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| __NOTOC__
| | ===Famous Cases=== |
| == Irritable Bowel Syndrome == | | The following are a few famous cases of narcolepsy: |
| {{WikiDoc CMG}}{{AE|AE=}}{{MWH}}
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| '''''Synonyms and Keywords:''''' Spastic colon, functional bowel disorder, IBS | | *'''Jimmy Kimmel''', American late-night talk show host, actor, producer, comedian, and writer |
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| | *'''Harold M. Ickes''', former deputy White House chief of staff for President Bill Clinton and a leading figure in the His administration's [[healthcare]] reform initiative |
| | *'''Arthur Lowe''', a British actor who played iconic Captain Mainwaring in the British sitcom ''Dad's Army'' |
| | *'''Nastassja Aglaia Kinski''', German actress, and former model |
| | *'''George M. Church''', molecular geneticist, molecular engineer, and chemist, who is a Professor of Genetics and Professor of Health Sciences at Harvard |
| | *'''Teresa Nielsen Hayden''', American science fiction editor, fanzine writer, and essayist who has a famous weblog, named Making Light |
| | *'''Franck Bouyer''', French former road racing cyclist who was unable to compete or train without treatment with Modafinil |
| | *'''Gabe Barham''', former Drummer for American post-hardcore band Sleeping With Sirens |
| | *'''Jinkx Monsoon''' (real name is Jerick Hoffer), Seattle Drag Queen, stage performer, comedian and singer who is the winner of the fifth season of ''RuPaul's Drag Race'' |
| | *'''Aaron Flahavan''', former English (Portsmouth) football Goalkeeper |
| | *'''Paul Gonsalves''', Jazz tenor saxophonist |
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| == Historical Perspective ==
| | <br />__NOTOC__ |
| Irritable Bowel syndrome (IBS) was first mentioned in the Rocky Mountain Medical Journal in 1950. IBS was described as a psychosomatic disorder, not explained by any biochemical or structural abnormalities. Apley and Nash conducted a famous study on 1000 children in Bristol, United Kingdom and were the first to describe recurrent abdominal pain (RAP) as the predominant feature of IBS. In 1978, the first diagnostic criteria i.e. the Manning criteria was described. It did not specify any required duration for the symptoms of IBS. The subsequent criteria saw a reduction in the required duration of symptoms to facilitate early diagnosis and treatment. In Rome in 1995, an international group of gastroenterologist defined the diagnostic criteria for IBS and this was published in 1999 under the title of the Rome II criteria. This criteria underwent modification and was described as the Rome III criteria. Since June 2016, the criteria being followed is the Rome IV criteria.
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| === Discovery ===
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| * In 1950, the concept of irritable bowel syndrome (IBS) was mentioned for the first time without the recognition of any particular etiology, in the ''Rocky Mountain Medical Journal.''
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| * IBS was described as a psychosomatic disorder, not explained by any biochemical or structural abnormalities.
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| * In 1958, Apley and Nash conducted a study on 1000 children in Bristol, United Kingdom and were the first to describe Recurrent abdominal pain (RAP), as the predominant feature of IBS.
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| * Recurrent abdominal pain was defined as pain in the abdomen occurring over a duration of at least 3 months, with the severity enough to cause significant impairment of function.<br />
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| <references />
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| == Classificatiion ==
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| Irritable bowel syndrome (IBS) may be classified according to Rome IV criteria into 4 sub-types based on predominant type of bowel habits:
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| * IBS with predominant constipation
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| * IBS with predominant diarrhea
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| * IBS with mixed bowel habits:
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| ** Alternating patterns of stool passage which is not in conjuncture with the normal bowel movements.
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| * IBS unclassified:
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| ** Patients who meet the diagnostic criteria for IBS but whose bowel habits do not fit into any of the above subtypes.
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| * Post infectious IBS (PI-IBS):
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| ** Post-infectious IBS is an additional sub-type that is acute in onset and occurs subsequent to an infectious illness of the gastrointestinal tract. Post-infectious IBS is characterized by two or more of the following:
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| *** Vomiting
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| *** Fever
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| *** Positive stool culture
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| *** Diarrhea
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| {| class="wikitable"
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| |+
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| !Subtype
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| !Hard or Lumpy Stools
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| !Soft (Mushy) or Watery Stools
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| |-
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| |IBS with Constipation
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| |≥ 25 percent
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| |≤ 25 percent
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| |-
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| |IBS with Diarrhea
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| |≤ 25 percent
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| |≥ 25 percent
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| |-
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| |Mixed IBS
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| |≥ 25 percent
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| |≥ 25 percent
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| |-
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| |Unsubtyped IBS
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| |colspan="3" align="center"| Insufficient abnormality of stool consistency to meet criteria for IBS with constipation, diarrhea or mixed sub types
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| |}
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| == Pathophysiology ==
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| === Pathogenesis ===
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| IBS occurs as a result of an interplay between four main factors:
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| {{Family tree/start}}
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| {{Family tree||||||||||A01||||||||||A01= '''CNS dysregulation and psychosocial factors'''}}
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| {{Family tree||||||||||!||||||||||}}
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| {{Family tree||||||||||!||||||||||}}
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| {{Family tree||||||||||!||||||||||}}
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| {{Family tree|B01|-|-|-|-|-|-|B02|-|-|-|-|-|B03|B01= '''Intrinsic gastrointestinal factors''':<br>• Motor abnormalities<br>• Visceral hypersensitivity<br>• Immune activation and mucosal inflammation<br>• Altered gut microbiota<br>• Abnormal serotonin pathways|B02= '''Irritable Bowel Syndrome'''|B03= '''Genetic factors''':<br>• Twin concordance<br>• Familial aggregation<br>• Single nucleotide polymorphisms(SNPs)<br>• TNF polymorphism}}
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| {{Family tree||||||||||!||||||||||}}
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| {{Family tree||||||||||!||||||||||}}
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| {{Family tree||||||||||!||||||||||}}
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| {{Family tree||||||||||C01||||||||||C01= '''Environmental factors''':<br> •Diet<br> •Infections}}
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| {{Family tree||||||||||||||||||||}}
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| {{Family tree||||||||||||||||||||}}
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| {{Family tree||||||||||||||||||||}}
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| {{Family tree/end}}<br />
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| === Environmental factors ===
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| === Diet ===
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| * Fermentable oligosaccharides, monosaccharides, disaccharides, and polyols (FODMAPs) are present in stone fruits, artificial sweeteners, lactose-containing foods, and legumes. Changes in diet such as increased amounts (FODMAPs) can alter gut microflora.
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| * Fermentation and osmotic effects of FODMAPs produce abdominal discomfort and diarrhea in IBS.
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| * FODMAPs yield carbon dioxide, methane, and hydrogen that are responsible for bloating.
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| * Osmotically active carbohydrate by products lead to diarrhea by enhancing intestinal contractions and precipitating fluid secretion.
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| '''<big>Infection</big>'''
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| * Infectious gastroenetritis triggers micro inflammation and up to one third of irritable bowel syndorme cases follow acute gastroenteritis[[Gastroenteritis|.]]
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| * Micro inflammation of the gut causes activation of the lymphocytes, mast cells and pro inflammatory cytokines that stimulate the enteric nervous system and lead to abnormal visceral and motor responses within the gastrointestinal tract.
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| === Intrinsic gastrointestinal factors[edit | edit source] ===
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| * '''Motor abnormalities:'''
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| ** IBS is referred to as ‘spastic colon’ due to changes in colonic motor function.
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| ** Manometry recordings from the transverse, descending and sigmoid colon have shown that IBS leads to altered colonic and small intestinal tumor function, such as increased frequency and irregularity of luminal contractions.
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| ** Motor changes lead to symptoms of diarrhea and constipation.
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| *** Diarrhea-prone IBS patients have increased responses to ingestion, CRH ([[Corticotropin-releasing hormone|corticotropin releasing hormone]]), CCK ([[cholecystokinin]]), which increase the peak amplitude of high-amplitude propagating contractions (HAPCs) and lead to abdominal discomfort with accelerated transit through the colon.
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| *** Constipation-prone IBS patients show fewer high-amplitude propagating contraction (HAPCs) as compared to diarrhea prone IBS patients, delayed transit through the colon and decreased motility.
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| '''<big>Visceral hypersensitivity:</big>'''
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| * IBS is associated with a decreased threshold for perception of visceral stimuli (i.e. visceral hypersensitivity)
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| * Rectal distension produces painful and non-painful sensations at lower volumes in [[Irritable bowel syndrome|IBS]] patients as compared to healthy controls, suggesting the presence of afferent pathway disturbances in visceral innervation.
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| * Visceral hypersensitivity contributes to IBS by involving the following:
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| ** '''Spinal hyperexcitability'''
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| *** Secondary to activation of neurotransmitters such as:
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| *** NDMA receptor
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| *** Nitric oxide
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| ** '''Activation of specific gastrointestinal mediators''' that lead to afferent nerve fiber sensitization:
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| *** Kinins
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| *** Serotonin
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| ** '''Central (brainstem and sortical) modulation''' with increased activation of anterior cingulate cortex, thalamus and insula.
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| *** These structures are involved in processing of pain.
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| *** Cortical and brainstem modulation translate into long term hypersensitivity due to neuroplasticity.
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| *** Semi permanent changes(seen on functional MRI and PET scan) in the neural response to visceral stimulation contribute to visceral hypersensitivity.
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| ** '''Recruitment of peripheral silent nocireceptors''' cause increased end organ sensitivity due to
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| *** Hormonal activation ( increased serotonin affects gastrointestinal and visceral pain perception)
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| *** Immune activation(recruitment of inflammatory mediators)
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| {{Family tree/start}}
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| {{Family tree ||||||||||||||||||||}}
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| {{Family tree ||||||||||||||||,|-|A01|-|A02|||||||A01= Spinal hyperexcitability|A02= Activation of<br>• N-methyl D aspartate (NMDA) receptor<br>• nitric oxide}}
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| {{Family tree ||||||||||||||||!||||}}
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| {{Family tree ||||||||||||||||)|-|B01|-|B02|||||||B01= Central (brainstem and cortical) modulation|B02= Increased activation of:<br>• Anterior cingulate cortex<br>• Thalamus<br>• insula}}
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| {{Family tree ||||||||||||||||!||||}}
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| {{Family tree ||||||||||||C01|-|(||||C01= Visceral Hypersensitivty}}
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| {{Family tree ||||||||||||||||!||||}}
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| {{Family tree ||||||||||||||||)|-|D01|-|D02||||||||||D01= Activation of specific gastrointestinal mediators|D02= Kinins and serotonin activation lead to afferent nerve fiber sensitization}}
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| {{Family tree ||||||||||||||||!||||}}
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| {{Family tree ||||||||||||||||`|-|E01|-|E02||||||||||E01= Recruitment of peripheral silent nociceptors|E02= Increased end organ sensitivity due to hormonal or immune activation}}
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| {{Family tree ||||||||||||||||||||}}
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| {{Family tree/end}}
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| '''<big>Immune activation and mucosal inflammation</big>'''
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| <br />
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| {{Family tree/start}}
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| {{Family tree|A01|-|-|-|A02|-|-|-|A03|||||||||A01= '''Mast cells'''|A02= '''IMMUNE ACTIVATION AND MUCOSAL INFLAMMATION'''|A03= '''Lymphocytes'''|}}
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| {{Family tree||||||||!||||||||||}}
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| {{Family tree||||||||!||||||||||}}
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| {{Family tree|||||||B01||||||||||B01= '''Proinflammatory cytokines'''}}
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| {{Family tree||||||||||||||||||||}}
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| {{Family tree/end}}
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| * IBS in patients with history of inflammatory bowel disease, celiac disease or microscopic colitis points towards the fact that immune activation and local gastrointestinal mucosal inflammation play an important role in its pathogenesis.
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| * IBS patients have high mucosal counts of lymphocytes (T cells, B cells), mast ''cells'' and immune ''mediators'' such as prostanoids, proteases, cytokines and histamines.
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| '''<big>Lymphocytes:</big>'''
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| * Activation of humoral immunity in IBS is specific for the gastrointestinal tract. Increased number of lymphocytes have been found in the small intestine and colon of IBS patients.
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| * IBS patients with diarrhea have enhanced mucosal humoral activity, associated with activation and proliferation of B cells and immunoglobin production, identified by microarray profiling.
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| * IBS patients with severe disease have an increase in lymphocyte infiltration in the myentric plexus.
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| '''<big>Mast cells:</big>'''
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| * IBS leads to an increased number of mast cells in IBS patients in the jejunum, terminal ileum and colon.
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| * Higher numbers of activated mast cells are found in proximity to colonic nerve fibres in the mucosa of the gastrointestinal tract of IBS patients
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| '''<big>Proinflammatory cytokines:</big>'''
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| * Cytokines are protein mediators of the immune response. Increased levels of cytokines have been found in IBS patients.
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| * Higher amounts of TNF are produced by the peripheral blood mononuclear cells of IBS patients.
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| * Other cytokines such as interleukin 6, interleukin 10, and TNF alpha are raised in IBS patients.
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| * Increased concentration of cytokines is directly proportional to the severity and frequency of pain.
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| * The TNF antagonist infliximab counteracts pain in IBS patients, proving TNF involvement in mechanical hypersensitivity of the colonic afferent nerve endings.
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| <br />
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| == Associated conditions ==
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| Several medical comorbidities appear with greater frequency in IBS patients.
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| === Headache, Fibromyalgia, and Depression ===
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| IBS patients may be identified with comorbidities such as headache, fibromyalgia and depression.
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| === Inflammatory Bowel Disease ===
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| * IBS and IBD are interrelated diseases, as patients with IBD experience IBS-like symptoms when their IBD is in remission.
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| * IBS is believed to be a type of low-grade IBD as serum markers associated with inflammation have also been found in patients with IBS.
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| * IBS patients are 16.3 times more likely to develop IBD.
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| === Abdominal Surgery ===
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| * IBS patients are 87% more likely to undergo abdominal and pelvic surgery, and three times more likely to undergo gallbladder surgery.
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| * IBS patients were twice as likely to undergo hysterectomy.
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| === Endometriosis[edit | edit source] ===
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| There is a statistically significant link between migraine headaches, IBS, and endometriosis.
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| == Gross Pathology ==
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| * On gross pathology, the GI tract appears normal in IBS.
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| == Microscopic Pathology ==
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| Microscopic changes that may be found in IBS patients are as follows:
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| <br />
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| {| class="wikitable"
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| |+
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| !Location
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| !Layer of Intestine involved
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| !Mast Cells
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| !T Lymphocytes
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| !Enterochromaffin Cells
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| |-
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| |Rectum
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| |Mucosa
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| | +++/-
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| | +/-
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| | +/-
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| |-
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| |Terminal Ileum
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| |Mucosa
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| | -
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| | ++
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| | -
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| |-
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| |Cecum
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| |Mucosa
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| | ++
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| | -
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| | -
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| |-
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| |Colon
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| |Muscularis Externa
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| | +/-
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| | -
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| | -
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| |-
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| |Jejunum
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| |Myenteric Plexus
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| | ++
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| | -
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| | -
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| |}
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| == Risk Factors ==
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| Common risk factors in the development of IBS may be categorized as psychological, epidemiological, genetic, and infections.
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| === Common risk factors ===
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| Common risk factors in the development of IBS include:
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| '''Psychological risk factors''':
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| * Stress
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| * Anxiety
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| '''Psychiatric risk factors:'''
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| * Depression
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| * Panic disorders
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| * History of physical or sexual abuse or adverse early life events
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