INFLAMMATORY BOWEL

DISEASE

-DR.PARASHURAM
PROFESSOR
DEPARTMENT OF INTERNAL MEDICINE
DR BRAMCH,BENGALURU.

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 CONTENTS
 INTRODUCTION
 ETIOLOGY AND PATHOGENESIS
 CLINICAL PRESENTATION
 DIFFERENTIAL DIAGNOSIS
 EXTRAINTESTINAL MANIFESTATIONS
 MANAGEMENT

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INRODUCTION
 IBD is an immune mediated chronic intestinal
condition,characterised by recurrent inflammatory involvement
of specific bowel segments.
 Two major categories are ulcerative colitis(UC) and crohns
disease(CD).
 Incidence and prevalence are traditionally high in industrialised
nations like USA and in europe.
 IBD is emerging in countries that are becoming more
westernised including China,India,Thailand and Africa.

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 Peak incidence of UC and CD is in 2nd to 4th decade,with
second modest rise between 7th and 9th decades of life.
 Pediatric IBD (<18yrs) comprises 20-25% of all IBD pts and

about 5% are <10yrs of age.

 Greatest incidence is seen among white and jewish people and

is increasing in hispanic and asians.

RISK/PROTECTIVE FACTORS
 Smoking may prevent UC,but may cause CD.

 Previous appendectomy is protective in UC.

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 Infectious GE with salmonella,shigella,C.difficile increases
IBD risk by 2-3 times.

 Diets high in animal protein,sugars,fish and dietary fat increase

risk of IBD.

 IBD is familial in 5-10% of pts,if both parents have IBD,each

child has 36% chance of being affected.

 Pancolic disease is more common in asian pts.

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DEFINING UC and CD
 ULCERATIVE COLITIS
 Inflammation and morphological changes remain confined to

colon.
 Rectum is involved in 95% pts,with variable degrees of

proximal extension.
 Inflammation primarily limited to mucosa,consisting of

PANCOLITIS with ulceration,edema and hemorrhage.

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 CROHNS DISEASE
 Can involve any part of gi tract from oropharynx to perianal
area,with diseased segments,separated by normal bowel leading
to SKIP areas.
 Inflammation can be transmural,resulting in sinus tracts or
FISTULA formation.
 Presence of mucosal GRANULOMAs.
 Most common location is ILEOCECAL region,followed by
terminal ileum alone.
 CD of small intestine is called regional enteritis.

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COMPARING FEATURES…

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ETIOLOGY AND PATHOGENESIS
 Commensal microbiota,intestinal epithelial cells and immune
cells

 Affected by environmental(smoking,antibiotics,enteromicrobes
and genetic factors)

 In susceptible host leads to dysregulated inflammation ,which

leads to IBD.
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GENETIC CONSIDERATIONS
-Mutations in genes encoding IL-10,cytotoxic T-lymphocyte
associated protein-4(CTLA4),Nucleotide-binding
oligomerisation domain containing 2(NOD2) etc
-Can be monogenic or polygenic.
-Associated genetic disorders include
• Turners syndrome
• Wiskott-Aldrich syndrome
• Immune dysregulation polyendocrinopathy,enteropathy X-

linked(IPEX synd.)

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COMMENSAL MICROBIOTA:
-Commensal microbiota in IBD pts is different from that of non
affected individuals,i.e in state of dysbiosis.
-Presence of microbes that drive disease(E.coli) or loss of
protective microbes(Firmicutes).

DEFECTIVE IMMUNE REGULATION:

-This leads to T cell activation,which further activates IL-1,IL-6
and TNF.
-This explains role of antibodies to block cytokines,5-
ASA(aminosalicylic acid) and glucocorticoids in
treatment,which inhibit inflammatory mediators.
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PATHOLOGY:
1)UC:
Macroscopic features
 40-50% have involvement of rectosigmoid,30-40% beyond

sigmoid and 20% have total colitis.

 Mucosa may appear erythematous,hemorrhagic,edematous or

ulcerated.
 Pseudopolyps may be present.
 Pts with fulminant disease can develop toxic colitis or

megacolon.

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2)CD:
Macroscopic features:
 30-40% have small bowel disease alone,40-55% have

involvement of both small and large bowel and 15-25% have

colitis alone.
 Terminal ileum is involved in 90% pts,with RECTUM being

often SPARED.
 Perirectal fissures,fistulas,abscesses and anal stenosis are

common.
 TRANSMURAL process.

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GRANULOMA IN CROHNS DISEASE.

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CLINICAL PRESENTATION
1)ULCERATIVE COLITIS
SIGNS AND SYMPTOMS:
 Major symptoms are diarrhea,bleeding PR,tenesmus,passage
of mucus and crampy abdominal pain.
 In severe cases,pts pass liquid stool containing blood,pus and
fecal matter.
 Diarrhea is often nocturnal and/or postprandial.
 Other features include anorexia,vomiting,fever and wt.loss.
 Pts with toxic colitis hv severe pain and bleeding

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LAB FEATURES
-Active disease is associated with increased CRP,ESR and
decreased Hb.
-Fecal lactoferrin and calprotectin are markers of inflammation
which are used to r/o inflamn vs symptoms of IBS.
-Diagnosis relies on history,symptoms,negative stool
examination for bacteria,C.difficile toxin and
ova,sigmoidoscopy and histology of colonic biopsy.
-Sigmoidoscopy/colonoscopy is used to assess disease activity
which shows erythema,vascular pattern and ulcerations.

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COMPLICATIONS OF UC:
-Massive hemorrhage

-Toxic megacolon leading to perforation.

-Strictures.

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2) CROHNS DISEASE:
SIGNS AND SYMPTOMS:
 Can cause fibrostenotic obstructing pattern or penetrating

fistulous pattern,with diff. treatment and prognosis.

 ILEOCOLITIS
 H/O recurrent right lower quadrant pain and diarrhea.
 Colicky abd. pain and low grade fever are seen.
 Symptoms of bowel obstruction.
 Enterovesical/Enterocutaneous fistulas may develop.

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 JEJUNOILEITIS:
 Causes malabsorption and steatorrhea.
 Anemia,hypoalbuminemia,hypocalcemia can occur.
 Pellagra and Vit B12 deficiency can occur,hence most pts should
take daily multivitamin,calcium and vitamin D tablets.

 COLITIS AND PERIANAL DISEASE

 Pts present with fever,diarrhea and abdominal pain.
 Colonic disease may fistulize into stomach or duodenum,causing
feculent vomiting.
 Perianal disease causes incontinence,strictures and abscesses.
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 GASTRODUODENAL DISEASE
-symptoms and signs include vomiting,epigastric pain and
features of chronic gastric outlet obstruction.

LAB FEATURES
-Similar to UC with elevated ESR,CRP and fecal calprotectin
levels.
-Endoscopic features include rectal sparing,fistulas and skip
lesions.
-Early radiographic findings in small bowel include thickened
folds and apthous ulcerations.
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-Other diagnostic radiographic modalities for CD include
 Wireless capsule endoscopy
 CT and
 MR enterography.

COMPLICATIONS
• Fistula formation
• Intraabdominal and pelvic abscesses
• Intestinal obstruction and massive hemorrhage.

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SEROLOGIC MARKERS:
 Increased titres of Anti-saccharomyces cerevisiae antibodies

are seen in CD.

 Increased titres of p-ANCA are seen in UC pts.

INDETERMINATE COLITIS
-In abt 15% cases,differentiating between UC and CD is not
possible.

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DIFFERENTIAL DIAGNOSIS
INFECTIOUS:
1)BACTERIAL
-Salmonella,shigella,E.coli and C.difficile.
2)TUBERCULOSIS
3)VIRAL
-CMV,HSV and HIV.
4)PARASITIC
-Amebiasis and hookworm infections.

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NONINFECTIOUS DDs:
1)Inflammatory
-Diverticulitis,Neutropenic colitis.

2)Neoplastic
-Lymphoma,Metastatic.

3)Drugs
-NSAIDs,Oral contraceptives etc.

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EXTRAINTESTINAL MANIFESTATIONS
 DERMATOLOGIC

-Erythema nodosum,pyoderma gangrenosum.

 RHEUMATOLOGIC
-Peripheral arthritis,Ankylosing spondylitis

OCULAR
-Conjunctivitis,anterior uveitis and episcleritis.

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HEPATOBILIARY
-Hepatic steatosis,Primary sclerosing cholangitis and
cholelithiasis.
UROLOGIC
-Calculi,ureteral obstruction and fistulas.
METABOLIC BONE DISORDERS
-Osteoporosis and osteonecrosis.
THROMBOEMBOLIC DISORDERS
-Both venous and arterial thrombosis can occur.

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TREATMENT
1)5-ASA agents:
-These are effective at inducing and maintaining remission in
UC,but have limited role in CD.
 Sulfasalazine(3-6g/day).
 Mesalamine(2.4-4.8g/day).

2)GLUCOCORTICOIDS(oral or parenteral)
-Used in mod. to severe UC,unresponsive to ASA therapy.
-Prednisone(40-60mg/day),hydrocortisone(300mg/day).
-Budesonide(9mg/day for 8wks without tapering.)
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3)ANTIBIOTICS:
-Used in cases of pouchitis.
-Metronidazole(15-20mg/kg/day)tid
-Ciprofloxacin(500mg bid).

4)AZATHIOPRINE AND 6-MERCAPTOPURINE

-Immunosuppressants.
-Azathioprine(2-3mg/kg/day) and 6-MP(1-1.5mg/kg/day)

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5)METHOTREXATE
 Inhibits dihydrofolate reductase.
 IM or SC doses range from 15-25mg/week.

6)CYCLOSPORINE(CSA) and TACROLIMUS

-Inhibits both cellular and humoral immune systems,by blocking
IL-2 production.
-DOSE OF CSA(2-4mg/kg/day i.v),monitor RFTs.
-Used in iv glucocorticoid refractory UC cases.

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7)BIOLOGIC THERAPIES:
-Used in mod. to severe CD and UC cases.
o ANTI-TNF therapies

-Infliximab(5mg/kg i.v)
-Adalimumab(40mg s.c, weekly)
-Certolizumab pegol(s.c)
-Golimumab(s.c)
-Side effects of these include Non hodgkins
lymphoma,reactivation of LATENT TB.
-Before initiating anti-TNF,do PPD and CHEST X-RAY.

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8)ANTI-INTEGRINs(In pts refractory to anti-TNF treatment):
-Natalizumab
-Vedolizumab
-Ustekinumab

9)NUTRITION:Mainly used in remission of CD pts.

-Bowel rest+TPN

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 SURGICAL MANAGEMENT

1)UC:
-Toxic megacolon
-Colonic obstructtion
-Ca colon.
2)CD:
-Stricture and obstruction
-Refractory fistula
-Abscess
-Ca colon.

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TREATMENT PLAN IN ULCERATIVE COLITIS

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TREATMENT PLAN IN CROHNS DISEASE.

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SUMMARY

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THANK YOU

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REFRENCES
 HARRISONS TEXTBOOK OF INTERNAL MEDICINE
 IBD AND ITS TREATMENT,SCIENCE DIRECT.

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