USMLE/COMLEX 1 - Pulmonary Embolism and Deep Vein Thrombosis

Here are key facts for USMLE Step 1 & COMLEX-USA Level 1 from the Pulmonary Embolism & Deep Vein Thrombosis tutorial, as well as points of interest at the end of this document that are not directly addressed in this tutorial but should help you prepare for the boards. See the tutorial notes for further details and relevant links.

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1. Definition: Pulmonary embolism (PE) occurs when pulmonary arteries are obstructed, most commonly by emboli from deep veins of thighs/pelvis. 2. Venous thromboembolism (VTE): Combined term for deep vein thrombosis (DVT) and pulmonary embolism. 3. Virchow's Triad: Three factors predisposing to thrombosis:

• Endothelial injury: Due to fracture, surgery, trauma, or previous DVT; triggers clotting cascade
• Venous stasis: Caused by immobility, elevated central venous pressure, heart failure, obesity
• Hypercoagulable states: Pregnancy, postpartum period, smoking, cancer, hormonal contraceptives/therapies, coagulation disorders (Factor V Leiden)

4. Pathogenesis: Clot forms in deep vein → fragment breaks off → travels through IVC → right heart → pulmonary arteries → obstructs blood flow → impaired gas exchange and perfusion. 5. Consequences: Pulmonary hypertension, right heart failure, pulmonary infarction, and potentially death. 1. Definition: Formation of blood clot in deep veins, most commonly in lower extremities. 2. Primary cause: Leading cause of pulmonary embolism. 3. Clinical features: When symptomatic, presents with unilateral leg swelling, tenderness, and venous dilation. 4. Complications:

• Post-thrombotic syndrome due to venous valve damage
• Pulmonary embolism (most serious complication)

5. Risk factors: Multiple predisposing factors increase risk (e.g., pregnant women on bed rest). 1. Definition: Obstruction of pulmonary arteries, usually by thrombi from deep veins. 2. Nonthrombotic sources: Air, fat, amniotic fluid, bacterial (septic), foreign bodies, and tumors. 3. Classification:

• By risk: Massive (high risk), intermediate (submassive), and low risk
• By location: Saddle emboli (at pulmonary trunk bifurcation), lobar, segmental, or subsegmental

4. Pathophysiologic consequences:

• Ventilation-perfusion mismatch
• Hypoxemia
• Respiratory alkalosis
• Pulmonary hypertension
• Right heart failure

5. Clinical presentation: Dyspnea, tachypnea, chest pain, tachycardia, altered mental status (especially in elderly). 1. DVT diagnosis:

• Wells Score for DVT (considering swelling, edema, alternative diagnoses)
• D-dimer testing (to rule out low-probability DVT)
• Imaging: Contrast venography or venous ultrasonography with compression

2. PE diagnosis:

• Wells Score for PE (heart rate, signs/symptoms, alternative diagnoses)
• D-dimer: >500 ng/mL suggests possible PE
• Imaging: CT angiography, ventilation-perfusion scan
• ECG: May show sinus tachycardia, S1Q3T3 pattern (S in lead I, Q and inverted T in lead III)
• Chest X-ray: May show atelectasis, Hampton hump (pulmonary infarction), Westermark sign (oligemic areas), pleural effusion

1. Supportive therapy: Oxygen, saline, vasopressors. 2. Anticoagulation:

• Acute: Heparin, enoxaparin, or fondaparinux
• Long-term: Warfarin

3. Advanced interventions: Embolectomy or clot dissolution for severe cases. 4. Prophylaxis:

• Sequential compression devices (SCDs) to prevent venous stasis
• Prophylactic anticoagulants (low-dose enoxaparin or heparin)

5. Complication awareness: Heparin-induced thrombocytopenia.

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1. Endothelial injury:

• Trauma stimulates clotting cascade
• Surgery, especially orthopedic
• Previous DVT damages vessel walls
• Inflammation causes endothelial dysfunction

2. Venous stasis:

• Immobility (long flights, bedridden patients)
• Heart failure reduces forward flow
• Compression of veins (e.g., May-Thurner syndrome, pregnancy)
• Obesity increases intra-abdominal pressure

3. Hypercoagulability:

• Pregnancy (also causes IVC compression)
• Malignancy (especially pancreatic, lung)
• Hormonal contraceptives increase clotting factors
• Genetic disorders (Factor V Leiden, Protein C/S deficiency)

5. Multiple risk factors: Significantly increase thrombotic risk in combination. 1. DVT symptoms: Often unilateral leg swelling, tenderness, venous dilation. 2. PE symptoms: Dyspnea (85%), chest pain (40-75%), tachypnea, tachycardia. 3. Silent presentation: Both DVT and PE can be asymptomatic. 4. Massive PE: Presents with hemodynamic instability (hypotension). 5. Altered mental status: Important clue in elderly patients. 1. D-dimer:

• Fibrin degradation product
• High sensitivity, low specificity
• Negative predictive value in low-probability patients

2. Wells Score for PE:

• <2: Low probability
• 2-6: Moderate probability
• >6: High probability

3. Imaging findings:

• Hampton hump: Wedge-shaped pulmonary infarction, usually in lower lobes
• Westermark sign: Focal oligemia (hypoperfusion)
• Saddle embolus: Visible at bifurcation of main pulmonary artery

4. Pathologic findings: Premortem thrombi display lines of Zahn (layers of fibrin, RBCs, and platelets). 5. ECG: S1Q3T3 pattern in acute PE (though nonspecific). 1. Mechanism: Small emboli obstruct blood flow causing tissue ischemia. 2. Location: Most common in lower lobes. 3. Radiographic finding: Wedge-shaped "Hampton Hump" on chest X-ray. 4. Clinical significance: Indicates tissue death from prolonged ischemia. 5. Pathology: Hemorrhagic necrosis of lung parenchyma. 1. Anticoagulation contraindications: Active bleeding, recent surgery, thrombocytopenia. 2. Thrombolysis indications: Massive PE with hemodynamic instability. 3. Inferior vena cava filters: When anticoagulation is contraindicated. 4. Prophylaxis importance: High-risk patients should receive appropriate prophylaxis. 5. Post-thrombotic syndrome: Long-term complication of DVT requiring management.

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Below is information not explicitly contained within the tutorial but important for USMLE & COMLEX 1. 1. Intrinsic pathway: Activated by contact with collagen via Factor XII. 2. Extrinsic pathway: Activated by tissue factor (Factor III) exposure. 3. Common pathway: Both pathways converge at Factor X activation. 4. Fibrinolytic system: Plasmin degrades fibrin to produce D-dimers. 5. Natural anticoagulants: Protein C, Protein S, Antithrombin III inhibit clotting. 1. Right ventricular failure: Acute pressure overload causes RV dilation and dysfunction. 2. Pulmonary hypertension: Acute from mechanical obstruction; chronic from repeated emboli. 3. Dead space ventilation: Areas ventilated but not perfused, wasting respiratory effort. 4. Hypoxemic mechanisms: V/Q mismatch, shunting, impaired diffusion. 5. Platelet activation: Contributes to propagation of thrombus. 1. Inherited thrombophilias: Antithrombin deficiency, protein C/S deficiency, prothrombin gene mutation. 2. Antiphospholipid syndrome: Autoimmune disorder causing hypercoagulability. 3. Heparin-induced thrombocytopenia: Paradoxical thrombosis due to antibodies against heparin-PF4 complex. 4. Malignancy-associated: Especially mucin-producing adenocarcinomas (Trousseau syndrome). 5. Inflammatory bowel disease: Increases thrombotic risk through multiple mechanisms. 1. Gross appearance: Red-blue obstructive material in pulmonary arteries. 2. Lines of Zahn: Alternating layers of platelets/fibrin and red cells in organized thrombi. 3. Pulmonary infarcts: Typically wedge-shaped, hemorrhagic, and subpleural. 4. Resolution process: Thrombolysis and recanalization over days to weeks. 5. Chronic changes: Organization and fibrosis of unresolved thrombi. 1. CT pulmonary angiography: Gold standard showing filling defects in pulmonary arteries. 2. Echocardiography: May show right ventricular strain, McConnell's sign (RV free wall akinesis with apical sparing). 3. Elevated troponin: Indicates myocardial injury from RV strain. 4. BNP/NT-proBNP: Elevated in right heart failure. 5. Normal A-a gradient: Rare in PE, making a low A-a gradient useful in excluding PE from differential.