Endocrine Response : To Stress and Injury Stress is the ‘wear and tear on the body’… -Hans Selye
The men who STRESSED us: Hans Selye researched the effects of stress on rats and other animals by exposing them to unpleasant or harmful stimuli introduced the stress response mechanism known as General Adaptation Syndrome in 1936
published in 1974 a model dividing stress into eustress and distress. His model argues that cognitive processes of appraisal are central in determining whether a situation is potentially threatening or harmful
usually for short time and may be due to work pressure, meeting deadlines pressure or minor accident, over exertion, increased physical activity, searching something but you misplaced it, or similar things.
Symptoms of this type of tension are headaches, back pain, stomach problems, rapid heartbeat, muscle aches or body pain.
Hypothalamus indirectly orders adrenals to release cortisol via the corticotropin releasing hormone (CRH).
Why indirect? CRH goes to the pituitary gland sends the message on to the adrenals by releasing adrenocorticotropic hormone (ACTH)
When ACTH reaches the adrenals, the adrenal cortex releases cortisol into the blood. Cortisol makes the body release stored chemicals into the blood.
With ADH and aldosterone helping the body preserve blood volume, and cortisol and growth hormone providing food for the cells, the body should recover. But if this isn't enough help, the body could become exhausted and suffer organ damage.
Primary adrenal insufficiency is due to adrenal gland failure and thus both baseline and post stimulation concentrations are abnormal.
Secondary adrenal insufficiency is due to hypothalamic or pituitary failure and, in the acute setting, the adrenal glands respond well to stimulation while the baseline cortisol concentration is low.
(Clinical Endocrinology, March 2001)
The impact of the nonpeptide corticotropin -Releasing Hormone Antagonist Antalarmin on Behavioral and Endocrine Responses to Stress.
CRH is a 41-amino acid peptide initially identified as a hypothalamic factor responsible for stimulating ACTH from the anterior pituitary
(1). Stressors induce the synthesis and release of CRH from cells of the paraventricular nucleus, into the portal blood, initiating the hypothalamopituitary-
adrenal (HPA) response to stressors. CRH isalso involved in the mediation of autonomic and behavioral sequelae of exposure to stressors.
The intracerebroventricular (icv) administration of CRH produces autonomic activation and many of the same behavioral, neurochemical, and electrophysiological alterations that are produced by stressors.
Furthermore, the icv administration of CRH antagonists, such as a helical CRH9–41 and D-Phe CRH, can blunt or block these stress-induced alterations in behavior and autonomic activity.
(Endocrine Society, April 1998)
Posttraumatic Inflammation Is a Complex Response Based on the Pathological Expression of the Nervous, Immune, and Endocrine Functional Systems M. A. Aller et al.
The nervous, immune and endocrine functional system integrates with each other to play important roles in local and systemic posttraumatic acute inflammatory response. In the nervous functional system, the phenomenon of ischemia-revascularization secondary to arteriolar vasomotor activity which involves vasoconstriction and vasodilatation would produce interstitial edema and permit selective cellular nutrition by diffusion.
Effective circulating volume- stimulates baroreceptor and stretch receptors, maximal NE response is when the effective circulating volume has been decreased by 30-40%, further decrease cannot be handled be compensatory systems, and shock follows
Decrease in oxygen, increase in carbon dioxide and hydrogen ions chemoreceptor activation causes an increase in heart rate and cardiac contractility.
Pain-NE response is not activated unless the neural pathways are intact
The neuroendocrine response (NER) is an essential component of the adaptive process to trauma, brain injury, and major surgery Chiolero R, et al.
While receiving additive humoral and neural afferent inputs, the brain nuclei responsible for the NER act mainly by efferent pathways to the hypothalamic-pituitary-adrenal (HPA) axis and the sympathoadrenal system, the activations of which induce subsequent circulatory and metabolic responses.
The outcome after brain injury is closely correlated with the intensity of these changes, particularly with catecholamine plasma levels and the severity of the low triiodothyronine syndrome.
Alterations of the thyroid hormones are largely related to a reduction in peripheral deiodination of thyroxin. Recent research shows that increased free-radical production and decreased selenium (an antioxidant) serum levels play an important role in thyroid metabolism.
(Endocrine Review, October 2004)
Hypopituitarism after traumatic brain injury Bondanelli Marta et al.
Traumatic brain injury (TBI) is from an external mechanical insult on the cephalic area that can direct mechanical injury to pituitary gland, stalk or hypothalamus and can lead into temporary or permanent neurological dysfunction, resulting to impairment of cognitive, physical and psychosocial functions.
Pituitary dysfunction can follow after a TBI and can be classified into two namely, functional alterations during the acute phase post-TBI, which result in a temporary increase or decrease in blood pituitary hormone concentrations, alterations in pituitary hormone secretion that may occur at any time after TBI, resulting in permanent hypopituitarism caused by damage at pituitary and/or hypothalamic level. Changes in the circulating hormone levels such as adrenocorticotropin (ACTH), prolactin (PRL) and growth hormone (GH) levels increase and luteinizing hormone (LH), follicle-stimulating hormone (FSH) and thyrotropin (TSH) levels may either decrease or remain unchanged, associated with a decreased activity of their target organ become apparent during the first hours or days after trauma, and may persist for the duration of the acute critical illness.
(Medline, July 2001)
Growth hormone deficiency occurs in approximately 20% of all individuals who suffer from a moderate to severe traumatic brain injury
This study shows that individuals with traumatic brain injury with normal GH secretion have below normal aerobic capacity and those patients who have GH insufficiency/deficiency are further deconditioned. Studies of GH replacement in these subjects should be conducted to assess whether GH therapy can improve cardiorespiratory fitness and prevent secondary disability.
(The Journal of Clinical Endocrinology & Metabolism, July 2008)
Sevoflurane improves the neuroendocrine stress response during laparoscopic pelvic surgery.
ACTH and cortisol are sensitive indicators of stress: plasma increase of ACTH and the subsequent increase of plasma cortisol are known to correlate with the severity of surgical injury.These hormones cause specific metabolic alterations (the best known is an increase of muscle catabolism, with net negative nitrogen balance), but also affect humoral and cellular immune responses)
(American Society of Anesthesiologist, July 2000)
Incidence of adrenal insufficiency after severe traumatic brain injury varies according to definition used: clinical implications Bernard Francis et al.
The stress response to surgery comprise a number of hormonal changes initiated by neuronal activation of the hypothalamic-pituitary-adrenal axis. The overall metabolic effect is one of catabolism of stored body fuels. In general, the magnitude and duration of the response are proportional to the surgical injury and development of complications such as sepsis. Other changes also occur following surgery, notably an increase in cytokine production which is triggered locally as a tissue response to injury.
Regional anaesthesia with local anaesthetic agents inhibits the stress response to surgery and can also influence postoperative outcome by beneficial effects on organ function.