Pain is a complex physiological and psychological experience that occurs when tissue injury or potential damage stimulates specialized sensory receptors known as nociceptors. Altered pathophysiology of pain develops when normal pain mechanisms become disrupted due to injury, inflammation, nerve damage, or chronic disease conditions. Under normal circumstances, pain serves as a protective mechanism, alerting the body to harmful stimuli. However, when pathological changes occur, pain perception may become exaggerated, prolonged, or occur even in the absence of tissue damage. The pathophysiology of pain begins with transduction, where noxious stimuli such as mechanical, thermal, or chemical injury activate nociceptors. These receptors convert harmful stimuli into electrical impulses. In altered conditions such as inflammation or trauma, chemical mediators like prostaglandins, bradykinin, serotonin, and substance P are released at the injury site, increasing sensitivity of nerve endings and lowering the pain threshold. This process results in hyperalgesia, where the patient experiences increased pain response to normally painful stimuli. The next phase is transmission, in which pain impulses travel through peripheral nerves to the spinal cord and then to higher brain centers. Damage or dysfunction in nerve pathways may lead to neuropathic pain, characterized by