week 8 Flashcards
Unchangeable CVD risks ?
Gender
Family history
Age
Race
Changeable CVD risk factors?
Smoking
Physical inactivity
Obesity
Diet
High cholesterol
high blood pressure
insulin resistance
Current physical activity recommendation from the Department of Health? % below?
30 minutes of moderate intensity physical activity on five or more days of the week
65% men below, 76% women below
Structure of artery ?
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.
What can initiate atherosclerosis ? plaque?
Atherosclerosis Initiation: Endothelial cell damage, often due to factors like high cholesterol, hypertension, or smoking, triggers the process.
Plaque Formation: Endothelial damage exposes underlying connective tissue, which promotes the accumulation of lipids and the development of plaque.
Inflammatory Response: Inflammatory cytokines trigger immune cell infiltration (diapedesis), leading to further plaque growth and instability.
Plaque progression? Causes of Plaque Growth?
Cellular Activation: Platelets, endothelial cells, and macrophages release growth factors (e.g., PDGF), promoting smooth muscle cell migration from the media to the intima.
Lipid Deposition: Oxidized LDL-C (oxLDL) is deposited in the plaque, contributing to its growth.
Plaque Growth: As the plaque expands, it narrows the arterial lumen, restricting blood flow.
Plaque erosion?
Plaque erosion occurs when macrophages and smooth muscle cells release matrix metalloproteinases (MMPs) and reactive oxygen species (ROS), which destabilize the plaque.
This process leads to cellular cytotoxicity and the formation of a necrotic core, contributing to the erosion of the plaque and potentially increasing the risk of thrombosis(blood clot) as there is a gap in surface which plaetelets cover.
Types of lipoproteins?
- Chylomicrons and
Very-low-density lipoproteins (VLDL) = Rich in TAG, >30nm - Low-density-lipoprotein (LDL) = Rich in Cholesterol, 20-22nm
1/2 Contain Apolipoprotein B = Atherogenic
- High-density-lipoprotein
(HDL) = Rich in protein and
phospholipid, 9-15nm
3 Contain Apolipoprotein A1= Anti-Atherogenic
Pathophysiology of Atherosclerosis?
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.
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.
Complications: Plaque rupture can cause thrombosis, leading to events like heart attacks or strokes.
Lipoproteins Progression in Atherosclerosis?
Low-Density Lipoproteins (LDL) particles penetrate the endothelium and accumulate in the arterial intima.
Once in there 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.
Lipoproteins Regression in Atherosclerosis?
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.
How do triacylglycerol (TAG) levels affect cholesterol transport?
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.
Oral Fat Tolerance Test (OFTT)?
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
Postprandial Lipaemia and Aerobic Exercise?
Aerobic exercise reduces post-meal triglyceride (TAG) levels by increasing lipid clearance and enhancing fatty acid oxidation. Regular exercise improves the efficiency of enzymes like lipoprotein lipase (LPL), which are crucial for TAG metabolism, leading to better overall lipid management.
Acute Changes of Lipid Metabolism Changes After Exercise?
TAG is cleared due to:
- Increased LPL activity.
- Enhanced fatty acid oxidation
A temporary reduction in circulating TAG increases HDL functionality promoting better lipid metabolism and cardiovascular health.
Chronic Adaptations of Lipid Metabolism Changes After Exercise?
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.
