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BRS YR2 > Coronary Heart Disease > Flashcards

Coronary Heart Disease Flashcards

1
Q

what are the modifiable risk factors of artherosclerosis?

A
  • smoking
  • lipid intake
  • blood pressure
  • diabetes
  • obesity
  • sedentary lifestyle
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2
Q

what are the non-modifiable risk factors of atherosclerosis?

A
  • age
  • sex
  • genetic background
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3
Q

How much does only hypertension increase your risk of developing atherosclerosis?

A

x 3

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4
Q

How much does only high cholesterol increase your risk of developing atherosclerosis?

A

x 4

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5
Q

How much does only smoking increase your risk of developing atherosclerosis?

A

x 1.6

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6
Q

How much does both hypertension and smoking increase your risk of developing atherosclerosis?

A

x 4.5

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7
Q

How much does both hypertension and high cholesterol increase your risk of developing aetherosclerosis?

A

x 9

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8
Q

How much does both smoking and high cholesterol increase your risk of developing atherosclerosis?

A

x 6

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9
Q

How much does smoking, hypertension and high cholesterol increase your risk of developing atherosclerosis?

A

x 16

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10
Q

Where does atherosclerosis tend occur?

A

at branches, bends and bifurcations

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11
Q

Why does atherosclerosis occur at branches and bends?

A

turbulent blood flow vortices cause damage to artery and causes inflammation

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12
Q

What does the endothelium do?

A
  • controls contraction

- maintain the blood pressure

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13
Q

What happens in atherosclerosis?

A

LDLs deposit in the subintimal space and binds to matrix proteoglycans

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14
Q

How does atherosclerosis start?

A

adaptive thickening of the smooth muscle cells

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15
Q

What happens in a Type II lesion?

A

macrophage foam cells enter the adaptive thickening and ‘eat up’ the collected LDLs

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16
Q

What happens in a Type III (preatheroma) lesion?

A

the macrophage foam cells die due to fat overload, causing the formation of small pools of extracellular lipid

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17
Q

What happens in Type IV (atheroma) lesions?

A

the small pools of extracellular lipid join to for a core of extracellular lipid

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18
Q

What happens in Type V (fibroatheroma) lesions?

A

the core of extracellular lipid causes a inflammatory reaction which triggers the smooth muscle cells forming a fibrous thickening using collagen

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19
Q

What happens in Type VI (complicated) lesions?

A

the fibrous thickening breaks down killing the collagen cells - fissure and hematoma which eventually causes the formation of a thrombus.
Cholesterol crystals can form too.
Stratificiation due

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20
Q

What happens in Type V lesions in terms of plaque disruption?

A

stratification caused by the multiple breaking and reformation of different plaques

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21
Q

When is the window of opportunity for primary intervention of atherosclerosis?

A

Intermediate and advanced lesions (WITHOUT complications)

  • life style changes
  • risk factor management
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22
Q

What clinical interventions are available when complications of atherosclerosis occur?

A
  • secondary prevention
  • catheter based interventions
  • revascularisation surgery
  • heart failure treatment
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23
Q

What are the main cell types involved in the inflammation of the arteries and the progression of atherosclerosis?

A
  • vascular endothelial
  • monocyte-macrophages
  • vascular smooth muscle cells
  • T lymphocytes
  • Platelets
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24
Q

What are the role of vascular endothelial cells?

A
  • barrier function (lipoproteins)

- leukocyte recruitment

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25
Q

What are the role of platelets?

A
  • thrombus generation

- secrete cytokines and growth factor release

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26
Q

What are the role of monocyte-macrophages?

A
  • foam cell formation
  • cytokine and growth factor release
  • major source of free radicals
  • metalloproteinases
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27
Q

What are the role of vascular smooth muscle cells?

A 
- migration and proliferation 
(from media to plaque)
- collagen synthesis
(strengthens the plaques)
- remodelling and fibrous cap formation
- can lead to unstable angina due to narrowing lumen
28
Q

What are the role of T-lymphocytes?

A

macrophage activation

29
Q

What is the relationship between macrophages and the T lymphocytes?

A

both activation each other

30
Q

What are the 2 main functions of macrophages?

A
  • inflammatory

- resident

31
Q

What do inflammatory macrophages do?

A

adapted to kill microorganisms

32
Q

What do resident macrophages do?

A
  • homeostatic (suppress anti-inflammatory activity)
  • alveolar resident macrophages (lipid surfactant homeostasis)
  • osteoclasts (calcium and phosphate homeostasis)
  • spleen (iron homoeostasis)
33
Q

What characterises atherosclerosis?

A

macrophage inflammatory cells

34
Q

What do LDLs do?

A

carries cholesterol from the liver to the rest of the body (including arteries)

35
Q

What do HDLs do?

A

carries cholesterol from peripheral tissues (including arteries) back to the liver

36
Q

What are oxidised/modified LDLs?

A

families of highly inflammatory and toxic forms of LDLs found in the vessel wall - caused by the action of free radicals on LDLs

37
Q

How are LDLs modified?

A
  • LDLs leak through the endothelial barrier
  • LDLs are trapped by binding to the sticky matrix proteoglycans in the sub-endothelial layer
  • LDL becomes oxidatively modified by free radicals
38
Q

How can oxidised LDLs cause chronic inflammation?

A

it is phagocytosed by macrophages (making them foam cells) which stimulates chronic inflammation

39
Q

What is familial hyperlipidemia?

A
  • massively elevated cholesterol (>20mmol/L)

- autosomal genetic disease (dominant)

40
Q

What causes familial hyperlipidemia?

A

failure to clear LDL from the blood

41
Q

What the effects of familial hyperlipidemia?

A
  • xanthomas
  • early atherosclerosis
    untreated:
  • fatal MI <20
42
Q

What gene causes familial hyperlipidemia?

A

LDLR (accidently bind OxLDL) + scavenger receptor

43
Q

What does macrophage scavenger receptor A (CD204) do?

A
  • binds to oxidised LDL
  • binds to gram positive bacteria
  • binds to dead cells
44
Q

What does macrophage scavenger receptor B (CD36) do?

A
  • binds to oxidised LDL
  • binds to malaria parasites
  • binds to dead cells
45
Q

What oxidative enzymes activated macrophages can modify LDL?

A 
NADPH oxidase (superoxide)
Myeloperoxidase (hypochlorous acid)
46
Q

What are the negative impacts of macrophages

A
  • generate free radicals that further oxidise lipoproteins
  • phagocytose modified lipoproteins and become foam cells
  • express cytokine mediators that recruit monocytes
  • express chemoattractants and growth factors
  • express proteinases that degrade tissue
47
Q

What are cytokines?

A

protein immune hormones that activate endothelial cell adhesion molecules

48
Q

What are chemokines?

A

small proteins chemoattractant to monocytes

49
Q

What cytokines are released by macrophages?

A

IL-1 stimulate endothelial cells over the plaque to express called VCAM-1 (mediates tight monocyte binding)

50
Q

What happens if IL-1 or VCAM-1 aren’t present?

A

no atherosclerosis formed (seen in mice)

51
Q

What chemokines are released by macrophages and what do they do?

A

MCP-1 binds to G protein coupled receptor CCR2

52
Q

What happens if MCP-1 or CCR2 aren’t present?

A

atherosclerosis is reduced (in mice)

53
Q

What is the wound healing role of macrophages?

A

release of complementary protein growth factors that recruit VSMC and stimulate them to proliferate and deposit matrix

54
Q

What is the impact of platelet derived growth factor (PDGF)?

A
  • vascular smooth muscle cell chemotaxis
  • vascular smooth muscle cell survival
  • vascular smooth muscle cell division (mitosis)
55
Q

What is the impact of transforming growth factor beta (TGF-b)?

A
  • increased collagen synthesis

- matrix deposition

56
Q

What are the main 2 types of growth factors released?

A
  • platelet derived growth factor

- transforming growth factor beta

57
Q

What happens in atherosclerotic vascular smooth muscle cells?

A
  • reduced contractile filaments

- increased matrix deposition genes

58
Q

Which proteinases are expressed by macrophages?

A

metalloproteinases (MMPs)

59
Q

What are Metalloproteinases?

A
  • family of 28 homologous enzymes

- zinc based enzymes

60
Q

What do Metalloproteinases do?

A
  • activate eachother via proteolysis
  • degrade collagen
  • catalytic mechanism based on zinc
61
Q

What happens when MMPs breakdown collagen?

A
  • plaque erosion/rupture
    (no longer trapped in smooth muscle)
  • blood coagulation may cause an occlusive thrombus
62
Q

What are the characteristics of vulnerable and stable plaques?

A
  • large, soft eccentric lipid-rich necrotic core
  • increased VSMC apoptosis
  • reduced VSMC and collagen content
  • thin fibrous cap
  • infiltrate of activated macrophages expressing MMPs
63
Q

What happens in macrophage apoptosis?

A
  • Ox LDLs are toxic
  • Macrophage foam cells have protective systems that maintain survival when toxic lipid loading
  • when overwhelmed, apoptosis
  • then release tissue factors and toxic lipids forming a lipid necrotic core
  • thrombogenic and toxic material accumulates until plaque rupture
64
Q

What is Nuclear Factor kappa B (NFkB)?

A

transcription factors that regulates inflammation

65
Q

What activates NFkB?

A
  • scavenger receptors
  • toll-like receptors
  • cytokine receptors (IL-1)
  • cholesterol crystals
  • toxic OxLDL
  • cell stress
66
Q

What genes does NFkB activate?

A
  • matrix metalloproteinases
  • inducible nitric oxide synthase
  • IL-1
67
Q

What happens in atherosclerotic inflammation?

A
  • LDLs are converted into OxLDLs that activate macrophages
  • activated macrophages damage artery walls
  • all regulated by NFkB

BRS YR2 (70 decks)

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