2nd Exam: Vascular Diseases - Part 2 Flashcards by Tedman McMahon

Leading cause of death in U.S.

CV d.

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Earliest change in ath:

fatty streak, thickening of intima

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wavy pink lines in normal aorta:

elastic laminae

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all plaques are in this layer of blood vessels:

tunica intima

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Fatty streaks are commonly distributed around these structure:

ostia of small branches

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ath pls are more common here:

branch points, due to turbulence and shear stress on vessel surface

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What happens after fatty streak formation?

development of fibro-fatty plaques

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fibro-fatty plaques are made of:

dense tissue and lipid

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Most advanced plaques:

“complicated” by ulceration, hemmorhage, thrombosis, or calcification

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atheroma:

Vessel wall degeneration, due to fat build up and scar formation, restricts blood, can lead to thrombus formation

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intima below a complicated plaque:

increased spaces, needle like clefts, cholesterol crystals dissolved out (cholesterol clefts)

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TF? Fatty deposits are more common in adults.

F. children, highest at 12 yo

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Fatty fibrous plaque are commonly seen in this age range:

10-65yo, 32yo most common

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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

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Intima includes:

endo and subendothelial layers

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Adventitia is related to:

vasovorum (?)

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Media of normal muscular artery is composed of:

sm (meaty-a)

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Closer to the endothelium, internal or external elastic lamina:

internal

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Pathogenesis of ath:

chronic endo injury

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Causes of chronic endo injury:

hyperlipidemia, hypertension, smoking, homocysteine, blood flow, toxins, viruses, immune reactions, shear stress

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Causes of endo dysfunction:

inc permeability, WBC adhesion

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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

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When can you see the fatty streak with the naked eye?

Once macs and sm cells engulf the lipid in the intima

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Earliest form of sclerosis:

rigid internal elastic, straight, thickened intima

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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:

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.

HD kills __ times as many WNY women as breast cancer.

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