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anesthetic drugs Flashcards

1
Q

CNS drugs must ….(according to structure_

A
  1. be lipid soluble (cross BBB)

or 2. be actively transported

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2
Q

anesthetic drugs - solubility in blood / lipids

A

low solubility in blood –> rapid induction and recovery times
increased solubility in lipids –> increased potency

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3
Q

inhaled anesthetics - MAC? (definition)

A

minimal alveolar concentration (of inhaled anesthetic) required to prevent 50% of subjects from moving in response to noxious stimulus (e.g. skin incision)

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4
Q

potency vs minimal alveolar concentration (EQUATION)

A

potency = 1 / MAC

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5
Q

example of inhaled anesthetic with low blood and lipid solubility

A

nitrous oxide

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6
Q

example of inhaled anesthetic with increased blood and lipid solubility

A

halothane

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7
Q

inhaled anesthetic with increased blood and lipid solubility –> …. (potency and induction)

A

high potency

low induction

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8
Q

inhaled anesthetic with low blood and lipid solubility –> …. (potency and induction)

A

low potency

high induction

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9
Q

inhaled anesthetics - drugs

A

(HALOTHANE, -FLURANE, N20)

  1. halothane 2. enflurane 3. isoflurane
  2. sevoflurane 5. methoxyflurane
  3. nitrous oxide (N2O) 7. desflurane
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10
Q

inhaled anesthetics - mechanism of action

A

unknown

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11
Q

inhaled anesthetics - side effects (and which drug) and other effects

A
  1. fulminant hepatic necrosis (halothane)
  2. nephrotoxicity (methoxyflurane)
  3. proconvulsant (enflurane)
  4. expansion of trapped gas in body cavity (N20)
  5. malignant hyperthermia (all)
  6. Myocardial and resp depression
  7. nausea/emesis
  8. increased cerrebral blood flow (decreased metabolic demands)
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12
Q

malignant hyperthermia - definition/causes/manifestation ….

A

rare, life threatening condition in which inhaled anesthetics or succinylcholine induce fever and severe muscle contraction

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13
Q

malignant hyperthermia - manifestations / susceptibility

A

fever and severe muscle contraction
Susceptibility is AD with variable expression –> mutation in voltage-sensitive ryanodine receptor cause increase Ca+ release from sarcoplasmic reticulum

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14
Q

malignant hyperthermia - treatment

A

dantrolene

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15
Q

Intravenous anesthetics - groups/drugs?

A
  1. barbiturates - thiopental
  2. benzodiazepines - midazolam
  3. arylcyclohexylamines - ketamine
  4. opioids - morphine, fentanyl
  5. propofol
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16
Q

Intravenous anesthetics - thiopental - properties

A

high potency, high lipid solubility, rapid entry BBB

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17
Q

Intravenous anesthetics - thiopental - clinical uses

A

induction of anesthesia and and short surgical procedures

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18
Q

Intravenous anesthetics - thiopental’s effect terminated by

A

rapid redistribution into tissue and fat

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19
Q

Intravenous anesthetics - thiopental - side effects

A

decreases cerebral flow

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20
Q

Intravenous anesthetics - benzodiazepines - drugs?

A

midazolam

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21
Q

Intravenous anesthetics - midazolam - clinical uses

A
  1. MC drug used for endoscopy

2. adjunctively with gaseous anesthetics and narcotics

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22
Q

Intravenous anesthetics - midazolam - side effects

A
  1. severe postoperative respiratory depression
  2. low BP
  3. anterograde amnesia
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23
Q

Intravenous anesthetics - treat midazolam overdose with

A

flumazenil

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24
Q

Intravenous anesthetics - arylcyclohexylamines - drugs

A

ketamine

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25
Q

Intravenous anesthetics - ketamine - mechanism of action

A

PCP analog that act as a dissociative anesthetics
Block NMDA receptors
cardiovascular stimulant

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26
Q

Intravenous anesthetics - ketamine - side effects

A
  1. hallucination
  2. bad dreams
  3. disorientation
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27
Q

Intravenous anesthetics - ketamine - except its action an anesthetic is also a

A

cardivascular stimulant –> useful for patients in cardiogenic of septic shock

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28
Q

Intravenous anesthetics - ketamine effect on cerebral arteries

A

increase cerebral blood flow

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29
Q

Intravenous anesthetics - opioids - drugs

A
  1. morphine

2. fentanyl

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30
Q

Intravenous anesthetics - opioids - clinical use

A

uses with other CNS depressants during general anesthesia

31
Q

Intravenous anesthetics - propofol - mechanism of action

A

potentiates GABA-A

32
Q

Intravenous anesthetics - propofol - side effects

A
  1. low BP

2. chemical pancreatitis

33
Q

Intravenous anesthetics - propofol vs thiopental according side effects

A

propofol –> less postoperative nausea

34
Q

Intravenous anesthetics - propofol clinical use

A
  1. used for sedation in ICU
  2. rapid anesthesia induction
  3. short procedures
35
Q

malignant hyperthermia - treatment

A

dantrolene

36
Q

Intravenous anesthetics - groups/drugs?

A
  1. barbiturates - thiopental
  2. benzodiazepines - midazolam
  3. arylcyclohexylamines - ketamine
  4. opioids - morphine, fentanyl
  5. propofol
37
Q

local anesthetics - groups

A
  1. esters

2. amides

38
Q

local anesthetics - groups/drugs

A
  • CAINE
    1. esters –> procaine, cocaine, trtracaine, benzocaine
    2. amides –> lidocaine, mepivacaine, bupvacaine (AMIDES HAVE 2 Is in name)
39
Q

local anesthetics - mechanism of action

A
  • block Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so must effective in rapidly firing neurons.
  • They penetrate membrane in uncharged form, then bind to ion channels as charged form (3ry amines)
40
Q

local anesthetics - clinical use

A
  1. minor surgical procedure

2. spinal anesthesia

41
Q

local anesthetics - toxicity (and which drugs)

A
  1. CNS excitation
  2. severe cardiovascular toxicity (bupivacaine)
  3. hypertension 4. hypotension
  4. arrhythmias (cocaine)
  5. methemoglobinemia (benzocaine)
    IF ALLERGIC TO TO ESTERS –> GIVE AMIDES
42
Q

local anesthetics can be given with … (why)

A

vasoconstrictors (usually epinephrine) to enchance local action - decrease bleeding, increase anesthesia by decrease systemic concentration

43
Q

local anesthetics in infected (acidic) tissue

A

alkaline anesthetics are charged and cannot penetrate membrane effectively –> need more anesthetic

44
Q

local anesthetics - order of nerve predominates

A

small myelinated fibers > small unmyelinated fibers > large myelinated fibers > large unmyelinated fibers

45
Q

local anesthetics - order sensation loss

A
  1. pain 2. temperature 3. touch 4. pressure
46
Q

local anesthetics - groups/drugs

A
  • CAINE
    1. esters –> procaine, cocaine, trtracaine, benzocaine
    2. amides –> lidocaine, mepivacaine, bupvacaine
47
Q

neuromuscular blocking drugs - purpose

A

muscle paralysis in surgery or mechanical ventilation

48
Q

neuromuscular blocking drugs - muscle paralysis in

A

surgery or mechanical ventilation

49
Q

neuromuscular blocking drugs - selective for

A

motor (vs autonomic) nicotinic receptors

50
Q

neuromuscular blocking drugs - receptors

A

motor nicotinic receptors

- selective for motor (vs autonomic) nicotinic receptors

51
Q

neuromuscular blocking drugs are divided to (and drugs)

A
  1. depolarizing –> succinylcholine
  2. nondepolarizing –> (-CURARINE, -CURIUM, -CURONIUM)
  3. Tubocurarine 2. Atracurium 3. Mivacurium
  4. Pancurorium 5. Vecuronium 6.Rocuronium
52
Q

neuromuscular blocking drugs - depolarizing - drugs

A

succinylcholine

53
Q

succinylcholine - mechanism of action

A

strong ACh receptor agonist –> produce sustained depolarization and prevents muscle contraction

54
Q

succinylcholine - complications

A
  1. hypercalcemia
  2. hyperkalemia
  3. malignant hyperthermia
55
Q

depolarizing neuromuscular blockage - phases and characteristic

A

phase I - prolonged depolarization

phase II - repolarized but blocked. ACh receptros are available but desensitized

56
Q

depolarizing neuromuscular blockage - phase II - receptor’s condition

A

ACh receptros are available but desensitized

57
Q

depolarizing neuromuscular blockage - reversal of blockage by … (antidote?)

A

phase I –> no antidote

phase II –> cholinestarase inhibitor

58
Q

depolarizing neuromuscular blockage - action of cholinestarase inhibitor

A

phase I –> potentiates the block

pase II –> antidote

59
Q

nondepolarizing neuromuscular blockage - drugs?

A

(-CURARINE, -CURIUM, -CURONIUM)

  1. Tubocurarine 2. Atracurium 3. Mivacurium
  2. Pancurorium 5. Vecuronium 6.Rocuronium
60
Q

nondepolarizing neuromuscular blockage - mechanism of action

A

competitive antagonists - compete with ACh for receptors

61
Q

nondepolarizing neuromuscular blockage - reversal of blockage?

A

cholinesterase inhibitors

  1. edrophonium
  2. neostigmine (with atropine)
  3. other cholinesterase inhibitors drugs
62
Q

nondepolarizing neuromuscular blockage - reversal of blockage - neostigmine featrues

A

must be given with atropine to prevent muscarinic effects such as bradycardia

63
Q

dantrolene - mechanism of action

A

prevents release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle

64
Q

dantrolene - clinical use

A
  1. malignant hyperthermia

2. neuroleptic malignant syndrome (a toxicity of antipsychotic drugs)

65
Q

Baclofen - mechanism of action

A

Activate GABA -B receptors at spinal cord level –> induces skeletal muscle relaxation

66
Q

Baclofen - clinical use

A

muscle spasms (eg. acute low back pain)

67
Q

cyclobenzaprine - mechanism of action

A

centrally acting skeletal muscle relaxant

structural related to TCAs

68
Q

cyclobenzaprine - clinical use

A

muscle spasm

69
Q

cyclobenzaprine is stractural related to

70
Q

cyclobenzaprine - side effects

A

similar to anticholinergic side effects

71
Q

neuroleptic malignant syndrome is a toxicity of

A

antipsychotic drugs

72
Q

Intravenous anesthetics - groups/drugs?

A
  1. barbiturates - thiopental
  2. benzodiazepines - midazolam
  3. arylcyclohexylamines - ketamine
  4. opioids - morphine, fentanyl
  5. propofol
73
Q

local anesthetics - groups/drugs

A
  • CAINE
    1. esters –> procaine, cocaine, trtracaine, benzocaine
    2. amides –> lidocaine, mepivacaine, bupvacaine
74
Q

inhaled anesthetics - drugs

A

(HALOTHANE, -FLURANE, N20)

  1. halothane 2. enflurane 3. isoflurane
  2. sevoflurane 5. methoxyflurane
  3. nitrous oxide (N2O) 7. desflurane

neurology FA (31 decks)

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