Thrombogenesis Module

Module thrombogenesis 9 disorders Pathograph 7

A conserved pathophysiology module representing conventional platelet-assisted, thrombin/fibrin thrombogenesis across venous and arterial thrombotic disorders. One or more Virchow-triad conditions - vessel-wall perturbation, altered or stagnant blood flow, and hypercoagulability - can create the prothrombotic context. Platelet adhesion, activation, secretion, and aggregation participate alongside tissue-factor-initiated thrombin generation and fibrin formation. The evidence used here does not establish a fixed platelet contribution, thrombus composition, or sequence across arterial and venous settings, so those features remain disease-specific. The defining output is pathological intravascular fibrin-platelet thrombus formation. A formed thrombus may remain nonocclusive or may later grow and obstruct local blood flow. If obstruction compromises tissue perfusion, ischemic injury can follow as a conditional, site-dependent consequence. A venous thrombus may instead dislodge and travel to the pulmonary arteries; this narrowly evidenced embolic branch is separate from local ischemic injury. None of occlusion, ischemia, or embolization is required for conformance. Conformance is branch- and node-qualified: disorder entries map only the stages their evidence directly represents and do not imply the entire module chain from a downstream match.

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Pathophysiology Nodes

6 shared nodes are defined in this module.

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Cell Types

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Biological Processes

Notes

This is a mechanism module, not a specific disease. It is a pathological structure-formation ("Xogenesis") module. Xogenesis anchor: the terminal output is a thrombus, an OGMS:0000078 pathological anatomical structure produced by an OGMS:0000081 pathological derivation (a new intravascular formation); process genus OGMS:0000061 pathological bodily process; site UBERON:0001981 blood vessel. MPATH represents the process as MPATH:125 (thrombosis) but has no distinct "thrombus" continuant class, an OBO gap noted for upstream contribution. SNOMED "Morphologically abnormal structure" (49755003) is used only as an external census/gap guide and is not bound here. Disorder entries reference individual nodes via conforms_to (for example, "thrombogenesis#Coagulation Cascade Activation and Thrombin-Driven Fibrin Formation"). The module defines the expected pathophysiology structure; conforming nodes in disorder files should include the corresponding cell types, biological processes, and causal edges, specialized to their disease context. Operational conformance boundary: a disease branch is in scope when it directly represents pathological intravascular formation of a platelet-assisted, thrombin-generated fibrin thrombus. That formed fibrin-platelet thrombus is necessary and sufficient for branch-level qualification, but each conforms_to assertion remains local to the stage actually modeled. This is an operational curation boundary, not a formal Grouping criteria assertion. A Virchow-triad context, a separately represented platelet amplifier, and local occlusion, ischemic injury, or venous embolization are not all required as separate nodes. Conversely, ischemia, infarction, vessel occlusion, or embolism alone is not sufficient to infer thrombogenesis. The module evidence identifies platelet processes and thrombin/fibrin formation as interacting components but does not license fixed arterial-versus-venous composition or platelet dominance; conformers must specialize their relative contribution using disease-specific evidence. Physiologic hemostatic plugs, nonthrombotic emboli or occlusions, and VWF-platelet microangiopathy such as thrombotic thrombocytopenic purpura are out of scope unless a distinct conventional thrombin/fibrin thrombosis branch is explicitly evidenced. Key disease-specific substitutions include venous stasis in immobilization, arterial plaque disruption, and systemic hypercoagulability in cancer, thrombophilia, or thrombotic antiphospholipid syndrome. The module's treatment is a mechanistic target pattern, not an inherited treatment recommendation; agent selection and contraindications remain disease-specific. Pathophysiology nodes bind GO biological processes, CL cell types, and, where needed, UBERON anatomy; they do not bind CHEBI chemicals or MONDO diseases. The treatments block may bind a therapeutic agent per the treatment schema.

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Used By Disorder Entries

Amniotic Fluid Embolism via Coagulation Activation and Fibrinogen Consumption → Coagulation Cascade Activation and Thrombin-Driven Fibrin Formation

Antiphospholipid Syndrome via Platelet activation → Platelet Adhesion, Activation, and Aggregation , Coagulation cascade activation and thrombin-driven fibrin formation → Coagulation Cascade Activation and Thrombin-Driven Fibrin Formation , Arterial and venous thrombosis → Pathological Fibrin-Platelet Thrombus Formation , Acute thrombotic vascular occlusion and ischemic tissue injury → Thrombotic Vascular Occlusion and Ischemic Tissue Injury

Dilated Cardiomyopathy 1A via Intracardiac Thrombus Formation → Pathological Fibrin-Platelet Thrombus Formation

HELLP Syndrome via Platelet Activation and Consumptive Thrombocytopenia → Platelet Adhesion, Activation, and Aggregation , Hepatic Sinusoidal Microthrombosis and Fibrin Deposition → Pathological Fibrin-Platelet Thrombus Formation

Heparin-Induced Thrombocytopenia via FcgammaRIIA-Mediated Platelet Activation by Immune Complexes → Platelet Adhesion, Activation, and Aggregation , Explosive Thrombin Generation → Coagulation Cascade Activation and Thrombin-Driven Fibrin Formation , Venous and Arterial Thrombosis → Pathological Fibrin-Platelet Thrombus Formation , Thrombotic Occlusion and Ischemic Tissue Injury → Thrombotic Vascular Occlusion and Ischemic Tissue Injury

Infective Endocarditis via Endothelial injury and sterile thrombus formation → Platelet Adhesion, Activation, and Aggregation , Vegetation maturation with biofilm-like protection → Pathological Fibrin-Platelet Thrombus Formation , Systemic embolization of vegetation fragments → Thrombotic Vascular Occlusion and Ischemic Tissue Injury

Posterior Myocardial Infarction via Coronary thrombosis and occlusion → Pathological Fibrin-Platelet Thrombus Formation , Posterior myocardial ischemic cell death → Thrombotic Vascular Occlusion and Ischemic Tissue Injury

Pulmonary Embolism via Prothrombotic venous context → Virchow-Triad Prothrombotic Context , Deep venous thrombus formation → Pathological Fibrin-Platelet Thrombus Formation , Embolization to the pulmonary arterial tree → Venous Thrombus Embolization to Pulmonary Arteries

Thrombophilia via Coagulation Cascade Activation and Thrombin-Driven Fibrin Formation , Pathological Venous Thrombus Formation → Pathological Fibrin-Platelet Thrombus Formation , Venous Thrombus Embolization to Pulmonary Arteries

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Pathograph

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Pathophysiology

Virchow-Triad Prothrombotic Context

trigger

An optional upstream context in which one or more of vessel-wall perturbation, altered or stagnant blood flow, and hypercoagulability predisposes to thrombosis. The dominant limb and its concrete cells and processes are disease-specific. This generic context node intentionally has no endothelial-cell or coagulation-process binding; those belong on a specialized disease trigger or the downstream coagulation node when directly evidenced.

Used by disorders

Pulmonary Embolism as Prothrombotic venous context

Downstream

Platelet Adhesion, Activation, and Aggregation
Coagulation Cascade Activation and Thrombin-Driven Fibrin Formation

Platelet Adhesion, Activation, and Aggregation

amplifier

Platelet adhesion, activation, secretion, and aggregation participate in thrombus formation alongside tissue-factor-initiated thrombin generation and fibrin formation. This amplifier node represents platelet participation and its interaction with coagulation without asserting a fixed sequence, abundance, composition, or dominance in arterial versus venous thrombi.

platelet CL:0000233

platelet activation GO:0030168 INCREASED platelet aggregation GO:0070527 INCREASED

Used by disorders

Antiphospholipid Syndrome as Platelet activation

HELLP Syndrome as Platelet Activation and Consumptive Thrombocytopenia

Heparin-Induced Thrombocytopenia as FcgammaRIIA-Mediated Platelet Activation by Immune Complexes

Infective Endocarditis as Endothelial injury and sterile thrombus formation

Downstream

Coagulation Cascade Activation and Thrombin-Driven Fibrin Formation

Coagulation Cascade Activation and Thrombin-Driven Fibrin Formation

central effector

The central coagulation convergence step of thrombogenesis. Tissue factor exposed by injury forms the extrinsic tenase complex, driving assembly of the prothrombinase complex (FXa-FVa) that converts prothrombin to thrombin; intrinsic tenase amplifies thrombin generation on the activated platelet surface. Thrombin then cleaves fibrinogen into fibrin monomers that polymerize and crosslink into an insoluble fibrin network. This thrombin-driven fibrin formation solidifies the thrombus and is the module's principal anticoagulant target, without claiming that one universal rate-limiting step applies across every arterial and venous context.

platelet CL:0000233

blood coagulation GO:0007596 INCREASED fibrin clot formation GO:0072378 INCREASED

Used by disorders

Amniotic Fluid Embolism as Coagulation Activation and Fibrinogen Consumption

Antiphospholipid Syndrome as Coagulation cascade activation and thrombin-driven fibrin formation

Heparin-Induced Thrombocytopenia as Explosive Thrombin Generation

Thrombophilia

Downstream

Pathological Fibrin-Platelet Thrombus Formation

Pathological Fibrin-Platelet Thrombus Formation

effector

The crosslinked fibrin network and aggregated platelets assemble into a pathological intravascular thrombus, the atomic structure-formation output of this Xogenesis module. Subsequent growth, propagation, narrowing, or complete vascular occlusion are conditional later states and are not part of the defining formation claim.

platelet CL:0000233

blood coagulation, fibrin clot formation GO:0072378 INCREASED

Used by disorders

Antiphospholipid Syndrome as Arterial and venous thrombosis

Dilated Cardiomyopathy 1A as Intracardiac Thrombus Formation

HELLP Syndrome as Hepatic Sinusoidal Microthrombosis and Fibrin Deposition

Heparin-Induced Thrombocytopenia as Venous and Arterial Thrombosis

Infective Endocarditis as Vegetation maturation with biofilm-like protection

Posterior Myocardial Infarction as Coronary thrombosis and occlusion

Pulmonary Embolism as Deep venous thrombus formation

Thrombophilia as Pathological Venous Thrombus Formation

Downstream

Thrombotic Vascular Occlusion and Ischemic Tissue Injury
Venous Thrombus Embolization to Pulmonary Arteries

Thrombotic Vascular Occlusion and Ischemic Tissue Injury

consequence

A conditional local consequence, distinct from the thrombus formed by the Xogenesis module. A formed thrombus may grow and obstruct local blood flow; when the affected vessel supplies perfusion-dependent tissue, the obstruction can cause ischemia or infarction. Nonocclusive thrombi may cause neither, so this consequence is not required for every conforming branch.

Used by disorders

Antiphospholipid Syndrome as Acute thrombotic vascular occlusion and ischemic tissue injury

Heparin-Induced Thrombocytopenia as Thrombotic Occlusion and Ischemic Tissue Injury

Infective Endocarditis as Systemic embolization of vegetation fragments

Posterior Myocardial Infarction as Posterior myocardial ischemic cell death

Venous Thrombus Embolization to Pulmonary Arteries

consequence

A separate, conditional venous consequence in which a formed thrombus dislodges and travels to the pulmonary arteries, producing pulmonary embolism. This narrow node does not generalize the evidence to arterial embolization, every distant vascular bed, or every formed thrombus.

Used by disorders

Pulmonary Embolism as Embolization to the pulmonary arterial tree

Thrombophilia