🧠 STEP 10 — Student Memory Support
🃏 1️⃣ High-Yield Flashcards
What is thrombosis?
Pathological formation of a solid mass from blood constituents within the cardiovascular system during life.
What are the three components of Virchow triad?
Endothelial injury, abnormal blood flow and hypercoagulability.
Which component of Virchow triad is most important in venous thrombosis?
Venous stasis.
Which blood-flow abnormality is more important in arterial and cardiac thrombosis?
Turbulence.
What is the mechanism of Factor V Leiden thrombophilia?
Resistance of factor V to inactivation by activated protein C.
Which inherited anticoagulant deficiencies increase venous thrombosis risk?
Antithrombin, protein C and protein S deficiencies.
What are lines of Zahn?
Alternating pale platelet-fibrin layers and dark red-cell layers in an antemortem thrombus.
What are the major possible outcomes of a thrombus?
Propagation, embolization, dissolution, organization and recanalization.
What is an embolus?
A detached intravascular solid, liquid or gaseous mass carried to a distant site.
What is a paradoxical embolus?
A venous embolus that enters systemic arterial circulation through a right-to-left shunt.
What is the most common source of pulmonary thromboembolism?
Proximal deep veins of the lower limb.
How does a large pulmonary embolus produce hypotension?
Pulmonary vascular resistance rises, causing acute right-ventricular failure and reduced left-ventricular filling.
What is the typical gross morphology of a pulmonary infarct?
Hemorrhagic, wedge-shaped, peripheral and pleural-based.
What are the common clinical features of pulmonary embolism?
Sudden dyspnea, pleuritic chest pain, tachypnea, tachycardia, hypoxemia and sometimes hemoptysis or syncope.
What is the main use of D-dimer in suspected pulmonary embolism?
To help exclude pulmonary embolism in selected patients with low or intermediate clinical probability.
Which investigation commonly confirms pulmonary embolism in a stable patient?
CT pulmonary angiography.
What is the treatment foundation for most patients with pulmonary embolism?
Anticoagulation.
When is systemic thrombolysis mainly considered in pulmonary embolism?
When pulmonary embolism causes persistent hypotension, shock or cardiac arrest.
How does mitral stenosis cause pulmonary hypertension?
Raised left-atrial pressure is transmitted backward into the pulmonary circulation.
What is the main management principle in pulmonary hypertension due to left-heart disease?
Treat the underlying cardiac disease and relieve congestion.
🧠 2️⃣ Mnemonics
Mnemonic Title: Virchow Triad
Mnemonic Word: E-S-H
Meaning:
- E — Endothelial injury
- S — Stasis or abnormal flow
- H — Hypercoagulability
Mnemonic Title: Fate of a Thrombus
Mnemonic Word: PEDO
Meaning:
- P — Propagation
- E — Embolization
- D — Dissolution
- O — Organization and recanalization
Mnemonic Title: Major Pulmonary Embolism Clues
Mnemonic Word: STOP
Meaning:
- S — Sudden dyspnea
- T — Tachycardia and tachypnea
- O — Oxygen saturation falls
- P — Pleuritic chest pain
Mnemonic Title: Acquired Thrombosis Risks
Mnemonic Word: SIMPLES
Meaning:
- S — Surgery
- I — Immobilization
- M — Malignancy
- P — Pregnancy
- L — Long-distance travel
- E — Estrogen exposure
- S — Smoking
📋 3️⃣ Memory Tables
Table 1 — Antemortem Thrombus vs Postmortem Clot
| Feature | Antemortem Thrombus | Postmortem Clot |
|---|---|---|
| Attachment | Attached to vessel wall | Not attached |
| Consistency | Firm and friable | Gelatinous |
| Surface | Rough or laminated | Smooth |
| Lines of Zahn | May be present | Absent |
| Formation | During life | After circulation stops |
Table 2 — Pulmonary Embolism Risk Categories
| Category | Key Finding | Main Management Logic |
| High risk | Hypotension, shock or cardiac arrest | Supportive care plus urgent reperfusion assessment |
| Intermediate risk | Stable BP with RV dysfunction or raised biomarkers | Anticoagulation and close monitoring |
| Low risk | Stable with no major RV strain | Anticoagulation; selected early discharge |
⚡ 4️⃣ Rapid Revision Points
Must Remember
- Virchow triad explains most pathological thrombosis.
- Stasis is the key mechanism in deep-vein thrombosis.
- Factor V Leiden causes activated protein C resistance.
- Lines of Zahn support an antemortem thrombus.
- Most pulmonary emboli arise from proximal lower-limb DVT.
- Pulmonary embolism causes hypoxemia through ventilation-perfusion mismatch.
- Massive pulmonary embolism causes shock through acute right-ventricular failure.
- A pulmonary infarct is hemorrhagic, wedge-shaped and pleural-based.
- A positive D-dimer does not confirm pulmonary embolism.
- CT pulmonary angiography is the main confirmatory investigation in stable patients.
- Anticoagulation prevents thrombus extension and recurrent embolization.
- Cardiac pulmonary hypertension is treated by managing the underlying heart disease.
🩺 5️⃣ Clinical Memory Hooks
Clinical Hook 1
Recent surgery + swollen calf + sudden dyspnea → Deep-vein thrombosis with pulmonary embolism
Clinical Hook 2
Pulmonary embolism + hypotension + raised JVP → Acute right-ventricular failure causing obstructive shock
Clinical Hook 3
Pleuritic pain + hemoptysis + peripheral wedge-shaped opacity → Pulmonary infarction
Clinical Hook 4
Recurrent thrombosis + prolonged phospholipid-dependent clotting test → Antiphospholipid antibody syndrome
Clinical Hook 5
Mitral stenosis + loud P2 + raised JVP + edema → Pulmonary hypertension with right-heart failure
⭐ 6️⃣ Starred High-Yield Exam Points
- ⭐ Virchow triad: endothelial injury, abnormal blood flow and hypercoagulability.
- ⭐ Lines of Zahn: hallmark of thrombus formation in flowing blood during life.
- ⭐ Most pulmonary emboli arise from proximal deep veins of the lower limb.
- ⭐ Pulmonary infarct: hemorrhagic, wedge-shaped and pleural-based.
- ⭐ Negative D-dimer: useful for excluding pulmonary embolism in appropriately selected low-risk patients.
- ⭐ Anticoagulation: foundation of treatment for most pulmonary emboli.
- ⭐ Systemic thrombolysis: mainly for pulmonary embolism with hemodynamic instability.
- ⭐ Mitral stenosis: classic cardiac cause of pulmonary hypertension through raised left-atrial pressure.