Pain PAT 201 - FALL 2025 - WEEK 4

Flashcards covering key definitions and concepts related to pain, its mechanisms, classifications, and pharmacological and non-pharmacological management strategies, based on lecture notes from PAT 201, Fall 2025, Week 4.

Pain 

An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage. It is a subjective and complex phenomenon made up of dynamic interactions among physical, cognitive, spiritual, emotional, and environmental factors.

Gate control theory

Explains the complexities of the pain phenomenon, stating that pain is modulated by a 'gate' in the cells of the substantia gelatinosa in the spinal cord. Nociceptive transmissions (A-delta and C fibers) 'open' the gate, while nonnociceptive transmissions (touch, A-beta fibers) 'close' or partially close it.

Afferent pathways (pain)

Pathways that begin in the periphery, travel to the spinal cord, and then ascend to the central nervous system (CNS).

Interpretive centers (pain)

Located in the brain, responsible for processing and interpreting pain signals.

Efferent pathways (pain)

Pathways that descend from the CNS to modulate pain signals.

Nociception

The processing of pain, involving four phases: transduction, transmission, perception, and modulation.

Transduction (pain)

The first phase of nociception, where tissue is damaged by exposure to thermal, mechanical, or chemical noxious stimuli and is converted to electrophysiologic activity.

Transmission (pain)

The second phase of nociception, involving the conduction of pain impulses along the A-delta and C fibers into the dorsal horn of the spinal cord and eventually to the reticular formation, hypothalamus, thalamus, and limbic system.

Perception (pain)

The third phase of nociception, defined as the conscious awareness of pain, which occurs in the reticular and limbic systems and cerebral cortex. Its interpretation can be influenced by genetics, cultural preferences, sex roles, age, level of health, and past pain experiences.

Sensory-discriminative system (pain)

One of the three systems interacting to produce pain perception; responsible for identifying the presence, character, location, and intensity of pain.

Affective-motivational system (pain)

One of the three systems interacting to produce pain perception; determines an individual's conditioned avoidance behaviors and emotional responses to pain.

Cognitive-evaluative system (pain)

One of the three systems interacting to produce pain perception; overlays learned behavior concerning the experience of pain and can modulate perception.

Pain threshold

The point at which a stimulus is perceived as pain.

Pain tolerance

The duration of time or the intensity of pain that an individual will endure before initiating overt pain responses.

Modulation (pain)

The fourth phase of nociception, involving the process of increasing or decreasing transmission of pain signals throughout the nervous system, with both excitatory and inhibitory mechanisms.

Excitatory neurotransmitters (pain)

Neurotransmitters involved in pain modulation that facilitate pain signals, often associated with tissue injury and inflammation.

Inhibitory neurotransmitters (pain)

Neurotransmitters involved in pain modulation that decrease pain signals, such as gamma-aminobutyric acid (GABA), glycine, norepinephrine, and serotonin.

Endogenous opioids

Morphine-like neuropeptides (e.g., enkephalins, endorphins, dynorphins, endomorphins) that inhibit the transmission of pain impulses in the periphery, spinal cord, and brain by binding with specific opioid receptors.

Enkephalins

The most prevalent natural opioids, binding to delta (δ) opioid receptors.

Endorphins

Natural opioids that provide substantial pain relief, binding to mu (μ) receptors.

Dynorphins

The most potent of the endogenous opioids, binding strongly with kappa (κ) receptors.

Endomorphins

Endogenous opioids that bind with mu (μ) receptors.

Nociceptin/orphanin FQ

An opioid that induces pain or hyperalgesia but does not interact with classic opioid receptors.

Segmental Pain Inhibition

A pathway of pain modulation where non-noxious stimuli can inhibit pain in the same spinal cord segment.

Diffuse Noxious Inhibitory Control (DNIC)

A pathway of pain modulation where noxious stimulation in one part of the body inhibits pain in another, often distant, part.

Nociceptive pain

Pain resulting from normal tissue injury from a known cause, categorized as somatic or visceral.

Non-nociceptive pain

Pain that includes neuropathic pain, which can be peripheral or central.

Somatic pain

Nociceptive pain that arises from skin, muscle, or bone.

Visceral pain

Nociceptive pain that arises from the internal organs and lining of body cavities.

Acute referred pain

Pain perceived at a site different from its point of origin but innervated by the same spinal segment.

Neuropathic pain

Pain that is the result of a primary lesion or dysfunction in the nervous system, often chronic, described as burning, shooting, shock-like, or tingling, and associated with hyperalgesia and allodynia.

Peripheral neuropathic pain

A type of neuropathic pain where injured nerves become hyperexcitable.

Central neuropathic pain

A type of neuropathic pain caused by a lesion or neuroplastic changes in the brain or spinal cord.

Hyperalgesia

An increased response to a stimulus that is normally painful, often seen in neuropathic pain.

Allodynia

Pain caused by a stimulus that normally does not cause pain, often seen in neuropathic pain.

Acute pain

A protective mechanism that alerts an individual to a condition or experience immediately harmful to the body, lasting less than 3 months.

Acute somatic pain

Acute pain arising from joints, muscle, bone, and skin; transmitted by A-delta fibers (sharp, well-localized) or C fibers (dull, aching, throbbing, poorly localized).

Acute visceral pain

Acute pain arising from the internal organs and lining of body cavities, transmitted by C fibers, and often poorly localized (aching, gnawing, throbbing, or intermittent cramping).

Chronic pain

Pain that lasts at least 3 months; poorly understood, serves no protective purpose, and is thought to be caused by dysregulation of nociception and pain modulation processes (peripheral and central sensitization). It may cause behavioral and psychologic changes.

Myofascial pain syndrome (MPS)

A chronic pain syndrome characterized by deep, aching, localized to generalized pain due to injury to the muscle, fascia, and tendons.

Chronic postoperative pain

A chronic pain syndrome involving plastic changes in the PNS and CNS that contribute to allodynia and hypersensitivity following surgery.

Cancer pain

Pain associated with the presence of cancer, which can be acute or chronic, nociceptive or neuropathic.

Central poststroke pain

A chronic pain syndrome characterized by hypersensitivity on one half of the body following a stroke.

Phantom limb pain

A chronic pain syndrome involving pain felt in a limb that has been amputated, often due to regeneration or hyperactivity of injured/cut peripheral nerves.

Complex regional pain syndrome (CRPS)

A chronic pain syndrome (Types I and II) associated with limb injury, characterized by severe pain, swelling, and changes in skin temperature/color.

Analgesics

Medications used to relieve pain, broadly categorized into opioids, non-opioids, and adjuvant analgesics.

Opioids (Analgesics)

Narcotic substances (natural or synthetic) that produce analgesia and CNS depression by interacting with mu and kappa receptors, altering the emotional and sensory response to pain.

Non-opioid Analgesics

Medications like acetaminophen that relieve pain by inhibiting prostaglandin synthesis in the CNS and influencing the hypothalamus, often used for mild to moderate pain and fever without anti-inflammatory action.

Adjuvant analgesics

Drugs initially developed for other conditions (e.g., antidepressants, antiepileptics) but also used to enhance pain relief or treat specific types of pain like neuropathic pain.

Amitriptyline

A tricyclic antidepressant indicated for neuropathic pain (in addition to depression), which inhibits the reuptake of norepinephrine and serotonin into presynaptic nerve terminals.

Gabapentin

An anti-epileptic and GABA analogue used for neuropathic pain, postherpetic neuralgia, and as an adjunct for partial seizures. It stimulates an influx of chloride ions that interact with the GABA receptor-chloride channel complex.

Naloxone

An opioid antagonist used to reverse the symptoms of opioid toxicity or overdose, such as sedation and respiratory depression.

Acetaminophen

A non-opioid analgesic that inhibits the synthesis of prostaglandins in the central nervous system and directly acts at the level of the hypothalamus to cause peripheral vasodilation; used for fever and mild to moderate pain, metabolized by the liver, and has no anti-inflammatory action.

Cannabinoids

Substances found in cannabis (e.g., THC, CBD) that stimulate cannabinoid receptor type 1 (CB1) and type 2 (CB2) within the body's endocannabinoid system, used for pain, muscle spasms, nausea, and vomiting.

THC (Tetrahydrocannabinol)

A cannabinoid from the cannabis plant that produces psychoactive properties ('feeling high').

CBD (Cannabidiol)

A non-psychotropic cannabinoid from the cannabis plant that has low affinity for CB1 and CB2 receptors but interacts at low concentrations.

Endocannabinoid system (ECS)

A system within the human body consisting of cannabinoid receptors (CB1, CB2), endocannabinoids (anandamide, 2-arachidonoyl-glycerol), and their metabolic enzymes. It plays a key role in homeostasis and regulates processes like inflammation and pain perception.

CB1 receptors

Cannabinoid receptors predominantly located in the brain and central nervous system.

CB2 receptors

Cannabinoid receptors most densely found in immunological tissues, modulating cell fate.