Valley: Neuromuscular Physiology & Pharmacology Flashcards
(141 cards)
1
Q
Motor neurons to skeletal muscle originate in the ——- of the spinal cord
A
anterior (ventral) horn
2
Q
Sensory neurons from skeletal muscle carry action potentials to the spinal cord via the —-
A
dorsal horn
3
Q
These motor and sensory nerves are —— nerves
A
somatic
4
Q
Motor nerves exit the ventral cord via —-
A
Efferent way
5
Q
Sensory nerves enter dorsal cords via —-
A
Afferent
6
Q
5 steps process of release of ACh from nerve terminal
A
- The motor nerve action potential arrives at and depolarizes a nerve terminal.
- Depolarization causes voltage-gated calcium channels to open.
- Calcium (Ca++) diffuses down a concentration gradient into the nerve terminal.
- Inside the nerve terminal, Ca ++ causes vesicles to fuse with the nerve cell membrane and open to the exterior.
- ACh spills out into the synaptic cleft (exocytosis).
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.
8
Q
Acetylcholine —— down a concentration gradient from the presynaptic membrane to the motor end- plate of the postsynaptic membrane.
A
diffuses
9
Q
5 events at the Postsynaptic membrane:
A
- ACh combines with nicotinic receptors of the protein channel.
- 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.
- The diffusion of these three types of ions through the channel causes the motor end-plate to depolarize.
- At a critical level of depolarization (threshold), an action potential is initiated.
- The action potential sweeps across the skeletal muscle cell and triggers contraction.
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.
11
Q
3 steps to termination of neurotransmitter action:
A
- Acetylcholinesterase (AChE), also known as “true” cholinesterase, breaks down acetylcholine to choline and acetate.
- As ACh is metabolized, the motor end-plate repolarizes and the muscle cell becomes ready for another squirt of ACh from the nerve terminal.
- The choline is transported back into the nerve terminal where it is used to re-synthesize ACh.
12
Q
Hypocalcemia is associated with a —- in amount of neurotransmitter released.
A
Decrease
13
Q
Hypercalcemia is associated with a —- in amount of neurotransmitter released.
A
Increase
14
Q
Hypomagnesemia is associated with a —- in amount of neurotransmitter released.
A
Increase
15
Q
Hypermagnesemis is associated with a —- in amount of neurotransmitter released.
A
Decrease
16
Q
Calcium and magnesium are —— at nerve terminals.
A
Antagonistic
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
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
19
Q
How many ACh molecules are needed to open each nicotinic acetylcholine receptor (nAChR).
A
2
20
Q
Where do the ACh molecules attach to on the Postsynaptic receptors?
A
2 identical 40k subunits
21
Q
5 step sequence for opening of channels by ACh:
A
- Two molecules of acetylcholine (represented by open triangles above) combine with two nicotinic
receptors on the channel. - The ion channel opens and becomes permeable to Na+, K+, Ca ++.
- The motor end-plate depolarizes; a local, sub-threshold depolarization occurs at the end-plate.
- When threshold is reached, an all-or-none action potential is initiated in the muscle fiber.
- An action potential passes over the muscle cell and into the transverse tubules and triggers the contraction.
22
Q
Nondepolarizing agents are —— inhibitors.
A
Competitive
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
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
25
Do nondepolarizing agents have a direct effect on the channel?
No
26
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 ——.
Polarized
27
Succinylcholine (sux) is composed of two —— molecules linked together.
Acetylcholine
28
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.
Open
29
Action potentials cannot be initiated in the skeletal muscle cell until the cell ——.
repolarizes
30
When an action potential cannot be initiated in the skeletal muscle cell, the —- gates are in the —— state.
Sodium, inactivated
31
Succinylcholine is metabolized by an enzyme in the plasma called —— ——.
plasma cholinesterase
32
Plasma cholinesterase is known by two other names: —— and ——.
pseudocholinesterase, butyrocholinesterase
33
When the channel of the motor end-plate opens, what diffuses into the cell?
Sodium and calcium
34
When the channel of the motor end-plate opens, what diffuses out of the cell?
Potassium
35
As long as succinylcholine maintains the —— state, the voltage-gated sodium channels remain ——, and action potentials cannot be elicited.
depolarized, inactivated
36
When the gated sodium channel is in the inactivated state, another action potential —— be fired no matter how intense the stimulus.
cannot
37
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.
absolute refractory period
38
At the neuromuscular junction, does the presynaptic action of succinylcholine enhance or antagonize its postsynaptic action?
presynaptic action of succinylcholine enhances its postsynaptic action.
39
Which neuromuscular blockers are very short?
Succinylcholine; anectine
40
Which neuromuscular blockers are short?
Mivacurium; mivacron
41
Which neuromuscular blockers are intermediate?
Atracurium (tracrium), cisatracurium (nimbex), vecuronium (norcuron), Rocuronium (zemuron)
42
Which neuromuscular blockers are long?
D-tubocurarine (tubarine), metocurine (metabine), pancuronium (pavulon), gallamine (flaxedil), pipecuronium (arduan), doxacurium (nuromax)
43
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. Ionized
B. Very highly
C. Do not
D. Do not
E. renal tubule
44
Route of elimination for succinylcholine?
Metabolism
45
Route of elimination for mivarcurium?
Metabolism
46
Route of elimination for atracurium?
Metabolism
47
Route of elimination for cisatracurium?
Metabolism
48
Route of elimination for vecuronium?
Biliary excretion
49
Route of elimination for rocuronium?
Biliary excretion
50
Route of elimination for d-tubocurarine?
Renal excretion
51
Route of elimination for metocurine?
Renal excretion
52
Route of elimination for pancuronium?
Renal excretion
53
Route of elimination for gallamine?
Renal excretion
54
Route of elimination for pipecuronium?
Renal excretion
55
Route of elimination for doxacurium?
Renal excretion
56
Atracurium is eliminated by —— ——(nonspecific esterases, unrelated to plasma cholinesterase, perform ester hydrolysis) and —— —— (pH and temp dependent degradation)
ester hydrolysis , Hofmann elimination
57
Cisatracurium is eliminated by —— —— only
Hofmann elimination
58
Mivacurium is eliminated by —— ——.
Plasma cholinesterase
59
Which 2 neuromuscular blockers produce autonomic ganglionic blockade?
D-tubocurarine and metocurine
60
Which 5 neuromuscular blockers elicit the release of histamine?
Sux, Mivacurium, atracurium, d-tubocurarine, and metocurarine
61
Which 3 neuromuscular blockers produce reflex tachycardia?
Atracurium, d-tubocurarine, and metocurine
62
Which 2 neuromuscular blockers cause direct vagolytic (antimuscarinic) by competitively antagonize ACh?
Pancuronium and gallamine
63
Which 3 neuromuscular blockers produce hypotension?
Sux, d-tubocurarine, and metocurine
64
Which 2 neuromuscular blockers produce HTN?
Pancuronium and gallamine
65
How does rocuronium affect peds?
Increase HR
66
How does sux effect plasma K?
Increase 0.5 mEq/L in normal pts and 5-10 mEq/L in burn, trauma, or head-injury pts
67
How does sux effect muscles?
Muscle pain (myalgia)
68
How does sux effect HR?
Bradycardia
69
How does sux effect heart conduction?
AV conduction block
70
How does sux effect eyes?
Increase intraocular pressure
71
How does sux effect MH?
Can cause it
72
How does sux effect intracranial pressure?
Increase it
73
How does sux effect pts with atypical plasma cholinesterase?
Prolonged respiratory paralysis
74
How does sux effect urine?
Myoglobinuria
75
How does sux effect muscle movement at induction?
Fasciculations
76
How does sux effect intragastric pressure?
Increase
77
What are the 4 conditions that accentuate sux-induced hyperkalemia?
1. Burn
2. Paraplegia or hemiplegia
3. Skeletal muscle trauma
4. Upper motor neuron injury (head, cerebrovascular, Parkinson’s disease)
78
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?
The twitch on the right will be greater than on the left!! Nicotinic receptors are up-regulated on the right, hemiplegic side.
79
What are the 5 diagnosis of MH?
1. Pyrexia (fever)
2. Tachycardia
3. Cyanosis
4. Rigidity
5. Failure of masseter to relax (trismus)
80
What are the 5 chances in serum composition that are found in MH?
Increased: protons, potassium, calcium and CO2
Decreased: O2
81
The defect in malignant hyperthermia is in the —— —— of skeletal muscle.
sarcoplasmic reticulum
82
In MH, the sarcoplasmic reticulum fails to sequester ——, so sustained contractions with increased metabolism result.
calcium
83
—— is used to treat malignant hyperthermia.
Dantrolene
84
Dantrolene acts on the sarcoplasmic reticulum to decrease the release of —— to contractile proteins.
calcium
85
One of the earliest and most sensitive signs of malignant hyperthermia is an unexplained doubling or tripling in —— ——.
end-expiratory CO2
86
In MH, the initial signs of tachycardia and tachypnea result from —— nervous system stimulation secondary to underlying —— and ——.
sympathetic , hypermetabolism and hypercarbia
87
In MH, sympathetic hyperactivity manifested by increased —— is also an early sign of increased
——.
heart rate , metabolism
88
In MH, an increase in end-tidal CO2 —— the increase in heart rate.
precedes
89
In MH, increased PaC02 (possibly > —— mmHg) and decreased pH (possibly < ——)
100 , 7.0
90
What 2 things can trigger MH?
Sux and halogenated inhalational agents (iso, des, halothane, enflurane, sevo)
91
Factors that alter the degree of NDMB: antibiotics
Block increased EXCEPT for penicillin, chloramphenicol, and cephalosporins
92
Factors that alter the degree of NDMB: local anesthetics
Block increase by amides
93
Factors that alter the degree of NDMB: volatile inhalational agents
Block increased
94
Factors that alter the degree of NDMB: hypokalemia
Block increased
95
Factors that alter the degree of NDMB: mypermagnesemia
Block increased
96
Factors that alter the degree of NDMB: respiratory acidosis
Block increased
97
Factors that alter the degree of NDMB: hypothermia
Block increased
98
Factors that alter the degree of NDMB: anti-arrhythmic agents
Block increased
99
Factors that alter the degree of NDMB: renal disease
Block increase for those agents that are eliminated by renal excretion (gallamine)
100
Factors that alter the degree of NDMB: hepatic disease
Block increased for those agents that are eliminated in the bile (vec and roc)
101
Factors that alter the degree of NDMB: myasthenia gravis
Block increased
102
Factors that alter the degree of NDMB: age
Block increased (>60-65) bc organs of elimination are less effective
103
Factors that alter the degree of NDMB: lithium
Block increased
104
Factors that alter the degree of NDMB: diuretics
Block increased
105
Factors that alter the degree of NDMB: calcium channel blockers
Block increased
106
Factors that alter the degree of NDMB: corticosteriods
Block unchanged
107
Factors that alter the degree of NDMB: anticonvulsants
Block decreased in pts treated chronically with anticonvulsants
108
Factors that alter the degree of NDMB: thermal (burn) injury
Block decreased; manifests 10 days after injury, peaks at 40 days and declines after 60 days
109
Factors that alter the degree of DMB: antibiotics
Block increased EXCEPT with penicillin, chloramphenicol, and cephalosporins
110
Factors that alter the degree of DMB: local anesthetics
Block increased by amides
111
Factors that alter the degree of DMB: volatile inhalational agents
Block unchanged
112
Factors that alter the degree of DMB: anticholinesterase agents
Block increased
113
Factors that alter the degree of DMB: hyperkalemia
Block increased
114
Factors that alter the degree of DMB: hypermagnesemia
Block increased
115
Factors that alter the degree of DMB: inherited pseudocholinesterase defect (atypical pseudocholinesterase)
Block increased
116
Factors that alter the degree of DMB: lithium
Block increased
117
Factors that alter the degree of DMB: calcium channel blockers
Block increased
118
Characteristics of NDMB: Amplitude of single twitch contractions —— with increasing intensity of block.
decreases
119
Characteristics of NDMB: Fade occurs during ——stimulation and —— stimulation.
Train of four and tetanic
120
Characteristics of NDMB: The train-of-four ratio (amplitude of fourth beat to amplitude of first beat) is less than ——%.
70
121
Characteristics of NDMB: (T4/T1 < ——%).
70
122
% Receptors occupied with NDMB: Complete paralysis - flaccid patient (no twitches in train-of- four)
99-100
123
% Receptors occupied with NDMB: Diaphragm moves (no twitches in train-of-four)
95
124
% Receptors occupied with NDMB: Abdominal relaxation adequate for most intra-abdominal procedures (one twitch present in train-of-four)
90
125
% Receptors occupied with NDMB: Tidal volume returns to normal (>5 mL/kg); single twitch as strong as baseline (not an indicator of recovery)
75-80
126
% 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
70-75
127
% Receptors occupied with NDMB: No palpable fade in double burst stimulation, more sensitive than TOF as indicator
60-70
128
% 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.
50
129
Data suggest that conditions for intubation with NDMB are appropriate if greater than ——% of nicotinic receptors at the motor end-plates are occupied.
95
130
Characteristics of DNMB: Block is —— by cholinesterase inhibitors (edrophonium, neostigmine, pyridostigmine).
enhanced (augmented)
131
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.
does not
132
Characteristics of DNMB: The train-of-four ratio (amplitude of fourth beat to amplitude of first beat) is greater than ——% (T4/T1 >——% = T4/T1 >——).
70 , 70 , 0.7
133
Characteristics of DNMB: Post-tetanic facilitation (post-tetanic potentiation) is ——.
absent
134
Characteristics of DNMB: Block is —— by nondepolarizing muscle relaxants.
antagonized
135
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.
phase I block
136
Treatment with higher doses of succinylcholine and/or prolonged exposure of the motor end-plate to
succinylcholine leads to the development of ——.
phase II, or desensitization, block.
137
very complex phenomenon; ion channels of the motor end-plate close for reasons that are unknown, and the motor end-plate repolarizes.
Phase II (desensitization) block
138
Phase II block has the characteristics of a nondepolarizing block; use of a peripheral nerve stimulator during phase II block will show —— and ——.
fade and post-tetanic facilitation
139
Refers to simultaneous existence of both depolarizing (Phase I) and Phase II blockade.
Dual Blockade
140
"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.
One
141
In general, antagonism should not be initiated before at least ——, preferably —— or ——, responses are observed?
2 , 3 , 4
