Temporal arteritis pathophysiology: Difference between revisions
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==Microscopic Pathology== | ==Microscopic Pathology== | ||
*On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name]. | *On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name]. | ||
==References== | ==References== | ||
Revision as of 01:27, 5 April 2018
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Temporal Arteritis Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Temporal arteritis pathophysiology On the Web |
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American Roentgen Ray Society Images of Temporal arteritis pathophysiology |
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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
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
- 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. [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.
Genetics
- There is no known genetic cause of temporal arteritis.
Associated Conditions
- Temporal arteritis may coexist (in one quarter of cases) with polymyalgia rheumatica (PMR), which is characterized by a sudden onset of pain and stiffness in muscles (pelvis, shoulder) of the body and seen in the elderly.[22, 23] Other diseases related with temporal arteritis are systemic lupus erythematosus, rheumatoid arthritis and severe infections.[26, 27, 28]
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].