STEMI Pathophysiology Quiz

What is the pathophysiology of STEMI?

• The pathophysiology of STEMI involves a partial blockage of a coronary artery due to a blood clot forming on a ruptured plaque, leading to ischemia and cell death in the heart muscle.

• The pathophysiology of STEMI involves a complete blockage of a coronary artery due to a blood clot forming on an intact plaque, leading to ischemia and cell death in the heart muscle.

• The pathophysiology of STEMI involves a narrowing of a coronary artery due to a blood clot forming on a ruptured plaque, leading to ischemia and cell death in the heart muscle.

• The pathophysiology of STEMI involves a complete blockage of a coronary artery due to a blood clot forming on a ruptured plaque, leading to ischemia and cell death in the heart muscle.

What causes the occlusion of a coronary artery in STEMI?

• Viral infection

• High blood pressure

• Atherosclerosis

• Blood clot or thrombus

What happens to the myocardium during a STEMI?

• The myocardium becomes hyperemic and undergoes apoptosis.

• The myocardium becomes atrophic and undergoes inflammation.

• The myocardium becomes ischemic and undergoes necrosis.

• The myocardium becomes hypertrophic and undergoes fibrosis.

What are the key steps in the pathophysiology of STEMI?

• Plaque rupture or erosion, thrombus formation, complete occlusion, ischemia and necrosis

• Plaque rupture or erosion, thrombus formation, no occlusion, ischemia and necrosis

• Plaque rupture or erosion, thrombus formation, partial occlusion, ischemia and necrosis

• Plaque rupture or erosion, thrombus formation, delayed occlusion, ischemia and necrosis

How does ischemia lead to myocardial infarction in STEMI?

• Ischemia leads to myocardial infarction by causing a blockage or reduction in blood flow to the heart muscle.

• Ischemia leads to myocardial infarction by causing a decrease in blood pressure.

• Ischemia leads to myocardial infarction by increasing blood flow to the heart muscle.

• Ischemia leads to myocardial infarction by causing a decrease in heart rate.

What role does plaque rupture play in the pathophysiology of STEMI?

• Plaque rupture leads to the formation of a blood clot and subsequent myocardial infarction (STEMI).

• Plaque rupture triggers the release of enzymes that break down the blood clot and restore blood flow.

• Plaque rupture results in the narrowing of the coronary arteries, leading to reduced blood flow.

• Plaque rupture causes the release of inflammatory mediators that lead to vasodilation and increased blood flow.

What are the consequences of prolonged ischemia in STEMI?

• Irreversible damage to the heart muscle

• Increased risk of arrhythmias

• Improved cardiac function

• Decreased risk of heart failure

How does the body respond to myocardial infarction in STEMI?

• The body responds to myocardial infarction in STEMI by decreasing blood pressure and heart rate.

• The body responds to myocardial infarction in STEMI by activating the sympathetic nervous system, releasing inflammatory mediators, and initiating an immune response.

• The body responds to myocardial infarction in STEMI by releasing anticoagulant substances.

• The body responds to myocardial infarction in STEMI by reducing oxygen supply to the heart.

What are the potential complications of STEMI?

• pulmonary embolism

• pericarditis

• heart failure, arrhythmias, cardiogenic shock, ventricular septal rupture, and death

• myocardial infarction

How does reperfusion therapy affect the pathophysiology of STEMI?

• Reperfusion therapy has no effect on the pathophysiology of STEMI.

• Reperfusion therapy increases myocardial damage in STEMI.

• Reperfusion therapy delays patient outcomes in STEMI.

• Reperfusion therapy restores blood flow to the blocked coronary artery in STEMI, reducing myocardial damage and improving patient outcomes.