Unit 1 Exam CMN 574: Chest Pain & Heart Failure
Questions with Accurate Answers
1. What pathophysiological event primarily triggers Acute
Coronary Syndrome (ACS)?
ANSWERS>: Atherosclerotic plaque rupture or erosion, exposing
the lipid core to the bloodstream, triggering platelet adhesion,
aggregation, and thrombus formation.
2. How does Prinzmetal (vasospastic) angina differ from classic
angina in terms of ECG findings and timing?
ANSWERS>: Prinzmetal angina occurs at rest (often midnight to
early morning) and is characterized by transient ST-segment
elevation due to coronary artery spasm, whereas classic angina
occurs with exertion and typically shows ST-segment
depression.
3. A patient presents with chest pain. ECG shows ST depressions
in leads V1-V4. Which area of the myocardium is experiencing
ischemia?
ANSWERS>: The posterior wall of the left ventricle. (V1-V4 are
anterior leads, but ST depressions in these leads are a reciprocal
mirror image of posterior ST elevation).
,4. What is the mechanism of action of Aspirin in the
management of ACS?
ANSWERS>: Aspirin irreversibly acetylates and inhibits
cyclooxygenase-1 (COX-1), preventing the formation of
thromboxane A2, thereby inhibiting platelet aggregation.
5. Why are second-generation P2Y12 inhibitors (like Ticagrelor
or Prasugrel) preferred over Clopidogrel in ACS?
ANSWERS>: They have a faster onset of action, more potent
platelet inhibition, and less variability in patient response
compared to clopidogrel, which requires hepatic conversion and
is subject to genetic polymorphisms.
6. A patient with STEMI is being considered for fibrinolytic
therapy. What are absolute contraindications to administration?
ANSWERS>: Prior intracranial hemorrhage, known structural
cerebral vascular lesion, ischemic stroke within 3 months,
suspected aortic dissection, active bleeding or bleeding
diathesis, or significant closed-head or facial trauma within 3
months.
, 7. What is the pharmacological mechanism of Nitroglycerin in
relieving anginal pain?
ANSWERS>: Nitroglycerin is metabolized to nitric oxide, which
activates guanylate cyclase, increasing cGMP. This leads to
smooth muscle relaxation, causing venodilation (decreasing
preload) and arteriolar dilation (decreasing afterload), reducing
myocardial oxygen demand.
8. A patient receives Nitroglycerin and develops reflex
tachycardia. What is the appropriate pharmacological
intervention to counteract this?
ANSWERS>: Administer a beta-blocker to blunt the reflex
sympathetic nervous system response and decrease myocardial
oxygen consumption.
9. Why is the combination of Nitroglycerin and
Phosphodiesterase-5 (PDE5) inhibitors (e.g., sildenafil) strictly
contraindicated?
ANSWERS>: PDE5 inhibitors prevent the breakdown of cGMP.
When combined with Nitroglycerin (which increases cGMP
production), it causes severe, synergistic vasodilation resulting
in profound, life-threatening hypotension.
Questions with Accurate Answers
1. What pathophysiological event primarily triggers Acute
Coronary Syndrome (ACS)?
ANSWERS>: Atherosclerotic plaque rupture or erosion, exposing
the lipid core to the bloodstream, triggering platelet adhesion,
aggregation, and thrombus formation.
2. How does Prinzmetal (vasospastic) angina differ from classic
angina in terms of ECG findings and timing?
ANSWERS>: Prinzmetal angina occurs at rest (often midnight to
early morning) and is characterized by transient ST-segment
elevation due to coronary artery spasm, whereas classic angina
occurs with exertion and typically shows ST-segment
depression.
3. A patient presents with chest pain. ECG shows ST depressions
in leads V1-V4. Which area of the myocardium is experiencing
ischemia?
ANSWERS>: The posterior wall of the left ventricle. (V1-V4 are
anterior leads, but ST depressions in these leads are a reciprocal
mirror image of posterior ST elevation).
,4. What is the mechanism of action of Aspirin in the
management of ACS?
ANSWERS>: Aspirin irreversibly acetylates and inhibits
cyclooxygenase-1 (COX-1), preventing the formation of
thromboxane A2, thereby inhibiting platelet aggregation.
5. Why are second-generation P2Y12 inhibitors (like Ticagrelor
or Prasugrel) preferred over Clopidogrel in ACS?
ANSWERS>: They have a faster onset of action, more potent
platelet inhibition, and less variability in patient response
compared to clopidogrel, which requires hepatic conversion and
is subject to genetic polymorphisms.
6. A patient with STEMI is being considered for fibrinolytic
therapy. What are absolute contraindications to administration?
ANSWERS>: Prior intracranial hemorrhage, known structural
cerebral vascular lesion, ischemic stroke within 3 months,
suspected aortic dissection, active bleeding or bleeding
diathesis, or significant closed-head or facial trauma within 3
months.
, 7. What is the pharmacological mechanism of Nitroglycerin in
relieving anginal pain?
ANSWERS>: Nitroglycerin is metabolized to nitric oxide, which
activates guanylate cyclase, increasing cGMP. This leads to
smooth muscle relaxation, causing venodilation (decreasing
preload) and arteriolar dilation (decreasing afterload), reducing
myocardial oxygen demand.
8. A patient receives Nitroglycerin and develops reflex
tachycardia. What is the appropriate pharmacological
intervention to counteract this?
ANSWERS>: Administer a beta-blocker to blunt the reflex
sympathetic nervous system response and decrease myocardial
oxygen consumption.
9. Why is the combination of Nitroglycerin and
Phosphodiesterase-5 (PDE5) inhibitors (e.g., sildenafil) strictly
contraindicated?
ANSWERS>: PDE5 inhibitors prevent the breakdown of cGMP.
When combined with Nitroglycerin (which increases cGMP
production), it causes severe, synergistic vasodilation resulting
in profound, life-threatening hypotension.
