ILA 1 - atherosclerosis Flashcards
describe the structure of the walls of a normal arterial vessel
- Tunica external / adventitia
Collagen and elastic fibres - structural support
Vasa vasorum – smaller vessels supplying vessel wall
Nerve fibres - Tunica media
Smooth muscle cells
Elastic and Collagen fibres
external elastic lamina - Tunica intima / interna
Endothelial cells
Subendothelial layer
Internal elastic lamina
what does the left coronary artery divide into and what areas of the heart does this supply?
Left coronary artery divides into:
Left anterior descending – supplies the anterior wall of the left ventricle
Left circumflex – supplies the lateral and posterior walls of the left ventricle
what does the right coronary artery divide into and what areas of the heart does this supply?
- Right marginal artery – supplies the right ventricle
- Posterior descending artery – supplies the posterior interventricular septum and inferior wall of the left ventricle
where does the blood that supplies the heart muscle drain?
Coronary veins – drain deoxygenated blood from the myocardium into the coronary sinus, which then empties into the right atrium
outline coronary artery dominance
- Right dominance – RCA supplies the posterior descending artery
- Left dominance - LCx supplies the posterior descending artery
- Co-dominant circulation – both right and left coronary arteries contribute to the PDA
- the posterior descending artery supplies the majority of the left ventricle
- most people 80-85% have right dominance
- this is good because if there is a block in either L or R coronary artery, the other unblocked branch would still supply the ventricle, keeping it alive
explain why the majority of embolisms which lead to cardiac infarction are from the systemic system
- because any embolisms in the pulmonary system get trapped in the small arterioles in the lung and filtered away, or cause damage
outline the main stages in the formation of an atherosclerotic plaque
- Endothelial cells will become damaged, causing gaps to form in the wall of the vessel (becoming leaky)
- LDL (cholesterol) gets into the wall of the vessel from the lumen – it typically only gets into the tunica intima and media and will never really reach the externa. – it usually gathers in areas of turbulent flow – where the flow isn’t lamina flow – so for example at curves and bends
- Damaged endothelial cells release pro-inflammatory molecules such as cytokines, these attract macrophages
- Macrophages then engulf the oxidised LDL and over time they become overloaded with LDL particles and turn into foam cells
- Foam cells then accumulate and form fatty streaks
- The continued accumulation of foam cells, lipids and cellular debris leads to the formation of a plaque
- Smooth muscle cells which form deeper layers of the artery wall, migrate into the plaque and secrete collagen and other fibrous materials, forming a cap over the plaque
- Over time the plaque contains smooth muscle cells, calcium deposits and fibrous tissue as well – it also becomes calcified
- As the plaque grows, a fibrous cap growth to contain it – ongoing inflammation can weaken this cap, making it likely to rupture, this means all these things will be exposed to the bloodstream, causing a clot formation, this may obstruct an artery and cause infarction to tissues.
- If the fibrous cap ruptures, this can lead to a thrombus forming – this can grow and potentially obstruct the vessel causing ischemia or infarction, or it can break off and become lodged in a different vessel, causing an embolism
- Damaged epithelial cells produce less nitric oxide which keeps blood vessels dilated and prevents excess clotting, with less of this the vessels tend to constrict more and are more prone to clots
what are the modifiable risk factors for atherosclerosis?
- Smoking – free radicals, nicotine, carbon monoxide damages endothelium allowing for more LDLs to stick
- Hypertension – force can damage the endothelium making it easier for cholesterol to build up
- Poorly controlled diabetes and insulin resistance– superoxide anions and glycosylation products
- Hyperlipidaemia – direct damage because of the higher amount of LDLs, the more likely they are to build into plaques
- Physical inactivity – contributes to hypertension, high LDLs, insulin resistance ect
- Diet high in saturated fats – increase levels of LDL
- Obesity
what are the non-modifiable risk factors for atherosclerosis?
- Old age – stiffer arteries so plaques more likely to form
- Men have a higher risk up to when women go through the menopause – this is because oestrogen increases HDL cholesterol which help to remove LDLs
- Ethnicity – African americans may tend to have higher blood pressure
- family history - genetics
outline how smoking causes endothelial damage
- free radicals and oxidative stress - break down cell lipids, proteins and dna
- can trigger apoptosis
- causes upregulation of adhesion molecules causing vessels to become sticku which weakens endothelium barrier
- inactivate proteins and enzymes - lead to less production of NO leading to vasoconstriction which increases the inflammatory responce
- carbon monoxide and nicotine: Blocks oxygen, Causes cell damage, Stops vessel relaxation, Triggers inflammation, Kills cells, Raises blood pressure
what are co-benefits, and give an example?
- things which better your health and wellbeing, as well as bettering the planet
- an example is cycling, better because it produces less greenhouse gasses and gives the patient more exercise than driving
is calcium found in vessel walls
yes lol
chemoattractants and inflam cytokines found in plaques
il-1
il-6
il-8
IFN-y
TGF-B
MCP-1
C reactive protein
is CAD dynamic
yes
