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Cardiology > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

What are 3 endothelial cell adhesion mcs?

A

VCAM 1
ICAM 1
E-selectin

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2
Q

What is a foam cell?

A

Macrophage rich in cholesterol and cholesterol esters

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3
Q

Which kinds of T cells play a role?

A

Inflammatory TH1 lymphocytes play a role in lesion initiation, progression and instabilty-plaque rupture. Express IL-12, INF-gamma and TNF alpha which perpetuates macrophage and T cell proliferation.

*Also inc MMPs that degrade matrix and cap, while reducing sm cell proliferation and formation of the cap

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4
Q

What is obligatory for lesion initiation and prog?

A

Macrophages and LDL

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5
Q

Are lymphocytes obligatory for lesion initiation and prog?

A

No, but they exert a net pro atherogenic effect under less atherogenic pressures

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6
Q

What is HDL’s role in atherosclerosis?

A
  • Antiinflammatory effects (dec in adhesion mcs)
  • HDL enters sub-endo space and effluxes cholesterol from macrophages/foam cells and then returns to plasma and carries that cholesterol to the liver for excretion
  • inhibits LDL ox
  • Upregulates prostacyclin and NO in endothelium and suppresses thrombosis
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7
Q

What signals for the change in sm phenotype?

A

Intigrins, adhesion mcs and chemokines produced in early lesions signal to medial smooth muscle cells

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8
Q

What changes in phenotype do sm’s have?

A
  • Switch from contractile to synthetic
  • Migrate into neointima
  • Undergo limited proliferation
  • Secrete lareg amt of matrix
  • Secrete cytokines, chemokines, growth factors and inflammatory prostaglandins
  • Migrate to subendo location at sites of greatest hemodynamic stress and form fibrous cap
  • Synthetic sm cells express scavenger receptors that can take up ox lipids and form sub pop of non macrophage foam cells
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9
Q

What growth factors do synthetic sm cells secrete?

A

PDGF, FGF, angiotensin II

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10
Q

Can foam cells contribute to lesion growth?

A

Yes, secrete all the things macrophages sec

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11
Q

What happens within the intermediate atherosclerotic lesion?

A
  • Neo-intimal calcification (can image this)

- Remodeling (compensatory expansion with lumen occlusion)

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12
Q

Are intermediate lesions symptomatic?

A

Usually sub-clinical and asymptomatic but are most common lesion to cause plaque rupture at shoulder regions (large hemodynamic stress and most inflamm content)

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13
Q

Are intermediate lesions reversible?

A

Yes, or at least decreasable. Lipid lowering and BP control reduce CV events leading to stabilization and regression of the plaque

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14
Q

Is rupture related to vessel stenosis?

A

NO!

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15
Q

List the properties of a vulnerable plaque

A
  • Thin fibrous cap
  • Lots of macrophages and T cells
  • Large lipid pool
  • High ox LDL content
  • Thin shoulder region
  • Greater neovasc (brings in inflamm cells)
  • Low VSMC count (vasc sm)
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16
Q

What overlapping mechanisms contribute to plaque instability?

A
  • Impaired endoth fxn
  • Thrombus formation
  • Inflammation
  • Impaired plaque stabilization
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17
Q

How do advanced lesions occur?

A

They are clinically silent and continue to grow or they rupture without clinical presentation. Some complex lesions can be contained and absorbed into an expanding lesion

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18
Q

Stage 1 of atherosclerotic lesions

A

Monocyte adhesion/migration

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19
Q

Stage 2 of atherosclerotic lesions

A

Foam cells in intima

20
Q

Stage 3 of atherosclerotic lesions

A

Extracellular lipid appears (ie apoptotic macrophages release fat cells)

21
Q

Stage 4 of atherosclerotic lesions

A

Core formation begins (can go straight to stage 6)

-also called atheroma lesion

22
Q

Stage 5 of atherosclerotic lesions

A

Cap and core formed

-also called fibroatheroma lesion

23
Q

Stage 6 of atherosclerotic lesions

A

Thrombosis

24
Q

What is a fatty streak?

A
  • Intracellular lipid filled foam cells
  • Response to injury/inflammation
  • Secrete pro-inflammatory cytokines that amplify inflammatory response
25
Q

Within which vessels do atherosclerotic plaques form?

A

Elastic arteries, large and medium sized arteries

26
Q

What are the components of a plaque?

A
  • Cells (SMCs, macrophages, leukocytes)
  • ECM (collagen, elastic fibers PGs)
  • Lipid (intracellular and free)
27
Q

What are some consequences of plaque rupture?

A
  • Hemorrhage into the plaque
  • Superimposed thrombosis due to exposure of ECM
  • Aneurysmal dilation
28
Q

What is percutaneous coronary intervention (PCI)?

A

Stick a balloon in the stenosis, then a stent

29
Q

What is an unwanted consequence of PCI?

A

Restenosis (smc activation and constrictive remodeling)

30
Q

Why does restenosis occur?

A
  • The ECM is exposed due to the stress of the PCI procedure leading to platelet activation, release of cytokines and GFs
  • SMcs are activated and become synthetic to secrete ECM into the intima forming a neointima within 7 days of injury
  • Vascular remodeling occurs (shrinkage of lumen)–>this is what the stent stops (vessel contracts, but stent does not stop SMCs from migrating in)
31
Q

What does PDGF do?

A

Induces SMC migration

32
Q

What secretes PDGF?

A

Platelets, endothelial cells, macrophages, SMCs in response to vessel wall injury

33
Q

What does basic FGF do?

A

induces SMC proliferation

34
Q

What releases basic FGF?

A

SMCs in response to stretch or crush injury (both of which occur with PCI)

35
Q

What is bFGF antibody?

A

It blocks 80% of SMC proliferation

36
Q

What does ang II do with atherosclerosis?

A

Induces SMC proliferation

37
Q

What can you give to attenuate neointimal formation?

A

ACE inhibitors

38
Q

What does TGF-beta do in atherosclerosis?

A

ECM secretion which makes up most of the restenotic region

39
Q

What secretes TGF beta?

A

SMCs, endothelial cells, and platelets following PTCA

40
Q

What do we do to inhibit SMC proliferation after PCI?

A

Put drugs on the stent like rapamycin or paclitaxel that inhibits its proliferation

41
Q

What do the stent drugs target?

A

They inhibit the cell cycle in some way

42
Q

What is a dangerous complication of PCI and stents?

A

Late thrombosis and neointimal atherosclerosis because you mess with the endothelial cells that are req to heal the artery. This allows blood clots to form occur

43
Q

Is restenosis predictable?

A

Yes, if it doesn’t occur within 6 mo of procedure it prob won’t

44
Q

Name the actions of AT1 receptor

A

AT1 receptor is a receptor for angioII

  • Vasoconstriction
  • Inflammation
  • Remodeling
  • Thrombosis
  • Inc ox stress
45
Q

Name the actions of AT2 receptor

A

AT2 receptor is a receptor for angio II, less densely distributed in the body than AT1

  • Vasodilation
  • Reduction in inflammation
  • Reduction in remodeling
  • Inc NO release
  • Tissue repair
46
Q

What are the effects of angio II on atherosclerosis?

A
  • Increases LOX-1 receptor on ECs to inc uptake of oxidized LDL
  • Activates NAD(P)H oxidase which inc ROS and therefore macrophage mediated LDL activation and uptake
  • EC dysfxn due to inc oxidative stress and uptake of ox LDL
  • Activates NFkappaB (inc monocyte adhesion and recruitment)
  • Vasoconstriction, inflammation, remodeling, thrombosis

Cardiology (16 decks)

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