2nd Exam: Vascular Diseases - Part 2 Flashcards
Leading cause of death in U.S.
CV d.
Earliest change in ath:
fatty streak, thickening of intima
wavy pink lines in normal aorta:
elastic laminae
all plaques are in this layer of blood vessels:
tunica intima
Fatty streaks are commonly distributed around these structure:
ostia of small branches
ath pls are more common here:
branch points, due to turbulence and shear stress on vessel surface
What happens after fatty streak formation?
development of fibro-fatty plaques
fibro-fatty plaques are made of:
dense tissue and lipid
Most advanced plaques:
“complicated” by ulceration, hemmorhage, thrombosis, or calcification
atheroma:
Vessel wall degeneration, due to fat build up and scar formation, restricts blood, can lead to thrombus formation
intima below a complicated plaque:
increased spaces, needle like clefts, cholesterol crystals dissolved out (cholesterol clefts)
TF? Fatty deposits are more common in adults.
F. children, highest at 12 yo
Fatty fibrous plaque are commonly seen in this age range:
10-65yo, 32yo most common
Greatest increase risk for complicated plaques are between these years:
33yo-43yo and 58yo-65yo, % affected always increasing after 32yo, steeper increases bw those age ranges
Intima includes:
endo and subendothelial layers
Adventitia is related to:
vasovorum (?)
Media of normal muscular artery is composed of:
sm (meaty-a)
Closer to the endothelium, internal or external elastic lamina:
internal
Pathogenesis of ath:
chronic endo injury
Causes of chronic endo injury:
hyperlipidemia, hypertension, smoking, homocysteine, blood flow, toxins, viruses, immune reactions, shear stress
Causes of endo dysfunction:
inc permeability, WBC adhesion
Response to endo injury:
platelet aggregation at site of developing plaque, monocyte adhesion and emigration to intima, lipids accumulate in intima, sm emigration from media to intima, mac activation, macs and sm cells engulf lipid, lymphos also present
When can you see the fatty streak with the naked eye?
Once macs and sm cells engulf the lipid in the intima
Earliest form of sclerosis:
rigid internal elastic, straight, thickened intima
How is an artery affected with early plaque build up?
fibers don’t recoil, hardening of artery
Red staining in adventitia surrounding artery:
collagen (stains blue in other images)
Appearance of internal elastic in artery unaffected by plaque:
wavy appearance, black stained (healthy or unhealthy)
TF? Plaques are either circumferential or eccentric.
F. not circumferential
Plaques formation and location in layer of vesssl
eccentric almost always, intima
Composition of core of eccentric plaquez;
lipid/ cellular debris
Composition of fibrofatty atheroma/ eccentric plaque:
fibrous ct, fibroblasts, sm cells, lymphos, collagen, lipid debris, other ECM deposition, extracellular lipid
Complications that can arise from complicated plaques:
calcification, ulceration, thrombosis, hemorrhage, or rupture CUTHR
why do bvs grow into plaque during atheroma development?
part of inflammatory response
vasovasorum should be in this layer:
outer media, adventitia
Type of cap around lipid core of atheroma:
fibrous
Cause of rapid increase in plaque volume:
hemmorhage
Complications arising from hemmorhagic plaque:
decrease lumen diameter and blood flow
What splits when a plaque ruptures:
fibrous cap
Clefts are formed by:
cholesterol and lipids (removal of?)
ulceration, used to be:
a soft core of plaque
This can cause further embolization of material, likely to form a thrombus at this site
flow of blood into ulcerated plaque
Indication of dangerous plaque:
calcification, seriously afflicted with atherosclerosis
When might dentists see calcified plaque in the carotid artery?
panos
Calcifications almost always occur:
at bifurcations
Site of plaque formation is a characteristics of:
local blood flow in the area, determines location
Laminar flow is slower here:
boundary of vessel: stagnation point, separation zone, surface of separation
Sites of stagnation and “separation” of boundary layer:
in areas of curvature, esp distal to curvature
Eccentric ath plaques form in these zones:
zones of separation, outer border at beginning of curve, inner border past the curve
How could you test to see where eccentric plaque build up will occur?
iron particles and strobe light
Narrowing will happen in these sites of a vessel first with ath plaque:
areas of curvature, branch points
Location of static zone at branch points:
lateral walls that are contiguous w main branch
How to visualize narrowing a heart vessels:
angiogram
3 overlapping disease that contribute to atherothrombotic disesase
coronary a. d., cerebrovascular d., peripheral arterial d.
stroke, what type of d.?
cerebrovascular d.
heart attack, what type of d.?
coronary a. disease
Cx pres of chronic blockage in carotid and vertebrobasilar aa.:
transient ischemic attacks, atherosclerotic dementia
Cx pres. of acute blockage in carotid and vertebrobasilar aa.:
cerebral infarct (stroke)
Cx pres. of acute blockage in coronary artery:
MI
Cx px of chronic blockage in coronary artery:
angina pectoris
Cx px of chronic blockage in celiac and sup mes. a.:
intestinal angina
Cx px of acute blockage in celiac and sup mes. a.:
intestinal infarct
Cx px of chronic blockage in lower extremity:
intermittent claudication (cramping in leg induced by exercise)
Cx px of acute blockage in lower extremity:
limb gangren
Cx px of chronic blockage in aorta:
aneurysm
Cx px of acute blockage in aorta:
rupture, plaque embolism
TF? Chronic blockage in carotid and vertebrobasilar aa.: often leads to permanent brain damage.
F. symptoms disappear w/in 24h
True aneurysm:
sacular (eccentric) or fusiform (circumferential), lumen must enlarge
False aneurysm:
extravasation of blood forming hematoma, entire circ of vessel widened but not lumen, dissection can cause
Any blockage visible in an x-ray is:
complicated, die to calcification (check)
Effect on bv w calcification of atherosclerotic plaque:
enlarged and dilated
syphilytic aneurysm is more common in this vessel:
thoracic aorta
Where do most atherosclerotic aneurysms occur?
below the renal artery, abdominal aorta
Angiogram highlights these aspects of aortic aneurysm:
dilated lumen, fusiform swelling of vessel distal to the site, branch point constriction
Common finding in distal iliacs and femorals:
aneurysm chamber w large mural thrombus, calcification found in vessel walls and thrombus
As elastic tissues are pressurized further, what happens?
converted to fibrous scar tissue
Tx for abdominal aortic aneurysm:
sew endovascular stent graft into place after it is released from catheter
Dissecting hematoma is aka:
dissecting aneurysm
If blood leaves the lumen and enters the media of the aorta how can it spread?
by separating the elastic layers
Dissecting hematoma:
blood enters media of aorta from the lumen, separates elastic layers and spreads, can also come from bleeding from vasorum in the media
Where does dissection most often begin?
tear in intima
Type A Dissecting hematoma:
ascending, proximal aorta, may extend entire length
Type B Dissecting hematoma:
distal to origin of L subclavian a.
HD kills __ times as many WNY men as prostate cancer.
13
HD kills __ times as many WNY women as breast cancer.
10
Risk factors for HD:
high cholesterol, high BP, smoking, inactivaty
Risk factors for HD that can’t be changed:
family history, increasing age, male, race
Risk factors for HD that can be changed:
Smoking, inactivity and obesity, high fat and calorie diets, alcohol
5 components of successful wellness-promotion programs:
quit smoking, eat better, excercise, know numbers, take meds
Risk factors for HD that can be changed w meds:
BP, chol, blocked aa., diabetes, tendency to form thrombi, chronic inflammation
Med to prevent trhombi formation:
anticoagulant
TF? Acute perio disease is assoc with risk of heart attack.
F. chronic
Greatest risk factor for stroke and heart attack:
high BP
Lowering BP by 5mm reduces disease rates by:
30%
Fraction of WNYers that don’t know they have hypertension
1/2
Statin tx:
reduce plaque size, inc lumen size
Factors associated with increased rates of premature death (40s/50s):
childhood obesity, glucose intolerance (insulin resistance), hypertension
Smoking prevalence in WNY is __% higher than national avg:
4% (U.S.:23%, NY:24%, WNY:27%)
How long does risk of death due to smoking take to decrease to non-smoker rates after quitting?
2 y
