Hemostasis & Coagulation Tournament
Two onboarding diagrams orient you in hemostasis. Then eight MCAT-DoK quiz rounds: tissue factor + factor VIIa, vitamin K-dependent factors II/VII/IX/X, warfarin + heparin + DOACs, hemophilia A vs B, von Willebrand disease, factor V Leiden, antiplatelets (aspirin, clopidogrel, abciximab), and heparin-induced thrombocytopenia.
Where the Coagulation pathway fits in Hemostasis
Reactome's Hemostasis overview shows how primary hemostasis (platelet plug) integrates with secondary hemostasis (fibrin clot) to seal vascular injury. The COAGULATION PATHWAY box highlights the cascade that culminates in thrombin and fibrin. Click it to enter the tournament.
Click the highlighted Coagulation pathway box to continue.
What this tournament tests
Each task maps to a distinct MCAT cognitive demand. The first two orient you in the broader topology; the next eight test the high-yield mechanism, regulation, sequence and quantitative reasoning that consistently appear on test day.
The Bigger Picture
Anchor the coagulation cascade within Reactome's Hemostasis overview alongside platelet adhesion, fibrinolysis, and the kallikrein-kinin system.
Whole-Pathway Overview
Pan and zoom the curated WikiPathways blood-clotting cascade figure before answering questions.
Fill in the Blank
Recall that tissue factor (TF, factor III) is the physiologic initiator of the extrinsic pathway.
Warfarin / TMP-SMX Disruptor
Predict why TMP-SMX potentiates warfarin via CYP2C9 inhibition + gut flora disruption.
Sequence Ordering
Order vascular injury -> platelet adhesion -> aggregation -> tissue factor -> Xa -> thrombin -> fibrin cross-linking by factor XIII.
Match the Pairs
Pair warfarin, heparin, LMWH, DOACs, aspirin, clopidogrel, and GPIIb/IIIa inhibitors with their precise targets.
Numeric Input
Count the four vitamin K-dependent coagulation factors.
Select All That Apply
Identify true statements about vWF, hemophilia A vs B, and protein C/S anticoagulants.
Odd One Out
Distinguish vitamin K-dependent factors (II, VII, IX, X) from factor V (cofactor only).
HIT Disruptor
Predict why heparin-induced thrombocytopenia paradoxically causes thrombosis despite low platelets.
Public leaderboard
Your score posts to a global, persistent leaderboard scored by points first, time as tiebreaker.
Hemostasis in 60 seconds
Primary hemostasis: vascular injury exposes collagen + tissue factor. Platelets adhere via vWF + GPIb, activate, release granules (ADP, TXA2), and aggregate via GPIIb/IIIa + fibrinogen bridges. This is the platelet plug.
Secondary hemostasis: tissue factor + factor VIIa activates factor X (extrinsic pathway). The intrinsic pathway (XII -> XI -> IX -> VIII) amplifies the same Xa output. Xa + Va converts prothrombin (II) to thrombin (IIa).
Thrombin is the central effector: cleaves fibrinogen to fibrin, activates platelets, amplifies factors V/VIII/XI, and (eventually) triggers anticoagulation via thrombomodulin + protein C. Factor XIIIa cross-links fibrin into a stable mesh.
Pharmacology: warfarin blocks vitamin K recycling (VKORC1 -> II, VII, IX, X + protein C/S); heparin activates antithrombin (-> IIa + Xa); DOACs directly inhibit Xa (apixaban, rivaroxaban) or thrombin (dabigatran); aspirin irreversibly acetylates platelet COX1.
FAQ
Why does PT measure 'extrinsic' but aPTT measures 'intrinsic'?
PT (prothrombin time) adds tissue factor + Ca2+ to plasma - it activates the extrinsic pathway and tests factors VII + the common pathway (X, V, II, fibrinogen). aPTT (activated partial thromboplastin time) adds a contact activator + phospholipid + Ca2+ - it activates the intrinsic pathway and tests factors XII, XI, IX, VIII + the common pathway. Warfarin prolongs PT first (factor VII has the shortest half-life); heparin prolongs aPTT.
What is factor V Leiden?
A common mutation (R506Q) in factor V that prevents protein C from cleaving and inactivating factor Va. Heterozygotes have ~5-fold higher venous thromboembolism risk; homozygotes ~50-fold. It is the most common hereditary thrombophilia in people of European ancestry. Combined with oral contraceptives or pregnancy, the risk is multiplied further.
Why is HIT type II 'paradoxical'?
Heparin-induced thrombocytopenia type II is immune-mediated: antibodies against heparin-PF4 complexes cross-link FcγRIIa on platelets, causing massive platelet activation. Platelets are consumed faster than the marrow can replace them (low count) but the activated platelets release microparticles that drive thrombosis. Treatment: STOP all heparin (no warfarin alone), switch to a direct thrombin inhibitor (argatroban) or fondaparinux until platelets recover.
Do I need an account to play?
No. The tournament is fully public. You get a randomized handle and your score posts to the public leaderboard at the bottom of this page.
Keep going
Caspase cascades + intrinsic / extrinsic pathways - similar 'cascade with multiple amplification points' logic.
Cyclin-CDK regulation; useful contrast in 'staged amplification' biology.
Overview diagram: Reactome Pathway R-HSA-109582, licensed CC BY 4.0.