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PHRM 100 – APPP > APPP 16: Pain > Flashcards

APPP 16: Pain Flashcards

1
Q

What are the 2 anatomical classifications of pain?

A
  • somatic pain: pain that originates in peripheral tissues such as skin, bone, muscles, tendons, or ligaments
  • visceral pain: originates in body’s internal organs (ie. heart, intestines, appendix, kidneys)
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2
Q

What are the 3 classifications of pain by duration?

A
  • acute
  • episodic: may occur at irregular intervals
  • chronic: lasts for 3+ months or beyond expected healing time, can sometimes occur for no known reason
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3
Q

What are the 3 classifications of pain by mechanism?

A
  • nociceptive pain
  • neuropathic
  • nociplastic pain
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4
Q

What is nociceptive pain?

A

caused by tissue damage and/or inflammation

  • sensation can be sharp, pricking, dull, or aching
  • ie. paper cut, infection, broken bone
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5
Q

What is neuropathic pain?

A

caused by nerve damage due to injury or disease

  • burning, tingling, shooting, or like electric shocks
  • ie. diabetic neuropathy, shingles, sciatica
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6
Q

What is nociplastic pain?

A

caused by changes in how the nervous system processes pain

  • not linked with a clear injury, tissue damage, inflammation, or disease
  • sensations related to this kind of pain vary widely
  • ie. fibromyalgia, complex regional pain syndrome
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7
Q

Psychological Effects of Pain

What are the physical effects of pain? (3)

A
  • fatigue and sleep disturbances
  • inability to keep up with daily activities
  • adverse side effects of medications
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8
Q

Psychological Effects of Pain

What are the psychological effects of pain? (3)

A
  • mood swings
  • irrational thinking or behaviour
  • helplessness
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9
Q

Functional Effects of Pain

What are the effects of pain on the brain? (2)

A
  • anxiety, fear, depression
  • inhibition or promotion of pain
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10
Q

Functional Effects of Pain

What are the effects of pain on the cardiovascular system? (2)

A
  • increased heart rate and blood pressure
  • water retention
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11
Q

Functional Effects of Pain

What are the effects of pain on the gastrointestinal system? (2)

A
  • nausea and vomiting
  • constipation
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12
Q

Functional Effects of Pain

What are the effects of pain on the respiratory system? (2)

A
  • increased respiratory rate
  • increased risk for infection
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13
Q

What are the 4 processes for modulation of pain sensation?

A
  • transduction
  • transmission
  • perception
  • modulation
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14
Q

What is transduction?

A

nociceptors detect noxious stimuli from somatic and visceral tissues (mechanical, chemical, etc.)

  • painful stimuli is converted to energy (neuronal action potential)
  • stimulus sends an impulse across peripheral nerve fibres
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15
Q

What are the types of nociceptors involved in transduction? (3)

A
  • mechanical nociceptors
  • thermal nociceptors
  • chemically sensitive nociceptors
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16
Q

What are mechanical nociceptors?

A
  • high threshold mechanoreceptors
  • respond to strong mechanical stimulation (ie. pinching, pressure) – Piezo2: mechanically-activated ion channel crucial for touch and proprioception
  • TRPA1: primarily known for its role in chemical nociception, can also be activated by mechanical stretch
17
Q

What are thermal nociceptors?

A
  • activated by skin temperatures above 42ºC or by severe cold
  • TRPV1: activated about 42ºC, also sensitive to capsaicin and acidic conditions
  • TRPM8: activated by cold temperatures below 25ºC
18
Q

What are chemically sensitive nociceptors?

A

respond to various chemicals and environmental irritants

  • prostaglandins: produced by cyclooxygenases acting on arachidonic acid
  • bradykinin: forms from kininogen via kallikreins
  • serotonin: releases from clotting platelets
  • histamine: originates from mast cells and basophils
  • cytokines (ie. TNF-a and IL-1b): emitted by immune cells
19
Q

Transduction: Nociceptor Activation

What substances are involved in nociceptor activation? (7)

A
  • globulin and protein kinases
  • arachidonic acid
  • histamine
  • nerve growth factor (NGF)
  • substance P (SP) and calcitonin gene-related peptide (CGRP)
  • other substances
20
Q

Transduction: Nociceptor Activation

Globulin and Protein Kinases

A

damaged tissue releases globulin and protein kinases

  • ie. kallikrein cleaves kininogen to release bradykinin
21
Q

Transduction: Nociceptor Activation

Arachidonic Acid

A
  • released during tissue damage
  • metabolized into prostaglandin and cytokines
  • through G protein and protein kinase A cascade, prostaglandins block K+ outflow from nociceptors, increasing their sensitivity
22
Q

Transduction: Nociceptor Activation

Histamine

A
  • released from mast cells when tissue is damaged
  • stimulates nociceptors
23
Q

Transduction: Nociceptor Activation

Nerve Growth Factor (NGF)

A
  • released during inflammation or tissue damage
  • binds to TrkA receptors on nociceptors, activating them
24
Q

Transduction: Nociceptor Activation

Substance P (SP) and Calcitonin Gene-Related Peptide (CGRP)

A
  • released due to injury
  • excite nociceptors
  • both cause blood vessels to dilate, spreading swelling around the injury
25
Q

Transduction: Nociceptor Activation

Other Substances

A

released during tissue damage:

  • serotonin (5-HT)
  • acetylcholine (ACh)
  • low pH solutions
  • ATP
26
Q

Opioids

A
  • opiates include natural plant alkaloids (ie. morphine, codeine, and many semisynthetic derivatives)
  • opioid receptor in CNS is an endogenous opioid
  • endogenous opioid peptides include enkephalins, endorphins, and dynorphins
27
Q

What are the 2 common opiate agonists?

A
  • morphine
  • codeine
28
Q

What is the common opiate antagonist?

A

naloxone

  • affinity for all known opioid receptors
29
Q

What are the 3 principle opioid receptors?

A

members of GPCR family

  • μ (mu)
  • Κ (kappa)
  • 𝛿 (delta)
30
Q

What does the activation of opioid receptors lead to? (3)

A
  • reduced cAMP (and PKA activity) – coupled to inhibitory G-protein (Gi)
  • reduce neuronal cell excitation and transmission – closing of voltage sensitive Ca2+ channels (decreased neurotransmitter release), and stimulation of K+ efflux (hyperpolarization)
  • euphoria – involves dopaminergic pathways
31
Q

What are the 2 pathways underlying rewarding properties of opiates?

A
  • MOR (μ opioid receptor) agonists reduce excitability and transmitter release
  • opiate-induced inhibition in ventral tegmental area (VTA) on GABAergic interneurons or in nucleus accumbens (NAc) reduce GABA-mediated inhibition and increase outflow from ventral pallidum (VP), which correlate with a positive reinforcing state (enhanced reward)
32
Q

Non-opioid Analgesics

What is NSAID anti-inflammatory activity mediated by?

A

through inhibition of prostaglandin biosynthesis

33
Q

Non-opioid Analgesics

What is paracetamol?

A
  • one of the most widely used analgesics
  • mechanism by which it elicits pain relief is not fully understood
  • primarily COX-independent
  • weak anti-inflammatory activity
  • raises threshold to painful stimuli
34
Q

Non-opioid Analgesics

What are topical analgesics?

A

relief of mild to moderate muscle and joint pain

  • topical local anesthetics
35
Q

What is transmission?

A

nociceptive message is transmitted to CNS of actual or impending tissue injury

  • A-delta fibres send sharp, localized, and distinct sensations
  • C fibres relay impulses that are poorly localized, burning, and persistent
36
Q

What is perception?

A

person is aware of the pain

  • somatosensory cortex identifies location and intensity
37
Q

What is modulation?

A

modulation of pain (positively or negatively) by the body

  • excitatory neurotransmitter (ie. glutamate, substance P, CGRP) mediate synaptic transmission in dorsal horn
  • inhibitory neurotransmitters (ie. GABA, glycine, enkephalins, dynorphin, noradrenaline) work to hinder pain transmission

PHRM 100 – APPP (23 decks)

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