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Related Concept Videos

Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Disorders of Hemostasis01:24

Disorders of Hemostasis

Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
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Venous Thrombosis I: Introduction01:30

Venous Thrombosis I: Introduction

Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
Venous Thrombosis III: Interprofessional Care01:29

Venous Thrombosis III: Interprofessional Care

Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

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Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
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Pulmonary Embolism I: Introduction01:29

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Pulmonary embolism (PE) occurs when a thrombus, fat or air embolus, amniotic fluid, or tumor tissue blocks one or more pulmonary arteries. These blockages originate in the venous system or the right side of the heart.EtiologyPE primarily arises from deep vein thrombosis (DVT) and other hypercoagulable states, such as inherited thrombophilias. Additional etiological factors include venous stasis, commonly seen in obesity, and endothelial injury from surgery and trauma. Less common causes include...

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Updated: May 27, 2026

Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)
04:56

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Published on: August 4, 2023

Hypercoagulable states.

Julia A M Anderson1, Jeffrey I Weitz

  • 1Department of Clinical and Laboratory Hematology, Royal Infirmary of Edinburgh, Scotland EH16 4SA, UK.

Critical Care Clinics
|November 16, 2011
PubMed
Summary
This summary is machine-generated.

Hypercoagulable states, inherited or acquired, increase venous thromboembolism risk. This risk, influenced by genetic factors and acquired conditions, often requires a trigger to exceed a critical threshold.

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Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
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Published on: September 9, 2012

Area of Science:

  • Hematology
  • Thrombosis Research

Background:

  • Hypercoagulable states represent an increased tendency to develop blood clots.
  • These states can be inherited (genetic) or acquired (environmental/disease-related).
  • Understanding these states is crucial for managing venous thromboembolism (VTE).

Purpose of the Study:

  • To elucidate the mechanisms and risk factors contributing to hypercoagulable states.
  • To explain the interplay between inherited and acquired factors in VTE development.
  • To define the threshold at which hypercoagulability leads to thrombosis.

Main Methods:

  • Review of existing literature on inherited and acquired hypercoagulable states.
  • Analysis of genetic and environmental risk factors for thrombosis.
  • Conceptual framework development for VTE risk assessment.

Main Results:

  • Inherited hypercoagulability arises from impaired anticoagulant pathways or enhanced procoagulant pathways.
  • Acquired risk factors include prior thrombosis, obesity, pregnancy, cancer, antiphospholipid antibody syndrome, heparin-induced thrombocytopenia, and myeloproliferative disorders.
  • The combination of inherited and acquired factors determines an individual's intrinsic VTE risk.

Conclusions:

  • Venous thromboembolism (VTE) occurs when the cumulative hypercoagulable risk surpasses a critical threshold.
  • External triggers like surgery, pregnancy, or estrogen therapy can elevate risk above this threshold.
  • Individual VTE risk is a complex interplay of genetic predisposition and acquired risk factors.