Pain Meds Flashcards
Strong/full opioid agonists
- Morphine
- Hydromorphone/Dilaudid
- Oxymorphone
- Methadone –> long acting, Tx of opioid addiction
- Fentanyl, Meperidine –> short acting
mild-moderate/partial agonists
- Codeine ( + acetaminophen = Tylenol #2, 3, 4 )
- Hydrocodone ( + acetaminophen = Vicodin) - most widely prescribed
- Oxycodone ( + acetaminophen = Percocet)
Fentanyl
- IV or transdermal
- only for persistent pain in patients already opioid tolerant
- contra-indicated < 2y/o or under 18 < 110 lbs
Buprenorphine
- partial agonist used as tx for addiction
- analgesia if used alone; if paired with opioid (as in someone with opioid addiction) can precipitate withdrawal reactions
- low abuse potential
Naloxone
- pure opioid antagonist
- used in overdose situations
- IV, IM, Sub Q, Nasal Spray
Opioids IV vs PO
- PO dosage will be higher than IV/IM
- PO is higher dose b/c higher 1st pass effect
Opioids MoA for analgesia
- mimic actions of endogenous opioid peptides; agonists at the mu receptor
Opioid AEs
- respiratory depression (fatal in infants & elderly)
- cough suppression
- constipation/urinary retention
- emesis
- euphoria/dysphoria
- drowsiness/sedation
- orthostatic hypotension
- miosis (pupillary constriction)
Naloxegol Moa/use
- peripherally acting opioid receptor antagonist
- blocks opioid effects in the gut while preserving centrally mediated analgesia; helps with opioid induced constipation
NSAIDs moa
- inhibits COX enzyme that converts arachidonic acid into prostaglandins and related compounds
NSAIDs desired target/outcome
- COX-2 enzyme specificlaly @ sites of inflammation, parts of brain and kidneys
- inhibition causes reduced inflammation, pain and fever
- AEs: renal impairement
ASA moa/AEs
- non-selective irreversible COX-1/2 inhibitor/NSAID
- mild/moderate pain + antipyretic; protects against thrombotic disorders
- AEs: heartburn, nausea, ulceration; bleeding; renal impairment; Reye’s syndrome (avoid ASA use in children < 16 y/o)
ASA interactions & poisoning
- increased bleeding with warfarin, glucocorticoids, alcohol, ibuprofen
- acidosis, hyperthermia, sweating dehydration, resp. failure; treat by cooling, IV bicarbonate to accelerate excretion and reduce acidosis
Ibuprofen moa/use
- non-selective reversible COX-1/2 inhibitor/NSAID
- used for dysmenorrhea, if risk for MI/stroke, arthritis
Ketorolac moa/use
- non-selective reversible cox-1/2 inhibitor/NSAID, powerful analgesic, less anti-inflammatory
- for post operative pain, as effective as morphine
other non-selective/reversible nsaids & BBW
- naproxen
- meloxicam –> some COX-2 selectivity, arthritis; less GI AEs
BBW for all NSAIDs –> increased risk of CV thrombotic events and serious GI bleed
Celecoxib moa/use
- COX-2 specific inhibitors
- analgesic and anti-inflamm
*lower GI toxicity
Celecoxib AEs
- less risk of CVD, but should be avoided
- impaired renal function –> avoid in CKD patients
Acetaminophen/Tylenol moa/use
- moa not fully understood, possible cox-2 inhibition in the CNS
- no anti-inflamm/anti platelet/gastric effects
- used as analgesic & antipyretic; DOC in pregnancy
Acetaminophen/Tylenol AEs
- chronic hepatitis effects (with 4g/day for 14 days)
- overdose –> serious liver injury. esp if heavy alcohol use
*antidote: acetylcystiene/mucomyst which inactivated toxic metabolites
Abortive therapy drugs for migraines
- Triptans (moderate to severe) –> Sumatriptan PO, SQ, nasal spray, transdermal patch
- Ergots (moderate to severe) –> Ergotamine SL & Dihydroergotamine SubQ, IM, IV, nasal
Triptans (sumatriptan) moa
- 5-HT agonist –> potent peripheral vasoconstrictor; blocks development of neurogenic inflammation
- selective for 5HT 1B/1D receptor agonists
Ergots (ergotamine/dihydroergotamine) moa & BBW
- can alter seritoninergic, dopaminergic and alpha adrenergic transmission
- BBW - contraindicated with potent CP3A4 inhibitors –> risk of vasospasm and cerebral ischemia
*contraindicated with ischemic heart disease and in pregnancy (can induce abortion)
Other abortive therapies
- NSAIDs –> mild to moderate migraine, less commonly used acutely
- Acetaminophen + ASA
- Opioids analgesics –> for severe migraine that has not responded to first-line medication
Preventative therapy purpose/types
- to reduce frequency of episodes, esp. when acute medications fail/are being overused
- Beta-blockers –> propranolol
- Tri-cyclic antidepressants –> amitriptyline
- anticonvulsants –> divalproex sodium & topiramate
- Botox
Tri-cyclic antidepressants (amitriptyline) use in migraines
- used at lower dose
- inhibit 5-HT re-uptake which increases serotonin, reducing re-occurrance
Beta-blockers (propranolol) use in migraines
- depresses action potentials
- bind to beta-adrenergic receptors on pial vessels
Anti-convulsants (divalproex sodium & topiramate) use in migraines
- GABA agonist, neuronal hyper-polarization
- usually requires lower dose, slowly taper off
Botox in migraines
- migraine prophylaxis
- acts pre-synaptically –> inhibits ACh release at the NMJ –> cause temporary local paralysis of injected muscle
CGRP agents for migraines
- Erenumab (subQ)
- Ubrogepant & remegepant (PO)
Erenumab
up to 50% reduction in episodes; monoclonal antibody that antagonizes CGRP receptor function
for prevention
Ubrogepant & remegepant
small molecule CGRP receptor antagonist
for acute use
AEs: N/V, tiredness
Anti-emetics
Metoclopramide & Prochlorperazine
(see slide)
