What is the initiating event that leads to the development of atherosclerosis?
Injury to the endothelial cells that line the artery walls
Release of the platelet-deprived growth factor
Macrophages adhere to vessel walls
Release of the inflammatory cytokines
The Correct Answer is A
A. Injury to the endothelial cells that line the artery walls: The development of atherosclerosis begins with damage to the endothelial cells of the arterial wall. This injury can be caused by various factors, including hypertension, smoking, high cholesterol, and diabetes. Once the endothelium is injured, it becomes more permeable, allowing lipids and inflammatory cells to penetrate and accumulate, leading to the formation of atherosclerotic plaques.
B. Release of the platelet-derived growth factor: While platelet-derived growth factor (PDGF) plays a role in the proliferation of smooth muscle cells and the progression of atherosclerosis, it is not the initiating event. PDGF is released in response to endothelial injury and inflammation but does not cause the initial damage itself.
C. Macrophages adhere to vessel walls: The adherence of macrophages to the vessel walls occurs after the initial endothelial injury. Once the endothelium is damaged, macrophages migrate to the site and contribute to the inflammatory response and plaque formation, but this is not the initiating event.
D. Release of inflammatory cytokines: Inflammatory cytokines are part of the response that follows endothelial injury and play a role in the progression of atherosclerosis. However, the release of these cytokines is a consequence of the initial injury rather than the initiating event.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is B
Explanation
A. Norepinephrine causes bronchial smooth muscle contraction and mucus secretion but it also causes high blood pressure: This statement is misleading in the context of asthma. Norepinephrine primarily acts on alpha and beta receptors, influencing blood pressure and bronchodilation but is not the main mediator in asthma pathophysiology. The focus should be on inflammation and airway responsiveness.
B. Uncontrolled inflammation leads to increased bronchial hyperresponsiveness and eventual scarring: This statement accurately describes the pathophysiologic process in asthma. Persistent inflammation in asthma can cause increased bronchial hyperresponsiveness, leading to airway narrowing and potential long-term remodeling and scarring of the airways if not controlled. Effective management is essential to prevent these adverse outcomes.
C. Immunoglobulin G causes smooth muscle contraction which will eventually weaken the respiratory muscles: Immunoglobulin E (IgE) is primarily involved in allergic reactions and asthma, and it does not directly cause smooth muscle contraction that weakens respiratory muscles.
D. The release of epinephrine leads to development of cardiac dysrhythmias: While epinephrine can have cardiovascular effects, including increased heart rate and potential for dysrhythmias, this is not directly relevant to the pathophysiology of asthma. The focus in asthma management is on controlling airway inflammation and bronchoconstriction rather than on cardiac issues.
Correct Answer is C
Explanation
A. Atherosclerotic lesion: An atherosclerotic lesion can lead to reduced blood flow to the myocardium, but it is not the direct trigger for angina pectoris. Rather, it is a contributing factor to the development of conditions that cause angina.
B. Myocardial necrosis: Myocardial necrosis refers to irreversible cell damage due to prolonged ischemia, such as in a myocardial infarction. This is not a trigger for angina pectoris but rather a consequence of severe and prolonged ischemia.
C. Myocardial ischemia: Myocardial ischemia is the primary trigger for angina pectoris. It occurs when there is an imbalance between the oxygen supply and demand in the heart muscle, typically due to narrowed coronary arteries. This insufficient blood flow results in chest pain or discomfort characteristic of angina.
D. Hyperlipidemia: Hyperlipidemia is a risk factor for atherosclerosis and subsequent coronary artery disease but does not directly trigger angina pectoris. It contributes to the underlying processes that lead to myocardial ischemia.
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