elizabeth mentzer, pa-s robert d. hadley, advisor
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•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
1. Post - Infectious IBS
2. Interstitial Cells of Cajal
3. 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 significant
reductions in expression of the SERT transcript when compared to control subjects as well as a reduction in the rate limiting enzyme TpH, which is essential for the biosynthesis of 5-HT
Is there a connection between IBS and UC?
5-HT and the relationship to ICCs 5-HT may indirectly regulate proliferation of
ICCs Impaired and/or decreased numbers of ICCs
have been associated with bowel dysfunction A study by Gershon (2005), showed that
decreased expression of SERT (required for the termination of 5-HT) could have negative downstream effects on 5-HT As a result, constipation and diarrhea type
symptoms were seen due to 5-HT desensitization or 5-HT amplification
Decreased SERT expression was also found in biopsies of UC patients -> Possible connection?
It may even be a mild form of UC
So far there have been strong arguments for IBS being an inflammatory response
There is no single definitive answer for the pathogenesis of IBS yet.
IBS is real It is not a psychological problem Stay up-to-date on drug therapies Realize that patients with IBS need a tailored
treatment plan. Exclude other possibilities like celiac disease and
endometriosis. Treat based on a patient’s history
For example: presence or history of enteric infection, do other family members have it etc.
Be sympathetic and understanding as IBS can be life-altering
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