High-Yield (Robbins Pathology): The hallmark of pulmonary infarction is hemorrhagic infarction with preservation of the underlying alveolar architecture — at least in the early/acute phase. Key microscopic features include:
| Feature | Description |
|---|---|
| Necrosis type | Coagulative necrosis — cell outlines preserved, nuclei lost (ghost outlines) |
| Hemorrhage | Extensive intra-alveolar hemorrhage filling alveolar spaces |
| Alveolar architecture | Intact/preserved — the alveolar walls and septal framework remain recognizable |
| Inflammatory response | Minimal early; neutrophilic infiltration appears at the margins later |
| Timing | Hemorrhagic infarct visible within 24–48 h; organization begins day 5–7 |
This is why Option A — hemorrhagic infarction with intact alveolar architecture — is the correct answer. The lung, unlike solid organs, undergoes hemorrhagic (not pale) infarction, and the preserved alveolar scaffold is the key distinguishing histological feature.
Option B describes "coagulative necrosis with neutrophilic infiltration and fibrin deposition." While coagulative necrosis is indeed the underlying necrosis type, the defining and distinguishing histological hallmark of pulmonary infarction is the hemorrhagic character with preserved alveolar architecture — not neutrophilic infiltration (which is more characteristic of bacterial pneumonia/abscess) or prominent fibrin deposition (more characteristic of DAD/ARDS). Option B's description more closely resembles an organizing pneumonia or early abscess than a classic pulmonary infarct.
| Condition | Key Histological Feature |
|---|---|
| PE with infarction | Hemorrhagic infarction, preserved alveolar outline, coagulative necrosis |
| Bacterial pneumonia | Purulent (neutrophilic) exudate, organisms, no preserved architecture |
| Tuberculosis | Caseous (cheese-like) necrosis, granulomas, Langhans giant cells, AFB |
Mnemonic: HIPA — Hemorrhagic infarction, Intact alveolar architecture, Pulmonary embolism, Acute coagulative necrosis.
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