analgesics Flashcards
(22 cards)
narcotic analgesics
narcotic, opiate/opioid terms are reserved for drugs(natural & synthetic) derived from the unripe opium poppy
eg. morphine, codeine
opiate analgesics
opium contains >20 alkaloids- morphine was the first extracted, more addictive than opium as a whole
primary use is to relieve intense pain
MOA- bind to specific opioid receptors to produce similar effects as endogenous transmitters- opiopeptins(including endorphins & enkephalins). interfere directly with the transmssion & the perception of pain
hyperpolarization of nerve cells = inhibition of nerve firing
pre-synaptic ihibition of pain mediators- substance-P
opioid receptors
distributed widly in brain, spinal cord, peripheral nervous system & GI
5 families of receptors with varying specificity for the drugs:
mu- primarily analgesic receptors
kappa
sigma- least selective, hallucinogen & phencyclidine
delta- enkephalins
epsilon
morphine/ MS contin
opioid analgesic
for pain relief, anxiety/pain relief in acute MI
potent opioid agonist, high affinity for Mu receptors. raises pain threshold at brain stem, thalmic & spnal cord. also alters brains perception of pain.
PO, PR, IM, IV- duration varies by route- tolerance to dosing lvl develops
SE- resp. depression- decreased sensory neurons to carbon dioxide(MC death), enhanced parasympathetic stim = pinpoint pupils(miosis), itching from histamine release, N/V, constipation
fentanyl/ duragesic
opioid analgesic
pain relief, anesthesia
MOA- similar to morphine but with 80x the analgesic property- used for anesthesia & intractable pain
IV, trandermal patch, lollypop, onset w/in minutes, duration 15-30min
SE- resp. depression, N/V, constipation, highly addictive
danger for use with CYP450 drugs, may cause fatal blood levels
codeine
opioid analgesic
pain relief, anti-tussive
MOA- opioid agonist, much weaker than morphine
PO, IV, IM, SQ- lower abuse potential- supresses cough at much lower dosing than needed for anlagesic dose
SE= sedation, constipation
tramadol/ ultram
centrally acting anagesic- for moderate to severe pain
MOA- ***mild Mu receptoragonist, affects reuptake at noradrenergic & serotonergic systems
SE resp. depression
acetaminophen containing narcotic analgesics
acetaminophen +: codeine = tyelonol 3 & 4 hydrocodone = vicodin, lortab oxycodone= percocet, roxicet propoxyphene= darvocet tramadol= ultraset
NSAID containing narcotic analgesics
oxycodone + aspirin= percodan
oxycodone + ibuprofen= combunox
hydrocodone + ibuprofen= vicoprofen
heroin
does not exsist naturally
produced by the acetylation of morphine = 2-3 fold increase in its potentcy, more lipid soluble(easier to cross the BBB)= greater sense of euphoria than morphine
CATEGORY I
methadone
synthetic opioid
less potent, less feeling of euphoris
used for controlled withdrawl of heroin & morphine addicted pts
dependence can devlop, but has less withdrawl ssx
naloxone/ narcan
opioid antagonist
for opioid OD. reverses coma & resp. depression
MOA- bind with high affinity to opioid receptors, but do not activate the mediated response
PO, IV. onset within 30 sec. 60-100 min half life, may need several doses to get the drug out of system
dextromethorphan
dextro-isomer of codeine
effective antitussive used in OTC cough neds
**little to no analgesic, sedative or GI effects
NSAIDS
inhibit synthesis of prostaglandins(eicosanoids) from aracadonic acid via inhibition of COX 1 & 2.
COX 1 is primarily involved in the production of prostaglandins that support platelets & protect the stomach
aspirin/ acetylsalicylic acid(ASA)
NSAID
for inflammation, pain, fever
PO, PR, readily absorbed, metabolized by liver, excreted in urine
SE- primarily GI iritation, PUD, N/V, inc risk of bleeding, renal insuff, REYE’s SYNDROME
**salicylism- dizziness, tinnitus, hyperventilation, mental status chx potential for coma & death- tx = IV hydration, alkalinization of urine & dialysis if renal insufficiency occurs
aspirin MOA
irreversible inhibiton of COX 1 & 2 enzymes. blockade of prostaglandin synthesis at target tissues. anti-pyretic effect due to blokade of prostaglandins at thermoregulatory centers in hypothalamus
prostaglandin E2 sensitizes nerve endings to bradykinins, histamine & other inflammatory mediators- so ASA diminishes pain by decreasing tissue sensitivity to the sensation of pain
Ibuprofen/ motrin, advil
NSAID
for inflammation, fever, pain
MOA- reversible inhibition of COX 1 & 2.
PO, PR- no risk for reye’s
celecoxib/celebrex
NSAID
inflammation, pain, tx of adenomatous polyps
MOA- reversible, SELECTIVE COX-2 inhibition
PO, minimal GI effects, less bleeding & no inhibition of platelet agg
SE- unclear if there is inc risk for CVD
Acetaminophen/ tylenol
NSAID
for pain, fever
MOA- not fully understood. weak peripheral blockade of prostaglandin synthesis, stronger in hypothalmus- **NO action on COX 1&2 inhib
PO, PR
SE- OD or taken with alcohol can lead to severe hepatic necrosis= liver failure & death
NEVER MIX ALCOHOL & TYLENOL!!
max safe dose for healthy adults= 4gm/24hrs
category B
acetominophen toxicity
metabolized via P450 in liver to toxic N-acetyl-p-benzoquinone-imine(NAPQI)- has a short half life, normally conjugated by glutathiaone(sulfhydryl donor)and excreted in urine. reduced glut stores & NAPQI will bind to vital proteins & the lipid bilayer of hepatocytes= hepatocellular death & liver necrosis
the course of acetaminophen toxicity
4 stages- directly correlates to hepatocyte death:
stage 1: 12-24hrs- N/V
stage 2: 24-48hrs- rising AST, ALT, bilirubin levels
stage 3: 72-96hrs- peak hepatotoxicity, AST may exceed 20,000
stage 4: 96hrs+ - recovery, need for liver transplant, or death
antidote- NAC by IV ASAP(within 8hrs)- augments glutathione stores
relative potency to morphine
less potent: aspirin< dextropropoxyphene< tramadol< hydrocodone
greater potency:
oxycodone< methadone< morphine(IV/IM)< diacetylmorphine(heroin)< hydromorphone< oxymorphone< levorphanol< buprenorphine< FENTANYL< sufentanyl
**fentanyl is 80X more potent than oral morphine
