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Pharmacology > Skeletal Muscle Relaxants > Flashcards

Skeletal Muscle Relaxants Flashcards

1
Q

What type of transmission process will evoke a skeletal muscle contraction?

A

Nicotinic cholinergic

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2
Q

What are neuromuscular blocking drugs normally used for?

A

Adjuncts to general anesthesia, to facilitate intubation and optimize surgical conditions

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3
Q

Which areas of the body do skeletal muscle relaxants NOT have effect on?

A

Cardiac and smooth muscles

Central nervous system

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4
Q

What are spasmolytic or “centrally-acting’ muscle relaxants used for?

A

Treat chronic back pain

Painful fibromyalgic conditions

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5
Q

Difference in muscle reaction and central activity between neuromuscular blocking agents vs spasmolytic drugs

A

Neuromuscular blocking agents: Cause paralysis with NO central effect
Spasmolytic drugs: Reduces spasticity WITH central effects

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6
Q

Which receptors are not normally involved in neuromuscular transmission but proliferate in pathologic conditions like prolonged immobilization in CVS and thermal burns?

A

Perijunctional/extrajunctional receptors

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7
Q

Stimulation of __________ receptors mobilizes addtional NT towards synaptic membrane to increase Ach at the synapse.

A

Presynaptic motor axon terminal receptors

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8
Q

Where can you find Nicotinic cholinergic receptors

A

NMJ

Peripheral autonomic ganglia

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9
Q

In the CNS, nicotinic cholinergic receptors controls _______ release from the ________ sites.

A

Neurotransmitter; presynaptic

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10
Q

What does binding of Ach to nicotinic cholinergic receptors initiate in muscle? in peripheral ganglia?

A

End plate potential (EPP); Excitatory postsynaptic potential (EPSP)

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11
Q

Nicotinic cholinergic receptors are composed of how many subunits? And what subunits are these?

A

5; 2 alpha subunits, 1 beta, 1 gamma, 1 delta

1 gamma is switched to 1 epsilon in adults

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12
Q

In what subunit(s) does Ach bind to in order to cause a conformational change in the nicotinic cholinergic receptor?

A

Alpha subunits (particularly alpha-beta and alpha-delta

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13
Q

The 2 molecules of Ach must bind ________ in order to cause conformational change in nicotinic cholinergic receptor.

A

Simultaneously

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14
Q

True or False. A conformational change in the nicotinic cholinergic receptor can be elicited with the binding of 1 molecule of Ach.

A

False. 2 molecules MUST bind simultaneously in order to elicit a conformational change.

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15
Q

What are the 2 types of muscle relaxants?

A

Neuromuscular blockers and Spasmolytics

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16
Q

What are the 2 types of neuromuscular blockers?

A

Nondepolarizing and Depolarizing neuromuscular blockers

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17
Q

What are the 2 subdivisions of nondepolarizing neuromuscular blockers?

A

Steroidal (“-curonium”) and Isoquinoline derivatives (“-curium”)

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18
Q

What are the steroidal nondepolarizing neuromuscular blockers?

A 
Pancuronium
Pipecuronium
Rocuronium
Papacuronium
Vecuronium
(PPRRV "-curonium")
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19
Q

What are the isoquinoline derivative nondepolarizing neuromuscular blockers?

A 
Tubocurarine (prototype, first NMB synthesized)
Metocurine
Doxacurium
Atracurium
Mivacurium
Cistacurium
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20
Q

What is are examples of depolarizing neuromuscular blockers? Which is the only one used clinically?

A

Succinylcholine (only one used clinically)

Decamethonium

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21
Q

Structural difference between Ach and succinylcholine

A

Presence of additional 1 or 2 quaternary nitrogens

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22
Q

What ring structure do steroidal derivatives have? Isoquinoline derivatives?

A

4 ring (steroid nucleus) structure; Basic ring structure

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23
Q

Nondepolarizing neuromuscular blockers are ________ antagonists to the __________ receptors at the __________ of skeletal muscles.

A

Competitive; Nicotinic cholinergic; NMJ

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24
Q

Nondepolarizing neuromuscular blockers cause the release of _________ to cause bronchospasm, peripheral vasodilation with subsequent hypotension.

A

Histamine

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25
Q

What route must NMB be given?

A

Parenteral; they are inactive orally.

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26
Q

NMB exhibit (rapid / slow) initial distribution phase and (rapid / slow) elimination phase

A

RAPID initial distribution

SLOWER elimination

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27
Q

Steroidal derivatives are mainly metabolized in the __________.

A

Liver.

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28
Q

What are the metabolites of steroidal derivatives in general? Which is most important and why?

A

3-hydroxy, 17-hydroxy, 3,17-dihydroxy;
3-hydroxy is 40-80% are potent as the parent drug and therefore produces neuromuscular blockade (accumulation causes prolonged paralysis)

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29
Q

Atracurium and cistacurium produce this metabolite.

A

Laudanosine

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30
Q

What is “Hoffman elimination”?

A

Spontaneous deactivation of atracurium (and cisatrucurium) to laudanosine.

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31
Q

What is the half-life of laudanosine? Why is this of importance?

A

150 minutes. It can therefore accumulate and cause cerebral side effects (high concentrations readily cross BBB) = SEIZURES

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32
Q

Advantage of cisatracurium (potent isomer of atracurium) over atracurium.

A

Less side effects

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33
Q

Nondepolarizing neuromuscular blockers with liver excretion? Significance?

A

Rocuronium
Vecuronium
**Shorter 1/2 lives and duration of action

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34
Q

Nondepolarizing neuromuscular blockers with renal elimination? Significance?

A

Pipecuronium (60%)
Doxicurium, Pancuronium (80% - long 1/2 life)
Tubocurarine (40%)
Metocurarine (40%)

**Longer 1/2 lives and duration of action

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35
Q

Nondepolarizing neuromuscular blockers with plasma elimination? Significance?

A

Atracurium
Cisatracurium
Mivacurium
**Can be given to patients with liver and kidney dysfunction

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36
Q

Which of the nondepolarizing neuromuscular blockers have the fastest time of onset?

A

Rocuronium (60-120 seconds)

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37
Q

Nondepolarizing neuromuscular blockers with short duration (10-20 minutes)?

A

Mivacurium

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38
Q

Nondepolarizing neuromuscular blockers with intermediate duration (20-35 minutes)?

A

Atracurium
Vecuronium
Rocuronium

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39
Q

Nondepolarizing neuromuscular blockers with long duration (>35 mins)?

A 
Pancuronium
Tubocurarine
Gallamine
Doxacurium
Metocurine
Pipercurium
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40
Q

Mechanism of action of nondepolarizing neuromuscular blockers in low dose?

A

Low: compete for binding to postsynaptic nicotinic receptor sites in NMJ of skeletal muscle, Interfere with presynaptic release of Ach

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41
Q

Mechanism of action of nondepolarizing neuromuscular blockers in high doses?

A

More intense motor blockade by blocking the pore of the nicotinic receptor channel complex

42
Q

Which muscles are affected first in neuromuscular blockade?

A

Small muscles (face, had, foot) –> large muscles (abdominals, trunk, paraspinous, diaphragm) last

43
Q

Which muscle is paralyzed last by NMBs? Which recovers first?

A

Diaphragm; Diaphragm =D

44
Q

Recovery of the muscles in NMB is in what order?

A

Reverse. Last ones affected are first to recover, etc…

45
Q

Nondepolarizing neuromuscular blockers have a ______ volume of distribution?

A

Limited (will only be slightly above blood volume (80-140 ml/kg)

46
Q

Nondepolarizing neuromuscular blockers with mininmal effects on the CVS?

A

Vecuronium
Pipecuronium
Doxacurium
Rocuronium

47
Q

Nondepolarizing neuromuscular blockers that cause hypotension 2/2 histamine release causing vasodilation (in order of most to least)

A

Tubocurarine&raquo_space; Metocurine > Atracurium > Mivacurium > (Cisatracurium)

48
Q

Nondepolarizing neuromuscular blockers that cause ganglionic blockade in large doses

A

Tubocurarine

Metocurarine

49
Q

Nondepolarizing neuromuscular blockers that increase HR, CO with increased systemic vascular resistance?

A

Pancuronium

50
Q

Characteristics of selected nondepolarizing neuromuscular blockers: Rapacuronium

A

Shortest onset and duration
Alternative to succinylcholine
High incidence of severe bronchospasm
OUT OF CLINICAL USE (Hello!?!?! picka different one to teach us then!!!)

51
Q

Characteristics of selected nondepolarizing neuromuscular blockers: Mivacurium

A

High doses cause histamine release

Caution: Pt with hx of allergies, asthma

52
Q

Characteristics of selected nondepolarizing neuromuscular blockers: Atracurium

A

Primary inactivation is by Hoffman Elimination (metabolite: laudanosine)
Cause seizures at high concentration of laudanosine metabolite

53
Q

Mechanism of action of depolarizing neuromuscular blockers (Succinylcholine)

A

Nicotinic AGONIST causing twitching and fasciculations initially

54
Q

What enzyme(s) degrade succinylcholine?

A

Butyrylcholinesterase (liver enzyme)

Pseudocholinesterase (plasma enzyme)

55
Q

Difference between succinylcholine and acetylcholine

A

Slower hydrolysis therefore stays at receptor site longer and repeated opening and closing of receptor channel

56
Q

Why is succinylcholine given in continuous infusion?

A

Only small doses reach the NMJ d/t hydrolysis in the plasma by pseudocholinesterase

57
Q

What is the onset of action of succinylcholine? duration of action?

A

60-90 seconds; 5-10 minutes

58
Q

What conditions prolong succinylcholine blockade?

A 
Decreased pseudocholinersterase levels
Atypical pseudocholinesterases (abnormal gene variant)
59
Q

What kind of patients will have decreased pseudocholinesterase levels?

A 
Liver disease
Pregnant
Burn 
Patients on oral contraceptives
Patients on MAOI, echothiopate, cytotoxic drugs, neoplastic disease, anticholinesterases, tetrahydroamacrine, hexafluorenium
60
Q

What is the dibucaine number and how does it predict paralysis time?

A

Dibucaine # is the % enzyme that is inhibited by dibucaine. It predicts the ability of the patient to metabolize succinylcholine; The lower the dibucaine number, the longer the paralysis time

61
Q

What is the normal dibucaine number (homozygous typical)

A

70-80

62
Q

Dibucaine number for heterozygous ATYPICAL? How much longer is the neuromuscular blockade in response to mevacurium/Sch?

A

50-60; increased by 50-100%

63
Q

Dibucaine number for homozygous ATYPICAL? How much longer is the neuromuscular blockade mevacurium/Sch?

A

20-30; increased by 4-8 hours

64
Q

What are the 2 phases in depolarizing neuromuscular blockade?

A

Phase I or Depolarizing block

Phase II or Desensitizing block

65
Q

Describe the Phase I block

A

Sch binding to 2 alpha subunits cause opening of the channel with subsequent repetitive depolarization
Repetitive firing causes fasciculations until action potential cannot occur (depolarizing block = no end plate repolarization)
No excitation-contraction coupling causing flaccid paralysis

66
Q

True or False. Cholinesterase inhibitors augment phase I block.

A

True.

67
Q

Describe the Phase II block

A

Higher doses = prolonged closed state

There is gradual repolarization but NM transmission remains blocked d/t desensitized membrane (channel block)

68
Q

Phase II block is (sensitive / not sensitive) to cholinesterase inhibitors?

A

Sensitive

69
Q

Effects of Sch on CVS

A
  • Cardiac arrythmias with halothane (sinus bradycardia, ventricular arrythmias)
  • Stimulation of ALL cholinoreceptors ((-) ionotropic & chronotropic effects)
  • Direct myocardial effects (increased muscarinic and ganglionic stimulation)
70
Q

How to prevent effects of Sch on CVS

A

Thiopental
Atropine
Ganglionic blocking drugs
Nondeoplarizing NMB

71
Q

Adverse effects of Depolarizing NMBs

A 
Hyperkalemia
Cardiac arrest especially in children with subclinical Duchenne's muscular dystrophy
Malignant hyperthermia
Increased IOP
Increased intragastric pressure
Muscle pains (myalgia) 2/2 fasciculations
Masseter spasm
Increased(?) ICP
72
Q

Effect of tubocurarine (0.1-0.4 mg) infusion

A

Initially motor weakness flaccidity and inexcitable to motor stimulation

73
Q

Effect of Sch (1-2 mg/kg) infusion

A

Transient muscle fasciculations (chest, abdomen, arm, neck, legs) and then paralysis of respiratory muscles

74
Q

When do you monitor effects of NMB?

A

1) Before intubation
2) Intraoperatively
3) During recovery - spontaneous and after reversla of cholinesterase inhibitor

75
Q

How do you assess neuromuscular transmission?

A

By nerve stimulation (transdermal electrical stimulation of peripheral nerve of the hand and recording the pattern of contractions/twitches

76
Q

What is the TOF (train of four) ratio?

A

After application of four stimuli of 2Hz, TOF ratio is the ratio of the strength of the 4th contraction to the 1st contraction.

77
Q

In late phase II, the blockade characteristics are identical to those of _________ block. Describe. How is this reversed?

A

NONdepolarizing block; Nonsustained twitch response to a tetanic stimulus; Reversal by acetylcholinesterase inhibitors.

78
Q

What does the single twitch pattern of electrical stimulation determine?

A

Determines peak effect

79
Q

What does the TOF pattern of electrical stimulation determine?

A

Differentiates nondepolarizing vs depolarizing block

80
Q

What does the double burst pattern of electrical stimulation determine?

A

It detects residual of neuromuscular block

81
Q

A TOF ratio of 0.15-0.25 is indicative of?

A

Adequate surgical relaxation

82
Q

A TOF ratio of ______ is needed for safe extubation adn recovery after surgery?

A

> 0.9

83
Q

Pancuronium is contraindicated in tachycardic patients because?

A

it is a sympathetic stimulator

84
Q

Drug interactions that augment or enhance neuromuscular block

A

Anesthetics
Antibiotics: aminoglycosides
Local anesthetics (high doses block neuromuscular transmission)

85
Q

Drug interactions that increase duration of Sch

A

Sch given after administration of neostigmine

86
Q

Drug interactions that prevent fasciculations from Sch

A

Nondeoplarizers given before Sch increase dose requirement of Sch

87
Q

Effect of Myasthenia gravis (Sch infusion)

A

Enhanced neuromuscular blockade

88
Q

Effect of age (elderly >70 YO) (Sch infusion)

A

Prolonged duration d/t decreased clearnce

decreased dose needed

89
Q

Effect of UMN disease, burns

A

DO NOT USE in burns
Resistance to nondepolarizing blocker
Dose increase needed

90
Q

How do you reverse the blockade of nondepolarizing blockers

A 
Competitive antagonism
Provide cholinesterase inhibitors (increase Ach) - neostigmine, pyridostigmine, edrophonium
Anticholinergic added (atropine) to counter cholinergic effects
91
Q

What is Suggamedex?

A

Novel cyclodextrine drug, rapidly inactive steroidal NMB drug, it is a selective relaxant binding agent

92
Q

How do spasmolytics relieve muscle spasms?

A

Modify the stretch reflex arc or by interfering directly with the skeletal muscle

93
Q

Which spasmolytic does not act on the CNS?

A

Dantrolene

94
Q

Examples of centrally-acting spasmolytics

A 
Diazepam
Baclofen
Cyclobenzaprine
Carisoprodol
Methocarbamol
Chlorophenasin carbamate
Chlorozoxasone
Orphenadrine citrate
Menphanasin
95
Q

Examples of peripherally-acting spasmolytics

A

Dantrolene
Episirone HCl
Pheniramidone

96
Q

Mechanism of action of diazepam

A

Binds with components of GABA(A) to facilitate GABA mediated presynaptic inhibition

97
Q

Mechanism of action of baclofen

A

Agonist of GABA(B) receptor resulting to hyperpolarization

Reduces pain by inhibition of substance P

98
Q

Mechanism of action of Tizanidine

A

Significant alpha2 adenoreceptor agonist with fewer CVS effects

99
Q

Mechanism of action of Dantrolene

A

Interferes with the release of calcium from SR by binding to the ryanodine receptors (prevents channel opening)
Prevents excitation-contraction coupling

100
Q

What is the drug of choice for malignant hyperthermia?

A

Dantrolene

101
Q

Malignant hyperthermia is a result of?

A

Massive release of calcium from SR leading to uncontrolled contraction and stimulation of metabolism in skeletal muscles

Pharmacology (14 decks)

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