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Daddy Pharm > Sedatives/Hypnotics > Flashcards

Sedatives/Hypnotics Flashcards

1
Q

first recorded parenteral agent to produce a hypnotic state

A

Christopher Wren
1657
injecting an aqueous opium solution into a dog

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2
Q

first hollow needles

A

Francis Rynd
1845
injected a morphine solution around nerves to treat neuralgia

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3
Q

Why were hollow needles significant?

A

could now be sterilized

instead of using porcupine needles lol

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4
Q

first recorded IV anesthetic

A

chloral hydrate

Pierre Ore’
1872

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5
Q

IV administration of inhalational anesthetics

A

unsuccesful

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6
Q

changed everything in the early 1900’s

A

specific agents
barbiturate testing

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7
Q

opened the era of IV anesthesia

A

first administration of thiopental in 1934

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8
Q

When was ketamine released?

A

1970

“ketamine: hallucin8ing is very 70s”

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9
Q

When was etomidate released?

A

1974

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10
Q

When was midazolam released?

A

mid 70’s

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11
Q

most used benzo in anesthesia

A

Midazolam

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12
Q

T/F
inhalationals are the preferred anesthetic

A

False
IV preferred
partially d/t less equipment needed

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13
Q

When was propofol released in its current form?

A

1986
Diprivan
problems with formulation d/t its high lipid solubility

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14
Q

Drugs take about ____ years to bring to market, costing about ____ dollars

A

10-15 Y
~1 billion

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15
Q

T/F
“Sedative/Hypnotics” accurately describe the class of medications it encompasses.

A

False
old terms
not specific

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16
Q

Sedative

A

mild suppression of arousal and behavior
slight decrease in alertness and response to stimuli

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17
Q

T/F
Sedatives produce certain degrees of CNS depression, but not anesthetic levels.

A

True

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18
Q

Hypnotic

A

pronounced sedative effects
induction of sleep

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19
Q

T/F
Sedatives can cause sleep in the proper dose

A

False
hypnotics cause LOC in proper doses

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20
Q

T/F
Hypnotics can provide anesthesia level LOC

A

False
not quite anesthesia level b/c still arousable to strong stimuli

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21
Q

T/F
Most sedatives become hypnotics in higher doses

A

True

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22
Q

Sedative/Hypnotics
example agents

A

alcohols
barbs
BZD
misc (meprobamate, meathqualone, Droperidol, etomidate, propofol)

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23
Q

T/F
Alcohol is considered a sedative/hypnotic.

A

True

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24
Q

Why can’t ethanol alone be used for anesthesia?

A

level that causes LOC can cause death
too many side effects

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25
Q

Chloral Hydrate is still often used in which pt population?

A

children

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26
Q

Thiopental was optimal for (short/long) duration cases.

A

short

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27
Q

T/F
Thiopental and methohexital are considered similar.

A

true

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28
Q

T/F
Pentobarbital & Phenobarbital are part of different families but have the same effects.

A

False
same family
different effx

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29
Q

T/F
Phenobarbital was once commonly used a sleeping pill, but not as common now d/t side fx.

A

False
Pentobarbital

Phenobarb: seizures, psych disorders

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30
Q

induces its own metabolism

A

phenobarbital

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31
Q

T/F
The phenobarbital dose for a chronic user may be fatal to a person who has never taken it before.

A

True
phenobarbital induces its own metabolism
body builds resistance

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32
Q

BZDs have largely supplanted the BARBs, except for ____

A

methohexital

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33
Q

T/F
BZDs can be the solo agent used in short procedures.

A

False
used as an adjunct

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34
Q

Use of preop BZDs (increases/decreases) anesthetic requirement.

A

decreases
produces some CNS depression

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35
Q

Known as Quaaludes

A

Methaqualone

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36
Q

T/F
Methaqualone is still available on the market.

A

False
heavy abuse caused issues in distribution

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37
Q

T/F
Sedative/Hypnotics’ MoA is similar, but not identical.

A

True

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38
Q

Sed/Hyps mainly act on _____.

A

polysynaptic pathways

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39
Q

Sed/Hyps usually fxn to _____.

A

increase presynaptic inhibition

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40
Q

T/F
Sedative/Hypnotics all lead to CNS depression.

A

True

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41
Q

Why is our understanding of sed/hyps limited?

A

it works in the brain
anything working in brain is hard to ID all mechanisms

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42
Q

T/F
Different brain areas have different levels of susceptibility

A

True

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43
Q

Most Sedative/Hypnotics are believed to enhance…

A

pre- and post-synaptic effects of GABA (gamma-aminobutyric acid)

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44
Q

polysynaptic pathways

A

go thru multiple nerves

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45
Q

monosynaptic pathways

A

one nerve going one place to another

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46
Q

We tend to block thses with compounds

A

interneurons

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47
Q

GABA is an (excitatory/inhibitory) (compound/NT) because it…

A

inhibitory
NT (neurotransmtr)
decreases the ability of depolarization

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48
Q

Sedative/Hypnotics Mechanism of action:
GABA ___ Augmentation

A

Ionophore

(ionophore = ligand gated)

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49
Q

How many GABA sites on the GABA receptor?

A

2

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50
Q

Which GABA binding site are we most concerned with?

A

GABA A

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51
Q

GABA receptors came from …

A

5 subunit protein structure

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52
Q

T/F
GABA receptors are quadrameric in structure.

A

False
pentameric

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53
Q

Cl- is higher in the (ICF/ECF)

A

ECF

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54
Q

Na is higher in the (ICF/ECF)

A

ECF

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55
Q

K is higher in the (ICF/ECF)

A

ICF

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56
Q

Ca is higher in the (ICF/ECF)

A

ECF

extremely small amount in ECF and ICF

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57
Q

At which voltage can Cl- no longer move into the cell?

A

-90

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58
Q

Na stops moving into cells @ which voltage?

A

-30/-40

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59
Q

When ICF is extremely (+/-), it is harder to depolarize.

A

negative

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60
Q

T/F
Cl- ions cannot flow into the cell if the ICF is at -70 mv.

A

False
the Cl gradient (ECF vs ICF) is so large, that it overcomes the repelling - charge from ICF
until about -90 mv

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61
Q

Depolarization occurs when membrane potential is closer to ___.

A

0

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62
Q

BZDs ___ GABA fxn by….

A

augment
increasing CNS depression

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63
Q

Lowering ICF voltage makes it (easier/harder) to depolarize.

A

harder

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64
Q

T/F
A single GABA molecule can open the channel completely.

A

False
need two! Two sites

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65
Q

T/F
A single molecule of GABA can bind and cause some Cl- to enter the cell.

A

True
not as much Cl- will enter as when 2 GABA molecules bind tho

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66
Q

How many GABA molecules need to bind to change the ionophores structure?

A

only 1

1 =changes structure; some Cl- influx
2 = full effect

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67
Q

T/F
most ionophores need 2 molecules to bind for full effect

A

True

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68
Q

T/F
Most brain pathways are excitatory.

A

False
inhibitory

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69
Q

Too much excitatory activity may result in…

A

excessive neuron firing
epileptic conditions

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70
Q

Picrotoxin

A

strong stimulant
prevents GABA from binding
epilieptic type/stimulatory effects

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71
Q

Anything blocking GABA causes…

A

epilieptic type/stimulatory effects (ie: picrotoxin)

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72
Q

T/F
GABA only acts when we introduce sed/hyps into the body.

A

False
GABA acts brain all the time by providing inhibition at certain times

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73
Q

T/F
The GABA A receptor complex spans the membrane.

A

True
allows Cl- to pass thru bilayer & enter ICF

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74
Q

T/F
The GABA A receptor complex is mostly composed of B-pleated sheets inside the channel.

A

False
Mostly alpha helices inside channel

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75
Q

Form the “mouth” of the GABA A receptor complex.

A

spiral helices

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76
Q

Ach receptors at the NMJ are ____.

A

ionphores

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77
Q

Twist more or less to open/close channel of GABA A receptor complex.

A

spiral helices

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78
Q

T/F
Glutamate is an inhibitory neurotransmitter.

A

False
Glutamate is an excitatory neurotransmitter

glutamate = excite
GABA = inhibit

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79
Q

voltage-dependent ionophoric system

A

Glutamate

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80
Q

Sed/Hyps works by (agonizing/antagonizing) the Glutamate Receptor.

A

antagonizing

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81
Q

NMDA glutamate receptor complex
Which ions to enter?
Which exit?

A

Calcium and Sodium IN
Potassium OUT

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82
Q

T/F
NMDA glutamate receptor complex works independently of the membrane potential

A

False
allows Ca & Na in; K out
depending on local membrane potential

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83
Q

T/F
Ketamine appears to act primarily at the PCP binding sites on the GABA A receptor complex

A

False

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84
Q

Which receptor has a QUADRAmeric structure (4 subunits)?

A

NMDA

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85
Q

Ca and Na entering cell causes (repolar/depolarization)

A

depolarization
they’re + ions

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86
Q

Ketamine and PCP both cause hallucinations. Why?

A

Ketamine and PCP act on same site = hallucin8 with ketamine

(gen class: Ketamine is an analog of PCP)

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87
Q

angel dust

A

PCP

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88
Q

glycine allows ___ to act properly

A

glutamate

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89
Q

Glycine vs. GABA
which is most present in the brain?
which is most present in the SC?

A

brain: GABA
SC: glycine

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90
Q

T/F
Nicotinic receptors have a pentameric structure.

A

True

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91
Q

Glycine receptor

A

Inhibitory neurotransmitter complex similar to GABAA

2 sites for glycine

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92
Q

2 phases of sleep (that we discussed)

A

Slow wave sleep (SWS)
Rapid eye movement sleep (REM)

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93
Q

Rapid eye movement sleep (REM)

A

skeletal muscles are relaxed (inhibited) and the eyes move back and forth rapidly.

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94
Q

Slow wave sleep (SWS)

A

EEG shows mainly high-voltage synchronous activity

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95
Q

How much of sleep is REM?

A

~25%

1-2 H

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96
Q

Hypnotic sleep differs…

A

SWS altered & shortened
REM depressed
Total sleep time longer

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97
Q

T/F
Without SWS, people can become psychotic.

A

False
REM

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98
Q

Which drug class is known to inhibit REM sleep?

A

BZDs

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99
Q

T/F
Hypnotics can produce longer, deeper sleep.

A

False
longer but not very deep
inhibited REM

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100
Q

Twitching/movement seen during REM sleep

A

Breakthrough

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101
Q

Barbiturates
Onset and duration of effect generally predictably based on…

A

lipid solubility (higher partition coefficient)

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102
Q

Barbiturates
more lipid soluble agents (higher partition coefficient) usually have the more ___ onset and ___ duration

A

rapid
shorter

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103
Q

Inhibits oxidative phosphorylation

A

BARBs
cell fxns requiring energy slows down
Slows down whole body

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104
Q

Overdoses with BARB sleeping pills

A

awaken thinking they didnt take pill
could happen multiple times in a night
OD

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105
Q

T/F
BARBs have a wider T.window than BZDs.

A

False
BZDs have wide TW; harder to OD

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106
Q

Barbiturates MoA

A

-Bind to GABAA receptor
-(diff site than BZDs)
-Decreases the dissociation rate of GABA
-increase Cl conductance
-inhibits excitatory glutamate AMPA receptors
-inhibits Ca mediated glutamate release

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107
Q

T/F
BZDs and BARBs bind to the same site on the GABA receptor.

A

False
they have separate sites

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108
Q

Barbiturates MoA
outside of GABA receptor

A

inhibits:
1) excitatory glutamate AMPA receptors
2) calcium mediated glutamate release

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109
Q

T/F
Barbiturates mimic the action of GABA at the GABAA receptor to the same extent.

A

False
mimicking is minimal
major effects require GABA

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110
Q

T/F
Barbituric acid has no sedative powers of the parent compound.

A

True

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111
Q

structure we get all BARBS from

A

Barbituric acid
Exists in keto and enol forms (tautomers)

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112
Q

Replacement of C-2 oxygen with sulfur results in (2)

A

thiobarbiturates
&
greater lipid solubility

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113
Q

Addition of various functional groups onto position ___ alters sedative/hypnotic properties

A

5

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114
Q

Addition of a ___ group at C-5 enhances anticonvulsant activity and produces ___.

A

phenyl
Phenobarbital

phenyl @ 5 = pheno

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115
Q

Addition of a ___ group to the ring N atom shortens duration of action and produces ___.

A

methyl
Methohexital

Methyl to N =methohex

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116
Q
A
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117
Q
A
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118
Q

which positions are 1, 2 & 5?
what are their significance?

A

sites of substitution

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119
Q

Which class exists in tautomer forms?

A

BARBs

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3
4
5
Perfectly
120
Q

Barbiturates by duration

A

Long: Phenobarbital

Intermediate: Pentobarbital & Secobarbital

Short/Ultra-short: Methohexital & Thiopental

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

T/F
Complications and side effects lead to the discontinuation of Thiopental by the FDA.

A

False
DC’ed by manufacturer
refused to sell to US b/c we use it to kill ppl

122
Q

Position 5 increases …

A

lipid solubility/mvmt into tissues

123
Q

T/F
Barbiturates are weak bases.

A

False
Barbiturates = weak acids

124
Q

What is the basic form of BARBs?

A

sodium salt (carboxylate form)

125
Q

BARBs are packaged as ___.

A

sodium salt, which is the basic form
(carboxylate form)

126
Q

The ___ pH of BARB sodium salt solution makes it ____.

A

high
bacteriostatic

126
Q

T/F
We can remove multiple doses of a BARB out of its packaging.

A

True
pH = bacteriostatic

however, only stable for a couple weeks or else precipitates

127
Q

lipid soluble agents
__ onset due to rapid increase in ____ concentration, followed by rapid ___ to other body fatty tissues.

A

shorter
brain
redistribution

128
Q

T/F
BARBs are lipid soluble.

129
Q

As a drug redistributes, the brain [ ] (increases/decreases)

130
Q

primary mechanism of cessation of action of lipid sol Rx in the brain

A

Redistribution (to fat)

131
Q

What does this chart tell us?

A

Thiopental
brain uptakes the fastest
balances with plasma [ ]
moves into other tissues
brain [ ] drops
Fat [ ] increases as [ ] in all other compartments drop

132
Q

Thiopental
As fat [ ] increases, [ ] in other tissues (increases/decreases)

133
Q

Primary metabolic pathway for BARB metabolism is…

A

hydroxylation to inactive metabolites
(Phase I)

134
Q

phenobarbital t1/2

A

86 hours
slowly metabolized

135
Q

BARB metabolism
occurs to a larger extent in oriental populations

A

N-glucosylation

136
Q

Potent inducers of the hepatic microsomal enzyme system

137
Q

BARBs can increase metabolic rates of drugs metabolized by ____. These include….

A

hepatic microsomal enzyme (CYPs)
oral anticoagulants, phenytoin, TCA’s

138
Q

Hydroxylation is a Phase ___ reaction.

A

I
its a CYP

139
Q

Your pt is taking phenobarbital regularly for epilepsy. For their anesthesia, you would use drugs that …

A

Use phase II/renal metab

140
Q

Cerebral edema occurs when…

A

prolonged hypoxia
cell damage/death causes swelling

141
Q

What can cause cerebral edema?

A

drowning
OD
ilicit drugs

142
Q

How does cerebral edema cause an impedance to blood flow?

A

Brain swelling impinges upon bony structure
closes off blood flow d/t pressure

143
Q

Do BARBs cross the placenta?

144
Q

BARB is mostly Phase ___ metabolism.

145
Q

BARBs are less used now b/c…

A

BZDs safer and equally effective
Drug interactions (enzyme induction)
Tolerance development
Greater abuse potential
Less CNS specificity than BZDs

146
Q

BZDs advantages over BARBs

A

higher specificity
safer (wider T.window)
equally effective

147
Q

BARBs primary use

A

-Therapeutic/diagnostic (psych)
-cerebral edema (surgery, head injury, cerebral ischemia)
-Antiepileptic

148
Q

What causes BARB tolerance

A

enzyme induction (CYP)

149
Q

T/F
BARBs offer extensive pain relief and muscle relaxation.

150
Q

Repeated administration of thiopental

A

will fill the body’s storage sites (fats) and can lead to long duration of action

(already some in fat, less [ ] differential btwn blood and fat; does not go into fat as quickly
Additional doses = longer duration
Not so much on second dose)

151
Q

T/F
Thiopental increases sensitivity to pain

A

True
lowers pain threshold

152
Q

Thiopental can induce in ____

A

10-15 seconds

153
Q

2-3 times as potent as Thiopental

A

Methohexital

154
Q

Methohexital metabolism

A

primarily via P-450 oxidation

metab faster than thio
(due to less lipid solubility)

155
Q

T/F
Thiopental is more lipid soluble than methohexital.

156
Q

Which has longer effect?
Methohexital
Thiopental

A

Thiopental

methohexital = less lipid-sol
-metabolized faster
-redistribution

157
Q

Methohexital is more potent than thiopental, but its effect is lost mainly d/t …

A

due to re-distribution (even though less lipid soluble)

158
Q

Which has faster recovery?
Thiopental
Methohexital

A

Methohexital

metabolized faster (due to less lipid solubility) primarily via P-450 oxidation

159
Q

BZDs were first introduced for the treatment of

160
Q

BZD properties (4)

A

sedative
antianxiety
anticonvulsant
muscle relaxant

161
Q

T/F
BZDs can achieve hypnosis and unconsciousness in large doses

162
Q

BZDs used to supplement or to induce and maintain anesthesia

A

Diazepam (VALIUM)
lorazepam (ATIVAN)
midazolam

163
Q

1/2 L of midazolam vs diazepam

A

M: 1H
D: >24 H

164
Q

T/F
BZDs are mostly metabolized via glucuronide conjugation.

A

False
Many = microsomal N-demethylation (diazepam)

some (oxazepam) rapidly via glucuronide conjugation.

Midazolam: microsomal hydroxylation

165
Q

Midazolam metabolism

A

rapidly mainly via microsomal hydroxylation

166
Q

T/F
Caution with liver Dz pts & BZDs

167
Q

T/F
1/2 life determines how long the effects of a medication will last.

A

False
1/2 life of effect

168
Q

T/F
Lorazepam (Ativan) does not undergo Phase I metabolism.

169
Q

⭐️
BZD receptor site

A

specific receptor sites
GABA receptor α and γ subunits
CNS

(ONE BZD site
Has TWO GABA sites)

170
Q

BZDs primarily affects cells in the ___

171
Q

BZD MoA

A

-α and γ subunits (GABA receptor; CNS)
-enhance GABA binding to its receptor
-more Cl- in
-hyperpolarization
-resistant to excitation

(Vs BARBs: decrease GABA dissociation rate)

172
Q

T/F
BZD receptors are found only in post-synaptic regions in the CNS

A

False
almost exclusively

173
Q

T/F
BZDs have minimal effects in other areas of the body other than the CNS.

A

True
(except effects caused via CNS control)

174
Q

BZDs receptor is greatest in the ______ & areas associated with ____.

A

cerebal cortex
memory formations

175
Q

T/F
BARBs cause amnesia

A

False
BZDs do

176
Q

T/F
BZDs have a smaller side effect profile

177
Q

Area responsible for memory/consciousness/thinking

A

Neo Cortex

178
Q

T/F
Anesthetic agents work in a bottom-up fashion.

A

False
work top-down
Neo cortex to lower brain

179
Q

T/F
neo cortex regulates breathing/autonomic fxns

A

False
lower brain/lizard brain

180
Q

Benefits of anesthetics affecting neo cortex before lower brain

A

affects memory/consciousness/thinking
before breathing & autonomic fxns

181
Q

What do patients forget when we give then BZDs in preop?

A

don’t remember things just prior to surgery (exposure to OR)

182
Q

BZD
CV effects

A

mild
minor decrease BP & SVR

183
Q

T/F
BZDs increases heart rate.

A

True
Heart rate may decrease or increase somewhat, probably reflexively

depends on a person’s state

184
Q

Rapid infusion of ____ risks ____, so resp support should be available.

A

Diazepam
transient apnea
(BZDs all carry risk of transient apnea, but rapid IV Diazepam especially)

185
Q

BZDs induces relaxation of spastic skeletal muscle activity via ____

A

central inhibition

186
Q

T/F
BARBs treat delirium tremens

187
Q

BZD Clinical Uses

A

Pre-op meds
Induction
sedation
Anticonvulsant
delirium tremens
Skeletal muscle relaxation

188
Q

T/F
BZDs provide smooth muscle relaxation.

A

False
skeletal

189
Q

T/F
BZDs are used as anesthetics.

190
Q

T/F
BZDs cross the placenta well and leads to fetal depression.

191
Q

Which BZD can lead to true physical dependance?

A

diazepam (long DoE d/t desmethyl metabolite)

“Diazepam dependance”

192
Q

Flumazenil (Romazicon)

A

Competitive Benzo antagonist
IV
treat OD
almost immediate reversal

193
Q

We must give Flumazenil (Romazicon) cautiously b/c…

A

give too much = seizure

194
Q

astringent

A

Locally cause dehydration of cell protoplasm

195
Q

Alcohol produces a cooling effect on skin due to

A

rapid evaporation

196
Q

Applying alcohol & rubbing the skin

A

Rubbing: increases blood flow
alcohol: cools more blood at a time

197
Q

T/F
Alcohol efficiently makes your body warmer in cold weather.

A

False
cutaneous vasodilation brings heat closer to surface = feel warmer
but
cold environment can suck this heat off you quickly
deadly

198
Q

High dose alcohol injections near nerves

A

blocks conduction by decreasing Na+ and K+ conductance
but
we don’t do this b/c high doses needed

199
Q

Alcohol bactericidal effect

A

ethanol penetrates lipid BL
increases fluidity of membrane
friction/shear tears bacterial membranes

200
Q

T/F
Alcohol is considered a potent CNS depressant

201
Q

Ethanol has a (wide/narrow) T.window as a general anesthetic.

A

narrow
why we dont use it for that

202
Q

Raises pain threshold and causes euphoria

203
Q

Ethanol
resp effects

A

Depresses medullary sensing of plasma CO2

Long periods between respirations

204
Q

T/F
Ethanol has anticonvulsant activity and may be used for these purposes if the patient is unresponsive to other means.

A

False
Anticonvulsant at [ ]s that depress other CNS functions

205
Q

T/F
Ethanol causes cardiac depression by both central and direct mechanisms at high plasma [ ].

A

True
cardiac depression
central & direct

206
Q

T/F
Ethanol can damage your muscles.

A

True

Small doses: increase work ability via central mechanisms

larger doses: decrease work; directly damage

207
Q

T/F
Ethanol [ ] 10% and higher increases gastric blood flow and secretions

208
Q

What causes vomiting from ethanol?

A

large ingestions due to local irritant effect (gastric irritation and erosion)

209
Q

Why do alcoholics have problems with fatty livers?

A

Increases synthesis of fat in liver

210
Q

Cirrhosis seen in (short/long) term abuse

211
Q

____ [ ] ethanol suppresses appetite.

212
Q

Ethanol metabolism

A

ethanol –alcohol dehydrogenase–> acetaldehyde

213
Q

alcohol dehydrogenase

A

liver enzyme
contains zinc
requires NAD cofactor

214
Q

Acetaldehyde metabolism

A

using aldehyde dehydrogenase
becomes acetic acid

215
Q

T/F
acetaldehyde is an energy source

A

False
acetic acid

216
Q

T/F
Methanol is converted via same enzymes as ethanol.

A

True
Give ethanol drip for methanol poisoning
Occupies eznymes for methanol metab and use for ethanol instead
Excrete methanol in urine

217
Q

Using alcohol dehydrogenase, methanol becomes _____ . It then becomes ____ using the enzyme ____.

A

formaldehyde
formic acid
aldehyde dehydrogenase

218
Q

T/F
Ethanol can cause blindness in a dose of 15 ml.

A

False
METHanol

219
Q

Formic acid cannot be used by the body, and its build up causes…

A

acidosis, which can be fatal

220
Q

fomepizole (Antizol)

A

inhibitor of alcohol dehydrogenase
may replace ethanol use

resistance d/t cost = longer stay using ethanol drip

221
Q

Why is making alcohol yourself dangerous?

A

methanol is produced in the process

222
Q

Why is alcohol high in calories?

A

converted directly to acetic acid, an energy source

223
Q

Which is most potent?
Zaleplon (Sonata)
Zolpidem (Ambien)
Eszopiclone (Lunesta)

224
Q

Zaleplon (Sonata)
Zolpidem (Ambien)
Eszopiclone (Lunesta)

have similar action to ____ in action on ____ receptor complex

A

BZD
omega 1 portion of GABA A receptor (on alpha 1 subunit)

225
Q

governs anti-anxiety and anticonvulsant effects

A

weak alpha-2 agonist

226
Q

What did these medications have over BZDs for sleep?

Zaleplon (Sonata)
Zolpidem (Ambien)
Eszopiclone (Lunesta)

A

did not interfere with tomorrow’s activities

vs. “benzo hangover”

227
Q

Which medications’ side fx included sleep eating/driving?

A

Zaleplon (Sonata)
Zolpidem (Ambien)
Eszopiclone (Lunesta)

228
Q

the first hollow needles were used to treat

A

neuralgia using a morphine solution

229
Q

Release date (earliest to latest):
Thiopental
midazolam
propofol
etomidate
ketamine

A

1934: thiopental
1970: ketamine
1974: etomidate
1975: midazolam
1986: propofol

TKEMP

230
Q

Sedative

A

cause mild suppression of arousal and behavior, and a slight decrease in alertness and response to stimuli

231
Q

Hypnotic

A
  • pronounced sedative effects (ex: inducing sleep)
  • usually arousable by strong stimuli (ie pain)
232
Q

Most hypnotics are…

A

-most agents are sedatives given in larger doses

233
Q

Which BARB was used as a sleeping pill?

234
Q

Which BARB induces its own metabolism?

A

Phenobarb

doses for chronic user could be fatal to novel user

235
Q

Misc. category of Sed/hyps

A

Meprobamate
Methaqualone
Droperidol
Etomidate
Propofol

236
Q

T/F
Most anesthetic agents work via same mechanism as the sed/hyps.

237
Q

Most act mainly on

A

polysynaptic pathways (interneurons)

goes thru multiple nerves to get one place to another

more nerves = more receptors = greater chance drug can inhibit

238
Q

presynaptic inhibition

A

2 methods:
1) NT released acts on receptor on presynaptic membrane to shut off/reduce release

2) neuron impinges on another (at terminal, axon, etc) to prevent signal passage

239
Q

Can help control amount of NT released

A

presynaptic inhibition

240
Q

SNS can shut off PNS via

A

presynaptic inhibition

241
Q

T/F
Most sed/hyps work by inhibiting excitatory signaling via post-synaptic inhibition.

A

False
pre synaptic

242
Q

T/F
Similar receptors in the brain work the same throughout the brain.

A

False
the different areas of the brain respond differently to the same compound, even if the receptors are similar

243
Q

most are believed to enhance

A

the pre- and post-synaptic effects of GABA (gamma-aminobutyric acid)

244
Q

ICF usual voltage

A

-50 to -70 mv

245
Q

Cl influx brings ICF voltage to ____ mv. At this voltage…

A

-90
no more Cl- can flow in; repulsive force too strong

246
Q

GABA receptors are located

A

between A1 and B2 subunits

247
Q

prevents GABA from binding

A

Picrotoxin

248
Q

T/F
90% of brain mechanisms are inhibitory.

249
Q

T/F
the BZD site only allows antagonists to bind.

250
Q

T/F
Steroids can augment GABA fxn.

251
Q

Does ethanol excite or inhibit?

A

affects both “evenly”
but since most of brain is inhibitory, the inhibitory processes are affected the most

“drinking diminishes inhibitions”

252
Q

the GABA receptor complex is similar to

A

ACh at the NMJ
both ionophores & pentameric

253
Q

Glutamate acts at which receptors?

254
Q

NMDA receptor structure

A

voltage-dependent ionphoric system
QUADRAmeric structure (4 subunits)

different than GABA ionophore!

255
Q

Ways we can control ion passage thru channel

A

change charge at both ends of the channel (will repel/attract)

change diameter of channel

256
Q

Ketamine MoA

A

primarily at PCP binding sites on NMDA glutamate receptor complex

blocks Calcium entrance → blocks excitation

257
Q

similar to GABA and allows glutamate to act properly

258
Q

T/F
Glycine attaches the the NMDA glutamate receptor allosteric site to alter Ketamine’s ability to bind and block Ca.

A

false
glycine has its own site
other ligands can bind to allosteric site and cause this effect tho

259
Q

increased K outflow will cause

A

hyperpolarization (losing + charge)

260
Q

the different mechanisms of action (7)

A

-GABA Ionophore Augmentation
-Glutamate Receptor Antagonism
-Two-pore domain K leakage channel activation
-Glycine receptor augmentation
-Sodium and Calcium ionophore inhibition
-Nicotinic ACh receptor inhibition
-Opiate Receptors

261
Q

Sodium and Calcium ionophore inhibition

A

block these + ions that depolarize

262
Q

Nicotinic ACh receptor inhibition

A

blocks action at NMJ
muscle relaxation
esp BZDs

263
Q

nerves that go to skeletal muscle are ___ in nature

A

cholinergic

uses NT ACh to start contraction
using nicotinic ionophore (pentameric)

264
Q

T/F
The muscle relaxant effect seen esp from BZDs is d/t muscarinic ACh receptor inhibition.

A

False
Nicotinic ACh receptor inhibition

265
Q

T/F
Some sed/hyps act on opioid receptors

266
Q

T/F
A dream (REM sleep) in which you’re running uses the same pathways as if you’re actually running IRL.

A

True
the brain inhibits the motor pathways during sleep; twitches = breakthrough

267
Q

Long-term BZD & sleeping pill use affects sleep by…
Which- leads to…

A

inhibiting REM sleep
developing certain psychiatric disorders

REM sleep deprivation = psychotic

268
Q

T/F
Hypnotics prolong sleep and enhance overall sleeping

A

True
but
not very deep
REM inhibited

269
Q

Sleeping pills now vs back then

A

50’s/60’s: BARBs
now: BZDs d/t wider T. window

270
Q

T/F
The primary effect of BARBs is their inhibition of oxidative phosphorylation.

A

False
BARBs do this, but isn’t primary effect

primary effect:
Bind to GABA receptor
Decrease dissociation of GABA
increase duration of action of GABA
increase chloride conductance

271
Q

conductance

A

movement of ions thru a channel

272
Q

Which position affects lipid solubility and DoA?

273
Q

How do we achieve salt form of BARBs?

A

Remove H+ and replace with Na+
Na+ attaches to O-
O-[Na+]

274
Q

What happens when we draw up additional doses from the same vial? (BARBs)

A

inserts air:
CO2 dissolves in water –> carbonic acid
H ions protonate –> back to (weak) acid form (RCOOH)
BARB structure can precipitate out (its no longer ionized)
&
decrease bacteriostatic effects

275
Q

RCOOH vs RCOO-
which is water soluble?

A

RCOO-
ionized
(will make solutions basic; mechanism used to make BARB into salt form)

276
Q

Use of BARBs in the Wada speech test

A

inject BARB into either L or R carotid
garbled speech = dominant language hemisphere

shows us which side NOT to use when doing NeuroSx

277
Q

BARB coma mechanism

A

decreases [O] phosphryltn > decreased metabolism > decreases swelling

gives tissues time to heal
reduces swelling (which causes ichemia)

278
Q

Should BARBs be used in pregnancy? why?

A

avoid
fetal elimination slower than mom’s

279
Q

T/F
BZD receptors are found in fewer places than BARBs.

A

True
BZD have higher specficity

280
Q

T/F
redistribution is an alteration of duration.

A

False
alteration of effect

281
Q

Which causes greater skeletal muscle relaxation?
BARBs
BZDs
neither

282
Q

Oxazepam
use
metabolism

A

sleep indxn
eliminated rapidly primarily via glucuronide conjugation (phase II)&raquo_space;> much shorter HL

283
Q

Should we give BARBs with BZDs?

A

No
BARBs induce CYP 450 (increased metab)
BZDs mostly use this system for metabolism

284
Q

T/F
Extended use of Versed may result in a -longer duration of effect d/t higher levels of inactive glucuronide.

A

True
high [ ] can increase duration of effect
also can happen in RF

285
Q

Midazolam –> 1-Hydroxymidazolam
is what type of rxn?

A

hydroxylation

286
Q

T/F
If a metabolite has Double the HL & half potency => doubles duration of effect

A

False
Double HL but half potency = extends effect but not greatly

287
Q

Shorter DoE of all BZDs

A

Midazolam (even tho Lorazepam does not have active metabolite)

288
Q

Region of brain distinctive to humans

A

neo cortex

289
Q

T/F
Amnesia effect of BZDs is considered beneficial

A

True
decreases anxiety for future procedure bc they don’t remember the scary OR

290
Q

Where do BZDs act?

A

interface of the α and γ subunits of the GABA receptor in the CNS

291
Q

T/F
BZDs will decrease BP to the same extent as propofol.

A

False
BZDs do not drop BP as much

292
Q

Drug of choice for status epilepticus

293
Q

T/F
BZDs are contraindicated in pregnancy

A

False
cross placenta; fetal depression
but
can be used

294
Q

Ethanol is ____ soluble

A

lipid
penetrates into lipid bilayer
increases fluidity

295
Q

When are Ethanol’s effects greatest?

A

“up-swing” of the plasma [ ] curve

On downswing, the brain becomes accustomed to the alcohol, and we can perform the same task at higher blood [ ]

(Same effect/outcome has lower [ ] on upswing vs downswing)

296
Q

T/F
acetic acid can greatly affect the body

A

False
formic acid; can lower pH; hard to remove

body mechanisms quickly removes acetic acid
(enters Krebbs cycle)

297
Q

How is methanol eliminated?

298
Q

Z class of sed/hyps

A

Zaleplon (Sonata) – potency = 1
Zolpidem (Ambien) – potency = 1
Eszopiclone (Lunesta) – potency = 7X

299
Q

T/F
Zaleplon (Sonata)
Zolpidem (Ambien)
Eszopiclone (Lunesta)

bind to alpha 2 receptors

A

False
they bind to the omega-1 portion of the GABA A receptor (on alpha 1 subunit)

“alpha 2 agonist” describes their actions on the SNS binding sites (norepi/epi type binding site)

Daddy Pharm (13 decks)

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