Haemodynamic Disorders for NEET PG Pathology: Oedema, Shock, Virchow Triad, Thrombophilia, Embolism, Infarction

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🎯 Exam priority: High. Expect: mechanism of oedema in a scenario, the type of shock, Virchow triad, factor V Leiden, the source of pulmonary emboli, paradoxical and amniotic fluid embolism, and why lung infarcts are uncommon.

CBME mapping: PA 5.1–5.6. Normal haemostasis and bleeding disorders are in article 14.

Oedema, shock, Virchow triad, thrombophilia and emboli. Drawn by TrackNation.

Oedema

• Oedema is extra interstitial fluid — mostly water, but protein- and cell-rich with infection or lymphatic block. Four mechanisms: raised hydrostatic pressure (heart failure: symmetric, dependent, pitting); low oncotic pressure (nephrotic syndrome, protein-losing enteropathy, liver failure, starvation); raised permeability (infection, toxins, inflammation); lymphatic obstruction (lymphoedema; filariasis in endemic areas, sometimes genital).

• Ascites = free fluid in the peritoneal cavity. Pulmonary oedema impairs gas exchange. Cytotoxic brain oedema (intracellular) follows hypoxic or ischaemic injury.

Hyperaemia, Congestion and Haemorrhage

• Hyperaemia (active, arterial) = more inflow; congestion (passive, venous) = blocked outflow.

• Haemorrhage = escape of blood from a vessel. Petechiae (pinpoint) < purpura < ecchymosis (> 2–3 cm, flat bruise); a haematoma is a collection of blood outside vessels.

Shock

Shock is failure to perfuse or oxygenate vital organs: cool clammy skin, confusion, lactate > 2 mmol/L, urine < 0.5 mL/kg/h. Hypotension (SBP < 90 or MAP < 65) is common but not required. Cells switch to anaerobic metabolism; if shock persists, damage becomes irreversible. In septic (distributive) shock the skin may be warm and flushed; septic shock is sepsis with hypotension or hypoperfusion despite fluids.

Thrombosis

• Virchow triad: stasis, endothelial injury, hypercoagulability. DVT begins in venous valve cusps; venous thrombi are red (fibrin and red cells, few platelets). Causes: immobility, leg fractures, cancer.

• Inherited thrombophilia: factor V Leiden (R506Q; factor Va resists activated protein C — the commonest cause of APC resistance), prothrombin 20210 mutation, deficiency of protein C, protein S or antithrombin, raised factors VIII, IX and XI.

Embolism and Infarction

Infarction is necrosis from local ischaemia, usually a thrombus or embolus. Pulmonary infarcts appear as pleural-based wedges but are uncommon because the lung has a dual (bronchial and pulmonary) supply. A negative D-dimer makes PE very unlikely when pre-test probability is low.

Traps the Examiner Sets

• Nephrotic or liver failure oedema = low oncotic pressure; heart failure = high hydrostatic pressure.

• Septic shock is distributive (warm skin early); tamponade is obstructive.

• Pulmonary emboli come from leg/pelvic veins; paradoxical emboli need a right-to-left shunt.

• Lung infarcts are rare: dual blood supply.

Memory Hooks & Shortcuts

Shortcuts to lock in this article's numbers and lists. Each one only re-packages facts proven above.

• 🧠 Pump, Pipe, Plasma, Plumbing — hydrostatic, permeability, oncotic, lymphatic oedema

• 🧠 HDCO: Hole (volume lost), Dilated, Can't pump, Obstructed — four shock types

• 🧠 Virchow's SEH: Stasis, Endothelium, Hypercoagulable — Virchow triad

• 🧠 Leiden Leaves Va alone (APC can't cut it) — factor V Leiden

• 🧠 Paradox needs a Passage (PFO/ASD) — paradoxical embolism

• 🧠 FAT after Femur, AIR after Ascent — fat and gas emboli

• 🧠 Two pipes save the lung — dual blood supply

Rapid-Revision Cards

• Oedema mechanisms

  ↑ hydrostatic, ↓ oncotic, ↑ permeability, lymphatic block.

• Nephrotic/liver oedema

  Low oncotic pressure.

• Heart-failure oedema

  Symmetric, dependent, pitting — high hydrostatic.

• Filariasis

  Lymphoedema, sometimes genital.

• Cytotoxic brain oedema

  Intracellular; hypoxia/ischaemia.

• Hyperaemia vs congestion

  Active inflow vs passive outflow block.

• Ecchymosis

  > 2–3 cm flat bleed.

• Shock types

  Hypovolaemic, distributive, cardiogenic, obstructive.

• Distributive

  Vasodilation, normal volume — sepsis, anaphylaxis, neurogenic.

• Obstructive

  Tamponade, tension pneumothorax.

• Shock markers

  Lactate > 2; urine < 0.5 mL/kg/h; SBP < 90 or MAP < 65.

• Virchow triad

  Stasis, endothelial injury, hypercoagulability.

• Venous thrombus

  Red; valve cusps; few platelets.

• Factor V Leiden

  R506Q; APC resistance.

• PE source

  Leg/pelvic DVT.

• Saddle embolus

  Pulmonary artery bifurcation.

• Paradoxical embolus

  ASD/PFO → stroke.

• Fat embolus

  Large-bone fractures.

• Amniotic fluid embolism

  Hypoxia, hypotension, coagulopathy in labour.

• Decompression sickness

  Nitrogen bubbles; recompression.

• Lung infarcts rare

  Dual blood supply.

Sources

Facts in this article were checked against these documents.

• MSD Manual Professional: Edema; Shock; Deep Venous Thrombosis; Pulmonary Embolism — Merck & Co. (MSD Manuals), reviewed 2025–26 (link)

• MSD Manual Professional: Amniotic Fluid Embolism; Decompression Sickness; Overview of Thrombotic Disorders — Merck & Co. (MSD Manuals), reviewed 2025–26 (link)

• Medical Subject Headings (MeSH) scope notes — US National Library of Medicine, accessed 2026 (link)

• Competency Based Undergraduate Curriculum, Pathology (PA 5) — National Medical Commission, 2024

Test Yourself: Practice Questions

Thirty questions in NEET PG style, most of them clinical vignettes.

Practice Questions (NEET PG pattern)

Original questions written in the style of the exam: +4 for a correct answer, −1 for a wrong one. Every answer was checked against the sources listed above. NEET PG papers are not published by NBEMS, so these are not past-paper questions.

Q1. A child with nephrotic syndrome has generalised oedema. The main mechanism is

• (a) increased capillary permeability from infection

• (b) low plasma oncotic pressure

• (c) lymphatic obstruction

• (d) raised capillary hydrostatic pressure

Q2. A man with right heart failure has symmetric, dependent, painless, pitting leg oedema. The mechanism is

• (a) raised capillary hydrostatic (venous) pressure

• (b) lymphatic obstruction

• (c) allergic permeability

• (d) low oncotic pressure

Q3. A man from a filaria-endemic area has long-standing swelling of one leg and the scrotum. The mechanism is

• (a) venous thrombosis

• (b) low oncotic pressure

• (c) right heart failure

• (d) lymphatic obstruction (lymphoedema)

Q4. Oedema fluid that is rich in protein and cells points to

• (a) nephrotic syndrome

• (b) infection or lymphatic obstruction

• (c) starvation

• (d) heart failure

Q5. After a severe hypoxic-ischaemic insult, the brain swells from fluid inside the cells. This is

• (a) vasogenic oedema only

• (b) cytotoxic brain oedema from hypoxic-ischaemic injury

• (c) lymphoedema

• (d) hydrocephalus

Q6. Increased blood in an organ because venous outflow is obstructed is called

• (a) active hyperaemia

• (b) passive (venous) congestion

• (c) infarction

• (d) haemorrhage

Q7. A flat purplish skin bleed larger than 2–3 cm is called

• (a) a petechia

• (b) purpura simplex only

• (c) an ecchymosis

• (d) a haematoma

Q8. A collection of blood outside blood vessels, within a tissue or space, is a

• (a) embolus

• (b) petechia

• (c) thrombus

• (d) haematoma

Q9. A patient with pneumonia has hypotension despite adequate fluids, warm flushed skin and a bounding pulse. The shock type is

• (a) hypovolaemic

• (b) obstructive

• (c) distributive (septic)

• (d) cardiogenic

Q10. Distributive shock differs from hypovolaemic shock because

• (a) the heart fails as a pump

• (b) blood volume is lost

• (c) blood volume is normal but vessels are dilated

• (d) great vessels are blocked

Q11. After a large myocardial infarction, a patient develops shock from failure of cardiac output. The shock type is

• (a) obstructive

• (b) cardiogenic

• (c) distributive

• (d) hypovolaemic

Q12. A trauma patient is in shock caused by cardiac tamponade. The shock type is

• (a) hypovolaemic

• (b) obstructive

• (c) cardiogenic

• (d) distributive

Q13. A patient with a high spinal cord injury (above T4) becomes hypotensive. The shock is

• (a) obstructive

• (b) cardiogenic

• (c) neurogenic — a form of distributive shock

• (d) hypovolaemic always

Q14. A laboratory marker of tissue hypoperfusion in shock is a blood lactate above

• (a) 10 mmol/L

• (b) 20 mmol/L

• (c) 0.5 mmol/L

• (d) 2.0 mmol/L

Q15. Hypotension in shock is usually defined as

• (a) systolic < 90 mm Hg or mean arterial pressure < 65 mm Hg

• (b) systolic < 120

• (c) diastolic < 80

• (d) mean arterial pressure < 100

Q16. Septic shock is defined as sepsis with

• (a) hypotension or hypoperfusion despite adequate fluid resuscitation

• (b) a raised white count

• (c) fever alone

• (d) bacteraemia alone

Q17. The three factors of Virchow's triad are

• (a) fever, pain and swelling

• (b) anaemia, jaundice and splenomegaly

• (c) stasis, endothelial injury and hypercoagulability

• (d) hypertension, diabetes and smoking

Q18. An immobilised patient after a leg fracture develops a calf DVT. The thrombus is typically

• (a) red — fibrin and red cells with few platelets, starting at valve cusps

• (b) made of fat

• (c) infected

• (d) white — platelets only

Q19. A young woman with recurrent DVT has a mutation that makes activated factor V resistant to activated protein C. This is

• (a) prothrombin 20210 mutation

• (b) haemophilia

• (c) factor V Leiden (R506Q)

• (d) antithrombin deficiency

Q20. Which of these is an inherited cause of venous thrombosis listed by MSD?

• (a) protein C or protein S deficiency

• (b) vitamin K deficiency

• (c) haemophilia A

• (d) von Willebrand disease

Q21. Nearly all pulmonary emboli arise from

• (a) the portal vein

• (b) the left atrium

• (c) deep vein thrombi in the legs or pelvis

• (d) arm veins

Q22. A large embolus is found straddling the bifurcation of the main pulmonary artery. This is a

• (a) fat embolus

• (b) paradoxical embolus

• (c) saddle embolus

• (d) air embolus

Q23. A man with a leg DVT suddenly has a stroke. Echocardiography shows a patent foramen ovale. This is

• (a) paradoxical embolism

• (b) fat embolism

• (c) septic embolism

• (d) air embolism

Q24. After a fracture of a large bone, a patient develops an embolus that is not a blood clot. The classic type is

• (a) air embolism

• (b) tumour embolism

• (c) amniotic fluid embolism

• (d) fat embolism

Q25. During labour, a woman suddenly develops hypoxia, hypotension and bleeding from a coagulopathy. The likely cause is

• (a) amniotic fluid embolism

• (b) pulmonary thromboembolism

• (c) placenta praevia

• (d) eclampsia

Q26. A diver who surfaced rapidly develops severe joint pain and confusion. The cause and treatment are

• (a) fat embolism — steroids

• (b) air in the pleura — chest drain

• (c) hypoglycaemia — glucose

• (d) nitrogen bubbles from rapid decompression — recompression therapy

Q27. Air embolism usually follows

• (a) large-bone fractures

• (b) labour

• (c) DVT

• (d) trauma, surgery or changes in atmospheric pressure

Q28. Pulmonary infarction is uncommon after pulmonary embolism because

• (a) the lung has no veins

• (b) emboli always dissolve

• (c) the lung has a dual blood supply (bronchial and pulmonary)

• (d) lung tissue does not need oxygen

Q29. An infarct is

• (a) fluid in tissues

• (b) a collection of blood outside vessels

• (c) necrosis from local ischaemia, usually due to a thrombus or embolus

• (d) a type of shock

Q30. In an outpatient with low pre-test probability of PE, a negative D-dimer

• (a) means DVT is present

• (b) makes pulmonary embolism very unlikely

• (c) is useless

• (d) confirms PE

Active Recall

From memory: give the four mechanisms of oedema with an example each; distinguish hyperaemia and congestion; classify the four types of shock with causes and markers; state Virchow triad and the inherited thrombophilias; and describe pulmonary, saddle, paradoxical, fat, air and amniotic fluid emboli, decompression sickness and why lung infarcts are uncommon.