Chapter 31 - Disorders of the adrenal cortex

Summary

During surgery there is a coordinated response to stress that includes the nervous, endocrine, and immune systems. Inappropriately low response or inappropriately excessive response to stress may lead to disease and possible premature death [1,2]. The hypothalamic–pituitary–adrenal (HPA) axis and the sympathetic nervous system react to stress by releasing hypothalamic CRH and vasopressin (AVP). These hormones synergistically stimulate systemic ACTH secretion, which, in turn, stimulates the adrenal cortexes to secrete glucocorticoids. Central activation of the sympathetic neurons leads to activation of both the systemic sympathetic nervous system and the adrenal medullae [2,3]. The immune system through inflammatory mediators, especially cytokines, stimulates the release of corticotropin-releasing factor from hypothalamic neurons. This central activation of the HPA axis and the direct stimulation of the adrenal glands by the sympathetic system may be a regulatory mechanism for preventing an excessive immune reaction [4,5].

Adrenocorticotropic hormone (ACTH) is released in quick, pulsatile bursts followed by a slower, more sustained rise in cortisol and metabolites [6,7]. Free cortisol is the active hormone and acts directly on tissues [6]. Normal ACTH release and production of cortisol follows a circadian rhythm and is connected to light. It is the highest on awakening in the morning (peaking about 8 hours after the onset of sleep), declines over the day, and is lowest in the middle of the night [7]. The cortisol secretory pattern is usually resistant to acute change. Prolonged bed rest, continuous feeding, or 5 days of fasting, do not alter the rhythm [8]. Occasionally, abrupt time changes of the sleep–awake cycle, as during shift work rotations and jet lag, may have some effect on the 24-hour cortisol patterns [9–11]. Critical illness, chronic inflammatory conditions, chronic insomnia, coronary artery disease, and severe stress often alter the daily rhythm [12–14]. These conditions exert their effect by cytokines, interleukins, and tumor necrosis factors. Circulating interleukin-6 is a potent activator of the HPA axis. By stimulating pituitary ACTH and therefore cortisol, response to inflammation can enhance resistance to inflammatory disease, while a decreased or defective response can increase susceptibility [4,5,13].