Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Disorders of Hemostasis

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.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.

Anticoagulant Drugs: Low-Molecular-Weight Heparins

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...

Venous Thrombosis III: Interprofessional Care

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 Hemostasis

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
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...

Clot Retraction and Fibrinolysis

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.

Formation of the Platelet Plug

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Exploring the Origin of Cells in the Progression of Primary Myelofibrosis to Acute Myeloid Leukemia Case Report.

Case reports in hematology·2026

Same author

Single dose antithymocyte globulin effectively reduces GVHD and improves survival in patient undergoing myeloablative matched sibling alloHCT.

Leukemia & lymphoma·2026

Same author

Avapritinib achieves long-term disease control with favorable safety in patients with indolent systemic mastocytosis over 3 years.

The Journal of allergy and clinical immunology·2026

Same author

Primary Indolent Acute Promyelocytic Leukemia.

Hematology reports·2026

Same author

Fluoroquinolone Prophylaxis Reduces Intensive Care Unit Admission and <i>Clostridioides difficile</i> Rates in Acute Myeloid Leukemia Induction Chemotherapy.

EJHaem·2026

Same author

Avapritinib improves cutaneous involvement in patients with indolent systemic mastocytosis: Results from the randomized, phase 2, interventional PIONEER study.

Journal of the American Academy of Dermatology·2026

Search research articles

Related Experiment Video

Updated: Mar 20, 2026

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

Prolonged Partial Thromboplastin Time Without Bleeding History; Fletcher Factor Deficiency.

Celalettin Üstün, Anand Jillella, Linda Hendriks

Turkish Journal of Haematology : Official Journal of Turkish Society of Haematology

|June 7, 2016

Summary

Fletcher factor deficiency, a rare cause of prolonged activated partial thromboplastin time (aPTT), should be considered in patients without a bleeding history. Surgical procedures are safe for individuals with this condition.

More Related Videos

Tail Vein Transection Bleeding Model in Fully Anesthetized Hemophilia A Mice

Tail Vein Transection Bleeding Model in Fully Anesthetized Hemophilia A Mice

Published on: September 30, 2021

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

Published on: February 14, 2017

Related Experiment Videos

Last Updated: Mar 20, 2026

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

Tail Vein Transection Bleeding Model in Fully Anesthetized Hemophilia A Mice

Tail Vein Transection Bleeding Model in Fully Anesthetized Hemophilia A Mice

Published on: September 30, 2021

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time

Published on: February 14, 2017

Area of Science:

Hematology
Coagulation Disorders

Background:

A 67-year-old patient presented with a lower esophageal lesion suspicious for cancer.
Preoperative laboratory tests revealed a prolonged activated partial thromboplastin time (aPTT) with a normal prothrombin time (PT).
The patient had no personal or family history of bleeding or thrombosis.

Purpose of the Study:

To investigate the cause of the prolonged aPTT in a patient undergoing esophagogastrectomy.
To determine the safety of surgical intervention in patients with Fletcher factor deficiency.

Main Methods:

Activated partial thromboplastin time (aPTT) and prothrombin time (PT) assays were performed.
Plasma mixing studies with normal plasma were conducted.
Incubation studies were performed to assess aPTT stability.
Fletcher factor activity was measured.

Main Results:

The patient's aPTT was prolonged (44 s), while PT was normal (11 s).
Plasma mixing corrected the prolonged aPTT, and prolonged incubation shortened it.
Fletcher factor activity was found to be 50%.
The patient underwent esophagogastrectomy without bleeding complications.

Conclusions:

Fletcher factor deficiency is a rare cause of isolated prolonged aPTT.
This deficiency should be considered in patients with unexplained prolonged aPTT and no bleeding history.
Surgical interventions, including esophagogastrectomy, are safe in patients with Fletcher factor deficiency.