Disasters and emergencies trigger sudden and systemic physiological responses in the body. The stress response is primarily regulated through the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system. The release of adrenaline and noradrenaline facilitates metabolic adaptation by inducing tachycardia, hypertension, bronchodilation, and increased gluconeogenesis. Cortisol secretion plays a role in protein catabolism, modulation of the immune response, and maintenance of energy balance. As part of the acute-phase response, the liver synthesizes proteins such as C-reactive protein and fibrinogen. Endothelial activation and the release of inflammatory cytokines (IL-1, IL-6, TNF-α) may lead to increased vascular permeability and the formation of edema. An excessive inflammatory response increases the risk of systemic inflammatory response syndrome (SIRS), disseminated intravascular coagulation (DIC), and multiple organ failure. Hypovolemia, hypoxia, and reperfusion injury can also cause significant pathophysiological changes at the tissue level. Understanding these physiological processes is critically important for the development of effective diagnostic and therapeutic strategies in disaster and emergency management.