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Pharmacology > Chapter 24: Pain > Flashcards

Chapter 24: Pain Flashcards

1
Q

Major contributors to the onset of pain

A

arthritis, back pain, cancer, headache

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2
Q

most common prescription meds used for pain relief

A

NSAIDs

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3
Q

Acute pain

A

nocioceptive pain that is a result of actual or pending tissue damage

duration is short

resolves with healing

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4
Q

chronic pain

A

Perception is a function of a person’s personality and character traits, cultural/ethnic backgound, presence of support systems, work/home satisfaction, and motivation

lasts longer than 3 months

cause is hard to identify

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5
Q

removing barriers that render pain management ineffective

A

stigma attached to certain medications like morphine

patient prefernce on strength

provider concerns about DEA reprisal

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6
Q

consequences of poorly managed pain

A

impaired function and quality of life

depression

polypharmacy from treated manifestations of pain (agitation, etc)

uncontrolled acute pain leading to chronic pain

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7
Q

properly assess pain before prescribing any drug

A

detailed history and physical

idetify the source of the pain

discuss realistic goals

re-examine and adjust therapy as needed

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8
Q

remeber the goal of using medications to manage acute pain

A

restore function as soon as possible

prevent the development of chronic pain syndrome

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9
Q

use different prescribing algorythms for mild, moderate, and severe acute pain

A

mild - NSAIDs and acetominophen with adjunct medications like capscaicin creams or topical salicylates (Ben-gay)

moderate - hydrocodone/APAP, hydrocodone/ibuprofen, oxycodone/APAP, or codeine

severe - pure opiates with dosages limited to less than 200mg morphine equivalent/day

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10
Q

use different algorythm when prescribing for chronic pain

A

usually requires adjunctive use of other medications for neuropathic component

comes about through hyperstimulation of NMDA receptors

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11
Q

remeber there is a role for adjunctive medications

A

drugs used to manage pain but whose primary action is ot analgesia

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12
Q

medications used to treat pain are generally grouped into what 2 categories

A

opioid and nonopioid

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13
Q

opiates

A

naturally occuring opium alkaloids or synthetic derivatives of them

multiple opiate receptor types throughout body to relieve pain

function as either agonists, partial agonists, or antagonists at one or more types of receptors

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14
Q

which opiate receptors are most snesitive and most important for managing general anethesia

A

Mu1 and Mu2

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15
Q

conscientious prescribing of opiates

A

equivalencies of using one opiate over another are approximate

when switching from oral to subQ or IV use 70-75% of dose

dose may be decreased d/t limited cross-tolerance

appropriate dose is the one that relieves pain with least side effects

schedule around the clock, not prn, especially for chronic pain

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16
Q

treatment of myoclonus reltaed to pain medication

A

change opioid or treat with lorazepam

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17
Q

typica dose of Narcan for overdose

A

0.2-0.8mg IV

up to 2mg is often given

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18
Q

prototype agent for antagonist agonist opiate analgesics

A

Morphine

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19
Q

morphine mechanism of action

A

have activity at pre- and post-synaptic mu receptors as well as pre-synaptic kappa and delta receptors

reduces neurotransmitter release from nociceptive primary afferent terminals

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20
Q

antagonist agonist opiate analgesic (morphine)

pharmacokinetics

A
  • Absorption: oral, subQ, and IV absorbed well. Fentanyl not given orally because it is broken down by mucosal and hepatic P450 and 3A4
  • Distribution: widely into CNS and other tissues, especially lipophillic
  • Metabolism: morphine/hydromorphone by glucuronidation, fentanyl by P450 and 3A4, most others by P450 2D6 isoenzyme
  • Excretion: urine
  • Half-life: 2-3 hours, prolonged with hepatic impairment
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21
Q

opiate adverse reactions

A
  • CV: ortho hypotension, decreased BP
  • DERM: occasional allergic rash/pruritus
  • EENT: visual changes
  • GI: constipation, n/v, abdominal cramps, dry mouth
  • GU: urine retention
  • META: decreased appetite, increased urine glucose
  • NEURO: sedation, diaphoresis, flushing, somnolence, dizziness
  • PUL: overdose=respiratory depression with skeletal muscle flaccidity, cold/clammy skin, cyanosis, extreme somnolence progressing to seizures, stupor, coma, death
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22
Q

opiate interactions

A

anything that causes respiratory depression

medications that prolong QT interval if using methadone or buprenorphine

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23
Q

mixed/partial agonist-antagonist analgesics

4 available agents

A

buprenorphine (Buprenex, Subutex)

pantazocine (Talwin)

nalbuphine (Nubain)

butorphanol (Stadol)

can precipitate withdrawal symptoms in patients taking chronic opiates

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24
Q

clinical use of buprenorphine

A

alters emotional perception of pain

sed as an alternative to methadone in opioid detox because of slow dissociation from mu receptor

antagonist at delta and kappa receptors

low analgesi activity

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25
Q

clinical use for pentazocine (Talwin) and nalbuphine (Nubain)

A

treat mod-severe pain

higher rate of hallucinations, nightmares, and anxiety than other opioids

Talwin is used as a supplement to surgical anethesia or pre-surgical sedative

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26
Q

clinical use of butorphanol (Stadol)

A

available as nasal spray and IV

treat mod-severe pain (migraines)

supplement anethsesia

pain during labor

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27
Q

synthetic opiate antagonists

A

bind to same opioid receptors as morphine but with higher affinity so it blocks effects of opioid

precipitates withdrawal symptoms in opioid-dependency

no effect on non-addicts

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28
Q

naloxone (Narcan)

A

fast onset (minutes)

will antagonize post-op analgesics

29
Q

Narcan mechanism of action

A

high affinity for mu sites

antagonistic effects at delta and kappa sites

30
Q

clinica use of Narcan

A

opioid overdose

31
Q

Narcan pharmacokinetics

A
  • Absorption: very poor from GI tract, well absorbed when given SC or IV
  • Distribution: rapidly to all tissues, crosses placenta
  • Metabolism: glucuronide conjugation in the liver
  • Excretion: urine
  • Half-life: 1-2 hours
32
Q

Narcan adverse reactions

A
  • CV: HTN, hypotension, v-fib, tachycardia
  • GI: n/v
  • MISC: severe opiate withdrawal
33
Q

methylnaltrexone (Relistor)

A

no risk for abuse/dependency

peripherally acting mu opioid receptor antagonist

does not cross blood brain barrier

34
Q

Relistor clinical uses and contraindication

A

treats opioid induced constipation (counteracts opioid effects like constipation and itching without effecting analgesia because it doesn’t cross the blood brain barrier)

contraindicated in GI obstruction

35
Q

Relistor pharmacokinetics

A
  • Absorption: admin SC w/ peak concentration in 30 minutes
  • Distribution: moderate
  • Metabolism: slightly via methylation in the liver
  • Excretion: 85% unchanged, half in urine, half in feces
  • Half-life: 8 hours
36
Q

Reistor adverse reactions

A
  • DERM: hyperhidrosis
  • GI: abdominal pain, gas, nausea, severe and/or persistent diarrhea
  • NEURO: dizziness
37
Q

nalmefene (Revex) and naltrexone (ReVia, Trexan)

A

similar chemical structures

used to decrease craving for opioids

naltrexone: used in “rapid detox” for opiate addicts and alcoholics
nalfmefene: long-acting injectable used to prevent alcoholic from relapsing

38
Q

examples of nonopiate analgesics

A

tramadol (Ultram)

ziconotide (Prialt)

tapentadol (Nucynta)

39
Q

tramadol (Ultram)

A

centrally acting synthetic agent with analgesic properties

used for mod-moderatly severe pain

can be subject to abuse

40
Q

tramadol (Ultram) mechanism of action

A

binds to mu receptors in CNS and

inhibits reuptake of serotonin and norepinephrine

to modify the acending pathways of pain

41
Q

tramadol pharmacokinetics

A
  • Absorption: good absorption through GI tract
  • Deistribution: widely
  • Metabolism: liver
  • Excretion: urine
  • Half-life: 6-8 hours
42
Q

tramadol adverse effects

A
  • CV: flushing
  • DERM: rash
  • EENT: burry vision, miosis
  • GI: nausea, constipation
  • MISC: flu-like symptoms
  • NEURO: dizziness, headache, insomnia, somnolence, weakness, and possible seizures
43
Q

tramadol contraindications

A

seizure disorders or concomittent use with medications that lower seizure threshold

44
Q

ziconotide (Prialt)

A

used for severe chronic pain when IT (intrathecal) therapy is warranted

administered directly into CSF

for patients who are intolerant of or refractory to other treatments

45
Q

Prialt mechanism of action

A

blocks excitatory neurotransmitter release and reduces their sensitivity to painful stimuli

46
Q

Prialt contraindications

A

history of psychosis, schizophrenia, clinical depression, bipolar disorder and seizures

47
Q

Prialt pharmacokinetics

A
  • Absorption: administered directly into CSF
  • Distribution: 50% bound to protein
  • Metabolism: by several enzymes inmultiple organs degrade it to peptide fragments and free amino acids
  • Excretion: urine
  • Haf-life: 2.9-6.5 hours
48
Q

Prialt adverse reactions

A
  • EENT: abnormal vision
  • GI: nausea, anorexia
  • NEURO: dizziness, confusion, headache, hypertonia, ataxia, somnolence, unsteadiness, memory impairment

most severe are hallucinations, suicidal idation, new/worsening depression ans seizures

49
Q

Tapentadol

A

similar to tramadol

similar to oxycodone inits ability to relieve severe pain, but very inexpensive

50
Q

NSAIDs

A

several available with similar pain alleviating effects and adverse reaction profiles

51
Q

NSAID mechanism of action

A
  • inhibit COX, resulting in decresed formation of prostaglandin precursors (PGE2, prostacyclin, and thromboxane) and an inhibition of phospholipids
  • may also inhibit lipoxygenase
  • extent of inhibition varies with each chemicla category
  • produces vasodilation by acting on the heat-regulation center of the hypothalamus
52
Q

Clinical uses of NSAIDs

A

pain relief

reduce inflammation

reduce fever

53
Q

NSAID contraindications

A

active peptic ulcers

chronic inflammation of the GI tract

GI bleeding

history of ulceration

history of sensitivity to ASA or other NSAIDs

54
Q

NSAID pharmacokinetics

A
  • Absorption: rapidly from GI tract
  • Distribution: 90% via protein binding
  • Metabolism: in liver to water soluble metabolite
  • Excretion: urine
  • Half-life: most are 2-4 hours
55
Q

NSAID adverse reactions

A
  • CV: edema
  • DERM: itiching, rash
  • ENDO: fluid retention
  • GI: abdominal pain. cramps, heartburn, constipation, gas, decreased appetite
  • NEURO: dizziness, headache, nervousness
56
Q

NSAID interactions

A

inhibits alpha blockers, ACE inhibitors, ARBs, beta blockers, and diuretics

decreased platelet aggregation with anticoagulants

decreased clearance with aminoglycosides

GI bleed with corticosteroids

57
Q

NSAID conscientious considerations

A

watch for hypersensitivity reactions and renal impairment

do not use in last trimester

stop one week before elective surgery

high doses do not increase effect

58
Q

ASA properties

A

analgesic, antipyretic, anti-inflammatory, antiplatelet

higher doses required for anti-inflammatory effect

59
Q

ASA antiplatelet effect

A

significantly reduces risk of MI and CVA

mearurable prolongation of bleeding time

inhibitory platelt aggregation effect lasts up to 8 days

60
Q

ASA mechanism of action

A

inhibits prostaglandin and thromboxane synthesis

61
Q

salicylism

A

mild, chronic salicylate intoxication after repeated administration of high doses

symptoms: headache, dizziness, tinnitus, hearing loss, mental disturbances, sweating, thirst, hyperventilation, n/v, occasional diarrhea

IMMEDIATE treatment required

62
Q

treatment of salicylism

A

gastric lavage

activated charcoal to absorb drug left in stomach

63
Q

ASA and Reye’s syndrome

A

association exists in children

no ASA under 16yo

64
Q

acetominophen mechanism of action

A

exact site and mechanism not known

possibly inhibits nitric oxide pathway mediated by multiple neurotransmitter receptors, most notable substance P and NMDA

blocks production and release of PGEs into CNS and blocks their effects in the heat-regulating areas of the anterior hypothalamus

65
Q

clinical uses of acetominophen

A

analgesic, antipyretic, mild arthritis, analgesic in those taking anticoagulants or children (not associated with Reyes syndrome)

66
Q

acetominophen contraindications

A

liver disease

allergy

67
Q

acetominophen conscientious considerations

A

risk for hepatotoxicity in malnourished and alcohol abusers

any drug that increases action of liver enzymes may nullify effect

safe in pregnancy and lactation

68
Q
A

Pharmacology (28 decks)

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