Pharmacotherapy of Severe Pain & Migraines Flashcards

1
Q

Goal of Pain Management

A

reduce pain to a level that allows a pt to perform reasonable ADL’s

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2
Q

Key Principles of Pain Management

A
  1. pt should be considered expert of their own pain
  2. pain management is a pt right and should be based on pt goals
  3. nonpharmacologic interventions should be encouraged in addition to pharmacotherapy
  4. dosing should be individualized/adjusted
  5. adverse effects should be anticipated & PREVENTED whenever possible
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3
Q

Is it easier to manage pain or prevent it?

A

Around-the-clock dosing helps to prevent exacerbations of pain which is easier to do than eliminate existing and escalating pain

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4
Q

nociceptor pain

A

sensory nerve fibers; somatic (sharp pain localized to muscles or joints); visceral (dull, throbbing, aching pain in the internal organs)

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5
Q

neuropathic pain

A

injury to nerves; burning, shooting, numbing pain that responds to adjuvant analgesics as anti seizure drugs and antidepressants

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6
Q

Should someone in pain look/act like they are in pain?

A

NO! Not all pt’s report pain because they don’t want to appear weak; pt’s will sometimes sleep even when in pain; VS not always good indicators

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7
Q

Gate Control Theory

A

proposes a gating mechanism for pain transmission to the spinal cord; signals from faster A-alpha and beta fibers reach spinal cord faster than slower C fibers; explain effectiveness of massage, transcutaneous electrical nerve stimulation, and possibly acupuncture in reducing pain

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8
Q

4 Phases of Pain Physiology

A
  1. Pain transduction (nociceptor nerve endings stimulated and chemical mediators released)
  2. Pain transmission (to spinal cord)
  3. Pain perception (in the brain)
  4. Pain modulation (descending nerve impulses inhibit afferent pain transmission via feedback mechanism; serotonin, norepinephrine, endorphins inhibit pain transmission)
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9
Q

NSAIDS

A

target peripheral NS; inhibit cyclooxygenase (enzyme responsible for formation of prostaglandin - mediator of inflammation); most adverse effects GI related; drugs of choice for mild to moderate pain, especially w/inflammation

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10
Q

Acetaminophen

A

nonopioid, not classified as NSAID; MAX DOSE: 4,000mg/day

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11
Q

Nonpharmacologic therapies

A

can be used instead of drugs or alongside drug therapy; allow for improved comfort, lower drug doses, and decreased potential for adverse drug effects

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12
Q

Combination drugs

A

opioid and nonopioid drugs

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13
Q

PCA

A

allows pt to self-administer pain meds, may reduce anxiety of waiting for meds; NURSES, FAMILY MEMBERS, OR VISITORS SHOULD NOT USE DEVICE TO GIVE PT MEDS

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14
Q

Opiates

A

natural substances obtained from opium (morphine & codeine)

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15
Q

Opioid

A

synthetic drug w/morphine-like activity; alter perception/emotional response to pain but not the actual pain impulses/threshold of pain

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16
Q

Narcotic

A

morphine-like drug used to relieve pain

17
Q

Opioid pain management

A

usually given for moderate-severe pain; when used for long-term, can cause physical and psychological dependence

18
Q

Opioid agonists

A

activate mu and kappa receptors; relieve moderate-severe pain

19
Q

Mixed opioid agonist-antagonists

A

work on one receptor but block/have no effect on another; treat moderate pain w/less risk of respiratory depression/dependence (although still possible)

20
Q

Opioid antagonists

A

block mu and kappa receptors; treat opioid overdose (Naloxone/Narcan)

21
Q

Opioid adverse effects

A

RESPIRATORY DEPRESSION (withhold med if respirations fall below 12/min; consider Narcan if they fall below 10/min)
ORTHOSTATIC HYPOTENSION
INCREASED ICP (due to vasodilation caused by increased CO2 and respiratory depression)
URINARY RETENTION
CONSTIPATION (no tolerance usually develops)
N/V
PHYSCIAL/PSYCHOLOGICAL DEPENDENCE
TYPE 1 HYPERSENSITIVITY REACTIONS

22
Q

Equianalgesic use

A

often necessary to change route of pain med/drug itself; what drug can be given by different route/different drug while still achieving same pain relief level

23
Q

morphine sulfate

A

narcotic analgesic; opioid agonist
USE: treat severe pain, preanesthetic sedation, relieve SOB w/end-stage conditions
MOA: occupies mu and kappa receptors = altered perception of pain/emotional responses - analgesia
AE: opioid adverse effects
BLACK BOX WARNING: Schedule II controlled substance w/high potential for physical/psychological dependence
Contraindications: pregnancy; caution in older adults, undiagnosed abd pain, kidney impairment, hepatic impairment & shock; conditions w/decreased respiratory reserve
Pregnancy: avoid chronic use - can cause poor fetal growth, stillbirths, preterm births, and possible birth defects

24
Q

buprenorphine (Buprenex)

A

partial agonist at mu receptors/antagonist at kappa receptors; Schedule III drug; relieve of moderate-to-severe pain

25
Q

adjuvant analgesics

A

diverse group of drugs used to enhance analgesia for specific indications; used to supplement pain relief; pain refractory to opioids & neuropathic pain

26
Q

antidepressants

A

TCAs and SSRIs; increase levels of inhibitory neurotransmitters resulting in increased pain modulation

27
Q

anti seizure drugs

A

ex. Gabapentin; act by suppressing neuronal discharges and reducing the hyper excitability that occurs after nerve injury

28
Q

corticosteroids

A

reduce inflammatory swelling, pressure on brain, spinal cord, and spinal nevers

29
Q

local anesthetics

A

ex. Lidocaine; caution for pt’s w/heart disease or dysrhythmias

30
Q

Naloxone administration

A
  1. hold opioid if respirations <12/min
  2. repeat small doses of naloxone (lasts about an hour)
  3. monitor to be sure drug effects outlast respiratory depression
    *naloxone reverses BOTH toxic and therapeutic effects of opioids
  4. maintain patent airway
  5. have resuscitation equipment ready
31
Q

migraine headache

A

throbbing, pulsating pain; preceded by aura, pt’s appear to have blood vessels that overreact to specific triggers; levels of serotonin decline, causing blood vessels to dilate/become inflamed = pain

32
Q

Goal of migraine pharmacotherapy

A
  1. terminate active migraine
  2. prevent/reduce frequency of migraines (most effective if begun before pain reaches severe level)
33
Q

mild migraines

A

occasional headaches w/no other functional impairment; tx: NSAIDs, acetaminophen, caffeine, triptans/ergot alkaloids

34
Q

moderate migraines

A

moderate headaches, nausea, some functional impairment; tx: oral, nasal, or SQ serotonin agonists (triptans/ergot alkaloids); can also use dopamine agonists

35
Q

severe migraines

A

severe headaches more than 3x/month, marked n/v, & functional impairment; tx: SQ, IM, or IV serotonin agonists OR dopamine agonist, narcotic analgesics for refractory pain

36
Q

Triptans

A

selective for 5-HT receptor subtype
MOA: constrict certain intracranial vessels
effective in ABORTING migraines w/or w/o auras; NOT EFFECTIVE AT PREVENTING MIGRAINES
Ex. sumatriptan (Imitrex)

37
Q

Ergot alkaloids

A

for pt’s not responsive to triptans (separate use by 24 hrs)
MOA: constrict both arteries and veins (CONTRAINDICATED IN PVD, CAD, AND SEVERE HTN)
Regular daily used can cause dependence
Pregnancy: can cause fetal harm
Ex. ergotamine (Ergostat)

38
Q

sumatriptan (Imitrex)

A

antimigraine, serotonin receptor agonist
USE: aborting active migraine attack
MOA: activates 5-HT1 serotonin receptors on intracranial and extra-cerebral blood vessels = cranial vessel constriction & reduced transmission in trigeminal pain pathways
AE: mild dizziness, nausea, diarrhea, myalgia, serious cardiac events
Contraindications: should not be used within 2 weeks of MAOIs and SSRIs; avoid use within 24 hrs of ergot alkaloids or other 5-HT1 agonists
Pregnancy: only if benefits outweigh risks
NC: administer drug at FIRST SIGN OF HEADACHE, monitor for cardiac events, and renal/liver function