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43 Cards in this Set

  • Front
  • Back
vascular wall components
endothelial cell

smooth muscle cells

extracellular matrix
vascular wall architecture
Tunica intima - endothelium + internal elastic lamina

Tunica media - mostly smooth muscle cells

tunica adventitia - external elastic lamina + extracellular matrix + vasa vasorum
neointima
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
pericytes
modified SMC on capillaries, precapilary arterioles, and postcapillary venules

support, contract and regulate endothelial cells

can atrophy or become neoplastic
arteriosclerosis
hardening of arteries due to thickening and loss of elasticity

atherosclerosis

monckeberg medial calcific sclerosis

arteriolosclerosis
Monckeberg medial calcific sclerosis
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
atheroma
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
Fatty dot/streak
see normally in aorta in childhood or coronary arteries in adolescence

these can progress to atheroma
2ndary changes of atheroma
atrophy of underlying media

neovascularization

calcification
worst consequence of atherosclerotic lesion in coronary artery
rupture of plaque -> thrombosis -> occulsion
consequences of atherosclerosis
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
chronic ischemic heart disease
state of reduced blood flow to heart muscle due to partial occlusion of coronary arteries
vascular interventions
balloon angioplasty - Percutaneous transluminal coronary angioplasty (PTCA)

stent placement

vascular placement

coronary artery bypass graft surgery
balloon angioplasty
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
proliferative restenosis
can get EC injury and SMC stimulation during balloon angioplasty

-> neointima
endovascular stents
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
hypertension
a multiorgan, systemic disorders which is a SIGN of high blood pressure (>140/90)

2types: primary or 2ndary
primary hypertension aka essential hypertension
indopathic, multifactorial cause
secondary hypertension
has a known cause

usually renal but can be endocrine, CV, neurological
arteriolosclerosis
thickening of walls of arterioles and small arteries

caused by hypertension
cell that is the number 1 player in the onset HTN
endothelial cells
benign hypertension
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
malignant hypertension
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
hyperplastic arteriolosclerosis
hyperplastic SMC caused by malignant hypertension

thickened basement membrane -> lumenal stenosis

ONION SKIN LESION
nephrosclerosis
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
benign hypertension
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
malignant hypertension
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
hyperplastic arteriolosclerosis
hyperplastic SMC caused by malignant hypertension

thickened basement membrane -> lumenal stenosis

ONION SKIN LESION
nephrosclerosis
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
hypertensive retinopathy (retinal arteriolosclerosis) - early lesions
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
hypertensive retinopathy (retinal arteriolosclerosis) - late lesions
flame hemorrhage

exudates

chroidal, retinal infarcts ->
1. cytoid bodies
2. cotton wool spots - collection of swollen axons

optic disk edema
small vessel vasculitis types
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
medium vessel vasculitis
immune complex:
polyarteritis nodosa

anti-endothelial cell antibodies:
kawasaki disease
large vessel vasculitis
mostly granulomatous disease:
giant cell (temporal) arteritis, Takayasu arteritis
giant cell (temporal) arteritis
>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
Takayasu arteritis
<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
Buerger disease
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
polyarteritis nodosa (PAN)
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
Kawasaki disease
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
Microscopic polyangiitis
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
Churg-Strauss Syndrome - allergic angiitis and granulomatosis
associated with asthma, eosinophilia

med to small arteries, veins - skin (palpable purpura), lungs, heart, kidney

see granulomas, eosinophils - necortizing vasculotis

p-ANCA
Wegener granulomatosis
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)
infectious arteritis
bacteria:
ricksetta - neutrophilic
pseuodomonas
spirochetes - plasmacytic

fungi:
aspergillosis, mucormycosis -> mycotic aneurysms