Metabolic response to stress

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Compared with the starving patient, the critically ill patient has a very different 'internal milieu' and exhibits greater and more prolonged negative nitrogen balance due to protein breakdown (gluconeogenesis). There is no adaptation to energy production from fat stores, and the basal metabolic rate is increased by 20 to 80 per cent. Metabolic and endocrine responses include stimulation of the sympathetic nervous system, release of epinephrine (adrenaline), glucocorticoids, and glucagon, suppression of prolactin, growth hormone, and thyroid hormone release, metabolic resistance to the effects of insulin, production of cytokine mediators, and release of eicosanoid precursors from membrane-bound phospholipids (Fig 1).

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Fig. 1 Nutritional and metabolic imbalance in critical illness: TNF, tumor necrosis factor; HGH, human growth hormone.

The body's initial response to stress is primarily controlled by the locus ceruleus in the brainstem and the paraventricular nucleus of the hypothalamus ( MichelsoD et al 1994). When stimulated, the former releases norepinephrine (noradrenaline), stimulates the autonomic nervous system, and increases arousal. The latter produces corticotropin-releasing hormone which activates the hypothalamo-pituitary-adrenal axis. The locus ceruleus and corticotropin- releasing hormone systems exhibit mutual feedback in that stimulation of either system will lead to activation of both pathways.

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