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Microscopy Endarteritis and periarteritis of vasa Fibrous cap with deeper core containing foam vasorum, perivascular infiltrate of plasma cells, cholesterol clefts and soft lipid cells and lymphocytes 4. However, some vasculitis, more often affecting arterioles, venules and usual clinical features are fever, malaise, weakness, weight capillaries, and hence also termed as small vessel vasculitis. The from many of patients with vasculitis of immunologic origin condition is believed to result from deposition of immune show the presence of following immunologic features: complexes and tumour-related antigens. While most cases of iii) Healed stage—In this stage, the affected arterial wall is immunologic vasculitis have immune complex deposits in markedly thickened due to dense fibrosis. The internal the vessel wall, there are some cases which do not have such elastic lamina is fragmented or lost. Healed stage may immune deposits and are termed as cases of pauci-immune contain haemosiderin-laden macrophages and organised vasculitis (similar to pauci-immune glomerulonephritis, thrombus. However, it may be mentioned here that various stages of the disease may be seen in different vessels and even Polyarteritis Nodosa within the same vessel. The tissues and organs most commonly involved order of frequency of involvement, are the kidneys, heart, are the skin, mucous membranes, lungs, brain, heart, gastrointestinal tract, kidneys and muscle. Most commonly involved 403 results from immunologic response to an identifiable antigen organs are the lungs, paranasal sinuses, nasopharynx and that may be bacteria (e. Typical features include pneumonitis with bilateral Hypersensitivity vasculitis includes clinicopathologic entities infiltrates in the lungs (Chapter 17), chronic sinusitis, naso such as serum sickness, Henoch-Schönlein purpura, mixed pharyngeal ulcerations (Chapter 18) and renal disease cryoglobulinaemia, vasculitis associated with malignancy, (Chapter 22). This is supported by the observation of subepithelial immunoglobulin deposits on the glomerular Microscopically, the lesions characteristically involve basement membrane and induction of remission by immuno smallest vessels, sparing medium-sized and larger suppressive therapy. Disseminated form of Wegener’s i) Leucocytoclastic vasculitis, characterised by fibrinoid granulomatosis differs from a related entity, idiopathic lethal necrosis with neutrophilic infiltrate in the vessel wall. This highly destructive and progressively necrotic disease of the form is found in vasculitis caused by deposits of immune upper airways. Histologically, the characteristic feature of Wegener’s ii) Lymphocytic vasculitis, in which the involved vessel granulomatosis is the presence of necrotising granulo shows predominant infiltration by lymphocytes. This type matous inflammation of the tissues and necrotising is seen in vascular injury due to delayed hypersensitivity vasculitis with or without granulomas: or cellular immune reactions. The granulomas consist of fibrinoid necrosis with extensive infiltration by neutrophils, mononuclear cells, Wegener’s Granulomatosis epithelioid cells, multinucleate giant cells and fibroblastic Wegener’s granulomatosis is another form of necrotising proliferation.

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