ULCERATIVE COLITIS.pptx in both ayurveda and modern

this presentation is about ulcerative colitis

1. ULCERATIVE COLITIS Dr Amritanshu Saroch Deptt. Of Rog Nidan

2. INFLAMMATORY BOWEL DISEASE Inflammatory Bowel Disease (IBD) is a group of chronic, relapsing inflammatory conditions that affect the gastrointestinal tract. The two main types of IBD are: 1. Ulcerative Colitis (UC) – Inflammation is limited to the colon and rectum, and involves only the mucosal and sub mucosal layer in a continuous pattern. 2. Crohn’s Disease (CD) – Can affect any part of the GI tract from mouth to anus, with patchy (skip) lesions and transmural (full-thickness) inflammation.

3. ✴ Key Features of IBD Autoimmune or immune-mediated nature Chronic and relapsing-remitting course Symptoms include abdominal pain, diarrhea, blood or mucus in stool, weight loss, and fatigue Associated with extraintestinal manifestations (joints, skin, eyes)

4. ULCERATIVE COLITIS DEFINITION Ulcerative Colitis (UC) is a chronic, idiopathic inflammatory bowel disease (IBD) characterized by continuous mucosal inflammation of the colon and rectum, starting from the rectum and extending proximally in a continuous pattern. Unlike Crohn’s disease, UC affects only the mucosa and submucosa, and is limited to the colon (large intestine).

5. Characterized by - Diffuse, continuous inflammation( starting from the rectum) Superficial mucosal ulceration Relapsing and remitting course

6. Epidemiology Prevalence: More common in Western countries but rising in developing nations (due to changes in diet, lifestyle, hygiene hypothesis). Age of onset: Bimodal – Peak at 15–30 years and second smaller peak at 50–70 years. Sex: Affects both males and females equally or with slight male predominance. Ethnicity: More common among people of Ashkenazi Jewish descent.

7. Anatomy of the Colon Parts : Cecum → Ascending colon → Transverse colon → Descending colon → Sigmoid colon → Rectum. Layers: Mucosa: Innermost, contains crypts of Lieberkühn, goblet cells (mucus secretion). Submucosa: Contains blood vessels, lymphatics, and immune cells. Muscularis propria: Circular & longitudinal muscles (peristalsis). Serosa (outermost).

8. Normal Physiology of Colon ( with UC relevance ) Water Absorption – Absorbs water/electrolytes → forms stool – In UC: ↓ absorption → diarrhea Mucus Secretion – Goblet cells secrete mucus → protects lining – In UC: goblet cells damaged → ulcers, bleeding Gut Flora Balance – Normal flora aids digestion & immune balance – In UC: dysbiosis → immune activation

9. Microbial Fermentation The colon hosts 100 trillion microbes, forming the gut microbiota. Functions of colonic microbes: Fermentation of undigested carbohydrates → Short-chain fatty acids (SCFAs) like acetate, propionate, butyrate. SCFAs are absorbed and used as energy (especially butyrate for colonocytes).Produce gas: H₂, CO₂, methane. Vitamin synthesis: Especially vitamin K, biotin, some B-complex vitamins.

10. Immune Regulation – GALT maintains tolerance to normal flora – In UC: immune overreaction → chronic inflammation Slow Motility – Allows time for absorption – In UC: inflammation disturbs motility → urgency, cramps

11. Normal Gut Immunity Gut has a mucosal barrier (epithelial cells + mucus + antimicrobial peptides). Gut-associated lymphoid tissue (GALT) maintains immune tolerance to food and commensals. Regulatory T-cells (Tregs) prevent overreaction to harmless antigens. IgA and macrophages help contain bacteria without inflammation.

12. In UC Barrier dysfunction allows microbes to enter mucosa. Dysbiosis (altered gut flora) triggers abnormal immune activation. Excessive activation of Th2-type immune response, especially IL-5, IL-13. Neutrophil infiltration → crypt abscesses. Chronic inflammation damages mucosa, causes ulcers, bleeding.

13. Etiology of UC Genetic Factors UC has a familial predisposition . Risk increases 10-15% if a first-degree relative is affected. Multiple genes are associated, such as: HLA alleles (especially HLA-DRB1*0103) Genes involved in immune regulation and epithelial barrier function (e.g., ECM1, IL23R, MUC2 etc.) Genetic overlap exists with Crohn’s disease but certain loci are unique to UC.

14. Immune Dysregulation UC involves abnormal immune response to colonic flora. Normally, the mucosal immune system tolerates gut microbes. In UC: Regulatory T cell dysfunction → loss of tolerance. Th2-mediated inflammation dominates (↑ IL-5, IL-13). Persistent activation leads to chronic mucosal inflammation and ulceration . Autoimmune component suspected (presence of pANCA antibodies in many UC patients).

15. Microbial Factors (Dysbiosis) Altered gut microbiota composition (" dysbiosis "): ↓ beneficial bacteria (e.g., Firmicutes, Faecalibacterium prausnitzii ) ↑ pathobionts (potentially harmful bacteria) Bacterial products may trigger immune response . Antibiotics, infections, or poor gut hygiene may initiate dysbiosis.

16. Environmental Triggers Factor Role 🧴 NSAIDs May increase intestinal permeability 🚬 Smoking Protective in UC (unlike Crohn's) 🧼 Hygiene Hypothesis Less microbial exposure → immune overreacts 💊 Antibiotics Disrupt microbiota 🍔 Diet High fat, low fiber may worsen gut inflammation 💉 Infections Some enteric infections may trigger first onset

17. Psychological Stress Stress does not cause UC , but it can worsen flares . Alters gut motility and immune function via brain-gut axis .

18. Epithelial Barrier Dysfunction Goblet Cell Damage: ↓ MUC2 expression → ↓ mucus production → thinner mucus layer IL-13 & TNF- α induce goblet cell apoptosis Tight Junction Breakdown : ↓ Occludin, Claudin-1, and ZO-1 ↑ Claudin-2 (forms leaky pores)=Barrier becomes permeable to antigens, microbes, toxins Result: “Leaky gut” → allows entry of luminal contents → stimulates inflammation.

19. Pathology The inflammation is limited to the mucosal layer of the colon. The rectum is always involved , with inflammation extending proximally in a confluent fashion. Dysregulation of the intestinal mucosa Increased permeability to gut bacteria Immune mediated attack of GIT.

20. PATHOPHYSIOLOGY Initiating Factors (Trigger Phase) In genetically susceptible individuals, certain environmental factors (infections, NSAIDs, diet, stress) and gut microbial imbalance (dysbiosis) act as triggers. These damage the intestinal epithelial barrier, leading to:↑ Mucosal permeability↑ Exposure of immune cells to luminal antigens (bacteria, food particles, toxins)

21. Breakdown of Epithelial Barrier The intestinal epithelial barrier normally prevents harmful substances from entering the lamina propria. In UC: Tight junction proteins (claudins, occludin , ZO-1) are disrupted Mucus layer (secreted by goblet cells) becomes thin and defective 🔁 This allows: Bacterial invasion Activation of immune system beneath the epithelium

22. Abnormal Immune Activation Once the mucosal barrier is breached: Dendritic cells and macrophages present antigens to T-helper cells. Instead of a controlled response, there's an exaggerated Th2-like immune reaction In UC :↑ IL-5 and IL-13 (cytokines associated with Th2-type immunity)↑ TNF- α, IL-1, IL-6 also contribute Neutrophils are recruited → form crypt abscesses> 📌 (In contrast, Crohn’s disease is more Th1/Th17-driven.)

23. Tissue Injury and Inflammation Activated immune cells release pro-inflammatory cytokines and reactive oxygen species (ROS) → cause: Mucosal ulceration Edema and hemorrhage Crypt architectural distortion Loss of goblet cells Formation of pseudopolyps (islands of regenerating mucosa)

24. Chronicity and Flare-Ups The inflammatory process is relapsing-remitting: Periods of flare (acute inflammation) Periods of remission (partial healing) Chronic inflammation leads to: Fibrosis (scarring)Muscle hypertrophy Risk of colorectal cancer (due to DNA damage from inflammation)

25. Extent and Pattern of Inflammation Characteristic Ulcerative Colitis Distribution Starts at rectum → spreads proximally in continuous pattern Layers involved Only mucosa and submucosa Depth of ulcers Superficial (not transmural) Skip lesions ❌ Absent

26. Trigger (genetic/enviro/microbial) → epithelial injury 2. Barrier breakdown → antigen exposure 3. Innate activation → cytokine storm (TNF, IL-1 β) 4. Th2/Th17 response → epithelial apoptosis, ulceration 5. Neutrophils invade → crypt abscesses 6. Cycle continues, leading to: Ulcers Bleeding Pseudopolyps Chronic mucosal damage

27. Summery of pathophysiology [Genetic Risk + Environment] ↓ [Dysbiosis + Barrier Breakdown] ↓ [Innate Immunity Activated (TLRs, cytokines)] ↓ [Th2-dominant Adaptive Immune Response] ↓ [Chronic Inflammation of Mucosa] ↓ [Ulcers, Bleeding, Crypt Abscess, Pseudopolyps ]

28. Classification Type Involvement Description E1: Ulcerative proctitis Rectum only Inflammation limited to rectum (≤15 cm from anal verge) E2: Left-sided colitis (distal UC) Rectum + sigmoid + descending colon (up to splenic flexure) Does not go beyond the splenic flexure E3: Extensive colitis (pancolitis) Extends proximal to splenic flexure May involve the entire colon

29. The disease is classified by the extent of proximal involved into Proctitis : Involvement limited to the rectum. Proctosigmoiditis : Involvement of the rectosigmoid. Left-sided colitis : Involvement of the descending colon up to the splenic flexure. Extensive colitis : Involvement extending proximal to the splenic flexure. Pancolitis (Universal colitis) : Involvement of the entire colon. It is may be associated with inflammation of the terminal ileum (backwash ileitis).

30. Gross Description Ulcerative inflammatory disease, usually limited to colon, disease from rectum proximally (pancolitis in some cases). Usually no deep fissuring ulceration, no strictures or fistulas, no sinus tract formation, no small intestinal involvement, no serositis, no bowel wall thickening, no fat wrapping. Early : mucosa is haemorrhagic, granular, friable, changes usually diffuse (similar intensity throughout). Late : extensive ulceration along bowel axis, have pseudopolyp (isolated islands of regenerating mucosa) and flat mucosa, usually normal wall thickness and normal serosa. severe cases may have megacolon or fibrotic, narrow or shortened colon

31. 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.

32. Signs 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

33. MONTREAL Classification Ulcerative Proctitis (E1) – Limited to rectum Left sided ulcerative colitis (E2)- limited to colon distal to splenic flexure. Extensive Ulcerative colitis (E3)- Extends proximal to splenic flexure.

34. Severity of the disease Mild disease: Stool frequency is less than 4 times/day with or without blood. No systemic signs of toxicity. Normal ESR. Moderate disease: Stool frequency is more than 4 times/day. Minimal signs of toxicity. Moderate abdominal pain.

35. Severe disease : Stool frequency > 6 times/day with blood +++. Fever > 37.5°C. Tachycardia > 90 per minute. ESR > 30 mm per hour. Anaemia < 10 g/dL haemoglobin. Albumin < 30 g/L.

36. Comparison between UC and CD Ulcerative colitis Crohn’s Disease ONSET Acute or subacute Insidious EXTENSION Affects only the colon Can affect any part of the GIT from the mouth to the anus RECTAL INVOLVMENT Always Rare DISTRIBUTION OF DISEASE Continuous area of inflammation Patchy areas of inflammation SKIP LESIONS Absent Present COBBLESTONE APPEARANCE Absent Present DEPTH OF IMFLAMMATION Shallow, mucosal May be transmural, deep into tissues

37. UC CD DIARRHEA Bloody Usually not bloody ABDOMINAL MASS Absent May be present FISTULA FORMATION Rare Common BILE DUCT INVOLVEMENT Higher rate of Primary Sclerosing Cholangitis Lower than UC CANCER RISK Higher than CD Lower than UC SMOKING Lower risk for smokers Higher risk for smokers

38. INVESTIGATION A) Laboratory findings : CBC – To rule out Anaemia, Leucocytosis, Thrombocytosis, LFT - Elevated ALP, GGT in PSC. pANCA – Elevated in 70% of pt Hypoalbuminemia – Associated with poor prognosis & severe disease . -loss of protein due to diarrhoea & inflammation -Also called protein enteropathy ( edema of face, feet & hand) Faecal calprotectin level :- Elevated NOTE :- Hypoalbuminemia & elevated CRP suggest a poor prognosis.

39. Patient with Hematochezia (blood in stool) < 1 month > 1 month e.g. Gastroenteritis Perform ileocolonoscopy Perform Esophagogastroduodenoscopy – to rule out CD

40. Toxic Megacolon (life threatening condition)

41. 2. Barium Enema It can be useful for detecting active ulcerative disease, polyps, or masses. -The colon typically appears granular and shortened.

42. Normal Colon On Barium Enema

43. 3. CT scan Typically reveals colonic wall thickening.

44. The wall of colon is hyper enhancing and slightly irregular in contour

45. C) Colonoscopy ➤ Allows assessment of the extent and severity of the disease. Multiple biopsies should be taken. ➤It helps to exclude alternative diagnoses, such as infectious or ischemic colitis. Findings include: Mucosal erythema, edema, and granularity and loss of normal vasculature. ➤Hemorrhages, ulcerations and a purulent exudate occurs with severe disease. ➤Pseudo polyps in patients with long-standing disease.

46. Colonic Pseudopolyp

47. Normal UC

48. Biopsy Findings Crypt abscess Neutrophil infiltration in crypts Mucosal atrophy

49. General Pattern Continuous, diffuse mucosal inflammation (always starting from rectum, extending proximally) Disease limited to mucosa & submucosa (unlike Crohn’s, which is transmural) Crypt architecture distortion, crypt abscesses, goblet cell depletion

50. Microscopic Features 1. Active Phase (Acute UC flare) Cryptitis → neutrophils infiltrating crypt epithelium Crypt abscesses → neutrophil accumulation inside glandular crypts Mucosal ulceration → superficial, not deep Granulation tissue at ulcer bases Diffuse mucosal infiltrate → neutrophils, lymphocytes, plasma cells

51. Chronic Phase Crypt architectural distortion Crypt branching, shortening, irregular arrangement Crypt atrophy → dropout of glands Basal plasmacytosis → plasma cells infiltrating base of mucosa (very characteristic) Goblet cell depletion → loss of mucin-producing cells Paneth cell metaplasia in left colon (normally Paneth cells present only in right colon)

52. Other Changes Diffuse lamina propria inflammation Mucosal edema Pseudopolyps → regenerative mucosa between ulcerated areas

53. Normal Colon Microscopy

54. Microscopic findings

55. Feature Description Stage Crypt distortion Branched, shortened, irregular crypts Chronic Cryptitis Neutrophils in crypt epithelium Active Crypt abscess Neutrophils in crypt lumen Active, classic Lamina propria inflammation Lymphocytes, plasma cells Chronic Goblet cell depletion Reduced mucin Chronic/active Granulomas Absent Helps differentiate from Crohn’s Basal plasmacytosis Plasma cells at base Early chronicity marker

56. 1- Severe haemorrhage. 2- Toxic megacolon. 3- Colorectal cancer (CRC). 4- Extraintestinal complications. 5- Pouchitis.

57. Severe haemorrhage.

58. Toxic Megacolon. Toxic megacolon ( transverse colon with a diameter of more than 5.0 cm to 6.0 cm with loss of haustration)

59. Colorectal Cancer (CRC) Risk Factors:- Duration, severity and extent of the disease. Positive family history. Concomitant Primary Sclerosing Cholangitis. CRC appears after 8-10 years of disease. So, screening colonoscopy is recommended with surveillance examination every 1-2 years with 4 quadrant biopsies every 10 cm throughout the colon.

60. Extraintestinal complications System or site Manifestation Hepatobiliary Primary sclerosing cholangitis Cholangiocarcinoma Gallstones Dermatological Erythema nodosum Pyoderma gangrenosum Sweet syndrome Oral Aphthous ulceration

61. System or site Manifestation Ocular Episcleritis Uveitis/iritis Musculoskeletal Enteropathic arthropathy Sacroiliitis Ankylosing spondylosis Osteopenia/osteoporosis Haematological Thromboembolic disease

62. Aphthous ulceration

63. Pouchitis Occurs in patients who have undergone an IPAA (ileal pouch–anal anastomosis). The etiology is unknown bacterial flora may play a role. Symptoms include diarrhoea, bleeding, urgency, incontinence, fever, and general malaise.

64. UC with backwash ileitis

65. Feature Ulcerative Colitis (UC) Crohn’s Disease (CD) Location Limited to colon and rectum (always involves rectum, extends proximally) Can involve any part of GIT (mouth → anus), most common = terminal ileum + colon Pattern of Involvement Continuous from rectum upwards Skip lesions (discontinuous, “cobblestone” mucosa) Depth of Inflammation Mucosa & submucosa only Transmural (full thickness) Gross Appearance - Loss of haustra → “lead pipe colon” on barium study - Pseudopolyps - Cobblestone mucosa - Strictures, fistulas, creeping fat Histopathology - Crypt abscesses (PMNs in crypts) - No granulomas - Non-caseating granulomas (pathognomonic but not always present) Bleeding Common (rectal bleeding, hematochezia ) Less common (usually occult bleeding)

66. Feature Ulcerative Colitis (UC) Crohn’s Disease (CD) Diarrhea Bloody diarrhea Non-bloody diarrhea (steatorrhea if ileum affected) Abdominal Pain LLQ pain RLQ pain (ileocecal disease) Perianal Disease Rare Common (fistula, fissure, abscess, skin tags) Strictures & Fistulas Rare Common (due to transmural inflammation) Toxic Megacolon Common complication Rare Cancer Risk High risk of colorectal carcinoma (risk ↑ with extent and duration of colitis) Risk ↑ with colonic involvement but less than UC

67. Feature Ulcerative Colitis (UC) Crohn’s Disease (CD) Smoking Protective (smoking lowers risk of UC) Risk factor (smoking worsens Crohn’s) Extraintestinal Manifestations Both can have: - Arthritis, Uveitis, Erythema Nodosum, Pyoderma gangrenosum Same spectrum, but more frequent in Crohn’s Radiology (Barium enema / Imaging) Lead pipe colon (loss of haustra) String sign of Kantor (narrowed terminal ileum) Treatment response Better response to 5-ASA (mesalamine) Less responsive to 5-ASA, often need immunosuppressants/biologics Surgery Curative (colectomy) Not curative (disease recurs in other parts of GIT)

68. Differential Diagnosis 1- Crohn colitis. 2- Infectious colitis. 3- Ischemic colitis. Acute, painful, self limited, localized, after meals. 4- Radiation colitis. Can cause proctitis, colitis or enteritis. 5- Diversion colitis. 6- Segmental colitis. Idiopathic focal colitis surrounding diverticulae . 7- GIT malignancies. Rectal bleeding, altered bowel habits, pain & anaemia. 8- Irritable bowel syndrome (IBS). Abdominal pain & diarrhea

69. Protective factors 1). Appendectomy (immune modulating effect) 2). Smoking (Nicotine may keep you getting UC including lowering the level of cytokines ,proteins that triggers inflammation) (NOTE :- SMOKING CAUSES CANCER)

70. Treatment of Ulcerative Colitis

71. Goals of Therapy for UC Inducing remission Maintaining remission Restoring and maintaining nutrition Maintaining patient’s quality of life Surgical intervention

72. A) Medical Treatment 1) 5- Aminosalicytes (5 ASAs) Used in mild to moderate disease Effective in induction and maintenance of remission. also, they may decrease the risk for CRC. e.g. – Mesalamine 250-500 mg TID , sulfasalazine (2-4 gm daily then 0.5 g 6 hourly).

73. Side Effects : are rare Interstitial nephritis. Pulmonitis. Pericarditis. Rash Pancreatitis. Worsening of colitis.

74. 2) Corticosteroids Used in acute treatment of moderate to severe colitis. About one third of patient with ulcerative colitis require steroids. Only about 50% of patients will achieve a remission and about 30% will have a response. They should be tapered off once a satisfactory maintenance medication has been started

75. Preparations - Prednisone 40-60 mg/day Methylprednisolone 40-60 mg/day Hydrocortisone 200-300 mg/day Rectally administered steroid enemas provide therapy for flares of distal ulcerative colitis without the systemic side effects.

76. 3) Thiopurines (Azathioprine & 6-mercaptopurine) Effective for the maintenance of remission but to their slow onset of action, they are not appropriate as solo induction agents for patients with severe disease. Dose :- Azathioprine 2 – 2.5 mg/kg/day 6-mercaptopurine 1 – 1.5 mg/kg/day Side effect- Leucopenia - Pancreatitis Hepatitis - Nausea

77. 4) Infliximab (Remicade 100 mg vial) Its an IgG monoclonal antibody against TNF. Its effective for the induction and maintenance of remission. Its offer a less toxic alternative to cyclosporine for patients with severe disease. Also it can be used in patients who are steroid refractory or steroid dependent and for patients who are failing to respond to azathioprine & 6 mercaptopurine. Dose:- -Induction of remission : 5 mg/kg IV at week 0,2,6. -Maintenance : 5 mg/kg IV every 8 weeks

78. 5) Cyclosporine Its used as last line medical therapy to treat hospitalized patients with severe ulcerative colitis. Dose: 2-4 mg/kg/day given as a continuous infusion Side effects: Nephrotoxicity. Opportunistic infection. Seizures.

79. Severity / Situation First-Line Treatment Dose Alternative / Next Step Maintenance Mild – Ulcerative Proctitis (rectum only) Topical 5-ASA (Mesalamine suppository) 1 g suppository once daily Rectal corticosteroid suppository/foam (Hydrocortisone 100 mg/day) Continue mesalamine suppository 500 mg–1 g OD Mild – Left-sided Colitis (up to splenic flexure) Oral 5-ASA (Mesalamine / Sulfasalazine) + Rectal 5-ASA enema - Mesalamine 2–4 g/day PO - Sulfasalazine 2–6 g/day PO - Rectal mesalamine enema 1–4 g HS Rectal steroid enema: Hydrocortisone 100 mg HS Oral ± rectal 5-ASA 1.6–2.4 g/day PO Mild – Extensive Colitis (beyond splenic flexure) Oral 5-ASA 2–4 g/day PO Add rectal mesalamine 1–4 g/day if distal symptoms Oral 5-ASA 1.6–2.4 g/day

80. Moderate UC Oral corticosteroids (Prednisolone) + Oral 5-ASA Prednisolone 40–60 mg/day PO (taper over 8–12 wks ) Mesalamine 2–4 g/day PO Budesonide MMX 9 mg/day PO as alternative - Oral 5-ASA (1.6–2.4 g/day) - Azathioprine 1.5–2.5 mg/kg/day PO - 6-MP 1–1.5 mg/kg/day PO if steroid-dependent Severe UC (hospitalized) IV corticosteroids (Hydrocortisone / Methylprednisolone) - Hydrocortisone 100 mg IV q8h - Methylprednisolone 60 mg IV daily If no response in 3–5 days → Rescue: ▪ Cyclosporine 2–4 mg/kg/day IV ▪ Tacrolimus 0.1–0.15 mg/kg/day PO ▪ Infliximab 5 mg/kg IV at 0, 2, 6 wks If remission: Continue infliximab or switch to azathioprine/6-MP Fulminant UC / Toxic Megacolon NPO, IV fluids, IV steroids, broad-spectrum antibiotics - Methylprednisolone 60 mg IV/day - Hydrocortisone 100 mg IV q8h If no response → Infliximab 5 mg/kg IV or Cyclosporine 2–4 mg/kg/day IV Surgery (subtotal colectomy with ileostomy) if not responding

81. Maintenance of Remission Oral ± rectal 5-ASA - Oral mesalamine 1.6–2.4 g/day - Rectal mesalamine suppository 500 mg–1 g daily or 3x/week Immunomodulators if steroid-dependent: ▪ Azathioprine 1.5–2.5 mg/kg/day PO ▪ 6-MP 1–1.5 mg/kg/day PO Biologics: ▪ Infliximab 5 mg/kg IV q8wks ▪ Adalimumab 160 mg SC day 1, 80 mg day 15, then 40 mg q2wks ▪ Vedolizumab 300 mg IV at 0, 2, 6 wks, then q8wks Surgery Indications — — Massive hemorrhage , perforation, toxic megacolon, refractory UC, cancer/dysplasia Curative surgery: Proctocolectomy with ileal pouch–anal anastomosis (IPAA)

82. Surgical options: Proctocolectomy and creation of IPAA. Proctocolectomy with end ileostomy. Proctocolectomy with continent ileostomy. Laparoscopic approach

83. Total Proctocolectomy with ileal Pouch-Anal Anastomosis : -Gold standard -Requires good anorectal function and sphincter tone -Generally performed on patients young than 65.

84. Complications of UC Surgery Mortality (<0.5%) 3-10 times stools/ 24 hrs so Bowel pattern not normal Impotence (1.5%) Pouchitis (10-60%) Small bowel obstruction (20%) Pouch-vaginal fistula (4%)

85. IBD conclusion Its is a chronic disorders Need to exclude other possibilities Need to differentiate between the two UC and CD Need long term management with primary goal to induce then maintain remission and prevent complications of both the disease and drugs

86. 2. Ghrita preperation a) Shatavari Ghrita : By taking the paste of Shatavari (Asparagus racemosus ) or ghee cooked with the same with milk and keeping on milk diet overcomes the bloody diarrhoea.It is useful in patient of Pittaatisara , Rakta- atisar , Grahani . Shatavari have Sheeta Veerya and Vaata Pitta Shamaka properties. It is Balya, Medhya and Rasayana . It has been suggested to heal the ulcers by potentiating defensive factors. b) Dravyadi Ghrit (Ghee prepared form Paste of Daruhaldi bark, Indrajau , Pipar , Sunthi , Munaka and Kutki ) with Peya and Manda is beneficial in the treatment of Pittatisar and Raktatisar . Due to its Vatanulomana and Agni dipana properties this Ghrita is beneficial in Raktatisar patients. c) Nyogradhi ghrita : Administration of Nyugradhi Ghrit (Ghee prepared from Bargad , Gular and Pipal) with honey and sugar is useful in the treatment of Raktatisar .

87. Kwatha (decoction) a) Cold decoction (Shit Kasaya ) of Shalmali vrinta with Yastimadu and honey cured Pittatisar and Raktatisar .[43] b) Administration of Bilvo Majja followed by honey is useful in Raktatisara patient.[44] c) Kutajadi kasaya : Bark of Kutaj, Bark of Dadim Fruit, Root of Nagarmotha , Flower of Dhataki , Bilvo Fruit majja , Sughandhabala , Red Chandan and Patha decoction with honey is useful in all types of diarrhoea especially in bloody diarrhoea.[45] d) Dadimadi kwath : Decoction of Dadim Fruit Bark and Kutaj Bark is useful in chronic bloody diarrhoea.[46]

88. Rasa Preperation : Vijaya Parpati , Panchamrit prapati It is useful in patients of Raktatisara (ulcerative colitis) by, enhancing the normal functioning of Pakwashaya due to its Rasayana property. As described in Bhaishajya Ratnavali in the chapter of Sangrahani Rogadhikar , Parpati acts on digestive system as Doshaghna , Jantughna and Balya. It settles the irritation and inflammation of colon mucosa. Parpati preperation Karpura rasa : Suddha Hingul , Suddha Aphim . Nagarmotha , Indrayav , Jayaphal , and Karpur take all the ingredients in equal amount and make 250mg Vati . Took this medicine two tablet twice a day. This medicine has a strong Stambhaka property which is useful in Jwaratisar , Raktatisar , Grahani Vikar.

89. Local application In case the anus gets inflamed by pitta due to frequent motions, one should sprinkle it with very cold decoction of Patola or decoction of Yestmadhu or decoction of Panchavalkala (Vata, Peepal, Udambar , Plaksha and Parisha). Often those having chronic diarrhoea suffer from weakness of anus, hence one should apply unctuous substance to their anus frequently.[52] Jatyadi Ghrita or Changeri Ghrita can also be used locally

90. Single Herbs: Kutaja ( Holarrhena antidysenterica ) – Grahī , Saṅgrahī Musta (Cyperus rotundus) – Dīpana , Pācana Bilva (Aegle marmelos ) – Grahī Udumbara , Lodhra , Nagakesara – Raktastambhaka Yashtimadhu – Vranaropaka , Pitta- shāmaka Arjuna – Raktaprasādaka , Stambhana