Inflammatory Bowel

Disease (IBD)

Dr.Arun Kumar K S
Asst.Professor
AUCOPS
 Introduction
There are two forms of inflammatory bowel
disease (IBD):
(a) Ulcerative Colitis: A mucosal
inflammatory condition confined to the
rectum and colon;
(b) Crohn’s disease: A transmural
inflammation of the gastrointestinal tract
that can affect any part, from the mouth to
the anus.
Etiology
• Infectious agents:
• Viruses (e.g., measles)
• L-Forms of bacteria
• Mycobacteria
• Chlamydia
• Genetics:
• Metabolic defects
• Connective tissue disorders
• Environmental Factors:
• Diet
• Smoking (Crohn’s disease)
 Etiology
• Immune defects:
• Altered host suceptibility
• Immune-mediated mucosal damage

• Psychologic factors:
• Stress
• Emotional or physical trauma
• Occupation
INFECTIOUS FACTORS
• Microorganisms are a likely factor in the
initiation of inflammation in IBD.

• Patients with inflammatory bowel diseases

have increased numbers of surface-adherent
and intracellular bacteria.

• Microbes may elaborate super antigens, which

are capable of stimulatingT-lymphocytes and
produce subsequent inflammatory response.
Genetic factors
• Genetic factors predispose patients to
inflammatory bowel diseases,
particularly Crohn’s disease.
• In studies of monozygotic twins, there
has been a high concordance rate, with
both individuals of the pair having an
IBD (particularly Crohn’s disease).
• Also, first-degree relatives of patients
with IBD had a 13-fold increase in the
risk of disease.
Immunologic Mechanisms
• With Crohn’s disease, the bowel wall is
infiltrated with lymphocytes, plasma cells,
mast cells, macrophages, and neutrophils.

• Similar infiltration has been observed in the

mucosal layer of the colon in patients with
ulcerative colitis.

• Inflammation in IBDs is maintained by an

influx of leukocytes from the vascular
system into sites of active disease.
Immunologic Mechanisms
• Many of the systemic manifestations of
IBD have an immunologic etiology
(e.g., arthritis or uveitis).

• IBD is responsive to
immunosuppressive drugs (e.g.,
corticosteroids and azathioprine).

• Potential immunologic mechanisms

include both autoimmune and non-
autoimmune phenomena.
PSYCHOLOGICAL FACTORS

• Mental health changes appear to

correlate with remissions and
exacerbations, especially of
ulcerative colitis, but are not
thought to be an etiologic factor.
DIET, SMOKING, AND NSAID USE

• Studies of increased intake of refined

sugars or chemical food additives and
reduced fiber intake have provided
conflicting results regarding risk for
Crohn’s disease.
• Smoking plays an important but contrasting
role in ulcerative colitis and Crohn’s
disease.
• Use of nonsteroidal anti-inflammatory
drugs (NSAIDs) can trigger disease
occurrence or lead to disease flares.
Pathophysiology
• Ulcerative colitis and Crohn’s disease differ in
two general respects:
1. Anatomic sites and
2. Depth of involvement within the bowel wall.

• The inflammatory response seen in IBD has

also been blamed for the systemic
complications seen in both Crohn’s disease and
ulcerative colitis.
Ulcerative colitis
• Ulcerative colitis is confined to the rectum and
colon, and affects the mucosa and the submucosa.

• In some instances, a short segment of terminal ileum

may be inflamed; this is referred to as backwash
ileitis.

• Unlike Crohn’s disease, the deeper longitudinal

muscular layers, serosa, and regional lymph nodes
are not usually involved.

• Fistulas, perforation, or obstruction are uncommon

because inflammation is usually confined to the
mucosa and submucosa.
Ulcerative colitis
• The primary lesion of ulcerative colitis occurs
in the crypts of the mucosa (crypts of
Lieberkuhn) in the form of a crypt abscess.

• Other typical ulceration patterns include a

“collar-button ulcer,” which results from
extensive submucosal undermining at the ulcer
edge.

• Ulcerative colitis can be accompanied by

complications that may be local (involving the
colon or rectum) or systemic (not directly
associated with the colon).
Ulcerative colitis
• Colonic perforation, however, may
occur with or without toxic
megacolon and is a greater risk with
the first attack.
• Another infrequent major local
complication is massive colonic
hemorrhage.
• Colonic stricture, sometimes with
clinical obstruction, may also
complicate long-standing ulcerative
colitis
HEPATOBILIARY COMPLICATIONS

• Approximately 11% of patients with

ulcerative colitis are reported to have
hepatobiliary complications with
frequencies ranging from 5% to 95% in
IBD patients overall.
• Hepatic complications include fatty liver,
pericholangitis, chronic active hepatitis,
and cirrhosis.
• Biliary complications include sclerosing
cholangitis, cholangiocarcinoma, and
gallstones.
JOINT COMPLICATIONS

• Arthritis commonly occurs in IBD

patients and is typically asymmetric
(unlike rheumatoid arthritis) and
migratory, involving one or a few
usually large joints.

• The joints most often affected, in

decreasing frequency, are the knees,
hips, ankles, wrists, and elbows.
OCULAR COMPLICATIONS

• Ocular complications including iritis,

uveitis, episcleritis, and conjunctivitis
occur in up to 10% of patients with IBD.

• The most commonly reported symptoms

with iritis and uveitis include blurred
vision, eye pain, and photophobia.
DERMATOLOGIC AND MUCOSAL
COMPLICATIONS

• Skin and mucosal lesions

associated with IBD include
erythema nodosum,pyoderma
gangrenosum, and aphthous
ulceration(blisters on mouth and
lips)
 Crohn’s Disease
• Crohn’s disease is best characterized as a
transmural inflammatory process.

• The terminal ileum is the most common site of

the disorder, but it may occur in any part of the
GI tract from mouth to anus.

• Fistula formation is common and occurs much

more frequently than with ulcerative colitis.

• Fistulae often occur in the areas of worst

inflammation, where loops of bowel have
become matted together by fibrous adhesions.
Complications
• Systemic complications of Crohn’s
disease are common, and similar to
those found with ulcerative colitis.
• Arthritis, iritis, skin lesions, and
liver disease often accompany
Crohn’s disease.
• Renal stones occur in up to 10% of
patients with Crohn’s disease
Clinical Presentations
• Mild—Fewer than four stools daily, with or
without blood, with no systemic disturbance
and a normal erythrocyte sedimentation rate
(ESR).
• Moderate—More than four stools per day
but with minimal systemic disturbance.
• Severe—More than six stools per day with
blood, with evidence of systemic
disturbance shown by fever, tachycardia,
anemia, or ESR of >30.
• It is also important to determine disease
extent; that is, which part of the colon is
involved—rectum, descending colon only,
or the entire colon.
Clinical Presentation of
Ulcerative Colitis
Signs and symptoms :
• Abdominal cramping
• Frequent bowel movements, often with blood
in the stool
• Weight loss
• Fever and tachycardia in severe disease
• Blurred vision, eye pain, and photophobia with
ocular involvement
• Arthritis
• Raised, red, tender nodules that vary in size
from 1 cm to several cms
• Physical examination
• Hemorrhoids, anal fissures, or perirectal abscesses
may be present
• Iritis, uveitis, episcleritis, and conjunctivitis with
ocular involvement
• Dermatologic findings with erythema nodosum,
pyoderma
• gangrenosum, or aphthous ulceration
• Laboratory tests
• Decreased hematocrit/hemoglobin
• Increased erythrocyte sedimentation rate
• Leukocytosis and hypoalbuminemia with severe
disease
Clinical Presentation of
Crohn’s Disease
• Signs and symptoms :
• Malaise and fever
• Abdominal pain
• Frequent bowel movements
• Hemotachezia
• Fistula
• Weight loss
• Arthritis
• Physical examination :
• Abdominal mass and tenderness
• Perianal fissure or fistula
• Laboratory tests :
• Increased white blood cell count and erythrocyte
sedimentation rate
 Treatment Goals
• These goals may relate to
• resolution of acute inflammatory
processes,
• resolution of attendant complications
(e.g., fistulas and abscesses),
• alleviation of systemic manifestations
(e.g., arthritis),
• maintenance of remission from acute
inflammation, or surgical palliation
or cure.
Treatment Goals
• Proper nutritional support is an
important aspect of the treatment of
patients with IBD,
• not because specific types of diets are
useful in alleviating the inflammatory
conditions,
• But because patients with moderate to
severe disease are often malnourished
either because the inflammatory process
results in significant mal absorption or
mal digestion or because of the catabolic
effects of the disease process.
 Treatment Goals
• Parenteral nutrition is an important
component of the treatment of severe
Crohn’s disease or ulcerative colitis.
• The use of parenteral nutrition allows
complete bowel rest in patients with
severe ulcerative colitis, which may
alter the need for proctocolectomy.
• Parenteral nutrition has also been
valuable in Crohn’s disease, because
remission may be achieved with
parenteral nutrition in about 50% of
patients
 Treatment Goals

• Probiotics involves the reestablishment

of normal bacterial flora within the gut
by oral administration of live bacteria
such as nonpathogenic Escherichia coli,
bifidobacteria, lactobacilli, or
Streptococcus thermophilus.
• Probiotic formulations have been
effective in maintaining remission in
ulcerative colitis
• Although surgery (proctocolectomy) is curative for ulcerative
colitis, this is not the case for Crohn’s disease. .

• For ulcerative colitis, colectomy may be necessary when the

patient has disease uncontrolled by maximum medical therapy
or when there are complications of the disease such as colonic
perforation, toxic dilatation (megacolon), uncontrolled
colonic hemorrhage, or colonic strictures.

• Colectomy may be indicated in patients with longstanding

disease (greater than 8 to 10 years), as a prophylactic measure
against the development of cancer, and in patients with
premalignant changes (severe dysplasia) on surveillance
mucosal biopsies
• The major types of drug therapy used in
IBD include aminosalicylates,
corticosteroids, immunosuppressive
agents (azathioprine, mercaptopurine,
cyclosporine, and methotrexate),
antimicrobials (metronidazole and
ciprofloxacin), and agents to inhibit
TNF-α (anti-TNF-α antibodies).
• Sulfasalazine, an agent that combines a
sulfonamide (sulfapyridine) antibiotic and
mesalamine (5-aminosalicylic acid) in the same
molecule, has been used for many years to treat
IBD.
• The active component of sulfasalazine is
mesalamine.
• Aminosalicylates may block production of
prostaglandins and leukotrienes, inhibit bacterial
peptide-induced neutrophil chemotaxis and
adenosine-induced secretion, scavenge reactive
oxygen metabolites, and inhibit activation of the
nuclear regulatory factor NF-κB.
• Corticosteroids and adrenocorticotropic
hormone have been widely used for the
treatment of ulcerative colitis and
Crohn’s disease, given parenterally,
orally, or rectally.
• Corticosteroids are believed to modulate
the immune system and inhibit
production of cytokines and mediators
• Azathioprine and mercaptopurine are
effective for long-term treatment of
Crohn’s disease and ulcerative colitis.
• These agents are generally reserved for
patients who are refractory to steroids,
and they may be associated with serious
adverse effects such as lymphomas,
pancreatitis, or nephrotoxicity
DRUGS DOSE ADR

Prednisolone 40 mg/day Moon face,sleep and mood

Reduse in 4 -6 disturbance,dyspepsia.
week
Sulfasalazine 2 -4g/day in div Nausea ,vomiting ,abdominal
dose pain ,metalic taste ,heamolytic
aneamia.
Azathioprine 2-2.5 mg/kg/day Flu like symptom,nausea,
Mercaptopurine 1-1.5mg/kg/day diarrhoea , leukopenia
Methotrexate 15 -25 mg once ,pancreatitis
weekly Nausea ,vomiting,stomatitis
Cyclosporin 2-5mg/kg/day Tremour ,headache ,gum
hyperplasia, hirsutism

Metronidazole 0.6 -1.5g/day Metalic taste, glossitis

,paraesthesia ,urticaria.
 Y o u
a nk
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