The document discusses inflammatory bowel disease (IBD), specifically ulcerative colitis, detailing its definition, classification, etiology, pathophysiology, symptoms, diagnosis, treatment options including pharmacological and surgical interventions, as well as Ayurvedic management. It emphasizes the chronic nature of the disease, the importance of differentiating it from other conditions, and the need for long-term management to induce and maintain remission. Complications of ulcerative colitis and various types and symptoms associated with it are also outlined.

1. IRRITABLE BOWEL SYNDROME
& ULCERATIVE COLITIS
GUIDED BY:
DR. NIBEDITA MAHAPATRA MAAM (HOD DEPT OF KAYA CHIKITSA)
DR. KABI CHANDRA SAHU SIR (LECTURER OF KAYA CHIKITSA)
PRESENTED BY:
ANKITA DASH
(4TH PROFESSIONAL BAMS)

19. IBD & ULCERATIVE COLITIS

20. DEFINITION
 Inflammatory bowel disease (IBD) represents a group of intestinal disorders that cause
prolonged inflammation of the digestive tract.
 It is a spectrum of chronic idiopathic inflammatory condition.
 It is a condition that can affect any part of the digestive tract and causes inflammation swelling
Redness & ulceration.

21. CLASSIFICATION
 Ulcerative colitis
 Crohn’s disease

22. ETIOLOGY
 Infectious agents
 Viruses (Measles)
 Bacteria (Mycobacteria)
 Genetics
 Environmental factors
 Diet
 Smoking
 Psychological factors
 Stress
 Emotional or physical trauma

23.  Mucosal immune response
 • Inflammatory cells
 • In IBD, activated CD4+Tcells are present in the lamina propria and in the peripheral blood
 • These cells either activate other inflammatory cells like macrophages, and B cells or recruit
more inflammatory cells by stimulation of homing receptors on leukocytes and vascular
endothelial cells

25. PATHOPHYSIOLOGY
1. Inflammatory process usually confined to rectum and sigmoid colon
2. Inflammation leads to mucosal hemorrhages and abscess formation, which
leads to necrosis and sloughing of bowel mucosa.
3. Mucosa becomes red, friable, and ulcerated; bleeding is common
4. Chronic inflammation leads to atrophy, narrowing, and shortening of colon.

26. PATHOPHYSIOLOGY
 Dietary and bacterial antigens penetrate into the
intestinal wall and activates the immune system.
 This causes increased production of pro-
inflammatory mediators which will lead to
inflammation of the mucosal layer.
ALTERED MUCOSAL IMMUNE RESPONSE

28. ULCERATIVE COLITIS
 Ulcerative colitis is an inflammatory bowel disease (IBD).
 Ulcerative colitis occurs when the lining of your large intestine (also called the colon),
rectum, or both becomes inflamed.
 This inflammation produces tiny sores called ulcers on the lining of your colon. It usually
begins in the rectum and spreads upward. It can involve your entire colon.
 Ulcerative colitis can be debilitating and can sometimes lead to life-threatening
complications. While it has no known cure, treatment can greatly reduce signs and
symptoms of the disease and bring about long-term remission.

29.  There is no difference between men and women.
 The worldwide incidence is 0.5~24 new cases per 100 000
 individuals, and prevalence is 100~200 cases per 100 000.

31. ETIOLOGY
 The cause of UC remains unclear, although interplay of genetic, microbial, and
immunologic factors clearly exists.
 A limited number of environmental factors have clearly been proven to either modify the
disease or regulate the lifetime risk of developing it.
 These include:
 Tobacco use. Appendectomy.
 Oral contraceptive pills. Antibiotic use.

33. SYMPTOMS
 Rectal bleeding and tenesmus are universally
present.
 Diarrhea and abdominal pain are more frequent
with proximal colon involvement.
 Nausea and weight loss in severe cases.
 Severe abdominal pain or fever suggests fulminant
colitis or toxic megacolon.

34. CLINICAL FEATURES
 Age: Ulcerative colitis presents at a young age, often in
adolescence. The median age of diagnosis is the fourth decade of
life.
 Onset: acute or subacute.
 Course: - Most patients experience intermittent exacerbations with
nearly complete remissions between attacks.
 About 5-10% of patients have one attack without subsequent
tsymptoms for decades

35. SIGN
 Pallor may be evident.
 Mild abdominal tenderness most localized in the hypogastrium or left lower quadrant.
 PR examination may disclose visible red blood.
 Signs of malnutrition.
 Severe tenderness, fever, or tachycardia suggests fulminant disease.

37. TYPES OF UC
 Ulcerative proctitis:limited nited to the rectum, diarrhea, bloody stool, pain in the rectal
area, and a sense of urgency to empty the bowel.
 Proctosigmoiditis: rectum and the sigmoid colon.diarrhea, bloody stool, cramps and pain
in the rectal area, and moderate pain on the left side of the abdomen
 Left-sided colitis: Left-sided colitis affects the entire left side of the colon, from the rectum
to splenic flexure. Diarrhea, bleeding, weight loss, loss of appetite, and sometimes severe
pain on the left side of abdomen.
 Pancolitis: If the entire colon is affected, the term pancolitis is used (“pan” meaning total).

39. COMPLICATIONS
 Severe bleeding
 A hole in the colon (perforated colon)
 Severe dehydration
 Bone loss (osteoporosis)
 Inflammation of the skin, joints and eyes
 An increased risk of colon cancer
 A rapidly swelling colon (toxic megacolon)
 Increased risk of blood clots in veins and arteries

40. WHEN DO WE SUSPECT INFLAMMATORY BOWEL DISEASE
Chronic diarrhoea
Rectal bleeding
Unexplained weight loss, joint problems & skin problems
Family history
Children with family history who exhibit any of the above symptoms

41. DIFFERENTIAL DIAGNOSIS

42. DIAGNOSIS
 Physical Examination
 Endoscopy
 Biopsy
 Radiology
 Blood Test

43.  PHYSICAL EXAMINATION
The main features to look for are: oral aphtosis, abdominal tenderness and masses, anal tags, fissure and
fistulae, nutritional deficiency.
An important feature in children retardation. Is growth
ENDOSCOPY/ COLONOSCOPY/SIGMOIDOSCOPY
Colonoscopy helps to determine the pattern and severity of colonic and terminal ileum inflammation and
allows biopsies to be obtained.
Endoscopic features are aphtous ulcers, deeper ulceration, postinflammatory polyps (which indicate previous
severe inflammation), but always accompanied by intervening normal mucosa, which is an important
differential feature between CD and UC.

44.  Biopsy
 Rectal and colonic biopsies should be examined to find the nature of the inflammation (ulcerative colitis
versus CD), collagenous colitis or microscopic inflammation if macroscopic appearance is normal, and
infection.

45.  Barium enema
 Barium inserted into rectum
 Fluoroscopy used to image bowel
 Rarely used due to colonoscopy
 Useful for identifying colonic strictures or colonic fistulae
Radiology

46.  Blood test
 Anemia may be present due to blood loss (iron deficiency), chronic
inflammation or B12 malabsorption (macrocytic)
 .Hypoalbuminemia suggests severe disease with denutrition.The best
markers of inflammation severity are elevation of the C-reactive protein
and platelet count.
 Anti-saccharomyces cerevisiae antibodies (ASCA) are positive in 50-
60% of CD patients while anti-neutrophil polynuclear antibodies
(ANCA) are positive in 50-60% of UC patients.

47. NON PHARMACOLOGICAL TREATMENT
 To avoid smoking cessation
 To reduce alcohol consumption
 To avoid the use of NSAIDs
 To avoid spicy and fried/oily food
 To take fiber rich diet as tolerated that include tender cooked vegetables, canned or cooked fruits,
and starches like cooked cereals and whole wheat noodles and tortillas.
 To incorporate more omega-3 fatty acids in the diet. These fats may have an anti-inflammatory
effect. They are found most probably in fish.

49. SURGERY FOR ULCERATIVE COLITIS
 Proctocolectomy (removing the colon and rectum) with ileostomy: If UC is severe, surgery may be
required to remove the entire colon and rectum, plus bring the ileum (end of the small intestine) through
a stoma (opening) in the abdominal wall to allow drainage of intestinal waste out of the body. The
second part of the procedure is called ileostomy. After the procedure, an external bag must be worn over
the opening to collect waste.
 Restorative proctocolectomy, also known as ileoanal pouch anal anastomosis (IPAA): It involves
removing the colon and rectum, but the patient can continue to pass stool through the anus in place of
an ileostomy, the ileum is fashioned into a pouch and pulled down and connected to the anus.

50. PHARMACOLOGICAL TREATMENT
 The major types of drug therapy used in IBD include
 Aminosalicylates
 Corticosteroids
 Immunosuppressive agents
 TNF-Tumor Necrosis Factor Inhibitor
 Antimicrobials

51. AMINOSALICYLATES/5-ASA
These agents have anti-inflammatory effects. They are used to maintain remission and to
induce remission of mild flares of disease.
Egs., Sulfasalazine, Mesalamine
Sulfasalazine and mesalamine are used to treat mild to moderate disease and to maintain
remission induced by corticosteroids.
Sulfasalazine is useful for ileocolonic and colonic disease.

52. CORTICOSTEROIDS
 Corticosteroids (1 mg/kg/day) are effective in decreasing disease activity and inducing
remission in most patients.
 Oral or parenteral corticosteroids are indicated for the treatment of ambulatory patients with
moderate to severe colitis whose symptoms cannot be controlled by aminosalicylates.
 The adverse effects include cosmetic effects, suppression of linear growth in children and
osteopenia.
 Egs., Prednisolone, Budenoside

53.  Ambulatory patients are usually treated with prednisolone.
 Budesonide, a potent steroid that undergoes extensive first- pass hepatic metabolism, is useful, but
approximately one- third of patients experience adverse effects related to budesonide use.

54. IMMUNE SUPRESSIVE AGENTS
If it is impossible to taper corticosteroids or frequent relapses occur, immunomodulating therapy should be
considered. However, the use of immunomodulators is not approved by the national health insurance
scheme.
Azathioprine and 6-mercaptopurine are used due to their steroid – sparing or steroid reducing effects, since
approximately 50% of patients experience adverse effects from corticosteroids.
Due to delayed onset of action, these agents are not used to treat acute colitis.
Cyclosporine and tacrolimus have been used to treat acute steroid-refractory UC when surgery seemed
inevitable.

56. TNF INHIBITORS
Increased production of inflammatory cytokines, especially tumor necrosis factor alpha
(TNF-α), has been described in both normal and inflamed mucosa.
These agents prevent the endogenous cytokine from binding to the cell surface
receptor and exerting biological activity. These agents adversely affect normal immune
responses.
The inhibitors are:
Thalidomide
Infliximab
Golimumab
Adalimumab

57. ANTI MICROBIAL AGENTS
 Metronidazole and ciprofloxacin are useful in the treatment of mild to moderate disease, particularly
in patients with perianal disease and infectious complications.
 Sensory neuropathy, which may be seen with long-term metronidazole use, usually resolves
completely or improves after discontinuation of the drug.

58. AYURVEDIC MANAGEMENT
 Deepaniya drugs: Pippali, Pippali-moola, Chavya, Chitrak, Shringavera, Amlavetas, Marich, Ajmoda,
Bhallatak asthi, and Hingu niryas.
 Ama pachaka drugs:
 Paneeya – Shunti,, Panchakola, Jeeraka + Dhanyaka
 Kashaya – Amrutottara kashaya, Drakshadi kashaya
 Churna-Taleesadi churna ,Hingvashtaka churna, Ajamodadi churna,
 Vati –Agnitundi vati, Chitrakaadi vati, Sanjeevini vati, Laghumalini vasanta
 Arishta –Amrutaarishta – the best
 Sthambaka drugs:
 Tulasi beeja,Mishri,kutaja,synoka,lodhradi gana etc.

59. IBD CONCLUSION
 It is a chronic disorders.
 Need to exclude other possibilities
 Need to differentiate between the two
 Need long term management with primary goal to induce then maintain remission and
prevent complications of both the disease and drugs.