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Cardiovascular System > Coronary Heart Disease > Flashcards

Coronary Heart Disease Flashcards

1
Q

What are the modifiable risk factors of coronary heart disease

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

What are the non-modifiable risk factors of coronary heart disease

A

Age
Sex
Genetic Background

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3
Q

What are the changes in epidemiology

A

Reduced hyperlipidaemia (statin treatment)
Reduced hypertension (antihypertensive treatment)
Increased obesity so increased diabetes
New improvements in diabetes treatment have doubtful effect on macrovascular disease
Changing pathology of coronary thrombosis possible related to altered risk factors

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4
Q

Describe the progression of atherosclerosis

A
  1. LDL deposits in the subintimal space and binds to matrix proteoglycans
  2. Macrophage foam cells form at the intima (type II lesion)
  3. Preatheroma where small pools of extracellular lipid accumulate (III)
  4. Atheroma where a core of extracellular lipid forms (IV)
  5. Fibroatheroma where there is fibrous thickening (V)
  6. Complicated lesion where a thrombus forms with tissue and haematoma (VI)
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5
Q

What is a myocardial infarction

A

blockage of the coronary artery by a thrombus

Stratifies layers are from multiple events triggering inflammation

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6
Q

What are the complications of atherosclerosis

A

Stenosis

Plaque rupture

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7
Q

What is primary prevention fro atherosclerosis

A

Lifestyle changes

Risk factor management

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8
Q

What are some clinical interventions for atherosclerosis

A

Secondary prevention
Catheter based interventions
Revascularisation surgery
Treatment of heart failure

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9
Q

What are the main cell types involved in atherosclerosis

A

vascular endothelial cells - barrier to lipoproteins and leukocyte recruitment

monocyte-macrophages - foam cell formation, cytokine and GF release, free radicals, metalloproteinases

Vascular smooth muscle cells - migration and proliferation, collagen synthesis, remodelling and fibrous cap

Platelets - thrombus and cytokine and GF release

T lymphocytes - macrophage activation

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10
Q

What are the main inflammatory cells in atherosclerosis

A

Macrophages (from blood monocytes)

Macrophages subtypes are regulated by combinations of transcription factors binding to regulatory sequences to DNA

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11
Q

Describe inflammatory macrophages

A

Adapted to kill microorganisms

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12
Q

Describe resident macrophages

A

Normally homeostatic to suppress inflammatory activity
Alveolar resident macrophages (Surfacent lipid homeostasis)
osteoclasts - calcium and phosphate homeostasis
Spleen - iron homeostasis

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13
Q

Compare LDL to HDL

A

LDL - synthesised in the liver, carries cholesterol from peripheral tissues to the liver
HDL - carries cholesterol from peripheral tissues to the liver

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14
Q

How is sub endothelial trapped LDL modified

A
  1. LDLs leak through the endothelial barrier
  2. LDL is trapped by binding to sticky matrix carbohydrates (proteoglycans) in the sub-endothelial layer and becomes susceptible to modification
  3. LDL becomes oxidatively modified by free radicals.
  4. Oxidised LDL is phagocytosed by macrophages and stimulates chronic inflammation
  5. Macrophages become foam cells
  6. Chronic inflammation
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15
Q

What binds to macrophage scavenger receptor A (CD204)

A

Binds to oxidised LDL
Binds to gram-positive bacteria like staphylococci and streptococci
Binds to dead cells

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16
Q

What binds to macrophage scavenger receptor B (CD36)

A

Binds to oxidised LDL
Binds to malaria parasites
Binds to dead cells

17
Q

What are the 5 functions of macrophages in plaques

A

Generate free radicals that further oxidise lipoproteins
Phagocytose modified lipoproteins and become foam cells
Express cytokine mediators that recruit monocytes
Express chemo-attractants and growth factors for VSMC
Express proteinases that degrade tissue

18
Q

Explain how macrophages in plaques generates free radicals

A

They have oxidative enzymes to modify native LDL
e.g. NADPH oxidase (superoxide) and myeloperoxidase (HOCl)
positive feedback loop
free radicals further oxidise lipoproteins

19
Q

Explain how macrophages become foam cells

A

In plaques they phagocytose modified lipoproteins and become foam cells (accumulate modified LDLs)

20
Q

where does ischaemic heart disease and cerebrovascular disease rank on world disease burden in 1990 and 2020

A

1990 - 5,6

2020 - 1,4

21
Q

Explain how macrophages in plaques express cytokine mediators that recruit monocytes

A

Expresses cytokines and chemokine

Inflammatory factors involved in monocyte recruitment

22
Q

Compare cytokines to chemokines

A

cytokines - protein immune hormones that activate endothelial cell adhesion molecules e.g. interleukin-1

chemokines - small proteins chemoattractant to monocytes e.g. MCP-1

23
Q

Explain how macrophages in plaques express chemo-attractants and growth factors for vascular smooth muscle cells

A

They release platelet derived growth factor and transforming growth factor beta
PDGF - vascular smooth muscle cell chemotaxis, survival and cell division
TGHB - increased collagen synthesis and matrix deposition

24
Q

What levels of contractile filaments and matrix deposition genes do atherosclerotic cells have

A

low contractile filament levels

high matrix deposition gene levels

25
Q

Explain how macrophages in plaques express proteinases that degrade tissue

A

Metalloproteinases activate each other by proteolysis which leads to the degradation of collagen
Based on zinc

26
Q

Describe the pathology of a vulnerable and stable plaque

A 
Large soft lipid rich necrotic core
Thin fibrous cap
increased smooth muscle cell apoptosis
reduced VSMC and collagen content
Infiltrate of activated macrophages expressing MMPs
27
Q

Describe the process of macrophage apoptosis

A
  1. OxLDL derived metabolites are toxic e.g. 7-keto-cholesterol
  2. Macrophage foam cells have protective systems that maintain survival in the face of toxic lipid loading
  3. Once overwhelmed, macrophages die via apoptosis
  4. Release macrophage tissue factors and toxic lipids into the central death zone called the lipid necrotic core
  5. Thrombogenic and toxic material accumulates, walled off until the plaque reuptures to cause it to meet blood
28
Q

What is nuclear factor kappa B (NFkB)

A

Transcription factor
Regulator of inflammation
Switches on numerous inflammatory genes e.g. matrix metalloproteinases and inducible NO synthase

29
Q

What is NFkB activated by

A

Scavenger receptors
Toll-like receptors
cytokine receptors
Break down of IkB (aspirin)

30
Q

What does Interleukin-1 do

A

Upregulates adhesion molecule VCAM-1

VCAM-1 mediates tight monocyte binding

31
Q

What does MCP1 do

A

Binds to a monocyte G-protein coupled receptor CCR2

Cardiovascular System (13 decks)

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