CEN Pathology Practice Questions (420 Flashcards)

STEMI involves a complete, persistent occlusion of a major epicardial coronary artery, usually caused by a fibrin-rich red thrombus following plaque rupture. This leads to transmural (full-thickness) myocardial ischemia. NSTEMI typically involves a partial or transient occlusion, often by a platelet-rich white thrombus, resulting in subendocardial (partial-thickness) ischemia. CEN Strategy: BCEN emphasizes complete vs. partial occlusion to determine the urgency of reperfusion therapy (PCI vs. medical management).

The subendocardial layer is affected. This is characteristic of an NSTEMI. Pathophysiologically, the subendocardium is most vulnerable to ischemia because it is the furthest from epicardial coronary blood supply and is subject to the highest intramyocardial wall tension during systole. In NSTEMI, the injury vector points toward the endocardium (away from the electrode), resulting in ST depression. Clinical Pearl: Subendocardial ischemia does not usually produce Q-waves, which are markers of transmural necrosis.

The Zone of Injury surrounds the central zone of infarction (necrosis). Cells in this zone are potentially salvageable but currently undergoing anaerobic metabolism and losing the ability to maintain membrane potential. This manifests as ST-segment elevation. Reperfusion (PCI/Fibrinolytics) targets this zone to prevent it from progressing to irreversible necrosis. BCEN Tip: Differentiate the three zones: Ischemia (T-wave inversion), Injury (ST elevation), and Infarction (Q-waves).

Type 1 MI is caused by acute atherothrombotic plaque rupture or erosion with thrombus formation. Type 2 MI is myocardial necrosis (elevated troponin) caused by a supply-demand mismatch without acute plaque rupture. Common triggers include severe tachycardia, sepsis, respiratory failure, or extreme hypertension. CEN Strategy: If the scenario involves a patient with a non-cardiac primary illness (e.g., GI bleed) and rising troponin, consider Type 2 MI pathophysiology rather than primary ACS.

Reciprocal changes are ST-segment depressions in leads anatomically opposite the area of transmural injury (STEMI). They represent the electrical mirror image of the ST-elevation vector. Their presence is a highly specific indicator of a STEMI and helps differentiate it from mimics like pericarditis (which typically shows diffuse STE without reciprocal changes). Distractor Alert: BCEN may ask you to identify reciprocal leads (e.g., ST depression in I and aVL during an inferior MI).