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MBBS viva

Venous Thromboembolism — Viva

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NEET-PGINICETUSMLEPLAB
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NEET-PGINICETUSMLEPLAB

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Opening (30 s)

"Venous thromboembolism — one-line definition and the single decision that separates anticoagulation from thrombolysis."

Model: VTE is DVT and PE as one disease. ESC: third acute cardiovascular syndrome after MI and stroke. The split is haemodynamic instability (systolic BP under 90 mmHg, shock, or arrest) — that patient gets systemic thrombolysis; the normotensive patient gets a DOAC.[1][2]

Station 1 — Pathophysiology (2 min)

Virchow's triad; red (fibrin-rich) venous clot; embolisation to the pulmonary arteries; acute RV pressure overload. High-risk imaging clue: RV/LV diameter ratio over 1.0.[1]

Station 2 — Clinical diagnosis (2 min)

Red flag cue: hypotension or syncope with clear lungs and a raised JVP.

Wells 1997 DVT prevalences: 3 / 17 / 75 percent (low / moderate / high). Wells 2001 PE: 1.3 / 16.2 / 37.5 percent. PERC-negative plus gestalt under 15 percent: false-negative 1.0 percent (Kline, 20 percent of outpatients).[5]

Station 3 — Investigations (2 min)

Christopher: PE-unlikely plus normal D-dimer — subsequent nonfatal VTE 0.5 percent. Age-adjusted D-dimer = age × 10 µg/L over 50 (ADJUST-PE / ESC). CTPA for PE; compression ultrasound for DVT; echo if unstable.[1]

Station 4 — Emergency management (3 min)

High-risk: rtPA 100 mg over 2 hours (ESC); ASH strong recommendation to lyse haemodynamic compromise. Accelerated option 0.6 mg/kg over 15 min, maximum 50 mg. PEITHO tenecteplase is not the routine intermediate-risk answer.[1][2][3]

Station 5 — Definitive / long-term care (2 min)

Apixaban 10 mg twice daily for 7 days then 5 mg twice daily (AMPLIFY). Extended apixaban 2.5 mg twice daily after unprovoked VTE (AMPLIFY-EXT 1.7 vs 8.8 percent). Indefinite anticoagulation for recurrent unprovoked VTE (ASH strong).[4][2]

Station 6 — Special populations (2 min)

Pregnancy: LMWH over UFH (ASH strong). Cancer: Caravaggio apixaban non-inferior to dalteparin; ESC caution with edoxaban/rivaroxaban in GI cancer. Severe CKD: VKA or UFH rather than an untested DOAC dose.[2][1]

Station 7 — Evidence and pitfalls (2 min)

PEITHO: 2.6 vs 5.6 percent decompensation, 6.3 vs 1.2 percent extracranial bleed, 2.4 percent stroke. Never anticoagulate a dissection. Never start warfarin without heparin in protein C deficiency.[3]

Station 8 — Rapid-fire pearls (1 min)

Pengo CTEPH 1.0 / 3.1 / 3.8 percent at 6 / 12 / 24 months — unexplained dyspnoea after PE gets a V/Q scan.[6]

References6ShowHide
  1. [1]Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS) Eur Heart J, 2020.PMID 31504429
  2. [2]Ortel TL, Neumann I, Ageno W, et al. American Society of Hematology 2020 guidelines for management of venous thromboembolism: treatment of deep vein thrombosis and pulmonary embolism Blood Adv, 2020.PMID 33007077
  3. [3]Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism N Engl J Med, 2014.PMID 24716681
  4. [4]Agnelli G, Buller HR, Cohen A, et al. Oral apixaban for the treatment of acute venous thromboembolism N Engl J Med, 2013.PMID 23808982
  5. [5]Kline JA, Courtney DM, Kabrhel C, et al. Prospective multicenter evaluation of the pulmonary embolism rule-out criteria J Thromb Haemost, 2008.PMID 18318689
  6. [6]Pengo V, Lensing AW, Prins MH, et al. Incidence of chronic thromboembolic pulmonary hypertension after pulmonary embolism N Engl J Med, 2004.PMID 15163775