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Anesthesia Pharm Exam 2 > Physiology of Pain > Flashcards

Physiology of Pain Flashcards

1
Q

2 Types of Pain:

A

Acute (somatic and visceral)

Chronic

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2
Q

Acute Pain

A
  • caused by noxious stimuli (nociceptive pain) and is a SYMPTOM
  • self-limited, resolves in days-weeks
  • Somatic: superficial (skin = sharp)

Visceral: internal organ (hard to identify = referred)

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3
Q

Chronic Pain

A
  • persists beyond “normal” time for pain
  • starts 6 weeks to 3 months post op
  • lasts 1-6 months or longer
  • nociceptive; neuropathic; cancer; unk etiology
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4
Q

Acute Pain 2

A

Result of tissue damage and is a symptom.

  • well defined onset, clear pathology
  • protective from tissue damage, allows healing time
  • observable tissue damage present
  • tx w pharmacologic means
  • acute pain is useful and protective… chronic pain is NOT!
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5
Q

Risk Factors for Increased Post Op Pain

A
  • poor pain control w prior surg
  • pain lasting >1 month
  • psychologically vulnerable
  • young pts
  • female
  • workman’s comp
  • genetics (cultural, pharmacogenomic issues)
  • diffuse noxious inhibitory control issues
  • chronic opioid use
  • physical dependence tolerance
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6
Q

Diffuse Noxious Inhibitory Control Issues (DNIC)

A
  • noxious stimuli activate C and A delta fibers
  • DNIC is where WDR neurons responsive to pain signals from one area may be inhibited by stimuli from another location
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7
Q

Compared to Opioid-Naive Patients, Pain is…

A
  • pain is 3x higher
  • post op opioid use is 3x higher
  • if epidural is placed, it stays in for 3 extra days
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8
Q

Independent Predictors for Development for Persistant Postsurgical Pain (PPP)

A
  • preop pain (those on opioids require more pain mgmt)
  • age (younger is worse)
  • type of surgery
  • preop anxiety
  • severity of immediate post op pain
  • size of incision (larger = more pain)
  • gender (femals > males)
  • need for information
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9
Q

Independent Predictors that do NOT indicate Development for Persistant Postsurgical Pain (PPP)

A
  • BMI has inconsistent effects
  • duration of surgery
  • type of anesthesia (regional vs general has no effect on pain)
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10
Q

Problems w poorly treated post-op pain

A
  • increased risk of PPS (persistant postsurgical pain)
  • increased CV complications
  • increased pulm complications
  • delays discharge
  • prolongs convalescent leave and return to work
  • increased risk of admission after ASC procedures
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11
Q

Model of Pain Transmission

A
  1. Pain impulse enters dorsal horn
  2. Glutamate or Substance P allow transmission (intrathecal morphine inhibits release of Sub. P into CSF)
  3. Transmission may be modulated by a descending inhibitory pathway that inhibits excitatory neurotransmitter (opioid receptors in substantia gelatinosa are probalby on Sub. P terminals and block its release, producing analgesia!)
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12
Q

NE is an ______ transmitter in the pain pathways

A

inhibitory

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13
Q

Non-Opioid Inhibitory Transmitters

A
  • endorphins
  • serotonin
  • NE
  • glycine
  • GABA
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14
Q

Clonidine is a _______ and produces ______ _______.

A

Clonidine is an alpha-1 agonist and produces spinal analgesia.

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15
Q

Neurotransmitters: Neuropeptides

A
  • substance P and calcitonin
  • opioids
  • glutamate
  • ion channels
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16
Q

Substance P and Calcitonin

A

neuropeptide neurotransmitters

  • Calcitonin Gene Related Peptide (CGRP)
  • inflammatory response = arthritic pain
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17
Q

Opioids

A

Neuropeptide Neurotransmitters

  • after peripheral inflammation there is an unregulation of the opioid receptors on the peripheral terminals of primary afferents
  • macrophages, monocytes, and lymphocytes all contain endogenous opioids
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18
Q

Glutamate

A

Neuropeptide Neurotransmitter

  • excitatory neurotransmitter
  • receptors found on primary afferent nociceptor terminals
  • injection of glutamate = hyperalgesia
  • upregulated in joints after inflammation
  • blockade of receptors = reduces pain and hyperalgesia
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19
Q

Injection of glutamate = ______

Blockade of gluatmate receptors = _______

A

Injection of glutamate = hyperalgesia

Blockade of gluatmate receptors = reduces pain and hyperalgesia

20
Q

Ion Channels

A

Neuropeptide Neurotransmitters

  • acid sensing channels = low pH in inflamed tissues
  • vanilloid rexeptor activated by capsaicin and mediates hyperalgesia
21
Q

Excitatory Neurotransmitter Effects on Pain:

Gluatmate

A
  • located in hippocampus, cerebral cortex, and substantia gelatinosa
  • learning and memory (recall)
  • central pain transduction
  • excitotoxic neuronal injury
22
Q

Ionotropic Gluatmate Receptors:

NMDA

A
  • ligand operated channel opens, influx of cation Na+, membrane depolarization
23
Q

Inhibitory Neurotransmitters

A
  • GABA
  • ACh
  • Dopamine
  • Epi and NE
  • Glycine
  • Endorphins
  • Serotonin
  • Histamine
24
Q

GABA

A
  • inhibitory NT
  • located in cortex, basal ganglia, cerebellum and SC
  • increase Cl- which HYPERpolarizes
25
Q

Glycine

A
  • inhibitory NT
  • located in SC
  • increases Cl- which HYPERpolarizes
  • strychnine and tetanus antagonize glycine’s postsynaptic inhibition which = sz activity
  • glycine solution used in TURPs may result in visual disturbances post-op d/t retinal inhibition
26
Q

ACh

A

Inhibitory NT

  • increased K+ conductance in peripheral PNS
27
Q

Dopamine

A
  • inhibitory NT by working on adenylate cyclase
28
Q

NE

A

inhibitory NT in RAS & hypothalamus

29
Q

EPI

A

inhibitory NT in hypothalamus

30
Q

Endorphins

A
  • inhibitory NT by being excitatory for th edescending pathways that inhibit pain transmission
31
Q

Serotonin

A
  • inhibitory NT in brain (ketamine may act on serotonin)
32
Q

Histamine

A

Inhibitory NT in hypothalamus and RAS

33
Q

Where do pain receptors (nociceptors) originate?

A
  • skin
  • skeletal structures
  • viscera
34
Q

3 Neuron System

A
  1. primary afferent
  2. spinothalamic tract
  3. thalamocortical neuron
35
Q

Excitatory Neurotransmitters

A
  • substance P (NK-1 receptors)
  • bradykinin
  • glutamate (NMDA and AMPA receptor)
  • calcitonin gene related peptide (CGRP)
36
Q

A-Delta fibers

A

myelineated, fast pain!

  • primarily releases glutamate which binds to AMPA and NMDA receptors
  • usually incisional pain or pain that causes rapid withdrawal of extremity from stimuli
37
Q

C-fibers

A

non-myelineated, slow, nagging pain

  • primarily relase substance P** which binds to **NK-1 receptors in the postsynaptic membrane
  • punch in the thigh, aching days later
  • slow in intensity, guarding effect
38
Q

Transmission of Pain

A
39
Q

Flaccid paralysis and absent stretch reflex indicate….

A

lower motor neuron lesion/injury

40
Q

Spastic paralysis with accentuated stretch reflex in the absence of skeletal muscle paralysis indicates…

A

upper motor neuron injury/destruction

41
Q

1st Generation Na+ channel blockers (fast pain, A-delta fibers)

A

disrupt transmissin

carbamazepine (Na)

Phenytoin (Na, K, GABA, Ca)

Valproic Acid (Na, K, GABA, Ca)

42
Q

2nd Generation Na+ channel blockers (fast pain, A-delta fibers)

A

oxcarbazepine (Na, Ca, K)

lamotrigine (Na, Ca, K, GABA)

topiramate (Na, Ca, GABA, glutamate)

43
Q

Drugs that block Ca+ Channels (slow pain, C-fibers)

A

gabapentin

pregabalin

44
Q

How do opioids block the VGaCa++ Channels?

A
  • enhance K+ efflus and enhance noradrenergic activity at the dorsal horn
  • alters the perception of pain (not blocking pain)
  • modulates nociceptive pathways and enhances endogenous opioids
  • mesolimbic dopamine system = reinforcing and rewarding properties
45
Q

Common Dermatome Levels

A

C4 - clavicle

T4 - nipples (and chemo. trigger zone)

T6 - xiphoid

T10 - umbilicus

T1 - T12 - SNS (sympathetic chain)

S2-4 - perineum

L4-5 - tibia

Anesthesia Pharm Exam 2 (5 decks)

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