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30 Cards in this Set

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fibromuscular dysplasia
focal irregular thickening of walls of medium-sized and large muscular artieries - see areas of thickening separated by aneurysm

idiopathic, effects young women most often

renal artery -> renovascular hypertension
aneurysm
localized abnormal dilation of a blood vessel or cardiac chamber

caused by a weakness in the wall - usually tunica media (muscular layer)

a true aneurysm is bounded by vascular wall components with luminal dilation
false aneurysm
pseudo-aneurysm

breach THROUGH WALL-> EXTRAvascular hematoma
dissection
split within vessel wall due to breach through endothelium - hematoma dissects BETWEEN layers of wall

doesnt necessarily cause a dilation
most common cause of arterial aneurysms
atherosclerosis
arterial aneurysm etiology and pathogenesis
due to atherosclerosis, connective tissue disease, or idiopathic

intimal thickening causing ischemia of media -> smooth muscle cell loss/dmg (erdheim medial degeneration) - replacement with ECM

inflammation -> MMP production of macrophage -> ECM degredation

overall: decrease in wall strength

made worse by hypertension which causes artheriolosclerosis of vasa vasorum -> ischemia of OUTER media
erdheim medial degeneration morphology
see elastic tissue fragmentation and separation of elastic and fibromuscular elements with cyst like spaces filed with ECM (GAGs)
abdominal aortic aneurysm
smokers > 65

located most often distal to renal arteries

most often due to atherosclerosis

also can be caused by altered ECM - scurvy, marfan

worry about ruptures - especially after > 5cm, high mortaility

also...can obstruct branches (renal a.), create emboli, impinge on other structure (duodenum)

doesn't get occluded because aorta is big

asymptomatic until you see one of these complications - dangerous
thoracic aortic aneurysm
rare compared to AAA

descending is same as AAA - atherosclerosis

ascending causes:
1. erdheim medial degeneration
2. atherosclerosis
3. syphilitic aortitis

#1 risk factor - hypertension

complications:
aortic ring dilation -> aortic insufficiency -> CHF

rupture, encroachment
syphilitic aneurysm
tertiary syphilis -> plasmacytic vasculitis of vasa vasorum

--> obliterative endarteritis -> ischemic necrosis of aortic media -> loss of elastic recoil -> dilation

"tree-barking" subintimal depression
aortic dissection
5-6th decade

hypertension is biggest factor

other factors: CT disease, marfans, pregnancy, iatrogenic

between middle and outer 1/3 of media

blood enters through a tear - most idiopathic, in ascending aorta

creation of a false lumen

worst complication - rupture through adventitia -> hemorrhage

intimal rupture (back into original lumen) -> "double barreled aorta" - not as bad

can extend dissection to the valves -> disruption
or
extend to other vessels -> obstruction (carotids, coronary)
aortic dissection classification
type A - proximal (arch) +/- distal

type B - distal descending
aneruyrsm repair
vascular replacement using dacron or gortex - but can lead to stenosis, occlusion due to thrombosis or neointima

stent graft - less invasive
endoluminal approach
varicose veins
most common venous lesion

abnormally dilated, tortuous veins, created by prolonged intraluminal pressure, loss of vascular wall support

often in superficial (saphenous veins) of lower extremity

increasing age -> prolonged upright position, degenerative veins, loss of CT

pregnancy, obesity

mostly a cosmetic issue, but can cause stasis -> decrased wound healing -> varicose ulcers
T/F primary tumors of large vessels are rare
True
benign vascular neoplasms
hemangioma

lymphangioma

glomus tumor
bacillary angiomatosis
nonneoplastic vascular tumor - REACTIVE

Bartonella infection (cat scratch disease)
-> vascular proliferation -> red papules/nodules

AIDS predisposed
Vascular ectasias
dilation of pre-existing vessles

examples:
nevus flammus (port-wine stain)

spider telangiectasia

hereditary hemorrhagic telangiectasia (osler-weber-rendu disease)
nevus flammeus
port wine stain - dilated dermal vessels

associated with sturge-weber syndrome and other syndromes
sturge-weber syndrome
nevus flammeus

leptomeningeal angiomas

mental retardation
spider telangiectasia
effects subcut arterioles and small arteries

often due to increased estrogen - pregnancy, cirrhosis
hereditary hemorrhagic telangiectasia (osler-weber-rendu disease)
auto dom

congenital dilated capillaries, veins in skin and mucous membranes

see mucosal bleeding - GI bleeds
hemangioma
most common vascular tumor
most common pediatric neoplasm

see well formed vascular channels

capillary type - superficial skin/mucous membranes - see pyogenic granuloma - pregnancy

cavernous type - see in deep soft tissues
lymphangioma
subcutaneous

capillary type - lymphangioma circumscriptum

cavernous - cystic hygroma
glomus tumor (glomangioma)
see in distal digit under the nail - very painful

from glomous body - arteriovenous thermoreceptor important for regulating arterial blood flow
karposi sarcoma
slit like cells

spindle cells

intermediate grade vascular neoplasms - minimal anaplasia, local invasion, low metastatic potential
hemangioendothelioma
see plump vacuolated cells

vessels are variable

few mitosis

intermediate grade vascular neoplasm - minimal anaplasia, local invasion

met rate 20-30%
angiosarcoma
malignancy of endothelial cells

hemangiosarcoma - vinyl chloride exposure

lymphangiosarcoma - chronic lymphedema

highly malignant

CD31 is endothelial cell marker

5 year survival 30%
hemangiopericytoma
neoplasm of pericytes

see in soft tissues - retroperitoneum and lower extremities

5 year survival 60-80%
CD31
distinguish angiosarcoma (CD31+) from hemangiopericyoma (CD31-)