Meningococcemia pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
* Transmission through respiratory secretions from a nasopharyngeal carrier case-patient. | * Transmission through respiratory secretions from a nasopharyngeal carrier case-patient. | ||
* Shock is due to lipooligosaccharide which is a potent toxin. This toxin initiates release of inflammatory cytokines, reactive oxygen radicals, prostaglandins, arachidonic acid, complement activated products, platelet aggregating factor, and perhaps nitric oxide. | * Shock is due to lipooligosaccharide which is a potent toxin. This toxin initiates release of inflammatory [[cytokines]], reactive oxygen radicals, [[prostaglandins]], [[arachidonic acid]], complement activated products, platelet aggregating factor, and perhaps [[nitric oxide]]. | ||
==References== | ==References== | ||
Revision as of 15:17, 25 February 2013
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Meningococcemia Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Meningococcemia pathophysiology On the Web |
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American Roentgen Ray Society Images of Meningococcemia pathophysiology |
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Risk calculators and risk factors for Meningococcemia pathophysiology |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Pathophysiology
- Transmission through respiratory secretions from a nasopharyngeal carrier case-patient.
- Shock is due to lipooligosaccharide which is a potent toxin. This toxin initiates release of inflammatory cytokines, reactive oxygen radicals, prostaglandins, arachidonic acid, complement activated products, platelet aggregating factor, and perhaps nitric oxide.