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APA 3 - Wolfe > Pain Management > Flashcards

Pain Management Flashcards

1
Q

Define: Algesia

A

Increased sensitivity to pain

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2
Q

Define: Algogenic

A

Pain producing

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3
Q

Define: Allodynia

A

A normally non harmful stimulus is perceived as painful

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4
Q

Define: Analgesia

A

The absence of pain in the presence of a normally painful stimulus

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5
Q

Define: Dysethesia

A

An unpleasant painful abnormal sensation, whether evoked or spontaneous

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6
Q

Define: Hyperalgesia

A

A heightened response to a normally painful stimulus

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7
Q

Define: Neuralgia

A

Pain in the distribution to a peripheral nerve(s)

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8
Q

Define: Neuropathy

A

An abnormal disturbance in the function of a nerve(s)

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9
Q

Define: Parasthesia

A

An abnormal sensation, whether spontaneous or evoked

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10
Q

What is the time length to be termed acute pain

A

< 1 month

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11
Q

What is the time length to be termed chronic pain

A

> 3 months

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12
Q

What is nociceptive pain

A

Stimulation of SPECIFIC nociceptors

  • Somatic
  • Visceral
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13
Q

What is non-nociceptive pain

A
  • Neuropathic

- Inflammatory

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14
Q

Describe Somatic pain

  • Identifiable _____
  • Tissue damage is from…
  • How is the pain described?
A

Identifiable focus
Tissue damage – chemical release modulates pain
Well localized, sharp, hurts at area

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15
Q

Describe Visceral pain

  • localized of diffuse?
  • How is pain described?
  • Associated with what autonomic reflexes
  • What is an example
A

Diffuse, referred
Dull, cramping, squeezing
Autonomic reflexes - nausea, vomiting, diarrhea

Ex. Distention of organ capsule, obstruction of a hollow viscus

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16
Q

Neuropathic pain - damage to peripheral or central neural structures resulting in…

A

an abnormal processing of painful stimuli

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17
Q

Neuropathic pain is dysfunction of the…

A

central nervous system

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18
Q

How is neuropathic pain described

A

Burning, tingling, shock like

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19
Q

Describe the process of inflammatory pain

A

Sensitization of the nociceptive pathway from multiple mediators being released at the site of the tissue inflammation WITHOUT neural injury

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20
Q

What is the order of nociceptive pain transmission

A

Transduction, Transmission, Perception, Modulation

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21
Q

Define: Transduction

A

Stimuli is converted to action potential

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22
Q

Define: Tranmission

A

Action potential conducted through nervous system

First-, second-, third-order neurons

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23
Q

Define: Perception

A

Integration of painful input into the somatosensory and limbic cortices

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24
Q

Define Modulation

A

Altering afferent transmission along pain pathway

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25
Q

Where does modulation take place at?

A

Most common in dorsal horn

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26
Q

Transduction is the transfer of ____ to an ___

A

noxious stimuli to action potential

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27
Q

During transduction, which fibers transmit sharp/fast pain?

A

A-delta fibers – myelinated, fast 6-30 m/s

reflex alert

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28
Q

During transmission, what fibers transmit dull, buring, throbbing, aching pain?

A

C fibers – unmyelinated, slow 0.5-2 m/s

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29
Q

C fibers respond to which type of injuries?

A

mechanical, thermal, and chemical injuries

known as “polymodal fibers”

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30
Q

When peripheral tissues (skin, bone, and viscera) receive chemical, thermal, or mechanical stimuli or are traumatized by either surgery or injury, a series of biochemical events takes place in peripheral pain transduction. These events include release of chemicals mediated from the inflammatory response and the release of neurotransmitters from _____

A

nociceptive nerve endings.

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31
Q

Transduction Chemical Mediator:
Substance P
1. Found & released from __ fibers and are involved in _____ pain

  1. G-protein linked ______
  2. What does it cause? (4 things)
A
  1. C fibers & slow/chronic pain
  2. G protein-linked neurokinin-1 receptor
  3. Vasodilation, extravasation of plasma proteins, degranulation of mast cells, sensitization of stimulated sensory nerve
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32
Q 
Transduction Chemical Mediator:
Glutamate
1.  CNS or PNS?
2. Which fibers?
3. Effect fast of slow?
4. What is the pain like?
A
  1. CNS
  2. A-delta, and C fibers
  3. Instantaneous effect
  4. Fast/sharp
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33
Q

Transduction Chemical Mediator:
Bradykinin
1. Peptide - notably _____
2. Direct stimulating effect on peripheral nociceptors via _____ receptors

A
  1. notably algesic

2. bradykinin (B1/B2)

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34
Q

Transduction Chemical Mediator:
Histamine
1. Amine is release from….. (3) via ____
2. Causes ____

A
  1. mast cells, basophils, and platelets - via substance P

2. Edema & vasodilation

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35
Q

Transduction Chemical Mediator:
Serotonin (5-hydroxytryptamine [5-HT])
1. Amine stored and released from ____ after tissue injury
2. Algesic effect on ______

A
  1. platelets

2. peripheral nociceptors

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36
Q 
Transduction Chemical Mediator:
Prostaglandins, thromboxanes, leukotrienes
1. Synthesized from \_\_\_\_
2. Hyperalgesia-PGs sensitize \_\_\_\_\_\_
3. Associated with \_\_\_\_\_ pain
A
  1. COX-1 and COX-2
  2. peripheral nociceptors
  3. Chronic
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37
Q 
Transduction Chemical Mediator:
Cytokines
1. Released in response to \_\_\_\_
2. Cytokines include \_\_\_\_
3. Leads to increased production of
A
  1. tissue injury
  2. interleukin-1B, interleukin-6, and tumor necrosis factor
  3. Prostaglandins
38
Q

Transduction Chemical Mediator:
Calcitonin gene-related peptide (CGRP)
1. Peptide released from AFFERENT __ fibers
2. Causes local cutaneous ____ (3)

A
  1. C fibers

2. vasodilation, plasma extravasation, and sensitization

39
Q

Transmission is action potential transmitted from

A

periphery to CNS

Multiple pathways (ex. Spinothalmic [anterolateral] tract)

40
Q

Perception occurs once signal is recognized by

A

various areas of the brain

Amygdala, somatosensory areas of cortex, hypothalamus, anterior cingulate cortex

41
Q

Modulation is altering neural afferent activity along pathway, how does it do this?

A

Suppress (inhibitory)

Enhance (excitatory)

42
Q

What is considered the bodys analgesia system?

A

Descending efferent pathways –> from the Suppress (inhibitory)

43
Q

Name the excitatory transmitters

A

Substance P

Glutamate

44
Q

Name the inhibitory neurotransmitters

A 
Glycine
GABA
Ankephaln
Serotonin
Norepinephrine
45
Q

NSAIDs
For what type of pain?
Has what properties?

A

mild to moderate pain

Anti-inflammatory, antipyretic, and analgesic properties

46
Q

What does NASIADs inhibit?

A

Inhibit COX, thereby stop conversion of arachidonic acid to prostaglandins

47
Q

Ketorlac (Toradol)

what is its MOA?

A

Nonselective COX inhibitor

48
Q

Ketorlac (Toradol)
30mg IM equivalent to
Dont admin longer than
Contraindications (7)

A

12 mg IM Morphine
5 days
coagulopathies, renal failure, active peptic ulcer disease, GI bleeding, Hx of asthma, hypersensitivity to NSAIDS, sx with high potential for post-op bleeding

49
Q 
Acetaminophen
Reduced \_\_\_\_\_ synthesis
What are the main properties
Has minimal \_\_\_\_
Contraindicated in
A

Prostaglandin
Analgesic and antipyretic
Minimal anti-inflammatory
Liver Failure

50
Q

What is the max daily doses for Acetaminophen

A

Max dose for 24 hrs is 4g

51
Q

Opioids bind to and activate ______ coupled receptors in the _____ and ____

A

G-protein

Periphery and CNS

52
Q

Where are the opioid receptors in the CNS

A

Dorsal Horn, specifically Rexed lamina II (substancia gelatinosa), periaqueductal grey, medial thalamus, amygdala, limbic system

53
Q

Where are the opioid receptors in the periphery

A

afferent sensory nerve fibers, GI tract, lungs, joints

54
Q

Opioids - what do the Mu, Delta & Kappa receptors do pre-synaptically?

A

decrease adenylate cyclase activity > inhibiting calcium channels >
decreased excitatory neurotransmitters

55
Q

Opioids - what do the Mu, Delta & Kappa receptors do post-synaptically?

A

Increased potassium conductance > hyperpolarizes >

Inhibits excitatory neurotransmission

56
Q

What is the NMDA antagonist we use?

A

Ketamine – prevents activation of NMDA receptor (NMDA is excitatory)

57
Q

NMDA is associated with

A

“wind-up”

58
Q

What are the alpha-2 adrenergic agonists

A

Clonidine and Precedex

59
Q

Clonidine & Precedex interact with ____ alpha 2 receptors, centrally and peripherally

Inhibits ____ and decreased ____

Activates postsynaptic ____ channels and inhibits presynaptic ____ channels which decrease neurotransmitter release

A

G protein-coupled

adenyl cyclase and decreased cAMP

potassium/calcium

60
Q

Anticonvulsants (gabapentin [Neurontin] and pregabalin [Lyrica]) are used for what type of pain? How does it work?

A

Neuropathic pain syndromes

Inhibit neuronal excitation and stabilize nerve membranes

61
Q

Should you continue Anticonvulsants (gabapentin/pregabalin) with surgery?

A

yes

62
Q

How do antidepressants work?

A

Block the reuptake of serotonin and norepinephrine in CNS, increasing availability

63
Q

Should you continue Antidepressants with surgery?

A

yes

64
Q

How do corticosteroids work?

A

Anti-inflammatory – decrease cytokine and prostaglandin release

65
Q

Should you continue corticosteroids with surgery?

A

yes - possible stress dose

66
Q

How does methadone work?

A

Synthetic opioid, NMDA and opioid receptor action

67
Q

Should you continue methadone with surgery?

A

continue?

68
Q

How long does it take to detox from methadone?

A

30 days to detox from methadone

20-40 mg range

69
Q

What are the 3 subdivisions of painful stimuli

A

Painful stimulation without tissue damage

Tissue damage without nerve damage

Nerve damage

70
Q

Painful stimulation without tissue damage:

Withdrawal from stimulation, stop damage, local event

A

…

71
Q

Tissue damage without nerve damage:

Pain persists after withdrawal, intensified response to tactile stimulation, sensation of pain will spread, release of response mediators

A

…

72
Q

Nerve damage:

Direct damage to nerve, can be ___ or ____

A

demyelinating or axonal

73
Q

3 anatomic regions associated with pain

A

Peripheral
Spinal
Cerebral

74
Q

Chronic pain treatment must do what?

A

Must address source!

The dysfunctional inhibitory mechanism in the peripheral and spinal nervous system

Address the dysfunctional pain perception in the cerebrum

75
Q

Types of chronic pain:

Psychogenic

A

unable to validate or find source

term falling out of favor

76
Q

Types of chronic pain:

Inflammatory

A

Tissue damage resulting in pain and release of inflammatory mediators

77
Q

Inflammatory produces capillary vasodilation, smooth muscle contraction and…

A

promote synaptic transmission of pain impulses to CNS (histamine, bradykinin, and substance P)**

78
Q

Types of chronic pain:

Neuropathic

A

Nerves damaged, pain radiates along dermatome

79
Q

Neuropathic pain commonly leads to …

Pain is ____ and not managed well with ___

A

Allodynia
persistant/NSAIDs

(ex. shingles)

80
Q

What is windup

A

Cyclic response to pain that leads to abnormal pain response

Patients often labeled as “drug seekers”, “chronic complainers”, “crazy”

While can be psychological, not always is

81
Q

Treating chronic pain is

A

Multimodal

  1. Remove or treat stimulus
  2. Reset the inhibitory mechanism of central spinal area
  3. Address psychological impact of pain in cerebral area
82
Q

In the periphery, neuropathic pain is thought to include both ___ and ___ fibers

A

A (fast) and C (slow) nerve fibers

83
Q

What is the normal sequence of response to pain in the periphery

A

Stimulation > Substance P > Neurokinins > Action potential sent to CNS

NMDA receptors inactive (stabilized by magnesium)

84
Q

What is the abnormal (chronic pain) sequence of response to pain in the periphery

A

Magnesium displace > NMDA activated > calcium ions enters cells

EXAGGERATED release of substance P and excitatory amino acids

85
Q

Spinal pain has many complex features. Chronic pain may trigger inappropriate activation of ____ creating negative consequences

A

neuropeptides

86
Q

Cerebral pain has various regions involved in pain modulation. There is a psychological component evident with

A

Placebo effect

87
Q

What medication may be helpful to prevent windup in chronic pain patients? what is the consequence to this med?

A

Windup is from NMDA activation
Pretreat with ketamine (blocks NMDA activity)
Concern for hallucination and vivid dreams

88
Q

Muscle Relaxants:
Cyclobenzaprine (Flexeril)

When does it become ineffective?
Used for..

A

ineffective in a few weeks

Short term symptomatic relief

89
Q

Muscle Relaxants:
Carisoprodol (Soma)

Has the potential for

A

dependence, tolerance, mental impairment

90
Q

Muscle Relaxants:
Baclofen

Is NOT for use in..
Specialized for
What can occur with use?

A

NOT for use in chronic pain

specialized (cerebral palsy, MS)

Withdrawal symptoms can occur
(Respiratory failure, hemodynamic changes, seizures, delirium)

APA 3 - Wolfe (11 decks)

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