Atherosclerosis and Heart Disease Flashcards

1
Q

Atherosclerosis characterization

A

characterized by raised fibrofatty plaques in intimal lining of medium and large-sized blood vessels

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2
Q

atheromas

A

fatty material that builds up inside arteries

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3
Q

what does atheromas consist of?

A

foam cells, proliferating smooth muscle cells, extracellular lipids, fibrous tissue

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4
Q

atherosclerosis symptoms

A

process is usually asymptomatic until vessel is approximately 75% occluded

  • at this time, heart can show signs of ischemia (eg. angina) particulary during times of physical exertion
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5
Q

lipid metabolism pathway

A
  1. chylomicron
  2. lymph
  3. subclavian veins => chylomicron circulates in blood
  4. adipose tissues => release triglycerides for storage
  5. liver => absorbed and broken down -> triglycerides, cholesterol, vitamins
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6
Q

what is liver responsible for

A

producing cholesterol for cells of the body

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7
Q

chylomicron

A

lipids absorbed from GI tract bound to a lipoprotein

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8
Q

how can lipids be metabolized

A

have to be transported by being bound to lipoprotein

since lipids CANNOT be readily dissolved in blood plasma

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9
Q

types of lipoprotein

A
  • VLDL
  • LDL
  • HDL
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10
Q

cholesterol pathway

A
  1. VLDL (synthesized cholesterol and cholesterol from chylomicron)
  2. adipose tissue - release triglycerides for storage
  3. VLDL -> LDL
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11
Q

what does LDL do once converted from VLDL

A

circulate around body and deliver cholesterol to tissues
or
taken up by liver and recycled

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12
Q

what occasionally happens to LDL

A

can get consumed by macrophages
- plays a role in development of atherosclerosis

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13
Q

HDL

A

high-density-lipoprotein

  • produced in liver
  • released into blood and is reponsible for picking up access cholesterol from tissues and plays a scavenger role
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14
Q

what does HDL do to cholesterol

A

“drops-off” cholesterol at liver and is returned to circulation

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15
Q

what happens in cholesterol removed by HDL?

A

excreted from body in bile

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16
Q

Atherogenesis

A

“Response to Injury Theory”
- mechanism of atherosclerosis development believed to begin w/ endothelial damage and inflammation

17
Q

two types of how intima of artery can be damaged

A

mechanical stress
oxidative stress

18
Q

mechanical stress

A

ie. shear stress
- ↑BP or ↑blood viscosity

19
Q

oxidative stress

A

certain metabolic processes result in generation of high levels of ROS
eg. ↑LDL, diabetes, smoking

20
Q

ROS

A

reactive oxygen species
- can damage lipids, proteins, DNA, intima or coronary arteries

21
Q

what does damage to endothelium induce

A

induces an inflammatory response
activates adhesion molecules, growth factors and ↑angiotensin II, ACE levels

22
Q

what does inflammation in atherogenesis result

A

accumulation of macrophages

23
Q

what does macrophages do in inflammation

A

consumes LDL and become foam cells that forms initial fatty streak

24
Q

foam cells

A

type of macrophage that localize to fatty deposits on blood vessel walls

25
angiotensin II in atherogenesis
=> vasoconstriction (vasospasm) and ↓NO levels
26
what does vasoconstriction and ↓NO levels r/t angiotensin II cause?
vascular smooth muscle proliferation enhanced inflammation vasoconstriction promotion of thrombosis
27
what does angiotensin II in atherogenesis promote
cardiac cell growth and contributes to cardiac hypertrophy
28
thrombi easily forms where
lesions
29
what happens to lesions as it grows?
- occludes lumen of vessel - may form a thrombus => complete occlusion quickly - weakens blood vessel wall => ↓activity - may calcify => further rigidity of blood vessel wall
30
as lesions grow what can it lead to?
aneurysms, rupture or hemorrhage in wall
31
stability of plaques is affected by what?
amount of lipid in plaque
32
stability of plaque w/ lots of lipid
very unstable, progress quickly and attract more macrophages and platelets
33
stability of plaque w/ more fibrous tissue and little lipid
more stable and less likely to rupture => ↓predisposition to thrombosis