Chapter 138 - Thromboangiitis obliterans Flashcards
Thromboangiitis obliterans define
1) Buerger disease 2) von Winiwarter-Buerger syndrome 3) inflammatory affecting infrapopliteal and infrabrachial medium small arteries and veins 4) age < 50 5) smoking related 6) male > female (5-10x more in men) 7) middle east, asia, mediterranean, eastern europe
Treatment for Buerger disease
1) smoking cessation 2) iloprost 3) endothelin receptor antagonist 4) immunoadsorption 5) growth factors 6) gene and stem therapy 7) bone fenestration to mobilize bone marrow
First full description of thromboangiitis obliterans
Buerger 1924 - the circulatory disturbances of the extremities
Risk factors for Buerger disease
1) smoking 2) low SES 3) poor oral hygiene 4) nutritional deficit 5) fungal/viral infection 6) cold injury 7) sympathomimetic drug abuse 8) arsenic intoxication
Possible pathways of immune-mediated injury in thromboangiitis obliterans
1) active smoking (urinary cotinine) 2) increased cellular sensitivity to collagen type I, III, IV 3) circulating immune complex 4) TNFalpha, IL1beta, IL5, IL6, IL12, IL17, IL23 increase 5) reduced IL10 6) Increased HMGB1, MMP9, ICAM1
Autoantibodies associated with TAO
1) antiphospholipid syndrome 2) anticardiolipin 3) antineutrophil cytoplasmic antibodies (ANCA) (controversial) 4) anti-endothelial cell antibodies
Genes associated with TAO
1) England: HLA-A9 and HLA-B5 2) Israel: HLA-DR4 and low HLA-DRW6 3) India: HLA-DRB1*1501
Hypercoagulable states in TAO
controversial 1) lower levels of urokinase-plasminogen activator 2) lower levels of plasminogen activator inhibitor 1 3) elevated platelet contractile force
Associated infectious cause of TAO
1) Treponema denticola 2) porphyromonas gingivalis 3) actinobacillus actinomycetemcomitans
Pathogenesis of TAO
1) endothelial cell damage 2) activation of APC 3) cellular and humoral inflammation 4) thrombotic occlusion
Which layer is affected in TAO
restricted to intima = endarteritis
Differentiating TAO from atherosclerosis in histology
Internal elastic lamina and architecture of vascular wall preserved in TAO
Three stages of TAO
1) acute phase: inflammation of small-medium (1-5mm) artery/vein - occlusive - cellular arterial thrombus - polymorphonuclear cell infiltrate - leukocytoclasis - giant cells - microabscess - inflammation of entire vessel wall - neurovascular bundle 2) intermediate/subacute phase: organization of occlusive thrombus - disappearance of microabscesses - CD3 pan, CD4 T cells, CD20 panB cells against internal elastic lamina - CD68 macrophage and S100 dendritic cells in intima - IgG, IgM, IgA, complement 3d 4c on internal elastic lamina 3) Chronic phase/end-stage: thrombus organization and recanalization - prominent vascularization of media - perivascular fibrosis
Phlebitis saltans define
Migrating phlebitis in 40-65% of TAO patients
How often are venous involvements in TAO
60% mostly superficial, DVT unusual
Symptoms of TAO and rate
TABLE 138.2