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MSK final > pharm of general and local anesthetics and muscle relaxants > Flashcards

pharm of general and local anesthetics and muscle relaxants Flashcards

1
Q

primary goals of anesthesia

A
  • induction of unconscious sedation
  • induction of intraoperative amnesia
  • analgesia
  • immobility
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2
Q

combination of drugs used is determined by

A

the specific requirements of each surgical procedure

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3
Q

area that unconsciousness/sedation targets

A

cortex thalamus reticular activation system

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4
Q

area that amnesia targets

A
  • hippocampus
  • amygdala
  • pre-frontal cortex
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5
Q

area targeted to induce immobility

A

spinal cord neuromuscular junction

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6
Q

analgesics act on the

A

spinal cord

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7
Q

analgesics act on the

A

spinal cord

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8
Q

anesthetics reduce the activity of neural circuits to produce _______ or _______

A

sedation or unconsciousness

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9
Q

mechanism of anesthetics

A
  • promote opening of GABAA receptor CL- channels and hyper polarize post-synaptic neurons - some other mechanisms not understood that well
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10
Q

mechanism of anesthetics

A
  • stimulate GABAergic synapses - inhibit glutaminergic synapses all to reduce neural output of circuits / AP promote opening of GABAA receptor CL- channels and hyper polarize post-synaptic neurons - some other mechanisms not understood that well
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11
Q

type of inhaled gas

A

nitrous oxide

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12
Q

volatile liquids

A

halothane, enflurane, isoflurane, sevoflurane, desflurane all ethers except halothane all halogenated

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13
Q

mechanism of benzodiazepine

A

increase CL- influx, hyper polarizing postsynaptic neurons and reduced neuronal firing

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14
Q

clearance of inhaled anesthetics is by

A

exhalation

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15
Q

no renal clearance or liver metabolism of inhaled anesthetics except for

A

halothane, whose metabolites are hepatotoxic

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16
Q

clearance from the body of IGAs is accomplished through _____ as the equilibria shift ____ after administration is stopped

A

exhalation left

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17
Q

clearance from the body of IGAs is accomplished through _____ as the equilibria shift ____ after administration is stopped

A

exhalation left

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18
Q

is halothane used?

A

no because it has hepatotoxic effects

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19
Q

the pharmacokinetic profile of IGA are strongly influenced by

A
  • the rate of ventilation during administration - the solubility of the drug in plasma
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20
Q

the most clinically relevant value associated with IGAs

A

the minimum alveolar concentration MAC

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21
Q

MAC

A

minimum alveolar concentration - the concentration of the drug that must be achieved in the alveoli in order to anesthetize 50% of patients

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22
Q

higher rate of ventilation _____ the onset time

A

decreases

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23
Q

FI

A

concentration of the drug in the inhaled gas

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24
Q

FA

A

concentration of the drug in the alveoli

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25
Q

higher rate of ventilation _____ the onset time

A

decreases (more quickly drug equilibrates in lungs)

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26
Q

FA

A

concentration of the drug in the alveoli

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27
Q

FA/FI = 1

A

the drug has reached equilibrium in the alveoli

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28
Q

FA/FI = 1

A

the drug has reached equilibrium in the alveoli

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29
Q

why does one gas have a different onset time as another?

A

depends on the solubility in plasma

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30
Q

why does one gas have a different onset time as another?

A

depends on the solubility in plasma

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31
Q

the _____ water soluble drugs have the fastest onset time

A

least

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32
Q

responsible for onset and recovery times of drugs

A

water solubility

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33
Q

highly soluble drugs take longer to _____ the blood and take longer to ______

A
  • saturate
  • enter the brain
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34
Q

Low B/G means

A

less water soluble and faster onset and recovery

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35
Q

high B/G means

A

more water soluble and slower onset and slower recovery

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36
Q

the drug can enter the brain when it is

A

fully saturated with dissolved drug

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37
Q

drugs with a faster recovery time

A

are less soluble in water/ have a low B/G coefficient

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38
Q

blood gas partition coefficient

A

expresses solubility as a ratio of the amount of drug that dissolves in blood vs the amount that remains a gas

39
Q

MAC produces of lack of movement in response to a surgical stimulus in

A

%50 of patients

40
Q

the lower the MAC, the ____ the potency

A

higher

41
Q

the IGAs must cross the epithelial cell layers in the ____, _____ and the ______ in order to reach the neurons of the brain

A

alveoli, the capillaries, and the blood-brain barrier

42
Q

the more hydrophobic

A

the more potent (requires a lower concentration to produce the same effect)

43
Q

This correlation shows that as * hydrophobicity increases from left to right, * potency increases from top to bottom

A

The Meyer-Overton correlation.

44
Q

MAC of 6% means that

A

6% of total alveolar gas volume must be the drug in order to anesthetize 50% of people

45
Q

MAC is not clinically useful because

A

it anesthetizes 50% of patients but we need 100% of patients

46
Q

the concentration of the drug that can anesthetize 99% of patients

A

1.3MAC

(30% higher than MAC for each drug)

47
Q

does nitrous oxide produce full unconsciousness in a patient?

A

no because the MAC is 104 so 1.3 MAC is so high

48
Q

phases of drugs

A

induction, maintainence, recovery

49
Q

inhaled anesthetics that can be used during the induction or mainenance phases

A

nitrous oxide and fluranes

50
Q

all of the fluranes, except ________, produce bronchodilation

A

nitrous oxide

advantageous for patients with obstructive lung disease

51
Q

suppopsed mechanism of fluranes

A

fluranes appear to to interfere with parasympathetic stimulation of bronchoconstriction by reducing the influx of Ca2+ into bronchiole smooth muscle cells either directly by blocking Ca2+ channels or indirectly by inhibiting the activity of protein kinase C.

52
Q

most potent coronary vasodilator of the fluranes

A

isoflurane

this is advantagous in patients with coronary artery disease or ischemic heart disease

53
Q

two important disadvantages of IGA

A
  • more likely to produce post operative nausea and vomiting (PONV) than IV anesthetics
  • malignant hyperthermia
54
Q

PONV in IV anesthetics

A

less than half the patients reported PONV side effects compared to inhaled anesthetics

55
Q

malignant hyperthermia

A

patients with rare polymorphisms of the ryanodine receptor

56
Q

inheritance mode of malignant hyperthermia

A

autosomal dominant

57
Q

mechanism of malignant hyperthermia

A

In patients with ryanodine receptor mutations, IGAs stimulate the opening of the Ca2+ channel causing persistent muscle contraction.

This leads to rigidity resulting from the muscle contraction, to acidosis resulting from the anaerobic breakdown of glycogen, and to hyperthermia, or high fever, resulting from the heat generated by these processes.

58
Q

ryanodine receptor is located in

A

skeletal muscle cells -

acts as a channel to release Ca2+ from the SR causing persistent muscle contraction

59
Q

symptoms of malignant hyperthermia

A

increased heart rate and respiratory rate

60
Q

treatment for malignant hypertermia

A

dantrolene

which is an inhibitor of the ryanodine receptor Ca 2+

61
Q

dantrolene

A

which is an inhibitor of the ryanodine receptor Ca 2+, prevents Ca2+ from being released

62
Q

inhaled anesthetics toxicities

A

there may be some chronic toxicities that result

  • mutagenicity
  • teratogenicity
  • carcinogenicity
63
Q

IV anesthetics enhance _____ ______ signals or inhibit ________ ______ signaling or both

A
  • inhibitory GABA
  • excitatory glutamate
64
Q

ketamine acts primarly as an ______ at ______ synapses

A
  • inhibitor
  • at stimulatory glutamate synapses
  • it is a non competitive NMDA (glutamate) receptor antagonist
65
Q

GABA-A positive modulators

A
  • propofol
  • thiopental
  • etomidate
66
Q

benzodiazeprine anxiolytics

A

midazolam

(similar to gaba pos modulators)

67
Q

IV anesthetics: hydrophobicity ______ with potency and _____ both onsent time and duration of action

A
  • correlates
  • shortens
68
Q

the more hydrophobic the drug is

A

the faster the onset time

also the faster it will redistribute out of the brain and shorter will be its duration of action

69
Q

After administration is stopped, the anesthetic…

A

diffuses out of the brain and redistributes to other tissues particularly those that are highly perfused, such as skeletal muscle, or that are lipid-rich, such as adipose tissue.

70
Q

unlike IGAs, IV antibiotics are metabolized

A

in the liver and/or kidneys

71
Q

where to IV anesthetics travel?

A

to lipophilic tissues such as the brain and spinal cord

over time - lipid rich and highly perfused, lipid poor and highly perfused, lipid rich and poorly perfused.

72
Q
A
73
Q

high volume of distribution

A

most drug is in the tissue not the plasma

74
Q

propofol

A

GABA positive modulator and powerful anti emetic

75
Q

propofol and PONV

A

anti emetic so it can help prevent nausea if used in conjuction with IGAs used in induction or maintenance stages

76
Q

propofol toxicity

A

hypersensitivity reactions - egg protein lecithin (highly hydrophobic, a soybean oil/lecithin emulsifyingagent)

77
Q

thiopental

A

more complex than a GABA-A positive modulator (like benzodiazepines)

78
Q

Thiopental is a GABAA positive modulator at ____ concentrations, and an _____ at higher concentrations (that produce unconsciousness)

A
  • low (just helps increase CL-)
  • agonist (releases the CL- itself)
79
Q

anesthetic effects of ketamine

A
  • amnesia
  • analgesia
  • unconsciousness/sedatoin
80
Q

unconsciousness/sedation

A

etomidate

ketamine

propofol

thiopental

81
Q

produces dissociative effects, disorientation, hallucinations, bad dreams

A

ketamine

(similar to ilicit drug PCP)

82
Q

ketamins dissociative effects can produce

A

psychosis like symptoms during recovery

83
Q

ketamine is contraindicated in

A

patients with schizophrenia

84
Q

thiopental and propofol (increase/decrease) systemic BP, respiratory rate, and cerebral blood flow

A

decrease

85
Q

ketamine (increase/decrease) systemic BP and blood flood

A

increases

86
Q

all of the IV anesthetics (GABA effectors) decrease

A

respiratory rate

87
Q

surgical amnesia is primarly achieved with

A

benzodiazepine anxiolytic drugs

like midazolam

88
Q

surgical analgesia is primarly the role of

A

opiods

89
Q

psychosis like symptoms

A

amnesia, derealization, depersonalizatoin, identity alteration, identity confusion

90
Q

benzodiazepine

A

(GABA A receptor positive modulators, not agonsits) so they increase GABA potency

91
Q

flumazenil

A

benzodiazepine reversal agent

can be used to treat BZ overdose

92
Q
A
93
Q

Inhibition of ascending pain pathways, stimulation of descending modulatory pain pathways

A

opiods

94
Q

at slide 42

A

MSK final (11 decks)

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