1.5, 1.6 Cardiovascular Disease Flashcards
1.5 Understand the course of events that leads to atherosclerosis (endothelial dysfunction, inflammatory response, plaque formation, raised blood pressure). 1.6 Understand the blood-clotting process (thromboplastin release, conversion of prothrombin to thrombin and fibrinogen to fibrin) and its role in cardiovascular disease (CVD).
What is atheroschlerosis?
where fatty deposits in the arteries block an artery or increase the chance of an artery being blocked by a blood clot (thrombosis)
Describe the process of athereoschlerosis:
- the endothelium is damaged (this could be due to high blood pressure or toxins)
- an inflammatory response occurs: white blood cells (mostly macrophages) move to the artery wall
- the WBCs accumulate cholesterol from the blood
- overtime, the fatty deposit builds up leading to the formation of an atheroma
- calcium salts and fibrous tissue build up at the site, resulting in a hard swelling called a plaque on the inner wall of the artery
- the artery wall loses some of its elasticity
- the plaques cause the lumen to narrow, increasing the blood pressure
- this increases the likelihood of endothelial damage
- this process is positive feedback: the formation of plaques will raise the blood pressure, increasing the likelihood of further plaque formation, which will further increase the blood pressure, and so on
Describe the blood clotting cascade:
- platelets stick to the exposed collagen on the damaged wall and to each other, forming a platelet plug
- thromboplastin (protein) is released from the damaged tissue and platelets
- thromboplastin activates an enzyme which catalyses the convertion of prothrombin (protein) into thrombin (enzyme)
- for this conversion to happen, protein factors, vitamin K, and Ca+ ions must be present in the blood plasma
- thrombin catalyses the conversion of fibrinogen (soluble protein) into fibrin (insoluble protein)
- a fibrin mesh forms, trapping more platelets and red blood cells
- this forms a clot
Why are clots necessary?
clots seal the break in the blood vessel, limiting blood loss and preventing entry of pathogens
Describe platelets:
- blood cell with no nucleus
- change from disks into spheres with projections when they come into contact with the damaged vessel wall
How does atheroschlerosis increase the chance of blood clotting?
atheromas can rupture, damaging the artery wall and leaving a rough surface, which causes thrombosis to occur
How do blood clots cause heart attacks?
- blood clots forming in coronary arteries cause the lumen to narrow, which decreases the oxygenated blood flowing to the heart
- this decreases the O2 supply of the cardiac muscles
- O2 is required for respiration, which releases energy for muscle contraction
- the cardiac muscles are then forced to respire anaerobically, which can cause angina (pain)
- if the artery is completely blocked, the blood supply to the heart muscle is completely cut off (the heart muscle is ischaemic)
- the lack of O2 leads to myocardial infarction, which can cause damage and death of the cardiac muscle
- therefore the heart cannot contract and pump blood (heart failure), leading to death
- blood clots can also become dislodged in other arteries and travel along the bloodstream to the heart, where it blocks a coronary artery
How do blood clots cause strokes?
- a blood clot blocks an artery that leads to the brain
- this limits the blood, and therefore O2 to the brain
- this causes a rapid loss of brain function, which can lead to death
How do blood clots cause deep vein thrombosis?
- prolonged inactivity can cause blood clots to form in veins
- this usually happens in the leg veins
How do blood clots cause aneurysms?
- blood clots blocking arteries can cause blood to build up behind it
- this causes the artery to bulge as it fills with blood
- this bulge can burst, which is fatal