What person is in the prodromal stage of influenza infection?

A. Opiate drugs cause respiratory acidosis by depressing the central nervous system, specifically the respiratory centers in the brainstem, leading to reduced ventilation and accumulation of carbon dioxide. This increases arterial PCO2, lowering blood pH. The patient’s exposure to opiates aligns with this mechanism, as it impairs the physiological need for adequate respiration, a key component of Maslow’s hierarchy.

B. Atelectasis results in respiratory acidosis due to collapsed alveoli, which reduces effective gas exchange and causes carbon dioxide retention. This elevates PCO2, decreasing pH. The patient’s condition of atelectasis directly contributes to hypoventilation, supporting this classification.

C. Hypoventilation leads to respiratory acidosis by decreasing alveolar ventilation, causing carbon dioxide buildup. Elevated PCO2 lowers blood pH. The patient’s hypoventilation directly correlates with this mechanism, as it disrupts the respiratory system’s ability to maintain acid-base balance.

D. Renal failure causes metabolic acidosis by impairing the kidneys’ ability to excrete hydrogen ions and reabsorb bicarbonate, leading to acid accumulation and reduced serum bicarbonate. This aligns with the patient’s renal failure, as it disrupts the renal regulation of acid-base homeostasis, a critical physiological need.

E. Airway obstruction results in respiratory acidosis by preventing adequate ventilation, leading to carbon dioxide retention and increased PCO2, which lowers pH. The patient’s airway obstruction directly causes this imbalance, impairing respiratory function.

F. Diarrhea causes metabolic acidosis due to excessive loss of bicarbonate-rich intestinal fluids, reducing serum bicarbonate and lowering pH. The patient’s diarrhea aligns with this mechanism, as it leads to a direct loss of base, disrupting acid-base equilibrium.

Choice A reason: Cortisol, a stress hormone, suppresses immune and inflammatory responses, slowing fibroblast activity and collagen synthesis, which impairs wound healing. This anti-inflammatory effect prioritizes energy allocation to stress response over tissue repair, making decreased wound healing a correct effect of cortisol during stress.

Choice B reason: Cortisol stimulates gastric acid secretion by enhancing gastrin release and reducing mucosal protection, increasing the risk of ulcers. This effect supports energy mobilization during stress by promoting digestion but can lead to gastrointestinal complications, making increased gastric acid secretion a correct effect.

Choice C reason: Cortisol promotes gluconeogenesis and glycogenolysis in the liver, elevating blood glucose levels to provide energy for the stress response. It also induces insulin resistance, ensuring glucose availability for critical tissues like the brain, making increased blood glucose a correct effect of cortisol.

Choice D reason: Cortisol suppresses the immune response by inhibiting cytokine production and lymphocyte proliferation, reducing inflammation and immune activity. This does not align with increased immune response, as cortisol’s immunosuppressive effects are well-documented, making this choice incorrect for the stress response.

Choice E reason: Cortisol increases blood pressure via mineralocorticoid effects, enhancing sodium retention and vascular tone. This supports cardiovascular stability during stress, not decreased blood pressure, which would be counterproductive in a fight-or-flight response, making this choice incorrect for cortisol’s effects.