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68 CASE 68


An 18-year-old girl comes to the university clinic complaining of fever, chills, headache, and aching joints.


Prior to today, the patient has been generally healthy and is up to date on all immunizations.






PATHOPHYSIOLOGY OF KEY SYMPTOMS


The patient’s major symptoms are tied to an infectious process. Increased activity of the immune system generates pyrogens that alter the hypothalamic temperature set point and cause an elevation in body core temperature. The changes in the vital signs are secondary to the fever.


Body core temperature results from the balance of heat gain and heat loss. Body core temperature is sensed in the anterior hypothalamus and regulated around a set point. If body core temperature falls below the set point, heat gain mechanisms are activated and heat lost mechanisms are inhibited. If body core temperature rises above the set point, heat lost mechanisms are activated and heat gain mechanisms are inhibited.


There are numerous pyrogenic substances that increase set point, including interleukin-1, interleukin-6, selected interferons, prostaglandins, and bacterial endotoxins. Many of these substances mediate the febrile response to infection. Prostaglandins, in particular, can play a central role in the resetting of the hypothalamic set point.


Influenza causes a transient increase in set point and, therefore, body core temperature. During the initial stages of the infection, temperature set point is elevated to 39°C. Body core temperature at 37°C is lower than the set point, and generating a “too cold” error signal, so heat gain mechanisms are activated. These include diminished cutaneous blood flow, shivering, and behavioral mechanisms such as putting on additional clothes or covering under blankets. Elevation of core temperature to 39°C brings the hypothalamic set point in body core temperature back into balance (Fig. 68-1).


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Jul 4, 2016 | Posted by in PHYSIOLOGY | Comments Off on 68

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