Plummer-Vinson syndrome pathophysiology: Difference between revisions
Jump to navigation
Jump to search
Akshun Kalia (talk | contribs) |
Akshun Kalia (talk | contribs) No edit summary |
||
| Line 41: | Line 41: | ||
**Iron replete cells with normal citric acid cycle have an increased formation of reducing equivalents (NADH) thus leading to increased ATP formation via oxidative phosphorylation. | **Iron replete cells with normal citric acid cycle have an increased formation of reducing equivalents (NADH) thus leading to increased ATP formation via oxidative phosphorylation. | ||
**In patients with iron deficiency, all these metabolic pathways (oxidative phosphorylation) are reduced. This promotes anaerobic metabolism with increased consumption of glucose and increased production of lactic acid. | **In patients with iron deficiency, all these metabolic pathways (oxidative phosphorylation) are reduced. This promotes anaerobic metabolism with increased consumption of glucose and increased production of lactic acid. | ||
** In patients with iron deficiency the | ** In patients with iron deficiency, the iron-dependent oxidative enzymes are unable to function at optimum level and may lead to myasthenic changes in muscles. | ||
** These myasthenic changes are often seen in muscles involved in swallowing and may lead to atrophy of the esophageal mucosa and formation of esophageal webs. | |||
*The dysphagia in Plummer-Vinson syndrome results from postcricoid web or stricture. However, | ** The dysphagia in Plummer-Vinson syndrome results from esophageal (postcricoid) web or stricture. However, patients who do not exhibit obstructive lesions may have dysphagia resulting from muscular in-coordination. | ||
OR | OR | ||
Revision as of 17:20, 25 October 2017
|
Plummer-Vinson syndrome Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Plummer-Vinson syndrome pathophysiology On the Web |
|
American Roentgen Ray Society Images of Plummer-Vinson syndrome pathophysiology |
|
Risk calculators and risk factors for Plummer-Vinson syndrome pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Please help WikiDoc by adding content here. It's easy! Click here to learn about editing.
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].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Pathogenesis
- Plummer-Vinson syndrome is a rare condition characterized by iron-deficiency anemia, glossitis and dysphagia.
- The exact pathogenesis of Plummer-Vinson syndrome is not fully understood. It is postulated that Plummer-Vinson syndrome results from iron deficiency. Other possible factors include malnutrition, genetic predisposition and autoimmune disorders.[1][2][3][4]
- Iron plays a major role in the expression of citric acid cycle enzymes such as citrate synthase, isocitric dehydrogenase, and succinate dehydrogenase.
- Iron replete cells with normal citric acid cycle have an increased formation of reducing equivalents (NADH) thus leading to increased ATP formation via oxidative phosphorylation.
- In patients with iron deficiency, all these metabolic pathways (oxidative phosphorylation) are reduced. This promotes anaerobic metabolism with increased consumption of glucose and increased production of lactic acid.
- In patients with iron deficiency, the iron-dependent oxidative enzymes are unable to function at optimum level and may lead to myasthenic changes in muscles.
- These myasthenic changes are often seen in muscles involved in swallowing and may lead to atrophy of the esophageal mucosa and formation of esophageal webs.
- The dysphagia in Plummer-Vinson syndrome results from esophageal (postcricoid) web or stricture. However, patients who do not exhibit obstructive lesions may have dysphagia resulting from muscular in-coordination.
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, Plummer-Vinson syndrome presents with the following findings:
- Epithelial atrophy
- Chronic submucosal inflammation
- Epithelial atypia or dysplasia (in advanced cases)
Pathophysiology
References
- ↑ Chisholm M (1974). "The association between webs, iron and post-cricoid carcinoma". Postgrad Med J. 50 (582): 215–9. PMC 2495558. PMID 4449772.
- ↑ Dantas RO, Villanova MG (1993). "Esophageal motility impairment in Plummer-Vinson syndrome. Correction by iron treatment". Dig. Dis. Sci. 38 (5): 968–71. PMID 8482199.
- ↑ Novacek G (2006). "Plummer-Vinson syndrome". Orphanet J Rare Dis. 1: 36. doi:10.1186/1750-1172-1-36. PMC 1586011. PMID 16978405.
- ↑ Ekberg O, Malmquist J, Lindgren S (1986). "Pharyngo-oesophageal webs in dysphageal patients. A radiologic and clinical investigation in 1134 patients". Rofo. 145 (1): 75–80. doi:10.1055/s-2008-1048889. PMID 3016824.