Constipation pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mugilan Poongkunran M.B.B.S [2]
Overview
The underlying pathophysiology of constipation involves several processes such as hardening of the stool, paralysis or slow transit, constriction in the lower gastrointestinal system or psychomotor factors.
Pathophysiology
Colonic Function
- Water absorbtion
- About 1.5 liter fluid is entered the colon from small intestine every day. Colon has to excrete out only 200-400 mL stool.
- Colon absorbed water and transit the stool into rectum to store and then expel. The amount of water that is absorbed in rectum is depend of the state of hydration.[1]
- Both sodium and chloride are the key elements in reabsorbing water in colon. The more time stool remained in colon, the drier it can become.[2]
- Motility
- There are two kinds of gross motility in colon, include:[1]
- Repetitive non-propulsive contractions: The main type of contraction in mixing and absorption of contents
- High-amplitude propagated contractions (HAPCs): Large coordinated contraction in charge of pushing the stool forward. Increased forms are seen in the morning and after drinking or eating.
- Normal colonic transition is about 20-72 hours.[3]
- HAPCs are decreased mainly in constipation, maybe as the main pathophysiology.[4]
- On molecular basis, the main movements of the gut (peristalsis) are regulated through serotonin (5-hydroxytriptamine [5HT]). 5HT is released from enterochromaffin cells in case bowel wall undergo traction (e.g., due to food or bolus). There are seven subtypes of the 5HT receptors, among which 5HT4 and 5HT3 are the most important ones. 5HT4 is to drive 5HT effect on the gut and 5HT3 is in charge of bowel sensation.[5]
- There are two kinds of gross motility in colon, include:[1]
Defecation
- The defecation process is consisted of three important stages, include:[6]
- Filling of the rectum
- Feeling the rectum filling
- Relaxation of pelvic floor muscles in a coordinated fashion
- Anal sphincters and puborectalis muscle are anatomical contributors to normal fecal consistency.
- Hardening of the feces: Improper mastication, low dietary fiber, dehydration and medications (aluminium, calcium, diuretic, iron).
- Paralysis or slowed transit: Hypothyroidism, hypokalemia, injured anal sphincter, medications (loperamide, codeine, morphine, tricyclic antidepressants) and severe systemic illness due to other causes.
- Constriction, where part of the intestine or rectum is narrowed or blocked: Diverticulosis, pelvic masses and stenosis.
- Psychosomatic constipation: Functional constipation and irritable bowel syndrome.[7]
Pathogenesis
- The exact pathogenesis of [disease name] is not fully understood.
OR
- It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Genetics
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
Associated Conditions
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ 1.0 1.1 Sleisenger, Marvin (2010). Sleisenger and Fordtran's gastrointestinal and liver disease : pathophysiology, diagnosis, management. Philadelphia: Saunders/Elsevier. ISBN 9781437727678.
- ↑ Andrews CN, Storr M (2011). "The pathophysiology of chronic constipation". Can J Gastroenterol. 25 Suppl B: 16B–21B. PMC 3206564. PMID 22114753.
- ↑ Southwell BR, Clarke MC, Sutcliffe J, Hutson JM (2009). "Colonic transit studies: normal values for adults and children with comparison of radiological and scintigraphic methods". Pediatr. Surg. Int. 25 (7): 559–72. doi:10.1007/s00383-009-2387-x. PMID 19488763.
- ↑ Dinning PG, Smith TK, Scott SM (2009). "Pathophysiology of colonic causes of chronic constipation". Neurogastroenterol. Motil. 21 Suppl 2: 20–30. doi:10.1111/j.1365-2982.2009.01401.x. PMC 2982774. PMID 19824935.
- ↑ Grundy D, Al-Chaer ED, Aziz Q, Collins SM, Ke M, Taché Y, Wood JD (2006). "Fundamentals of neurogastroenterology: basic science". Gastroenterology. 130 (5): 1391–411. doi:10.1053/j.gastro.2005.11.060. PMID 16678554.
- ↑ Bharucha AE (2006). "Pelvic floor: anatomy and function". Neurogastroenterol. Motil. 18 (7): 507–19. doi:10.1111/j.1365-2982.2006.00803.x. PMID 16771766.
- ↑ Caldarella MP, Milano A, Laterza F; et al. (2005). "Visceral sensitivity and symptoms in patients with constipation- or diarrhea-predominant irritable bowel syndrome (IBS): effect of a low-fat intraduodenal infusion". Am. J. Gastroenterol. 100 (2): 383–9. doi:10.1111/j.1572-0241.2005.40100.x. PMID 15667496.