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GIANT CELL (TEMPORAL) ARTERITIS

Giant cell (temporal) arteritis, the most common form of systemic vasculitis in adults, is an acute and chronic, often granulomatous, inflammation of arteries of large to small size.[54] It

affects principally the arteries in the head—especially the temporal arteries—but also the vertebral and ophthalmic arteries and the aorta, where it may cause thoracic aortic aneurysm.

Ophthalmic arterial involvement may lead to permanent blindness. Therefore, visual loss caused by giant cell arteritis is a medical emergency that requires prompt recognition

Figure 11-23Diagrammatic representation of the sites of the vasculature involved by the major forms of vasculitis. The widths of the trapezoids indicate the frequencies of involvement of

various portions. LCA, leukocytoclastic angiitis. (Reproduced from Jennette JC, and Falk RJ: Small-vessel vasculitis. New Engl J Med 337:1512, 1997.)

TABLE 11-5-- Classification and Characteristics of Selected Vasculitis

(Not Available)

Modified from Jennette JC, et al: Nomenclature of systemic vasculitides: the proposal of an international consensus conference. Arthritis Rheum 37:187, 1994.

Figure 11-24Temporal (giant cell) arteritis. A, H&E stain of section of temporal artery showing giant cells at the degenerated internal elastic membrane in active arteritis (arrow). B,

Elastic tissue stain demonstrating focal destruction of internal elastic membrane (arrow) and intimal thickening (IT) characteristic of long-standing or healed arteritis. C, Examination of

the temporal artery of a patient with giant-cell arteritis shows a thickened, nodular, and tender segment of a vessel on the surface of head (arrow). (C Reproduced from Salvarani C, et al.

Polymyalgia rheumatica and giant-cell arteritis. N Engl J Med 347:261, 2002.)

Figure 11-25Takayasu arteritis. A, Aortic arch angiogram showing narrowing of brachiocephalic, carotid, and subclavian arteries (arrows). B, Gross photograph of two cross-sections of

the right carotid artery taken at autopsy of the patient shown in A, demonstrating marked intimal thickening with minimal residual lumen. C, Histologic view of active Takayasu aortitis,

illustrating destruction of the arterial media by mononuclear inflammation with giant cells.

 

Figure 11-26Representative forms of systemic medium-sized to small vessel vasculitis. A, Polyarteritis nodosa. B, Leukocytoclastic vasculitis. C and D, Wegener granulomatosis. E,

Thromboangiitis obliterans (Buerger disease). In polyarteritis nodosa (A), there is segmental fibrinoid necrosis and thrombotic occlusion of the lumen of this small artery. Note that part of

the vessel wall at the upper right (arrow) is uninvolved. In leukocytoclastic vasculitis (B), shown here from a skin biopsy, there is fragmentation of neutrophils in and around blood vessel

walls. In Wegener granulomatosis (C), there is inflammation (vasculitis) of a small artery along with adjacent granulomatous inflammation, in which epithelioid cells and giant cells



(arrows) are seen. D, Gross photo from the lung of a patient with fatal Wegener granulomatosis, demonstrating large nodular lesions. In a typical case of Buerger disease (E), the lumen is

occluded by a thrombus containing two abscesses (arrow). The vessel wall is infiltrated with leukocytes. (A, and D, courtesy of Sidney Murphree, MD, Department of Pathology,

University of Texas Southwestern Medical School, Dallas, TX; B, courtesy of Scott Granter, M.D., Brigham and Women's Hospital, Boston.)

Figure 11-27Vasculitis with fibrinoid necrosis in a patient with active systemic lupus erythematosus.

Figure 11-28Raynaud phenomenon. A, Sharply demarcated pallor of the distal fingers resulting from the closure of digital arteries. B, Cyanosis of the fingertips. (Reproduced from

Salvarani C, et al.: Polymyalgia rheumatica and giant-cell arteritis. N Engl J Med 347:261, 2002.)

TABLE 11-6-- Classification of Vascular Tumors and Tumor-Like Conditions


Date: 2016-04-22; view: 661


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