Atherosclerosis Flashcards
Define atherosclerosis
A condition where the arteries narrow & harden due to the build-up of plaque made of calcium, fatty deposits etc. This plaque reduces the blood flow as the lumen narrows, creating higher pressure, increased afterload and reducing the heart’s efficiency as a pump. It creates a mismatch between supply and demand, less blood enters the heart so less blood is pumped out of the heart
What indicator suggests inflammation to endothelium lining
The release of nitric oxide by endothelial cells signals inflammation
Define a low density lipoprotein
A type of protein that carries cholesterol throughout the bloodstream, contributes to the build-up of plaques.
LDL is composed of a core of cholesterol and triglyceride. The primary role of LDL is to transport cholesterol from the liver to various tissues in the body, Where it is used to build cell membranes, produce hormones, and perform other vital functions. hen its levels are too high, it can deposit cholesterol in the walls of arteries, narrowing them and potentially blocking blood flow
Describe stage 1 in atherosclerosis: endothelial injury
Cells in the endothelial become damaged e.g., high BP/ smoking, this creates injury resulting in the endothelium becoming more permeable leading to the accumulation of substances
Describe stage 2 in atherosclerosis: Lipid accumulation
LDL’s penetrate endothelium, once inside they become oxidized, this is harmful as it triggers the formation of foam cells & an immune response
Foam cells contribute to plaque formation
Describe stage 3 in atherosclerosis: Migration of WBC/inflammatory cells
Presence of oxidized LDL’s cause WBC e.g., monocytes & macrophages to attempt to engulf them as they are seen as foreign to the body. WBC get stuck in the sub-endothelium and become foam cells, they cannot pass back into the vessel, cytokines stimulate smooth muscle proliferation, muscle expands but does not contract, forms a fibrous cap over damaged area
Describe stage 4 in atherosclerosis: plaque structure
Foam cells collect substances such as calcium & collagen & deposit them to form a fatty streak, over time streak thickens, more substances e.g., lipids are added, forming a plaque which bulges out into the lumen of the vessel, reducing blood flow
Describe what happens when the plaque ruptures
If plaque ruptures, platelets arrive to fix the damage, they are very sticky & may cause vessel occlusion, the blood clot can grow large enough to completely block the artery, leading to MI’s, strokes, PAD
Fibrous cap could break off and embolize e.g., pulmonary embolism
Where is atherosclerosis most likely to occur
The most common site is in medium to large arteries or arteries that have many kinks & turns.
Bifurcated vessels (into 2)
Renal, carotid & coronary
Describe the clinical manifestations of atherosclerosis
Atherosclerosis takes time to develop so often remains asymptomatic
1. Angina, pain in the chest caused by lack of blood flow, feels like tightness, pressure
2. MI, rupture of plaque forms a thrombus which travels and creates a blockage, SOB, chest pain, nausea
3. Stroke, reduced blood flow to the brain, if plaque breaks of can block carotid arteries causing a stroke, numbness, trouble speaking, dizziness
Describe coronary artery and peripheral artery disease
CAD: Atherosclerosis in carotid arteries leads less blood flow to the brain, increased risk of TIA’s & strokes, symptoms of numbness, paralysis, visual changes
PAD: peripheral artery disease, where arteries of limbs have reduced flow, leading to pain e.g., cramps, numbness etc
Describe non-modifiable risk factors associated with atherosclerosis & the impact on pathogenesis
- Age, risk increases after 45 in men & 55 in women, blood vessels become less elastic and more prone to damage
- Gender, males have a greater risk of atherosclerosis, and hormonal changes in women post-menopause increase risk
- Genetics, strong family history of cardiovascular disease, genetic predisposition to inflammation & high cholesterol
Describe modifiable risk factors associated with atherosclerosis & the impact on pathogenesis
- Hypertension, damages endothelium,which accelerates plaque formation and hardening of arteries
- Obesity, associated with high BP, cholesterol & LDL, this can increase lipid levels & inflammation
- poor diet, leads to obesity, high in fat & refined carbs, raises LDL & inflammation
- Smoking, raises LDL, damages endothelial cells, lowers HDL, inflammation, increases oxidative stress & vascular inflammation
- Excessive Drinking, leads to high BP & elevated triglycerides, risk of lipid build-up and endothelial damage
Describe the financial burden atherosclerosis has on the healthcare system
- increased costs: increased treatment & surgeries on strokes, MI’s etc, as well as treatment of chronic management of cardiovasc conditions
- Increased deman on specialist care: higher demand for surgeons, cardiologists etc, increased need for rehabilitation centres & services & follow-ups
- Strain: puts strain on emergency services, ambulances & emergency rooms
