Septic Shock Research Paper

833 Words2 Pages

Topic: The Controversy of using Corticosteroid in septic shock patients

Ranya Bafail

University of Michigan School of Nursing

Introduction:
Severe sepsis and septic shock are major public health problems globally and are associated with substantial morbidity and mortality. The role of corticosteroid treatment in patients with severe sepsis and septic shock remains controversial despite the studies that have been using since decades.
The issue:
HPA axis and septic shock:
The complex pathophysiologic changes in severe sepsis and septic shock are known to have important impact on endocrine organs with reported alterations in thyroid, pancreas, and adrenal function (1). By far the most controversial endocrine topic in …show more content…

Corticotropin-releasing hormone initiates the synthesis of adrenal corticotropin hormone (ACTH) from the anterior pituitary gland, which stimulates the adrenal to produce cortisol (4). Sufficient levels of cortisol production inhibit further production via a negative feedback mechanism. In addition, vasopressin, a neurohormone synthesized in the supraoptic and paraventricular nucleus of the hypothalamus and stored in the posterior pituitary, has been shown to regulate cortisol production via V1a and V1b receptors (4,5). The majority of cortisol in the circulation is bound to proteins, corticosteroid-binding globulin (70%), and albumin (20%), but the circulating free cortisol is the active form (4 ,5). Critical illnesses, such as severe sepsis, are associated with a decrease in albumin and corticosteroid-binding proteins, which may result in a decreased total cortisol measurement but a relative increase in the free cortisol level (4, 6, …show more content…

The dysfunction can be either inappropriately low production of glucocorticoids or an impaired response to cortisol in the systemic circulation. Molecular interactions, classified as either genomic or nongenomic pathways, may contribute to impaired cortisol response. The genomic pathways can affect the clinical interaction of cortisol with the glucocorticoid receptor (GR) via either transactivation or transrepression (4, 8). The GR plays an integral role in facilitating the activity of glucocorticoids, and GR-binding affinity has been demonstrated to be altered in severe sepsis and septic shock (4,8). The nongenomic effects include the interaction of glucocorticoids with vascular membranes, cellular junctions, and the various signaling pathways between cellular mediators

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