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Patho > Atherosclerosis and Heart Disease > Flashcards

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
Q

angiotensin II in atherogenesis

A

=> vasoconstriction (vasospasm) and ↓NO levels

26
Q

what does vasoconstriction and ↓NO levels r/t angiotensin II cause?

A

vascular smooth muscle proliferation
enhanced inflammation
vasoconstriction
promotion of thrombosis

27
Q

what does angiotensin II in atherogenesis promote

A

cardiac cell growth and contributes to cardiac hypertrophy

28
Q

thrombi easily forms where

A

lesions

29
Q

what happens to lesions as it grows?

A
  • 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
Q

as lesions grow what can it lead to?

A

aneurysms, rupture or hemorrhage in wall

31
Q

stability of plaques is affected by what?

A

amount of lipid in plaque

32
Q

stability of plaque w/ lots of lipid

A

very unstable, progress quickly and attract more macrophages and platelets

33
Q

stability of plaque w/ more fibrous tissue and little lipid

A

more stable and less likely to rupture => ↓predisposition to thrombosis

Patho (11 decks)

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