How does angiotensin II increase the workload of the heart after a myocardial infarction (MI)?
By causing dysrhythmias as a result of hyperkalemia
By increasing the peripheral vasoconstriction
By stimulating the sympathetic nervous system
By reducing the contractility of the myocardium
The Correct Answer is B
A. By causing dysrhythmias as a result of hyperkalemia: Angiotensin II does not directly cause dysrhythmias through hyperkalemia. While hyperkalemia can lead to dysrhythmias, angiotensin II primarily acts as a vasoconstrictor and does not directly influence potassium levels.
B. By increasing peripheral vasoconstriction: Angiotensin II increases peripheral vascular resistance through vasoconstriction, which raises blood pressure. This increased resistance requires the heart to work harder to pump blood, thereby increasing the workload on the heart following a myocardial infarction.
C. By stimulating the sympathetic nervous system: Angiotensin II does stimulate the sympathetic nervous system, which can increase heart rate and contractility; however, the direct effect on increasing workload is more prominently due to peripheral vasoconstriction.
D. By reducing the contractility of the myocardium: Angiotensin II does not reduce contractility; in fact, it can enhance contractility in some contexts. It primarily increases the workload of the heart through vasoconstriction and increased afterload rather than reducing contractility.
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Related Questions
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.
Correct Answer is A
Explanation
A. Actually, people who have the latent form of the disease won't be sick and can't spread it either: This response is accurate because individuals with latent tuberculosis infection (LTBI) do not exhibit symptoms and are not infectious. They carry the bacteria in their body, but it remains dormant and does not spread to others. Only those with active tuberculosis disease are capable of transmitting the infection through respiratory droplets.
B. Many people do manage to fight off the infection, but you are right: they can still spread it by coughing or sneezing: This statement is misleading because it implies that individuals with LTBI can spread the disease, which is not the case. Only those with active TB are contagious.
C. There isn't any real risk of them spreading it, but we would like to vaccinate everyone who's had any contact with it in the past: This response downplays the importance of understanding the difference between latent and active TB and could create confusion. Vaccination for tuberculosis (BCG vaccine) is not routinely given in the United States, and exposure alone does not necessitate vaccination.
D. If someone has been previously exposed to tuberculosis, they are particularly infectious because they are often unaware of the disease: This statement is incorrect, as individuals who have been exposed but have LTBI are not infectious. It is only those with active TB who pose a risk of spreading the infection.
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