Pain Physiology

Question 1

physiologic pain

Answer 1

Normal response to a noxious stimulus, producing protective behavioural responses to potential or actual tissue damage

Question 2

acute pain

Answer 2

sudden onset of pain, which may be severe but disappears when the stimulus is removed

Question 3

chronic pain

Answer 3

pain that lasts several weeks to months and persists beyond the expected healing time

Question 4

somatic pain

Answer 4

originates from damage to bone, joint, muscle, or skin;

well localized

Question 5

visceral pain

Answer 5

originates from internal organs – stretching or twisting of viscera, mesenteries, and ligaments;

poorly localized

Question 6

neuropathic pain

Answer 6

originates from injury to the peripheral or central nervous system (ex. nerve transection or compression)

Question 7

inflammatory pain

Answer 7

originates from tissue damage (ex. sx, trauma, ischemia, OA, laminitis, infection)

Question 8

referred pain

Answer 8

originates from one part of the body but perceived as occurring in another

ex: heart attach - presents as pain in left arm but damage is to the myocardium

Question 9

transduction

Answer 9

peripheral pain receptors activated by a stimulus

Question 10

transmission

Answer 10

signal communicated via Aδ and C-nerve fibers to spinal cord

Question 11

modulation

Answer 11

nociceptive input modified at the spinal cord

Question 12

perception

Answer 12

conscious recognition of pain at the cerebral cortex

Question 13

mechanoreceptors respond to

Answer 13

stretching, compression, crushing

Question 14

thermoreceptors respond to

Answer 14

heat and cold

Question 15

chemoreceptors respond to

Answer 15

Neurotransmitters, prostaglandins,

autocoids (ex. Bradykinin, histamine),

acids (ex. Lactic),

cytokines (ex. TNF, IL-1, 6,8),

leukotrienes, nerve growth factor

Question 16

Aδ-fibers

Answer 16

Myelinated, fast transmission

Acute, accurately localized, sharp, and rapid onset pain

Question 17

C-fibers

Answer 17

Nonmyelinated, slow transmission

Chronic, diffuse, dull, burning, aching pain

Question 18

spinal cord pathway

Answer 18

Afferent peripheral nerves (Aδ and C fibers) enter the spinal cord through the dorsal roots →

Synapse in Lamina II of the dorsal horn gray matter→

Ascend via spinothalamic and spinoreticular tracts to brain

Question 19

facilitory/excitatory substances

Answer 19

increase pain

Substance P → NK1 receptor

Glutamate → AMPA, NMDA, kainate receptors

Question 20

inhibitory substances

Answer 20

decrease pain

GABA, endogenous opioids

Question 21

spinothalamic tract

Answer 21

terminates at thalamus and somatosensory cortex

Transmits easily localized, superficial pain

Question 22

spinoretucular tract

Answer 22

Terminates in the reticular formation

Transmits deep and visceral pain

Question 23

descending inhibitory pain pathways

Answer 23

input recieved in midbrain (periaqueductal grey matter, nucleus raphe magnus) →

axons from PAG and NRM release endorphins (endogenous opioids - serotonin and NE)→

inhibit pain transmission at level of dorsal horn

Question 24

T/F head pain is different from peripheral pathways

Answer 24

True

mediated by trigeminal nerve (CN V)

Question 25

stress response

Answer 25

systemic consequence of unmanaged pain mediated by SNS release **hormones** (ACTH, cortisol, vasopressin, growth hormone) and **neurtotransmitters** (epi, NE)

Question 26

GI consequences of unmanaged pain

Answer 26

delayed gastric emptying, nausea, ileus

Question 27

hematologic consequences of unmanaged pain

Answer 27

hypercoaguability risk of thrombosis

Question 28

allodynia

Answer 28

Pain evoked by a stimulus that does not normally cause pain

Question 29

hyperalgesia

Answer 29

An increased or exaggerated response to a stimulus that is normally painful (heightened sense of pain)

Question 30

T/F secondary hyperalgesia occurs in surrounding, undamaged tissue

Answer 30

**True**

Question 31

peripheral sensitization

Answer 31

An increase in the activity, excitability, and responsiveness of peripheral nerve terminals, leading to primary hyperalgesia

Question 32

wind up

Answer 32

Summation of painful stimulation **IN THE SPINAL CORD,** mediated by C-fibers. Contributes to central sensitization

Question 33

central sensitization

Answer 33

An increase in nerve excitability and responsiveness in the central nervous system, particularly the spinal cord, leading to **primary and secondary hyperalgesia, and allodynia**

Question 34

what results in "sensitizing soup"

Answer 34

release of H+, K+, and ATP from ruptured cells Release of NE, histamine, bradykinin, serotonin, prostaglandins, leukotrienes, cytokines, substance P increases intra cellular Ca and indices intracellulae signaling cascades

Question 35

in peripheral sensitization high threshold Aδ and C-fiber nociceptors→

Answer 35

low threshold (INCREASED SENSITIVITY) activation of silent nociceptors

Question 36

peripheral sensitization clinically results in

Answer 36

primary hyperalgesia

Question 37

what is wind up

Answer 37

Temporal summation and cumulative depolarization of dorsal horn neurons = Continuous stimulation of these neurons by a peripheral pain stimulus removes normal Mg++ block on NMDA receptors (gluatmate can bind→increases pain transmission)

Question 38

wind up contributes to \_\_\_\_\_\_\_sensitization

Answer 38

**central**

Question 39

MoA of increased dorsal horn excitability in central sensitization

Answer 39

Removal of Mg++ block on NMDA receptors (wind-up) Activation of NMDA receptors by glutamate Increased intracellular Ca++, triggering signalling pathways and gene expression

Question 40

disinhibition at the level of the spinal cord in central sensitization is due to

Answer 40

decreased GABA activity

Question 41

central sensitization results in:

Answer 41

hyperalgesia allodynia spontaneous pain pain memory (phantom limb pain)

Question 42

preemptive analgesia

Answer 42

The administration of analgesic therapy before painful stimulation, used to PREVENT WINDUP

Question 43

clinical goal of analgesia

Answer 43

reduce pain by interrupting nociception at one or multiple levels (transduction, transmission, modulation, perception)

Question 44

T/F pre-emptive analgesia can prevent peripheral and/or central sensitization

Answer 44

**true** depends on drug decreases total analgesic requirements

Question 45

interruption of nociception - transduction

Answer 45

Topical local anesthetics, tissue cooling Infiltration of local anesthetic, into pleural cavity or intra-articular (+ morphine) Systemic NSAIDS – decrease local production of inflammatory mediators

Question 46

interruption of nociception - transmission

Answer 46

Local anesthetic nerve blockade (peripheral, plexus) Epidural

Question 47

interruption of nociception - modulation

Answer 47

Opioids α-2 agonists NSAIDS NMDA antagonists

Question 48

interruption of nociception - perception

Answer 48

opioids α-2 agonists General anesthetics

Question 49

Which pain fiber would be most likely involved in transmitting sharp, fast pain?

Answer 49

Aδ fibers

Question 50

What are the major excitatory and inhibitory neurotransmitters involved with pain transmission?

Answer 50

**excitatory -** glutamate, subtance P **inhibitory -** GABA

Question 51

What strategies could be used to prevent peripheral sensitization?

Answer 51

local blocks, topical anesthetics, NSAIDs

Question 52

What strategies could be used to prevent central sensitization?

Answer 52

opioids alpha 2 agonists ketamine

Question 53

Does general anesthesia prevent either peripheral or central sensitization?

Answer 53

**No** - have to add analgesia