Temporal arteritis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
==Pathophysiology== | |||
The damage to the vasuclature is mediated by an attack on the internal elastica lamina by activated CD4+ [[T helper cell]]s. This occurs in repsonse to the presentation of an [[antigen]] by [[macrophages]]. The inciting antigen has not been identified. | |||
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:''' | |||
*Cervicocephalic arteries: [[carotid artery]] and [[vertebral artery]]. The [[vertebral artery]] is involved as frequently as the temporal artery in fatal cases. Involvement of the [[basilar artery]] is rare. | |||
*Intraorbital branches: Posterior ciliary artery and [[ophthalmic artery]]. | |||
*External common, external, and internal carotid artery involvement: It is less common for proximal intracranial arteries to be involved. | |||
*External vertebral arteritis: It is less common though for the disease to extend more than 5 mm beyond the dural penetration. | |||
*Subclavian, axially and proximal brachial artery: There can be typical vasculitic lesions with long, smooth, lesions with tapered occlusions. | |||
*Coronary arteries: for a full discussion of the involvement of the heart in this disorder see the chapter on [[The Heart in Temporal Arteritis / Giant Cell Arteritis]] | |||
'''Less commonly involved sites:''' | |||
*Descending aorta: Mesenteric, iliac, femoral and renal arteries are less often involved. In these cases there can be [[mesenteric ischemia]], [[renal infarction]], and ischemic [[mononeuropathy]] can occur. | |||
*Pulmonary artery | |||
===Associated Conditions=== | ===Associated Conditions=== | ||
Revision as of 20:41, 29 August 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Pathophysiology
The damage to the vasuclature is mediated by an attack on the internal elastica lamina by activated CD4+ T helper cells. This occurs in repsonse to the presentation of an antigen by macrophages. The inciting antigen has not been identified.
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:
- Cervicocephalic arteries: carotid artery and vertebral artery. The vertebral artery is involved as frequently as the temporal artery in fatal cases. Involvement of the basilar artery is rare.
- Intraorbital branches: Posterior ciliary artery and ophthalmic artery.
- External common, external, and internal carotid artery involvement: It is less common for proximal intracranial arteries to be involved.
- External vertebral arteritis: It is less common though for the disease to extend more than 5 mm beyond the dural penetration.
- Subclavian, axially and proximal brachial artery: There can be typical vasculitic lesions with long, smooth, lesions with tapered occlusions.
- Coronary arteries: for a full discussion of the involvement of the heart in this disorder see the chapter on The Heart in Temporal Arteritis / Giant Cell Arteritis
Less commonly involved sites:
- Descending aorta: Mesenteric, iliac, femoral and renal arteries are less often involved. In these cases there can be mesenteric ischemia, renal infarction, and ischemic mononeuropathy can occur.
- Pulmonary artery
Associated Conditions
The disorder may coexist (in one quarter of cases) with polymyalgia rheumatica (PMR), which is characterized by sudden onset of pain and stiffness in muscles (pelvis, shoulder) of the body and seen in the elderly. Other diseases related with temporal arteritis are systemic lupus erythematosus, rheumatoid arthritis and severe infections.