biopsy of temporal giant cell arteritis will show...
inflamed vessel wall with giant cells fibrosis between media and intima BUT negative biopsy doesn't exclude disease...might not have been in that segment
how to treat takayasu arteritis?
risk factors of essential HTN
age, race, obesity, smoking, stress, lack of physical activity, excess salt
caused by alcoholism
complications of HTN?
renal (renal failure) CV (MI) brain (stroke) eye (hypertensive retinopathy)
three pathogenesis that weaken wall and lead to aneurym
CT disorders matrix metalloprotease (MMP breaks down elastin) antherosclerosis
henoch schonlein purpura
vasculitis with all lesions same stage? varying stages?
same stage = microscopic polyangiitis varying = polyarteritis nodosa
why is henoch schonlein purpura usually after upper respiratory tract infection?
because IgA levels are increased to protect mucosal surfaces
what does smoking increase?
what tumor is associated with PVC, arsenic, and thorotrast exposure?
HSP henoch schonlein purpura
small vessel vasculitis due to IgA immune complex deposition; children; palpable purpura on buttocks and legs, GI pain/bleeding, hematuria, post-respiratory tract infection, proteinuria treat w steroid or will self-resolve
complications of atherosclerosis
stenosis --> impaired blood flow and ischemia --> peripheral vascular disease, angina (coronary a), and IBD (mesenteric a) rupture --> emboli or thrombosis --> MI, stroke, aneurysm
fatty streak histology =
foam cells (macrophages full of lipid) and t lymphocytes
medium vessel, necrotizing vasculitis involving DIGITS symptoms - ulcers, gangrene, autoamputation of digits, raynauds phenomenon treat - stop smoking
hemoglobin A1c indicates
diagnostic features of polyarteritis nodosa?
serum HBsAg (hep B surface antigen) segmental, lesions of varying stage string of pearls = dilatation + fibrous nodes(fibrinoid necrosis
churg strauss syndrome
small vessel necrotizing granulomatous vasculitis with eosinophils; multiple organs expecially lungs and heart serum p-ANCA
hyperplastic arteriolosclerosis is caused by
elevated CRP and cholesterol crystals and foam cells indicate
medium vessel necrotizing vasculitis involving most organs (LUNGS ARE SPARES) in young adults lesions of varying stages symptoms - HTN (renal a), abdominal symptoms (mesenteric a), neurologic issues, skin lesions
c reactive protein marker of inflammation
calcification of the media
monckeberg medial sclerosis
response to endothelium injury
injury --> lipid accumulation in intima --> t lymphocytes release interferon -->monocyte/platelet recruitment/adhesion/emigration --> macrophage activation and smooth m recruitment --> lipid/oxidized LDL is engulfed by both --> smooth m proliferation and ecm/collagen deposition + remodeling --> smaller lumen, weakened wall, scarring expansion encroaches on media and adventitia and narrows lumen --> nutrients not reaching full thickness --> necrosis
causes of aortic dissection
HTN is most common CT disorder - Marfans (fibrillin) or Ehlers Danlos (collagen)
two types of ANCA
cANCA is in cytoplasm periphery = Wegener granulomatosis pANCA is in nucleus periphery = microscopic polyangiitis and churg strauss syndrome
intima tears and blood dissects through media creating false channel sharp radiating chest pain to back, proximal 10 cm of aorta due to preexisting media weakness due to HTN or genetic CT disorder
intimal plaque that obstruct blood flow --> chronic inflammation and progressive accumulation
ulcers, gangrene, raynauds, autoamputation of digits
thickened vessel wall by hyperplasia of smooth muscle onion skinning appearance BP>20/120, leads to reduced vessel caliber and end organ ischemia, renal failure w flea bitten appearance