Pharm 11 Flashcards
MOA of local anesthetics (LA’s)
Block voltage-dependent sodium channels
This may enhance activity of local anesthetics
Hyperkalemia
This may antagonize activity of local anesthetics
Hypercalcemia
Almost all local anesthetics have this property and sometimes require the administration of vasoconstrictors (ex. Epinephrine) to prolong activity
Vasodilation
Local anesthetic with vasoconstrictive property, favored for head, neck, and pharyngeal surgery
Cocaine
Longer acting local anesthetics which are less dependent on vasoconstrictors
Tetracaine and bupivacaine
These LA’s have surface activity
Cocaine and benzocaine
Most important toxic effects of most local anesthetics
CNS toxicity
Commonly abused LA which has cardiovascular toxicity including severe hypertension with cerebral hemorrhage, cardiac arrhythmias, and myocardial infarction
Cocaine
LA causing methemoglobinemia
Prilocaine
Structurally related to acetylcholine, used to produce muscle paralysis in order to facilitate surgery or artifical ventilation. Full doses lead to respiratory paralysis and require ventilation
Neuromuscular blocking drugs
These drugs strongly potentiate and prolong effect of neuromuscular blockade (NMB)
Inhaled anesthetics, especially isoflurane, aminoglycosides, and antiarrhythmic
These prevent the action of Ach at the skeletal muscle endplate to produce a “surmountable blockade,” effect is reversed by cholinesterase inhibitors (ex. neostigmine or pyridostigmine)
Nondepolarizing type antagonists
Agent with long duration of action and is most likely to cause histamine release
Tubocurarine
Non-depolarizing antagonist has short duration
Mivacurium
Agent blocking muscarinic receptors
Pancuronium
Agent undergoing Hofmann elimination (breaking down spontaneously)
Atracurium
Depolarizing blocker –> continuous depolarization –> muscle relaxation and paralysis, also causes muscle pain postoperatively and myoglobinuria may occur
Succinylcholine
During Phase I these agents worsen the paralysis by succinylcholine, but during phase II they reverse the blockade produced by succinylcholine
Cholinesterase inhibitors
Agents acting in the CNS or in the skeletal muscle, used to reduce abnormally elevated tone caused by neurologic or muscle end plate disease
Spasmolytic drugs
Facilitates GABA presynaptic inhibition
Diazepam
GABA agonist in the spinal cord
Baclofen
Similar to clonidine and may cause hypotension
Tizanidine
Agent used for acute muscle spasm
Cyclobenzaprine
Agent used in drug therapy of Parkinson’s instead of Dopamine which has low bioavailability and does not cross the BBB
L-dopa
This is combined with L-dopa, inhibits DOPA decarboxylase (active only peripherally) which allows lower effective doses of L-dopa and allows for fewer SE’s (GI distress, postural hypotension, and dyskinesias)
Carbidopa
Clinical response that may fluctuate in tx of Parkinson’s dx
“On-off-phenomenon”
Anti-Parkinson’s drug which increases intraocular pressure and is contraindicated in closed angle glaucoma
Levodopa
Ergot alkaloid that is a partial agonist at D2 receptors in the brain, used for patients who are refractory or cannot tolerate levodopa, causes erythromelalgia
Bromocriptine
Non ergot agents used as first-line therapy in the initial management of Parkinson’s
Pramipexole and ropinirole
Sedative-Hypnotics action
Reduce inhibition, suppress anxiety, and produce relaxation
Additive effects when Sedative-Hypnotics used in combination with these agents
CNS depressants
Common mechanism by which overdose result in death
Depression of medullary and cardiovascular centers
The most important sign of withdrawal syndrome
Excessive CNS stimulation (seizures)
