Pathology Cheat Sheet
Vessel Block to Tissue Death
Embolism and infarction for NEET-PG: saddle, fat, air and amniotic emboli, paradoxical embolism, red vs white infarcts, and wedge-shaped organ infarcts.
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Vessel Block to Tissue Death
Embolism and infarction for NEET-PG: saddle, fat, air and amniotic emboli, paradoxical embolism, red vs white infarcts, and wedge-shaped organ infarcts.
Embolism, ischaemia and infarction, including special embolus types and the gross features of infarcts.
High-yield lines
- An embolus is a detached intravascular mass carried by blood to lodge at a distant site, and most emboli are thromboemboli.
- A saddle embolus lodges at the pulmonary artery bifurcation and can cause acute right heart failure and sudden death.
- Paradoxical embolism occurs when a venous thrombus crosses a patent foramen ovale or septal defect to reach the systemic circulation.
- Fat embolism follows long bone fractures and presents as respiratory distress, neurological signs, and a petechial rash.
- Amniotic fluid embolism presents with sudden collapse, respiratory failure, and disseminated intravascular coagulation during labour.
- Air embolism requires a large bolus (over 100 mL) to form a cardiac air lock, and decompression sickness releases nitrogen bubbles causing the bends.
- White (pale, anaemic) infarcts occur in solid organs with end-arterial supply such as heart, spleen, and kidney.
- Red (haemorrhagic) infarcts occur in loose tissues with dual blood supply such as lung and intestine, and in venous occlusion.
- Renal and splenic infarcts are pale wedge-shaped lesions with the apex pointing to the occluded vessel.
- Most infarcts show coagulative necrosis, but brain infarcts show liquefactive necrosis.
- Neurons suffer irreversible ischaemic injury within 3 to 5 minutes, while cardiomyocytes tolerate about 20 to 40 minutes.
- Amniotic fluid embolism is confirmed by fetal squames, mucin, and lanugo hair in maternal pulmonary vessels.
Mapped competency codes
- PA6.5
- PA6.6
- PA6.7
Continue into the full chapter
This summary maps to PA6-hemodynamic-disorders.
Frequently Asked Questions
What is the classic triad of fat embolism syndrome?
Respiratory insufficiency, neurological dysfunction, and a petechial rash, typically arising a day or two after a long bone fracture.
Which organs develop pale (white) infarcts?
Solid organs with an end-arterial supply such as the heart, spleen, and kidney, where collateral flow cannot re-perfuse the necrotic tissue.
Why does the lung develop red infarcts?
Because it has a dual blood supply and loose spongy tissue, allowing haemorrhage into the infarcted area.
What is paradoxical embolism?
Passage of a venous embolus into the systemic arterial circulation through a patent foramen ovale or septal defect, causing systemic embolism from a venous source.
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