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PHSL232 > Lecture 27 - Atherosclerosis > Flashcards

Lecture 27 - Atherosclerosis Flashcards

1
Q

What occurs after initial intima injury?

A

After initial intima injury, remodelling of media (atrophy, loss of SMC’s) occurs to accommodate plaque and preserve lumen diameter

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2
Q

Where does atherosclerosis begin?

A

In the intima

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3
Q

Where is the most common location for atherosclerosis?

A

Coronary arteries

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4
Q

What does atherosclerosis in the coronary arteries cause?

A

Coronary artery disease

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5
Q

What does atherosclerosis in the cerebral (carotid) arteries cause?

A

Transient ischemic attack (TIA) or stroke

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6
Q

What does atherosclerosis in the limb arteries cause?

A

Peripheral artery disease

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7
Q

What does atherosclerosis in the renal arteries cause?

A

Hypertension or kidney failure

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8
Q

What are aneurysms in atherosclerosis?

A

Bulge in artery which can be life threatening if burst

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9
Q

What is the process of atherosclerosis/endothelial dysfunction?

A

Initial injury
Fatty streak
Intermediate lesion
Atheroma
Fibroatheroma
Complicated lesion

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10
Q

What can be the initial injury of endothelium?

A

Hypercholesterolemia
- High cholesterol
Hypertension
High triglycerides (FFA)
Inflammation

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11
Q

What is the bad form of cholesterol?

A

LDL

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12
Q

What does LDL do?

A

Stick to artery walls leading to plaque formation

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13
Q

What does HDL do?

A

Carry LDL away from artery walls

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14
Q

What are the HDL cholesterol levels and risk classification?

A

< 1.0 mmol/L High Risk
> 1.6 mmol/L Desirable level

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15
Q

What are the LDL cholesterol levels and risk classification?

A

< 2.6 mmol/L Optimal
> 4.1 mmol/L High Risk

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16
Q

What is the formation of fatty streak?

A

Influx of LDL exceeds eliminating capacity – extracellular LDL pool
LDL migrate to subendothelial intima
oxLDL- expression leucocyte adhesion molecules - chemokine secretion to attract monocytes
LDL oxidized by radicals - oxLDL
Monocytes enter the intima
Monocytes turn into Macrophages to take up the excessive oxLDL
Macrophages internalise oxLDL
Dead macrophages - Foam cells
Foam cells attract more monocytes and form fatty streak

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17
Q

What is the formation of plaque?

A

Foam cells activating T-cell immune response
Smooth muscle cells (SMCs) migrate from media into the
intima, and turn into fibroblast like repair cells
Synthesise extracellular matrix: elastin and collagen
Developing calcium crystals
Inflammatory response (C-reactive protein)
Formation of fibrous cap
Isolating the stiffened lipid core prevents blood clothing
Plaque = lipid core and fibrous cap

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18
Q

What does lesions and fissures of endothelium cause?

A

Formation of thrombus (blood clot) on plaque

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19
Q

What is arterial/venous thrombosis?

A

Formation of a thrombus within artery or vein

20
Q

What is arterial/venous embolism?

A

Interruption of blood flow due to an embolus (free-moving thrombus), potentially causing infarction of almost any organ/part in body

21
Q

During the formation of a fibrous cap:
a. monocytes turn into macrophages and take up the excessive oxLDL particles.
b. smooth muscle cells migrate into the media.
c. the clinical risk for an arterial thrombus is very high.
d. calcium crystals are formed in the intima.

A

d. calcium crystals are formed in the intima

22
Q

What takes up the excessive oxLDL?

A

Monocytes which turn into macrophages in tissue
- Macrophages internalise oxLDL

23
Q

What do the foam cells do?

A

Attract more monocytes to form fatty streak
Activate T-cell immune response

24
Q

What do smooth muscle cells (SMCs) do during plaque formation?

A

Smooth muscle cells (SMCs) migrate from media into the intima, and turn into fibroblast like repair cells that synthesise extracellular matrix (elastin and collagen) - fibrosis

25
Q

What is the plaque composed of?

A

lipid core and fibrous cap

26
Q

What does the formation of fibrous cap do?

A

Isolate stiffened lipid core to prevent blood clotting

27
Q

What happens when there are abnormalities of blood vessel wall?

A

Vascular repair response

28
Q

What happens when there are abnormalities of blood constituents?

A

coagulation, platelet activation

29
Q

What happens when there are abnormalities of blood flow?

A

Shear stress

30
Q

What is shear stress in blood flow?

A

Force resulting from friction of flowing blood on luminal surface

31
Q

What happens with normal shear stress in blood flow?

A

NO production
- decrease expression of inflammatory response mediators, adhesion molecules, vasoconstrictors and oxidants

32
Q

What happens with low or turbulent shear stress in blood flow?

A

Reduced NO production
- enhanced monocyte adhesion, platelet activation, SMC proliferation, oxidant activity, vasoconstriction

33
Q

Relating to shear stress/turbulence, what areas have higher risk of atherosclerosis?

A

Local areas with low shear stress and altered flow directions during cardiac cycles have higher risk of atherosclerosis

34
Q

Which arteries have turbulent and pulsatile flow?

A

Elastic (Aorta, carotid arteries, iliac arteries)
Large-medium sized muscular arteries (coronary + femoral)

35
Q

Relating to pathophysiology, what are the carotid arteries susceptible to and why?

A

Particularly susceptible to plaque formation
Lower blood pressures - Head above the heart
Turbulent blood flow in the “fork”.

36
Q

Relating to pathophysiology, what are the coronary arteries susceptible to and why?

A

High(est) blood pressures from aorta
Ageing and Hypertension (Reflections)
Turbulent flow, constant compressive systolic force

37
Q

What are pharmacological treatments for atherosclerosis?

A

Statins
Cholesterol absorption inhibitors
Inclisiran
Bempedoic acid

37
Q

What are pharmacological treatments for atherosclerosis?

A

Statins
Cholesterol absorption inhibitors
Inclisiran
Bempedoic acid

38
Q

What are statins?

A

HMG-CoA reductase inhibitors - lowers LDL

39
Q

What do cholesterol absorption inhibitors do?

A

Block absorption of cholesterol in intestine

40
Q

What does inclisiran do?

A

Interfere with RNA to lower LDL levels

41
Q

What does bempedoic acid do?

A

Act as upstream target of statins

42
Q

What is endarterectomy?

A

Surgery for the removal of atheromatous plaque material

43
Q

What is restenosis?

A

Narrowing of arteries after angioplasty and stenting
- low flow areas

44
Q

Describe angioplasty and stent

A

Angioplasty is a procedure used to open blocked coronary arteries caused by coronary artery disease (Ballooning). Whilst stent is a contraption put in afterwards to keep vessel open

45
Q

What are aortic aneurysms?

A

Aorta dilatation (atherosclerosis – age) which can occur anywhere along aorta
Rupture is almost certain death
Symptoms are rare and non-specific

46
Q

How can we repair aortic aneurysms?

A

Stents

PHSL232 (31 decks)

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