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.
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.
Downstream
-
Platelet Adhesion, Activation, and Aggregation
-
Coagulation Cascade Activation and Thrombin-Driven Fibrin Formation
Show evidence (1 reference)
"Malignancy itself induces a thrombophilic state by increasing the risk of venous stasis, endothelial injury and an imbalance of pro and anti-thrombotic factors leading to a hypercoaguable state."
This cancer-specific review directly enumerates venous stasis, endothelial injury, and a pro-/antithrombotic imbalance as one disease example of the three-part context. It provides only partial support for this generic, optional module node and does not establish that every branch contains all three conditions. Evidence source is OTHER because this is a review.
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.
Used by disorders
HELLP Syndrome
as Platelet Activation and Consumptive Thrombocytopenia
Preeclampsia
as Platelet Activation and NET-Amplified Thrombus Propagation
Downstream
-
Coagulation Cascade Activation and Thrombin-Driven Fibrin Formation
Show evidence (1 reference)
"Thrombus formation, including platelet adhesion, activation, secretion and aggregation as well as tissue factor-initiated thrombin generation and fibrin formation, has been studied in the past using in vitro systems, often with isolated components."
Enumerates platelet adhesion, activation, secretion, and aggregation alongside tissue-factor-initiated thrombin and fibrin formation as the components of thrombus formation, supporting the platelet-activation amplifier and its coupling to coagulation. Evidence source is OTHER because this is a review.
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
Preeclampsia
as Microvascular Thrombosis and Maternal Organ Ischemia
Show evidence (1 reference)
"Platelet deposition and activation of the blood coagulation cascade in response to plaque disruption lead to the formation of a platelet-fibrin thrombus, which can grow rapidly, obstruct coronary blood flow, and cause myocardial ischemia and/or infarction."
Directly states that a platelet-fibrin thrombus can obstruct coronary blood flow and cause myocardial ischemia or infarction, supporting the local occlusion-to-injury arm. Evidence source is OTHER because this is a review.
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.
Show evidence (1 reference)
"Complications of venous thrombosis include pulmonary embolism (PE), where a dislodged thrombus travels to the pulmonary arteries, potentially leading to fatal outcomes"
Directly supports dislodgement and travel of a venous thrombus to the pulmonary arteries. The node is restricted to that pulmonary embolic branch because the source does not establish a generic distant-obstruction mechanism. Evidence source is OTHER because this is a review.
Anticoagulation via Heparin-Potentiated Antithrombin
Therapeutic heparins potentiate antithrombin-mediated inhibition of thrombin and activated coagulation factors, including factor Xa. This is a mechanism-level anticoagulation pattern aimed at the coagulation/thrombin node rather than a recommendation inherited by conforming disorders. Agent or class selection, dose, intensity, duration, bleeding risk, and other contraindications must be assessed and evidenced in each disease context.
Evidence: 1