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    1. Cortisol plays a key role in mobilizing substances needed for cellular metabolism and stimulates gluconeogenesis or the formation of glucose from noncarbohydrate sources, such as amino acids or free fatty acids in the liver. In addition, cortisol enhances the elevation of blood glucose levels that is promoted by other hormones, such as epinephrine, glucagon, and growth hormone. The effects of cortisol are considered to be permissive for the actions of other hormones. Cortisol also inhibits the uptake and oxidation of glucose by many body cells. Overall, the cortisol-induced increase in carbohydrate metabolism serves to energize the body to cope with the stressor.

      A middle-aged female is presented with COPD, respiratory failure, and prediabetes is being treated with systemic corticosteroids for acute bronchitis. Since starting steroid therapy, her blood glucose levels have remained around 190 mg/dL, and she has a slow-healing wound on her arm. She does not normally require insulin. Which pathophysiological mechanism best explains the delayed wound healing in this patient?

      A. Cortisol activation leads to increased insulin sensitivity and enhanced collagen production.

      B. Elevated cortisol levels cause insulin resistance, impaired leukocyte function, and decreased collagen synthesis.

      C. Acute hypoglycemia resulting in reduced tissue perfusion and delayed cellular repair.

      D. Increased parasympathetic nervous system activity causing accelerated tissue regeneration.

    2. Antiinflammatory effects (systemic effects)High levels of cortisol used in drug therapy suppress inflammatory response and inhibit proinflammatory activity of many growth factors and cytokines; however, over time some individuals may develop tolerance to glucocorticoids, causing an increased susceptibility to both inflammatory and autoimmune diseases

      A recent patient I have is a middle-aged female with respiratory failure, chronic COPD, pre-diabetes that is diet-controlled, and a slow-healing wound on her forearm. Her normal random blood glucose before lunch is around 100-120 mg/dL; it is now 190-210 mg/dL. She recently had bronchitis and needs corticosteroid therapy. This patient demonstrates how chronic physiological stress, combined with necessary medical intervention, can interact and alter clinical outcomes. Her chronic illness and acute bronchitis treatment with corticosteroids stimulates the sympathetic nervous system to increase the cortisol effects. The cortisol effects promote glucogenesis and insulin resistance. This elevated glycemic state impairs wound healing by reducing leukocyte function and collagen synthesis, contributing to the staling of her arm wound. The increased blood glucose also triggers overstimulation of mitochondrial respiration, leading to increased metabolic output. I noticed an increase in her respiratory rate from 16 to 19-20 and in oxygen usage from 2L to 3L to offset the metabolic output. The patient stated she hasn’t been sleeping well due to increased oxygen requirements and a higher respiratory rate. The combination of chronic illness, acute bronchitis, and medical intervention creates a domino effect that delays the patient from healing and maintaining homeostasis.