IRRITABLE BOWEL SYNDROME AND ITS HOMOEOPATHIC MANAGEMENT.
Department Of Practice of Medicine.
Father Muller Homoeopathic Medical College and Hospital
Irritable bowel syndrome is a functional disorder characterised by abdominal discomfort or pain. This article reviews about the epidemiology, etiology, types, pathophysiology, diagnosis, miasmatic interpretation general and Homoeopathic management of irritable bowel syndrome.
Irritable bowel syndrome, Pathogenesis, Diagnosis, miasmatic interpretation.
IBS is a functional disorder characterised by abdominal discomfort or pain that is accompanied by at least two of the following, relief by defecation, change in the frequency of stool or change in the consistency of stool.
• 3 – 22% world-wide
• Reason for 20 – 50% of gastroenterology visits.
• 26%prevalence among children with recurrent abdominal pain.
• 40%onset before age 35.
• 50%onset age 35 – 50.
• female > male (3:1)
ETIOLOGY OF IBS
5.sexual /physical abuse
1 Abnormal gastrointestinal (GI) tract movements.
2. A change in the nervous system communication between the GI and brain
3. Sensory and motor disorders of the colon.
4. Dietary allergies or food sensitivities.
5. Neurotransmitter imbalance“(decreased serotonin levels).
• IBS pathophysiology is not clear
• Many theories have been put forward , but the exact cause of IBS is still uncertain
Traditionally, IBS has been conceptualized as a condition of visceral hypersensitivity (leading to abdominal discomfort or pain) and gastrointestinal motor disturbances (leading to diarrhoea or constipation). Some have suggested that these abnormalities are secondary to psychological disturbances rather than being of primary relevance. However, not all patients with IBS have significant psychological overlay and referral bias may partly account for the psychological associations. Hints as to why visceral hypersensitivity and gastrointestinal motor disturbances may arise are emerging. There is increasing evidence that organic disease of the gastrointestinal tract can be identified in subsets of patients who fulfil the Rome criteria for IBS. Evidence for subtle inflammatory bowel disease, serotonin dysregulation, bacterial overgrowth and central dysregulation continue to accumulate.
Infection and Immune activation in IBS
There is increasing evidence regarding the role of immune activation in the etiology of IBS, Approximately 1 in ten patients with IBS believe their IBS began with an infectious illness. Prospective studies have shown that 3%-36% of enteric infections lead to persistent new IBS symptoms; the precise incidence depends on the infecting organism. Whereas viral gastroenteritis seems to have only short-term effects, bacterial enteritis and protozoan and helminthic infections are followed by prolonged IBS.Risk factors for developing IBS include, in order of importance, prolonged duration of initial illness, toxicity of infecting bacterial strain, smoking, mucosal markers of inflammation, female gender, depression, hypochondriasis, and adverse life events in the preceding 3 mo. Age older than 60 years might protect against IBS whereas treatment with antibiotics has been associated with increased risk. The mechanisms that cause IBS are unknown but could include residual inflammation or persistent changes in mucosal immunocytes, enterochromaffin and mast cells, enteric nerves, and the gastrointestinal microbiota. Exposure to intestinal infection induces persistent low-grade systemic and mucosal inflammation, which is characterized by an altered population of circulating cells, mucosal infiltration of immune cells and increased production of various cytokines in IBS patients.
Serotonin (5-HT), acting particularly through the 5-HT3 and 5-HT4 receptors, plays a significant role in the control of gastrointestinal motility, sensation, and secretion. Furthermore, observations that plasma 5-HT concentrations are reduced in IBS patients with constipation. But raised in those with diarrhoea especially those showing postprandial symptoms, provide further support for its involvement in the motor and sensory dysfunction associated with this condition. Thus there has been considerable interest in these receptors as possible therapeutic targets for IBS, with agonists at the 5-HT4 receptor predicted to enhance gastrointestinal propulsion (that is, to be prokinetics) and antagonists at the 5-HT3 receptor to slow gastrointestinal transit and reduce visceral sensation.
Studies indicate that small intestinal bacterial overgrowth (SIBO) is prevalent in IBS, it remains unclear whether SIBO causes IBS. Although, the bacterial overgrowth hypothesis of IBS may be biologically plausible, there is also a strong rationale for competing hypotheses. It is unlikely that SIBO is the predominant cause of IBS in all comers, because competing explanations are sensible and defensible. Moreover, data indicate that the test used to promulgate the SIBO hypothesis – the lactulose hydrogen breath test – may not have measured SIBO in the first place. We do not have evidence of SIBO being absent before IBS symptoms, and present after IBS emerges. There is not a dose-response relationship between small intestinal microbiota and IBS symptoms.. IBS does not behave like a traditional infectious disease, suggesting that microbes may not principally cause the syndrome. Other factors may confound the relationship between SIBO and IBS, including proton pump inhibitors. Whereas the brain-gut hypothesis is evolutionarily sensible, the bacterial hypothesis is harder to defend from an evolutionary perspective. So it can be said that bacteria may contribute to some IBS symptoms, but that bacteria cannot be the only explanation, and a causal link between SIBO and IBS is not secure.
Central dysregulation and brain-gut interaction
Psychosocial factors appear to be important in IBS, although whether these factors directly alter gastrointestinal function remains uncertain. It is also possible that gastrointestinal dysfunction modulates central processes too. For example, there is good evidence now that abuse in childhood or adulthood is associated with IBS, although whether it is of etiological importance remains in dispute. Anxiety and depression are also common in IBS.Some have conceptualized IBS as a somatization disorder, but the clear evidence for an organic pathophysiology in some cases of IBS makes this unlikely.
The central nervous system modulates various functions such as secretion, motility, and blood flow. Signals from the gut, in turn, are involved in regulating reflexes. Perception of events in the gut involves activation of afferent pathways, with information being modulated at different levels, peripheral as well as central. A major advance in our understanding of brain-gut interaction and its alteration in IBS occurred with the introduction of functional magnetic resonance imaging. This technique allowed assessment of the difference in cortical function in response to gut stimulation between healthy subjects and IBS patients opening the door for potential pharmacologic and behavioural interventions. There are differences in brain responses in patients with IBS that have been documented.
Studies have suggested that there is a genetic contribution to IBS, although the importance of this remains in dispute. A search for candidate genes continues, with the working hypothesis that environmental factors likely play an important role in the pathogenesis in the genetically primed individual.
1-Pain, distension or abdominal discomfort and bloating.
2-Abnormal bowel habits with periods of constipation and/or diarrhoea Sensation of incomplete bowel movement-
3 Mucus in the stool
4.Abnormal stool passage
Feeling of incomplete evacuation
6. Extra intestinal symptoms
o sleep disturbances
o chronic headache
TYPES OF IBS
The person tends to alternate constipation with normal stools.
Symptoms of abdominal cramping or aching are commonly triggered by eating.
• The person tends to experience diarrhoea first thing in the morning or after eating.
• The need to go to the toilet is typically urgent and cannot be delayed.
3-ALTERNATING CONSTIPATION AND DIARRHOEA
• It is also known as (IBS-A) , (IBS-M) or ( mixed IBS)
• This is characterised by the features of both constipation and diarrhoea predominant IBS.
DIAGNOSIS OF IBS
• 1. CLINICAL EVALUATION BASED ON.
Abdominal pain and discomfort lasting at least 12 weeks, though the weeks don’t have to occur consecutively. You also need to have at least two of the following:
A change in the frequency or consistency of your stool. –
o For example you may change from having one normal formed stool every day to three or more loose stools daily, or you may have only one hard stool every three to four days
Straining, urgency or a feeling that you can’t empty your bowels completely. Mucus in your stool.
Bloating or abdominal distension
• 2. BASIC LAB TESTS
Screening for organic causes
• 3. SIGMOIDOSCOPY
• 4. COLONOSCOPY
Strongly consider further testing
• Bloody stool
• Large volume diarrhoea
• Greasy stools
• Onset age >50
• Rectal bleeding
• Weight loss
• Palpable rectal mass
• Persistent diarrhoea and constipation
Drug induced diarrhea
Post –cholecystectomy diarrhea
1. SUPPORT AND UNDERSTANDING
Psychological stress , mood disorders should be identified , evaluated and treated
Physical activities helps to release stress,
Concentrating on hobbies
Reduce cabbage, beans , and other foods containing fermentable carbohydrates
Apple and grape juice, banana , nuts , and raisins – avoid
Low fat diet should take.
Dietary fiber supplements – soften stool and improves evacuation
A bland bulk producing agent may be used.– raw bran 15 ml (1tsp)
3. COGNITIVE –BEHAVIORAL THERAPY
4. STD. PSYCHOTHERAPY
PSORA: As the disease is only in the functional level and there is no structural pathological changes, IBS come under psoric miasm.
1. CONSTIPATION PRE DOMINANT IBS
- Obstinate constipation
- Hard crumbling stool
- Require great effort to expulsion
- Crumble from the verge of anus
- No stools alike
- Green mucus stools alternate with constipation
- Painful stool with spasm of sphincter
- Stool comes down with difficulty
- When partly expelled, recedes again
- Great straining
- Constipation before and after menses
- Obstinate constipation
- Feces protrudes and recedes
- Stool involuntary black, offensive, frothy
- Violent pain in rectum
- Hard , knotty stool, no desire
- Even a soft stool passed with difficulty
- Great straining
- Diarrhea on urinating
- Evacuation preceded by painful urging long before stool
- Watery, noisy, flatulent, green like chopped spinach
- Diarrhea immediately after drinking, or eating
- After any emotion with flatulence
- Dysentery , tenesmus , not relieved by stool
- Cutting pain with shreds of mucus membrane
- Incessant ,tenesmus of rectum not relieved by stool
- Frequent ,unsuccessful desire for stool
- Colic after drinking
- Morning diarrhea ,drives out of bed , painless
3-ALTERNATING CONSTIPATION AND DIARRHOEA
- Indigestion , vomiting of large quantities of offensive fluid
- Alternate diarrhea and constipation.
- Sensation as if bowels were sinking down
2. NUX VOM
- Constipation with frequent ineffectual urging
- Incomplete and unsatisfactory
- Feeling as if part remained unexcelled
- Constriction of rectum
- Irregular peristaltic action
- Passing small quantities at each attempt
- Alternate constipation and diarrhea
- Dysentery stool relieve pain for a time
- constipation alternate with diarrhea
- early morning long standing diarrhea
- prolapse of rectum before / with stool
- constipation clay colored , hard, dry , difficult
- painless, profuse, polychromatic , diarrhea
- great prostration
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Dr. Minimol.PE studied BHMS in father muller homoeopathic medical college and perusing MD in practice of medicine at father muller homoeopathic medical college.