Lecture 9 - Atheroma, thrombosis and embolism Flashcards
What do Atheroma, thrombosis and embolisms cause?
Major cause of morbidity and mortality
Myocardial infarction
Cerebral infarction
Pulmonary embolism
what is an atheroma?
Intimal lesion that protrudes into a vessel wall. It consists of a raised lesion with a soft core of lipid (mainly cholesterol and cholesterol esters) and is covered by a fibrous cap.
What is found in the fibrous cp?
Smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin
what is found in the necrotic centre?
Cell debris, cholesterol crystals, foam cells, calcium
(Can become calcified)
what are foam cells?
Macrophages that engulf the lipids
What do you get excess lipid in atheroma development?
Macrophages absorb lipids and turn into foam cells however they are good at absorbing it so there is left over lipids.
What are some commonly affected vessels of atheroma?
Bifurcations (sites of turbulent flow)
Abdominal aorta
Coronary arteries
Popliteal arteries
Carotid vessels
Circle of Willis
What are some non- modifiable risk factors?
Increasing age
Male gender
Family history
Genetic abnormalities
What are some modifiable risk factors?
Hyperlipidemia (LDL: HDL)
Hypertension
Cigarette smoking
Diabetes
C-reactive proteins
What does atherosclerosis start with?
Atherosclerosis starts with damage or injury to the inner layer of an artery.
What can damage to the inner layer of an artery be caused by?
High blood pressure
High cholesterol
An irritant, such as nicotine
Certain diseases, such as diabetes
How does atherosclerosis develop in response to endothelial injury?
Atherosclerosis develops as a chronic inflammatory response of the arterial wall to endothelial injury.
How does lesion progression occur?
Lesion progression occurs through interactions of modified lipoproteins, monocyte-derived macrophages, T-lymphocytes, and the normal cellular constituent of the arterial wall.
How is the contemporary view of atherosclerosis expressed?
response-to-injury hypothesis
What are the steps after the response to injury in atherosclerosis?
- Endothelial dysfunction (Increased permeability, leukocyte adhesion, monocyte adhesion and emigration)
- Smooth muscle emigration from media to intima. Macrophage activation.
- Macrophages and smooth muscle cell engulf lipid
- Smooth muscle proliferation, collagen and other ECM deposition, extracellular lipid
What is the fatty streak?
The earliest lesion in atherosclerosis
Composed of lipid filled foamy macrophages
Begins as multiple minute flat yellow spots that eventually coalesce into streaks >= 1cm
These lesions are not significantly raised and do not cause flow disturbance
Do all fatty streaks form a plaque?
Not all fatty streak are destined to progress to atheromatous plaque
Nevertheless coronary fatty streaks begin to form in adolescence at the same anatomical sites that later tend to develop plaques
Atherosclerotic plaque characteristics?
Consists of intimal thickening and lipid accumulation
Appears white yellow and superimposed thrombus on the plaque appears red
Plaque impinges on the vessel lumen
Sequelae of atherosclerosis:
Rupture, ulceration or erosion of the intimal surface exposes the blood to highly thrombogenic substances and induces thrombosis… Lumen occlusion…ischemia
Haemorrhage into plaque
Atheroembolism
Aneurysm formation
what is a thrombus?
A solid mass of blood constituents formed within the vascular system in vivo
What is the most common cause of arterial thrombosis?
Arterial thrombosis most commonly superimposed on atheroma
What is the most common cause of venous thrombosis?
Venous thrombosis is most commonly due to stasis
What are the three factors of Virchow’s triad?
- endothelial injury
- Abnormal Blood flow
- Hypercoaguliability
Mechanism of Arterial thrombosis?
Typically from rupture of atheromatous plaque
