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

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...

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...

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...

Structure and Function of Platelets

Structure and Function of Platelets

The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000...

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.

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.

You might also read

Related Articles

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

Sort by

Same author

Liaison haematology in the United Kingdom: Workforce perspectives of workload and labour demand.

British journal of haematology·2026

Same author

Use of andexanet alfa: A British Society for Haematology position statement.

British journal of haematology·2026

Same author

Thrombotic microangiopathy overlap syndrome in pregnancy.

Obstetric medicine·2026

Same author

Medical haematology: Repositioning haematology at the centre of medicine.

British journal of haematology·2026

Same author

Diagnosis without consent: A reply to Johnstone et al. "De-diagnosing chronic lymphocytic leukaemia: An ethical and scientific case for changing diagnostic criteria".

HemaSphere·2026

Same author

Trends and variation in the use of andexanet alfa for the reversal of direct oral anticoagulants in NHS trusts in England.

British journal of clinical pharmacology·2025

Search research articles

Related Experiment Video

Updated: Jun 19, 2025

Ferric Chloride-induced Murine Thrombosis Models

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

Anti-platelet factor 4 immunothrombotic syndromes.

Richard J Buka¹, Sue Pavord²

¹Institute of Cardiovascular Sciences, University of Birmingham, Birmingham, UK.

British Journal of Haematology

|July 26, 2024

Summary

Anti-platelet factor 4 immunothrombotic syndromes, including heparin-induced and vaccine-induced conditions, are prothrombotic disorders. Early suspicion and testing are crucial for diagnosing these immune-mediated conditions characterized by low platelets and clots.

Keywords:

PF4 antibodies heparin‐induced thrombocytopenia immunothrombosis platelet factor 4 vaccine‐induced immune thrombocytopenia and thrombosis

More Related Videos

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets

Published on: November 22, 2024

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

Related Experiment Videos

Last Updated: Jun 19, 2025

Ferric Chloride-induced Murine Thrombosis Models

Ferric Chloride-induced Murine Thrombosis Models

Published on: September 5, 2016

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets

Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets

Published on: November 22, 2024

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

Area of Science:

Immunology
Hematology
Pathology

Background:

Anti-platelet factor 4 (PF4) immunothrombotic syndromes are immune-mediated disorders.
These syndromes include heparin-induced thrombocytopenia (HIT) and vaccine-induced immune thrombocytopenia and thrombosis (VITT).
They are characterized by thrombocytopenia (low platelet count) and thrombosis (blood clots).

Purpose of the Study:

To review the pathophysiology of PF4 immunothrombotic syndromes.
To outline the clinical presentation and diagnostic criteria for these disorders.
To raise awareness for unexplained thrombocytopenia with thrombosis.

Main Methods:

Literature review of existing studies on PF4 immunothrombotic syndromes.
Synthesis of information on triggers, clinical features, and diagnostic approaches.
Discussion of pathophysiology, presenting features, and diagnostic criteria.

Main Results:

PF4 immunothrombotic syndromes are triggered by heparin and adenoviral vector vaccines, but other factors and spontaneous forms exist.
Key diagnostic features include thrombocytopenia and thrombosis.
Unexplained co-occurrence of these findings warrants suspicion and testing.

Conclusions:

Understanding the pathophysiology and diagnostic criteria is essential for managing PF4 immunothrombotic syndromes.
Prompt diagnosis and testing are critical for patients presenting with unexplained thrombocytopenia and thrombosis.
These disorders highlight the complex interplay between immune responses and thrombosis.