week 8

Question 1

Unchangeable CVD risks ?

Answer 1

Gender
Family history
Age
Race

Question 2

Changeable CVD risk factors?

Answer 2

Smoking
Physical inactivity
Obesity
Diet
High cholesterol
high blood pressure
insulin resistance

Question 3

Current physical activity recommendation from the Department of Health? % below?

Answer 3

30 minutes of moderate intensity physical activity on five or more days of the week

65% men below, 76% women below

Question 4

Structure of artery ?

Answer 4

Layers: Composed of three layers—intima, media, and adventitia.

Intima: Inner lining formed by endothelial cells, providing a smooth, protective barrier between the blood and the arterial wall.

Media: Middle layer containing smooth muscle, responsible for regulating blood pressure and flow.

Adventitia: Outer layer providing structural support and flexibility.

Question 5

What can initiate atherosclerosis ? plaque?

Answer 5

Atherosclerosis: Damage to endothelial cells triggers the process.

Plaque Formation: Endothelial damage exposes underlying connective tissue, initiating plaque development.

Inflammatory Response: Inflammatory cytokines induce diapedesis, promoting immune cell infiltration.

Question 6

Plaque progression?

Answer 6

Cellular Activation: Platelets, endothelial cells, and macrophages release growth factors (e.g., PDGF), promoting smooth muscle cell migration from the media to the intima.

Plaque Growth: As the plaque expands, it narrows the arterial lumen, restricting blood flow.

Lipid Deposition: Oxidized LDL-C (oxLDL) is deposited in the plaque, contributing to its growth.

Question 7

Plaque erosion?

Answer 7

Macrophages and smooth muscle cells release MMPs and ROS, which destabilize the plaque.

This leads to cellular cytotoxicity and necrotic core formation, contributing to plaque erosion.

Question 8

Types of lipoproteins?

Answer 8

1. Chylomicrons and
   Very-low-density lipoproteins (VLDL) = Rich in TAG, >30nm
2. Low-density-lipoprotein (LDL) = Rich in Cholesterol, 20-22nm

1/2 Contain Apolipoprotein B = Atherogenic

3. High-density-lipoprotein
   (HDL) = Rich in protein and
   phospholipid, 9-15nm

3 Contain Apolipoprotein A1= Anti-Atherogenic

Question 9

Pathophysiology of Atherosclerosis?

Answer 9

Initiation: Endothelial damage (due to smoking, hypertension, high cholesterol) leads to increased permeability and adhesion of inflammatory cells.

Lipid Accumulation: Low-density lipoprotein (LDL) cholesterol infiltrates the arterial wall, becoming oxidized and triggering immune responses.

Plaque Formation: Foam cells (from macrophages engulfing LDL) form fatty streaks, which grow into plaques.

Complications: Plaque rupture can cause thrombosis, leading to events like heart attacks or strokes.

Question 10

Lipoproteins Progression in Atherosclerosis?

Answer 10

Low-Density Lipoproteins (LDL):
LDL particles penetrate the endothelium and accumulate in the arterial intima.
Oxidized LDL (ox-LDL) triggers an inflammatory response, attracting monocytes and macrophages.
Macrophages engulf ox-LDL, forming foam cells and initiating fatty streaks.
Continued LDL accumulation promotes plaque growth and instability.

Very-Low-Density Lipoproteins (VLDL):
Contribute to plaque formation by delivering triglycerides and cholesterol to arterial walls.

Question 11

Lipoproteins Regression in Atherosclerosis?

Answer 11

High-Density Lipoproteins (HDL): HDL facilitates reverse cholesterol transport, removing cholesterol from plaques and returning it to the liver for excretion.
HDL reduces inflammation and oxidative stress, stabilizing plaques.

Therapeutic Influence:
Lowering LDL levels (e.g., via statins) and increasing HDL activity can reduce plaque size and risk of complications.

Question 12

Initiation of Atherosclerosis

Answer 12

Endothelial Injury: Damage to the artery lining caused by factors like hypertension, smoking, or high cholesterol.

Increased Permeability: Endothelial dysfunction allows LDL cholesterol to enter the arterial wall.

Oxidation of LDL: LDL becomes oxidized, triggering an inflammatory response.

Monocyte Recruitment: Inflammatory signals attract monocytes, which enter the arterial wall and differentiate into macrophages.

Foam Cell Formation: Macrophages engulf oxidized LDL, forming foam cells, which are the earliest sign of atherosclerotic plaque.

Question 13

Triacylglycerol (TAG) and Cholesterol Transport?

Answer 13

High TAG levels impair reverse cholesterol transport by HDL, reducing cholesterol removal.

TAG-rich lipoproteins (e.g., VLDL) compete with LDL and HDL for hepatic lipase and other enzymes, altering their composition and function.

Question 14

Oral Fat Tolerance Test (OFTT)?

Answer 14

Measures the body’s ability to clear lipids (TAG) after consuming a high-fat meal.

Identifies impaired fat metabolism, linked to cardiovascular disease risk and metabolic disorders

Question 15

Postprandial Lipaemia and Aerobic Exercise?

Answer 15

Exercise reduces post-meal TAG levels by increasing lipid clearance and fatty acid oxidation.

Regular aerobic exercise enhances the efficiency of enzymes like lipoprotein lipase (LPL), which metabolizes TAG

Question 16

Acute Changes of Lipid Metabolism Changes After Exercise?

Answer 16

Increased LPL activity improves TAG clearance.

Enhanced fatty acid oxidation reduces TAG levels.

Temporary reduction in circulating TAG and increase in HDL functionality.

Question 17

Chronic Adaptations of Lipid Metabolism Changes After Exercise?

Answer 17

Improved lipid transport enzyme function (e.g., LPL, hepatic lipase).

Increased HDL concentration and efficiency in cholesterol transport.

Reduced fasting and postprandial TAG levels, lowering cardiovascular risk.