N926 Pharmacology Final Exam Second Half Flashcards
MOA of Butorphanol
antagonism at mu receptor and antagonist at kappa receptor
MOA of nalbuphine
Antagonism at mu receptor
Nalbuphine is 1/4 antagonist of
morphine
Acetaminophen has both
analgesic and antipyretic properties
PK of Acetaminophen
metabolized in the liver
damage to liver results from N-acetyl-p-benzoquinonemine
liver failure by depleting gluthathione
Dose of Acetaminophen
325-600mg PO q6h
Total not to exceed 4000mg/24 hr
2000mg for chronic alcoholics
IV-1000mg q6h
Acetaminophen Anesthetic considerations
use in multimodal approach but not in liver patients
MOA of Ibuprofen
nonselective COX inhibitor
Dosing of Ibuprofen
200-800mg PO q4-6h
Anesthetic Considerations of Ibuprofen
use in multi-modal approach
Ketorolac is common
used for perioperatively
Dosing of Ketorolac
15mg IV q6h
Ketorolac must be avoided
in renally compromised patients
MOA of Celecoxib
Selective COX 2 inhibitor
Dosing of Celecoxib
400mg PO preoperatively
200mg BID x 5 days post op
Risks of Celecoxib
increased cardiovascular risk
When is Celecoxib used?
ERAS protocol
Part of multi-modal pain management; give in pre-op
MOA of Succinylcholine
Depolarizing neuromuscular blocked on nACHr
partial agonist
PK of Succinylcholine
low Vd d/t quaternary ammonium (polar molecule)
metabolized by PChE (succinylmonocholine and choline)
first order kinetics
PD of Succinylcholine
Neuro: increases ICP/ IOP
Cardiac: may cause bradycardia, tachycardia, ventricular dysrhythmias, and increased BP, junctional rhythm sinus arrest (action on muscarinic receptors)
Side Effects of Succinylcholine
increase K level by 0.5mg/dl
Risk for MH and don’t administer to children
increasing intragastic pressure (GERD pts)
Myalgias
masseter spasm
Dosing of Succinylcholine
1mg/kg of IBW
When can you intubate after administering Succinylcholine
60 seconds
Recover to 90% muscle strength of Succinylcholine
9-13 minutes
MOA of Atracurium
benzylisoquinium non-depolarizing NMD (antagonist)
PK of Atracurium
racemic mixture of 10 isomers
metabolized by ester hydrolysis and Hoffman elimination
(Laudanosine active metabolite implicated in convulsions)
non-liver dependent for metabolism, okay to use in liver pts
Small volume of distribution
PD of Atracurium
Histamine Release
May block peripheral nACHr causing bradycardia and hypotension
Dosing of Atracurium
0.5 mg/kg (intermediate acting onset)
MOA of Cisatracurium
Benzlisoquinium non-depolarizing NMBD (antagonist)
PK of Cisatracurium
cis isomer of atracurium
metabolized by Hoffmann elimination (good for liver and kidney patients)
Dose of Cisatracurium
0.1mg/kg (intermediate onset and action)
MOA of Pancuronium
Steroidal compoound nondepolarizing NMBD (antagonist)
PK of Pancuronium
deacetylated by liver
Accumulation of 3-OH metabolite prolongs block)
Cleared by Kidney
- don’t use in renal patient s
PD of Pancuronium
vagolytic (inhibits the vagus nerve/ blocks muscarinic receptors) and PChE-inhibiting properties
may block peripheral nAChR causing bradycardia and hypotension
Dose of Pancuronium
0.08mg/kg with onset time of 2.9 minutes (not for RSI)
MOA of Vecuronium
Steroid compound non-depolarizing NMBD (antagonist)
PK of Vecuronium
Pancuronium without quaternized methyl group (increased lipid solubility)
metabolized principally by the liver (3-deacteyl metbolite has 80% of neuromuscular potency)