Atherosclerosis Flashcards
- In which societies is atherosclerosis the major cause of death and premature disability?
- Which part of the arteriolar wall does atherosclerosis primarily effect?
- What characterizes atherosclerosis?
- Developed societies
- The intima of large and medium-sized arteries
- The presence of atherothrombotic plaques, atherosclerotic lesions, and atheromas (atheromata)
- What is the most current theory explaining the process of atherosclerosis?
- How should we think of atherosclerosis when defining it as a disease??
- Response to injury theory
- Both a chronic inflammatory disease and a lipid metabolism disorder
- What is the first step in initiating atherosclerotic disease?
- What are the two major risk factors for this triggering event?
- How is endothelial injury the triggering event for the development of atherosclerotic lesions?
- Endothelial injury acts as the triggering event
- Hemodynamic stress from HTN, and chronic hyperlipidemia
- When damaged the endothelium releases vWF, which aggregates platelets and mediates their adhesion to the subendothelium causing the formation of the platelet plug; the activation of platelets leads to inflammation which draws WBCs and macrophages to the ares
-What is the second step in the development of an atherosclerotic lesion?
-Infiltration of LDL: The more LDL you have, the more infiltrates the opening in the endothelium and gets deposited below the basement membrane of the tunica intima. This LDL gets oxidized and causes more endothelial inflammation. This recruits more macrophages and they become large and distended and are now called foam cells. Foam cell death plays an important role in the formation and growth of the atheroma.
- What is step 3 in the development of atherosclerosis?
- By what age are these usually seen?
- What do they consist of?
- The accumulation of foam cells in the intima develops into fatty streaks. These are the first grossly visible lesions in the devo of atherosclerosis
- Age 20!!
- Lipid-containing foam cells, T cells, aggregated platelets, smooth muscle cells
- What is step 4 in the development of atherosclerosis?
- As the plaque grows, what occurs before stenosis of the artery?
- What forms if the plaque remains stable?
- What is the purpose of this cap?
- Formation of a fibrous plaque. Over time, fatty streaks can remain stable, regress, or evolve into fibrous plaques
- Arteriolar wall thickening occurs before narrowing
- A fibrous cap forms and the lesions becomes calcified. Eventually vessel remodeling occurs and the lumen may become narrowed
- It provides stability to the plaque by walling off the lesions and preventing it from coming into contact with blood, which is good because the atheroma’s lipid core is soft, weak, and highly prothrombotic
- What does the development of clinical features of atherosclerosis depend on?
- What are the defining characteristics of a vulnerable plaque?
- The fate of the fibrous cap. As long as it is stable and intact, the plaques will remain stable or progress slowly
- A thin fibrous cap, a large lipid-rich necrotic core, a higher concentration of macrophages
-What is step 5 in the development of atherosclerosis?
-Rupture of the fibrous cap leading to intravascular thrombus. Once the cap ruptures, it allows blood to come into contact with the thrombotic core, blood flow becomes turbulent and a cascade of events culminate in intravascular thrombosis. This is the problem in most people
- What do the outcome of plaque rupture and thrombus formation depend on?
- What does a partial vessel occlusion lead to?
- What can a complete vessel occlusion lead to?
- When are these episode more common?
- Whether or not the vessel becomes occluded
- Stable angina/ischemia, claudication, or TIA, depending on vessel location
- ACS (unstable angina, STEMI, NSTEMI), claudication, stroke, depending on the vessel location
- In the early morning or shortly after rising
-What role does collateral circulation play in atherosclerosis?
- With it: In a patient with chronic multi-vessel occlusive CAD, collateral channels can form. In these cases, even a total arterial occlusion may not lead to a clinically significant outcome (MI) or it may produce an unexpectedly modest or a NSTEMI. The collateral vessels bypass the blockage in the main artery and supply enough O2 to allow the cardiac tissue to survive or recover.
- Without it: In a patient with less advanced disease and without substantial stenotic lesions to provide a stimulus for collateral vessel formation, sudden plaque rupture and arterial occlusion commonly produces an STEMI.
-What is the cause of most clinical manifestations of atherosclerosis?
-The rupture oa an atherosclerotic plaque, NOT artery stenosis
-What are the major risk factors for atherosclerosis?
Hyperlipidemia Hypertension Smoking DM Obesity Insulin resistance/metabolic syndrome Physical inactivity Unhealthy diet Gender (male) Age (women after 55, men after 45) Family history
-What are other risk factors?
High levels of CRP in blood (sign of inflammation) High triglycerides (especially in women) Sleep apnea Stress Persistent heavy alcohol use Elevated homocysteine levels
-What are the coronary heart disease risk equivalents?
- A 10-year risk of having heart disease greater than 20% according to the Framingham Cardiac Risk Calculator
- Clinical coronary heart disease (CHD)
- Symptomatic carotid artery disease (CAD)
- Peripheral arterial disease (PAD)
- Abdominal aortic aneurysm (AAA)
- Diabetes mellitus
- By what age do fully developed atheromatous plaques usually appear?
- Is atherosclerosis more common in men or women?
- Are there genetic and familial factors with atherosclerosis?
- 40
- Men
- Yes. Genetic derangements of lipoprotein metabolism predispose the individual to high blood lipid leves and familial hypercholesterolemia, also children of parents with heart disease are more likely to develop it themselves
