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Pharmacology > pain meds exam 4 > Flashcards

pain meds exam 4 Flashcards

1
Q

where is an endogenous opioid peptide found

A

in CNS and peripheral tissues

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2
Q

what are the opioid receptors

A

Mu, Kappa, Delta

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3
Q

what mu

A

activation causes analgesia, respiratory depression, euphoria, sedation, decreased GI motility, and eventual physical dependence

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4
Q

what is kappa

A

activation causes analgesia, sedation, and decreased GI motility

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5
Q

what effect does delta have

A

no effect

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6
Q

how are opioids classified

A

pure agonistis, agonist - antagonist, pure antagonists

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7
Q

what is a pure agonist

A

morphine, codeine, meperidine (Demerol)

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8
Q

what is an agonist - antagonists

A

Pentazocine (Talwin), Nalbuphine (Nubain)

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9
Q

what are pure antagonists

A

Naloxone (Narcan), naltrexone

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10
Q

what is a strong opioid agonist

A

morphine

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11
Q

what is the MOA of morphine

A

mimic endogenous opioids and activate mu and kappa receptors

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12
Q

clinical uses of morphine

A

relief of moderate to sever pain

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13
Q

pharmacokinetics of morphine

A

any route
best to be schedules

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14
Q

metabolism of morphine

A

affected by first-pass effect
liver inactivation

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15
Q

adverse effects of morphine

A

respiratory depression

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16
Q

drug interactions with morphine

A

CNS depressants, anticholinergics, antihypertensives, agonist-antagonists, antagonists

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17
Q

fentanyl (Duragesic)

A

strong opioid agonists

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18
Q

parenteral administration of fentanyl for?

A

induction and maintenance of anesthesia

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19
Q

transdermal administration of fentanyl for?

A

postoperative pain in patients who are opioid tolerant

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20
Q

metabolism of fentanyl

A

hepatic bt CYP3A4

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21
Q

moderate strong opioid agonist examples

A

codeine, oxycodone, hydrocodone

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22
Q

main difference of moderate strong opioid agonists

A

less effective , less abuse potential

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23
Q

codeine uses

A

relief of pain, cough suppressant

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24
Q

codeine pharmacokinetics

A

PO most common method

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25
Q

metabolism of codein

A

liver

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26
Q

adverse effects of codeine

A

sim to morphine, increase with higher dosage

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27
Q

agonist- antagonist opioid activate what

A

kappa receptor, and block mu receptors

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28
Q

agonist- antagonist opioid provide?

A

analgesia without as many side effects as pure agonist, less potential for abuse

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29
Q

agonist- antagonist opioid could cause?

A

withdrawal symptoms

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30
Q

pentazocine (talwin)

A

agonist-antagonist

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31
Q

pentazocine (talwin) MOA

A

activates kappa receptors causing analgesia, sedation, and limited respiratory depression

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32
Q

pentazocine (talwin) pharmacokinetics

A

PO admin

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33
Q

pentazocine (talwin) metabolism

A

short T1/2 ; frequent dosing

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34
Q

pentazocine (talwin) adverse effects

A

sim to morphine but less resp depression
increases cardiac workload

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35
Q

naloxone (Narcan)

A

opioid anatogonist

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36
Q

naloxone (Narcan) MOA

A

block the opioid receptor to reverse opioid overdose

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37
Q

naloxone (Narcan) metabolism

A

hepatic, T1/2 about 2 hours

38
Q

naloxone (Narcan) adverse effects

A

none on its own

39
Q

severe forms of headache

A

tension type
cluster
migraine

40
Q

tension type headaches

A

headband, non throbbing pain, tightness in head and neck

41
Q

abortive tmt for tension type headaches

A

ibuprofen, naproxen, aspring

42
Q

preventative tmt for tension type headaches

A

coping, relaxation

43
Q

cluster headaches

A

less common, 15mnin-2hrs,
unlateratl pain near eye, lacrimation, ptosis, nasla congestion, rhinorrhea

44
Q

abortive tmt for cluster headaches

A

oxygen, sumatriptan

45
Q

preventative tmt for cluster headaches

A

betamethasone, verapamil, lithium

46
Q

migraine headaches

A

throbbing moderate -severe pain that may be unilateral or bilateral,
last for days
N/V

47
Q

patho of migraine headaches

A

neurovascular problem - vasodilation and inflammation of the cranial blood vessels

48
Q

abortive therapy of migraine headaches and prototype:

A

Triptans : Sumatriptan

49
Q

Sumatriptan uses

A

migraines and cluster headaches

50
Q

Sumatriptan MOA

A

bind to serotonin receptors causing vasoconstriction

51
Q

Sumatriptan pharmacokinetics

A

PO, SQ, inhalation
hepatic metabolism with 2.5 half life

52
Q

adverse effects of Sumatriptan

A

chest heaviness,
angina
teratogen

53
Q

abortive therapy ergot alkaloids protoype

A

ergotamine

54
Q

ergotamine uses

A

migraines and cluster headaches

55
Q

ergotamine MOA

A

activation of serotonin receptors
blockage of cranial inflammation
cranial vasoconstriction

56
Q

ergotamine pharmacokinetics

A

PO, SL, PR, inhalation
2 hr half life

57
Q

ergotamine adverse effects

A
58
Q

migraine preventative therapy options

A

1) Beta Blockers - propranolol ~ tiredness
2) Antiepileptics - topiramate ~ fatigue
3) Tricyclic antidepressant - amitriptyline ~ hypotension/ SLUDGE

59
Q

what is COX

A

Cyclooxygenase, an enzyme

60
Q

what does COX do in the stomach

A

COX 1 protects gastric mucosa

61
Q

what does COX do in plateletes

A

COX 1 stimulates aggregation

62
Q

what does COX do in uterus

A

COX 1 contractions at term

63
Q

what does COX do in kidney

A

COX 1 and 2 maintains renal blood flow

64
Q

what does COX do in tissue injury

A

COX 2 promotes inflammation and pain

65
Q

what does COX do in vessels

A

COX 2 vasodilation

66
Q

what does COX do in brain

A

COX 2 mediates fever and pain perception

67
Q

what does COX do in colon

A

COX 2 colorectal cancer problem

68
Q

cox inhibitors uses

A

mild/mod pain
inflammation
fever
pre mense symptoms
protection against colon cancer

69
Q

2 major categories of cox inhibitors

A

anti inflammatories (NSAIDS- aspirin, ibuprofen, naproxen, celecoxib)
non anti - inflammatories (acetaminophen)

70
Q

first gen NSAID prototype

A

aspirin

71
Q

aspirin uses

A

reduction of pain, fever, inflammation

72
Q

aspirin MOA

A

irreversibly inhibtes COX 1 and COX 2

73
Q

aspirin pharmacokinetics

A

PO short half life

74
Q

aspirin adverse effects

A

GI distress, bleeding, ulcers, renal impairment, salicylism syndrome, hypersensitivity

75
Q

aspirin interactions

A

warfarin, heparin, alcohol, NSAIDS

76
Q

aspirin toxicities

A

salicylism syndrome: tinnitus, sweating, headache, dizziness

77
Q

ibuprofen (advil, motrin)

A

first gen NSAID

78
Q

ibuprofen MOA

A

reversible inhibition of COX 1 and COX 2

79
Q

ibuprofen risk

A

renal impairment

80
Q

Naproxen (Aleve, Anaprox)

A

first gen NSAID

81
Q

Naproxen selective for

A

COX 1, less incidence of GI problems , half life 12-17hrs

82
Q

second gen NSAID Celecoxib (Celebrex) MOA

A

inhibit COX 2 only

83
Q

Celecoxib (Celebrex) uses

A

arthirits, acute pain, dysmenorrhea

84
Q

Celecoxib (Celebrex) not a good option for who

A

pts with heart disease

85
Q

Non- anti - inflammatory prototype:

A

acetaminophen (tylenol)

86
Q

acetaminophen (tylenol) uses

A

analgesia
antipyretic
no anti-inflammatory effects

87
Q

acetaminophen (tylenol) MOA

A

COX inhbition

88
Q

acetaminophen (tylenol) pharmacokinetics

A

PO, PR, IV

89
Q

acetaminophen (tylenol) metabolism

A

in liver in 2 pathways

90
Q

major pathway acetaminophen (tylenol) metabolism

A

simple, acetaminophen converted directly into nontoxic metabolites

91
Q

minor pathway acetaminophen (tylenol) metabolism

A

CYP450 converts acetaminophen to a toxic metabolite

92
Q

acetaminophen (tylenol) toxicity

A

Pharmacology (8 decks)

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