Gastroparesis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Madhu Sigdel M.B.B.S.[2]
Overview
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].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
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The progression to [disease name] usually involves the [molecular pathway].
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The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Pathogenesis
- The exact pathogenesis of gastroparesis is not fully understood. However, it is well known that gastric emptying process is the result of interaction of smooth muscles, extrinsic and enteric autonomic nervous system, and interstitial cells of Cajal (ICC).[1] The final process for delay of gastric emptying is increased tone of pylorus. Gastric emptying is mediated by the vagus nerve, which involves fundus accommodation, antrum contraction, and pyloric relaxation. Interstitial cells of Cajal are the pacemaker cells in the gut with unique ability to generate and propagate slow waves in gastrointestinal muscles. This electrical slow wave activity is the determinant of the characteristic frequency of phasic contractions of the stomach, intestine and colon as well as the direction and velocity of propagation of peristaltic activity, in coordination with the enteric nervous system.[2] Interstitial cells of Cajal regulate both gastric pacemaker activity and enteric neurons, which then initiate smooth muscle cell activity.[3] Slow wave activity in human stomach originates from a pacemaker region at the mid/upper corpus on the greater curvature. From this pacemaker region, a band of activity is formed rapidly and propagated in an organised fashion towards the distal antrum.[4] Hence, tone of pyloric sphincter plays an important role in the regulation of gastric emptying. Non-adrenergic, non-cholinergic (NANC) innervation to the pylorus is predominantly inhibitory and mediates relaxation of the sphincter.[5] A high density of Nitric Oxide Synthase-immunopositive nerve cells and fibres have been been demonstrated in the pylorus.[6] They are called inhibitory nitrergic neurons. Expression of neuronal nitric oxide synthase (nNOS) activity from nitrergic neurons in gastric wall secrete nitric oxide (NO). Majir function of NO from these nitrergic enteric nerves include accommodation of the fundus and relaxation of pylorus through smooth muscle relaxation. These enteric nerves (nNOS) also control the muscle tone of the lower esophageal sphincter, the sphincter of Oddi, and the anus.[7] As per research and understood to date most important mechanism in pathogenesis of gastroparesis appears to be:[8]
- Loss of expression of neuronal nitric oxide synthase (nNOS)
- Loss of interstitial cells of Cajal (ICC)
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
- ↑ Oh JH, Pasricha PJ (2013). "Recent advances in the pathophysiology and treatment of gastroparesis". J Neurogastroenterol Motil. 19 (1): 18–24. doi:10.5056/jnm.2013.19.1.18. PMC 3548121. PMID 23350043.
- ↑ Camborová P, Hubka P, Sulková I, Hulín I (2003). "The pacemaker activity of interstitial cells of Cajal and gastric electrical activity". Physiol Res. 52 (3): 275–84. PMID 12790758.
- ↑ Parkman HP (2015). "Idiopathic gastroparesis". Gastroenterol Clin North Am. 44 (1): 59–68. doi:10.1016/j.gtc.2014.11.015. PMC 4324534. PMID 25667023.
- ↑ Cheng LK (2015). "Slow wave conduction patterns in the stomach: from Waller's foundations to current challenges". Acta Physiol (Oxf). 213 (2): 384–93. doi:10.1111/apha.12406. PMC 4405773. PMID 25313679.
- ↑ Anuras S, Cooke AR, Christensen J (1974). "An inhibitory innervation at the gastroduodenal junction". J Clin Invest. 54 (3): 529–35. doi:10.1172/JCI107789. PMC 301585. PMID 4152775.
- ↑ Ekblad E, Mulder H, Uddman R, Sundler F (1994). "NOS-containing neurons in the rat gut and coeliac ganglia". Neuropharmacology. 33 (11): 1323–31. PMID 7532815.
- ↑ Sivarao DV, Mashimo H, Goyal RK (2008). "Pyloric sphincter dysfunction in nNOS-/- and W/Wv mutant mice: animal models of gastroparesis and duodenogastric reflux". Gastroenterology. 135 (4): 1258–66. doi:10.1053/j.gastro.2008.06.039. PMC 2745304. PMID 18640116.
- ↑ Oh JH, Pasricha PJ (2013). "Recent advances in the pathophysiology and treatment of gastroparesis". J Neurogastroenterol Motil. 19 (1): 18–24. doi:10.5056/jnm.2013.19.1.18. PMC 3548121. PMID 23350043.