Temporal arteritis pathophysiology: Difference between revisions

Jump to navigation Jump to search
No edit summary
Line 4: Line 4:


==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
Temporal arteritis is caused by transmural inflammation of elastic arteries. It is understood that temporal arteritis is the result of cell mediated immunity which arises as a response to endothelial injury. Temporal arteritis granulomatous histopathology has suggested the presence of an antigen-driven disease with local T-cell and macrophage activation in or near elastic tissue in the arterial walls with an important role of the proinflammatory cytokines. The adventitia of the vessel is the initial site of immunologic injury. The activation of dendritic cells in the adventitia causes a production of chemokines that recruit CD4+ T helper cells. The CD4+ T helper cell convert in to Th17 cells which produce interleukin 17 and Th1 cells which produce interferon gamma. Giant cell are one of many inflammatory cells that are recruited and produce growth factor which narrows and obstructs the vessels. The concentric inflammation occurs in segments. Macrophages in the adventia produce interleukin 6. While in the intima and media of the vessel, macrophages produce vascular endothelial growth factor (VEGF) and metalloproteinases which destroy the internal elastic lamina. An increased activated platelets express P-selectin which may cause vessel inflammation and thromboembolic events. Temporal arteritis arises from giant cells, which are fused monocytes cells that are normally involved in the body immune response. Because the disease involves only arteries with internal elastic lamina, the [[aortic arch]] and its branches are often involved. Intracranial arteries do not have internal elastic lamina and are not involved.  
 
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==
==Pathophysiology==

Revision as of 02:34, 5 April 2018

Temporal Arteritis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Temporal Arteritis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography or 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

Temporal arteritis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Temporal arteritis pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Temporal arteritis pathophysiology

CDC on Temporal arteritis pathophysiology

Temporal arteritis pathophysiology in the news

Blogs on Temporal arteritis pathophysiology

Directions to Hospitals Treating Temporal arteritis

Risk calculators and risk factors for Temporal arteritis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2]

Overview

Temporal arteritis is caused by transmural inflammation of elastic arteries. It is understood that temporal arteritis is the result of cell mediated immunity which arises as a response to endothelial injury. Temporal arteritis granulomatous histopathology has suggested the presence of an antigen-driven disease with local T-cell and macrophage activation in or near elastic tissue in the arterial walls with an important role of the proinflammatory cytokines. The adventitia of the vessel is the initial site of immunologic injury. The activation of dendritic cells in the adventitia causes a production of chemokines that recruit CD4+ T helper cells. The CD4+ T helper cell convert in to Th17 cells which produce interleukin 17 and Th1 cells which produce interferon gamma. Giant cell are one of many inflammatory cells that are recruited and produce growth factor which narrows and obstructs the vessels. The concentric inflammation occurs in segments. Macrophages in the adventia produce interleukin 6. While in the intima and media of the vessel, macrophages produce vascular endothelial growth factor (VEGF) and metalloproteinases which destroy the internal elastic lamina. An increased activated platelets express P-selectin which may cause vessel inflammation and thromboembolic events. Temporal arteritis arises from giant cells, which are fused monocytes cells that are normally involved in the body immune response. Because the disease involves only arteries with internal elastic lamina, the aortic arch and its branches are often involved. Intracranial arteries do not have internal elastic lamina and are not involved.

Pathophysiology

Pathogenesis

  • It is understood that temporal arteritis is the result of cell mediated immunity which arises as a response to endothelial injury.[21]
  • Temporal arteritis granulomatous histopathology has suggested the presence of an antigen-driven disease with local T-cell and macrophage activation in or near elastic tissue in the arterial walls with an important role of the proinflammatory cytokines. [29, 30]
  • The adventitia of the vessel is the initial site of immunologic injury. The activation of dendritic cells in the adventitia causes a production of chemokines that recruit CD4+ T helper cells. The CD4+ T helper cell convert in to Th17 cells which produce interleukin 17 and Th1 cells which produce interferon gamma.
  • Giant cell are one of many inflammatory cells that are recruited and produce growth factor which narrows and obstructs the vessels.[10][13]
  • The concentric inflammation occurs in segments.[11]
  • Macrophages in the adventia produce interleukin 6.[13] While in the intima and media of the vessel, macrophages produce vascular endothelial growth factor (VEGF) and metalloproteinases which destroy the internal elastic lamina.[12][13]
  • An increased activated platelets express P-selectin which may cause vessel inflammation and thromboembolic events. [16]
  • Temporal arteritis arises from giant cells, which are fused monocytes cells that are normally involved in the body immune response.
  • Because the disease involves only arteries with internal elastic lamina, the aortic arch and its branches are often involved. Intracranial arteries do not have internal elastic lamina and are not involved. The distribution of involved arteries are as follows:

Commonly involved sites: [3, 4][7]18]

  • External vertebral arteries: It is less common though for the disease to extend more than 5 mm beyond the dural penetration.

Less commonly involved sites:

Genetics

  • There is no known genetic cause of temporal arteritis.

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

Template:WikiDoc Sources