2. • INFLAMMATORY BOWEL DISEASE (IBD) IS AN UMBRELLA TERM
USED TO DESCRIBE DISORDERS THAT INVOLVE CHRONIC
INFLAMMATION OF YOUR DIGESTIVE TRACT.
• TYPES OF IBD INCLUDE:
1) ULCERATIVE COLITIS
2) CROHN'S DISEASE
3. • ULCERATIVE COLITIS.
• THIS CONDITION INVOLVES INFLAMMATION AND SORES
(ULCERS) ALONG THE SUPERFICIAL LINING OF YOUR
LARGE INTESTINE (COLON) AND RECTUM.
• CROHN'S DISEASE.
• THIS TYPE OF IBD IS CHARACTERIZED BY INFLAMMATION
OF THE LINING OF YOUR DIGESTIVE TRACT, WHICH
OFTEN CAN INVOLVE THE DEEPER LAYERS OF THE
DIGESTIVE TRACT.
4. • DIGESTIVE SYSTEM
• CROHN'S DISEASE AND ULCERATIVE COLITIS ARE BOTH FORMS OF INFLAMMATORY
BOWEL DISEASE. CROHN'S DISEASE MOST COMMONLY AFFECTS THE COLON AND
THE LAST PART OF THE SMALL INTESTINE (ILEUM). ULCERATIVE COLITIS AFFECTS
ONLY THE COLON.
5. • BOTH ULCERATIVE COLITIS AND CROHN'S DISEASE
USUALLY ARE CHARACTERIZED BY DIARRHEA, RECTAL
BLEEDING, ABDOMINAL PAIN, FATIGUE AND WEIGHT
LOSS.
• IBD CAN BE DEBILITATING AND SOMETIMES LEADS TO
LIFE-THREATENING COMPLICATIONS.
6. • SYMPTOMS
• INFLAMMATORY BOWEL DISEASE SYMPTOMS VARY,
DEPENDING ON THE SEVERITY OF INFLAMMATION AND WHERE
IT OCCURS.
• SYMPTOMS MAY RANGE FROM MILD TO SEVERE.
• YOU ARE LIKELY TO HAVE PERIODS OF ACTIVE ILLNESS
FOLLOWED BY PERIODS OF REMISSION.
7. • SIGNS AND SYMPTOMS THAT ARE COMMON TO BOTH CROHN’S
DISEASE AND ULCERATIVE COLITIS INCLUDE:
• DIARRHEA
• FATIGUE
• ABDOMINAL PAIN AND CRAMPING
• BLOOD IN YOUR STOOL
• REDUCED APPETITE
• UNINTENDED WEIGHT LOSS
8. • ETIOLOGY
• THE EXACT CAUSE OF INFLAMMATORY BOWEL DISEASE REMAINS UNKNOWN.
PREVIOUSLY, DIET AND STRESS WERE SUSPECTED, BUT NOW DOCTORS KNOW THAT
THESE FACTORS MAY AGGRAVATE BUT AREN'T THE CAUSE OF IBD.
• ONE POSSIBLE CAUSE IS AN IMMUNE SYSTEM MALFUNCTION.
• WHEN YOUR IMMUNE SYSTEM TRIES TO FIGHT OFF AN INVADING VIRUS OR
BACTERIUM, AN ABNORMAL IMMUNE RESPONSE CAUSES THE IMMUNE SYSTEM TO
ATTACK THE CELLS IN THE DIGESTIVE TRACT, TOO.
• HEREDITY ALSO SEEMS TO PLAY A ROLE IN THAT IBD IS MORE COMMON IN PEOPLE
WHO HAVE FAMILY MEMBERS WITH THE DISEASE. HOWEVER, MOST PEOPLE WITH
IBD DON'T HAVE THIS FAMILY HISTORY.
9. • RISK FACTORS
• AGE. MOST PEOPLE WHO DEVELOP IBD ARE DIAGNOSED BEFORE THEY’RE
30 YEARS OLD.
• RACE OR ETHNICITY. ALTHOUGH WHITES HAVE THE HIGHEST RISK OF THE
DISEASE, IT CAN OCCUR IN ANY RACE.
• FAMILY HISTORY. YOU'RE AT HIGHER RISK IF YOU HAVE A CLOSE RELATIVE —
SUCH AS A PARENT, SIBLING OR CHILD — WITH THE DISEASE.
10. • CIGARETTE SMOKING. CIGARETTE SMOKING IS THE MOST IMPORTANT
CONTROLLABLE RISK FACTOR FOR DEVELOPING CROHN'S DISEASE.
• NONSTEROIDAL ANTI-INFLAMMATORY MEDICATIONS. THESE INCLUDE IBUPROFEN
(ADVIL, MOTRIN IB, OTHERS), NAPROXEN SODIUM (ALEVE), DICLOFENAC
SODIUM AND OTHERS. THESE MEDICATIONS MAY INCREASE THE RISK OF
DEVELOPING IBD OR WORSEN THE DISEASE IN PEOPLE WHO HAVE IBD.
11. • COMPLICATIONS
• ULCERATIVE COLITIS AND CROHN'S DISEASE HAVE SOME COMPLICATIONS
IN COMMON AND OTHERS THAT ARE SPECIFIC TO EACH CONDITION.
• COMPLICATIONS FOUND IN BOTH CONDITIONS MAY INCLUDE:
• COLON CANCER. HAVING ULCERATIVE COLITIS OR CROHN'S DISEASE THAT
AFFECTS MOST OF YOUR COLON CAN INCREASE YOUR RISK OF COLON CANCER.
• SKIN, EYE AND JOINT INFLAMMATION. CERTAIN DISORDERS, INCLUDING
ARTHRITIS, SKIN LESIONS AND EYE INFLAMMATION (UVEITIS), MAY OCCUR
DURING IBD FLARE-UPS.
12. • MEDICATION SIDE EFFECTS. CERTAIN MEDICATIONS FOR IBD ARE ASSOCIATED
WITH A SMALL RISK OF DEVELOPING CERTAIN CANCERS.
• CORTICOSTEROIDS CAN BE ASSOCIATED WITH A RISK OF OSTEOPOROSIS, HIGH
BLOOD PRESSURE AND OTHER CONDITIONS.
• BLOOD CLOTS. IBD INCREASES THE RISK OF BLOOD CLOTS IN VEINS AND
ARTERIES.
13. • PATHOGENESIS
• 1) IBD PATHOGENESIS IS INITIATED BY BACTERIAL PEPTIDOGLYCAN, WHICH
INDUCES CASPASE-1-DEPENDENT MECHANISM BY NOD1 AND NOD2, WHICH
ENHANCED THE EXPRESSION OF IL-32.
• IL-32 INITIATES THE NF-KB ACTIVATION AND A SPECTRUM OF VARIOUS
OTHER INFLAMMATORY CYTOKINES, AND THIS ACTIVATION ULTIMATELY
RESULT IN IBD.
• 2) PRESENCE OF THE MICROORGANISMS IN GUT TRIGGERS THE IMMUNE
RESPONSE AGAINST THESE MICROBS, THESE ANTIBODIES SOMETIMES
ATTACKS ON THE BOWEL LININGS CAUSING INFLAMMATION.
• 3) THIS INFLAMMATION CAUSES ABNORMALITIES IN THE INTESTINAL WALL
(BARRIER) RESULTS IN BREACHES IN THIS BARRIER. BREACHES (THE
INTESTINAL EPITHELIUM) ALLOW FURTHER INFILTRATION OF
MICROORGANISMS THAT, IN TURN, ELICITE FURTHER IMMUNE RESPONSES.