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IRRITABLE BOWEL SYNDROME presentation.pptx
- 1. IRRITABLE BOWEL SYNDROME Dr. AliKhurshid Bhalli PGR Gastroenterology
- 2. What is IBS? •IBS is a disorder of gut-brain interaction • Characterized by: • Chronic or recurrent abdominal pain (usually lower abdomen) • Altered bowel habits: diarrhea, constipation, or both • Associated features: bloating, distention, disordered defecation • Involves abnormalities in: • GI motility • Visceral sensation • Intestinal microbiome • Immune activation
- 3. Rome IV DiagnosticCriteria • Recurrent abdominal pain at least 1 day/week in the last 3 months • Associated with two or more: • Related to defecation • Change in stool frequency • Change in stool form • Criteria must be met for 3 months with symptom onset at least 6 months prior
- 4. How Common isIBS? • Prevalence (Rome IV): 1.3% to 5.9%, average 4.1% • More common in individuals <50 years • Can begin in childhood • Higher prevalence in females (2:1 overall) • IBS-C: higher in females • IBS-D: ~equal in males and females • Females more likely to seek medical care
- 5. Effect of IBSon Quality of Life • Significant impact on Health-Related Quality of Life (HR-QOL) • Lower SF-36 scores across all domains vs general population • HR-QOL comparable or worse than in diabetes or depression • Often underestimated by clinicians
- 6. Economic Burden ofIBS • 25%-50% of IBS sufferers seek medical care • IBS is: • One of the top 10 reasons for primary care visits • The leading reason for gastroenterology consultations • ~2.7 million U.S. healthcare visits per year (2007-2015) • Patients often undergo unnecessary diagnostic and therapeutic procedures • Work productivity loss: ~14 hours/week per patient
- 7. Causes and RiskFactors of IBS • IBS is due to a complex gut-brain axis interaction • Pathogenesis is multifactorial: • Genetics and family history • Early life experiences (abuse, loss) • Psychosocial factors (stress, coping skills) • Gut dysmotility and visceral hypersensitivity • Intestinal microbiota and immune response • Diet and environmental factors
- 8. Intestinal Dysmotility inIBS • IBS patients may have increased or decreased colonic contractions • Motility abnormalities don’t correlate well with symptoms
- 9. Central Pain Processingin IBS • Altered brain activation during rectal distention • Failure to activate pain-inhibiting areas (e.g., perigenual ACC) • Heightened pain perception and unpleasantness • Upregulation of pain signals from gut to brain
- 10. Role of GutMicrobiota in IBS • Reduced microbial diversity in IBS • Increased Klebsiella and enterococci; decreased Lactobacillus, Bifidobacteria • DNA sequencing shows shifts in genera (Coprococcus, Collinsella, Coprobacillus) • IBS-D and IBS-C have distinct microbiomes
- 11. Visceral Hypersensitivity inIBS • Lower pain thresholds to GI distention • Mechanisms: • Altered serotonin and cytokine release • Pain memory (neural sensitization) • Stress-induced sigmoid contractions
- 12. Postinfectious IBS (PI-IBS) •Follows GI infections (e.g., Campylobacter, Salmonella, Shigella, viral, bacterial, protozoal). • Persistent immune and neuroendocrine activation • Risk factors: • Female, <60 years, prolonged diarrhea, no vomiting • Anxiety, stress, somatization • Biomarkers: CdtB and antivinculin antibodies
- 13. Stress and ComorbidConditions • Stress exaggerates GI responses in IBS • IBS often triggered by major life events • Common comorbidities: • Dyspepsia, heartburn, urinary urgency, fatigue, headache • Sleep issues, low back pain, rheumatologic symptoms
- 14. Diagnosis of IBS •Positive diagnosis based on symptoms and exclusion of alarm features • Rome IV criteria: abdominal pain ≥1 day/week in past 3 months with stool changes • Physical exam and basic labs are usually sufficient
- 15. Common IBS Symptoms •Abdominal pain (lower abdomen) • Altered bowel habits (diarrhea, constipation, or both) • Bloating, urgency, incomplete evacuation • Symptoms often more frequent than Rome IV threshold
- 16. Recommended Testing • CBCfor all suspected IBS cases • IBS-D: • Test for celiac disease (serology) • Fecal calprotectin, CRP • IBS-C: • Consider TSH if clinically indicated • Avoid routine colonoscopy if <45 years without alarm features • Consider biopsies if colonoscopy performed (rule out microscopic colitis)
- 17. Alarm Features NeedingFurther Workup • Rectal bleeding • Unintended weight loss • Fever • Nocturnal symptoms • Family history of colon cancer or IBD • Onset after age 50
- 18. Fructose and LactoseIntolerance • Fructose: • Common in sweets and fruits • Malabsorption common but not causal in most IBS • Lactose: • Slightly more common in IBS • Trial of lactose-free diet or hydrogen breath test • Ensure adequate calcium intake (yogurt, supplements)
- 19. Role of SIBOin IBS • SIBO = bacterial overgrowth in the small intestine • More common in IBS patients • Detected via breath tests (glucose or lactulose) • May contribute to bloating and diarrhea
- 21. Role of Foodin IBS •Most patients report food-related symptom flares •Common triggers: milk, wheat, onions, beans, cabbage, caffeine etc •No clear link with IgE-mediated food allergies •Risk of excessive dietary restriction (e.g., ARFID) •Importance of individualized food tracking and elimination trials
- 22. FODMAP Overview • FODMAPs= Fermentable Oligo-, Di-, Monosaccharides, and Polyols Examples: • Fructose, Lactose (fruits, honey, milk) • Fructans, Galactans (wheat, onions, legumes) • Polyols (sorbitol, mannitol in sugar-free foods) Effect: Poor absorption → fermentation → bloating & discomfort
- 23. The Low FODMAPDiet •Phases: •Elimination (4–6 weeks): Remove all high FODMAP foods •Reintroduction: Systematic testing of food groups •Personalization: Long-term, less restrictive plan •Effectiveness: ~76% find symptom relief •Caution: Not ideal for patients with eating disorders or low baseline FODMAP intake
- 25. Gluten-Free Diet inIBS • Many report improvement on gluten-free diets • Controlled evidence limited • Key finding: Fructans (not gluten) may be the real triggers • Often overlaps with low FODMAP interventions
- 26. Role of Fiberin IBS •Soluble fiber (e.g., psyllium): Improves global symptoms •Insoluble fiber (e.g., bran): Can worsen bloating, pain •Start slow: Gradual increase to 20–25g/day •Alternatives: Methylcellulose, polycarbophil if psyllium not tolerated
- 27. Cognitive Behavioral Therapy(CBT) • Best-studied psychological therapy for IBS • Combines cognitive restructuring + behavioral techniques • Delivery methods: • In-person sessions (4 –15) • Home-based or app-based CBT (FDA-approved) • Other therapies: Gut-directed hypnotherapy, relaxation training
- 28. Exercise in IBSManagement •Increases gut motility & improves psychological well-being •Study: 12 weeks of moderate exercise → symptom improvement •Suggested regimen: 20–60 min, 3x/week •No major impact on stool form but helps overall symptom burden
- 29. Pharmacologic Management ofIrritable Bowel Syndrome (IBS) •Pharmacologic therapy is symptom-targeted: •Diarrhea (IBS-D) •Constipation (IBS-C) •Abdominal pain
- 30. Treatment of IBS-D(1/3) •Loperamide (Imodium®): •Opioid agonist; reduces stool frequency & urgency by reducing gut motility. •Dose: 2–4 mg/day (max 16 mg/day); taken after bowel movements. •Duration: As needed; chronic use possible. •Cholestyramine (Questran®): •Bile acid sequestrant for bile acid malabsorption. •Dose: 4 g once or twice daily. •Duration: Ongoing in bile acid diarrhea.
- 31. Treatment of IBS-D(2/3) •Eluxadoline (Viberzi®): •µ- and κ-opioid receptor agonist, δ-antagonist; reduces GI motility. •Dose: 100 mg BID with food (lower dose 75 mg if needed). •Duration: Chronic; avoid in post-cholecystectomy, alcoholism(pancreatitis risk, spasm of sphincter of oddi).
- 32. Treatment of IBS-D(3/3) • Alosetron (Lotronex®): • 5-HT3 antagonist; slows colonic transit. • Dose: Start at 0.5 mg BID; titrate to 1 mg BID. • Duration: For severe IBS-D in women; ongoing use. • Side effect: severe constipation, ischemic colitis • Rifaximin (Xifaxan®): • Minimally absorbed antibiotic; alters gut flora. • Dose: 550 mg TID for 14 days; repeat up to 2 courses. • Duration: 2-week course; re-treat if symptoms recur.
- 33. Treatment of IBS-C(1/4) • Polyethylene glycol (Miralax®): • Osmotic laxative; improves stool frequency. • Dose: 17 g daily. • Duration: Long-term use if tolerated. • Lubiprostone (Amitiza®): • Chloride channel activator; increases intestinal secretion. • Dose: 8 mcg BID (IBS-C in women). • Duration: Chronic.
- 34. Treatment of IBS-C(2/4) • Linaclotide (Linzess®): • GC-C agonist; increases fluid and reduces pain. • Dose: 72, 145 or 290 mcg daily. • Duration: Long-term. • Plecanatide (Trulance®): • GC-C agonist. • Dose: 3 mg once daily. • Duration: Chronic use.
- 35. Treatment of IBS-C(3/4) • Tenapanor (Ibsrela®): • NHE3 inhibitor; increases water secretion. • Dose: 50 mg BID before meals. • Duration: Long-term. • Tegaserod (Zelnorm®): • 5-HT4 partial agonist; prokinetic. • Dose: 6 mg BID before meals. • Duration: Ongoing; women <65 yrs.
- 36. Treatment of IBS-C(4/4) • Prucalopride (Motegrity®): • 5-HT4 agonist; increases motility. • Dose: 2 mg once daily. • Duration: Chronic idiopathic constipation; IBS off-label.
- 37. Treatment for PredominantPain • Hyoscyamine (Levsin®), Dicyclomine (Bentyl®): • Anticholinergic; reduce smooth muscle spasm. • Dose: Hyoscyamine 0.125–0.25 mg up to QID; Dicyclomine 20–40 mg QID. • Peppermint Oil (IBgard®): • Calcium channel blocker; antispasmodic. • Dose: 180–225 mg TID.
- 38. • TCAs (Amitriptyline,Desipramine): • Visceral analgesia, slows GI transit. • Dose: 10–50 mg nightly. • SSRIs (Fluoxetine, Paroxetine): • Improve mood; mixed effect on IBS. • Dose: Varies per agent. • Other agents: SNRIs (Duloxetine), Mirtazapine, Buspirone – limited data.
- 39. Probiotics in IBS •Modulate gut microbiota and immune function. • Evidence for efficacy is inconsistent. • 2018 meta-analysis: Some benefit for global symptoms. • Not recommended by current guidelines due to variable data.
- 41.