•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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