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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.
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...
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...
Pulmonary Embolism I: Introduction01:19

Pulmonary Embolism I: Introduction

A blood clot, or thrombus, is a semi-solid mass composed of fibrin, platelets, and red blood cells. When it forms within a vessel, it can obstruct blood flow, known as thrombosis. If part of the clot detaches, it becomes an embolus that can travel and block distant vessels. When this occurs in the pulmonary arteries, it causes a condition known as pulmonary embolism (PE).Origin and ImpactMost often, the embolus originates from a thrombus in the deep veins of the lower limbs, a condition called...
Pulmonary Embolism I: Introduction01:29

Pulmonary Embolism I: Introduction

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...
Venous Thrombosis II: Clinical Manifestations and Diagnostic Studies01:20

Venous Thrombosis II: Clinical Manifestations and Diagnostic Studies

The key difference between Superficial Vein Thrombosis (SVT) and Deep Vein Thrombosis (DVT) lies in their location and severity.Clinical ManifestationsSVT typically presents with localized pain, tenderness, and redness along the course of a superficial vein, often accompanied by a palpable, cord-like structure under the skin. This condition is usually less dangerous than DVT but can be uncomfortable and may lead to complications such as cellulitis or, rarely, a clot extension into the deep...

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Updated: Jun 3, 2026

Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States
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Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States

Published on: April 1, 2015

Thrombosis and sickle cell disease.

Lucia De Franceschi1, Maria Domenica Cappellini, Oliviero Olivieri

  • 1Department of Medicine, University of Verona, Verona, Italy. lucia.defranceschi@univr.it

Seminars in Thrombosis and Hemostasis
|April 2, 2011
PubMed
Summary

Sickle cell disease (SCD) involves sickle hemoglobin polymerization, leading to dehydrated red cells and a hypercoagulable state. This review explores coagulation, platelet, endothelial, and inflammatory factors contributing to SCD complications.

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

Published on: March 14, 2017

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Last Updated: Jun 3, 2026

Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States
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Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States

Published on: April 1, 2015

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

Area of Science:

  • Hematology
  • Vascular Biology
  • Pathophysiology

Background:

  • Sickle cell disease (SCD) is defined by sickle hemoglobin polymerization upon deoxygenation.
  • Dense, dehydrated red blood cells are central to SCD's acute and chronic manifestations.
  • SCD is associated with a hypercoagulable state, driving vaso-occlusive events and organ damage.

Purpose of the Study:

  • To review the multifaceted pathophysiology of hypercoagulability in sickle cell disease.
  • To examine the interplay of coagulation abnormalities, platelet dysfunction, endothelial issues, inflammation, and nitric oxide metabolism in SCD.
  • To discuss current and potential therapeutic strategies for managing hypercoagulability in SCD.

Main Methods:

  • Literature review of recent studies on SCD pathophysiology and hypercoagulability.
  • Analysis of the roles of coagulation factors, platelet activation, and endothelial function.
  • Examination of inflammatory responses and nitric oxide metabolism in SCD.
  • Synthesis of information on therapeutic approaches for hypercoagulability in SCD.

Main Results:

  • Abnormalities in the coagulation system are a key feature of SCD.
  • Perturbations in platelet activation and aggregation contribute to vaso-occlusion.
  • Vascular endothelial dysfunction and inflammatory responses are significantly involved.
  • Nitric oxide metabolism is altered, impacting vascular function in SCD.

Conclusions:

  • Hypercoagulability is a critical component of sickle cell disease pathophysiology.
  • Understanding these complex interactions is essential for developing effective treatments.
  • Targeting hypercoagulability offers a promising avenue for managing SCD complications.