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43 Cards in this Set
- Front
- Back
vascular wall components
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endothelial cell
smooth muscle cells extracellular matrix |
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vascular wall architecture
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Tunica intima - endothelium + internal elastic lamina
Tunica media - mostly smooth muscle cells tunica adventitia - external elastic lamina + extracellular matrix + vasa vasorum |
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neointima
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proliferation of smooth muscle cells and extracellular matrix within the intma -> thickening of the intima
occurs due to vascular intimal injury can cause stenosis or occlusion |
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pericytes
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modified SMC on capillaries, precapilary arterioles, and postcapillary venules
support, contract and regulate endothelial cells can atrophy or become neoplastic |
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arteriosclerosis
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hardening of arteries due to thickening and loss of elasticity
atherosclerosis monckeberg medial calcific sclerosis arteriolosclerosis |
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Monckeberg medial calcific sclerosis
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dystrophic calcification of media or internal elastic lamina of muscular arteries
> 50yo unknown etiology - more frequent with diabetes mellitus hard, dialated arterys can are palpable and seen on radiograph see concentric dystrophic calcification and osseous metatplasia - no encroachment on vascular lumen |
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atheroma
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intemal thickening leading to fibrous cap and a lipid accumulation leading to a lipid core
composed of ECM, cells (macrophages, lymphocytes), lipids seen in abdominal aorta (MC), coronary arteries, popliteal arteries, internal carotid, circle of willis |
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Fatty dot/streak
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see normally in aorta in childhood or coronary arteries in adolescence
these can progress to atheroma |
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2ndary changes of atheroma
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atrophy of underlying media
neovascularization calcification |
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worst consequence of atherosclerotic lesion in coronary artery
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rupture of plaque -> thrombosis -> occulsion
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consequences of atherosclerosis
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hemorrhage into plaque -> stenosis or ruptures plaque -> thrombosis and/or embolism (of the thrombus or of cholesterol)
aneurysmal dilation due to media weakening - most common abdominal aorta near bifurcation of illiac stenosis/occlusion due to a plaque leargement -> MI, stroke, peripheral artery disease (often in leg -> gangrene), infarcts, chronic ischemic disease embolization |
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chronic ischemic heart disease
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state of reduced blood flow to heart muscle due to partial occlusion of coronary arteries
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vascular interventions
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balloon angioplasty - Percutaneous transluminal coronary angioplasty (PTCA)
stent placement vascular placement coronary artery bypass graft surgery |
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balloon angioplasty
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aims to expand a narrowed part of a vessel
can cause: ruptures plaque, stretches media, and can cause medial dissection often recloses chronic complications: proliferative restenosis through simulation of EC and SMC -> neointima |
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proliferative restenosis
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can get EC injury and SMC stimulation during balloon angioplasty
-> neointima |
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endovascular stents
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provides a scaffold to damaged blood vessels, limits vascular reactions
but, can get endothelial damage and medial stretching complications: thrombosis and intimal thickening -> restenosis need to use drugs |
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hypertension
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a multiorgan, systemic disorders which is a SIGN of high blood pressure (>140/90)
2types: primary or 2ndary |
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primary hypertension aka essential hypertension
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indopathic, multifactorial cause
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secondary hypertension
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has a known cause
usually renal but can be endocrine, CV, neurological |
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arteriolosclerosis
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thickening of walls of arterioles and small arteries
caused by hypertension |
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cell that is the number 1 player in the onset HTN
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endothelial cells
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benign hypertension
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systolic BP < 200 mmHg
diastolic BP < 120 mmHg hemodynamic stress -> EC injury -> leakage of plasma across endothelium + excessive ECM production by SMC -> thickening of arterial walls and loss of architecture (arteriolosclerosis) eventually luminal stenosis |
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malignant hypertension
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5% of htn patients
RAPID rise in BP systolic > 200 mmHg diastolic > 120 mmHg very dangerous leads to hyperplastic arteriolosclerosis - hyperplastic SMC with thickened basement membrane - onion skin lesion also see necrotizing arteriolitis - fibrinoid necrosis |
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hyperplastic arteriolosclerosis
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hyperplastic SMC caused by malignant hypertension
thickened basement membrane -> lumenal stenosis ONION SKIN LESION |
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nephrosclerosis
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renal scarring due to ischemia - associated with sclerosis and eventually stenosis
associated with chronic htn, or diabetes mellitus look for: arteriolonephrosclerosis (aterniolosclerosis of renal vessels) cortical scars and granular renal surface sclerosis of interlobular and acruate arteries severe form associated with malignant hypertension -> renal failure |
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benign hypertension
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systolic BP < 200 mmHg
diastolic BP < 120 mmHg hemodynamic stress -> EC injury -> leakage of plasma across endothelium + excessive ECM production by SMC -> thickening of arterial walls and loss of architecture (arteriolosclerosis) eventually luminal stenosis |
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malignant hypertension
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5% of htn patients
RAPID rise in BP systolic > 200 mmHg diastolic > 120 mmHg very dangerous leads to hyperplastic arteriolosclerosis - hyperplastic SMC with thickened basement membrane - onion skin lesion also see necrotizing arteriolitis - fibrinoid necrosis |
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hyperplastic arteriolosclerosis
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hyperplastic SMC caused by malignant hypertension
thickened basement membrane -> lumenal stenosis ONION SKIN LESION |
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nephrosclerosis
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renal scarring due to ischemia - associated with sclerosis and eventually stenosis
associated with chronic htn, or diabetes mellitus look for: arteriolonephrosclerosis (aterniolosclerosis of renal vessels) cortical scars and granular renal surface sclerosis of interlobular and acruate arteries severe form associated with malignant hypertension -> renal failure |
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hypertensive retinopathy (retinal arteriolosclerosis) - early lesions
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mural thickening ->
1. arteriovenous nicking -> where arteriole and venule cross - due to thickened walls of artery -> compression of vein 2. copper wiring look due to thickened walls 3. silver wiring is seen as the walls become so thick the vessel is now completely opaque also see vascular damage - leak and exudates can see this through opthalmascope |
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hypertensive retinopathy (retinal arteriolosclerosis) - late lesions
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flame hemorrhage
exudates chroidal, retinal infarcts -> 1. cytoid bodies 2. cotton wool spots - collection of swollen axons optic disk edema |
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small vessel vasculitis types
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non-immune complex:
microscopic polyangitis (no asthma or granulomas) wergner granulomatosis (granulomas, no asthma) churg-strauss syndrome (granulomas + asthma + eosiniophilia) immune complex mediated: SLE vasculitis Henoch-Schonlein (IgA) cryoglobulin vascuilitis goodpasture disease |
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medium vessel vasculitis
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immune complex:
polyarteritis nodosa anti-endothelial cell antibodies: kawasaki disease |
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large vessel vasculitis
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mostly granulomatous disease:
giant cell (temporal) arteritis, Takayasu arteritis |
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giant cell (temporal) arteritis
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>50yo
most common systemic vasculitis in US adults large to medium sized arteries: mostly temporal artery, also vertebral, OPTHTHALMIC, aorta possible blindness due to effect on opththamic jaw claudication morphology: -granulomatous medial inflammation -fragmentation of internal elastic lamina -mural thickening, luminal narrowing -see giant cells |
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Takayasu arteritis
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<40 year asian female
large to med size arteries -> aortic arch and its branches, pulmonary arteries --> see "pulseless disease", cold fingers, low BP, pulm htn, ocular problems, stroke, MI may involve renal arteries -> systemic htn may involve distal aorta -> leg claudication see alternating aneurysms and luminal stenosis mononuclear cells invade from adventitia toward the intima -> thickened intima -> possible arthersclerosis +/- granuloma |
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Buerger disease
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see in SMOKERS age <35
med to small arteries of distal extremities - possible involvement of veins and NERVES - pain transmural, segmental vasculities -> progressive vascular insufficiency -> claudication, pain, ulcers, GANGRENE |
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polyarteritis nodosa (PAN)
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any age but peak in young adults, M>F
med to small vessels - *kidneys*, heart, liver, GI SPARES pulmonary artery associated with HBV and HCV, no association with ANCA acute inflammation with mixed cells attracted to immune complex -> necrosis chronic-> fibrous mural thickening -ongoing due to continuous circulation of antigen - see all stages of activity present in different vessels or parts of vessels see thrombosis, stenosis, weakening of wall -> ischemia, infarct, aneurysm clinical manifestation depends on organ: renal failure major cause of death |
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Kawasaki disease
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endemic to Japan
most common type of acquired heart disease in North American children medium sized arteries - CORONARY ARTERIES thought to be caused by unknown antigen/superantigen -> delayed type hypersensitivity -> B cell activation -> autoantibody looks like polyarteritis nodosa morphology KEY: coronary artery aneurysms -> thrombosis, rupture -> MI also see mucocutaneous disease - high fever, conjunctivitis, oral/oralpharyngeal, palms and soles |
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Microscopic polyangiitis
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adults usually
arterioles, capillaries, venules skin - palpable papura multisystemic effects drug etiology most often but can see with henoch-schonlein purpura, cryoglobulinemia, vasculitis associated with autoimmune disease most are type II - p-ANCA (anti-MPO, MPO-ANCA) type III - immune complex neutrophilic vasculitis - leukocytoclasis, no granulomas erythrocyte extravasation late changes - necrotizing glomerulonephritis, pulmonary capillaritis (see hematuria, hemoptysis) all lesions will be the same stage - suggests single exposure |
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Churg-Strauss Syndrome - allergic angiitis and granulomatosis
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associated with asthma, eosinophilia
med to small arteries, veins - skin (palpable purpura), lungs, heart, kidney see granulomas, eosinophils - necortizing vasculotis p-ANCA |
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Wegener granulomatosis
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triad of organs: kidney, upper respiratory (ENT), lower respiratory (lung)
lesion triad: respiratory - parenchymal granulomas (noncaseating), pneumonitis, aerodigestive tract ulcers vascular - necrotizing granulomatous vasculitis renal med to small vessels M>F 5th decade c-ANCA (PR3-ANCA) |
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infectious arteritis
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bacteria:
ricksetta - neutrophilic pseuodomonas spirochetes - plasmacytic fungi: aspergillosis, mucormycosis -> mycotic aneurysms |