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Pharmacology > MSK Pain > Flashcards

MSK Pain Flashcards

1
Q

Acute pain is primarily ___

A

nociceptive (somatic> visceral)

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2
Q

Compare Nociceptive vs neuropathic pain

A

Nociceptive: somatic or visceral, activation of nociceptive nerve fibers

Neuropathic: persists and has become disengaged from noxious stimuli or the healing process

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3
Q

Describe Somatic pain

A
  1. arising from skin, bone, joint, CT or muscle due to MSK condition, inflammation or mechanical problems
  2. Decribed as throbbing and well localized
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4
Q

Describe visceral pain

A
  1. arising from internal organs

2. referred pain or well localized

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5
Q

Describe neuropathic pain

A
  1. burning/tingling/shock like
  2. shooting
  3. exaggerated response to normal painful stimuli (hyperalgesia)
  4. and/or painful response to nomrally nonnoxious stimuli (allodynia)
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6
Q

What effect do prostaglandins have on chemoreceptors

A

do not stimulate them directly, but act to increase the sensitivity of the nerve endings to the other neurochemicals resulting in an increased pain response for any given stimulus

  • NSAIDs inhibit PG synthesis
  • GC decrease PG synthesis and have anti-inflammatory effects
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7
Q

How do local anesthetics help with blocking transduction-transmission of pain stimulus

A

Local anesthetics block VSSC along the spinothalamic tract and interrupt the transmission of pain impulses at any site in the pain pathway

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8
Q

Somatosensory cortex receives input from ___ and is involved in sensory-discriminative aspects of pain (where and how much?)

A

ascending pathway of spinothalamic tract

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9
Q

Stimulation gives rise to localized, sharp, stinging pain via ___ fibers. Describe the adaptation of these fibers

A

rapidly conducting A-δ nerve

*The pain receptors in this pathway adapt very little allowing the person to remain apprised of damaging pain-inducing stimuli as long as it persists

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10
Q

info from ___ + ___ forms subjective pain experience

A

discriminatory (somatosensory cortex) +

emotional (limbic system)

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11
Q

compare different pain nerve fibers

A

A-delta: sharp, stinging, fast conducting, little adaptation

C: slow, diffuse, achy,

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12
Q

How do opioid analgesics affect pain

A
  1. act on dorsal horn of SC to alter subjective reaction/response to pain (emotional- can feel pain but don’t care)
  2. act on endogenous enkephalin receptors at this site resulting in a subsequent decrease in ascending pain impulse transmission. (raises the pain threshold and decreases the patient perception of pain (intensity level))
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13
Q

The descending pain-inhibitory pathway originates in neurons of the ___ and descends (i.e., from the CNS to the periphery) to synapse on primary pain afferent neurons in the dorsal horn of the spinal cord (C and A-δ).
-The neurotransmitters that are released from [__] neurons include:

A

periaqueductal gray region (PAG) of the midbrain

PAG

  1. opioid peptides (enkephalins),
  2. norepinephrine, and
  3. serotonin.
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14
Q

Uses for:
Aspirin (acetylsalicylic acid, ASA) / Nonsteroidal anti-Inflammatory Drugs (NSAIDs) / Acetaminophen, COX-2 Selective agents

A
  1. most frequently used drugs for pain relief (analgesia)
  2. all but acetaminophen are also effective for tx of inflammation
  3. used as antipyretic or antiplatelet (ASA) actions
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15
Q

How do local anesthetics block pain

A

block all sensory afferents

*commonly used in combo w/ vasoconstrictors such as epi

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16
Q

Anti-inflammatory drugs and NOT analgesics – BUT block of inflammation is associated with pain relief

A

Glucocorticoid anti-inflammatory agents

17
Q

How should you treat mild pain (rated 1-3)

A
  1. non-opioid (NSAIDS or acetaminophen)

2. +/- adjuvant analgesics (useful, not classified as analgesics)

18
Q

How should you treat acute moderate pain (rated 4-6)

A
  1. Immediate-release, short-acting opioids with slow titration
    • Non-opioid (NSAIDs more effective)
  3. +/- adjuvant analgesics
19
Q

How should you treat acute severe pain (rated 7-10)

A
  1. Immediate-release, short-acting opioids with rapid titration
    • Non-opioid
  3. +/- adjuvant analgesics (most commonly LocalAs)
  4. Commonly managed with multimodal analgesia approach
20
Q

___ remains a cornerstone of treatment for acute severe pain- BUT idiosyncratic and dose-limiting side effects curtail practical efficacy

A

Opioid monotherapy

21
Q

Benefits of combining other agents with opioids

A
  1. greater analgesic efficacy from synergistic actions of agents w/ different mechanisms
  2. synergism btwn agents allows use of lower doses limiting dose related SE
22
Q

what is neuropathic and functional pain

A

neuropathic–> result of nerve damage

functional–> abnormal operation of nervous system

23
Q

Tissue inflammation may change chemical environment at terminals of nociceptor. Damaged cells release-synthesize proinflammatory mediators that can directly activate the terminal and produce pain or render the terminal hypersensitive to subsequent stimuli.

A

peripheral sensitization

24
Q

NMDA receptor is central to the amplification of synaptic transfer from terminal to dorsal horn neurons. Initial sensitization is activity dependent, then later sustained by transcriptional changes (via COX-2, BDNF, substance P, NK1).

A

central sensitization

25
Q

Increased excitability of injured sensory neurons can generate pacemaker-like extra discharges that result in sensory inflow that is independent of any peripheral stimuli

A

ectopic activity

26
Q

neuropathic adjuvants

A
  1. Anticonvulsants
  2. antidepressants
  3. local anesthetics
27
Q

Adjuvants for muscle spasms, anxiety and inflammation

A

Muscle spasms- antispasmodics

anxiety- benzodiazepines

inflammation- glucocorticoids

28
Q

____ to drug selection is most often employed with chronic pain managment, rather than an emphasis on ____ as is used with acute pain

A

A mechanistic approach

therapeutic class stratification

29
Q

Enhancement of descending inhibitory pathway via

A
  1. activation of opioid receptors

2. block of NE-5HT reuptake

30
Q

What meds:

  1. activation of opioid receptors
  2. block of NE-5HT reuptake
A
  1. activation of opioid receptors: opioid analgestics, tramadol
  2. block of NE-5HT reuptake: Antidepressants, TCAD, SNRI, SSRI
31
Q

Decrease in central sensitization via

A
  1. Block of VSCC/ decrease excess NT release
  2. Block of NMDA-Glu receptors
  3. Block of COX-2
32
Q

What meds:

  1. Block of VSCC
  2. Block of NMDA-Glu receptors
  3. Block of COX-2
A
  1. Block of VSCC: anticonvulsants
  2. Block of NMDA-Glu receptors: ketamine
  3. Block of COX-2: NSAIDs, Celecoxib, acetaminophen
33
Q

Decrease in peripheral sensitization via

A
  1. Block of VSSC- inhibit excess NT
34
Q

What meds

1. Block of VSSC- inhibit excess NT

A
  1. Block of VSSC- inhibit excess N: local anesthetics, anticonvulsants
35
Q

TCADs are good adjuvant meds for what chronic pain conditions

A
  1. diabetic neuropathy
  2. postherpetic neuralgia
  3. low back pain
  4. migraine
36
Q

SNRIs are good adjuvants for what chronic pain conditions

A
  1. Fibromyalgia
37
Q

anticonvulsants/ VSCC ligands are good adjuvants for what chronic pain conditions

A
  1. SC injury
  2. trigeminal neuralgia
  3. diabetic neuropathy
38
Q

local anesthetics (topical) are good adjuvants for what chronic pain conditions

A
  1. post herpetic neuralgia

2. allodynia if pain localized

39
Q 
Antidepressants and antiepileptics are commonly used to treat: 
A.  Postherpetic neuralgia 
B.  Diabetic nephropathy 
C.  Fibromyalgia pain 
D.  All of the above
A

D.  All of the above

Pharmacology (31 decks)

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