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• Most feared complication: blindness -permanent!!

• Histology:
• This produce elastic lamina fragmentation

• Pulseless disease
• Marked weakening of the pulses in the upper extremities
•
Giant Cell Arteritis / Takayasu Arteritis/ Polyarteritis Nodosa (PAN)
Temporal Arteritis Pulseless disease

Chronic Inflammatory disorder of • Granulomatous vasculitis of Systemic vasculitis of small – medium

large to small-sized arteries
(L-S)
• Mainly temporal, ophthalmic
arteries; also vertebral
-may include aorta
*most feared sequelae: BLINDNESS
• pathogenesis: T-cell mediated
immune response against vessel
wall antigens which cause
subsequent proinflammatory
cytokine production
medium and larger arteries sized arteries
(L-M) (M-S)
Characterized by ocular disturbances , Involves renal and visceral vessels but
and marked weakness of the pulses in the sparing the pulmonary circulation;
upper extremities No association with ANCA, but patients
with PAN have chronic HEP B
• Pathogenesis: Transmural fibrous
thickening of the aorta; Particularly
the aortic arch and great vessels-
and severe narrowing of the major
branch vessels
• Pulmonary involvement –half cases
• May affect coronary and renal
arteries
• Affects females <40

• • Clinical Manifestations: Malaise

• Fever, nigh sweats

Histology: Granulomatous
inflammation -diagnostic; this
produce elastic lamina
fragmentation
Intimal thickening -> reduces
luminal diameter
Laboratory: marked Increase ESR
(Polymyalgia Rheumatica)
Often AN AB’s (+)
• Arthralgias, anorexia, weight loss
Histology: indistinguishable from giant Histology: segmental, Transmural
cell necrotizing inflammation of small -to
medium sized arteries
Frequently accompanied by Fibrinoid
necrosis
Diagnosis: Aortic Arteriography
*shares many attributes with giant cell-
If px <50 – Takayasu
>50 – Giant cell
Management: Glucocorticoid therapy
40-6- mg prednisone/day
Surgery/angioplasty