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Pharmacology Exam 2 > NMBD > Flashcards

NMBD Flashcards

1
Q

What is the principle effect(s) of NMBDs?

A

interrupt transmission of nerve impulses at the NMJ; to optimize surgical conditions and augment patient safety

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2
Q

Is succinylcholine an agonist or antagonist?

A

Agonist, causes depolarization

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3
Q

Are Non-depolarizing NMBs agonists or antagonists?

A

Competitive Antagonists, prevent depolarization

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4
Q

The terminal of the ________ motor nerve releases __________ to the motor end plate at the NMJ.

A

presynaptic; acetylcholine

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5
Q

What is embedded in the lipid bilayer of the presynaptic nerve terminal?

A

Voltage gated Ca channels and nicotinic Ach receptors

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6
Q

True/False: Nicotinic receptors are at both pre and postsynaptic membranes.

A

True

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7
Q

What breaks down/metabolizes Ach?

A

Acetylcholinesterase (AChE)

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8
Q

What makes up Acetylcholine? and which enzyme?

A

Acetyl-CoA and Choline with the enzyme Choline Acetyltransferase (ChAT).

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9
Q

What do synaptic vesicles contain? how many?

A

Quanta of ACh molecules, 1-50k per vesicle

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10
Q

The motor nerve action potential enters and ________ the nerve terminal.

A

depolarizes

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11
Q

What happens after depolarization of the nerve terminal?

A

voltage sensitive Ca channels open, calcium diffuses down conc gradient within nerve terminal.

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12
Q

What does the released Ca inside the nerve terminal do?

A

causes synaptic vesicles of ACh to fuse with nerve cell membrane.

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13
Q

Release of Neurotransmitter ACh depends on entry of _________ into the terminal

A

Calcium

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14
Q

What happens after the vesicles fuse with the nerve cell membrane?

A

Exocytosis of Ach, released into synaptic cleft.

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15
Q

What does the presynaptic nicotinic ACh receptor do?

A

responds to ACH by increasing synthesis and release of ACh; positive feedback mechanism preventing depletion of ACh at NMJ

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16
Q

What does ACh combine with at the postsynaptic membrane?

A

nicotinic ACh receptors.

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17
Q

How many subunits are on a nicotinic ACh receptor and what are they?

A

5; 2 alpha, 1 beta, 1 delta, 1 epsilon

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18
Q

How many molecules of ACh must combine with what type of subunits?

A

2 molecules of ACh with 2 alpha subunits

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19
Q

What causes the nicotinic ACh receptor to open?

A

when both nicotinic receptor proteins are occupied by ACh.

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20
Q

What happens when the channels of the nicotinic ACh receptor snap open?

A

Na and Ca INTO cell, K OUT OF cell, making the cell more positive, causes motor end plate to depolarize–Action potential sweeps across skeletal muscle and triggers contraction.

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21
Q

How many of the 5 million postsynaptic receptors need to be occupied by ACh in order to generate an end plate potential?

A

250-500k

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22
Q

What does AChE split ACh into?

A

choline and acetate, which terminates the action of ACh

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23
Q

Is the half life of ACh long or short?

A

very short due to high conc of AChE at synapse

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24
Q

What happens to choline after metabolism?

A

transported back to nerve terminal where it is reconverted to ACh

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25
Q

What happens to acetate after metabolism?

A

diffuses away

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26
Q

Name the steps of the main events at the NMJ

A

1.action potential depolarizes motor neuron. 2.triggers calcium channels to open and influx. 3.facilitates exocytosis of ACh vesicles. 4. ACh molecules released into synaptic cleft. 5. ACh binds with nicotinic receptors on motor end plate causing opening of Na/K channels; Na and Ca in, K out. 6.change in membrane potential sweeps and causes Na channels of adjacent membranes to open thus propagation. 7. ACh rapidly hydrolyzed by AChE. 8. channels close and motor end plate repolarizes. 9. muscle relaxes

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27
Q

Describe extrajunctional nicotinic receptors.

A

proliferate in response to paralysis, dystrophies, upper/lower motor neuron injury, major burns. channels stay open 4x longer and upregulate –hyper K

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28
Q

What type of receptor is a nicotinic receptor at the NMJ?

A

ligand gated ion channel

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29
Q

Where is ChAT located? AChE?

A

ChAT is in presynaptic nerve terminal; AChE is in the synaptic cleft.

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30
Q

What are the other names for Acetylcholinesterase?

A

True cholinesterase, specific cholinesterase, genuine cholinesterase, type I cholinesterase

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31
Q

What’s the difference between depolarizing muscle relaxants and non-depolarizing muscle relaxants?

A

Depolarizing are ACh receptor AGONISTS, Non-depolarizing are COMPETETIVE ANTAGONISTS

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32
Q

What is an example of a depolarizing muscle relaxant?

A

Succinylcholine

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33
Q

What are examples of non-depolarizing muscle relaxants and the durations?

A

Long: pancuronium; Intermediate: atracurium, cisastracurium, rocuronium, vecuronium; short: mivacurium

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34
Q

Succinylcholine is ______ bound together.

A

2 ACh molecules

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35
Q

Why is succinylcholine longer acting than ACh?

A

It’s broken down by a different enzyme that isn’t as available in the synaptic cleft.

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36
Q

What does succinylcholine do?

A

mimics ACh but causes a sustained depolarization of the cell with an absolute refractory period. As long as the motor end plate doesn’t repolarize it can’t have additional action potentials or contractions.

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37
Q

Why is the duration of Succ so short?

A

rapid hydrolysis by plasma cholinesterase

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38
Q

What are the other names for plasma cholinesterase?

A

Pseudocholinesterase or Butyrocholinesterase, false, non-specific, type II cholinesterase

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39
Q

What is the metabolite of succinylcholine?

A

succinylmonocholine

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40
Q

How much of the injected dose of Succ reaches the NMJ?

A

10%, most is rapidly metabolized

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41
Q

Where is plasma cholinesterase synthesized?

A

liver

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42
Q

Why might you have a prolonged Succ blockade?

A

decreased hepatic production of plasma cholinesterase, drug-induced decreases in plasma cholinesterase, genetically determined presence of atypical plasma cholinesterase

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43
Q

Name factors that lower plasma cholinesterase.

A

liver disease, advanced age, malnutrition, pregnancy, burns, oral contraceptives, MAOIs, cytotoxic drugs, anticholinesterase drugs, high estrogen levels

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44
Q

Name drugs that decrease pseudocholinesterase activity.

A

echothiophate, neostigmine, pyridostigmine, phenelzine, cyclophosphamide, metoclopramide, esmolol, pancuronium, oral contraceptives

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45
Q

Atypical plasma cholinesterase is a __________ defect.

A

qualitative, pseudocholinesterase is produced in sufficient quantity, however the enzyme that is produced is not functional.

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46
Q

What is dibucaine?

A

a local anesthetic that inhibits normal plasma cholinesterase activity

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47
Q

Does dibucaine have any effect on atypical plasma cholinesterase?

A

no

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48
Q

What does a dibucaine number reflect?

A

the percentage of normal enzyme that is inhibited by dibucaine. Blood test assessing QUALITY of enzyme, not routinely drawn.

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49
Q

What does a dibucaine number of 80 and above mean?

A

normal response to Succ, recover 5-10 min

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50
Q

What does a dibucaine number of 40-60 mean?

A

response to Succ prolonged 50-100% (20-30 min)

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51
Q

What does a dibucaine number of 20 and below mean?

A

response to Succ prolonged by 4-8 hours.

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52
Q

Where are postoperative myalgias common from Succ?

A

neck, back, abdomen

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53
Q

Who does postoperative myalgias tend to affect?

A

young muscular adults

54
Q

How long do postoperative myalgias last?

A

24-48 hours

55
Q

What is the mechanism of postop myalgias?

A

muscle damage from fasciculations, prostaglandins and cyclooxygenases.

56
Q

How do you minimize postop myalgias?

A

meds: pretreat with NDMR 1/10th of ED95. (2mg roc, 0.3mg vec) 3-5 min before Succ. Prostaglandin inhibitors, NSAIDS, lidogaine 1.5mg/kg. Prevent: perform deep intubation, avoid Succ.

57
Q

What are the side effects of Succinylcholine?

A

Bradycardia, Tachycardia & HTN, HyperK, Myalgias, Myo-globinuria, Increased intra-gastric pressure ICP IOP, MH trigger, masseter spasm, prolonged resp paralysis

58
Q

How much does K increase after Succ administration?

A

plasma K conc may increase 0.5-1 mEq/L in normal patients for 10-15 min and 5-10 mEq/L in burn/trauma/head injury patients

59
Q

Why can Succ cause bradycardia?

A

muscarinic cardiac receptor activity

60
Q

Why can Succ cause tachycardia/HTN?

A

modest stimulation of autonomic ganglia Nicotinic receptors.

61
Q

What factors increase a Succ block?

A

antibiotics (esp aminoglycosides), local anesthetics, anticholinesterase agents (ACh increased), increased extracellular K, increased extracellular Mg, inherited pseudocholinesterase defect, lithium

62
Q

What accentuates Succ-induced HyperK?

A

unrecognized muscular dystrophy, burns (7-10 days post), conditions with upregulation of extra-junctional ACh receptors (paraplegias, hemiplegia, MD, guillain-barre, upper motor neuron lesions/injury, CVA), severe abd infections, severe metabolic acidosis.

63
Q

What’s the big deal with extra-junctional nicotinic receptors?

A

Subunits on nicotinic receptors structurally different, impacts how nicotinic receptor responds to ACh & Succ (increased sensitivity, stays open 4x longer, INCREASED INFLUX OF K.

64
Q

What do NDMR do at the presynaptic membrane?

A

inhibit mobilization of ACh to be ready for exocytosis, mechanism for FADE

65
Q

What do NDMR do at the postsynaptic membrane?

A

Combine with ACh receptors, competitively blocking ACh from attaching to receptors, channels stay closed so no electrolyte influx or efflux and postsynaptic membrane stays polarized.

66
Q

Which type of NMBDs have direct effects on the channels?

A

Depolarizing, non-depolarizing have NO direct effect.

67
Q

Discuss the pharmacokinetics of NDMR: solubility/elimination/protein binding.

A

highly ionized, water soluble, limited lipid solubility, no CNS effects (doesn’t cross BBB), minimal renal tubular reabsorption, no effect of fetus, renal and hepatic elimination. 50% bound to plasma protein. ALL MUSCLE RELAXANTS CAN BE EXCRETED BY KIDNEYS OF OTHER ROUTES UNAVAILABLE.

68
Q

Name the steroidal NDMRs.

A

panCURONIUM, veCURONIUM, roCURONIUM

69
Q

Name the benzylisoquinolinium NDMRs.

A

atraCURIUM, cisatraCURIUM, mivaCURIUM

70
Q

Which types of NDMRs are dependent on hepatic/renal function for metabolism and which aren’t?

A

Aminosteroids DEPENDENT, benzyls NOT dependent–undergo spontaneous degradation in plasms

71
Q

How is atracurium metabolized?

A

66% ester hydrolysis, 33% Hoffman

72
Q

What % is renal elimination for atracurium?

A

10-40%, high

73
Q

What is atracurium’s metabolite?

A

Laudanosine, increase CNS–>seizures

74
Q

How is cisatracurium metabolized?

A

77% Hoffman, no ester hydrolysis

75
Q

What % is renal elimination for cisatracurium?

A

16% of total, low

76
Q

What is cisatracurium’s metabolite?

A

laudanosine increase, 5x less

77
Q

How is Rocuronium metabolized?

A

None

78
Q

What % is renal elimination for rocuronium/

A

10-25%

79
Q

What is rocuronium’s metabolites?

A

none

80
Q

What % of Rocuronium is eliminated by liver?

A

70%…avoid in liver disease.

81
Q

How is vecuronium metabolized?

A

liver 30-40%

82
Q

What % of vecuronium is eliminated by liver?

A

40-50% cleared in bile

83
Q

What % of vecuronium is eliminated renally?

A

25-30%

84
Q

What is vecuronium’s metabolite?

A

3-OH vecuronium 1/2 potency

85
Q

How is pancuronium metabolized?

A

liver 10-20%

86
Q

What % of pancuronium is eliminated by the liver?

A

15%

87
Q

What % of pancuronium is eliminated renally?

A

85% …avoid in renal disease

88
Q

What is Pancuronium’s metabolite?

A

3-OH pancuronium 1/2 potency

89
Q

What NMBD is is primarily excreted renally?

A

Pancuronium

90
Q

What NMBDs are primarily excreted biliary?

A

vecuronium and rocuronium

91
Q

What NMBDs primarily undergo metabolism?

A

Succinylcholine, Atracurium, and Cisatracurium (and mivacurium)

92
Q

Which NDMR has histamine release?

A

atracurium, can cause hypotension/tachycardia, dependent on doe/speed of injection

93
Q

In hoffman elimination alkalosis and hyperthermia cause ______metabolism and ______DOA.

A

faster metabolism, shorter DOA

94
Q

In hoffman elimination _______ and __________ cause slower metabolism and longer DOA.

A

acidosis and hypothermia

95
Q

Which NMBD has a slight effect on vagal blockade?

A

Rocuronium

96
Q

Which NMBD has a moderate effect on vagal blockade?

A

Pancuronium, blocks muscarinic receptors at SA node, avoid if trying to avoid tachycardia

97
Q 
What is the primary event terminating the drug's effects?
Roc
Vec
Panc
Atra
Cisatra
A 
roc--biliary
Vec--biliary
Panc--renal
Atra--ester hydrolysis
Cisatra--hoffman elim
98
Q

Why are NMBD associated with anaphylaxis?

A

chemical structure has an antigenic quaternary NH4+1 group that interacts with IgE causing mast cell and basophil degradation which increases tryptase (primary mediator for anaphylaxis.

99
Q

What is the order the NMBD are associated with anaphylaxis?

A

Succ>atra>cisatra>roc>vec

100
Q

Does Succ cause histamine release?

A

yes

101
Q

How would you dose vecuronium for maintenance of paralysis after succinylcholine was used for intubation?

A

1/2 intubation dose, 4mg Vec. CHECK TWITCHES FIRST!

102
Q

How do you calculate an intubating dose for NMBDs?

A

2-3x the ED95

103
Q

What drugs potentiate NDMR?

A

Aminoglycoside antibiotics (polymixins, clindamycins), local anesthetic large doses, volatiles (des>sevo>iso>n2o), mag sulfate, lithium, loop diuretics, antiarrhythmics (quinidine, propranolol, procainamide)

104
Q

What patient factors potentiate NDMRs?

A

hypothermia, gender (women more sensitive) Electrolytes: high Mg, low Ca, low K

105
Q

What factors decrease the effects of NDMRs?

A

Chronic anticonvulsants, hyperparathyroidism and hypercalcemia (increased Ca enhances ACh release which competes with NDMRs), hyperkalemia

106
Q

What affect does myasthenia gravis have on NMBDs?

A

Fewer functional ACh receptors due to degradation from antibodies so INCREASED SENSITIVITY to NDMRs and
RESISTANCE TO SUCC.

107
Q

What affect does muscle denervation injuries have on NMBDs?

A

chronic decrease in ACh release with compensatory increase in ACh-N postsynaptic receptors (upregulation) so RESISTANCE TO NDMRs (more to be blocked) and
EXAGGERATED SUCC RESPONSE

108
Q

Where is the best location to monitor a PNS for RECOVERY?

A

Ulnar nerve, adductor pollicis muscle

109
Q

Where is the best location to monitor a PNS for ONSET of blockade?

A

Facial nerve, orbicularis oculi muscle or corrugator supercilii

110
Q

What nerve and muscle adducts thumb?

A

ulnar nerve, adductor pollicis muscle

111
Q

What nerve and muscle causes eyebrow twitch?

A

temporal branch of facial nerve, corrugator supercilii muscle

112
Q

What nerve and muscle causes eyelid squint?

A

zygomatic branch of facial nerve, orbicularis oculi muscle

113
Q

What nerve and muscle causes plantar flexion of great toe?

A

posterior tibial nerve, flexor hallucis brevis muscle

114
Q

What is the order of most resistant (last to block, 1st to recover) to most sensitive (1st to block, last to recover) areas to measure blockade?

A

Vocal Cords Die Out After Adding Muscle Paralysis Externally.
Vocal cords; Diaphragm, Orbicularis Oculi, Abdominal Rectus Adductor Pollicis, Masseter, Pharyngeal, Extra-ocular

115
Q

What type of TOF response does a depolarizing block cause?

A

Constant but diminished response

116
Q

What type of TOF response does NDMR cause?

A

FADE, gradual decrease in twitch height as ACh is depleted.

117
Q

What mechanism is responsible for FADE with TOF monitoring when using PNS and NDMRs?

A

ANTAGONISM of presynaptic nicotinic receptors: so no mobilization of stored ACh inside vesicles which limits ACh supply to only what is available in synaptic cleft. So with each successive nerve stimulation there’s less ACh released

118
Q

What 2 situations could cause a phase II Succ block?

A

Succ dose >7-10mg/kg

30-60 min of continuous IV infusion of Succ

119
Q

What is the difference between a phase I and phase II Succ block?

A

Phase I normal, Phase II from high doses, mimics nondepolarizing FADE

120
Q

Why do phase II blocks occur?

A

high doses of Succ: impair ACh mobilization and release through inhibition of presynaptic nicotinic receptors, possibly create change in postsynaptic nicotinic receptors–causing to resemble FADE.

121
Q

The presence or absence of __________ distinguishes a phase I and phase II block.

A

FADE

122
Q

Describe characteristics of a phase I block.

A

Depolarizing, preceded by fasciculations, decrease in twitch tension, no fade during repetitive stimulation, no post-tetanic potentiation

123
Q

Describe characteristics of a phase II block.

A

Non-depolarizing, decrease in twitch tension, fade during repetitive stimulation, post-tetanic potentiation

124
Q

What TOF ratio is needed for safe extubation/recovery?

A

> 0.9, <0.9 associated with impaired swallowing, pharyngeal dysfunction, increased risk for aspiration, decrease in hypoxic ventilatory drive

125
Q

What is the equation for TOF ratio?

A

ht of 4th twitch/ht of 1st twitch x100. can’t use PNS

126
Q

What % of receptors are blocked with 1 abolished TOF response(3/4 twitches)?

A

75%

127
Q

What % of receptors are blocked with TOF 2/4?

A

80%

128
Q

What % of receptors are blocked with TOF 1/4?

A

90%

129
Q

What test most closely indicates TOF ratio of 0.9?

A

sustained jaw clench on tongue blade sustained for 5 sec (max of 50% of receptors occupied)

130
Q

What test represents TOF ratio of 0.5-0.6.

A

head lift >5 sec.

Pharmacology Exam 2 (5 decks)

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