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Clinical Pharmacology > Local anesthetics > Flashcards

Local anesthetics Flashcards

1
Q

What blocks sensory transmission from a specific region of the body to the CNS?

A

local anesthetic

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2
Q

What was the first local anesthetic?

A

cocaine

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3
Q

What’s the MOA of local anesthetics?

A

reduce influx of sodium ions

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4
Q

What is the order of the sensory blockade?

A

sympathetic function –> pain (pinprick) –> temperature –> touch/deep pressure –> motor

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5
Q

What are local anesthetics clinically utilized?

A

minor surgical procedures (lidocaine) commonly with vasoconstrictors (epinephrine) to prolong duration which is more afe

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6
Q

What can repeated epidural injection in anesthetic doses lead to?

A

tachyphylaxis

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7
Q

What are CNS effects of local anesthetics?

A

light-headedness sedation, restlessness, nystagmus, tonic-clonic convulsions
severe = respiratory/cardiovascular depression

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8
Q

What are cardiovascular effects?

A

vasodilators (except cocaine)
bupivacaine = severe toxicity, hypotension

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9
Q

What are other effects to consider?

A

allergic responses, or neurotoxic action

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10
Q

What are neuromuscular blockers?

A

bind to nicotinic receptors at neuromuscular junction, either polarizing or nondepolarizing
(only de = succinylcholine)
nonde=”cur” = antagonists

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11
Q

What is malignant hyperthermia?

A

hyperthemia from massive release of calcium from sacroplasmic reticulum = uncontrolled contraction and metabolism stimulation in skeletal muscle

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12
Q

What are depolarizing NMBs?

A

2ACh molecules linked end to end
initial: twitching and fasciculations –> muscle relaxation and paralysis

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13
Q

How does the effect of succinylcholine change in depolarizing NMBs?

A

continuous depolarization –> gradual repolarization w/ resistance to depolarization

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14
Q

What is key about depolarizing NMBs?

A

two phases: transient fascicultations from depolarization followed by flaccid paralysis and then when membrane repolarizes it is desentizied

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15
Q

how to reverse depolarizing NMBs?

A

paralysis is INCREASED by cholinesterase inhibitors (phase 1) –> reversible in phase II

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16
Q

What are ADRs of depolarizing NMBs?

A

muscle pain, hyperkalemia, increase in intragastric pressure, HR decrease

17
Q

Do nondepolarizing NMBs cross blood brain barrier?

A

no

18
Q

What’s a good nondepolarizing NMB for kidney disease?

A

cisatracurium, also most commonly used

19
Q

What’s the nondepolarizing NMB MOA?

A

prevent action of ACh at skeletal muscle, competing with AcH

20
Q

What’s the fastest nondepolarizing NMB?

A

rocuronium has the most rapid onset time

21
Q

What’s the antagonist/reversal for nondepolarizing NMB?

A

increasing AcH, or sugammadex for rocuronium

22
Q

What are ADRs of nondepolarizing NMBs?

A

respiratory paralysis — MUST PROVIDE MECHANICAL VENTILATION!!!!!
tachycardia
histamine release

23
Q

What are spasmolytics?

A

drugs that reduce abnormal elevated muscle tone (spasm) w/o paralysis or reduction of strength

24
Q

Do spasmolytics act in CNS or cell?

A

CNS

25
Q

What are some spasmyolitc drugs?

A

diazepam (benzo), baclofen (GABA agonist), tizanidine, dantrolene, botulinum toxin, gabapentin/pregabalin
most PO
acute = cyclobenzaprine

26
Q

How does diazepam work?

A

GABAa synapses, partly in spinal cord, but strong sedation

27
Q

How does baclofen work?

A

orally GABA-mimetic and agonist at GABAb receptors – less sedation, reduces spasticity, but can be drowsy and increased seizure and risk with pregnancy

28
Q

How does tizanidine work?

A

a2 agonist, less muscle weakness, with drowsiness, hypotension, dizziness, dry mouth, dose must be adjusted in patients w/ hepatic or renal impairment

29
Q

How does dantrolene work?

A

reduces muscle strength, used to treat malignant hyperthermia (succinylcholine/tubocurarine)

30
Q

How does cyclobenzaprine work?

A

in brain stem, interfering w/ polysynaptic reflexes, marked sedative and antimuscarinic actions, serotonin syndrome, NOT in cerebral palsy

Clinical Pharmacology (14 decks)

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