PA5.6 | Infarction & Thrombus Morphology — Practical — Summary & Reflection

REFLECT

Before you move to the summary, take 2 minutes to sketch your own '4-step reading framework' from memory — organ, colour/shape, age, mechanism. Then answer:

1. A pulmonary infarct is haemorrhagic. A renal infarct is pale. Both are caused by arterial occlusion (embolism). Why is one red and the other white?

1. You are given a slide with coagulative necrosis + dense collagen replacing the entire field, and no viable cells. How old is this lesion, and what does it tell you about the patient's clinical course?

1. On a viva, how would you distinguish a postmortem clot from an antemortem thrombus using only gross features (no microscopy)?

If you can answer all three confidently, you are ready for the examination on this module.

KEY TAKEAWAYS

Key take-aways from this module:

Gross classification:
• Pale infarcts — solid organs, end-arterial supply (heart, kidney, spleen). Firm, grey-white, wedge-shaped.
• Red infarcts — dual supply, venous occlusion, or loose tissue (lung, intestine). Haemorrhagic, dark.
• Wedge shape — base at organ surface, apex toward occluded vessel (hilum in kidney).

Gross ageing:
Hyperemic rim (hours) → pale/yellow-white (days) → granulation tissue margin (1–2 weeks) → fibrous scar (weeks–months).

Microscopy — necrosis pattern:
• Coagulative necrosis (most infarcts): ghost cells with intact outlines, nuclear loss, neutrophils → macrophages → granulation tissue → scar.
• Liquefactive necrosis (brain only): cystic softening, no ghost cells.

Thrombus morphology:
• Lines of Zahn = alternating pale (fibrin-platelet) + dark (red cell) layers = antemortem thrombus, attached.
• Chicken-fat / currant-jelly = no layering = postmortem clot, not attached.

Reading approach: Organ → Gross colour/shape → Micro necrosis type → Age the lesion → State mechanism.