Why is the attack of COVID-19 on ACE II detrimental to health?

Study for the Pathophysiology Pulmonary Exam. Explore detailed questions with hints and explanations. Prepare thoroughly for your exam and enhance your respiratory pathophysiology knowledge!

Multiple Choice

Why is the attack of COVID-19 on ACE II detrimental to health?

Explanation:
The attack of COVID-19 on ACE2 receptors is detrimental to health primarily because it results in the dominant fibrotic and inflammatory effects of ACE. ACE2 plays a critical role in the renin-angiotensin system, where it helps to balance the effects of angiotensin II, which can cause vasoconstriction and inflammatory responses when in excess. When the virus binds to and diminishes the availability of ACE2, it disrupts this balance. With lower ACE2 levels, there is an increase in angiotensin II activity, which promotes vasoconstriction, inflammation, and fibrosis in the lungs. This can lead to acute respiratory distress syndrome (ARDS) and other severe pulmonary complications. Essentially, the receptor’s loss amplifies the damaging effects of angiotensin II, resulting in increased inflammation and fibrosis, which can significantly impair lung function and overall cardiovascular health. Maintaining ACE2 function is key to supporting lung health, and its disruption contributes to the severe respiratory symptoms and long-term health implications seen in COVID-19 patients. Therefore, the correct answer emphasizes the detrimental consequences of this pathway alteration.

The attack of COVID-19 on ACE2 receptors is detrimental to health primarily because it results in the dominant fibrotic and inflammatory effects of ACE. ACE2 plays a critical role in the renin-angiotensin system, where it helps to balance the effects of angiotensin II, which can cause vasoconstriction and inflammatory responses when in excess. When the virus binds to and diminishes the availability of ACE2, it disrupts this balance.

With lower ACE2 levels, there is an increase in angiotensin II activity, which promotes vasoconstriction, inflammation, and fibrosis in the lungs. This can lead to acute respiratory distress syndrome (ARDS) and other severe pulmonary complications. Essentially, the receptor’s loss amplifies the damaging effects of angiotensin II, resulting in increased inflammation and fibrosis, which can significantly impair lung function and overall cardiovascular health.

Maintaining ACE2 function is key to supporting lung health, and its disruption contributes to the severe respiratory symptoms and long-term health implications seen in COVID-19 patients. Therefore, the correct answer emphasizes the detrimental consequences of this pathway alteration.

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