Spasmodigestin tablets composition:
Each tablet contains:
Papain 100 mg
Sanzyme 3500 36mg
Sodium dehydrocholate 10 mg
Dicyclomine hydrochloride 5 mg
Povidone K90, Crospovidone, Microcrystalline cellulose, Colloidal silicon dioxide, Dibasic calcium phosphate dihydrate.
Hydroxypropylmethylcellulose, Eudragit, Sodium hydroxide, Titanium dioxide, Talc powder, Triethyl citrate, Dimethicone, colouring agent.
Spasmodigestin tablets properties:
It is a well balanced combination with specific digestive, choleretic, spasmolytic and antiflatulent properties. It provides the body with papain, the proteolytic enzyme, in addition to sanzyme 3500 which is a multienzyme complex containing mainly protease, amylase, lipase and cellulase. These enzymes act upon food contents of the GIT and catalyze their conversion into simpler and easily digestible and absorbable components. Spasmodigestin also exerts choleretic effect through sodium dehydrocholate which improves the flow of bile necessary for emulsification and digestion of fats. The spasmolytic effect of Spasmodigestin is due to dicyclomine hydrochloride which rapidly and effectively relieves spastic pain of the GI musculature and intestinal hypermotility. The antimuscarinic and direct antispasmodic actions of dicyciomine hydrochloride account for its high efficacy in irritable bowel syndrome (spastic colon). The antiflatulence effects of Spasmodigestin is due to simethicone, the powerful defoaming agent. Simethicone reduces surface tension to gas bubbles of the GIT causing them to colesce and be easily expelled. At the same time, simethicone prevents formation of mucus surrounded gas pockets in the GIT. These properties collectively make it the drug of choice for rapid relief of indigestion, GI spasms and flatulence. .
Spasmodigestin tablets pharmacokinetics:
For Dicyclomine :
Dicyclomine hydrochloride is rapidly absorbed from gastrointestinal tract also enter the circulation through the mucosal surfaces to the body.
It appears to be distributed throughout the entire body and readily cross the blood-brain barrier .
Hepatic, by enzymatic hydrolysis.
Elimination : 1.8 hours (initial phase) and 9 to 10 hours (secondary phase) It is assumed to be eliminated unchanged either by renal or lecal.
For Simethicone :
Fecal, as unchanged drug.
Spasmodigestin tablets indications :
– Dyspepsia, abdominal discomfort and flatulence.
– Gastro-intestinal spasm particularly, associated with irritable bowel syndrome (more drugs used for treatment of irritable bowel syndrome: Coloverin D Tablets and Gast Reg).
– Following surgery on the stomach, small intestine or pancreas, and postgastrectomy syndrome.
-Irritable bowel syndrome (spastic colon) with such symptoms as anorexia, intestinal spasm, flatulence, constipation or diarrhea.
– Loss of appetite.
– Anorexia nervosa.
Spasmodigestin tablets dosage & administration:
1 – 2 tablets to be taken immediately, before each meal.
Spasmodigestin tablets contraindications :
Hypersensitivity to any ingredients of the product
It is contra-indicated in patients with prostatic enlargement, in whom it may lead to urinary retention, and in those with paralytic ileus or pyloric stenosis.
Spasmodigestin tablets side effects:
The side effects are dose-related and are usually reversible when therapy is discontinued.
The peripheral side effects of anti-muscarinics are a consequence of their inhibitory effect on muscarinic receptors within the autonomic nervous system. At therapeutic doses, adverse effects include dryness of the mouth with difficulty in swallowing, thirst, reduced bronchial secretions, dilatation of the pupils (mydriasis) with loss of accommodation (cycloplegia) and photophobia, flushing and dryness of the skin, transient bradycardia followed by tachycardia, with palpitations and arrhythmias, and difficulty in micturition, as well as reduction in the tone and motility of the gastrointestinal tract leading to constipation.
Spasmodigestin tablets drug interactions :
The effects of antimuscarinics may be enhanced by the concomitant
administration of other drugs with anti muscarinic properties, such as amantadine, some antihistaminics, phenothiazine antipsychotics, and tricyclic antidepressants. Inhibition of drug-metabolising enzymes by MAOls may possibly enhance the effects of antimuscarinics. The reduction in gastric motility caused by antimuscarinics may affect the absorption of other drugs.
Spasmodigestin tablets pregnancy & lactation:
In retrospective studies there has been no evidence of dicyclomine having any untoward effect on the embryo Although a causal relationship has not been established, the use of dicyclomine in nursing mothers is not recommended.
Spasmodigestin tablets precautions & warnings:
Caution is generally advisable in any patient with diarrhea It should not be gillen to patients with myasthenia gravis except to reduce
adverse muscarinic effects of an anti-cholinesterase.
A box containing 30 enteric coated tablets in ( AI/transparent PVC) strips, each of 10 tablets and an inner leaflet.
keep at temperature not exceeding 30 c in dry place away from light keep out of the reach of children
Produced by :
pharco Pharmaceuticals – alexandria
Union of Arab Pharmacies.
Irritable bowel syndrome PPT power point presentation :
1. Irritable Bowel Syndrome Dr Junaid Saleem
2. Conflict of Interest Statement • Sponsored by Abbott for this lecture • No other conflicts of interest 2
3. Short Version • Irritable Bowel Syndrome – Definition? – Aetiology? – Pathology? – Clinical Features – Diagnosis? – Treatment? – Prognosis +/- 3
4. Introduction • First described in 1771. • 50% of patients present <35 years old. • 70% of sufferers are symptom free after 5 years. • GPs will diagnose one new case per week. • GPs will see 4-5 patients a week with IBS. • Point prevalence of 40-50 patients per 2000 patients. 4
5. What Is IBS? • A syndrome. • One man’s constipation is another man’s normality. • Cause unknown. • 20% seem to start after an episode of gastroenteritis. 5
6. Psychosocial factors •IBS aetiology is multi-factorial •Emotions significantly affect colonic response in IBS – Stressful stimuli disrupt upper GI motility in several ways, including mean • oesophageal peristaltic amplitude, • rate of gastric emptying, • small bowel transit, and • increased upper oesophageal sphincter pressure Aetiology
7. Psychosocial factors •The response to stress is mediated by corticotrophin releasing factor (CRF) secreted by the enteric neurons, enteroendocrine cells and immune cells – CRF binds to CRF receptors present on smooth muscle cells and increase the number of discrete cluster contractions – Psychosocial factors exacerbate the symptoms of IBS but a definite link has not been established Aetiology
9. • Exact pathophysiology remains uncertain • Dysregulation within the brain gut axis, • interactions between genetics, • psychosocial factors, • post-inflammatory changes and • motor and sensory dysfunction are all likely to influence the development of IBS Pathophysiology Spiller R, Aziz Q, Creed F, et al. Guidelines on the irritable bowel syndrome: mechanisms and practical management. Gut 2007;56:1770-1798. Mawe GM, Coates MD, Moses PL. Intestinal serotonin signalling in irritable bowel syndrome. Aliment Pharmacol Ther 2006;23:1067-1076.
10. • Exact pathophysiology remains uncertain • Visceral hypersensitivity – enhanced pain sensitivity of the gut – may play an important role in the development of chronic pain and discomfort in IBS1 • Heightened sensitivity of the peripheral nervous system is caused by immune and inflammatory mediators acting at the site of tissue injury and inflammation Pathophysiology Spiller R, Aziz Q, Creed F, et al. Guidelines on the irritable bowel syndrome: mechanisms and practical management. Gut 2007;56:1770-1798. Mawe GM, Coates MD, Moses PL. Intestinal serotonin signalling in irritable bowel syndrome. Aliment Pharmacol Ther 2006;23:1067-1076.
11. • Exact pathophysiology remains uncertain • Serotonin (5-HT) – present extensively in the GI tract – is the most important neurotransmitter in the pathogenesis of IBS, • peripheral sensitisation causes an area of hypersensitivity to develop in the surrounding uninjured tissue – this phenomenon is called central sensitisation Pathophysiology Spiller R, Aziz Q, Creed F, et al. Guidelines on the irritable bowel syndrome: mechanisms and practical management. Gut 2007;56:1770-1798. Mawe GM, Coates MD, Moses PL. Intestinal serotonin signalling in irritable bowel syndrome. Aliment Pharmacol Ther 2006;23:1067-1076.
12. Disturbances in GI motility •A proportion of IBS patients, specifically those reporting constipation or dyspeptic symptoms, exhibit delayed gastric emptying, especially of solids, this correlates with absence of post-prandial increase in electrogastrography (EGG) amplitude Pathophysiology Hammerle CW, Surawicz CM. Updates on treatment of irritable bowel syndrome. World J Gastroenterol 2008;14(17):2639-2649.