L1: Cardiovascular Disease Flashcards

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1
Q

What percentage of UK deaths is attributable to CVD in 2018?

A

27%

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2
Q

What where the two experiments to identify the association between physical activity and CHD?

A

Morris et al, 1980: London bus conductors

Paffenbarger 1975: Work intensity

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3
Q

What curve does volume of physical activity follow as a risk factor for CVD mortality?

A

U-shaped curve

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4
Q

What range of physical activity (Met hours per week) is associated with the lowest risk of CVD mortality and what is the risk reduction?

A

15 - 40 MET hours per week reduces the risk of mortality from CVD by 42% compared to sedentary people

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5
Q

Other than physical activity, what other modifiable risk factor for CVD mortality is there>

A

Cardiorespiratory fitness

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6
Q

Who identified the association between cardiorespiratory fitness and CVD mortality?

A

Barlow et al

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7
Q

What reduction in risk is associated with a 1 MET increase in cardiorespiratory fitness?

A

18% CVD mortality reduction

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8
Q

What did Tikkenan et al, 2018 identify?

A
  • Cardiorespiratory fitness is capable of reducing the risk caused by high genetic risk.
  • Those with high cardiorespiratory fitness reduced there risk below 1 despite having high genetic risk.
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9
Q

What are the three layers of arteries?

A

Tunica intima, Tunica media and tunica externa

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10
Q

What is the tunica intima?

A

Inner muscular layer which contains a layer of endothelial cells

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11
Q

What is the Tunica Media?

A

Smooth muscular layer responsible for vasoconstriction and vasodilation

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12
Q

What is the Tunica Externa

A

Connective tissue composed of mainly collagen and elastin responsible for providing structure and support.

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13
Q

Describe the process of Atherosclerosis formation

A

1) Damage to the endothelial lining of blood vessels leads to increased permeability between the blood and vessel wall.
2) Increased diffusion of LDLs and VLDLs into the tunica media.
3) Immune response recruits circulating monocytes which differentiate into macrophages.
4) Macrophages engulf lipid molecules becoming foam cells which contribute to the formation of fatty streaks
5) Smooth muscle cells migrate and proliferate and collagen deposition occurs ultimately producing an advance fibrous cap lesion.
6) The AFC causes a thrombus that can either rupture causing an haemorrhage or break off causing a clot. This can lead to a myocardial infarction or stroke.

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14
Q

What causes damage to the endothelial lining?

A

1) High blood pressure
2) Diabetes
3) High cholesterol
4) Smoking
5) Chronic low grade inflammation

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15
Q

What is the clinical identification of CVD?

A

40% reduction in blood flow identifies as cardiovascular disease

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16
Q

When does atherosclerosis begin developing and how does this effect primary intervention?

A

Development has been identified in very early ages and so primary intervention needs to occur early in life.

17
Q

What are other risk factors for Cardiovascular Disease?

A
  1. Physical inactivity/activity
  2. Lipid metabolism
  3. Blood pressure
  4. Vascular function
  5. Inflammation
18
Q

How is physical inactivity a modifiable risk factor?

A
  1. Physical inactivity reduces GLUT-4 recruitment in muscle cells. GLUT-4 receptors are responsible for Glucose uptake, meaning the more insulin is required for a given glucose uptake.
  2. Physical inactivity leads to elevated blood pressure which increase arterial stress and contributes to endothelial damage.
19
Q

What are chylomicrons?

A

Transport molecules responsible for the transport of dietary triglycerides from the small intestines to peripheral adipose.

20
Q

What do VLDL do?

A

Transport of endogenous triglycerides from the liver to peripheral adipocytes

21
Q

What do LDL do?

A

Transport of cholesterol around the body

22
Q

What does HDL do?

A

Transport and removal of cholesterol from circulation

23
Q

What to lipid transport molecules can provide protective benefits against cardiovascular disease?

A

VLDL reduces in response to exercise which prevents the over accumulation of adipocytes and the development of chronic inflammation.

HDL increases in response to exercise which increases the removal of cholesterol from the circulating blood, reducing the effect of cholesterol of endothelial dysfunction and damage.

24
Q

How can acute and chronic exercise modify blood pressure and subsequently cardiovascular disease risk?

A

Acute
transient Reduction in systolic blood pressure hours after exercise caused by increased endothelial-dependent vasodilation. Vasodilation occurs in response to increased vascular resistance from exercise.

Arterial baroreflex resetting occurs which reduces parasympathetic nerve activity meaning reduced epinephrine responsible for vasoconstriction. Subsequently, vasodilation increases.

Chronic
chronic exercise promotes IL-10 anti-inflammatory cytokine release whilst decreasing IL-6 and TNF-Alpha thus changing the inflammatory profile of the body.

Angiogenesis occurs along with increase lumen size of blood vessels resulting in increased cross-sectional area. Wall thickness is also reduced and overall blood pressure is lower.

25
Q

Who’s study identified increased HDL from exercise and what year?

A

LaPorte et al, 1983

26
Q

What is the STRRIDE study ?

Slentz et al, 2007

A

Randomised control study on the effects exercise has on cholesterol composition.
Showed that High intensity exercise increases HDL and decreases LDL.
HDL increase is effected by both exercise duration and intensity.
This effect occurs 15 days after training session

27
Q

What sort of exercise and duration is needed to induce a reduction in blood pressure? Also how long does the effects last

A

low-intensity exercise such as standing and walking is enough to reduce arterial blood pressure, this is irrespective of intermittent or continuous exercise, with both causing the same effect.

This effect can last up to 24 hours, know as post-exercise hypotension.

28
Q

What is endothelial dysfunction?

A

The inability to interact with vascular smooth muscle to influence blood flow.

29
Q

What are the key processes of endothelial dysfunction?

A
  • decreased monocyte uptake reduces the ability to remove lipids via macrophages.
  • Reduced release of histamines and nitric oxide for endothelial-dependent vasodilation.
30
Q

What is the physiological process in which exercise induces endothelial-dependent vasodilation?

A

1) Exercise increases blood flow
2) Increased blood flow increases interaction between blood and endothelial (shear stress)
3) Increased nitric oxide synthase activity from endothelium responsible for catalysing nitric oxide
4) elevated nitric oxide release promotes vasodilation
5) Increase endothelial function

31
Q

What is the gold standard of measuring endothelial function?

A

Infusion of acetylcholine and measuring how much vasoconstriction occurs

32
Q

What is a non-invasive technique to measure endothelial function and how does it work?

A

Flow-mediated dilation
Ultrasound measures blood Flow and occlusion bands are used to restrict blood flow for a standardised period of time.
Measure the vasodilatory response to when occlusion bands are released.

33
Q

How does exercise effect endothelial function of vasodilation?

A

Initial 2 weeks of exercise increases nitric oxide production via endothelial stress caused by increased blood flow.
After 2 weeks endothelial function seems to decrease but in reality this is caused by angiogenesis which increases blood vessel diameter which ultimately reduces blood pressure.