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Function of pain
Warning signal about an unmet need, or malfunction of the nervous system secondary to a disease process
Motor, sensory, or emotional response to a subjective feeling
Warning/Symptoms of Disease
Function of pain
A symptom is a warning about a disease or condition
Disease entity that can be treated
Response to Injury
Function of pain
Reaction to different types of injury
Thermal injuries, e.g., sunburn
Mechanical injury, e.g., fracture
Chemical injury, e.g., inhalation of toxic fumes
Ischemic injury, e.g., lack of oxygen to body tissues
Cognitive factors influencing perception of pain
An alert, oriented patient can recognize pain, report pain, and implement behaviors to prevent or relieve pain.
Non-alert patients may have impaired ability to perceive, report, prevent, or relieve pain.
Patients with Alzheimer disease or other cognitive disorders may not be able to express the location of pain, prevent pain, or relieve pain, but they are capable of perceiving and experiencing pain.
Affective/Behavioral factors influencing perception of pain
behaviors include:
physical: grimaces, clenched teeth, guarding, bent posture, and restlessness
verbal: crying, moaning, screaming
psychological: anger, irritability, despair
Sensory factors influencing perception of pain
Any loss of sensory function directly influences the patient’s awareness of pain. When patients cannot sense pain, they cannot communicate pain, prevent it, or respond to it.
Patients in pain may feel like their senses are overstimulated or demonstrate sensitivity to light, sound, and smells
Pattern Theory
Theory of pain that proposed the physiologic basis of pain and provided the foundation for the gate control theory of pain
When injury occurs, sensations relay a unique pattern or sequence of signals to the brain.
The brain deciphers the pattern and correlates it with the sensation.
The pattern determines whether the brain interprets the stimuli as pain.
Gate Control Theory of Pain
Theory of pain that looked at pain via the mind-body perspective, explaining the influence of cognitive and emotional factors on pain perception
Tissue damage causes a stimulus to be sent to the brain, which first travels to three locations in the spinal cord.
One of these locations, the dorsal horn of the spinal cord, provides a gating mechanism.
The signals at this gate determine whether or not pain is felt. If the gate closes, the impulses are not transmitted to the brain and no pain is perceived. If the signals reach a specific level of intensity, the gate opens, allowing the signal to reach the brain and pain to be felt.
State-of-mind and lifestyle choices can affect the intensity of the stimuli. For example, depression may cause the gate to remain open more often
Neuromatrix Theory
Theory of pain that proposed that the central nervous system, rather than injury at the periphery, is responsible for pain sensation
Pain is a complex issue that cannot be explained solely by physical factors.
Perception of painful stimuli results from the neuromatrix, a unique genetically controlled network of neurons affected by an individual’s subjective physical, psychological, cognitive, and life experiences.
Input from the periphery, such as tissue trauma, can initiate or affect but not create a neurosignature (the signal created by the neuromatrix).
Specific neurosignatures elicit corresponding sensations, and alterations in signals yield memories of the experience, allowing the same sensation to be felt if the same circumstance occurs in the future
Nociceptors
a peripheral nerve ending, or sensory neuron, that initiates the sensation of pain by sending “threat” stimuli to the spinal cord and brain and is sensitive to thermal, mechanical, and chemical stimuli
distributed throughout the body in joints, muscles, skin, and viscera, but density differs in each area
Highest density: Skin, extremely sensitive to pain
Lower density: Joints and tissues, less sensitive than skin
Lowest density: Internal organs, respond only to painful stimuli, e.g., on palpation or when infection is present
Nociception
the process by which pain is conducted from the periphery to the central nervous system
begins with the conversion of the noxious stimuli (injury) to an electrical impulse, which is transmitted from one neuron (nerve) to the next with the help of neurotransmitters
Lobes involved in nociception
Brainstem: pain signals travel from the spinal cord to the brain, including the brainstem, thalamus, and cerebral cortex
Occipital lobe: processes the pain (cause of pain or reaction of pain) from the body and generates the actual experience of pain
Parietal lobe: helps the person localize where on the body injury occurred
Frontal lobe: conveys the degree of unpleasantness of the pain experience
Temporal lobe: allows the person to plan ways of removing or getting away from the pain
Cerebellum: the relay station that distributes sensory signals to several other regions of the brain
Four Steps of Nociception
transduction, transmission, perception, and modulation
Transduction
Injury occurs and nociceptors identify pain stimuli and convert it to an electrical impulse
Injured tissues release neurotransmitters that are part of the inflammatory response
Neurotransmitters assist with transmission of pain signals across neurons
Inflammatory response is a significant cause of generalized pain
Transmission
Pain signal is transmitted through the afferent nerve to the spinal cord and brain
Signals travel two pathways:
A-delta fibers:
Larger fibers and rapid conduction
Pain translated as sharp, acute pain
C fibers:
Smaller fibers and slow conduction
Pain translated as diffuse, dull, and longer-lasting pain
Both A-delta and C fibers carry pain impulses from the spinal cord to the cerebral cortex of the brain
Modulation
Once pain is recognized, the brain changes pain perception by sending inhibitory signals via the spinal cord
This signal results in the release of analgesic neurotransmitters called endogenous opioids
Enkephalins influence the emotional perception of pain.
Beta-endorphins reduce pain via the central and peripheral nervous systems.
Dynorphins modulate pain through stimulation or reduction, depending on which receptors are activated
Perception
Brain translates afferent nerve signals as pain and person perceives pain
Limbic system controls emotional reactions
Somatosensory cortex perceives location, intensity, and quality of pain
Pain threshold: lowest intensity at which the brain recognizes pain; varies per person
Pain tolerance: intensity or duration of pain that a person can, or is willing to, endure; varies per person
Bradykinin
A peptide produced in the blood that mediates the inflammatory response and stimulates pain receptors
Substance P
A neuropeptide that transports pain impulses from the periphery to the central nervous system
Histamine
An amine released by immune cells in response to inflammation
Serotonin
A neurotransmitter released from the brainstem and dorsal horn that inhibits pain transmission
Cytokines
Proteins secreted by immune system cells that control inflammation
Electrolytes
Molecules that activate nerve endings (synapses) that respond to painful stimuli by changing ionic movement into and out of nerve cells
Prostaglandins
Hormone-like compounds derived from fatty acids that are thought to increase sensitivity to pain by stimulating pain receptors on neurons (nerve cells)
Nociceptive pain
occurs when nociceptors encounter harmful stimuli such as trauma, inflammation, or tissue damage
most common type felt as sharp, burning, aching, cramping, or stabbing sensations
visceral pain - from organs. occurs from pancreatitis, inflammatory bowel disease, bladder distention, and cancer
somatic pain - from skin, muscles, joints, and bones. occurs from sunburn, lacerations, fractures, sprains, arthritis, bone cancer
referred pain - from location of the body other than where it originated
radiating pain - extends from the source of pain to an adjacent area of body
Neuropathic pain
nerve injury or impairment
serves no purpose in relation to the body’s warning system or defenses
felt as numbness, tingling, burning, aching, crushing, stabbing, or shooting
primary causes are inflammation or metabolic disease
caused by tumors, trauma, infection, chemotherapy, phantom limb pain
Psychogenic pain
no physical source and is caused, increased, or prolonged by mental, emotional, or behavioral factors
often presents as headache, back pain, or stomach pain
Acute pain
transient
< 3 months
fast onset
identifiable cause
diminishes as injury heals
associated with conditions such as acute injury or trauma, surgery, and childbirth
Chronic pain
persistent pain
> 3 months
intermittent or continuous pain
does not always have an identifiable cause
can lead to disability, affecting quality of life
associated with conditions such as arthritis, fibromyalgia, and neuropathy
can be further divided into cancer and noncancer pain
Breakthrough pain
can occur in patients with cancer or noncancer pain (acute or chronic), and it is associated with surgery, injury, or a fluctuation in pain from an existing condition
Transient, worsening pain exacerbation that generally lasts 30 minutes or less
exacerbation of pain even though background pain is controlled
Idiopathic pain
chronic pain with no identifiable cause or pain that remains beyond healing from a medical condition or injury
examples : migraine headache and fibromyalgia
Physiologic factors of pain
age, fatigue, genes, neurologic function
Social factors of pain
previous experience, family and social network, spiritual factors
Psychological factors of pain
attention (increased attention to pain is linked to increased pain), anxiety and fear, coping
Cultural factors of pain
gender, familial factors, ethnicity
SOCRATES for pain assessment and history
S = site
O = onset
C = character
R = radiation
A = associations
T = time course
E = exacerbating/relieving factors
S = severity
ABCDE method for pain management
Assess the patient about their pain frequently
Believe the patient and their family and how it can be relieved
Choose pain control that is appropriate
Deliver interventions in a timely manner
Evaluate how your intervention helped your patient