Multimodal Pain Management Flashcards

1
Q

What are the different types of a pain stimulus?

A

mechanical, thermal, chemical, sensitizing hormones

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2
Q

What are the 2 pathways from free nerve endings to CNS?

A

Fast (sharp) and Slow (chronic)

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3
Q

Describe fast pain signals.

A

sharp, to spinal cord by small alpha and delta fibers, velocities 6-30 m/sec, mechanical and thermal

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4
Q

Describe slow pain signals.

A

chronic, to spinal cord by C fibers, velocities 0.5-2 m/sec, chemical and/or persistent mechanical or thermal

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5
Q

What is multimodal pain management?

A

use of multiple classes of analgesic drugs to act on different receptors along the pain pathway. Drugs act synergistically to enhance analgesia and reduce side effects

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6
Q

What are the 4 elements of pain processing?

A

transduction–stimuli converted to action potential
transmission–AP conducted through nervous system
modulation–altering afferent transmission along pain pathway
perception–pain recognized and interpreted by the brain

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7
Q

Which element of pain processing should multimodal pain management try to affect?

A

all 4 elements

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8
Q

What type of receptors are opioid receptors and where are they located?

A

g-protein coupled, brain/spine/periphery

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9
Q

What is biased agonism?

A

distinct ligands can bind to g-protein coupled receptor activating differential signaling pathways. Same receptor but different physiologic outcomes. Activates a subset of signaling pathway. Goal to activate analgesic action without side effects.

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10
Q

What are the pharmacokinetics of NSAIDS?

A

absorbed completely with minimal first pass metabolism, tightly protein bound, small volume of distribution

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11
Q

What is the primary effect of NSAIDS?

A

inhibition of cyclooxygenase (COX) preventing transformation of arachidonic acid to prostaglandins

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12
Q

What is the fastest to slowest absorption by site?

A

intercostal->caudal epidural->lumbar epidural->brachial plexus->subq tissue

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13
Q

What are indications for regional/neuraxial analgesia?

A

acute post surgical pain, severe chronic pain

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14
Q

What are the physiologic effects of neuraxials?

A

blockade of sympathetic fibers peripheral T1-L2, cardiac T1-T4, splanchnic T6-L1. unopposed parasympathetic stimulation

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15
Q

What are contraindications to regional/neuraxial?

A

Pt refusal (only absolute), sepsis/infection, allergy to meds, inability to position, preexisting neuropathy, spinal stenosis, previous spine surgery, multiple sclerosis, spina bifida, aortic stenosis, coagulopathy

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16
Q

What are 2 types of commonly used NMDA antagonists?

A

magnesium, ketamine

17
Q

What’s the dose of magnesium?

A

1-23.5 grams

18
Q

What is the MOA of alpha 2 adrenergic agonists?

A

MOA unknown postulated release of Ach involved

19
Q

Is potency increased or decreased with concomitant use of opioids and alpha-2 adrenergics?

A

increased

20
Q

What’s the purpose of alpha-2 adrenergic agonists?

A

reduce undesirable physiological/psychological effects of opioid withdrawal

21
Q

What are cannabinoid receptor agonists?

A

endogenous/exogenous compounds binding to inhibitory cannabinoid receptors decreasing NT release

22
Q

Where are CB1 receptors?

A

CNS at nerve terminals mediating inhibition of NT

Brain multiple areas–cerebral cortex, hippocampus, cerebellum, brain stem

23
Q

Where are CB2 receptors?

A

mainly on immune cells modulating cytokine release (reducing inflammation)
Spleen, tonsils, thymus, and tissues responsible for immune cell production

24
Q

What are the side effects of cannabinoid receptor agonists?

A

sedation, dizziness, dry mouth, dysphoria, cognitive impairment, anxiety, orthostatic hypotension, tachycardia, bronchodilation, impairment in attention, decreased body temp, psychosis