GIT 4th ibd 2017

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Dr. Mohamed AlshekhaniProfessor in Medicine

MBChB-CABM-FRCP-EBGH2017

Inflammatory Bowel Disease(IBD):

Inflammatory Bowel Disease(IBD):

• IBD is idiopathic GIT inflammation ( no specific cause of inflammation as infections,ischemia,radiation, Vasculitis,etc) .

• 2 Main types: macroscopic & microscopic.• Microscopic: lymphocytic & collagenous.

• Macroscopic: 2 main subclasses: • Crohn disease (CD) • Uulcerative colitis (UC) • Minor subclass; Indeterminate colitis; 10-15%( clinical features &

test that do not allow a definitive sub-classification into above 2 types).

Risk Factors:

• Interplay between genetic & environmental factors. • Genetics:• Increased risk in family members. • Monozygotic twins have a higher risk than dizygotics or siblings. • The risk in an offspring is higher if both parents are affected. • Certain ethnic groups (Jewish) are at higher risk > others (blacks).

• Genes identified, but contribution to overall population is small.

Risk Factors:

• Interplay between genetic & environmental factors. • Environmental: • Smoking&appendisectomy is a risk factor for the development of

CD, protective factor for UC. • Dietary factors inconsistent. • IBD is more common in developed countries.• A north-south gradient, ? vitamin D.

Clinical Manifestations:Ulcerative Colitis

• Typically presents with bloody diarrhea & abdominal discomfort, the severity related to the extent / severity of inflammation.

• The distribution:• Proctitis 25%(involving the rectum only); can present with

constipation owing to rectal spasm & stasis of stool. • Left-sided colitis 25% (not extend beyond splenic flexure).• Pancolitis 50% (inflammation extends above the splenic flexure). • Because UC typically involves the rectum, so tenesmus, urgency,

rectal pain& fecal incontinence are common. • Fever& weight loss are uncommon, suggest severe disease.

Clinical Manifestations:Ulcerative Colitis

• PE:• With mild disease, physical exam may be normal. • Severe disease: fever, tachycardia, dehydration, abd tenderness, or

pallor. • Abdominal distention, hypoactive bowel sounds, & rebound

tenderness suggest fulminant colitis or perforation or toxic megacolon.

• Lab findings: significant anemia, leukocytosis, hypoalbuminemia& electrolyte abnormalities, reflect the severity of disease.

Severity in UC:

Clinical Manifestations:CD

• Common symptoms are abdominal pain, diarrhea, weight loss.• Fever & overt GIB are less common than is typical in UC. • Unlike UC,transmural inflammation in CD may predispose to fistula. • 30% have isolated SB disease.• 40% ileocolonic disease.• 25% isolated colonic disease• 5% isolated upper GI or perianal disease.


• Symptoms correlate with disease location:• SB disease usually presents with abdominal pain with or without

diarrhea; overt GI bleeding is uncommon. • Ileocolonic dis: RLQ pain is common, diarrhea & bleeding are less. • Colonic disease: bloody diarrhea more likely; also associated with

perianal disease, with perineal pain& seepage of stool or mucus from fistulas.

• Proctitis (very rare):Small-volume diarrhea with urgency& tenesmus.

• UGI disease: epigastric pain,nausea,vomiting& occasionally GOO.


• PE:• From normal to significantly abn depending on location& severity. • Patients may appear pale, malnourished, or chronically ill.• Fever; if high it suggests an abscess or peritonitis. • Abd tenderness, sometimes with a mass or fullness, is often located

in RLQ. • Perianal exam may reveal skin tags, induration, or fistulas.• As in UC, abnormal lab findings correlate with disease severity: • Leukocytosis, anemia, hypoalbuminemia, vitamin deficiencies. • The ESR& CRP are often elevated; if so, can be monitored as signs of

response to therapy & subsequent disease flare.

Clinical Manifestations:EIM

• In 10% of patients. • In both CD or UC, it may precede GI symptoms. • The most common:• Oral aphthous ulcers, arthralgia, back pain (ankylosing spondylitis

or sacroiliitis). • Eye symptoms (redness, pain, swelling) may be due to uveitis,

scleritis, or other causes of ocular inflammation & warrant immediate examination by an ophthalmologist.

• Skin manifestations are common include pyoderma gangrenosum & erythema nodosum.

• Liver involvement, most commonly ;primary sclerosing cholangitis.• In CD, EIMs are more common with colitis than SB disease.• Some EIMs correlate with IBD activity, whereas others do not.

Diagnosis: UC

• Colonoscopy & biopsy of the colon & ileum, is required. • All should undergo stool &lab exam to exclude infectious colitis,

including C. difficile & CMV & non-infectious colitis as ischemic&radiation COLITIS.

• Some patients with pancolitis extend into the ileum for a few centimeters(backwash ileitis) not indicative of CD.

• Mild UC is characterized by mucosal edema, erythema& loss of the normal vascular pattern.

• More significant disease produces granularity, friability, ulceration& bleeding.

• Histology shows altered crypt architecture with shortened, branched crypts, acute &chronic inflammation of the lamina propria.

Diagnosis:CD

• Endoscopic findings vary from superficial aphthous ulcers to discrete, deep ulcers that can be linear, stellate, or serpiginous & that may coalesce into a “cobblestone” appearance

• Rectal sparing is typical, as are areas of inflammation separated by normal mucosa (known as skip lesions).

• The ileum should be inspected during colonoscopy to detect ileal inflammation characteristic of CD.

• Histology may show patchy transmural inflammation, but more superficial inflammation does not rule out CD. Aphthous ulcers & granulomas are characteristic findings but are often not seen.

Diagnosis:CD

• CD can affect any part of GIT&in some patients inflammation is beyond the reach of colonoscopy.

• In these patients, supportive evidence can be obtained with CT or (MR) enterography, capsule endoscopy, or directly by deep enteroscopy.

• Enterography also rules out complications such as obstruction, perforation, fistulas, abscesses.

• Radiographs are more often used in CD than UC owing to the frequent involvement of the small intestine.

• Plain films can evaluate bowel obstruction & dilatation. • Small-bowel barium radiographs have largely been replaced by the

more sensitive CT or MR enterography.

Diagnosis:IDC• 10-15% have indeterminate colitis. • In these patients, serologic tests have been proposed as a way to

distinguish UC from CD,but are expensive,relatively insensitive or nonspecific&often do not add useful information to standard diagnostic tests such as colonoscopy & enterography.

Treatment:UC• For mild to moderate UC, the 5-ASA drugs are first-line therapy for

inducing & maintaining remission. • 5-ASA is delivered topically to the bowel lumen, primarily to the

colon, with the exception of the time-release formulation of mesalamine, which is able to deliver the drug throughout the small bowel & the colon.

• Sulfasalazine may cause folate deficiency& supplementation is recommended.

• More severe UC is often treated with oral glucocorticoids as prednisone, 40-60 mg/d.

Treatment:• Budesonide is a glucocorticoid with high first-pass metabolism

available in a controlled ileal-release formulation frequently used in CD, but (multi-matrix [MMX] system) formulation provides release of the drug throughout the colon useful in treating UC.

• It has similar efficacy as prednisone but has fewer side effects but high cost.

• Patients whose disease does not respond to oral glucocorticoids should be hospitalized&given IV glucocorticoids or biologic agent.

• Glucocorticoids are not effective for maintaining remission in UC. • In patients whose disease responds to glucocorticoids, the dose

should be tapered over 2 - 4 months while transitioning to a maintenance medication (AZA, 6-MP, or a biologic agent).

Treatment:• Patients whose symptoms do not respond to glucocorticoids are

treated with cyclosporine, a biologic agent, or colectomy. • Cyclosporine is effective for avoiding colectomy in the short term. • Many patients eventually require colectomy. • The three anti-TNF antibodies approved for inducing/ maintaining

remission in UC are infliximab, adalimumab&golimumab. • The integrin-blocking antibody vedolizumab blocks leukocyte

trafficking ,also approved for the treatment of UC.

Treatment:CD• 5-ASA drugs for CD little or no benefit. • Antimicrobial agents are important in patients with fistulas or

abscesses, but no treating luminal disease. • Patients with mild to moderate inflammatory CD are often treated

initially with glucocorticoids. Prednisone is often used. • For ileocolonic CD, controlled-release budesonide is an alternative

to prednisone, with fewer side effects but higher cost.• As in UC, glucocorticoids are not effective for maintaining remission

in CD,SO patients who responds to glucocorticoids should be transitioned to an immunomodulator while the glucocorticoid is tapered.

Treatment:CD• In addition to AZA / 6-MP, methotrexate is an option in CD.• AZA, 2 -3 mg/kg/d; 6-MP, 1.5 mg/kg/d; methotrexate, 25 mg/week,

are effective for inducing & maintaining remission. • AZA / 6-MP are effective for closing fistulas. • Some adverse events from methotrexate minimized by the use of

folic acid,but should not be used in pregnant or lactating women.

Treatment:CD• Patients with more severe disease are treated with a biologic agent.

The three anti-TNF agents approved for CD are infliximab, adalimumab, and certolizumab.

• These medications are effective for inducing / maintaining remission & closing fistulas, generally considered to be safe in pregnancy.

• Anti-TNF efficacy is better when used with an immunomodulator& risk of developing anti-TNF antibodies is lower.

Treatment:CD

• Patients whose disease does not respond to one anti-TNF agent are often switched to a second or third anti-TNF agent.

• Those with no response to or intolerance of anti-TNF agents should be treated with either surgery or a leukocyte trafficking blocker (natalizumab or vedolizumab).

• Natalizumab increases the risk of infections, including progressive multifocal leukoencephalopathy (PML), specially if JC virus sero +ve making the risk unacceptably high & should not be used.

IBD: Health maintinance

• CRC Surveillance: Patients with long-standing IBD are at increased risk for CRC & should undergo surveillance colonoscopy every 1- 2 years beginning after 8-10 years of disease.


• Nutritional support:• Patients with severely active disease, particularly CD, are at risk for

malnutrition & various vitamin deficiencies & should undergo screening for these conditions,sp distal ileal disease is associated with vitamin B12 malabsorption.


• Osteoporosis screen:• Steriod use for > 3 mons is a risk factor for osteoporosis &indication

to assess bone density.


• Vaccination:• Routine adult vaccines+annual killed influenza vaccine( not

attenuated vaccine) hepatitis A & B virus (if not already immune), pneumococcus&meningococcal vaccine.


• TB screen:• Before starting anti-TNF, patients assessed for TB (with Tuberculin or

IGRA) & for immunity to hepatitis A / B viruses.

Microscopic colitis:

• Accounts for 10- 15% of patients with chronic, watery diarrhea. • > Common in elderly. • Endoscopically normal. • The symptoms similar to other chronic causes of non-bloody

diarrhea, such as celiac disease & IBS which should be excluded.• Colonic mucosal biopsies are required for diagnosis. • Lymphocytic & collagenous colitis are the two subtypes &

distinguishable only by histology.• In some patients, certain medications (NSAIDs /PPI). • MC is associated with other AI diseases as DM & psoriasis.

Microscopic colitis:treatment

• Based on symptom severity. • Suspected drugs stopped if possible. • In mild disease, antidiarrheal as loperamide or diphenoxylate used. • In moderate disease, bismuth subsalicylate may be beneficial. • In severe cases or those that do not respond to antidiarrheal agents

or bismuth, budesonide is the treatment of choice,highly effective (response rates of ≥80%), but the risk of relapse is high once stopped (70%-80%); many patients require long-term low dose maintenance or an immunomodulator as AZA.

• The 5-ASA medications are not very effective for MC. • If not respond or not tolerate budesonide, cholestyramine effective. • In severe cases, treatment with an anti-TNF agent may be needed.

BO5:1

• 1.Inflammatory Bowel disease includes:• A.Ischemic colitis.• B.Infectious colitis.• C.Idiopathic inflammattory colitis.• D.Radiation colitis.• E.Behcet-associated colitis.

BO5:2

• 2.The following are Inflammatory Bowel disease except:

• A.Ulcerative colitis.• B.Crohns disease.• C.Intdermined colitis.• D.TB-induced colitis.• E.Microscopic colitis.

BO5:3

• 3.The least common subtype of IBD is:• A.Ulcerative colitis.• B.Crohns disease.• C.Intdermined colitis.• D.Collagenous colitis.• E.Lymphocytic colitis.

BO5:4

• 4.Hematochesia is more common with:• A.Ulcerative colitis.• B.Crohns disease.• C. Both above.• D.Collagenous colitis.• E.Lymphocytic colitis.

BO5:5

• 5.Skiped lesions are more characteristic of:• A.Ulcerative colitis.• B.Crohns disease.• C. Both above.• D.Collagenous colitis.• E.Lymphocytic colitis.

BO5:6

• 6.Transmural colonic involvement is characteristic of:

• A.Ulcerative colitis.• B.Crohns disease.• C. Both above.• D.Collagenous colitis.• E.Lymphocytic colitis.

BO5:7

• 7.Granuloma on histopathology is characteristic of:

• A.Ulcerative colitis.• B.Crohns disease.• C. Both above.• D.Collagenous colitis.• E.Lymphocytic colitis.

BO5:8

• 8.Extraintestinal features are characteristic of:• A.Ulcerative colitis.• B.Crohns disease.• C. Both above.• D.Collagenous colitis.• E.Lymphocytic colitis.

BO5:9

• 9.Standard drug treatment for crohn’s disease usually include all except:

• A.5 ASAs.• B. Steroides.• C. Infliximab.• D.Azathioprine.• E.Cyclosporine.

BO5:10

• 10.Patients with long-standing IBD require the following long-term interventions except:

• A.CRC surveillance.• B. Nutritional support.• C. Killed vaccine.• D. Attenuated vaccines.• E.TB screen.

BO5:11

• 11.The standard drug therapies for microscopic colitis include all except:

• A.Anti-diarrheals.• B. Bismuth.• C. Budosonide.• D. 5 ASA.• E.Cholecytramine.

BO5:12

• 12.The biological agent that increase the risk of CJD in IBD treated patients is:

• A.Infliximab.• B. Adalimumab.• C. Golizumab.• D. Natalizumab.• E. None of the above.

BO5:13

• 13.The IBD subtype that has a more complicated course is:

• A.Crohn’s disease.• B. Ulcerative colitis.• C. Indetermined colitis.• D. Lymphocytic colitis.• E. Collagenous colitis.

BO5:14

• 14.patients with long-standing active extensive disease should start surveillance colonoscopy after how many years:

• A. 15.• B. 5.• C. 7.• D. 20.• E. 8.

BO5:15

• 15.Important differential diagnosis of Microscopic colitis include:

• A. UC.• B. IBS.• C. Celiac disease.• D. Crohn’s disease.• E. The last 3.

BO5:16

• 16.Common extra-intestinal features of IBD involve the following organs except:

• A. Skin.• B. Eye.• C. Hepatobiliary system.• D. Heart.• E. Joints.

Health & Medicine

GIT 4th ibd 2017