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
Where does modulation take place at?
Most common in dorsal horn
26
Transduction is the transfer of ____ to an ___
noxious stimuli to action potential
27
During transduction, which fibers transmit sharp/fast pain?
A-delta fibers – myelinated, fast 6-30 m/s | reflex alert
28
During transmission, what fibers transmit dull, buring, throbbing, aching pain?
C fibers – unmyelinated, slow 0.5-2 m/s
29
C fibers respond to which type of injuries?
mechanical, thermal, and chemical injuries known as “polymodal fibers”
30
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 _____
nociceptive nerve endings.
31
Transduction Chemical Mediator: Substance P 1. Found & released from __ fibers and are involved in _____ pain 2. G-protein linked ______ 3. What does it cause? (4 things)
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
32
``` Transduction Chemical Mediator: Glutamate 1. CNS or PNS? 2. Which fibers? 3. Effect fast of slow? 4. What is the pain like? ```
1. CNS 2. A-delta, and C fibers 3. Instantaneous effect 4. Fast/sharp
33
Transduction Chemical Mediator: Bradykinin 1. Peptide - notably _____ 2. Direct stimulating effect on peripheral nociceptors via _____ receptors
1. notably algesic | 2. bradykinin (B1/B2)
34
Transduction Chemical Mediator: Histamine 1. Amine is release from..... (3) via ____ 2. Causes ____
1. mast cells, basophils, and platelets - via substance P | 2. Edema & vasodilation
35
Transduction Chemical Mediator: Serotonin (5-hydroxytryptamine [5-HT]) 1. Amine stored and released from ____ after tissue injury 2. Algesic effect on ______
1. platelets | 2. peripheral nociceptors
36
``` Transduction Chemical Mediator: Prostaglandins, thromboxanes, leukotrienes 1. Synthesized from ____ 2. Hyperalgesia-PGs sensitize ______ 3. Associated with _____ pain ```
1. COX-1 and COX-2 2. peripheral nociceptors 3. Chronic
37
``` Transduction Chemical Mediator: Cytokines 1. Released in response to ____ 2. Cytokines include ____ 3. Leads to increased production of ```
1. tissue injury 2. interleukin-1B, interleukin-6, and tumor necrosis factor 3. Prostaglandins
38
Transduction Chemical Mediator: Calcitonin gene-related peptide (CGRP) 1. Peptide released from AFFERENT __ fibers 2. Causes local cutaneous ____ (3)
1. C fibers | 2. vasodilation, plasma extravasation, and sensitization
39
Transmission is action potential transmitted from
periphery to CNS Multiple pathways (ex. Spinothalmic [anterolateral] tract)
40
Perception occurs once signal is recognized by
various areas of the brain Amygdala, somatosensory areas of cortex, hypothalamus, anterior cingulate cortex
41
Modulation is altering neural afferent activity along pathway, how does it do this?
Suppress (inhibitory) | Enhance (excitatory)
42
What is considered the bodys analgesia system?
Descending efferent pathways --> from the Suppress (inhibitory)
43
Name the excitatory transmitters
Substance P | Glutamate
44
Name the inhibitory neurotransmitters
``` Glycine GABA Ankephaln Serotonin Norepinephrine ```
45
NSAIDs For what type of pain? Has what properties?
mild to moderate pain | Anti-inflammatory, antipyretic, and analgesic properties
46
What does NASIADs inhibit?
Inhibit COX, thereby stop conversion of arachidonic acid to prostaglandins
47
Ketorlac (Toradol) | what is its MOA?
Nonselective COX inhibitor
48
Ketorlac (Toradol) 30mg IM equivalent to Dont admin longer than Contraindications (7)
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
``` Acetaminophen Reduced _____ synthesis What are the main properties Has minimal ____ Contraindicated in ```
Prostaglandin Analgesic and antipyretic Minimal anti-inflammatory Liver Failure
50
What is the max daily doses for Acetaminophen
Max dose for 24 hrs is 4g
51
Opioids bind to and activate ______ coupled receptors in the _____ and ____
G-protein | Periphery and CNS
52
Where are the opioid receptors in the CNS
Dorsal Horn, specifically Rexed lamina II (substancia gelatinosa), periaqueductal grey, medial thalamus, amygdala, limbic system
53
Where are the opioid receptors in the periphery
afferent sensory nerve fibers, GI tract, lungs, joints
54
Opioids - what do the Mu, Delta & Kappa receptors do pre-synaptically?
decrease adenylate cyclase activity > inhibiting calcium channels > decreased excitatory neurotransmitters
55
Opioids - what do the Mu, Delta & Kappa receptors do post-synaptically?
Increased potassium conductance > hyperpolarizes > | Inhibits excitatory neurotransmission
56
What is the NMDA antagonist we use?
Ketamine – prevents activation of NMDA receptor (NMDA is excitatory)
57
NMDA is associated with
“wind-up"
58
What are the alpha-2 adrenergic agonists
Clonidine and Precedex
59
Clonidine & Precedex interact with ____ alpha 2 receptors, centrally and peripherally Inhibits ____ and decreased ____ Activates postsynaptic ____ channels and inhibits presynaptic ____ channels which decrease neurotransmitter release
G protein-coupled adenyl cyclase and decreased cAMP potassium/calcium
60
Anticonvulsants (gabapentin [Neurontin] and pregabalin [Lyrica]) are used for what type of pain? How does it work?
Neuropathic pain syndromes | Inhibit neuronal excitation and stabilize nerve membranes
61
Should you continue Anticonvulsants (gabapentin/pregabalin) with surgery?
yes
62
How do antidepressants work?
Block the reuptake of serotonin and norepinephrine in CNS, increasing availability
63
Should you continue Antidepressants with surgery?
yes
64
How do corticosteroids work?
Anti-inflammatory – decrease cytokine and prostaglandin release
65
Should you continue corticosteroids with surgery?
yes - possible stress dose
66
How does methadone work?
Synthetic opioid, NMDA and opioid receptor action
67
Should you continue methadone with surgery?
continue?
68
How long does it take to detox from methadone?
30 days to detox from methadone | 20-40 mg range
69
What are the 3 subdivisions of painful stimuli
Painful stimulation without tissue damage Tissue damage without nerve damage Nerve damage
70
Painful stimulation without tissue damage: Withdrawal from stimulation, stop damage, local event
...
71
Tissue damage without nerve damage: Pain persists after withdrawal, intensified response to tactile stimulation, sensation of pain will spread, release of response mediators
...
72
Nerve damage: Direct damage to nerve, can be ___ or ____
demyelinating or axonal
73
3 anatomic regions associated with pain
Peripheral Spinal Cerebral
74
Chronic pain treatment must do what?
Must address source! The dysfunctional inhibitory mechanism in the peripheral and spinal nervous system Address the dysfunctional pain perception in the cerebrum
75
Types of chronic pain: | Psychogenic
unable to validate or find source | term falling out of favor
76
Types of chronic pain: | Inflammatory
Tissue damage resulting in pain and release of inflammatory mediators
77
Inflammatory produces capillary vasodilation, smooth muscle contraction and...
promote synaptic transmission of pain impulses to CNS (histamine, bradykinin, and substance P*)***
78
Types of chronic pain: | Neuropathic
Nerves damaged, pain radiates along dermatome
79
Neuropathic pain commonly leads to ... | Pain is ____ and not managed well with ___
Allodynia persistant/NSAIDs (ex. shingles)
80
What is windup
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
Treating chronic pain is
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
In the periphery, neuropathic pain is thought to include both ___ and ___ fibers
A (fast) and C (slow) nerve fibers
83
What is the normal sequence of response to pain in the periphery
Stimulation > Substance P > Neurokinins > Action potential sent to CNS NMDA receptors inactive (stabilized by magnesium)
84
What is the abnormal (chronic pain) sequence of response to pain in the periphery
Magnesium displace > NMDA activated > calcium ions enters cells EXAGGERATED release of substance P and excitatory amino acids
85
Spinal pain has many complex features. Chronic pain may trigger inappropriate activation of ____ creating negative consequences
neuropeptides
86
Cerebral pain has various regions involved in pain modulation. There is a psychological component evident with
Placebo effect
87
What medication may be helpful to prevent windup in chronic pain patients? what is the consequence to this med?
Windup is from NMDA activation Pretreat with ketamine (blocks NMDA activity) Concern for hallucination and vivid dreams
88
Muscle Relaxants: Cyclobenzaprine (Flexeril) When does it become ineffective? Used for..
ineffective in a few weeks Short term symptomatic relief
89
Muscle Relaxants: Carisoprodol (Soma) Has the potential for
dependence, tolerance, mental impairment
90
Muscle Relaxants: Baclofen Is NOT for use in.. Specialized for What can occur with use?
NOT for use in chronic pain specialized (cerebral palsy, MS) Withdrawal symptoms can occur (Respiratory failure, hemodynamic changes, seizures, delirium)