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Related Concept Videos

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...
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.
Clot Retraction and Fibrinolysis01:16

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.
Structure and Function of Platelets01:18

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 platelets, with...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

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...
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...

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Related Experiment Video

Updated: May 17, 2026

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
05:49

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets

Published on: November 29, 2024

Reduced platelet aggregation in a boy with scurvy.

F Dey1, A Möller, B Kemkes-Matthes

  • 1Department of Child Neurology, University of Giessen, Giessen, Germany. Friederike.Dey@paediat.med.uni-giessen.de

Klinische Padiatrie
|October 17, 2012
PubMed
Summary
This summary is machine-generated.

Pediatric scurvy, a vitamin C deficiency, can cause platelet dysfunction and bleeding. Supplementation with ascorbic acid normalized platelet aggregation, suggesting a link between vitamin C and blood clotting in children.

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Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
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Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation

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Microfluidics in Assessing Platelet Function
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Microfluidics in Assessing Platelet Function

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Last Updated: May 17, 2026

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
05:49

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets

Published on: November 29, 2024

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
09:13

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation

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Microfluidics in Assessing Platelet Function
06:47

Microfluidics in Assessing Platelet Function

Published on: November 8, 2024

Area of Science:

  • Biochemistry
  • Hematology
  • Pediatrics

Background:

  • Scurvy, a condition caused by vitamin C deficiency, is typically associated with impaired collagen synthesis, leading to symptoms like bruising and bleeding.
  • The exact mechanisms contributing to the hemorrhagic diathesis in pediatric scurvy are not fully understood, with collagen abnormalities being the primary focus.

Observation:

  • A case study of a 9-year-old autistic boy with a highly restricted diet presented with classic scurvy symptoms, including petechiae, gingival bleeding, and bone pain.
  • Platelet aggregometry in this patient revealed significantly reduced thrombocyte aggregation, a measure of platelet function.

Findings:

  • Vitamin C supplementation led to the normalization of platelet aggregation in the patient.
  • This suggests that platelet dysfunction is a contributing factor to the bleeding tendencies observed in scurvy.

Implications:

  • Ascorbic acid deficiency should be considered in the differential diagnosis of children presenting with unexplained acquired thrombocytopathy or bleeding disorders.
  • This finding broadens the understanding of scurvy's pathophysiology beyond collagen defects to include potential hematological abnormalities.