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HLB Cardiac > Atherogenesis > Flashcards

Atherogenesis Flashcards

1
Q

What is atherogenesis?

A
  • formation of fatty deposits in arteries
  • progressive inflammation follows
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2
Q

What are some risk factors that are not able to be modified for atherogenesis?

A
  • gender (male 10 years earlier)
  • genetic abnormalities
  • increasing age (MAIN RISK)
  • family history
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3
Q

What are some risk factors that are modifiable for atherogenesis?

A
  • smoking
  • high cholesterol
  • high blood pressure
  • diabetes
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4
Q

What are the 3 main layers of the arterial walls? (inner to out layers)

A
  • innermost = intima
  • middle = media
  • outermost = adventitia
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5
Q

What is the inner most layer of arterial walls composed of?

A
  • endothelium
  • squamous epithelial cells
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6
Q

What is the middle layer of arterial walls, called media composed of?

A
  • smooth muscle
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7
Q

What is the outer most layer of arterial walls, called adventitia composed of?

A
  • tough fibrous tissue
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8
Q

What does atherosclerosis mean?

A
  • athero = greek for gluey/fatty yellow
  • sclerosis = german for hardening
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9
Q

What are the 2 main parts of an atheromatous plaque?

A

1 - fibrous cap

2 - necrotic core

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10
Q

What is a fibrous cap?

A
  • layer of fibrous tissue connective tissue
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11
Q

What layer of the arterial walls does the fibrous cap form in?

A
  • below endothelium
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12
Q

Generally what cells are found within a fibrous cap?

A
  • smooth muscle cells
  • macrophages
  • lymphocytes
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13
Q

What are the fibres that contribute towards the fibrous cap?

A
  • elastin
  • collagen
  • proteoglycans
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14
Q

As fibrous cap formation is inflammation, what do arterial walls need to create to supply the fibrous cap with blood?

A
  • neovascularisation
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15
Q

What is the necrotic core formed in atherosclerosis?

A
  • forms inside the intima below fibrotic cap
  • necrotic components under fibrous cap
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16
Q

What are the main components of the necrotic core that also contribute to stiffening of the arteries?

A
  • cholesterol crystals
  • Ca2+ salts
  • foam cells (from macrophages)
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17
Q

In the lipid hypothesis, roughly when was LDL cholesterol linked with atherosclerosis?

A
  • 1980s
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18
Q

What is the lipid oxidation hypothesis in atherosclerosis?

A
  • free radicals modify LDL cholesterol
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19
Q

If free radicals have modified LDL cholesterol, what can that cause in the innate immune system?

A
  • macrophages absorb LDL, but do not normally
  • macrophages become foam cells and undergo necrosis
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20
Q

What was the main problem with the lipid oxidation hypothesis?

A
  • did not account for non lipid risk factors
  • age, genetics, smoking
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21
Q

What was the conclusion about the lipid oxidation hypothesis?

A
  • contributes
  • NOT primary cause
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22
Q

When looking at research into atherosclerosis, what is one important thing to keep in mind?

A
  • evidence is based on pre-clinical models
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23
Q

What is the response to injury hypothesis?

A
  • atherosclerosis in a chronic inflammatory process to endothelial injury
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24
Q

In order for fatty streaks to form and then go onto atherosclerosis, what is the first thing that must happen in the endothelium in the injury hypothesis?

A
  • endothelial are damaged and injuryed
  • endothelial dysfunction follows
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25
Q

Following the initial injury/dysfunction in endothelium in the response to injury hypothesis, what then accumulates at the site of injury/dysfunction?

A
  • lipoproteins
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26
Q

In a similar manner to acute inflammation, once there is an initial injury/dysfunction to endothelium what migrates to the area as part of the response to injury hypothesis?

A
  • leukocyte, specifically monocytes
  • margination, adhesion and migration into intima
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27
Q

What is primary leukocyte (WBCs) involved in the early phase of the response to injury hypothesis?

A
  • monocytes differentiate into macrophages
  • lipids accumulate and macrophages phagocytose them
  • macrophages become foam cells
  • macrophages undergo necrosis and release contents
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28
Q

Following macrophages becoming foam cells, what do smooth muscle cells of the media do?

A
  • recruited, migrate and proliferate into intima
29
Q

Once recruited, migrated and proliferating in the intima what do smooth muscles form?

A
  • extracellular matrix
30
Q

What are some basic day to day things that can cause endothelial injury/dysfucntion?

A
  • ageing
  • high BP
  • toxins (smoking)
  • hyperlipidaemia
31
Q

What are cytokines?

A
  • signalling proteins
  • signal inflammation, immunity and hematopoiesis processes
32
Q

What do nitric oxide and endothelium derived relaxing factor do to the endothelium?

A
  • contribute to vasodilation
33
Q

What are the 4 basic groups of small molecules involved in atherscleroisis?

A

1 - cytokines 2 - growth factors 3 - chemokines 4 - adhesion molecules

34
Q

What do common lipoprotein abnormalities commonly cause in the blood markers?

A
  • ⬆️ LDL - ⬇️ HDL - ⬆️ Lp (a) highly atherogenic sub-fraction of LDL
35
Q

What does endothelial injury cause a reduction in the production and release of in endothelial cells?

A
  • nitric oxide
36
Q

What does endothelial injury cause an increase in the production and release of in endothelial cells?

A
  • O2 free radicals
37
Q

What are the 2 forms of lipid that begin to accumulate in the intima?

A
  • oxidised LDL - cholesterol crystals
38
Q

Damage to the endothelial can cause an increase in the release of proteins that are involved in regulating inflammation, immunity and hematopoiesis, what are these proteins?

A
  • cytokines
39
Q

What is the first visible manifestation of atherosclerosis?

A
  • fatty streaks
40
Q

What are fatty streaks?

A
  • combination of foam cells and smooth muscle cells
41
Q

Do fatty streaks cause symptoms and are they common in everyone?

A
  • can be present with no symptoms - can be in anyone
42
Q

When looking at fatty streak formation, are macrophages or smooth muscle cells referred to as good?

A
  • smooth muscle cells = good - macrophages = bad
43
Q

What do smooth muscles secrete to form extra cellular matrix?

A
  • mainly collagen - elastin and proteoglycans
44
Q

Why are smooth muscle cells referred to as good in athersclerosis?

A
  • aim to stabilise plaque - aim to prevent rupture of plaque
45
Q

What is the main purpose of the extra cellular matrix in atherosclerosis?

A
  • stabilisation of the atherosclerotic plaque
46
Q

What are some examples of growth factors involved in stabilising the extra cellular matrix?

A
  • platelet derived growth factor (PDGF) - fibroblast growth factor (FGF) - tissue growth factor alpha (TGF-a)
47
Q

As the plaque develops more and more foam cells are formed that undergo necrosis and release their contents. What is the name of the cap that aims to maintain stability of this cap?

A
  • fibrous cap - lipid rich underneath
48
Q

Plaque formation generally expands inwards, but as it continues to grow and develop it can raise up from the vessel wall. What is the problem with this?

A
  • can block arteries
49
Q

As the plaque develops, what causes the hardening of the arteries?

A
  • Ca2+ salt deposition - phosphate and hydroxyapatite
50
Q

Roughly what amount of occlusion of the arteries begins to present with clinical problems?

A
  • 70%
51
Q

Is it easy to distinguish between a stable and unstable plaque?

A
  • no
52
Q

What is the main cause of a plaque becoming unstable and increasing the risk of rupture?

A
  • thinning of the fibrous cap
53
Q

If the plaque continues to expand in size, what can happen to the tunica media?

A
  • becomes thinner and weaker - ⬆️ risk of aneurysm
54
Q

What is an aneurysm?

A
  • weakening of an artery wall - artery wall bulges/distends - can rupture causing internal bleeding
55
Q

What is the main cause of the fibrous cap to begin to thin?

A
  • continued accumulation of cholesterol in necrotic core - expands fibrous cap and thins it
56
Q

If the plaque continues to increase in size it can eventually rupture. What will then be exposed into the circulating blood?

A
  • collagen, free cholesterol and Ca2+ salts
57
Q

Once a plaque ruptures, why is it bad if collagen, free cholesterol and Ca2+ salts from the necrotic core are released into the blood?

A
  • all are highly thrombogenic
58
Q

What does something mean if it is thrombogenic?

A
  • cause coagulation of the blood - leads to thrombosis, commonly known as blood clot
59
Q

If a thrombus that has been formed, how can this cause a myocardial infarction?

A
  • occlusion of an artery - limited or no blood flow - common in coronary arteries
60
Q

If a thrombus that has been formed, how can this cause unstable angina, which is essentially pain in chest even at rest?

A
  • partial occlusion of an artery - reduced blood flow to heart - intermittent pain in chest
61
Q

If a thrombus that has been formed due to rupture, but then becomes incorporated into fibrous cap, what is the most common clinical presentation of this?

A
  • partial occlusion of an artery - reduced blood flow to heart - chest pain upon exertion
62
Q

In a patient who is having or has previously had a myocardial infarction what may we expect to see on an ECG?

A
  • ST elevation
63
Q

If a thrombus that has been formed due to a rupture of a plaque, in addition to a central myocardial infarction, what could occur in the brain?

A
  • stroke due to blockage of blood supply
64
Q

If a thrombus that has been formed due to a rupture of a plaque, in addition to a central myocardial infarction, what could occur in the legs?

A
  • thrombus lands in legs - results in acute ischemia
65
Q

If a plaque continues to develop but does not rupture, it can continue through the media and into the adventitia. What can this cause?

A
  • aneurysm formation - artery walls become weakened and can rupture - can cause a haemorrhage and be life threatening
66
Q

In addition to acute presentations of atherosclerosis, there are a number of chronic conditions as well. How can atherosclerosis of the aorta impact renal system?

A
  • branches of aorta become narrowed - caused renal artery stenosis
67
Q

What does stenosis mean?

A
  • narrowing of a space
68
Q

In addition to acute presentations of atherosclerosis, there are a number of chronic conditions as well. How can atherosclerosis cause vascular dementia?

A
  • blood flow to brain is impaired - similar to dementia
69
Q

What are the most common symptoms patients with atherosclerosis can present with in the legs?

A
  • claudication (pain) - foot ulcers - gangrene

HLB Cardiac (24 decks)

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