Lecture 4 Vascular Disorders Flashcards
(41 cards)
What is atherosclerosis?
Is chronic inflammatory response to some triggering injury to endothelium. Also a build up of plaque in the arteries.
Initiation stage of atherosclerosis
Damage to endothelium
• LDL accumulates in intima and
becomes oxidized
• Endothelial cells express
adhesion molecules that
attract monocytes
• Monocytes enter the intima
and become macrophages
Progression stage of atherosclerosis
• Continual release of inflammatory
mediators recruit monocytes and
smooth muscle cells (SMCs) to
intima
• Macrophages and SMCs engulf
oxidized lipids and become foam
cells
• Foam cells undergo apoptosis and release contents within the
intima, triggering a continuous cycle of cell proliferation and death
• Accumulation of oxidized LDL, dead cells, extracellular debris→
formation of necrotic core
• SMCs produce extracellular matrix → formation of fibrous cap
• Erosion of vasa vasorum → hemorrhage into plaque
• Calcium salts deposited → blood vessels harden
What are some clinical consequences of atherosclerosisosclerosis
What are some clinical consequences of atherosclerosis
Plaque stability
- thickness and composition of fibrous cap
- size of atheroma
- degree of inflammation
- emotional or physical stress
Critical stenosis
Occlusion by thrombus
Aneurysm and rupture
Form mainly in elastic and muscular arteries
How to diagnose atherosclerosis
Imaging
Measure BP
Exercise or stress testing
Prevention of atherosclerosis
diet, exercise, no smoking, normal weight
Treatment of atherosclerosis
Medications
- statins
- antihypertensives
- anti platelets
- glycemic control
Surgery
- vascular bypass surgery
- angioplasty and stenting
- endarterectomy
What is PAD?
Narrowing of arteries other than the heart
Clinical presentation:
- intermittent claudication
- pale and blueish skin
- cold skin
- no healing ulcers
- abnormal hair growth
What is an aneurysm
- Abnormal localized dilation of the arterial wall
- classified by layers of vessel involved, shape, and location
Atherosclerotic Plaque / Atheroma
The lesion formed by atherosclerosis. Takes decades to create/grow
Basic Plaque Structure
Cells (SMC, macrophages) ECM (collagen, elastin) Lipids (intra/extracellular) May contain blood, calcium
Atherosclerosis Risk Factors
Male, older age Dyslipidemia, HTN, Diabetes, Smoking Obesity, inactivity, stress Endothelial damage
Dyslipidemia & Atherosclerosis
High cholesterol risk Lipids form lipoproteins (chylomicrons, VLDL, LDL) LDL carries ~75% cholesterol Too many LDL, not enough HDL is bad
Plaque Progression
Inflammatory mediators recruit cells Macrophages/SMCs engulf oxidized lipids → foam cells Foam cells die, release contents → necrotic core SMCs produce ECM → fibrous cap
Atherosclerosis Key Process
Inflammation of vessel wall
Aneurysm Types/Classification
Layers involved, shape, location True vs. false Berry aneurysms (intracranial)
Aneurysm Pathogenesis/Risk Factors
Compromised connective tissue in wall Atherosclerosis, hypertension Genetic (Marfan, Ehlers-Danlos) Inflammation Trauma
Aortic Aneurysm Types
Thoracic Aortic Aneurysm (TAA) Abdominal Aortic Aneurysm (AAA)
Abdominal Aortic Aneurysm (AAA)
90% aortic aneurysms Smoking major risk factor Usually asymptomatic May cause pain (abdomen/back), pulsatile mass
Thoracic Aortic Aneurysm (TAA)
<10% aortic aneurysms HTN major risk factor Usually asymptomatic May cause dyspnea, cough, dysphagia, hoarseness, pain
Aneurysm Complications
Rupture (medical emergency) Risk increases with size Rapid bleeding → shock Abrupt pain (chest, neck, back, abdomen) Often fatal Thrombi may form → emboli → organ ischemia
Aneurysm Diagnosis/Management
Incidental diagnosis by imaging AAAs by palpation Monitor growth with serial imaging Reduce risk factors (quit smoking, control HTN/cholesterol, avoid heavy lifting) Surgery for large aneurysms
