NURS113 Lecture 13: NURS113 - UNIT 7

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UNIT 7: CARDIOVASCULAR SYSTEM DISORDERS
Part 1
Coronary artery disease (CAD)
- Two sides to the heart they work independently and have different roles
- Umbrella term for ischemic heart disease and coronary heart disease
- Your oxygen demand is higher than the oxygen supply
- Imbalance between the oxygen being supplied to the heart and the demand (so the
myocardium needs a lot of oxygen but you do not have a lot of oxygen in the blood)
- Insufficient delivery of oxygenated blood to the myocardium due to atherosclerotic coronary
arteries
- When plaque (made from nutrients left back by the blood) builds up in the blood vessels
and causes it to harden and narrow the lumen
- As such, there is an imbalance between oxygen supply and demand
- Since the vessels are narrowing in diameter so it is harder to transport blood from
place to place
- This may lead to
- Angina pectoris
- Chest pain
- Myocardial infarction
- Myocardial ischemia
- Dysrhythmias
- Abnormal rhythms of the heart → sometimes called lethal because heart
is not working effectively at all
- Chronic heart failure (CHF) → or congestive heart failure
- Sudden cardiac death
- You have cardiac arrest and the heart stops working
- The main cause of CAD is atherosclerosis
- Aorta, coronary arteries or cerebral arteries (so ATHERO IS ONLY THESE THREE!)
- Pathogenesis of atherosclerosis
- Arteriosclerosis → hardening of the
arteries
- Atherosclerosis is a specific
type of arteriosclerosis
- It is when lipid
plaques from on the
inside of the aorta,
coronary arteries
(heart) , cerebral
arteries (brain)
which cause all of
them to become
narrowed and stiff
- What can cause this?
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-First step, damage to the endothelial cells of the artery (hypertension, smoking,
increased BG, hypercholesterolemia)
- The inner lining of the arteriole the endothelial gets damaged → so any
toxins that can damage the inner layer of the arteriole
-Second step, formation of foam
cells
- LDL and monocytes
move between the
endothelial cells into the
tunica intima
(diapedesis)
- After the endothelial
cells are damaged then
the endothelial cells and
monocytes move into the
arteries (the tunica intima)
- Then monocytes release free radicals that damage the endothelial
layer even more
- Monocytes release free radicals, which oxidize the LDL (low density
lipoproteins)
- So bad lipid
- Foam cells → monocytes that engulf the LDL
- The free radicals oxidize the LDL and then the monocytes engulf
this LDL and then become foam cells
- SO BASICALLY FIRST THE MONOCYTES GO INTO THE
ARTERIOLE AND RELEASES FREE RADICALS TO
FURTHER DAMAGE THE ENDOTHELIAL LAYER, WHICH
OXIDIZES LDL WHICH THEN CAUSES MONOCYTES TO
ENGULF THE LDL and then more monocytes come in and etc
etc
- Positive feedback system
- Spiralling production of foam cells -->nothing is stopping the
production of foam cells in this process
-Third step, formation of plaque
- Can partially or completely occlude the artery
- The foam cells are created and attract more things to them, such
as platelets, smooth muscle cells and the T lymphocytes →
which develops plaque (positive feedback system)
- The more big the plaque gets it attracts even MORE T
cells and platelets and smooth muscle cells → nothing to
stop it
- The plaque grows larger
- T cells, platelets and smooth muscle cells join the foam cells
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- Platelets get activated and form a blood clot over the plaque
- Overtime, calcium salts added and plaque hardens with a lipid core →
the calcium causes the plaque to be a big hard piece of material
- You get a blood clot forming over the plaque; the blood clot can
rupture and dislodge the clot over it
- If it blocks artery there called thrombus
- If moves and goes other places to occlude then it is
embolus
- Collateral circulation develops
- This takes 20-25 or 35 years (formation of plaque), but as it is
developing in the artery and slowly cutting off circulation, then it
is called collateral circulation
- The heart adapts to this blockage in the arterioles by
creating collateral circulation; so basically little
arterioles around the blocked artery develop so that they
can still be able to bring blood to the heart muscle (since
there is decreased blood flow in arteriole where the
plaque is)
- Minor vessels enlarge and join together to keep the blood flow
DISTAL to obstruction
- Eventually
- Blood clot may block the vessel wall
- Or break off and occlude another blood vessel
-TLDR: SO BASICALLY, endothelial cells get damaged, causes increased permeability and
allows LDLs and monocytes to enter from lumen to the tunica intima. Monocytes release free
radicals, free radicals oxidizes LDLs, and then oxidized LDLs are engulfed by monocytes, which
get bigger and reduce even more free radicals and the cycle goes on. These monocytes that have
engulfed a lot of LDLs = foam cells. Then, formation of the plaque occurs; so the foam cells start
to sequester other
stuff as well, such as
platelets and T cells
from the outside
which starts to get
bigger and bigger and
occludes the lumen.
Endothelial cell
grows on top and
calcium salts get
absorbed so the
plaque becomes
hardened. And then
because there is an
occlusion, platelets
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Document Summary

Two sides to the heart they work independently and have different roles. Umbrella term for ischemic heart disease and coronary heart disease. Your oxygen demand is higher than the oxygen supply. Imbalance between the oxygen being supplied to the heart and the demand (so the myocardium needs a lot of oxygen but you do not have a lot of oxygen in the blood) Insufficient delivery of oxygenated blood to the myocardium due to atherosclerotic coronary arteries. When plaque (made from nutrients left back by the blood) builds up in the blood vessels and causes it to harden and narrow the lumen. As such, there is an imbalance between oxygen supply and demand. Since the vessels are narrowing in diameter so it is harder to transport blood from place to place. Abnormal rhythms of the heart sometimes called lethal because heart is not working effectively at all. Chronic heart failure (chf) or congestive heart failure.

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