1. Irritable Bowel Syndrome

2. Irritable Bowel Syndrome
Functional bowel disorder characterized by abdominal pain or discomfort and altered bowel habits in the absence of structural abnormalities
Common cause of constipation with alternating bouts of diarrhea
Affects all ages, females diagnosed two to three times more often than males

3. Diagnostic Criteria for IBSa
Recurrent abdominal pain or discomfort b at least 3 days per month in the last 3 months associated with two or more of the following: 1. Improvement with defacation 2. Onset associated with a change in frequency of stool 3. Onset associated with a change in form (appearance) of stool
Criteria fulfilled for the last 3 months w/ symptom onset at least 6 months prior to diagnosis.
Discomfort means an uncomfortable sensation not described as pain. In pathophysiology research and clinical trials, a pain/ discomfort frequency of at least 2 days a week during screening evaluation is required for subject eligibility
Fauci et.al. Harrison’s principles of Internal Medicine th edition. McGraw-Hill USA

4. Rome II Criteria Used mainly in the context of research
Rome II criteria characterizes IBS as:
At least 12 weeks (which need not be consecutive), in the preceding 12 months, of abdominal discomfort or pain with two of the following three features:
(1) Relief by defacation
(2) Onset associated with a change in frequency of stool
(3) Onset associated with a change in stool appearance.
National Institute for Health and Clinical Excellence, 2008

5. Rome II Criteria
However, this criteria exclude some clinical features that are recognized by clinicians as part of IBS such as:
(1) prandial urgency and abdominal pain/diarrhea and
(2) diarrhea with borborigmi and sense of incomplete rectal evacuation and thus limit its use.
National Institute for Health and Clinical Excellence, 2008

6. IBS: Signs and Symptoms
All ages can be affected, but mostly, patients below 45 have their first symptoms
Women are diagnosed with IBS two to three times as often as men and make up 80% of the population with severe IBS
Pain or abdominal discomfort is a key symptom for the diagnosis of IBS

7. IBS: Signs and Symptoms
Abdominal pain or discomfort is a prerequisite clinical feature of IBS
Highly variable in intensity and location
In 25% of patients, pain is localized to the hypogastrium, the right side in 20%, to the left side in 20%, and the epigastrium in 10%
Frequently episodic and crampy, but it may be superimposed on a background of constant ache

8. IBS: Signs and Symptoms
Eating or emotional stress exacerbates pain, but passage of flatus or stool relieves it
Women commonly report worsening symptoms during the premenstrual and menstrual phases
The most consistent clinical feature of IBS is alteration in bowel habits; and constipation alternating with diarrhea, usually with one of these symptoms predominating as the most common pattern

9. IBS: Signs and Symptoms
Initially, constipation may be episodic, but eventually becomes continuous and increasingly intractable to treatment with laxatives
Stool characteristics:
Usually hard with narrowed caliber, possibly reflecting excessive dehydration caused by prolonged colonic retention and spasm
repeated attempts at defecation in a short time span are common, because most patients also experience a sense of incomplete evacuation

10. It is not IBS when there is:
Painless diarrhea or constipation
Defecation straining, urgency or a feeling of incomplete bowel movement, passing mucus, and bloating are supportive symptoms not part of the diagnostic criteria
Sleep deprivation – unusual because abdominal pain is almost uniformly present only during waking hours
There is bleeding on bowel movement

11. IBS: Signs and Symptoms
If constipation is the predominant symptom, patients may have it weeks or months, interrupted with brief periods of diarrhea
If diarrhea is the predominating symptom, it usually consists of small volumes of loose stools
Most patients have stool volumes of < 200 mL
Nocturnal diarrhea does not occur in IBS

12. IBS: Signs and Symptoms
Increased gas in IBS patients causes abdominal distention and increased belching or flatulence
Quantitative measurements reveal that most patients who complain of increased gas generate no more than a normal amount of intestinal gas
Most IBS patients have impaired transit and tolerance of intestinal gas loads; and tend to reflux gas from the distal to the more proximal intestine, which may explain the belching

13. IBS: Pathophysiology
Irritable bowel syndrome (IBS) is a functional GI disorder characterized by abdominal pain and altered bowel habits in the absence of specific and unique organic pathology.
Unknown Cause
Intestinal contractions may be stronger and last longer than normal
Food is forced through the intestines more quickly, causing gas, bloating and diarrhea
The walls of the intestines are lined with layers of muscle that contract and relax in a coordinated rhythm as they move food from your stomach through your intestinal tract to your rectum. If you have irritable bowel syndrome, the contractions may be stronger and last longer than normal. Food is forced through your intestines more quickly, causing gas, bloating and diarrhea.

14. IBS: Pathophysiology Traditional theories: 3-part complex
Altered GI motility
Visceral hyperalgesia
Psychopathology
A unifying mechanism is still unproven

15. IBS: Pathophysiology
Altered GI motility includes distinct aberrations in small and large bowel motility
Colonic dysmotility demonstrates variations in slow-wave frequency and a blunted, late-peaking, postprandial response of spike potentials
Clustered contractions in the duodenum and jejunum and prolonged propagated contractions in the ileum
Small bowel dysmotility manifests
delayed meal transit in patients prone to constipation
accelerated meal transit in patients prone to diarrhea.
shorter intervals between migratory motor complexes (the predominant interdigestive small bowel motor patterns). 
The myoelectric activity of the colon is composed of background slow waves with superimposed spike potentials. Colonic dysmotility in irritable bowel syndrome manifests as variations in slow-wave frequency and a blunted, late-peaking, postprandial response of spike potentials. Patients who are prone to diarrhea demonstrate this disparity to a greater degree than patients who are prone to constipation.
Small bowel dysmotility manifests in delayed meal transit in patients prone to constipation and in accelerated meal transit in patients prone to diarrhea. In addition, patients exhibit shorter intervals between migratory motor complexes (the predominant interdigestive small bowel motor patterns). 
Current theories integrate these widespread motility aberrations and hypothesize a generalized smooth muscle hyperresponsiveness. They describe increased urinary symptoms, including frequency, urgency, nocturia, and hyperresponsiveness to methacholine challenge.

16. IBS: Pathophysiology
Visceral hyperalgesia
Enhanced perception of normal motility and visceral pain characterizes irritable bowel syndrome
Patients who are affected describe widened dermatomal distributions of referred pain
Sensitization of the intestinal afferent nociceptive pathways that synapse in the dorsal horn of the spinal cord provides a unifying mechanism
Visceral hyperalgesia is the second part of the traditional 3-part complex that characterizes irritable bowel syndrome.
Enhanced perception of normal motility and visceral pain characterizes irritable bowel syndrome. Rectosigmoid and small bowel balloon inflation produces pain at lower volumes in patients than in controls. Notably, hypersensitivity appears with rapid but not gradual distention.
Patients who are affected describe widened dermatomal distributions of referred pain. 
Sensitization of the intestinal afferent nociceptive pathways that synapse in the dorsal horn of the spinal cord provides a unifying mechanism.

17. Visceral hyperalgesia
Visceral afferent dysfunction manifests as exaggerated sensory responses to visceral stimulation which influences postprandial pain in 74% of IBS patients after the entry of food bolus to the cecum
Lipids lower the threshold for the first sensation of gas, discomfort and pain in IBS
Increased area of referred pain after lipid ingestion
Postprandial symptoms may be explained in part by nutrient-dependent exaggerated sensory component of the gastrocolonic response
Afferent pathway disturbances appear to be selective for visceral innervations with sparing of somatic pathways.

18. IBS: Pathophysiology Psychopathology
Associations between psychiatric disturbances and irritable bowel syndrome pathogenesis are not clearly defined
Patients show preferential activation of the prefrontal lobe, which contains a vigilance network within the brain that increases alertness
These may present as a form of cerebral dysfunction leading to the increased perception of visceral pain.

19. IBS: Pathophysiology Small bowel bacterial overgrowth
Has been heralded as a unifying mechanism for the symptoms of bloating and distention common to patients with irritable bowel syndrome.
Campylobacter, Salmonella and Shigella
Patients with Campylobacter infections who are toxin-positive are more likely to develop postinfective IBS.
Increased rectal mucosal enteroendocrine cells, T lymphocytes and increased gut permeability could persist and may contribute to postinfective IBS.

20. IBS: Pathophysiology Serotonin
Imbalance in mucosal 5-HT availability caused by defects in 5-HT production, serotonin receptors, or SERT
May cause the increase in serotonin release contributing to the postprandial symptoms of patients and provide a rationale for the use of serotonin antagonist as treatment for this disorder.

21. IBS: Diagnosis The diagnosis of IBS relies on:
Recognition of positive clinical features
Rome II diagnostic criteria
Other supportive symptoms such as defecation straining, urgency or a feeling of incomplete bowel movement, passing mucus, bloating, lethargy, nausea, backache and bladder symptoms
Elimination of other organic diseases

22. IBS: Diagnosis
In people who meet the IBS diagnostic criteria, the following tests should be undertaken to exclude other diagnoses:
CBC, ESR or plasma viscosity, C-reactive protein (CRP), antibody testing for coeliac disease (endomysial antibodies [EMA] or tissue transglutaminase [TTG]), sigmoidoscopic examination, stool examination for ova and parasites.
The laboratory features that argue against IBS include evidence of anemia, elevated ESR, presence of leukocytes or blood in stool, and stool volume > mL/d
National Institute for Health and Clinical Excellence, 2008
Fauci et.al. Harrison’s principles of Internal Medicine th edition. McGraw-Hill USA

23. IBS: Management
Nonpharmacologic
Pharmacologic

24. Non-Pharmacologic Patient Counseling and Dietary Alterations
Reassurance and careful explanation of the functional nature of the disorder
Avoid food precipitants that aggravate symptoms
such as coffee, disaccharides, legumes, and cabbage
excessive fructose and artificial sweeteners, such as sorbitol or mannitol, may cause diarrhea, bloating, cramping or flatulence
dietary change (high fiber diet)

25. Pharmacologic Stool-Bulking Agents Antispasmodics Antidiarrheal Agents
Antidepressant Drugs
Antiflatulence Therapy
Serotonin Receptor Agonist and Antagonists
Chloride Channel Activators

26. Stool-Bulking Agents
bran or hydrophilic colloid or psyllium
The water-holding action of fibers may contribute to increased stool bulk because of the ability of fiber to increase fecal output of bacteria.
Fiber also speeds up colonic transit in most persons.
In diarrhea-prone patients, whole-colonic transit is faster than average; however, dietary fiber can delay transit.
stool-bulking agents bind water and thus prevent both excessive hydration or dehydration of stool.
The water-holding action of fibers may contribute to increased stool bulk because of the ability of fiber to increase fecal output of bacteria. Fiber also speeds up colonic transit in most persons. In diarrhea-prone patients, whole-colonic transit is faster than average; however, dietary fiber can delay transit. Furthermore, because of their hydrophilic properties, stool-bulking agents bind water and thus prevent both excessive hydration or dehydration of stool.

27. Antispasmodics Inhibits the gastrocolic reflex
Provides temporary relief for symptoms such as painful cramps related to intestinal spasm
Given 30 min before meals so that effective blood levels are achieved shortly before the anticipated onset of pain
Most anticholinergics contain natural belladonna alkaloids
may cause xerostomia, urinary hesitancy and retention, blurred vision, and drowsiness
Use with caution in elderly
dicyclomine (synthetic anticholinergics) – less effect on mucous membrane secretions and produce fewer undesirable side effects
Physiologic studies demonstrate that anticholinergic drugs inhibit the gastrocolic reflex. hence, postprandial pain is best managed by giving antispasmodics 30 min before meals so that effective blood levels are achieved shortly before the anticipated onset of pain. Most anticholinergics contain natural belladonna alkaloids, which may cause xerostomia, urinary hesitancy and retention, blurred vision, and drowsiness. They should be used in the elderly with caution. Some physicians prefer to use synthetic anticholinergics such as dicyclomine that have less effect on mucous membrane secretions and produce fewer undesirable side effects

28. 2–4 mg every 4–6 h up to a maximum of 12 g/d Less addictive
Antidiarrheal Agents
Increases in segmenting colonic contractions, delays in fecal transit, increases in anal pressures, and reductions in rectal perception
2–4 mg every 4–6 h up to a maximum of 12 g/d
Less addictive
most useful if taken before anticipated stressful events that are known to cause diarrhea
Peripherally acting opiate-based agents
the initial therapy of choice for IBS-D
loperamide
bile acid binder cholestyramine resin
Hehe. Napagtripan lang. :D
Nakakatawa kasi nakita ko ito sa net. Hehe!
Tanggalin ng reporter ang pic ah! Gusto ko lng ishare iyan. Ang twilight ng philippines. Hahaha! ^^ v

29. Antidepressant drugs
TCA
IBS - D
Imipramine- slows jejunal migrating motor complex transit propagation and delays orocecal and whole-gut transit.
Desipramine- 86% improved abdominal pain

30. Antidepressant drugs
SSRI
IBS-C
Paroxetine – accelerates orocecal transit
Citalopram – blunts perception of rectal distension and reduces gastrocolonic response
Mianserin with 5HT2 and 5HT3 receptor antagonist and α2-adrenoceptor antagonist effect – reduces pain, distress and functional disability
*efficacy needs further confirmation

31. Antiflatulence therapy
Patients are advised to eat slowly or not chew gum or drink carbonated beverages
Avoid flatogenic foods, exercise, lose weight, take activated charcoal
Β-glycosidase
May reduce rectal passage of gas without decreasing bloating and pain

32. Serotonin receptor antagonist
Serotonin receptor agonist and antagonist
Serotonin receptor antagonist
IBS-D
ALOSETRON
Reduces perception of painful visceral stimulation in IBS
Rectal relaxation, increases rectal compliance and colonic transit

33. Serotonin receptor agonist and antagonist
5HT-4 receptor agonist
Tegaserol
prokinetic activity stimulating peristalsis
Accelerate intestinal and ascending colon transit
* series of cardiovascular events

34. Chloride channel activators
Lubiprostone
bicylcic fatty acid
Stimulates chloride channels in apical membrane of intestinal epithelial cells.
* nausea and diarrhea

35. References:
Fauci et.al. Harrison’s principles of Internal Medicine th edition. McGraw-Hill USA
National Institute for Health and Clinical Excellence, 2008