Local anesthetics Flashcards
What blocks sensory transmission from a specific region of the body to the CNS?
local anesthetic
What was the first local anesthetic?
cocaine
What’s the MOA of local anesthetics?
reduce influx of sodium ions
What is the order of the sensory blockade?
sympathetic function –> pain (pinprick) –> temperature –> touch/deep pressure –> motor
What are local anesthetics clinically utilized?
minor surgical procedures (lidocaine) commonly with vasoconstrictors (epinephrine) to prolong duration which is more afe
What can repeated epidural injection in anesthetic doses lead to?
tachyphylaxis
What are CNS effects of local anesthetics?
light-headedness sedation, restlessness, nystagmus, tonic-clonic convulsions
severe = respiratory/cardiovascular depression
What are cardiovascular effects?
vasodilators (except cocaine)
bupivacaine = severe toxicity, hypotension
What are other effects to consider?
allergic responses, or neurotoxic action
What are neuromuscular blockers?
bind to nicotinic receptors at neuromuscular junction, either polarizing or nondepolarizing
(only de = succinylcholine)
nonde=”cur” = antagonists
What is malignant hyperthermia?
hyperthemia from massive release of calcium from sacroplasmic reticulum = uncontrolled contraction and metabolism stimulation in skeletal muscle
What are depolarizing NMBs?
2ACh molecules linked end to end
initial: twitching and fasciculations –> muscle relaxation and paralysis
How does the effect of succinylcholine change in depolarizing NMBs?
continuous depolarization –> gradual repolarization w/ resistance to depolarization
What is key about depolarizing NMBs?
two phases: transient fascicultations from depolarization followed by flaccid paralysis and then when membrane repolarizes it is desentizied
how to reverse depolarizing NMBs?
paralysis is INCREASED by cholinesterase inhibitors (phase 1) –> reversible in phase II
What are ADRs of depolarizing NMBs?
muscle pain, hyperkalemia, increase in intragastric pressure, HR decrease
Do nondepolarizing NMBs cross blood brain barrier?
no
What’s a good nondepolarizing NMB for kidney disease?
cisatracurium, also most commonly used
What’s the nondepolarizing NMB MOA?
prevent action of ACh at skeletal muscle, competing with AcH
What’s the fastest nondepolarizing NMB?
rocuronium has the most rapid onset time
What’s the antagonist/reversal for nondepolarizing NMB?
increasing AcH, or sugammadex for rocuronium
What are ADRs of nondepolarizing NMBs?
respiratory paralysis — MUST PROVIDE MECHANICAL VENTILATION!!!!!
tachycardia
histamine release
What are spasmolytics?
drugs that reduce abnormal elevated muscle tone (spasm) w/o paralysis or reduction of strength
Do spasmolytics act in CNS or cell?
CNS
What are some spasmyolitc drugs?
diazepam (benzo), baclofen (GABA agonist), tizanidine, dantrolene, botulinum toxin, gabapentin/pregabalin
most PO
acute = cyclobenzaprine
How does diazepam work?
GABAa synapses, partly in spinal cord, but strong sedation
How does baclofen work?
orally GABA-mimetic and agonist at GABAb receptors – less sedation, reduces spasticity, but can be drowsy and increased seizure and risk with pregnancy
How does tizanidine work?
a2 agonist, less muscle weakness, with drowsiness, hypotension, dizziness, dry mouth, dose must be adjusted in patients w/ hepatic or renal impairment
How does dantrolene work?
reduces muscle strength, used to treat malignant hyperthermia (succinylcholine/tubocurarine)
How does cyclobenzaprine work?
in brain stem, interfering w/ polysynaptic reflexes, marked sedative and antimuscarinic actions, serotonin syndrome, NOT in cerebral palsy
