Exam 3 - Lecture 4 Flashcards
(120 cards)
1
Q
Neuron nACHr
A
Autonomic/CNS nACHr
2
Q
Part of the synapse where there are NMJ
A
Junctional area
3
Q
Area JUST outside NMJ on skeletal muscle
A
Peri junctional area
4
Q
Area further down skeletal muscle outside the NMJ
A
Post junctional
5
Q
What are you doing with electrodes on ulnar nerve?
A
Generating an action potential by eliciting a negative charge outside the cell, which equalizes the negativity inside the cell which technically “depolarizes” the nerve, sending an action potential
6
Q
2 electrodes for nerve stimulation that are 1 _______ and 1 _________.
A
1 cathode and 1 anode
7
Q
Nerve stimulators work by taking away the _____ between outside and inside the cell
A
Polarity
8
Q
If we have a block on the nerve that we are trying to stimulate, and it’s a good block, we should expect:
A
To not see a muscle contraction
9
Q
Supramaximal stimulus
A
A stimulus strong enough to recruit all motor neurons in the underlying nerve and generate an AP/entire muscle activated
10
Q
Single twitch
A
One impulse to see if it triggers muscle
11
Q
Train of four (how many hertz and how many seconds?)
A
Repetitive stimuli that happens at a frequency of 2 hertz over 2 seconds
12
Q
Hertz
A
Something happening per second.
E.g. 2 hertz means 2 impulses over 1 second
13
Q
How many seconds does a train of four last?
A
2 hz per second, 4 twitches total… therefore 2 seconds.
14
Q
Non depolarizing paralytic B/A ratio
A
1st twitch is stronger than the following twitches which get weaker and weaker, equals a LOW ratio.
15
Q
Depolarizing blocking paralytic relation to B/A ratio
A
Each muscle twitch are just as strong as eachother, B/A ratio very close to 1
16
Q
Tetanic contraction
A
Repetitive high speed contraction, high frequency stimulation for a very short period of time
17
Q
Post-tetanic count
A
Impulses muscle generates after tetanic stimulation. Stimulate with high frequency, to check health of synapse.
18
Q
DBS: double-burst stimulation
A
Multiple tetanic bursts to look at different characteristics of the neuromuscular block.
Do it, lay off a couple seconds, do it again
19
Q
The ulnar nerve innervates what muscle?
A
Adductor pollicis
20
Q
What happens when the adductor pollicis is stimulated?
A
Thumb comes forward a little bit and pinky finger should twitch
21
Q
Why is the ulnar nerve used for TOF?
A
Easy to access and see
22
Q
Other places to monitor neuromuscular blockade?
A
Ophthalmic branch of facial nerve (oculi muscles outside eye socket), peroneal nerve in the butt area, posterior tibial nerve
23
Q
Characteristics of response time for NDMR
A
Slow to kick in (few minutes) and takes awhile to wear off. 26 minutes to hours depending on drug
24
Q
Depolarizing block paralytic is what drug?
A
Succinylcholine
25
Characteristics of succinylcholine timing and why is it used
Very quickly to take effect, and cheap to make. Very quick to wear off as well (starts to wear off after just a few minutes)
26
The twitches for NDMR will come back in
Stages.
First it'll just be one twitch, then 2, then 3, then 4... but they're all unequal in strength
27
B/A ratio
Train of four ratio, where A is the first twitch and B is the last twitch. The more uneven the strength of the twitches, the LOWER the ratio is
28
If A twitch is strong, and B is super weak, that would create a _____ B/A ratio
Very small
29
How many twitches do you need for a B/A ratio to be used?
All 4 muscles must twitch
30
TOF ratio
B/A
31
Do depolarizing paralytic twitches recover evenly over time?
Yes. Each twitch during the TOF will be an equal strength.
32
What is the TOF ratio (B/A) in the depolarizing block?
Almost always 1.0
33
NDMR act on both the
Motor neuron and skeletal muscle
Technically both paralytics do but NDMRs cause a different and more important effect
34
Second type of ACH receptor that is on the motor neuron
Alpha3, Beta2 (3 alpha subunits and 2 beta subunits)
35
What are the 3 alpha subunits on the ach receptor on motor neuron represents
Where ach can bind
36
When acetylcholine is dumped into synapse, most of it goes to the skeletal muscle to bind to those receptors, but a few go
Back up to the alpha3,beta2 receptors (also called auto receptors)
37
Autoreceptors
The name for alpha3 beta2 ach-r on the motor neurons
38
Secondary effect of ach release from motor neuron
The act of them routing back up to motor neuron to bind to autoreceptors
39
When autoreceptors open, what happens?
Causes sodium and calcium to flow into cell.
40
What happens when autoreceptors are bound and ions come in?
Alerts the VP1 vesicles to move forward to become VP2, since VP2 just got dumped.
41
NDMR drugs overall affects on skeletal muscle
Prevents end plate potential at NMJ, and they inhibit autoreceptors and inhibit acetylcholine release
42
So why is there a weaker subsequent contraction in NDMR? (Chart showing weaker and weaker contractions)
Due to fewer and fewer VP2 vesicles moving to cell wall to dump acetylcholine due to blocking of autoreceptors
43
Do less acetylcholine get released from motor neuron in depolarizing drugs?
No.. same amount get released.
44
How does non-depolarizing drugs bind to ach-r?
They park themselves on alpha subunits of autoreceptors and skeletal muscle NMJ ACH-r
45
How does sux break down and stop working?
Plasma cholinesterase clear sux from system over time
46
How many acetylcholine NTs are required to open autoreceptors?
Probably only need 2, but 3 can bind...?
47
What type of calcium channels do we have in addition to p-type calcium channels? Are they required?
L-type calcium channels.. They are fast to open unlike p-type calcium channels. They are not required for motor function, but if you give an l-type calcium channel blocker it will settle them down a little bit.
48
If we have skeletal muscle with nACHr post-junctional, what will happen if we dose someone with a depolarizing agent? (Succinylcholine)
Hemorrhaging potassium, since there are extra channels.
49
Do paralytics have the same sensitivity to every muscle? Why?
No. Certain muscles require higher doses due to nACHr receptor density in those muscles.
50
Which muscles require higher paralytic doses?
More important muscles such as the diaphragm.
51
Dose range for 10-90% effectiveness on the adductor pollicis?
20ish-40ish mcg/kg
52
Dose range for 10-90% effectiveness on the diaphragm?
40ish-100ish mcg/kg
53
The diaphragm is what kind of muscle?
Skeletal muscle
54
The motor neurons that control the diaphragm, where do they originate and what's the nerve called? (vertebra #'s)
Phrenic nerve, C3-C5 (You must know this forever)
55
If we break our neck and have a lesion above C3, what happens?
Cannot breathe on your own.
56
As the drug is wearing off, your TOF generates 2/4 twitches. Is the diaphragm working?
it likely is. The diaphragm requires much higher doses so if the ulnar nerve isnt fully paralyzed then the diaphragm likely isnt.
57
4th twitch disappears? %
75-80% nACHr's blocked
58
3rd twitch disappears? %
85% of nACHr's blocked
59
2nd twitch disappears? %
85-90% blocked
60
All twitches disappear? %
90-95% blocked
61
If a patient can reasonably lift their head, the nACHrs are what % blocked?
70%
62
Stimulator settings #'s
50-80 mA (milliampures), this will be the supramaximal stimuli, and it varies per hospital.
63
What does mA stand for?
Milliampures
64
A high voltage battery can push
alot of current
65
If you have a lesion/severed spinal cord at C4, what happens?
A partially affected diaphragm, will depend on patients physical health if they can survive it.
e.g. A 17 year old athlete vs a 70 year old man with comorbidities who smoked 10 packs a day
66
Ways K+ gets out during depolarization in succinylcholine?
primarily leak channels, secondary voltage gated channels around NMJ, 3rd through ach receptors but this is very minimal.
67
The succinylcholine will also allow what ion coming in? (other than sodium)
Calcium, causes minimal contraction but does allow calcium to leak in, only at NMJ.
68
Fetal receptors on skeletal muscle with succiynlcholine, this allows more K+ to flow out, more Na+ to leak in, and more __________
Calcium to leak in, which with this much calcium coming in it actually will allow muscle to contract, but this is only with people who have a ton of "bad" skeletal muscle.
69
Ocular muscles in the eyes have ________
Several neurons controlling a single muscle, leads to lots of NMJs.
70
If we hit ocular muscles with acetylcholine, what can happen?
They contract just enough to increase intraocular pressure.
71
Depolarizing muscle block in ocular muscles side effects and why?
Increased ocular pressure, loss of vision.
So if you got someone with an eye condition, head down, and on succinylcholine for a long period of time, it can pressurize the optic nerve and cause vision loss.
Due to multiple NMJs per muscle.
72
GABA characteristics
important NT in CNS, inhibitory in nature, increases chloride conductance, and the body has tons of GABA activity all the time to limit neural activity.
73
Glycine characteristics
important inhibitory NT in SPINAL CORD! Similar to GABA.
74
2 most important inhibitory NTs in spinal cord?
GABA and Glycine
75
Acetylcholine characteristics
Communication with skeletal muscles and smooth muscles.
76
Acetlycholine in CNS characteristics
Within CNS, it increases awareness. More ACH in brain, more awake we are, and the more we are aware of our surroundings.
77
If you have something that blocks ACH in our nervous system, it will
Cause drowsiness.
78
Anticholinergics will cause us to
be drowsy i.e. benadryl via acetylcholine inhibition.
79
Majority of awareness in CNS mediated through acetylcholine, is done through __________ receptors.
mACHr.
80
If we have agents that block mACHr, it will
make us drowsy
81
What common drug blocks mACHr? And what type of drug is it?
Benadryl, antihistamine/anticholinergics.
82
Antihistamines are cross reactive with
mACHr. They're very similar to CNS mACHr.
83
Whats another side effect of benadryl since its anticholinergic?
Spike of heart rate due to inhibition of mACHr at the heart.
84
How do we increase ACH at a central synapse?
Inhibit acetylcholinesterase.
85
What types of drugs inhibit ach-esterase and make us more aware?
drugs that can cross BBB. -stigmines.
86
If you want to wake a patient up and reverse paralytic, without waking them up, you would use a drug that:
is a acetylcholinesterase inhibitor that doesnt cross the BBB (if it crosses it would wake them up)
87
What drugs do pt's with alzheimers get?
Centrally acting acetylcholinesterase inhibitor to increase ach across the BBB
88
Do stigmines cross BBB?
Yes.
89
Side effects of inhibiting acetylcholinesterase across body?
-Increase ach at every receptor, including mACHr and a large decrease in heart rate (vagus nerve talking to heart, activity of that increases, lowers heart rate)
-Glands use acetylcholine as a NT to turn glands on (lungs, airways, mouth). Cholinergic activity increases from inhibited esterase, therefore more secretions and can inhibit gas exchange in the lungs.
90
Histamines
work similarly to ACH, more histamines in brain will result in more awareness.
91
If we have drugs that block histamine receptors, we would expect
drowsiness
92
Glutamate general characteristics
Stimulatory CNS NT that increases neuronal activity.
93
Patients on meth will have an increased ________ due to what?
awareness; glutamate.T
94
Too much glutamate will ________
Burn out brain cells and not be replaced.
95
Are meth users more sensitive to pain?
Acutely, no... but after, yes.
96
Dopamine
Pleasure/reward NT.
Can be a potent motor inhibitor
97
Dopamine can inhibit:
Motor activity.
98
If we have a difficult time producing enough dopamine, it results in:
an overactive nervous system
99
Norepi in CNS
increases awareness/mood.
100
Common antidepressants are:
norepi reuptake inhibitors. Those typically boost norepi in brain/spinal cord and increases awareness. A big chunk of older antidepressant drugs.
101
Norepi reuptake inhibitors can be used for antidepressants but ALSO
chronic pain control.
102
Large reduction in pH (more acidotic) results in
Reduction of CNS activity
103
Large increase in pH (more alkalotic) results in
increased CNS activity.
104
Why does increased/decreased pH result in alterations in CNS activity?
Everything to do with calcium levels
105
Our body uses chemical reactions to control
acid-base issues
106
How does the body buffer acids in the blood?
With bicarb. Combines bicarb with H+ (excess during acidosis) and produces carbonic acid (h2CO3)
107
When carbonic acid dissociates, what does it become?
CO2 and H2O
108
Carbonic acid formula
H2CO3
109
Most significant plasma protein
albumin
110
Albumin has a ton of ________ associated with it and they buffer _____.
Negative charges; positively charged things.
111
What ions are attracted to albumin?
Ca++ and H+ due to its negative nature
112
The amount of free calcium is dependent upon how many ________ we have hanging around.
Protons
113
If we have lots of protons hanging around and hogging real estate of albumin, what happens to calcium?
Ends up freely circulating in the blood.
114
Increased free calcium results in _________ CNS activity
Reduced
115
A deficit of free calcium will result in __________ CNS activity.
Increased.
116
Calcium will _________ CNS activity
inhibit
117
If we get rid of all the H+, this allows calcium to
Bind to albumin, resulting in less free floating calcium. increased CNS.
118
If someone hyperventilates, CO2 blows off and this will favor
Less CO2 in blood -> less protons binding to albumin -> more room for calcium to bind in albumin -> less calcium in blood inhibiting CNS activity -> result in overactivity of CNS/seizures
119
if someone hypoventilates, there will be an increase in CO2
Increased CO2 -> more protons binding to albumin -> more calcium in free blood -> results in more inhibited CNS activity.
120
Chemical buffering in pH (chemical formulas he wrote on board)
H+ binds with HCO3- ---> H2CO3 ---> CO2 + H2O
