Acute Pain Flashcards
What is acute pain and how long does it usually last?
Acute pain is a type of long-lasting pain that may or may not require clinical intervention. It usually subdues within a few days after the cause of pain is resolved, but can persist for weeks if it necessitates medical attention. It becomes chronic pain if it lasts longer than three months.
What are some examples of acute pain conditions?
Examples of acute pain include pain from tooth extraction, inflammation of respiratory passageways during a viral infection, post-traumatic pain, post-surgery pain, and burn injury pain. These types of pain may persist for weeks and require continuous medical attention.
When does acute pain become classified as chronic pain?
Acute pain is classified as chronic pain when it persists for longer than three months, which is an arbitrarily agreed period for categorizing pain as either acute or chronic.
What are three major types of acute pain necessitating clinical interventions?
The three major types of acute pain necessitating clinical interventions are post-traumatic pain, post-surgery pain, and burn injury pain. These conditions may require continuous medical attention and have a risk of transforming into chronic pain.
What are the three phases of acute pain?
The three phases of acute pain are:
Emergency phase: Between injury and stabilization, characterized by nociceptive pain from tissue damage, anxiety, and fear.
Healing phase: Lasts several weeks, characterized by fluctuating background pain, breakthrough pain from therapeutic interventions, and potential PTSD.
Rehabilitation phase: The longest phase, with pain becoming more localized, deep, and aching.
What are the physiological mechanisms involved in acute pain
The mechanisms involved include direct stimulation of C and A-delta nociceptors, primary hyperalgesia, secondary hyperalgesia, sympathoadrenal activation, and neuroendocrine responses.
How does direct stimulation of nociceptors occur in acute pain?
Direct stimulation of nociceptors occurs due to tissue disruption from cutting, tearing, pressure, or heat. In burn injury patients, pain results from environmental exposure, debridement procedures, and physiotherapy. Surgery can also cause nociceptor stimulation, leading to muscle contractions and reduced ventilation.
How does primary hyperalgesia manifest in acute pain?
Primary hyperalgesia involves a decreased pain threshold in C and A-delta nociceptors to heat and mechanical stimuli near the injury site. It is caused by ions like H+ and K+, local mediators (bradykinin, serotonin, histamine), substance P, and pro-inflammatory cytokines (e.g., interleukin 1-beta, interleukin 6). Primary hyperalgesia develops within minutes after injury.
What is secondary hyperalgesia and its phases?
Secondary hyperalgesia occurs in non-traumatized tissues surrounding the injury. It has two phases: an initial phase characterized by strengthened firing in wide-dynamic-range neurons (wind-up) and a long-term potentiation phase with prolonged enhanced responses. The long-term potentiation phase starts 15-20 minutes after injury and outlasts the initial nociceptive stimulation.
What role do excitatory neuromediators play in secondary hyperalgesia
Excitatory neuromediators such as glutamate and N-methyl-D-aspartate (NMDA) receptors play essential roles in secondary hyperalgesia. These mediators contribute to the central nervous mechanisms underlying secondary hyperalgesia.
What is the sympathoadrenal response to acute pain?
The sympathoadrenal response is a physiological adaptation to stress involving activation of the hypothalamus and sympathetic neurons, leading to increased heart rate, respiration, and blood flow in muscles and brain. This response aims to support tissue repair and survival but may impair healing by reducing blood flow to injured areas.
How does the sympathoadrenal response affect acute pain patients
Activation of the sympathoadrenal system aggravates pain by sensitizing nociceptors. Reduced blood flow in injured areas impairs healing, increases muscle spasms, and can cause visceral ischemia, which further increases pain.
What is the neuroendocrine response to acute pain?
The neuroendocrine response involves increased secretion of catabolic hormones like cortisol, glucagon, growth hormone, and catecholamines, which increase energy availability but may impair healing and cause muscle wasting and immunosuppression if prolonged.
What role do interleukins play in the neuroendocrine response to acute pain?
Interleukins (e.g., IL-1 beta, IL-6) stimulate the secretion of adrenocortical hormones, contributing to the neuroendocrine response to acute pain. This response is characterized by increased levels of catabolic hormones to cope with injury.
How do individual characteristics affect responses to acute pain?
Factors like age, sex, ethnicity, cultural background, anxiety, pain catastrophizing, locus of control, and history of substance abuse all influence responses to acute pain and management strategies.