Week 7 Flashcards
What are common cardiac pathologies?
- angina pectoris, myocardial infarction, heart failure, valve dysfunction, arrhythmias, inflammation
What are common vascular pathologies?
- atherosclerosis, peripheral artery disease, coronary disease, varicose veins, hypertension/hypotension
What is arteriosclerosis?
hardening & thickening of arterial wall (cause of CAD)
What is the most common type of arteriosclerosis?
artherosclerosis
What is atherosclerosis?
- an inflammatory response to endothelial cell injury
- characterized by the build-up of atherosclerotic ‘plaques’ (atheroma) within the vessel wall
What are the atherosclerotic plaques (atheroma) made of?
lipids (cholesterol), cell debris, fibrin, thrombus vessel wall
What are the most common arteries in descending order for atherosclerosis?
- abdominal aorta and iliac arteries
- proximal coronary arteries
- thoracic aorta, femoral and popliteal arteries
- internal carotid arteries
- vertebral basilar, and middle cerebral arteries
What are the risk factors for atherosclerosis?
- age
- family history
- hypertension
- diabetes mellitus
- dyslipidemia
- smoking, diet, sedentary lifestyle
What is dyslipidemia?
- an imbalance of lipid components in the blood
- can be classified by any of the following:
→ high triglycerides
→ high cholesterol
→ high levels of low-density lipoproteins
→ low levels of high-density lipoproteins
Lipids are transported in combo with….
proteins
Describe low-density lipoproteins
- transports cholesterol from liver to cells
- major factor contributing to atheroma formation
Describer high-density lipoproteins
- transport cholesterol away from peripheral cells o liver
- breakdown in liver & excretion
Describe the pathogenesis of atherosclerosis
damage to endothelial cells → LDL enters into the intimal layer & become oxidized → macrophages eat up lipids; foam cells; creates a fatty streak → inflammatory response; growth factor released → smooth muscle cell proliferation & migration from tunica media into the tunica intima, fibroblasts recruited → growth of extracellular matrix; formation of fibrous cap over a lipid core = fibrous plaque
What happens with the pathogenesis of atherosclerosis over time?
the foam cells within the lipid core undergo necrosis → release of enzymes that eat at fibrous cap → eventual rupture → platelets activated & adhere to site → thrombus forms at site of rupture → thrombus occludes the lumen of the artery & can detach & travel to occlude a distal artery
What are the potential consequences from atherosclerosis?
- ischemia (at least 70% of lumen occluded)
→ CAD → angina pectoris
→ PAD → claudication - total occlusion/plaque rupture → clot detachment
→ myocardial infarction, ischemic stroke - weakened vessel wall
→ aneurism
How can atherosclerosis be diagnosed?
screening tests to asses risk
→ blood cholesterol level (HDL, LDL)
→ blood pressure
→ exercise stress testing
imaging
→ coronary angiography - visualize blood flow in coronary arteries
→ ultrasound - visualize blood flow in peripheral vessels
What is the treatment for atherosclerosis?
risk reduction
→ dietary/lifestyle intervention
→ pharmaceutical measures: antihypertensives, cholesterol-lowering, anticoaugulants
→ maintenance of existing conditions (e.g. type 2 diabetes, hypertension)
surgical intervention
→angiplasty
→ bypass
Describe the two types of angioplasty
- balloon angioplasty: catheter with an inflatable balloon flattens the atheroma when inflated
- laser angioplasty: catheter with a laser → inserted into a narrow part of the artery → laser disintegrates the plaque
- a stent may be inserted after the angioplasty to maintain opening
What is a coronary artery bypass graft?
- open heart surgery
- heart is arrested and cooled
- circulation bypass using a heart-lung machine
- artery with plaques physically removed
- replaced with a piece of saphenous vein from leg or mammary artery
What is angina pectoris?
- chest pain due to myocardial ischemia
- due to vessel occlusion and/or inability to vasodilate to meet perfusion demand
- stable (transient, usually due to exertion) or unstable (prolonged pain at rest)
- angina can be treated with rest, lifestyle, modification, nitroglycerin, surgical intervention
- can be a warning sign for MI (especially when unstable)
What is a myocardial infarction?
coronary artery is completely blocked → ischemia → cell necrosis → infarction
- size, location, & duration determine severity of damage
- damage may be reversible if blood supply is restored within 1 hour
- enzymes are released from the damaged/dead myocardial cells → released into the blood
What are the common ways to develop a infarction?
- atheroma progresses to obstruct artery
- thrombus breaks away and lodges in small branch
What are the signs and symptoms of myocardial infarction?
pain:
- sudden, severe crushing - substernal chest pain with radiation to left arm, shoulder, jaw or neck
- can be milder & present as indigestion, jaw pain
pallor, sweating, nausea, dizziness, dyspnea
anxiety
hypotension, rapid & weak pulse due to decreased cardiac output
How is myocardial infarction diagnosed?
- ECG changes
- blood markers (released by necrotic cells): myoglobin, CPK-MB, AST, LDH-1, cardiac specific troponin
