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This document provides a schematic diagram of the pathophysiology of toxic shock syndrome. It shows that certain bacteria like Staph. Aureus and Strep. Pyogenes can produce superantigen toxins that bind to T-cell receptors and MHC II, leading to excessive T-cell proliferation and activation of proinflammatory mediators. This causes activation of the coagulation system and endothelial damage, resulting in hypotension, microvascular thrombi, disseminated intravascular coagulation, and decreased tissue perfusion. Ultimately, this pathophysiological process can lead to organ damage in multiple organ systems and symptoms of the toxic shock syndrome.
Description originale:
Pathophysiology of Toxic Shock Syndrome
Titre original
Schematic Diagram of the Pathophysiology of Toxic Shock Syndrome
This document provides a schematic diagram of the pathophysiology of toxic shock syndrome. It shows that certain bacteria like Staph. Aureus and Strep. Pyogenes can produce superantigen toxins that bind to T-cell receptors and MHC II, leading to excessive T-cell proliferation and activation of proinflammatory mediators. This causes activation of the coagulation system and endothelial damage, resulting in hypotension, microvascular thrombi, disseminated intravascular coagulation, and decreased tissue perfusion. Ultimately, this pathophysiological process can lead to organ damage in multiple organ systems and symptoms of the toxic shock syndrome.
This document provides a schematic diagram of the pathophysiology of toxic shock syndrome. It shows that certain bacteria like Staph. Aureus and Strep. Pyogenes can produce superantigen toxins that bind to T-cell receptors and MHC II, leading to excessive T-cell proliferation and activation of proinflammatory mediators. This causes activation of the coagulation system and endothelial damage, resulting in hypotension, microvascular thrombi, disseminated intravascular coagulation, and decreased tissue perfusion. Ultimately, this pathophysiological process can lead to organ damage in multiple organ systems and symptoms of the toxic shock syndrome.
Schematic Diagram of the Pathophysiology of Toxic Shock Syndrome
Continued
Staph. Aureus Strep. Pyogenes Production of superantigen toxins and absorption into the systemic circulation Binding of Tcell receptor to MHC II Excessive Tcell proliferation and activation Proinflammatory mediators activation Activation of complement system Cytokines proliferation Activation of Coagulation system Binding to endothelial tissues Vasodilatation, increased vascular permeability Activation of clotting factors; decreased ATIII, protein C and S Endothelial damage Hypotension Microvascular thrombi; DIC Clot formation, thrombosis of small vessels, Decreased tissue perfusion
Pyrogenic effect on the hypothalamus Fever Chills
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Continuation
Clot formation, thrombosis of small vessels, Decreased tissue perfusion
Brain Heart Skin Gastrointestinal Lungs Kidneys Liver Altered mental status, confusion, headaches, seizures Increased dead space Impaired gas exchange Hypoxemia Tachycardia Salt and water retention Decreased urine output Weakening of the intestinal wall barrier Bacterial/endooxin translocation Nausea, vomiting, diarrhea Damage to hepatocytes Increased liver enzymes, inability to excrete toxins Diffuse rash, desquamation Tachypnea Sepsis Increasd levels of ammonia Encephalopathy