pain meds exam 4 Flashcards by Ashley Maley

where is an endogenous opioid peptide found

in CNS and peripheral tissues

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what are the opioid receptors

Mu, Kappa, Delta

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what mu

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

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what is kappa

activation causes analgesia, sedation, and decreased GI motility

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what effect does delta have

no effect

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how are opioids classified

pure agonistis, agonist - antagonist, pure antagonists

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what is a pure agonist

morphine, codeine, meperidine (Demerol)

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what is an agonist - antagonists

Pentazocine (Talwin), Nalbuphine (Nubain)

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what are pure antagonists

Naloxone (Narcan), naltrexone

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what is a strong opioid agonist

morphine

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what is the MOA of morphine

mimic endogenous opioids and activate mu and kappa receptors

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clinical uses of morphine

relief of moderate to sever pain

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pharmacokinetics of morphine

any route
best to be schedules

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metabolism of morphine

affected by first-pass effect
liver inactivation

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adverse effects of morphine

respiratory depression

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drug interactions with morphine

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

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fentanyl (Duragesic)

strong opioid agonists

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parenteral administration of fentanyl for?

induction and maintenance of anesthesia

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transdermal administration of fentanyl for?

postoperative pain in patients who are opioid tolerant

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metabolism of fentanyl

hepatic bt CYP3A4

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moderate strong opioid agonist examples

codeine, oxycodone, hydrocodone

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main difference of moderate strong opioid agonists

less effective , less abuse potential

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codeine uses

relief of pain, cough suppressant

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codeine pharmacokinetics

PO most common method

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metabolism of codein

liver

adverse effects of codeine

sim to morphine, increase with higher dosage

agonist- antagonist opioid activate what

kappa receptor, and block mu receptors

agonist- antagonist opioid provide?

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

agonist- antagonist opioid could cause?

withdrawal symptoms

pentazocine (talwin)

agonist-antagonist

pentazocine (talwin) MOA

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

pentazocine (talwin) pharmacokinetics

PO admin

pentazocine (talwin) metabolism

short T1/2 ; frequent dosing

pentazocine (talwin) adverse effects

sim to morphine but less resp depression increases cardiac workload

naloxone (Narcan)

opioid anatogonist

naloxone (Narcan) MOA

block the opioid receptor to reverse opioid overdose

naloxone (Narcan) metabolism

hepatic, T1/2 about 2 hours

naloxone (Narcan) adverse effects

none on its own

severe forms of headache

tension type cluster migraine

tension type headaches

headband, non throbbing pain, tightness in head and neck

abortive tmt for tension type headaches

ibuprofen, naproxen, aspring

preventative tmt for tension type headaches

coping, relaxation

cluster headaches

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

abortive tmt for cluster headaches

oxygen, sumatriptan

preventative tmt for cluster headaches

betamethasone, verapamil, lithium

migraine headaches

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

patho of migraine headaches

neurovascular problem - vasodilation and inflammation of the cranial blood vessels

abortive therapy of migraine headaches and prototype:

Triptans : Sumatriptan

Sumatriptan uses

migraines and cluster headaches

Sumatriptan MOA

bind to serotonin receptors causing vasoconstriction

Sumatriptan pharmacokinetics

PO, SQ, inhalation hepatic metabolism with 2.5 half life

adverse effects of Sumatriptan

chest heaviness, angina teratogen

abortive therapy ergot alkaloids protoype

ergotamine

ergotamine uses

migraines and cluster headaches

ergotamine MOA

activation of serotonin receptors blockage of cranial inflammation cranial vasoconstriction

ergotamine pharmacokinetics

PO, SL, PR, inhalation 2 hr half life

ergotamine adverse effects

migraine preventative therapy options

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

what is COX

Cyclooxygenase, an enzyme

what does COX do in the stomach

COX 1 protects gastric mucosa

what does COX do in plateletes

COX 1 stimulates aggregation

what does COX do in uterus

COX 1 contractions at term

what does COX do in kidney

COX 1 and 2 maintains renal blood flow

what does COX do in tissue injury

COX 2 promotes inflammation and pain

what does COX do in vessels

COX 2 vasodilation

what does COX do in brain

COX 2 mediates fever and pain perception

what does COX do in colon

COX 2 colorectal cancer problem

cox inhibitors uses

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

2 major categories of cox inhibitors

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

first gen NSAID prototype

aspirin

aspirin uses

reduction of pain, fever, inflammation

aspirin MOA

irreversibly inhibtes COX 1 and COX 2

aspirin pharmacokinetics

PO short half life

aspirin adverse effects

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

aspirin interactions

warfarin, heparin, alcohol, NSAIDS

aspirin toxicities

salicylism syndrome: tinnitus, sweating, headache, dizziness

ibuprofen (advil, motrin)

first gen NSAID

ibuprofen MOA

reversible inhibition of COX 1 and COX 2

ibuprofen risk

renal impairment

Naproxen (Aleve, Anaprox)

first gen NSAID

Naproxen selective for

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

second gen NSAID Celecoxib (Celebrex) MOA

inhibit COX 2 only

Celecoxib (Celebrex) uses

arthirits, acute pain, dysmenorrhea

Celecoxib (Celebrex) not a good option for who

pts with heart disease

Non- anti - inflammatory prototype:

acetaminophen (tylenol)

acetaminophen (tylenol) uses

analgesia antipyretic no anti-inflammatory effects

acetaminophen (tylenol) MOA

COX inhbition

acetaminophen (tylenol) pharmacokinetics

PO, PR, IV

acetaminophen (tylenol) metabolism

in liver in 2 pathways

major pathway acetaminophen (tylenol) metabolism

simple, acetaminophen converted directly into nontoxic metabolites

minor pathway acetaminophen (tylenol) metabolism

CYP450 converts acetaminophen to a toxic metabolite

acetaminophen (tylenol) toxicity