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STEP 1 > Anesthetic Drugs > Flashcards

Anesthetic Drugs Flashcards

1
Q

How does lipid solubility impact anesthesia

A

CNS drugs must be lipid soluble (cross the BBB) or be actively transported

drugs with low solubility in blood = rapid induction and recovery times
drugs with high solubility in lipids = increased potency = 1/MAC

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2
Q

What is MAC?

A

minimal alveolar concentration required to prevent 50% of subjects from moving in response to noxious stimulus

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3
Q

Inhaled anesthetic examples

A

N2O has decreased blood and lipid solubility and thus fast induction and low potency
Halothane has high lipid and blood solubility and thus high potency and slow induction

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4
Q

Name the inhaled anesthetics

A

halothan, enflurance, isoflurance, sevoflurane, methoxyflurane, N2O

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5
Q

Effects of inhaled anesthetics

A

myocardial depression
respiratory depression
nausea/emesis
increased cerebral blood flow (decreased cerebral metabolic demand)

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6
Q

Toxicity of halothane

A

hepatotoxicity

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7
Q

Toxicity of methoxyflurane

A

nephrotoxicity

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8
Q

Toxicity of enflurane

A

proconvulsant

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9
Q

Toxicity of N2O

A

expansion of trapped gas in body cavity (not good for GI surgeries)

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10
Q

What is malignant hypertermia?

A

rare, life-threatening hereditary condition in which inhaled anesthetics and succinylcholine induce fever and severe muscle contractions (can see cyanotic skin mottling)

Tx: dantrolene

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11
Q

Properties of barbiturates as IV anesthetic

A

thiopental - high potency, high lipid solubility, rapid entry into brain

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12
Q

Use of barbiturate for IV anesthetic

A

induction of anesthesia and short surgical procedures
effect terminated by rapid redistribution into tissue and fat
decreased cerebral blood flow

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13
Q

Use of benzos for IV anesthetic

A

midazolam for endoscopy

adjunctively with gaseous anesthetics and narcotics

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14
Q

Effects of benzos for IV anesthetic

A

may cause severe postoperative respiratory depression, decreased BP (tx with flumazenil), anterograde amnesia

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15
Q

Mechanism of ketamine for IV anesthetic

A

PCP analogs that acts as dissociative anesthetics

blocks NMDA receptors

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16
Q

Effects of ketamine for IV anesthetic

A

cardiovascular stimulants
cause disorientation, hallucination, bad dreams
increase cerebral blood flow

17
Q

Use of propofol for IV anesthetic

A

sedation in ICU, rapid anesthesia induction, short procedures
less postoperative nausea than thiopental
potentials GABAa

18
Q

Name the local ester anesthetics

A

procaine, cocaine, tetracaine (one I)

19
Q

Name the local amide anesthetics

A

lidocaine, mepivacaine, bupivacaine (two I)

20
Q

Mechanism of local anesthetics

A

block Na+ channels by binding to specific receptors on inner portion of channel
bind to activated Na+ channels so most effective in rapidly firing neurons
3 degree amine local anesthetics penetrate membrane in uncharged form, then bind ion channels as charged form

21
Q

Use of local anesthetics

A

minor surgical procedures, spinal anesthesia

if allergic to esters give amides

22
Q

Toxicity of local anesthetics

A

CNS excitation, severe cardiovascular toxicity (bupivicaine), HTN, hypotension, arrhythmias (cocaine), methemoglobinemia (benzocaine)

23
Q

Use of neuromuscular blocking drugs

A

muscle paralysis in surgery or mechanical ventilation

selective for motor (vs. autonomic) nicotinic receptors

24
Q

Name the depolarizing agent and mechanism

A

succinylcholine
strong ACh receptor agonist
produces a sustained depolarization and prevents muscle contraction

25
Q

Reversal of succinylcholine blockade

A

phase I - prolonged depolarization - NO ANTIDOTE
- the block is potentiated by AChE inhibitors

phase II - repolarized but blocked - ACH receptors are available but desensitized - ANTIDOTE is AChE inhibitors

26
Q

Complications of succinylcholine

A

hypercalcemia, hyperkalemia, malignant hyperthermia

27
Q

Name the nondepolarizing agents

A

tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

28
Q

Mechanism of nondepolarizing agents

A

competitive antagonists - compete with ACh for receptors

29
Q

Reversal of nondepolarizing blockade

A

neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors

30
Q

Mechanism of dantrolene

A

prevents release of Ca2+ from sarcoplasmic reticulum of skeletal muscle

31
Q

Use of dantrolene

A

malignant hypertermia and neuroleptic malignant syndrome (toxicity of antipsychotic drugs)

32
Q

Mechanism of baclofen

A

activates GABAb receptors at spinal cord level, inducing skeletal muscle relaxation

33
Q

Use of baclofen

A

muscle spasms (e.g. acute low back pain)

34
Q

Mechanism of cyclobenzaprine

A

centrally acting skeletal muscle relaxant

structurally related to TCAs, similar anticholinergic side effects

35
Q

Use of cyclobenzaprine

A

muscle spasms

STEP 1 (26 decks)

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