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Cardiovascular System > 16. Atherosclerosis and coronary heart disease > Flashcards

16. Atherosclerosis and coronary heart disease Flashcards

1
Q

6 Modifiable risk factors that contribute to coronary heart disease

A 
Smoking
Lipids intake
Blood pressure
Diabetes
Obesity
Sedentary lifestyle
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2
Q

3 Non-modifiable risk factors that contribute to coronary heart disease

A

Age
Sex
Genetic background

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3
Q

How has epidemiology of contributory factors to coronary heart disease changed?

A 
Reduced hyperlipidaemia (statin treatment)
Reduced hypertension (antihypertensive treatment)
Increased obesity = Increased diabetes
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4
Q

If risk factors are general, why is atherosclerosis focal?

A

Carotid artery bifurcates into internal and external
When blood hits outer wall a vortex is created by the disturbance in geometry
Plaque forms where there is more disordered blood flow

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5
Q

Describe the development of atherosclerosis

A
  1. Lesion prone location, develops increase in interstitial matrix in intima
    2.Becomes more inflammatory with macrophage foam cells
  2. Some macrophages start to die and release the fat = Fat in artery wall
  3. Pools of fat coalesce, form core of extracellular lipid and dead macrophage= necrotic core
  4. Inflammation triggers fibrotic thickening/ scarring
  5. If fibrous thickening does not happen enough, fibrous cap can crack apart mechanically, triggers a thrombus to form
    Thrombi can block coronary artery and cause MI
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6
Q

What are the main inflammatory cells in atherosclerosis?

A

Macrophages

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7
Q

Which form of lipoprotein is ‘bad’? What does it do?

A

Low density Lipoproteins (LDL)

Carries cholesterol from liver to rest of the body including arteries.

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8
Q

What are Oxidised/ modified LDL(s)?

A

Due to action of free radicals on LDL.

Families of highly inflammatory and toxic forms of LDL found in vessel walls.

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9
Q

What are the 2 classes of macrophages and how are their roles different?

A

Resident: involved in maintaining homeostasis
Inflammatory: kill microorganisms

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10
Q

What causes the oxidation of LDLs?

A

Free radicals

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11
Q

Describe what happens to LDLs after endothelial activation

A

Endothelial activation increases membrane permeability
LDLs enter and are oxidised by free radicals and become stuck in the subendothelial layer
OxLDLs are phagocytosed by macrophages to form foam cells
Foam cells accumulate and stimulate chronic inflammation

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12
Q

What is Familial Hyperlipidaemia? State 2 clinical features.

A

Autosomal recessive disease
Massively elevated blood cholesterol level (20 mmol/L)
Failure to clear LDL from blood
Xanthoma (accumulations of foam cells in the skin)
Early atherosclerosis

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13
Q

What is the LDLR regulated by?

A

It is negatively regulated by intracellular cholesterol

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14
Q

What is the second LDL receptor? (not LDLR)

A

Scavenger receptor
Not under feedback control by intracellular cholesterol
Pathogen receptors that ‘accidentally’ binds to OxLDLs

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15
Q

Other than OxLDL what does Macrophage scavenger receptor A bind to? What is it AKA?

A

AKA: CD204
Gram-positive bacteria
Dead cells

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16
Q

Other than OxLDL what does Macrophage scavenger receptor B bind to? What is it AKA?

A

AKA: CD36
Malaria parasites
Dead cells

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17
Q

What determines the function of the second LDL receptor?

A

Level of OxLDL present
Low levels: abnormal materials are taken up by macrophages and cleared safely by reverse cholesterol transport.
High levels: it triggers an inflammatory reaction

18
Q

How do macrophages within plaques generate free radicals that further oxidise lipoproteins? Which 2 enzymes are involved?

A

Have oxidative enzymes that can modify native LDL, causes a cycle
(Macrophages think OxLDL a bug, oxidise it further= further inflammation)
NADPH Oxidase
Myeloperoxidase

19
Q

How do macrophages within plaques become foam cells?

A

Phagocytose OxLDLs
OxLDLs accumulate
Become enlarged foam cells

20
Q

What do plaque macrophages express? Why?

A

Express inflammatory factors

To recruit monocytes

21
Q

What cytokines are released by macrophages?

A

IL-1: upregulates VCAM-1

VCAM-1 mediates tight monocyte binding

22
Q

What chemokines are released by macrophages?

A

Monocyte chemotactic protein-1 (MCP-1)
MCP-1 binds to a monocyte G-protein coupled receptor CCR2
Attracts monocytes

23
Q

What 2 growth factors are produced by macrophages and how do they affect vascular smooth muscle cells (VSMCs)? (“wound healing” role)

A

Platelet derived growth factor (PDGF): stimulates VSMC chemotaxis, survival and division
Transforming growth factor-beta: stimulates collagen synthesis and matrix deposition, makes fibrous cap thicker

24
Q

Describe how the normal function of a VSMC is different to the atherosclerotic VSMC

A

Normal: more contractile filaments and less collagen deposition
Atherosclerotic: fewer contractile filaments and more collagen deposition

25
Q

What do the matrix metalloproteinases (MMPs) expressed by macrophages do?

A

Degrade collagen in the ECM and hence weaken the plaque

26
Q

Effect of plaque erosion/rupture

A

Blood coagulation at the site of rupture may lead to an occlusive thrombus and cessation of blood flow.

27
Q

What are the characteristics of unstable plaques?

A

Thin fibrous cap
Increased VSMC apoptosis
Reduced VSMC and collagen content
Infiltration of activated macrophages expressing MMPs
Large, soft, eccentric lipid-rich necrotic core

28
Q

How do macrophages cope with the toxic OxLDL metabolites?

A

Have protective systems that maintain their survival in the face of toxic lipid loading
Once overwhelmed, they die via apoptosis

29
Q

What is the consequence of atherosclerotic macrophage apoptosis?

A

Release macrophage tissue factors and toxic lipids into the ‘central death zone’

30
Q

What is a master transcription factor involved in atherosclerosis and what does it stimulate?

A

Nuclear Factor Kappa B

Stimulates matrix metalloproteinases and inducible nitric oxide synthase

31
Q

What is Nuclear Factor Kappa B activated by?

A

Scavenger receptors
Toll-like receptors
Cytokine receptors

32
Q

What does atherosclerosis lead to?

A

Coronary heart disease

33
Q

What 2 categories to patients presenting with sudden onset chest pain fall into?

A

Acute myocardial infarction

Progressive (unstable) angina

34
Q

How has the mortality from cardiovascular disease changed over the past 50 years?

A

It has decreased by 50%

35
Q

What is the main biochemical test for myocardial infarction?

A

Troponin

36
Q

Coronary heart disease

A 
Occlusion of coronary arteries
Less O2 to myocytes 
Myocytes die 
Less heart to perform same function 
Need more O2 (which they don’t have)
37
Q

What is the pain and discomfort from lack of oxygen-rich blood to the heart in CHD called?

A

Angina

38
Q

List 3 clinical features of coronary heart disease

A

Angina
Breathlessness
Heart attack

39
Q

What can be used to diagnose coronary heart disease?

A 
Electrocardiogram (ECG)
Exercise stress tests
Echocardiogram
Coronary angiography 
Blood test
40
Q

List 4 approaches for treating coronary heart disease

A

Lifestyle changes: exercise, stop smoking
Medication: Antiplatelets, Statins, Beta blockers, ACE inhibitors
Coronary angioplasty: using balloons/ stents to treat narrow heart arteries
Surgery: Coronary artery bypass graft, Heart transplant

Cardiovascular System (16 decks)

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