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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...
Introduction to Hemostasis01:05

Introduction to Hemostasis

Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized, and...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

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 forms a...
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...
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...
Formation of the Platelet Plug01:22

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...

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Updated: Jun 18, 2026

Polyelectrolyte Complex for Heparin Binding Domain Osteogenic Growth Factor Delivery
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Polyelectrolyte Complex for Heparin Binding Domain Osteogenic Growth Factor Delivery

Published on: August 22, 2016

"Heparinization" and hyperfibrinogenolysis by wasp sting.

Cristina Lombardini1, Robert-Ebadi Helia, Françoise Boehlen

  • 1Service of Intensive Care, Department of Anesthesiology, Pharmacology and Intensive Care, University Hospitals of Geneva, 1211 Geneva, Switzerland. cristina.lombardini@hcuge.ch

The American Journal of Emergency Medicine
|November 26, 2009
PubMed
Summary

Wasp sting anaphylaxis can cause unusual bleeding disorders by activating mast cells. These cells release heparin and tryptase, leading to anticoagulation and fibrinogen degradation, mimicking heparin therapy.

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Basophil Activation Test for Allergy Diagnosis
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Basophil Activation Test for Allergy Diagnosis
07:22

Basophil Activation Test for Allergy Diagnosis

Published on: May 31, 2021

Area of Science:

  • Hematology
  • Immunology
  • Toxicology

Background:

  • Anaphylaxis, a severe allergic reaction, can trigger complex physiological responses.
  • Coagulation abnormalities are not typically considered a primary manifestation of anaphylaxis.

Observation:

  • A patient presented with an unclottable activated partial thromboplastin time and significant anti-Xa activity post-wasp sting, despite no heparin administration.
  • The patient also exhibited an extremely low fibrinogen level with a normal platelet count and only a slight increase in D-dimers.

Findings:

  • Mast cell activation during anaphylaxis released endogenous heparin, causing "heparinization" and anticoagulant effects.
  • Serum tryptase cleaved fibrinogen and activated fibrinolysis, leading to hyperfibrinogenolysis and low fibrinogen levels.
  • These combined mechanisms explained the observed coagulation abnormalities, distinct from disseminated intravascular coagulation.

Implications:

  • This case highlights a novel mechanism of coagulation derangement in human anaphylaxis.
  • Understanding these mechanisms is crucial for managing anaphylaxis patients, especially in settings with potential bleeding risks like trauma or surgery.
  • Further research into in vivo anaphylaxis-induced coagulopathy is warranted.