Atherosclerosis Flashcards
What is atheroma?
Fatty plaque/deposit
What is sclerosis?
Hardening
How is arteriosclerosis different from atherosclerosis?
Arteriosclerosis is the hardening and loss of elasticity of the vessels with out the fatty deposits e.g. vascular remodelling
Atherosclerosis leads to stenosis and ischaemia in distal tubules. What do these 2 terms mean?
Stenosis = narrowing of vessels Ischaemia = Lack of O2
What sized arteries does this condition often present in?
Medium- large sized arteries
What are the 5 components of the body that atherosclerosis affect (3 are arteries)? Name a condition related to these effects.
- ) Coronary arteries - MI, angina
- ) Cerebral arteries & carotid arteries - stroke
- ) Renal arteries - renovascular disease
- ) Aorta - aortic aneurysm
- ) Arms and legs - gangrene, claudication = refered pain when exercising (o2 demand)
What is one of the initiating factors in the development of atherosclerosis?
Endothelium dysfunction/ injury. Will see changes here before any changes are seen in the vasculature
How does a defect in the production of NO effect endothelium dysfunction?
A defect in the production of NO impairs on the endothelium dependent vasodilation. This then cause an increase in the production of ET-1 (endothelin) which is a vasoconstrictor and ROS which decreases the body’s ability to produce NO further.
Explain the injury hypothesis
- ) Injury = Due to endothelium dysfunction/injury, the endothelium becomes more permeable
- ) lipids = lipoproteins start to accumulate in the sub-endothelial space. Leukocytes come along and adhere. Then the monocytes start to adhere in the gaps in the endothelium. They develop into macrophages that try to phagocytose the LDL. In this process, they become foam cells and leave fatty streaks in the endothelium. Fatty streaks are reversible but are one of the first signs of atherosclerosis.
Describe the development of an atheroma
- ) Following the development o fatty streaks and initial endothelium damage, we get continued plaque growth as more LDL is deposited in the intima.
- ) We get a compensatory mechanism where the adventita tries to absorb the plaque as not to affect the radius of the lumen = fatty build up in the elastic outer wall
- ) Eventually the plaque will become so big that it protrudes into the lumen where a fibrous cap forms on it and calcium deposits.
- ) If the fibrous cap weakens, we get a plaque rupture into the blood - this is a clot.
- ) Usually the bigger the plaque the more stable but will take up more room in the lumen
Atheromas usually develop over decades but the speed of development and size usually depends on their anatomical location (coronary, cerebral, peripheral) and exposure to risk factors. What are the risk factors and how to they affect atheroma development?
1.) Diabetes - increase glucose interferes with endothelium regulation
2.) Hypertension- vasculature remodelling
3.) Hyperlipidaemia - high cholesterol
4.) Metabolic syndrome - increase in abdominal fat
5.) Smoking - increase in exposure to ROS and free radicals which causes endothelial damage
6.) Infection
All of these stimulate inflammatory processes, lipid accumulation and calcification = endothelial damage = all of which predispose you and may initiate the production of plaques which will lead to the development of an atheroma or Coronary artery disease (if in the coronary arteries)
What are the three major blood vessels that supply the heart?
- ) Right coronary artery
- ) Left anterior descending coronary artery
- ) circumflex coronary artery
* occlusion in any one of these = heart attack *
Where are atheromas most likely to form in coronary arteries?
At hair pin bends or where the artery branches = where there is turbulent flow = where shear stress is at its highest
What is collateral vessel formation?
When there is an occlusion to a major coronary artery, the body will try and adapt and find another pathway for blood flow (and oxygen). Will supply around 25% of original supply = ok at rest
What is the myocardial oxygen balance?
The ratio between oxygen supply and oxygen demand.
To increase o2 supply we would either increase arterial oxygen content (RBC’S) or increase coronary blood flow (increase heart rate/stroke volume = CO)
if have an occlusion the body’s ability to reach demand will be compromised
