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Related Concept Videos

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.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
Disorders of Erythrocytes01:27

Disorders of Erythrocytes

Disorders of erythrocytes, or red blood cells (RBCs), include a range of conditions affecting their number, shape, or function.
Erythrocyte disorders can be broadly categorized into two main types: anemic and polycythemic conditions.
A low oxygen-carrying capacity of the blood due to the loss, lower production, or destruction of erythrocytes is termed anemia. Hemorrhagic anemia, for example, occurs when bleeding from an external wound or internal ulcer reduces erythrocyte counts.
On the other...
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...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Blood Pressure Imbalances and Circulatory Shock01:24

Blood Pressure Imbalances and Circulatory Shock

Disorders affecting blood volume, vascular tone, or vascular function can disrupt vascular homeostasis, including conditions like hypertension, hemorrhage, and shock.
Blood Pressure: Hypertension and Hypotension
Normal blood pressure is 120/80 mm Hg. Elevated blood pressure is 120-129/under 80 mm Hg. Hypertension, warranting treatment at 130/80 mm Hg, is often asymptomatic and can lead to severe cardiovascular events, aneurysms, peripheral arterial disease, chronic renal disease, or cardiac...
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...

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Updated: May 10, 2026

Continuous Manual Exchange Transfusion for Patients with Sickle Cell Disease: An Efficient Method to Avoid Iron Overload
05:23

Continuous Manual Exchange Transfusion for Patients with Sickle Cell Disease: An Efficient Method to Avoid Iron Overload

Published on: March 14, 2017

Hemostatic abnormalities in sickle cell disease.

Ming Y Lim1, Kenneth I Ataga, Nigel S Key

  • 1Division of Hematology/Oncology, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.

Current Opinion in Hematology
|July 3, 2013
PubMed
Summary
This summary is machine-generated.

Sickle cell disease (SCD) increases the risk of venous thromboembolism (VTE) due to chronic hypercoagulation. Hemolysis and blood cells play a key role in this thrombophilic state, requiring further study for effective therapies.

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Characterization of Sickling During Controlled Automated Deoxygenation with Oxygen Gradient Ektacytometry
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Characterization of Sickling During Controlled Automated Deoxygenation with Oxygen Gradient Ektacytometry

Published on: November 5, 2019

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Last Updated: May 10, 2026

Continuous Manual Exchange Transfusion for Patients with Sickle Cell Disease: An Efficient Method to Avoid Iron Overload
05:23

Continuous Manual Exchange Transfusion for Patients with Sickle Cell Disease: An Efficient Method to Avoid Iron Overload

Published on: March 14, 2017

Characterization of Sickling During Controlled Automated Deoxygenation with Oxygen Gradient Ektacytometry
08:23

Characterization of Sickling During Controlled Automated Deoxygenation with Oxygen Gradient Ektacytometry

Published on: November 5, 2019

Area of Science:

  • Hematology
  • Vascular Biology
  • Thrombosis Research

Background:

  • Sickle cell disease (SCD) is linked to chronic hypercoagulation.
  • Venous thromboembolism (VTE) complications in SCD are increasingly recognized.
  • Hemolysis is implicated in the hypercoagulable state of SCD.

Purpose of the Study:

  • To review the evolving epidemiology of VTE in SCD.
  • To explore the mechanistic role of hemolysis in SCD-associated hypercoagulation.
  • To understand the complex pathways underlying the thrombophilic state in SCD.

Main Methods:

  • Review of recent literature on SCD and VTE.
  • Utilized global coagulation assays (thromboelastography, thrombin generation assays).
  • Analysis of mechanistic studies in human and mouse models.

Main Results:

  • Recent literature strengthens the evidence for SCD as a thrombophilic state.
  • Global coagulation assays suggest a role for peripheral blood cells and microparticles.
  • Inconsistent results from global assays may be due to technical differences.

Conclusions:

  • VTE is an underappreciated complication of SCD.
  • The hypercoagulable state in SCD is complex and multifactorial.
  • Understanding these mechanisms may guide novel antithrombotic therapies for SCD.