musculoskeletal and connective tissue disorders
Overview of Vasculitis
Pathophysiology of Vasculitis
Histologic description of an affected vessel should include the following: A description of vessel wall damage (eg, type and location of inflammatory infiltrate, extent and type of damage, presence or absence of fibrinoid necrosis) A description of healing responses (eg, intimal hypertrophy, fibrosis) Certain features (eg, predominant inflammatory cell type, location of inflammation) suggest particular vasculitic processes and may aid in the diagnosis. For example, in many acute lesions, the predominant inflammatory cells are polymorphonuclear leukocytes; in chronic lesions, lymphocytes predominate. Inflammation may be segmental or involve the entire vessel. At sites of inflammation, varying degrees of cellular inflammation and necrosis or scarring occur in one or more layers of the vessel wall. Inflammation in the media of a muscular artery tends to destroy the internal elastic lamina. Some forms of vasculitis are characterized by giant cells in the vessel wall. In some vasculitic disorders, such as Granulomatosis with Polyangiitis (GPA) or Leukocytoclastic vasculitis is a histopathologic term used to describe findings in small-vessel vasculitis. It refers to breakdown of inflammatory cells that leaves small nuclear fragments (nuclear debris) in and around the vessels. Inflammation is transmural and nongranulomatous. Polymorphonuclear leukocytes predominate early; later, lymphocytes predominate. Resolution of the inflammation tends to result in fibrosis and intimal hypertrophy. Intimal hypertrophy or secondary clot formation can narrow the vessel lumen and cause tissue ischemia or necrosis. 