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4th Quarter > Pain Management Final Exam > Flashcards

Pain Management Final Exam Flashcards

1
Q

Where does morphine cause analgesia which rexed?

A

Rexed 2 associated with the substantia gelatinousa

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2
Q

Which neurotransmitter is responsible for hyperalgesia?

A

Prostaglandins

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3
Q

What are two types of Nociceptive pain?

A
  • Somatic

- Visceral

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4
Q

What are types of Non-nociceptive?

A
  • Neuropathic

- Idiopathic/Psychogenic

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5
Q

What is Somatic pain?

A

pain that has an identifiable locus as a result of tissue damage causing the release of chemicals from injured cells that mediate pain. well localized, sharp in nature, generally hurts at the point of stimulus.
i.e. sharp, well localized, hurts in area of stimulus

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6
Q

What is Visceral pain?

A

diffuse and can be referred to another area. It is often associated with distention of an organ capsule or the obstruction of a hollow viscus. Also, it is often accompanied with autonomic reflexes such as N/V/D.
i.e. dull, cramping, squeezing, vague in nature

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7
Q

What is Neuropathic pain?

A

caused by damage to peripheral or central neural structures resulting in ABNORMAL processing of painful stimuli.
i.e. burning, tingling, shock-like

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8
Q

What is Idiopathic or Psychogenic pain?

A

associated with chronic pain states and is used to describe pain that has no apparent cause. Neither nociceptive or non-nociceptive mechanisms can be identified as a cause for pain and psychological symptoms are commonly present.Still real pain.

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9
Q

What is transduction?

A

the transformation of a noxious stimulus(chemical, mechanical or thermal) into an action potential.

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10
Q

Describe A-delta nerve fibers.

A

Large, myelinated, primary afferent neurons conduct action potentials at velocities between 6 and 30 m/sec and elicit sharp pain (mechanical and chemical?thermal?)

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11
Q

Describe C nerve fibers.

A

Nonmyelinated C fibers Smaller, conduct at velocities between 0.5 and 2 m/sec, aka polymodal fibers because they respond to mechanical, thermal, and chemical injuries, slow pain, chronic pain, dull, burning, throbbing, aching

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12
Q

Chemical mediators and neurotransmitters stimulate peripheral nociceptors causing an influx of ___ ions to enter the nerve fiber membranes. This is called ___. There is a subsequent efflux of ___ ions from the nerve fiber membrane which is called ___. An action potential is the result and a pain impulse is generated.

A
  • sodium
  • depolarization
  • potassium
  • repolarization
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13
Q

What are the primary afferent neurons?

A
  • A delta fibers

- C fibers

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14
Q

Primary afferent neurons have cell bodies in the…..?

A

dorsal root ganglia of the spinal cord, ascend or descend several spinal segments in the Tract of Lassoer

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15
Q

In the Spinothalamic(anterolateral) system what are the two types of second-order neurons?

A
  • nociceptive neuron

- wide-dynamic-range(WDR) neurons

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16
Q

What is the function of the nociceptive neurons of the Spinothalamic system?

A

receive input solely from primary afferent A delta and C fibers

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17
Q

What is the function of the WDR neurons of the Spinothalamic system?

A

receive input from both nociceptive and non-nociceptive primary afferents. WDR neurons are activated by a variety of stimulants(innocuous and noxious).

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18
Q

What is the Spinothalamic (anterolateral) system?

A

a sensory pathway from the skin to the thalamus.

Primary afferent nuerons(a delta and C fibers) have cell bodies in the dorsal root ganglia of the spinal cord
after leaving the tract of Lissauer, the axons of the primary afferents enter the gray matter of the dorsal horn where they synapse with second-order neurons and terminate primarily in LR I, II, V

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19
Q

first order neurons terminate primarily in

A

LR I, II, V

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20
Q

Where are third order neuron?

A

in thalamus to cortex where perception takes place

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21
Q

Where does pain modulation take place?

A

descending efferent pathways

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22
Q

what is considered the body’s analgesic system/pain control system

A

the descending efferent modulatory pathways from the brain

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23
Q

descending axons from the cerebral cortex, hypothalamus, thalamus, periaquaductal gray, nucleus raphe magnus, and locus corealus via the _____ ______ synapse with and suppress pain transmission to the ____ and the ___ ___ ____ ____.

A
  • dorsolateral funiculus
  • brainstem
  • spinal cord dorsal horn
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24
Q

What is the efferent pathway?

A

descending dorsolateral funiculus- body’s analgesic system

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25
Q

What is Central Sterilization?

A

inadequately controlled acute pain that recruits Beta fibers, constantly barraged with nociceptive input, threshold decreases d/t spasticity of upper brain centers, then turns into plasticity– the reconfiguring of upper brain centers to painful stimulus

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26
Q

Excitatory neurotransmitters?

A
  • glutamate

- substance P

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27
Q

Substance P receptors?

A

Neurokinin 1 and 2

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28
Q

Glutamate receptors?

A

NMDA, AMPA, kainate

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29
Q

another name for tract

A

funiculus

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30
Q

primary afferent neuron originates in the periphery and terminates in the

A

lamina rexed I-V

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31
Q

secondary neurons transmitting pain terminate in the

A

thalamus

32
Q

which funiculus modulates pain

A

dorsolateral

33
Q

perception of pain occurs once the signal is recognized by the

A

cerebral cortex

34
Q

two types of second order neurons exist. one is nociceptive, the other is

A

WDR

35
Q

What are the physiologic effects of pain on the GI system?

A
  • decreased gastric emptying—>N/V
  • decreased intestinal motility—>paralytic ileus
  • increased smooth muscle sphincter tone
36
Q

NSAIDs all possess these three properties.

A
  • anti-inflammatory
  • antipyretic
  • analgesic
37
Q

Prostaglandins(primarily PGE1 and PGE2( are responsible for ___ and ___ peripheral nociceptors to the ___ ___ which are released when tissue is traumatized. What are some examples of these mediators?

A
  • sensitizing
  • amplifying
  • inflammatory mediators
  • substance P, bradykinin and serotonin

PROSTAGLANDINS LOWER THE PAIN THRESHOLD…WE WANT TO PREVENT FORMATION OF PROSTAGLANDINS

38
Q

What is the only COX-2 selective NSAID available in the US?

A

Celebrex(celecoxib)

39
Q

In what situations is Celebrex contraindicated?

A
  • contraindicated in known hypersensitivity to sulfonamides or ASA.
  • CAUTION in asthmatics b/c COX-2 inhibitors can convert arachidonic acid to the precursor of leukotrienes, potentially causing bronchoconstriction.
40
Q

What are the specifics of Ofirmev dosing?

A
  • > 50 kg: 1000mg every 6 hrs or 650mg every 4 hours infused over 15 minutes to a maximum of 4000mg/day
  • > 2 years old
41
Q

What is the onset of action and duration of action of Ofirmev?

A
  • ~10 minutes

- ~4-6 hours

42
Q

Where are central opioid receptors found?

A

centrally, receptors are found in the dorsal horn of the spinal cord, specifically Rexed’s lamina II of the substantia gelatinous, and supra spinally in the preaqueductal gray area(PAG), thalamus, amygdala and limbic cortex.

43
Q

What is the duration of action of Fentanyl intrathecally?

A

2 - 4 hours

44
Q

What are the active and inactive metabolites of Morphine?

A
  • inactive: morphine-3-glucuronide
  • active: morphine-6-glucuronide

both are excreted by the kidneys

45
Q

What is the opioid of choice for renal patients?

A

hydromorphone

-metabolism via hepatic conjugation(inactive metabolites)

46
Q

NMDA receptors at rest remain closed due to a ___ ___. They are activated by ____?

A
  • magnesium plug

- glutamate

47
Q

Because Clonidine exert is its effects on both alpha1 and alpha2 receptors(220:1 a2:a1), side effects such as ___, ___, and ___ can occur.

A
  • sedation
  • hypotension
  • bradycardia—>go slow
48
Q

How does Precedex compare to Clonidine in its selectivity for alpha 2 receptors?

A

Precedex(Dexmedetomidine) is 7-10 times more selective for alpha 2 receptors(1620:1 alpha2:alpha2) as compared to Clonidine

GO SLOW IT CAUSES BRADYCARDIA

49
Q

Like Clonidine, Precedex exhibits sedative, anxiolytic, analgesic, sympatholytic and vagomimetic effects with little or no ___ ___.

A

respiratory depression

50
Q

PCA is usually used at ___ only and not with a ___ rate.

A
  • demand only

- basal rate

51
Q

PCA have a ___ and ___ max dose limit.

A

1 hour and 4 hour max dose limit

52
Q

What is the PCA bolus dose and lock out interval for Morphine?

A

> 0.5-2.5mg

>5-10 minutes

53
Q

What is the PCA bolus dose and lock out interval for Fentanyl?

A

> 10-20mcg

>4-10 minutes

54
Q

What is the PCA bolus dose and lock out interval for Hydromorphone?

A

> 0.05-0.25mcg

>5-10 minutes

55
Q

Peripheral sensitization contributes to chronic pain states due to exposure to substances in the periphery which renders high-threshold nerve ending ___ to normally ___ stimuli.

A
  • responsive

- non-noxious

56
Q

Sensitization of ___ neurons as well an an increase in the release of excitatory neurotransmitters, specifically ___ results in the phenomenon termed ___ ___.

A
  • WDR neurons
  • glutamate
  • wind up
57
Q

___ is the primary excitatory neurotransmitter in wind up.

A

glutamate

58
Q

What is the mechanism of action of the 2nd generation chronic pain analgesics Gabapentin and Neurontin?

A

block alpha 2 delta subunit of the PREsynaptic voltage-gated calcium channels in the CNS, thereby preventing excitatory neurotransmitter release.

59
Q

How doe antidepressants affect chronic pain analgesia n the presence of central sensitization?

A

-blocks re-uptake of serotonin and norepinephrine in the CNS, thereby increasing availability.

60
Q

How long does it take for analgesic effects after starting treatment with antidepressants due to neuropathic pain?

A

4-10 days

61
Q

3 examples of SNRIs?

A
  • Velafaxine(Effexor)
  • Duloxetine(Cymbalta)
  • Milnacipran(Savella)
62
Q

3 examples of SSRIs?

A
  • Fluoxetine(Prozac)
  • Citalopram(Celexa)
  • Lexapro
63
Q

What drug class is ideal for chronic pain analgesia for those patients with cardiac disease?

A

Selective Norepinephrine Re-uptake Inhibitors(SNRIs)

64
Q

Concomitant use of SNRIs with SSRIs is not recommended why?

A

may precipitate serotonin syndrome which can be life-threatening

65
Q

Neither SNRIs or SSRIs should be ____ abruptly.

A

stopped

66
Q

A sigle epidural steroid injection can cause HPA suppression from _____ days of injection and lasting up to ___ weeks.

A
  • 4 to 5 days

- 5 weeks

67
Q

Depression can be a side effect of _____?

A

steroids

68
Q

Methadone is a synthetic opioid used for the treatment of opioid addiction in detox. What is the function of its d-isomer(S-methadone)?

A

antagonized NMDA receptor and inhibits serotonin and norepinephrine uptake with aids in the treatment of neuropathic pain, avoid tolerance and hyperalgesia.

69
Q

Preop management of patients with chronic pain:

A

prior to surgery determine severity of chronic pain syndrome as well as types of meds, duration of therapy, and dosages.

if patient has not received usual opioid on the day of surgery, an equivalent should be administered prep.

fentanyl patches should remain ON preoperatively, if need to remove start fentanyl gtt or morphine admin. continue all chronic and acute pain meds including infusion pump, tcas, ssris, etc

ALL chronic pain meds should continue on the day of surgery to prevent withdrawal, administer preop if missed dose

realistic expectations, benzos, multimodal analgesia, start 1-2 hrs prior to surgery. regional is also a great option

70
Q

Intraoperative management of patients with chronic pain:

A

Intraoperative opioids may need to be increased 30 to 100% as compared with opioid-naive because of receptor down-regulation and/or tolerance.

Titrate opioids to HR, BP, RR, resp depth, pupil size

Opioid antagonists and agonist-antagonists should be avoided because these will precipitate an acute withdrawal syndrome

Nonopioid analgesic adjuncts (ketamine, clonidine, and dexmedetomidine) also should be part of a multimodal approach to perioperative pain management, opioid sparing effects.

In the COT patient, use RA with LA whenever possible but continue baseline opioid admin

peripheral nerve blocks with continuous catheter infusions is also an excellent alternative

opioid rotation recommendation if one not seeming to work. cross tolerance between opioids is incomplete, so different tolerance levels.

71
Q

Postop management of patients with chronic pain.

A

If patient is not a candidate for RA/continuous peripheral
nerve block, or did not benefit from it, then IV PCA should be considered.

A basal continuous infusion should be implemented to
cover daily requirements.

Remember to gradually wean COT patients to previous daily regimen prior to abrupt discharge of therapy to prevent withdrawal syndrome.

72
Q

Describe the physiologic effects of dependance:

A

pharmacologic property of opioid drugs defined by the manifestation of a “withdrawal syndrome” after abrupt discontinuation of the opioid, or after the administration of an opioid antagonist (naloxone) or a mixed agonist-
antagonist. CAUSED BY REBOUND DISINHIBITION OF CAMP. Assume it exists after opioid admin more than a few days. To prevent: taper before d/c, daily scheduled opioids should be continued periop.

withdrawal symptoms: ANS responses ie increased irritability, restlessness, tremors, chills, muscle cramps, sweating, mydriasis, abdominal pain, diarrhea, and tachycardia.

73
Q

Describe the psychological effects of dependance:

A

characterized by the craving for an opioid drug to achieve a psychological effect, resulting in the continual use of the drug despite harm to self or others. Component of addiction rather than addiction.

74
Q

What is Pseudoaddiction?

A

often confused with psychological dependence because the
behavior can be the same.

patients exhibit what appears to be drug seeking behavior

in the patient who is pseudoaddicted, the origin of the behavior is inadequate analgesia.

when these patients receive adequate analgesia, they no
longer demonstrate drug-seeking behavior

75
Q

What is tolerance?

A

refers to a change in the dose-response relationship induced by repeated exposure to the drug and manifested as a need for a higher dose to maintain an analgesic effect.

may be due to enzyme induction or opioid receptor down-
regulation.

when tolerance occurs, opioid rotation is suggested

opioid rotation involves switching from one opioid to another in an effort to improve analgesia and decrease side effects.

normal physiologic response.

76
Q

What is Opioid-Induced Hyperalgesia (OIH)?

A

phenomenon that occurs with chronic opioid therapy, which attributes worsening pain to high, escalating doses of opioids.

manifestations of OIH: complaints of pain in locations different from the original pain area, whole-body hyperesthesia, allodynia, agitation, multifocal myoclonus jerks, and seizures.

treatment: reduce or discontinuance of the opioid as well as starting non-opioid analgesics (e.g., NMDA receptor antagonists, NSAIDs, COX-2 inhibitors).

central activation of NMDA via glutamate may play a role s well as shifting in pain modulation from descending inhibitory pathway to facilitating pronociceptive pathway. prostaglandins stimulate glutamate release.

dx is difficult because it resembles tolerance.

77
Q

What is COT?

A

may have higher levels of postop pain, slower resolution of pain

4th Quarter (11 decks)

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