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Vasculitis
Vasculitis and Atherosclerosis
| Question | Answer |
|---|---|
| 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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