Final Exam Drug MOA, indications, side effects, PK/PD Flashcards
agonist antagonist drugs
pentazocine butorphanol nalbuphine buprenorphine nalorphine
Mu1 receptor effects
analgesia euphoria miosis bradycardia urinary retention
Mu2 receptor effects
analgesia
respiratory depression
physical dependence
constipation
Kappa Receptor Effects
analgesia dysphoria, sedation low abuse potential miosis diuresis
delta receptor effects
analgesia respiratory depression physical dependence constipation urinary retention
Morphine MOA Onset T1/2 Vd metabolism metabolite SE contraindications
agonist at opioid receptors at presynaptic and postsynaptic sites in CNS (brain and SC) that are normally activated by endogenous ligands. opioids mimic these ligands to modulate pain.
ex) enkephalins, endorphins, dynorphins. most effective against slow dull pain.
Onset 15-30min
elimination t1/2 1.5-3h
Vd large
poor lipid solubility
mostly ionized
conjugated by the liver
metabolite morphine 6 glucoronide
-histamine release, accumulation of metabolite in impaired renal function, respiratory depression.
contraindications: acute pancreatitis, cholecystectomy, renal patients, older population
Meperidine MOA, uses potency Elimination t1/2 Vd duration of action metabolism SE contraindications
kappa and mu agonist
anti shivering postop
1/10 as potent as morphine
elimination t1/2 3-5h
duration of action 2-4h
large
first pass metabolism demethylization (normeperidine) and hydrolysis (meperidinic acid) (phase 1)
-normeperidine metabolite t1/2 15h (greater than 30h in renal failure)
structurally similar to atropine. increased HR, mydriasis, delirium, seizures. in high doses, negative inotropic effects or histamine release
-contraindications: renal patients, patients taking MAOI’s or fluoxetine r/t serotonin syndrome
fentanyl t1/2 context sensitive half time Vd metabolism SE
elimination t1/2 3-6h
increases with infusions greater than 2h, or 260minutes
large Vd
lipid soluble
redistribution
first pass uptake in lungs
secondary peaks
metabolized by n dealkylation and hydroxylation (phase 1)
no active metabolites
-can see bradycardia, increased ICP, myoclonus
alfentanil potency t1/2 context sensitive t1/2 Vd duration of action metabolism SE contraindications
elimination half time 1.5h
least potent, fastest onset due to high fraction of un ionization
60 minutes
small
nonionized
short duration of action
metabolized by piperidine n dealkylation and amide n dealkylation (phase 1)
-hypotension, dystonia, less potent than fent
-contraindicated in parkinsons
remifentanil t1/2 metabolism Vd context sensitive half time SE
t1/2 15-30min
- hydrolysis by nonspecific plasma esterases, no active metabolites, ester linkage
- small Vd
- context sensitive half time 4 minutes
- SE: can induce seizure like activity, decrease BP, hyperalgesia (give ketamine or mag)
sufentanil potency t1/2 metabolism metabolite Vd context sensitive half time SE contraindications
t1/2 2.4-5h -5-10x more potent than fentanyl -Protein binding (alpha 1 glycoprotein) Highly lipid soluble Metabolized by N-dealkylation and O-demethylation (phase 1) Some activity Clearance sensitive to hepatic flow -metabolite desmethyl sufentanil -Vd large -context sensitive t1/2 30min -SE: more potent than fentanyl. may cause chest wall rigidity. first pass pulm uptake contraindications: avoid in renal patients
butorphanol MOA, SE**
-Low affinity for Mu receptor – produces antagonism
Moderate affinity for Kappa receptor – analgesia and anti-shivering
-Dysphoria “doesn’t feel right”
Increase in catecholamine response (increased HR, CO, BP)
Limits effects of concomitant opioid agonists
nalbuphine MOA, SE
-Antagonist effect at Mu receptor
chemically related to naloxone
If given before opioid – diminish effects of morphine-like drugs
If given after opioid – can reverse depression of ventilation effects but maintain analgesia
-Catecholamine stimulation effects – beneficial for cardiac patients
Less dysphoria than pentazocine and butorphanol
edrophonium MOA, t1/2, SE, onset
build up Ach at NMJ, give with atropine.
t1/2 30min-2h
-SE: bronchoconstriction, salivation, lacrimation, bradycardia
-onset 30-60seconds
neostigmine MOA, half life, SE, onset
build up ach at NMJ. give with glycopyrrolate
t1/2: 1-2h
SE: increased bowel motility, urination, bradycardia
onset: 1 minute
acetaminophen MOA, uses metabolism metabolites half life consideration
antagonism of NMDA, substance P and NO pathways. activates serotonergic pathway.
- analgesic and antipyretic
- metabolized in liver
- n acetyl p benzoquinoneimine=liver failure by depleting glutathione
- t1/2 2-3h
- IV form is expensive
ibpruphen
metabolism
half life
through oxidation
t1/2 2-2.5h
ketorlac Vd metabolism half life considerations
- weak acid, increased protein binding
- low Vd
- conjugated
- 2.5-8.5h
- most commonly used periop
