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Cert Prep > Valley: Neuromuscular Physiology & Pharmacology > Flashcards

Valley: Neuromuscular Physiology & Pharmacology Flashcards

1
Q

Motor neurons to skeletal muscle originate in the ——- of the spinal cord

A

anterior (ventral) horn

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2
Q

Sensory neurons from skeletal muscle carry action potentials to the spinal cord via the —-

A

dorsal horn

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3
Q

These motor and sensory nerves are —— nerves

A

somatic

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4
Q

Motor nerves exit the ventral cord via —-

A

Efferent way

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5
Q

Sensory nerves enter dorsal cords via —-

A

Afferent

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6
Q

5 steps process of release of ACh from nerve terminal

A
  1. The motor nerve action potential arrives at and depolarizes a nerve terminal.
  2. Depolarization causes voltage-gated calcium channels to open.
  3. Calcium (Ca++) diffuses down a concentration gradient into the nerve terminal.
  4. Inside the nerve terminal, Ca ++ causes vesicles to fuse with the nerve cell membrane and open to the exterior.
  5. ACh spills out into the synaptic cleft (exocytosis).
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7
Q

What type of feedback is the release of ACh from nerve terminal?

A

Positive; presynaptic nicotinic receptors responds to ACh by increasing the synthesis and release of ACh to prevent depletion of ACh at neuromuscular junction.

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8
Q

Acetylcholine —— down a concentration gradient from the presynaptic membrane to the motor end- plate of the postsynaptic membrane.

A

diffuses

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9
Q

5 events at the Postsynaptic membrane:

A
  1. ACh combines with nicotinic receptors of the protein channel.
  2. When both alpha subunits of the nicotinic receptor channel are occupied by ACh, the channel snaps open, and sodium, calcium and potassium ions diffuse through the channel.
  3. The diffusion of these three types of ions through the channel causes the motor end-plate to depolarize.
  4. At a critical level of depolarization (threshold), an action potential is initiated.
  5. The action potential sweeps across the skeletal muscle cell and triggers contraction.
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10
Q

When both alpha subunits of the nicotinic receptor channel are occupied by ACh, the channel snaps open, and sodium, calcium and potassium ions diffuse through the channel. How do Na, Ca, and K ions diffuse?

A

Sodium and calcium ions diffuse into the cell and potassium ions diffuse out to the extracellular space.

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11
Q

3 steps to termination of neurotransmitter action:

A
  1. Acetylcholinesterase (AChE), also known as “true” cholinesterase, breaks down acetylcholine to choline and acetate.
  2. As ACh is metabolized, the motor end-plate repolarizes and the muscle cell becomes ready for another squirt of ACh from the nerve terminal.
  3. The choline is transported back into the nerve terminal where it is used to re-synthesize ACh.
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12
Q

Hypocalcemia is associated with a —- in amount of neurotransmitter released.

A

Decrease

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13
Q

Hypercalcemia is associated with a —- in amount of neurotransmitter released.

A

Increase

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14
Q

Hypomagnesemia is associated with a —- in amount of neurotransmitter released.

A

Increase

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15
Q

Hypermagnesemis is associated with a —- in amount of neurotransmitter released.

A

Decrease

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16
Q

Calcium and magnesium are —— at nerve terminals.

A

Antagonistic

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17
Q

The release of neurotransmitter from all nerve terminals, including the motor nerve terminals, depend on the entry into the terminal of ——.

A

Calcium ions

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18
Q

An —— molecule must attach to each of these two identical subunits where the nicotinic receptors are located in order to open the channel

A

ACh

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19
Q

How many ACh molecules are needed to open each nicotinic acetylcholine receptor (nAChR).

A

2

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20
Q

Where do the ACh molecules attach to on the Postsynaptic receptors?

A

2 identical 40k subunits

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21
Q

5 step sequence for opening of channels by ACh:

A
  1. Two molecules of acetylcholine (represented by open triangles above) combine with two nicotinic
    receptors on the channel.
  2. The ion channel opens and becomes permeable to Na+, K+, Ca ++.
  3. The motor end-plate depolarizes; a local, sub-threshold depolarization occurs at the end-plate.
  4. When threshold is reached, an all-or-none action potential is initiated in the muscle fiber.
  5. An action potential passes over the muscle cell and into the transverse tubules and triggers the contraction.
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22
Q

Nondepolarizing agents are —— inhibitors.

A

Competitive

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23
Q

When a nondepolarizing agent binds to either ACh-binding site on a nicotinic receptor, ACh —— attach to that receptor and the channel —— open.

A

Cannot, cannot

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24
Q

Because succinylcholine is not metabolized by true acetylcholinesterase, the channels stay —— and depolarization is maintained for an extended period of time.

A

Open

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25
Q

Do nondepolarizing agents have a direct effect on the channel?

A

No

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26
Q

The nondepolarizing agent competitively blocks acetylcholine from attaching to its receptors so the channel cannot open. The channel stays closed, and the postsynaptic membrane remains ——.

A

Polarized

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27
Q

Succinylcholine (sux) is composed of two —— molecules linked together.

A

Acetylcholine

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28
Q

Because true acetylcholinesterase does not metabolize succinylcholine, the succinylcholine remains attached to the receptors, and the channels stay —— until the succinylcholine diffuses back into the circulation; depolarization is maintained for several minutes.

A

Open

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29
Q

Action potentials cannot be initiated in the skeletal muscle cell until the cell ——.

A

repolarizes

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30
Q

When an action potential cannot be initiated in the skeletal muscle cell, the —- gates are in the —— state.

A

Sodium, inactivated

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31
Q

Succinylcholine is metabolized by an enzyme in the plasma called —— ——.

A

plasma cholinesterase

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32
Q

Plasma cholinesterase is known by two other names: —— and ——.

A

pseudocholinesterase, butyrocholinesterase

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33
Q

When the channel of the motor end-plate opens, what diffuses into the cell?

A

Sodium and calcium

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34
Q

When the channel of the motor end-plate opens, what diffuses out of the cell?

A

Potassium

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35
Q

As long as succinylcholine maintains the —— state, the voltage-gated sodium channels remain ——, and action potentials cannot be elicited.

A

depolarized, inactivated

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36
Q

When the gated sodium channel is in the inactivated state, another action potential —— be fired no matter how intense the stimulus.

A

cannot

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37
Q

The —— —— ——corresponds to the time when the fast voltage-gated sodium channels are in the inactivated state. Depolarization of the motor end-plate by succinylcholine causes the voltage-gated sodium channels to become inactivated, thereby electrically arresting skeletal muscle.

A

absolute refractory period

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38
Q

At the neuromuscular junction, does the presynaptic action of succinylcholine enhance or antagonize its postsynaptic action?

A

presynaptic action of succinylcholine enhances its postsynaptic action.

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39
Q

Which neuromuscular blockers are very short?

A

Succinylcholine; anectine

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40
Q

Which neuromuscular blockers are short?

A

Mivacurium; mivacron

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41
Q

Which neuromuscular blockers are intermediate?

A

Atracurium (tracrium), cisatracurium (nimbex), vecuronium (norcuron), Rocuronium (zemuron)

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42
Q

Which neuromuscular blockers are long?

A

D-tubocurarine (tubarine), metocurine (metabine), pancuronium (pavulon), gallamine (flaxedil), pipecuronium (arduan), doxacurium (nuromax)

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43
Q

Physiological Properties of Neuromuscular Relaxants A. 100% —— at physiologic pH
B. —— —— protein bound
C. —— cross the blood-brain barrier (ions do not cross lipid bilayers)
D. —— cross the placental barrier (ions do not cross lipid bilayers)
E. Trapped in the —— —— after filtration because of high degree of ionization (NB: muscle relaxants can be excreted by the kidney if other routes are unavailable)

A

A. Ionized
B. Very highly
C. Do not
D. Do not
E. renal tubule

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44
Q

Route of elimination for succinylcholine?

A

Metabolism

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45
Q

Route of elimination for mivarcurium?

A

Metabolism

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46
Q

Route of elimination for atracurium?

A

Metabolism

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47
Q

Route of elimination for cisatracurium?

A

Metabolism

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48
Q

Route of elimination for vecuronium?

A

Biliary excretion

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49
Q

Route of elimination for rocuronium?

A

Biliary excretion

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50
Q

Route of elimination for d-tubocurarine?

A

Renal excretion

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51
Q

Route of elimination for metocurine?

A

Renal excretion

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52
Q

Route of elimination for pancuronium?

A

Renal excretion

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53
Q

Route of elimination for gallamine?

A

Renal excretion

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54
Q

Route of elimination for pipecuronium?

A

Renal excretion

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55
Q

Route of elimination for doxacurium?

A

Renal excretion

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56
Q

Atracurium is eliminated by —— ——(nonspecific esterases, unrelated to plasma cholinesterase, perform ester hydrolysis) and —— —— (pH and temp dependent degradation)

A

ester hydrolysis , Hofmann elimination

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57
Q

Cisatracurium is eliminated by —— —— only

A

Hofmann elimination

58
Q

Mivacurium is eliminated by —— ——.

A

Plasma cholinesterase

59
Q

Which 2 neuromuscular blockers produce autonomic ganglionic blockade?

A

D-tubocurarine and metocurine

60
Q

Which 5 neuromuscular blockers elicit the release of histamine?

A

Sux, Mivacurium, atracurium, d-tubocurarine, and metocurarine

61
Q

Which 3 neuromuscular blockers produce reflex tachycardia?

A

Atracurium, d-tubocurarine, and metocurine

62
Q

Which 2 neuromuscular blockers cause direct vagolytic (antimuscarinic) by competitively antagonize ACh?

A

Pancuronium and gallamine

63
Q

Which 3 neuromuscular blockers produce hypotension?

A

Sux, d-tubocurarine, and metocurine

64
Q

Which 2 neuromuscular blockers produce HTN?

A

Pancuronium and gallamine

65
Q

How does rocuronium affect peds?

A

Increase HR

66
Q

How does sux effect plasma K?

A

Increase 0.5 mEq/L in normal pts and 5-10 mEq/L in burn, trauma, or head-injury pts

67
Q

How does sux effect muscles?

A

Muscle pain (myalgia)

68
Q

How does sux effect HR?

A

Bradycardia

69
Q

How does sux effect heart conduction?

A

AV conduction block

70
Q

How does sux effect eyes?

A

Increase intraocular pressure

71
Q

How does sux effect MH?

A

Can cause it

72
Q

How does sux effect intracranial pressure?

A

Increase it

73
Q

How does sux effect pts with atypical plasma cholinesterase?

A

Prolonged respiratory paralysis

74
Q

How does sux effect urine?

A

Myoglobinuria

75
Q

How does sux effect muscle movement at induction?

A

Fasciculations

76
Q

How does sux effect intragastric pressure?

A

Increase

77
Q

What are the 4 conditions that accentuate sux-induced hyperkalemia?

A
  1. Burn
  2. Paraplegia or hemiplegia
  3. Skeletal muscle trauma
  4. Upper motor neuron injury (head, cerebrovascular, Parkinson’s disease)
78
Q

If you use a nerve-muscle stimulator on the right wrist of the patient with right-sided hemiplegia, will the twitch be less than, the same as, or greater than the twitch on the left?

A

The twitch on the right will be greater than on the left!! Nicotinic receptors are up-regulated on the right, hemiplegic side.

79
Q

What are the 5 diagnosis of MH?

A
  1. Pyrexia (fever)
  2. Tachycardia
  3. Cyanosis
  4. Rigidity
  5. Failure of masseter to relax (trismus)
80
Q

What are the 5 chances in serum composition that are found in MH?

A

Increased: protons, potassium, calcium and CO2
Decreased: O2

81
Q

The defect in malignant hyperthermia is in the —— —— of skeletal muscle.

A

sarcoplasmic reticulum

82
Q

In MH, the sarcoplasmic reticulum fails to sequester ——, so sustained contractions with increased metabolism result.

A

calcium

83
Q

—— is used to treat malignant hyperthermia.

A

Dantrolene

84
Q

Dantrolene acts on the sarcoplasmic reticulum to decrease the release of —— to contractile proteins.

A

calcium

85
Q

One of the earliest and most sensitive signs of malignant hyperthermia is an unexplained doubling or tripling in —— ——.

A

end-expiratory CO2

86
Q

In MH, the initial signs of tachycardia and tachypnea result from —— nervous system stimulation secondary to underlying —— and ——.

A

sympathetic , hypermetabolism and hypercarbia

87
Q

In MH, sympathetic hyperactivity manifested by increased —— is also an early sign of increased
——.

A

heart rate , metabolism

88
Q

In MH, an increase in end-tidal CO2 —— the increase in heart rate.

A

precedes

89
Q

In MH, increased PaC02 (possibly > —— mmHg) and decreased pH (possibly < ——)

A

100 , 7.0

90
Q

What 2 things can trigger MH?

A

Sux and halogenated inhalational agents (iso, des, halothane, enflurane, sevo)

91
Q

Factors that alter the degree of NDMB: antibiotics

A

Block increased EXCEPT for penicillin, chloramphenicol, and cephalosporins

92
Q

Factors that alter the degree of NDMB: local anesthetics

A

Block increase by amides

93
Q

Factors that alter the degree of NDMB: volatile inhalational agents

A

Block increased

94
Q

Factors that alter the degree of NDMB: hypokalemia

A

Block increased

95
Q

Factors that alter the degree of NDMB: mypermagnesemia

A

Block increased

96
Q

Factors that alter the degree of NDMB: respiratory acidosis

A

Block increased

97
Q

Factors that alter the degree of NDMB: hypothermia

A

Block increased

98
Q

Factors that alter the degree of NDMB: anti-arrhythmic agents

A

Block increased

99
Q

Factors that alter the degree of NDMB: renal disease

A

Block increase for those agents that are eliminated by renal excretion (gallamine)

100
Q

Factors that alter the degree of NDMB: hepatic disease

A

Block increased for those agents that are eliminated in the bile (vec and roc)

101
Q

Factors that alter the degree of NDMB: myasthenia gravis

A

Block increased

102
Q

Factors that alter the degree of NDMB: age

A

Block increased (>60-65) bc organs of elimination are less effective

103
Q

Factors that alter the degree of NDMB: lithium

A

Block increased

104
Q

Factors that alter the degree of NDMB: diuretics

A

Block increased

105
Q

Factors that alter the degree of NDMB: calcium channel blockers

A

Block increased

106
Q

Factors that alter the degree of NDMB: corticosteriods

A

Block unchanged

107
Q

Factors that alter the degree of NDMB: anticonvulsants

A

Block decreased in pts treated chronically with anticonvulsants

108
Q

Factors that alter the degree of NDMB: thermal (burn) injury

A

Block decreased; manifests 10 days after injury, peaks at 40 days and declines after 60 days

109
Q

Factors that alter the degree of DMB: antibiotics

A

Block increased EXCEPT with penicillin, chloramphenicol, and cephalosporins

110
Q

Factors that alter the degree of DMB: local anesthetics

A

Block increased by amides

111
Q

Factors that alter the degree of DMB: volatile inhalational agents

A

Block unchanged

112
Q

Factors that alter the degree of DMB: anticholinesterase agents

A

Block increased

113
Q

Factors that alter the degree of DMB: hyperkalemia

A

Block increased

114
Q

Factors that alter the degree of DMB: hypermagnesemia

A

Block increased

115
Q

Factors that alter the degree of DMB: inherited pseudocholinesterase defect (atypical pseudocholinesterase)

A

Block increased

116
Q

Factors that alter the degree of DMB: lithium

A

Block increased

117
Q

Factors that alter the degree of DMB: calcium channel blockers

A

Block increased

118
Q

Characteristics of NDMB: Amplitude of single twitch contractions —— with increasing intensity of block.

A

decreases

119
Q

Characteristics of NDMB: Fade occurs during ——stimulation and —— stimulation.

A

Train of four and tetanic

120
Q

Characteristics of NDMB: The train-of-four ratio (amplitude of fourth beat to amplitude of first beat) is less than ——%.

A

70

121
Q

Characteristics of NDMB: (T4/T1 < ——%).

A

70

122
Q

% Receptors occupied with NDMB: Complete paralysis - flaccid patient (no twitches in train-of- four)

A

99-100

123
Q

% Receptors occupied with NDMB: Diaphragm moves (no twitches in train-of-four)

A

95

124
Q

% Receptors occupied with NDMB: Abdominal relaxation adequate for most intra-abdominal procedures (one twitch present in train-of-four)

A

90

125
Q

% Receptors occupied with NDMB: Tidal volume returns to normal (>5 mL/kg); single twitch as strong as baseline (not an indicator of recovery)

A

75-80

126
Q

% Receptors occupied with NDMB: No palpable fade in TOF, useful as gauge of recovery; sustained tetanus at 50Hz for 5 seconds, reliable indicator of recovery

A

70-75

127
Q

% Receptors occupied with NDMB: No palpable fade in double burst stimulation, more sensitive than TOF as indicator

A

60-70

128
Q

% Receptors occupied with NDMB: Passes inspiratory pressure test, at least -40 cm H 20; head lift for 5 seconds; sustained strong handgrip; sustained bite, very reliable indicator of recovery.

A

50

129
Q

Data suggest that conditions for intubation with NDMB are appropriate if greater than ——% of nicotinic receptors at the motor end-plates are occupied.

A

95

130
Q

Characteristics of DNMB: Block is —— by cholinesterase inhibitors (edrophonium, neostigmine, pyridostigmine).

A

enhanced (augmented)

131
Q

Characteristics of DNMB: Fade —— occur during tetanic stimulation or train-of-four stimulation, although the amplitudes of the tetanic contraction and train-of-four beats are reduced.

A

does not

132
Q

Characteristics of DNMB: The train-of-four ratio (amplitude of fourth beat to amplitude of first beat) is greater than ——% (T4/T1 >——% = T4/T1 >——).

A

70 , 70 , 0.7

133
Q

Characteristics of DNMB: Post-tetanic facilitation (post-tetanic potentiation) is ——.

A

absent

134
Q

Characteristics of DNMB: Block is —— by nondepolarizing muscle relaxants.

A

antagonized

135
Q

Which phase block is this? The motor end-plate is depolarized; succinylcholine has activated the nicotinic receptors of the motor end-plate and the ion channels have opened and remained open.

A

phase I block

136
Q

Treatment with higher doses of succinylcholine and/or prolonged exposure of the motor end-plate to
succinylcholine leads to the development of ——.

A

phase II, or desensitization, block.

137
Q

very complex phenomenon; ion channels of the motor end-plate close for reasons that are unknown, and the motor end-plate repolarizes.

A

Phase II (desensitization) block

138
Q

Phase II block has the characteristics of a nondepolarizing block; use of a peripheral nerve stimulator during phase II block will show —— and ——.

A

fade and post-tetanic facilitation

139
Q

Refers to simultaneous existence of both depolarizing (Phase I) and Phase II blockade.

A

Dual Blockade

140
Q

“Antagonism of neuromuscular blockade should normally not be attempted when blockade is intense because reversal will often be inadequate, regardless of the dose of antagonist administered?’ Reversal can be attempted when —— twitch is elicited.

A

One

141
Q

In general, antagonism should not be initiated before at least ——, preferably —— or ——, responses are observed?

A

2 , 3 , 4

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