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Inflammation01:38

Inflammation

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Overview
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Inflammatory Response I: Vascular and Cellular01:30

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The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
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Psychoneuroimmunology: Cardiovascular Disease01:27

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Psychoneuroimmunology (PNI) is a multidisciplinary field that examines how psychological factors, particularly stress, interact with the immune system and impact physical health. Research in PNI has shown that chronic or traumatic stress can disrupt both the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. These disruptions contribute to serious health conditions, including cardiovascular diseases.
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Viscosity of Fluid01:19

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Viscosity measures the resistance a fluid offers to flow and deformation. It results from internal friction between layers of fluid moving relative to one another. Dynamic viscosity, denoted by the Greek letter mu (μ), quantifies the force needed to move one fluid layer over another. For Newtonian fluids like water and air, the relationship between the shearing stress and the rate of shearing strain is linear, meaning their viscosity remains constant regardless of the applied stress.
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COVID-19 Demonstrates That Inflammation Is a Hyperviscous State.

Gregory D Sloop1, Gheorghe Pop2, Joseph J Weidman3

  • 1Pathology, Idaho College of Osteopathic Medicine, Meridian, USA.

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|November 24, 2022
PubMed
Summary
This summary is machine-generated.

Severe COVID-19 causes blood hyperviscosity and hyperfibrinogenemia, increasing thrombosis risk and decreasing tissue perfusion. This contributes to organ damage and long-COVID symptoms.

Keywords:
blood viscositycovid-19fibrinogeninnate immunitymyocarditissars-cov-2silent hypoxemiatoll-like receptor 8

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Area of Science:

  • Hematology
  • Virology
  • Pathophysiology

Background:

  • Severe coronavirus disease-2019 (COVID-19) complications are linked to blood hyperviscosity.
  • Hyperviscosity arises from elevated fibrinogen levels, creating a syndrome affecting various blood flow conditions.
  • This condition increases thrombosis risk and impairs tissue perfusion.

Purpose of the Study:

  • To elucidate the mechanisms by which COVID-19-induced hyperviscosity contributes to disease severity and long-term effects.
  • To explore the role of viral genetic factors in triggering hyperviscosity and immune responses.

Main Methods:

  • Review of existing literature on COVID-19 pathophysiology, focusing on hematological changes.
  • Analysis of the severe acute respiratory syndrome coronavirus 2 genome for specific genetic sequences.
  • Correlation of hyperviscosity markers with clinical outcomes and organ-specific damage in COVID-19 patients.

Main Results:

  • COVID-19-associated hyperviscosity significantly increases arterial and venous thrombosis risk, counteracting anticoagulation.
  • Reduced tissue perfusion due to hyperviscosity leads to lung, heart, and brain damage, including hypoxemia, myocarditis, and demyelination.
  • Viral genetic factors, specifically oligonucleotide sequences, activate innate immunity, elevating fibrinogen and contributing to pathology.

Conclusions:

  • Blood hyperviscosity is a critical factor in severe COVID-19 pathogenesis, driving thrombosis and organ dysfunction.
  • Hyperviscosity contributes to long-COVID symptoms through mechanisms like capillary rarefaction and endothelial damage.
  • Targeting hyperviscosity and associated immune activation may offer therapeutic strategies for COVID-19 and its sequelae.