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Questions and Answers
Which step of the chronic inflammatory response involves the migration of lymphocytes into the intima?
What is the consequence of atherosclerosis that occurs when the lipid core of a plaque is exposed?
What is the macroscopic appearance of a fatty streak?
What is the microscopic appearance of a stable plaque?
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What is the consequence of plaque rupture in atherosclerosis?
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What is the consequence of an increase in lipid accumulation in atherosclerosis?
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What is the consequence of luminal narrowing in atherosclerosis?
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What is the consequence of plaque rupture in atherosclerosis?
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What is the consequence of luminal obstruction in atherosclerosis?
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What is the consequence of a blood clot formation in atherosclerosis?
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Which of the following is the correct sequence of events in the development of atherosclerosis?
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What is the main cause of endothelial damage in atherosclerosis?
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What happens to monocytes in the development of atherosclerosis?
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What are foam cells in the context of atherosclerosis?
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What is the earliest lesion of the atheroma called?
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What is the main role of smooth muscle cells in the development of atherosclerosis?
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What initiates the chronic inflammatory response in atherosclerosis?
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What causes the endothelium to become leaky in atherosclerosis?
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What is the role of monocytes in the development of atherosclerosis?
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What is the main factor that attracts monocytes in the development of atherosclerosis?
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Study Notes
Chronic Inflammatory Response and Lymphocyte Migration
- Migration of lymphocytes into the intima marks a critical step in the chronic inflammatory response in atherosclerosis.
Consequences of Atherosclerosis
- Exposure of the lipid core of a plaque can lead to thrombosis, resulting in blood vessel occlusion and potential ischemic events.
- Luminal narrowing restricts blood flow, potentially leading to angina or tissue ischemia.
- Increase in lipid accumulation contributes to plaque growth and instability, raising the risk of rupture.
- Plaque rupture can result in the release of thrombogenic material, leading to acute vascular events like myocardial infarction.
Fatty Streak and Plaque Appearance
- Macroscopically, a fatty streak appears as yellowish streaks on the arterial wall and is an early indicator of atherosclerosis.
- Microscopically, a stable plaque is characterized by a fibrous cap and lipid-rich necrotic core, with smooth muscle cells contributing to plaque stability.
Consequences of Obstructions and Clots
- Luminal obstruction due to plaque can diminish organ perfusion, resulting in ischemic symptoms.
- Formation of a blood clot (thrombus) at the plaque site can completely obstruct blood flow, leading to severe complications.
Sequence of Atherosclerosis Development
- The development of atherosclerosis follows a sequence: endothelial injury, monocyte recruitment, foam cell formation, and plaque maturation.
Endothelial Damage and Inflammatory Response
- Endothelial damage is primarily caused by factors such as hypertension, smoking, and elevated LDL cholesterol levels.
- Increased permeability of the endothelium allows lipoproteins and leukocytes to penetrate the arterial wall.
Role of Monocytes and Foam Cells
- Monocytes migrate into the arterial wall in response to inflammatory signals and differentiate into macrophages.
- Foam cells, formed from lipid-laden macrophages, are crucial contributors to plaque development and progression.
Early Lesions and Smooth Muscle Role
- The earliest lesion of the atheroma is called a fatty streak, marking the onset of atherosclerosis.
- Smooth muscle cells play a significant role by proliferating and forming a fibrous cap that stabilizes plaques.
Factors Attracting Monocytes
- Chemotactic factors such as oxidized LDL and cytokines attract monocytes to sites of endothelium damage, initiating inflammation and atherogenesis.
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Description
Test your knowledge on atherosclerosis and learn about the mechanisms involved in the development of atheroma, as well as the macroscopic and microscopic appearances of the condition. Explore topics such as chronic endothelial damage and the chronic inflammatory response.
