Arthersclerosis, Apoptosis, Necrosis, Hypertrophy, Hyperplasia, Atrophy, Metaplasia, Dysplasia Flashcards
What is Atherosclerosis?
A disease of the arteries characterised by the deposition of fatty material, cholesterol filled plaques on the inner walls that obstruct blood flow lengthways.
Build ups bulge into the lumen of vessels, occluding and blocking them off.
Hardening of the arteries & narrowing of the arteries due to plaque (waxy substance made predominantly of lipids) formation.
It is the main contributor to coronary heart disease/ heart attacks .
What is the first stage of Atherosclerosis formation and explain it…
- Endothelial dysfunction:
- Endothelium on inner vessel walls acts as a barrier between blood constituents and blood vessel wall, it also secretes proteins onto its surface that prevent clotting
- Damage to the endothelium can be cause by irritants such as cigarette toxins
- It is influenced by:
hypertension, hypercholesterolemia, hyperlipidaemia, obesity, insulin resistance, lack of physical activity, unhealthy diet, diabetes mellitus, age, family history, age, family history, immunodeficiency disorders, atrial fibrillation/ heart arrhythmia/ turbulent blood flow (any factors that increase likelihood of thrombus formation)
What are symptoms of atherosclerosis in the coronary arteries?
- Vomiting
- Anxiety
- Angina
- Coughing
- Feeling faint
and in severe cases ischaemia of cardiac muscle leading to heart attack/ heart failure/ myocardial ischaemia
What are symptoms of atherosclerosis in the carotid arteries?
- Weakness
- Dysphgia
- Headache
- Facial numbness/ paralysis
(as blood supply to brain is decreased)
What can atherosclerotic plaque also cause and what are its symptoms?
Peripheral vascular disease = reduced blood supply to any part of the body that is not the brain or heart.
Symptoms:
- hair loss
- erectile dysfunction
- weakening of that area
What are the symptoms of atherosclerosis in the renal arteries?
- reduction in appetite
- swelling of hands
- trigger renin release (which can in turn increase blood pressure)
In what direction does the plaque grow in the vessel wall in its initial stages?
Downwards, away from lumen of vessel, causes a bulge instead of cutting off the lumen.
Once the plaque has grown downwards in the vessel wall where does it go?
It starts to grow upwards, into the lumen of the vessel, narrowing it.
With continued growth, severity increases and vessel is extremely narrowed.
What happens if the mass of plaque formation ruptures?
When it ruptures, it causes a thrombus, which can in turn causes a clot, which stops/ impedes blood flow.
What is the normal structure of a vessel (its layers) and what does it contain that is in turn the cause of plaque formation?
- Have the lumen of the vessel that contains LDL’s and is in contact with the endothelium layer
- Beneath the endothelial layer, is the tunica intima then the tunica media (which contains smooth muscle cells) which is surrounded by adventitia
What can cause endothelial cell damage?
- A irritant present:
- Hyperlipideamia/ Hypercholesterolemia
- Toxins from cigarette smoking (carcinogens directly damage endothelial cells)
- Reactive oxygen species damage endothelium cells directly
- Nicotine is toxic to endothelial cells (strips them)
- Smoking causes higher LDL numbers
- Smoking increased blood clotting
- Hypertension
How are LDLs involved in plaque formation?
- Endothelial dysfunction; caused by high amounts of circulating LDLs, the high conc. of LDLs means that they are deposited into the tunica intima
- Once deposited in the tunica intima they become oxidised
- Oxidised LDLs activate endothelial cells, causing them to express receptors for white blood cells on their surface
- There is an aggregation of oxidised LDLs under the endothelial layer (which are activated; expressing adhesion molecules for white blood cells)
- Adhesion of leukocytes to activated endothelium allows passage of monocytes & T helper cells to move into tunica intima layer
- Once monocytes move into the tunica intima layer, they become macrophages
- Macrophages take up the oxidised LDLs and become foam cells
- Foam cells promote migration of smooth muscle cells from tunica media into tunica intima and promote smooth muscle cell proliferation
- Increased SMC proliferation = heightened synthesis of collagen = hardening of atherosclerotic plaque
- In this process, foam cells also die and release their lipid content = increased growth of plaque = building pressure that can cause rupture
Describe the structure of the vessel (specifically wall) during rupture
- Endothelial cells are damaged
- SMCs have accumulated in the tunica intima as well as collagen
- The tunica intima also contains many foam cells that have died and left behind lipid droplets (dead foam cells and their lipid content); which is the growth of the plaque
- The plaque can rupture and lead to thrombosis
What is thrombosis formation?
- When the plaque formed ruptures and coagulation happens to stop the plaque from spilling its content into lumen
- Which forms a clot/ thrombus, that impedes blood flow and can cause further complication
Why do the arteries harden in atherosclerosis?
- SMCs migrate out of the smooth muscle layer and into the fatty plaque
- The SMCs also secrete a fibrous cap of collagen and elastin over the thrombogenic plaque to prevent it from being exposed to blood
- Cytokines are also released by foam cells, which induce SMCs into depositing calcium into the plaque
What are the modifiable risk factors of atherosclerosis?
- Diet –> specifically affecting high blood pressure, and high triglyceride levels
- Exercise
- Tobacco smoking
- Lifestyle changes
- Diabetes mellitus (type 2)
- Pre diabetes
- Hypertension (increased pressure = increased plaque rupture)
- Hyperlipidaemia/ hypercholesterolemia
- high glucose levels; auto-oxidation, leading to many free radicals
What are the non-modifiable risk factors of atherosclerosis?
- Type 1 diabetes
- Age (specifically old age)
- Family history –> inheritance of other risk factors for atherosclerosis
- Gender (evidences suggests oestrogen protects endothelial cells and diet in men tends to be worse)
- Racial origin; south asian population is at much higher risk
What are primary preventative measures?
Preventative measures that come before the onset of illness or injury and before the disease process begins.
What are secondary preventative measures?
Preventative measures that lead to early diagnosis and prompt treatment of illness/ injury.
What is tertiary management?
It is the management of disease instead of preventative measures.
Not every scenario has a tertiary stage.
What is are the linear yellow lines that can be seen within vessel walls?
They are fatty streaks, collections of macrophages filled with yellow lipids.
What is the distribution of atherosclerosis?
It is much more prevalent in the systemic arterial side of the body.
