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Vasculitis and Atherosclerosis

Vasculitis: definition inflammation of blood vessels
Vasculitis: major divisions Infectious and noninfectious
Infectious vasculitis: what are the possible etiologies and common agents that cause them? Fungal: aspergillus; Bacterial: pseudomonas; Viral: cytomegalovirus
Why is it important to accurately diagnose infectious vasculitis? Misdiagnosing as primary (autoimmune) and treating with steroids ---> FATAL
What is the general pathogenesis of noninfectious vasculitis? Heterogeneous: 1) T-lymphocytes-->cytokines-->activate macrophages-->chew up elastic lamina. 2) immune complex deposition. 3) antibody-mediated attack 4) others not known
What very specific sign(s) should alert you to vasculitis? Palpable purpura (VERY SPECIFIC) and Fever (very sensitive, especially if of unknown origin). Many nonspecific symptoms
Hypersensitivity angiitis: definition • Definition: an acute necrotizing inflammatory disease of the smallest vessels (arterioles, capillaries, venules), especially in the skin and commonly limited to skin.
Leukocytoclastic vasculitis o Leukocytoclastic vasculitis is the term used for cutaneous hypersensitivity angiitis, and 10% is due to drugs (quinolones, penicillins, sulfonamides, retinoids, etc.) while some cases are due to infections or tumors
Microscopict polyangiitis (the term used for hypersensitivity angiitis involving internal organs), renal involvement (glomerulonephritis) occurs in 90%, musculoskeletal in 60%, lungs (capillaritis) 50%, gut 50%, skin 40%, and ear-nose-throat 35%.
What is the pathogenesis of hypersensitivity angiitis? immune complex deposition and complement activation 7-10 days following exposure to an antigen
Hypersensitivity angiitis: pathological hallmarks o Infiltration of blood vessels by neutrophils o Breakdown (leukocytoclasia) dispersing nuclear dust, o Fibrinoid change, thrombosis, rupture and hemorrhage. o Lymphocytic infiltration, but it is characteristic that all lesions are in the same phase
Hypersensitivity angiitis: signs and symptoms “palpable purpura” especially in the lower legs, livedo reticularis, urticaria, hematuria, proteinuria, arthralgias, myalgias, hemoptysis, gastrointestinal bleeding
Hypersensitivity angiitis: diagnosis biopsy, usually of skin.
Hypersensitivity angiitis: treatment o Skin: generally no specific therapy (except stopping drug, treating infection, or excising tumor if one of these is causing it). o Microscopic polyangiitis + major organ damage: immunosuppressive therapy (steroids plus cyclophosphamide) is indicated.
Temporal arteritis: definition granulomatous inflammatory disease of medium and larger arteries, especially in the head; occasional involvement of thoracic aorta + branhces
Temporal arteritis: epidemiology o It affects 1 in 750 persons age 50 or older in the US. o Female predominance (female/male ratio 2/1) o Much more common in whites (especially those of northern European ancestry).
Temporal arteritis: pathogenesis o Autoimmune (deranged cell-mediated immunity
Temporal arteritis: pathology o Segmental transmural chronic granulomatous inflammation with multinucleated giant cells o Destruction of internal elastic lamina o Intimal thickening, cell proliferation and luminal stenosis (but the inflammation is sometimes not granulomatous).
Temporal erteritis: signs and symptoms o Abrupt or insidious o Headache (75%), visual disturbances (50%), jaw claudication (50%), swollen tender artery (50%), scalp tenderness (50%), fever (25%), malaise, and weight loss.
How do fever, malaise, and weight loss affect the diagnosis + prognosis of temporal arteritis? Presence of fever, malaise, and weight loss make blindess less likely
How do diplopia, jaw claudication, and swollen tender arteris affect the diagnosis of temporal arteritis? Diagnosis 4x more likely
What is the typical presentation of patients with temporal arteritis? Elderly white female patients with headaches
What immune mediated comborbidity does temporal arteritis often copresent? Part of the same spectrum of diseases as polymyalgia rheumatica (40% of cases)
What complications are associated with temporal arteritis? BLINDNESS (20% of cases, half bilateral). Aortic aneurysm, arterial dissection and arterial rupture.
Temporal Arteritis: diagnosis o Erythrocyte sedimentation rate (“ESR,” “sed rate”) is over 40 mm/hour in 97% of cases o Biopsy is positive in 90%.
Tempoeral Arteritis: treatment Steroids and sometimes aspirin
Kawasaki's disease: definition o Mucocutaneous lymph node syndrome. Acute childhood primary vasculitis of medium arteries, especially coronaries, with aneurysm formation (in 20%).
Kawasaki's disease: epidemiology o Uncommon o 1-2 year old children. o Male predominance of 1.5/1 o More common in Asians, especially Japanese.
Kawasaki's disease: proposed pathogenesis o Aberrant immune reaction to a ubiquitous RNA virus that can become persistent in genetically predisposed individuals.
Kawasaki's disease: pathology o Endothelial necrosis o Transmural inflammation with neutrophils, lymphocytes, necrosis, aneurysms, and thrombosis.
Kawasaki's disease: signs and symptoms o Persistent high fever o Conjunctivitis o Mucosal and skin erythema and edema (involving palms and soles, with peeling) o Erythematous maculopapular skin rash o Cervical lymphadenopathy. o Erythematous swollen tongue may resemble a strawberry.
Kawasaki's disease: complications o Arterial rupture o Myocardial infarction o Death (1%).
Kawasaki's disease: diagnosis history and physical examination
Kawasaki's disease: o Aspirin + intravenous immunoglobulin o Tx reduces the rate of cardiovascular sequelae from 20% to less than 5%.
Artherosclorosis: definition a chronic inflammatory disease of the inner layer (tunica intima) of arteries, causing narrowing and hardening of the arteries
ARtherosclerosis: response to injury hypothesis 1) injury to endothelial cells 2) accumulation of lipid in tunica intima 3) leukocyte recuitment into tunica intima 4) foam cell formation 5) extracellular matrix deposition
Artherosclerosis: what changes are seen initially after injury to endothelial cells? Impairment to the permeability barrier; Release of inflammatory cytokines; Increased adhesion of monocytes; Decreased secretion of vasodilators nitric oxide and prostacyclin; Decreased release of antithrombotic substances.
Artherosclerosis: how + why does lipid accumulate in tunica intima? What does it cause? Especially low density lipoprotein (LDL); Hypertension-->increased production of pretoglycans; LDL trapped by binding to extracellular matrix proteoglycans; LDL modified; Modified LDL promotes leukocyte recruitment and foam cell formation
What cell markers and proteins cause the leukocyte recruitment into the tunica intima during artherosclerosis? Mediated by endothelial expression of: Leukocyte adhesion molecules (LAM), Monocyte chemotactic protein 1, Interferon-inducible protein 10 and interleukin-8 (IL-8)
What cell markers and proteins cause the recruitment of smooth muscle cells into the tunica intima during artherosclerosis? Platelet-derived growth factor (PDGF); Tumor necrosis factor-alpha (TNF-alpha); Transforming growth factor-beta (TGF-beta); Interleukin-1 (IL-1).
What steps are seen that lead to foam cell formation in artherosclerosis? 1. Transformation of monocytes into macrophages 2. Phagocytosis of modified LDL via scavenger receptors 3. Evasion of negative feedback inhibition 4. Become engorged foam cells.
What proteins mediate the deposition of extra-cellular matrix during artherosclerosis? Due to smooth muscle cell production of ECM mediated by IL-1, TNF-alpha, TGF-beta Fibroblast growth factor (FGF).
Laying down of ____ represents an irreversible component of artherosclerosis collagen
What pathological findings do you see in artherosclerosis? Fatty streaks (reversible); artheromatous plaques with yellow lipid core (artheroma) and white fibrous cap; neovascularization
How do the artheromatous plaques change over time? • Early: atherosclerosis is all atheroma and no sclerosis • End-point: all sclerosis and no atheroma.
Why do you see neovascularization in artherosclerosis? o Cells in the expanded tunica intima signal need for blood vessels within the vasa vasorum to serve them. o Ingrowth of capillaries from the outer layer (tunica adventitia) through the middle layer (tunica media) into the tunica intima.
What complications do you see in artherosclerosis? SUPERIMPOSED THROMBOSIS, o Calcification, fissures (cracks in the surface), erosion, ulceration, rupture, atheroembolism, intraplaque hemorrhage
How do you reduce the risk of superimposed thrombosis? Aspirin
When is superimposed thrombosis most likely? Younger patients, especially women; due to erosion and more likely organizing
Created by: karkis77



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