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33 Cards in this Set

  • Front
  • Back
tunica media – rich in elastic tissue
aorta and its major branches (Large elastic Arteries)
tunica media – concentric layers of smooth muscle cells, outer limit is external elastic lamina.
Medium sized muscular arteries (greater than 2 mm diameter)
rich in autonomic nerves for maintenance of blood pressure.
small arteries and arterioles
Veins histology
thin walled vessels with relatively large lumina; tunicas not well defined; valves found in many veins.
Veins are predisposed to
dilatation, compression, penetration by tumors and inflammatory processes because of thin walls.
Lymphatics histology
extremely thin walled vessels lined by endothelial cells not containing red cells.
Lymphatics major functions
drainage system.
Lymphatics play a role in pathogenesis in
dissemination of disease (bacteria, tumor).
VASCULAR WALL RESPONSE TO INJURY
The response is carried out by endothial cells and smooth muscle cells. Damage of endothelium and then smooth muscle from the tunica media migrates into the intima and proliferates. This proliferation is not of smooth muscle cells but as fibroblast which lay collagen. Intima thickens which is bad because it causes narrowing of the lumen-atherosclorosis, hypertension
Congenital Anomalies-e.g aneurysms are often asymptomatic but, play an important role in
in surgical operative technique
Young guy lies down, dies.
Berry Aneurysm
developmental weakness in cerebral vessels (circle of Willis) which yield to thrust of blood pressure leading to formation of a small saccular aneurysmal outpouchings
Berry Aneurysm
Where does Berry aneurysm usually happen?
bifurcation or branching points
The developmental weakness that leads to berry aneurysm is due to
poorly developed musculature in tunica media with eventual degeneration of elastic lamina
Berry aneurism leads to death when
rupture leading to subarachoid or intracerebral hemorrhage.
what are the classifications of Atherosclerosis
1) Atherosclerosis.(most significant form of arteriosclerosis)
2) Monckeberg medial calcific sclerosis.
3) Arteriolosclerosis. (hardening of the arterioles)
Involves elastic arteries (e.g. aorta, carotid, iliac) and large and medium sized muscular arteries (e.g. coronary, popliteal).
Atherosclerosis. Formation of atheroma (fibrofatty plaques) protruding into lumen and weakens media.
Number one cause of death in Western world.
Atherosclerosis.
Atherosclerosis can damage other organ systems like
1) Ischemic heart disease – myocardial infarction.
2) Cerebral infarction.
3) Aortic aneurysms.
4) Gangrene of legs.
5) Mesenteric ischemia.
Atheromatous plaque which occur mainly in the Abdominal aorta, coronary, popliteal, descending thoracic aorta, cerebral. morphology is
raised focal plaque within intima, having a core of lipid (mainly cholesterol) covering fibrous cap (smooth muscle cells, macrophages, new vessels) and underlying smooth muscle proliferation-lumen narrowing.
Atherosclerosis complications
1) Calcification.
2) Rupture or ulceration.
3) Hemorrhage.
4) Thrombosis.
5) Aneurysm.
1) Precursor of atherosclerosis.
2) No vascular disturbance.
Fatty streak.
Atherosclerosis Nonmodifiable.-(nothing we can do about these) risk factors.
1) Age
2) Sex-males more predisposed due to estrogen, females catch up after menopause
3) Genetics-diabetes, hypertension
Potentially Controllable
Atherosclerosis factors
1) Hyperlipidemia.-most important of the controllable factors

2) Hypertension.
3) Smoking.
4) Diabetes.
5) Homocysteine.
a) Elevation caused by low folate.
6) Obesity.
7) Physical inactivity.
8) Stress (Type A personality).
9) Post menopausal estrogen deficiency?- at first it was thought that givin estrogen was protective, but this is controversial.
=Hyperlipidemia levels of cholesterol are
Increased LDL cholesterol
Decreased HDL cholesterol
When cholesterol is floating around bound to proteins is known as
lipoproteins. These exists as low density lipoprotein and high density lipoprotein.
the protein part of the lipoprotein
Apolipoprotein A.-found in HDL-good
Apolipoprotein B.-found in the LDL-bad
Total cholesterol and HDL cholesterol can be directly tested, but how is LDL calculated?
Total cholesterol = HDL chol + LDL chol + VLDL chol.

VLDL chol = triglycerides/5.
LDL chol = (Total chol)-(HDL chol)-(tryglycerides/5).
LDL calculation is usually effective except when
there is abnormality in lipid levels so then a test to directly measure LDL is ordered.
What is the tx of hyperlipedemia
LDL cholesterol levels.
Other risk factors.
Ischemic heart disease.
Atherosclerosis risk factors are divided into
Nonmodifiable
Potentially Controllable

Factors affecting Hemostasis and Thrombosis.
Factors affecting Hemostasis and Thrombosis.
1) C reactive protein.-identifies patients with atherosclerotic inflammation.
Atherosclerosis pathogenesis
a. Chronic endothelial injury.

b. Lipoproteins (LDL cholesterol) into vessel wall.

c. Blood monocytes →macrophages → foam cells.

d. Platelet adhesion.

e. Migration of smooth muscle cells from media into intima.

f. Proliferation of smooth muscle cells in intima with accumulation of collagen and proteoglycans – intimal thickening.

g. Enhanced accumulation of lipids.

h. Stenosis or occlusion of vessel.