PathogenesisofIBS-UniversityofKentucky.pptVIP

Elizabeth Mentzer, PA-S Robert D. Hadley, Advisor IBS is a diagnosis of exclusion with a female predominance Affects at least 20% of the American population Classic Symptoms: Chronic abdominal pain or discomfort associated with chaotic bowel motility Heightened visceral sensitivity Constipation dominant IBS, diarrhea dominant IBS or mixed At least 12 weeks or more, with onset of at least 6 months previously of recurrent abdominal pain or discomfort associated with two or more of the following: Improvement with defecation; and/or Onset associated with a change in frequency of stool; and/or Onset associated with a change in form (appearance) of stool Common Treatments Fiber Supplements Antispasmodics Ex. dicyclomine, hyoscyamine Anti-diarrheals Tricyclic Antidepressants Amitryptaline for d-IBS Probiotics Lactobacillus plantarum or the combo. L. plantarum + L. acidophilus or Bifidobacterium Antibiotics New Possibilities Mesalamine derivative (ATB-429) Budesonide Post - Infectious IBS Interstitial Cells of Cajal Serotonin Pathway How do GI –Infections Lead to IBS? Genetics Polymorphisms of gene coding for cytokine production of Interleukin 10 (IL-10) Increased Production of Tumor Necrosis Factor –α (TNF-α) Mast Cell Activation Mast cell release of inflammatory mediators could alter gastrointestinal motility Relationship to IBS and Pain Spacial relationships between mast cells and gastrointestinal nerves Pacemakers of the Gastrointestinal System Play roles in intestinal motor activity, balanced control of gut motility and a functional role in neuronal motor activity Located within close proximity to enteric nerve endings Damaged ICCs (ex., immune reactions or endometriosis) could lead to disruption of musculature electrical activity leading to IBS symptoms Defects in 5-HT signaling could lead to colonic aberrations and sensations typical of IBS and Ulcerative Colitis (UC). A 2004 study by Coates et al., found that: IBS and UC patients all had significan