3 - Acute Pain Flashcards

(90 cards)

1
Q

Allodynia

A

painful response to a normally non-painful stimuli

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2
Q

Hyperalgesia

A

exaggerated pain response to a normally painful stimuli

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3
Q

Neuronal Plasticity

A

Acute pain induced changes in the brain

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4
Q

What are nociceptors?

A

Free nerve endings located in the skin, muscle, bone

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5
Q

The nociceptice pathway is an ________ ascending system, made up of which two Nerve fiber types?

A

Afferent

A delta

Polymodal C

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6
Q

A delta fibers transmit _______

A

First pain

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7
Q

Polymodal C fibers transmit

A

Second Pain

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8
Q

What is the difference between first and second pain?

A

First pain is sharp and stinging

Second pain is dull/diffuse pain

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9
Q

What are the three primary afferent nerve fibers types?

A

A beta

A delta

C

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10
Q

What is the smallest afferent nerve fiber?

Largest?

Slowest?

Fastest?

A

C

A beta

C

A beta

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11
Q

A delta fibers carry signals from _______ receptors

C fibers carry signals from _______ receptors

A

specialized sensory

Free nerve ending

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12
Q

What are first order and second order neurons?

A

1st order neurons are located in the specialized sensors and carry impulses to the dorsal horn where they synapse with second order neurons on the same level

OR

ascend via lissauer’s tract to the second order neurons above

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13
Q

Where are third order neurons located?

A

in the reticular formation

periaqueductal gray

thalamus

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14
Q

What is the function of the efferent modulating pathway?

A

It sends impulses from the brain down to the level of the dorsal horn and modulates the response transmitted by afferent nerve fibers

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15
Q

What are the four elements of pain processing?

A
  1. Transduction
  2. Transmission
  3. Modulation
  4. Perception
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16
Q

Define:

Transduction

Transmission

A

Transduction is when a stimuli sparks an action potential in receptors

Transmission is when they action potential is passed to the first, second and third order neurons

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17
Q

Identify the location of cell bodies for the following:

First order neurons

Second order neurons

Third order neurons

A

Dorsal root

Dorsal Horn

Thalamus

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18
Q

Modulation involves altering ________

A

afferent neural transmission along the pain pathway

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19
Q

What is the most common site of modulation?

A

Dorsal Horn

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20
Q

List two types of spianl inhibitory modulation:

A
  1. Release inhibitory neurotransmitters (GABA)
  2. activation of efferent pathway (norepinephrine, serotonin 5HT, Enkephalin endorphin)
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21
Q

Traditional analgesic therapies targeted only _________

A

pain perception

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22
Q

IV fentanyl will affect which element of the pain pathway?

A

Perception

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23
Q

Ketamine will affect which element of the pain pathway?

A

Modulation

NMDA receptor antagonist

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24
Q

Duramorph will affect which element of the pain pathway?

A

Modulation

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25
A peripheral nerve block will affect which element of the pain pathway?
Transmission
26
A bupivicaine epidural will affect which element of the pain pathway?
Transmission
27
How is preventive analgesia accomplished?
preventing NMDA receptor activation in the dorsal horn (associated with windup, facilitation, central sensitization expansion of receptive fields, and long-term potentiation, all of which can lead to a chronic pain state)
28
What are the three necessities for preventive analgesia to be effective?
1. Must block ALL nocicpetive stimulation during surgery 2. Must include the entire surgical field 3. Duration must span both operative and postoperative periods
29
What causes neuropathic pain?
Damage to the nerves themselves may be delayed and may not be dermatomal
30
What are the top five surgeries that are known to cause neuropathic pain?
1. Limb amuptation 2. breast surgery 3. gallbladder surgery 4. thoracic 5. inguinal repair
31
Codeine and tramadol are examples of \_\_\_\_\_\_\_\_
prodrugs Require metabolism by CYP2d6 to be activated
32
Three primary mechanisms of opiods at the level of the spinal cord:
(1) inhibition of calcium influx presynaptically, resulting in inhibition of depolarization of the cell membrane and decreased release of neurotransmitters and neuropeptides into the synaptic cleft (2) enhanced potassium efflux from the cell postsynaptically, resulting in hyperpolarization of the cell and a decrease in pain transmission (3) activation of a descending inhibitory pain circuit via inhibition of GABAergic transmission in the brainstem
33
What are the signs of inadequate dosing of opiods during surgery?
dilated pupils increased HR and BP increased RR
34
multimodal perineural analgesia is a cocktail of:
buprenorphine bupivicaine clonidine dexmedetomidine
35
NSAIDs inhibit:
Cyclooxygenase (COX) enzymes
36
Why do NSAIDs shred your stomach?
Cox 1 is responsible for gastric protection and hemostasis Cox 2 produces prostaglandins which lead to pain and inflammation If you inhibit cox to inhibit COX2, you also end up inhibiting COX1
37
Why do NSAIDS and COX2 inhibitors cause fluid retention and hypertension?
Prostaglandins play a crucial role in renal function because they are potent local and humoral vasodilators If you block them, you get constriction in the afferent arterioles of the glomerulus, leading to fluid retention and high blood pressure
38
How do inhaled volatiles effect neuromuscular function? (2)
1. directly relax skeletal muscle (dose dependent) 2. Potentiate the action of NMBA agents
39
How is uterine muscle tone effected by inhaled anesthetics?
Decreased uterine tone
40
When administering volatile anesthetics for an emergent c-section under general, what can be done to prevent uterine atony?
Use 05-0.75 MAC of gas in combination with N2O
41
Experienced nurses tend to ________ pain Inexperienced nurses tend to ________ pain
underestimate overestimate
42
What is glutamate?
Major excitatory neurotransmitter released from A delta and C nerve fibers Fast, sharp pain
43
What is nociceptive pain?
caused by the stimulation of specific nociceptors
44
What are the two types of nociceptive pain?
Somatic (identifiable locus, sharp, stinging) - i.e. first pain Visceral (dull, cramping, diffuse - i.e. second pain)
45
Visceral pain is often associated with \_\_\_\_\_\_\_\_
distention of an organ capsule obstruction of a hollow viscus
46
Visceral pain is often accompanied by which autonomic reflexes?
Nausea vomiting diarrhea
47
Non-nociceptive pain is categorized as \_\_\_\_\_\_\_
neuropathic
48
What causes inflammatory pain?
multiple mediators released from the site of inflammation cause sensitization of the nociceptive pathway
49
Pain transmitted by Polymodal C fibers is often described as \_\_\_\_\_\_\_\_\_
burning, throbbing, dull, aching
50
What is Substance P?
released from C fibers Involved in slow, chronic pain
51
What is histamine?
Released from mast cells, basophils, and plateletes via substance P Produces edema and vasodilation Potentiates bradykinin pain
52
What is serotonin?
Amine stored and released from platelets after tissue injury Algesic effect on peripheral nociceptors potentiates bradykinin pain
53
What are prostaglandins?
metabolite synthesized from COX-1 and COX-2 Associated with chronic pain Sensitizes peripheral nociceptors, causing hyperalgesia
54
What are cytokines?
Mediators released by tissue damage and inflammation lead to increased production of prostaglandin, causing excited and sensitized nociceptive fibers
55
What is CGRP?
Calcitonin gene-related peptide released from C fibers causes sensitization of sensory nerves
56
What happens when chemical mediators and neurotransmitters stimulate peripheral nociceptors?
sodium channels open nerve is depolarized action potential develops into a pain impuse
57
What are the two types of second order neurons?
Nociceptive (received from A delta and C fibers) Wide-dynamic Range (WDR) that receive from A delta, C, *and A beta*
58
What is the other name for serotonin?
5HT
59
Where do second order neurons synapse with third order neurons? What happens once they do?
In the thalamus Thalamus sends projection of pain to the cerebral cortex, the hypothalamus, and anterior cingulate
60
The descending efferent modulatory pathways are considered the body's \_\_\_\_\_\_\_\_\_\_
pain control system
61
What are the excitatory neurotransmitters?
Substance P Gultamate
62
What receptor does Glutamate bind to in order to cause excitation?
NMDA receptor This is how ketamine works
63
What are the inhibitory neurotransmitters?
Glycine GABA Enkephalin Serotonin Norepinephrine
64
Norepinephrine is an inhibitory neurotransmitter. How does this relate to regional anesthesia?
This is why A2 agonists cause analgesia. They bind to the Alpha 2 receptors, just like norepinephrine would, and inhibit pain transmission
65
What are four predictors of post op pain?
Presence of preop pain patient fear regarding the outcome of their surgery patients who catastrophize pain if post op pain is expected
66
All NSAIDs possess what properties?
anti-inflammatory anti-pyretic analgesic
67
Why does inhibiting COX decrease pain and inflammation?
By inhibiting COX, they prevent conversion of arachindonic acid to prostaglandins Prostaglandins are responsible for sensitizing and ampliying peripheral nociceptors to the inflammatory mediators
68
How do prostaglandins influence pain?
They do not directly cause pain they contribute to hyperalgesia by increasing the sensitivity of nociceptors to inflammatory mediators
69
30mg IM ketorolac is equivalent to how much morphine?
12mg IM
70
When should ketorolac not be given?
Beyond five days coagulopathy, renal failure, active ulcers, GI bleed, asthma
71
Tylenol is not a true NSAID. So why does it decrease pain?
Reduces prostaglandin synthesis somehow minimal anti-inflammatory effects
72
How do opioids inhibit pain?
bind to and activate G-protein coupled receptors (GPCR) both peripherally and in the CNS This inhibits calcium channels and decreases release of excitatory neurotransmitters (like substance P) presynaptically It also hyperpolarizes the post-synaptic junction and inhibits response to excitatory neurotransmission
73
What does NMDA stand for?
N-Methyl-D-Aspartate
74
What is the resting state of the NMDA receptor?
Closed plugged by magnesium
75
What causes the NMDA receptor to open? What happens once it does?
Glutamate binding causes an influx of calcium, resulting in second messengers Second messengers causes hyperexcitability of the NMDA receptors, which amps up algesia Hence ketamine's role in preventing "wind-up"
76
Clonidine and Precedex are \_\_\_\_\_\_\_agonists
A2 adrenergic
77
What do clonidine and precedex bind with?
GCPA A2 receptors in dorsal horn and peripherally activation results in inhibition of cAMP 2nd messenger
78
What happens when A2 agonists bind with GPCA?
decreased cAMP presynaptic: inhibits voltage gated Ca channels postsynaptic: activates potassium channels to hyperpolarize
79
Which is more selectively an A2 adrenergic agonist, precedex or clonidine?
Precedex
80
What would be the effect of A1 adrenergic agonist action?
sedation, hypotension, bradycardia
81
How do local anesthetics block transmission?
block sodium channels in afferent and efferent neuronal membranes
82
Which anticonvulsants are often used to treat pain?
gabapentin and lyrica
83
Which antidepressants help with pain?
SNRIs duloxetine, venlafaxine
84
What is a unique side effect of methadone that isn't seen with other opiods?
QT prolongation
85
Define opioid tolerance
a change in the dose-response relationship
86
What is opioid induced hyperalgesia?
escalating doses of opioids result in increasing hyperalgesia and allodynia
87
What is the difference between opioid addiction and pseudoaddiction?
addiction is pathologically pursuing reward/relief by substance use (cravings, obsessive thoughts, compulsive use) Pseudoaddiction in drug seeking behavior that is actually due to inadequate analgesia. when they receive higher doses, they no longer demonstrate drug seeking behavior
88
Should you leave or remove an implanted intrathecal or epidural opioid infusion system preop?
It should stay and continue perioperatively
89
In neonates, how well developed is the nociceptive pathway? Descending pathway?
Well Poorly Leads to increased pain perception and stress response
90
85% of ascending C fibers terminate in the:
Reticular Formation