Related Experiment Video
Updated: Jun 25, 2026

Ferric Chloride-induced Murine Thrombosis Models
Published on: September 5, 2016
Mechanisms of thrombosis related to hormone therapy
Per Morten Sandset1, Else Høibraaten, Anette Løken Eilertsen
1Oslo University Hospital at Ullevål, Department of Hematology, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway. p.m.sandset@medisin.uio.no
Abstract:
Combined oral contraceptives and combined oral postmenopausal hormone therapy are associated with a weak, but clinically significant risk of arterial and venous thrombosis (VT). The effects are related to dose of estrogen and type of progestin. The main effects are increase in markers of activated coagulation, reduction in coagulation inhibitors, and acquired activated protein C resistance. Reduction in tissue factor pathway inhibitor (TFPI) is probably an important mechanism, which predicts activation of coagulation and acquired resistance to activated protein C. Coagulation markers should be used as intermediate or surrogate markers in early pharmacodynamic studies to evaluate the risk associated with new formulations.
Related Concept Videos
Anticoagulant Drugs: Low-Molecular-Weight Heparins
Venous Thrombosis I: Introduction
Disorders of Hemostasis
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
Venous Thrombosis III: Interprofessional Care
Extrinsic and Intrinsic Pathways of Hemostasis
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
