therapy after corticosteroid induction therapy, often an immunomodulator such as 6-mercaptopurine or its prodrug azathioprine is warranted; these agents are corticosteroid-sparing & maintain remission.
If corticosteroid therapy does not induce remission, patients may be treated with either infliximab or cyclosporine; in hospitalized patients, these medications are considered after a 7- to 10-day trial of corticosteroids.
Cyclosporine requires close monitoring for hypertension, neurologic& renal toxicity, infliximab may be favored despite its increased risk for opportunistic infection & possibly malignancy.
Medically refractory UC is treated surgically with curative total proctocolectomy with either end-ileostomy or ileal pouch-anal anastomosis, in which a neorectum is constructed from a segment of ileum and connected to the anus to retain continence.
Total proctocolectomy may also be warranted in patients with neoplasia, toxic megacolon, perforation, and refractory bleeding.