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3rd Quarter > Pharm Quiz #4 > Flashcards

Pharm Quiz #4 Flashcards

1
Q

How does the number of twitches correlate with degree of neuromuscular block?

A

T4 disappears at 75% depression
T3 disappears at 80-85% depression
T2 disappears at 90% depression
Twitch suppression of 90% would equate to a TOF count of 1 or less

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2
Q

When is reversal of residual NMB safely achieved?

A

When TOF is => 3 twitches

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3
Q

Traditionally, it had been accepted that a TOF ratio of 0.7 or greater was an indication of adequate reversal however……..

A

it is now that that a TOF ratio of 0.9 should be achieved before tracheal extubation(at least 3 twitches)

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4
Q

Is TOF more useful monitoring depolarizers or non-depolarizers?

A

non-depolarizers; with depolarizers, each twitch is decreased equally in size with NO fade

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5
Q

What is the normal set time for tetanic stimulation?

A

5 seconds

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6
Q

In non-paralyzed skeletal muscle, tetanic response is…..

A

maintained tetanic contraction

Once given a non-depolarizer, the muscle shows fade and is unable to sustain muscular contraction

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7
Q

The degree of fade corresponds to the…..

A

degree of NMB

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8
Q

What limits the use of Tetanic stimulation?

A

pain

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9
Q

Tetanus fade is the effect of non-depolarizing agent on _____ nerve membranes.

A

presynaptic

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10
Q

With non-depolarizers, what contributes to fade during tetanic stimulation?

A

competitive block of presynaptic receptors that decreases mobilized and released acetylcholine

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11
Q

Is fade seen with tetanic stimulation during partial depolarizing block?

A

no

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12
Q

Single twitch nerve stimulations gives what information?

A

Post synaptic/junctional information(muscle side)

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13
Q

Tetanus and TOF gives what information?

A

Pre synaptic/junctional membranes

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14
Q

Tetanic stimulation should not be repeated for how many minutes?

A

6 minutes

*Tetanic stimulus affects NMJ of stimulated nerves for a significant time

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15
Q

What drug class is acetylcholine?

A

Quaternary ammonium ester

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16
Q

How many molecules are in a quanta?

A

1000 molecules

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17
Q

First twitch is only accurate if ____ seconds have elapsed since previous stimulation.

A

10

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18
Q

What is the main disadvantage of tetanus?

A

Post-tetanic facilitation(pain)

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19
Q

Increased sensitivity to non-depolarizers due to extra juctional proliferation is seen in what type of patients?

A

Paraplegia/quadriplegia

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20
Q

Greater than 30% body surface area burns acquire non-depolarizing NMB resistance. Explain

A

Begins 10 days after injury
Peaks at 40 days
Declines after 60 days

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21
Q

What are the cardiovascular effects of non-depolarizers?

A

Actions from histamine release
Effects at cardiac muscarinic receptors
Effects at autonomic ganglia nicotinic receptors
Rarely has clinical significance

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22
Q

Non-depolarizing NMB have enhanced activity due to perioperative drugs including….?

A 
Volatile anesthetics(enhance effects)
Aminoglycosides**
Local anesthetics
Anti-dysrhythmics
Diuretics
Mg++
Lithium
Ganglionic blockers(arthenand)
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23
Q

Non-deplarizing NMB effects are altered by what?

A 
Hypotension
Acidosis/alkalosis
Serum K levels
Adrenocortical dysfunction
Thermal injury
Allergic reactions
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24
Q

Non-depolaring NMB enhancement is greatest with(3) and least with(2)?

A

Iso, Sevo, Des

Nitrous, Opioids

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25
Q

Non-Depolarizing NMB enhancement by VA leads to what?

A

probable volatile anesthetic induced depression of CNS-decreased skeletal muscle tone

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26
Q

By what function do Aminoglycosides enhance non-depolarizing NMB?

A

due to pre-junctional release of acetylcholine and decreased post-junction membrane sensitivity

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27
Q

Will there be any TOF or single twitches noted with profound non-depolarizing NMB?

A

no

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28
Q

With profound NMB, what is the best reversal?

A

time

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29
Q

What is the characteristics of Post-tetanic count?

A

5 second tetanic stimulus at 50 hz administered, followed 3 seconds later by single twitches

response seen in the early stages of recovery, before TOF reappears

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30
Q

After tetanic stimulus, acetylcholine synthesis and mobilization continues this leads to……

A

there is increased acetylcholine causing enhanced response to subsequent single twitch stimulation

number of post-tetanic twitches indicates when first twitch of TOF reappears

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31
Q

What is the mode of action of non-depolarizers?

A

Bind to post-junctional nicotinic cholinergic alpha subunit receptors sites without any activation of ion receptor channels

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32
Q

Is there any evidence of NMB with occupancy of < 70% of nicotinic cholinergic receptors?

A

No evidence of block by single twitch test

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33
Q

Neurotransmission fails when ___-___% of alpha subunit post-junctional nicotinic cholinergic receptors are blocked.

A

80-90%

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34
Q

What are the characteristics of non-depolarizing NMB?

A
  • decreased response to single twitch
  • fade during tetanus
  • TOF ratio less than 0.7
  • Post-tetanic potentiation
  • potentiation of other non-depolarizing NMB
  • antagonism by anti cholinesterase drugs
  • NO fasciculations
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35
Q

Skeletal muscle response is ___ or ___.

A

all or nothing;

Skeletal muscle fibers contract maximally or not at all.
Therefore, when twitch response is decreased, some fibers are normally contracting & some are completely blocked.

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36
Q

There is no detectable block until how much of the receptors are occupied?

A

75-85%

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37
Q

Paralysis is complete at how much receptor occupancy?

A

90-95%

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38
Q

Adequate muscle relaxation corresponds to a narrow range of how much receptor occupancy?

A

85-90%

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39
Q

What is the definition of the ED95 of a drug?

A

dose producing 95% single twitch depression

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40
Q

First twitch accurate only if…….

A

10 seconds have elapsed since previous stimulation

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41
Q

Disappearance of 4th response after TOF stimulation correspond to…..

A

70-75% single twitch depression

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42
Q

With TOF, four successive stimuli are delivered at?

A

2 Hz every 0.5 seconds

*immediately available stores of acetylcholine are depleted and amount released by nerves decreases with successive stimuli

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43
Q

During _____ NMB TOF does not fade.

A

depolarizing

the height of all the four twitches decreases simultaneously

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44
Q

With non-depolarizing NMB what is the response of TOF with increasing degree of block?

A
  • The twitches in TOF progressively fade starting with the fourth and one by one eventually disappear.
  • The ratio of the height of the fourth response to the first has been defined as the TOF ratio.
  • In the absence of non-depolarizing block, the T4/T1 ratio is approximately one.
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45
Q

There is no need for a control measurement before using TOF to measure relaxant?

A

true

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46
Q

Is there post-tetanic facilitation with TOF?

A

No; so can be repeated every 10 - 12 seconds

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47
Q

With tetanus, fade is first noted at what % receptor occupancy?

A

70%

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48
Q

What is the main disadvantage of post tetanus?

A

post-tetanic facilitation(very painful)

less useful than TOF

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49
Q

With hemiplegia, resistance to non-depolarizers develops with how many days?

A

2-3 days

May be due to central inhibition

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50
Q

Should the unaffected or affected side be monitored with those with hemiplegia?

A

the unaffected side

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51
Q

What response to non-depolorizers will be seen to those with Parkinsons and multiple sclerosis?

A

Normal response to NMB monitoring

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52
Q

Those with myotonia and muscular dystrophies have what response to non-depolarizers?

A

mostly normal response

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53
Q

What effect does succinylcholine given for intubation have on twitch suppression produced by non-polarizing NMB dosing?

A

increases twitch suppression even when succinylcholine effects have gone

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54
Q

What is the definition of autonomic margin of safety?

A

difference between NMB dose and dose producing circulatory effect

*ED95 dose of pancuronium producing NMB also produces increased HR, so autonomic margin of safety is low

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55
Q

Non-depolarizing NMB enhancement by volatile agent is caused by?

A

probable volatile anesthetic induced depression of CNS—>decreases skeletal tone as an additive effect

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56
Q

How does the co-administration of aminoglycosides effect non-depolarizing NMB function?

A

decreased pre-junctional release of acetylcholine & decreased post-junction membrane sensitivity to acetylcholine

reversal of non-depolarizing of NMB less predictable on patients receiving aminoglycosides
QUIZ QUESTION

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57
Q

Are intermediate non-depolarizers most or less expensive than succinylcholine or pancuronium?

A

more expensive

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58
Q

Do intermediate non-depolarizers have CV effects?

A

minimal to absent

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59
Q

What is the drug class of Vecuronium?

A

Monoquaternary aminosteroid non-depolarizer

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60
Q

What is the onset of vecuronium?

A

3-5 minutes

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61
Q

What is the duration of action of vecuronium?

A

20-35 minutes

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62
Q

What is the structure of vecuronium?

A

Structurally its pancuronium without the quaternary methyl group in the A-ring of the steroid nucleus

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63
Q

What is the intubating dose of vecuronium?

A

0.1 mg/kg

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64
Q

What is the physiologic effect of the absence of quaternary methyl group in vecuronium?

A

it reduces the acetylcholine-like character, decreasing vagolytic effects by 95%

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65
Q

Vecuronium undergoes _____ metabolism & _____ excretion.

A

hepatic, renal

66
Q

Is vecuronium more or less lipid soluble than pancuronium?

A

More lipid soluble which facilitates its entrance into hepatocytes.

67
Q

What are the 3 metabolites of vecuronium?

A
  1. 3-desacetyl vecuronium- 1/2 as potent as vecuronium
  2. 17-desacetyl vecuronium- 1/10 as potent as vec
  3. 3,17-desacetyl vecuronium- 1/10 as potent
68
Q

How much of the vecuronium dose is present in the liver 30 minutes after administration?

A

50%

69
Q

What aids in vecs rapid reduction in plasma concentration and short duration of action?

A

Extensive hepatic uptake

70
Q

Is elimination 1/2 time prolonged in ESRD with vecuronium?

A

yes

71
Q

Doubling the vec dose to _____ mg/kg prolongs duration of action & elimination 1/2 times in hepatic dysfunction patients.

A
  1. 2 mg/kg

* Vecuronium doses of 0.1 mg/kg not associated with prolonged duration of action in hepatic dysfunction

72
Q

What acid base changes can be seen with vecuronium?

A

hypoventilation occurring in the post period may enhance residual neuromuscular blockade from vec

73
Q

Does vec have a small or large Vd?

A

large Vd due to significant tissue uptake

74
Q

With single doses of vec, plasma {} decline rapidly due to ?

A

redistribution

  • with repeated doses, peripheral compartments become saturated & redistribution is limited*
  • Cumulative effects are present, less then pancuronium*
75
Q

How does onset of action/duration of action of vec in children compare to adults?

A
  • onset of action-more rapid in infants than adults
  • duration of action-longest in infants/shortest in children

infants high CO speeds onset of blockade-immature neonate enzyme systems and greater Vd lengthen duration of action

76
Q

Why would you decrease vec dosing in the elderly?

A
  • lower plasma clearance from reduced renal/hepatic blood flow
  • lower microsomal enzyme activity

recover of single twitch response prolonged in elderly with vec infusions-with single dose vec, elimination 1/2 time and dose responses are no different in the elderly

77
Q

Are there any effects on the newborn when vec is given to the OB patient

A

no-insufficient {} cross placental barrier

78
Q

How does vec affect the patient over 130% of ideal body weight?

A

duration of action may be prolonged

79
Q

Unlike Succ, vecuronium does not(2).

A
  1. does alter intraocular pressures

2. does not trigger MH

80
Q

What is the drug classification of Rocuronium?

A

Monoquaternary aminosteroid non-depolarizer

81
Q

What is the onset and DOA of rocuronium?

A

onset-1-2 minutes

DOA- 20-35 minutes

82
Q

What is the structure of Rocuronium?

A

like vecuronium except rocuronium has a hydroxyl group rather than an acetyl group on the A-ring of the steroid nucleus

83
Q

What contributes to the speed of onset of Rocuronium?

A

lack of potency—>more drug available to bind to receptors

84
Q

The onset of max doses(3-4xED95) of Roc resembles ____?

A

succinylcholine;Rocuronium the only non-depolarizer that serves as an alternative to succinylcholine for RSI

85
Q

Which set of muscles are more resistant to roc?

A

Laryngeal muscles more resistant to roc than adductor pollicis muscles

86
Q

Since laryngeal muscles are resistant to rocuronium, large doses of rocuronium will resemble _____ at adductor pollicis but _____ at laryngeal adductors.

A

succinylcholine; delayed

  • complete suppression of twitch response @ adductor pollicis does NOT confirm laryngeal & diaphragm paralysis*
  • Initiating laryngoscopy @ peak laryngeal muscle paralysis may result in diaphragm movement during tube placement*
87
Q

For best intubation conditions monitor _____, for best return of breathing monitor _____.

A

obicularis occuli; adductor pollicis

88
Q

How is rocuronium cleared by the body?

A

up to 50% exerted unchanged in bile

89
Q

How does rocuronium affect ESRD patients?

A

will have longer DOA

90
Q

How does rocuronium affect patients with impaired liver function?

A

longer DOA especially with infusions and multiple doses due to their larger Vd.

Elderly have similar onset but longer DOA due to impaired hepatic clearance

91
Q

Does roc have histamine release or vagolytic effects?

A

no histamine release, only a slight vagolytic effect

92
Q

What is the drug classification of Cisatracurium?

A

Benzylisoquinolinium non-depolarizer

93
Q

What is the intubating dose of Cisatracurium?

A

0.1 mg/kg

94
Q

What is the onset of action and duration of action of Cis?

A

OoA- 3-5 minutes

DoA- 20-35 minutes

95
Q

How does Cisatracurium compare to Atracurium?

A

has a NMB profile similar to atracurium except a slightly lower onset and much lower histamine release.

Cis is one of 10 stereoisomers of Atracurium, accounting for 15% of the mixture

96
Q

Is the rate of recovery of Cis influenced by prolonged infusion?

A

no; NM block is easily maintained by constant rate infusion without diminishing over time.

NO cumulative effects!

97
Q

What is the principle mechanism of degradation of Cis and what is the byproduct?

A

Hoffman elimination

98
Q

What are the two byproducts of the degradation of Cis?

A

at physiologic pH and temp, it forms laudanosine and a mono quaternary acrylate

99
Q

What are the two ways Cis is cleared from the body and the percentages related?

A

77% clearance by Hoffman elimination

16% clearance by the kidneys

100
Q

Unlike atracurium, _____ _____ do NOT help cisatracurium clearance.

A

plasma esterases

101
Q

Is there any alterations in the NMB profile of cisatracurium with ESRD?

A

no

pharmacokinetics minimally altered by advanced age-only slightly slower onset is noted

102
Q

Cisatracurium metabolites are _____ at the NMJ.

A

inactive

103
Q

Plasma {} of principle metabolite laudanosine, are _____ with cis due to greater potency.

A

lower

104
Q

What is the only depolarizing NMB?

A

Succinylcholine

105
Q

What is the OoA and the DoA of Succinylcholine?

A

DoA 3-5 minutes

OoA 30-60 seconds

106
Q

What is the intubating dose of Succinylcholine?

A

1 -1.5 mg/kg

107
Q

What is the mechanism of action of Succinylcholine?

A
  • attaches to alpha subunits of nicotinic cholinergic receptors
  • mimics action of acetylcholine
  • depolarizes the post-junctional membrane
108
Q

Compared to acetylcholine, _____ of succinylcholine is _____, resulting in _____ depolarization- receptor ion channels remain open.

A

hydrolysis, slow, sustained

109
Q

How does succinycholine cause NMB?

A

occurs because depolarized post-junctional membranes can not respond to new acetylcholine release

depolarizing block = Phase I block

110
Q

How is succinylcholine degraded?

A

degraded by pseudocholinesterase, a plasma cholinesterase(as opposed to acetylcholinesterase)

Hydrolysis by pseudocholinesterase much slower than acetylcholine by acetylcholinesterase

111
Q

In succinylcholine, sustained receptor ion channel opening and depolarization of post-junctional membranes causes _____ leakage from cell interiors. This causes an increase in what ion, and by what margin?

A

potassium, 0.5 mEq/L in serum K+

hyperkalemia is contraindicated in succinylcholine

112
Q

Succinylcholine dosing with doses > 2mg/kg, repeated doses or succinylcholine infusions may cause…..

A

post-junctional membranes that will not respond to succinylcholine(phase II block)

mechanism for desensitization NMB unknown, hence the name phase II block which docent imply a mechanism

113
Q

What are the characteristics of a phase I block?

A
  • reduced response to single twitch
  • reduced but sustained response to tetanus
  • TOF ratio > than 0.7
  • no post-tetanic facilitation
114
Q

Succinylcholine’s short DoA is due to?

A

hydrolysis by plasma cholinesterase made in the liver

115
Q

What is the initial metabolite of succinylcholine?

A

succinylmonocholine—> very weak neuromuscular activity

116
Q

What is succinylmonocholine broken down to?

A

succinct acid and choline

117
Q

Plasma cholinesterase capacity is _____ - most succinylcholine _____ before reaching neuromuscular junction.

A

huge, hydrolyzed

118
Q

Plasma cholinesterase not found in large amounts at the NMJ, so ending of succinylcholine NMB due to…..?

A

diffusion away from neuromuscular action

119
Q

Plasma cholinesterase affects succinylcholine DoA by….?

A

controlling amounts hydrolyzed before reaching NMJ

120
Q

Succinylcholine rapidly hydrolyzed by plasma cholinesterase to?

A

succinylmonocholine

121
Q

Succinylmonocholine metabolized to?

A

succinic acid and choline(QUIZ QUESTION)

10% of the succinylcholine excreted unchanged in the urine

122
Q

With succinylcholine, depolarization may be observed as?

A

fasciculations

subsequent NM transmission inhibited as long as adequate {} of succinylcholine remain @ receptors

123
Q

What is the onset of paralysis and DoA of Succinylcholine?

A

< 1 minute and DoA= 4-6 minutes

124
Q

When both alpha subunits are bound =?

when pretreatment used only 1 bound =?

A

fasiculations

no fasiculations

125
Q

What are two affects of longer effects of succinylcholine?

A
  • higher doses cause the effects to last somewhat longer
  • when plasma levels of cholinesterase are greatly diminished or an atypical form of cholinesterase is present paralysis may last longer
126
Q

What is the IV/IM pediatric dose of succinylcholine?

A

IV=2 mg/kg

IM=3-4 mg/kg

127
Q

The onset of succinylcholine given IM is usually observed in about?

A

2-3 minutes

128
Q

IV bolus succinylcholine in infants or children may result in?

A

profound bradycardia or asystole

129
Q

The incidence of bradycardia in children is higher following a?

A

second dose of succinylcholine

130
Q

The occurrence of bradyarrhythmias in infants/children may be reduced by?

A

pretreatment with atropine

131
Q

What are 4 conditions that are contraindications of Succinylcholine and why?

A
  1. major burns
  2. multiple trauma
  3. extensive denervation of skeletal muscle
  4. upper motor neuron injury

Succinylcholine administration may result in SEVERE HYPERKALEMIA which may result in cardiac arrest

132
Q

Risk of hyperkalemia in patients with the 4 contraindications _____ over time and usually peaks at day ___ to ____ after the injury.

A

peaks; 7 to 10

risk is dependent on the extent and location of the injury, precise time of onset and duration of the risk period are not known

133
Q

What are the adverse effects of succinylcholine?(8)

A
  • dysrhythmias
  • hyperkalemia
  • myalgia
  • myoglobinuria
  • increased intragastric pressure
  • increased intraocular pressure
  • increased ICP
  • sustained skeletal muscle contractions
134
Q

All of the adverse effects of succinylcholine may be minimized with pre-treatment except for?

A

hyperkalemia

135
Q

What are 10 adviser effects of succinylcholine?

A
  • hypotension
  • hypertension
  • initial muscle fasciculations
  • excessive salivation
  • MH
  • rare allergic reactions
  • phase II block
  • anaphylaxis
  • jaw rigidity—>one of the first signs of MH with such
  • rhabdomyolysis with possible myoglobinuric renal failure
  • rash
  • prolonged resp depression or apnea
136
Q

Pre-treatment with non-depolarizers may prevent dysrhythmias, myalgia, increased intragastric pressures, increased intraocular pressures, but not ___.

A

hyperkalemia

137
Q

Succinylcholine is associated with MH. Risk increases with co-administration of volatile anesthetics. MH presents as?

A
  • intractable spasms of the jaw muscles
  • generalized rigidity
  • increased O2 demands
  • tachycardia
  • tachypnea
  • profound hyperpyrexia
138
Q

Incomplete jaw relaxation or masseter muscle rigidity occurs most often with?

A

peds-not necessarily abnormal

  • may occur in up to 4% of peds population
  • the question is normal variant or MH?
139
Q

Sustained muscle contraction may also occur with these two conditions which may make ventilation impossible when administering Succ to the pediatric population.

A
  1. myotonia congentia

2. myotonia dystrophia

140
Q

Succinylcholine should be administered with GREAT CAUTION to patients suffering from(2)?

In these circumstances succinylcholine may induce(2)…..due to?

A
  • electrolyte abnormalities
  • DIGOXIN TOXICITY
  • serous cardiac arrhythmias
  • or cardiac arrest

-hyperkalemia

141
Q

Does non-depolarizer pre-treatment prevent hyperkalemia?

A

NOPE

142
Q

Succinylcholine has fallen out of favor in part due to the small % of male peds patients with undiagnosed _____, typically _____.

With these undiagnosed conditions, what 3 adverse events are possible if given succinylcholine?

A
  • myopathies
  • Duchenne MD
  • rhabdomyolysis
  • hyperkalemia
  • cardiac arrest
143
Q

Succinylcholine has no direct effect on the myocardium(t/f).

A

true

144
Q

Succinylcholine stimulates(2)…….which can cause changes in cardiac rhythm including cardiac arrest.

A
  • autonomic ganglia

- muscarinic receptors

145
Q

Changes in cardiac rhythm may result from(2)……., particularly in children.

A
  • vagal stimulaiton

- hyperkalemia

146
Q

The effects upon the human heart by succinylcholine may be enhanced by?

A

halogenated anesthetics

147
Q

What 3 dysrhythmias may occur with succinylcholine dosing?

A
  • sinus brady
  • junctional rhythms
  • sinus arrest
148
Q

These cardiac dysrhythmias with succinylcholine dosing are due to?

A
  • Succinycholine actions at cardiac muscarinic cholinergic receptors where succinylcholine mimics acetylcholine effects.
  • most likely to occur when a second dose follows 5 minutes after first dose*
149
Q

Will atropine prevent second dose bradycardia in succinylcholine?

A

no;but pretreatment with a non-depolarizing muscle relaxant may.

150
Q

IV succinylcholine in children may result in deadly arrhythmias due to(2)?
When this occurs, what should be suspected?

A
  • rhabdomyolysis & hyperkalemia

- underlying myopathy

151
Q

If a healthy appearing kid develops cardiac arrest after succinylcholine not due to inadequate ventilation, oxygenation or anesthesia OD, what 4 IMMEDIATE treatments for hyperkalemia should be instituted?

Quiz Question

A
  1. IV calcium
  2. bicarbonate
  3. glucose with insulin
  4. hyperventilation
152
Q

It is recommended that the use of succinylcholine in children be reserved for(5)?

A
  • emergency intubation
  • laryngospasm
  • difficult airway
  • full stomach
  • IM use when a suitable vein is inaccessible
153
Q

What 2 conditions may occur related to the head/eyes immediately after injection of Succ and during fasciculation’s?

A
  • increase in intraocular pressure

- increase in ICP

154
Q

Succ maximally increases IOP how many minutes post administration? This IOP last only how long?

A

2-4 minutes

5-10 minutes

155
Q

The mechanism of action for IOP with such administration is due to(2)?

A
  • contraction of extra-ocular muscles
  • Succinylcholine cycloplegic actions with deepened anterior chamber and increased resistance to aqueous humor flow

SUCCINYLCHOLINE SHOULD BE AVOIDED WITH OPEN GLOBE INJURES

156
Q

Succinylcholine produces inconsistent increases in intragastric pressures related to?

A

fasciculations

Pretreatment with non-depolarizers prevents increases in intragastric pressures

Children do not have intragastric pressures > 20 cm H2O even without pre-treatment

157
Q

TOF = No response
What % blockade
What clinical significance?

A

100% blocked; suitable for intubation

158
Q

TOF = one twitch(response)
What % blockade
What clinical significance?

A

90% blocked; suitable for ventilation

159
Q

TOF = two twitches(responses)
What % blockade
What clinical significance?

A

80-90% blocked; suitable for short term relaxation

160
Q

TOF = three twitches(responses)
What % blockade
What clinical significance?

A

75-80% blocked; maintenance doses needed

161
Q

TOF = four twitches(responses)
What % blockade
What clinical significance?

A

0-75% blocked; rapid cholinesterase inhibitors reversal

3rd Quarter (22 decks)

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