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Levi 3 2019 > Pain Management > Flashcards

Pain Management Flashcards

1
Q

Define Algesia

A

Increased sensitivity to pain

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2
Q

Define Alogenic

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 of peripheral nerves

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8
Q

Define Neuropathy

A

An abnormal disturbance in the function of nerves

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9
Q

Define Paresthesia

A

An abnormal sensation, whether spontaneous or evoked

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10
Q

What is acute pain?

A
  • unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
    • <1 month
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11
Q

What is chronic pain?

A
  • Persistent pain associated with a distinct period of uninterrupted pain f 3 months or more, that includes negative sensory and emotional experiences
    • > 3 months
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12
Q

What is considered nociceptive pain?

A

Stimulus of specific nociceptors

  • somatic
  • visceral
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13
Q

What is considered non-nociceptive pain?

A
  • neuropathic

- inflammatory

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14
Q

What occurs with somatic pain?

A
  • identifiable focus
  • tissue damage
  • chemical release modulates pain
  • Well localized area, sharp, hurts at area
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15
Q

What occurs with visceral pain?

A
  • diffuse, referred
  • dull, cramping, squeezing
  • Example: distention of organ capsule, obstruction of hollow viscous
  • associated with autonomic reflexes such as N/V, diarrhea
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16
Q

What occurs with neuropathic pain?

A
  • Damage to peripheral or central neural structures resulting in abnormal processing of painful stimuli
  • dysfunction of CNS
  • Burning, tingling shock-like
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17
Q

What occurs with inflammatory pain?

A
  • sensitization of the nociceptive pathway from multiple mediators
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18
Q

What is transduction?

A

The transformation of noxious stimulus (chemical, mechanical, thermal) into an action potential

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19
Q

Explain the A-delta fibers

A

Fast, sharp pain
6-30m/sec
Reflex alert

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20
Q

Explain the C-fibers

A

Slow
0.6-2m/sec
Dull, burning, throbbing, aching

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21
Q

What are the chemicals released during transduction?

A
  • substance P
  • glutamate
  • bradykinin
  • histamine
  • serotonin
  • prostaglandins
  • cytokines
  • calcitonin gene
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22
Q

What happens with the release of Substance P?

A
  • C fibers (slow chronic pain)
  • G protein linked neurokinin-1 receptor
  • vasodilation, extravasation of plasma proteins, degranulation of mast cells, sensitization of stimulated sensory nerve
  • *inflammation and algesia
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23
Q

What happens with the release of Glutamate?

A
  • CNS, A-delta and C fibers

- instantaneous effect, fast sharp pain

24
Q

What happens with the release of Bradykinin?

A
  • peptic algesic

- Direct stimulating effect on peripheral nociceptors via bradykinin receptors

25
Q

What happens with the release of Histamine?

A
  • Amine released from mast cells, basophils and platelets—> via Substance P
    • edema and vasodilation
26
Q

What happens with the release of Serotonin (5-hydroxytryptamine) [5-HT]?

A
  • Amine stored and released from platelets after tissue injury
  • Algesic
27
Q

What happens with the release of Prostaglandins, thromboxanes and leukotrienes?

A
  • made from COX-1 and COX-2

- Hyperalgesia

28
Q

What happens with the release of Cytokines?

A
  • released in response to tissue injury

* * increase production of prostaglandins—> HYPERalgesia

29
Q

What happens with the release of Calcitonin gene-related peptide (CGRP)?

A
  • peptide released from C fibers (afferent)

- causes local cutaneous vasodilation, plasma extravasation and sensitization

30
Q

What happens during transmission?

A
  • Action potential is conducted from periphery to CNS

- multiple pathways ( ex: spinothalmic (anterolateral) tract)

31
Q

What happens during perception?

A
  • occurs once signal is recognized by various areas of the brain
  • amygdala, somatosensory areas of cortex, hypothalamus, anterior cingulate cortex
32
Q

What happens during modulation?

A
  • altering neural afferent activity along pathway:
    Can either:
  • suppress (inhibitory)
  • enhance (excitatory)- mostly excitatory via substance P
33
Q

What are the inhibitatory neurotransmitters and which receptors do they work on?

A
  • Glycine —> Chloride linked (GlyR)
  • GABA—> GABAa, GABAb, GABAc
  • Enkaphalin—> mu, delta, kappa
  • Serotonin—> 5-HT
  • Norepinephrine—> alpha 2
34
Q

What do NSAIDs do?

A

Treat mild to moderate post-op pain

  • anti-infammatory, antipyretic, and analgesic properties
  • inhibit COX —> thereby stop conversion of arachidonic acid to prostaglandin
35
Q

What does Ketorolac (Toradol) do?

A
  • Non-selective COX inhibitor
  • 30mg IM equivalent to 12 mg morphine IM
  • do NOT give longer than 5 days
36
Q

What are contraindications for Toradol?

A
  • coagulopathies
  • renal failure
  • active P.U.D./GIB
  • history of asthma
  • hypersensitivity to NSAIDS
  • surgery with high potential for post-op bleeding
37
Q

What does Acetaminophen do?

A
  • decreases prostaglandin synthesis
  • analgesic, anti-pyretic, and minimally anti-inflammatory
  • contraindication—> liver failure
38
Q

What do NMDA antagonists do?

A

Ketamine:

  • prevents activation of NMDA receptor
  • NMDA is associated with “wind up”
39
Q

What do alpha 2 agonists do?

A

Clonidine and Precedex:

  • interact with G protein coupled and 2 receptors, centrally and peripherally
  • inhibit adenyl Cyclades and decrease cAMP
  • activate post-synaptic K+ channels and inhibit presynaptice Ca+ channels which decrease neurotransmitter release
40
Q

What do opioids do?

A

Bind to and activate G protein coupled receptors in periphery and CNS

  • CNS: opioid receptors in dorsal horn, specifically REXED LAMINA II (substantiated gelatinosa), periaqueductal grey, medial thalamus, amygdala, lambic system
  • Peripheral: afferent sensory fibers, GI tract, lungs, joints
41
Q

What medications are used for acute pain in chronic pain patients?

A
  • anti-convulsants
  • anti-depressants
  • corticosteroids
  • methadone
42
Q

What do anti-convulsants do?

A

Gabapentin (neurontin) and pregabalin (Lyrica):

  • neuropathic pain syndromes
  • inhibit neuronal excitation and stabilize nerve membranes
  • should continue on the day of surgery
43
Q

What do anti-depressants do?

A
  • block re-uptake of serotonin and norepinephrine, thus increasing availability
  • should continue
44
Q

What do corticosteroids do?

A
  • anti-inflammatory:
    Decrease cytokines and prostaglandin release
  • continue, possible stress dose
45
Q

What does methadone do?

A
  • synthetic opioid, NMDA, opioid receptor action

- continue * does have opioid effect

46
Q

When the source of pain cannot be identified we call it ________________.

A

Fibromyalgia

47
Q

What are the 3 heuristic subdivisions of painful stimuli?

A
  1. ) painful stimulation without tissue damage
    - withdrawal from stimulation, stop damage
    - local event
  2. ) tissue damage without nerve damage
    - pain persists after withdrawal, intensified response to tactile stimulation, sensation of pain will spread, release of response mediators
  3. ) nerve damage
    - direct damage to nerve
    - can be demyelinating, or axonal
48
Q

What are the 3 anatomic regions associated with pain?

A
  • peripheral
  • spinal
  • cerebral
49
Q

What are the goals in treating chronic pain?

A
  • must address the source
  • the dysfunctional inhibitory mechanism in the peripheral or spinal nervous system
  • address the dysfunctional pain perception in the cerebrum
50
Q

What are the 3 types of chronic pain?

A
  • psychogenic
  • inflammatory
  • neuropathic
51
Q

What is psychogenic chronic pain?

A

Term falling out of favor

Unable to validate or find source

52
Q

What is inflammatory pain?

A
  • tissue damage resulting in pain and release of inflammatory mediators
  • produce capillary vasodilation, smooth muscle contraction and promote synaptic transmission of pain implement to CNS (histamine, bradykinin, substance P)
53
Q

T/F Substance P and substance P receptors are specifically associated with inflammatory pain and are diminished or absence in neuropathic and cancer pain

A

TRUE

54
Q

What is neuropathic pain?

A
  • nerves damaged, pain radiates along dermatome
  • commonly leads to allodynia (painful stimuli that is normally not painful)
  • differs from inflammatory pain—> persistent allydonia is not managed well with NSAIDS
55
Q

What is wind up?

A
  • cyclic response to pain that leads to abnormal pain response
  • pts often labeled as drug seekers

Levi 3 2019 (1 decks)

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