Hypercoagulable States
Hypercoagulable States - Related Videos
06:03
Electrolytic Inferior Vena Cava Model (EIM) of Venous Thrombosis
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Cited by 39 •
2011
The electrolytic induction of endothelial activation to the internal surface of the Inferior Vena Cava results in venous type thrombus formation due to endothelial activation and partial blood stasis, two components of Virchow's triad.
06:59
Using Next Generation Sequencing to Identify Mutations Associated with Repair of a CAS9-induced Double Strand Break Near the CD4 Promoter
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Cited by 5 •
2022
Presented here is sgRNA/CAS9 endonuclease and next-generation sequencing protocol that can be used to identify the mutations associated with double strand break repair near the CD4 promoter.
08:20
Sexual Development and Ascospore Discharge in Fusarium graminearum
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Cited by 79 •
2012
Sexual crosses and isolation of recombinant progeny are important research tools for the filamentous fungus, Fusarium graminearum, The techniques necessary successfully carry out these processes are presented.
06:35
An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
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Cited by 2 •
2019
The protocol illustrates the use of histopathologic examination and immunohistochemistry to profile the folate receptor beta macrophage and its relationship with the total immune cell infiltrate in temporal artery biopsies in giant cell arteritis.
07:30
Protocol for Producing Three-Dimensional Infrared Video of Freezing in Plants
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Cited by 1 •
2018
Here, we present a protocol to image a strawberry plant freezing in 3 dimensions. Two infrared cameras positioned at slightly different angles are used to produce a red-blue anaglyph video to observe the freezing of the plant in 3 dimensions.
FAQs
The key mechanism is a shift in which procoagulant activity exceeds the protection provided by natural anticoagulant and fibrinolytic systems. This imbalance can reflect inherited abnormalities, acquired disease, medications, or physiologic conditions. Understanding which part of this balance is altered helps clinicians interpret why thrombosis risk is increased and consider whether the risk may persist.
Inherited abnormalities represent underlying predispositions that may contribute to thrombosis risk across a person’s life, whereas acquired causes arise from disease, medications, or physiologic conditions. This distinction helps place an event in context, particularly when clinicians review family history, personal history, and provoking factors. It also supports assessment of whether the risk reflects a persistent or situational tendency.
Medications and physiologic conditions can act as provoking factors that alter the likelihood of thrombosis without necessarily indicating a permanent abnormality. Identifying these circumstances gives clinicians a clearer explanation for a clotting event and helps distinguish transient risk from persistent thrombophilia. That distinction is important when considering prevention, follow-up, and the role of anticoagulation.
Evaluation combines personal and family history, known provoking factors, and laboratory findings. Personal history may show previous thrombotic events, while family history can point toward an inherited contribution. Clinicians interpret laboratory information alongside the clinical circumstances rather than in isolation, using the combined picture to assess risk and distinguish transient influences from persistent thrombophilia.
The distinction helps determine whether elevated thrombotic risk is linked to a temporary circumstance or an ongoing predisposition. A transient risk may be interpreted differently from persistent thrombophilia when clinicians plan prevention and follow-up. This assessment also contributes to decisions about anticoagulation and encourages attention to any underlying disease or other continuing contributor.
Assessment is useful when clinicians need to explain or anticipate venous or arterial thrombosis, including deep vein thrombosis, pulmonary embolism, or ischemic stroke. Reviewing risk factors and laboratory findings can support individualized risk assessment after or around these events. The resulting information may guide preventive strategies, treatment decisions, and management of contributing conditions.
Recognizing an increased clotting tendency supports efforts to prevent complications and informs treatment when thrombosis occurs. Clinical management may include decisions about anticoagulation, while addressing an underlying acquired cause can reduce or control a continuing source of risk. The approach is shaped by the balance between identified provoking factors, persistent thrombophilia, and the type of thrombosis involved.