Plummer-Vinson syndrome pathophysiology

Revision as of 17:20, 25 October 2017 by Akshun Kalia (talk | contribs)
Jump to navigation Jump to search

Plummer-Vinson syndrome Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Plummer-Vinson syndrome from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

Echocardiography and Ultrasound

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Plummer-Vinson syndrome pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Plummer-Vinson syndrome pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Plummer-Vinson syndrome pathophysiology

CDC on Plummer-Vinson syndrome pathophysiology

Plummer-Vinson syndrome pathophysiology in the news

Blogs on Plummer-Vinson syndrome pathophysiology

Directions to Hospitals Treating Plummer-Vinson syndrome

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

  1. Chisholm M (1974). "The association between webs, iron and post-cricoid carcinoma". Postgrad Med J. 50 (582): 215–9. PMC 2495558. PMID 4449772.
  2. 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.
  3. Novacek G (2006). "Plummer-Vinson syndrome". Orphanet J Rare Dis. 1: 36. doi:10.1186/1750-1172-1-36. PMC 1586011. PMID 16978405.
  4. 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.