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A&P 1 > Exam 3 - Lecture 4 > Flashcards

Exam 3 - Lecture 4 Flashcards

1
Q

Neuron nACHr

A

Autonomic/CNS nACHr

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2
Q

Part of the synapse where there are NMJ

A

Junctional area

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3
Q

Area JUST outside NMJ on skeletal muscle

A

Peri junctional area

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4
Q

Area further down skeletal muscle outside the NMJ

A

Post junctional

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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

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6
Q

2 electrodes for nerve stimulation that are 1 _______ and 1 _________.

A

1 cathode and 1 anode

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7
Q

Nerve stimulators work by taking away the _____ between outside and inside the cell

A

Polarity

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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

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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

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10
Q

Single twitch

A

One impulse to see if it triggers muscle

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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

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12
Q

Hertz

A

Something happening per second.

E.g. 2 hertz means 2 impulses over 1 second

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13
Q

How many seconds does a train of four last?

A

2 hz per second, 4 twitches total… therefore 2 seconds.

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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.

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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

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16
Q

Tetanic contraction

A

Repetitive high speed contraction, high frequency stimulation for a very short period of time

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17
Q

Post-tetanic count

A

Impulses muscle generates after tetanic stimulation. Stimulate with high frequency, to check health of synapse.

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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

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19
Q

The ulnar nerve innervates what muscle?

A

Adductor pollicis

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20
Q

What happens when the adductor pollicis is stimulated?

A

Thumb comes forward a little bit and pinky finger should twitch

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21
Q

Why is the ulnar nerve used for TOF?

A

Easy to access and see

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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

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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

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24
Q

Depolarizing block paralytic is what drug?

A

Succinylcholine

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25
Q

Characteristics of succinylcholine timing and why is it used

A

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)

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26
Q

The twitches for NDMR will come back in

A

Stages.

First it’ll just be one twitch, then 2, then 3, then 4… but they’re all unequal in strength

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27
Q

B/A ratio

A

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

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28
Q

If A twitch is strong, and B is super weak, that would create a _____ B/A ratio

A

Very small

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29
Q

How many twitches do you need for a B/A ratio to be used?

A

All 4 muscles must twitch

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30
Q

TOF ratio

A

B/A

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31
Q

Do depolarizing paralytic twitches recover evenly over time?

A

Yes. Each twitch during the TOF will be an equal strength.

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32
Q

What is the TOF ratio (B/A) in the depolarizing block?

A

Almost always 1.0

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33
Q

NDMR act on both the

A

Motor neuron and skeletal muscle

Technically both paralytics do but NDMRs cause a different and more important effect

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34
Q

Second type of ACH receptor that is on the motor neuron

A

Alpha3, Beta2 (3 alpha subunits and 2 beta subunits)

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35
Q

What are the 3 alpha subunits on the ach receptor on motor neuron represents

A

Where ach can bind

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36
Q

When acetylcholine is dumped into synapse, most of it goes to the skeletal muscle to bind to those receptors, but a few go

A

Back up to the alpha3,beta2 receptors (also called auto receptors)

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37
Q

Autoreceptors

A

The name for alpha3 beta2 ach-r on the motor neurons

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38
Q

Secondary effect of ach release from motor neuron

A

The act of them routing back up to motor neuron to bind to autoreceptors

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39
Q

When autoreceptors open, what happens?

A

Causes sodium and calcium to flow into cell.

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40
Q

What happens when autoreceptors are bound and ions come in?

A

Alerts the VP1 vesicles to move forward to become VP2, since VP2 just got dumped.

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41
Q

NDMR drugs overall affects on skeletal muscle

A

Prevents end plate potential at NMJ, and they inhibit autoreceptors and inhibit acetylcholine release

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42
Q

So why is there a weaker subsequent contraction in NDMR? (Chart showing weaker and weaker contractions)

A

Due to fewer and fewer VP2 vesicles moving to cell wall to dump acetylcholine due to blocking of autoreceptors

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43
Q

Do less acetylcholine get released from motor neuron in depolarizing drugs?

A

No.. same amount get released.

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44
Q

How does non-depolarizing drugs bind to ach-r?

A

They park themselves on alpha subunits of autoreceptors and skeletal muscle NMJ ACH-r

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45
Q

How does sux break down and stop working?

A

Plasma cholinesterase clear sux from system over time

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46
Q

How many acetylcholine NTs are required to open autoreceptors?

A

Probably only need 2, but 3 can bind…?

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47
Q

What type of calcium channels do we have in addition to p-type calcium channels? Are they required?

A

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.

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48
Q

If we have skeletal muscle with nACHr post-junctional, what will happen if we dose someone with a depolarizing agent? (Succinylcholine)

A

Hemorrhaging potassium, since there are extra channels.

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49
Q

Do paralytics have the same sensitivity to every muscle? Why?

A

No. Certain muscles require higher doses due to nACHr receptor density in those muscles.

50
Q

Which muscles require higher paralytic doses?

A

More important muscles such as the diaphragm.

51
Q

Dose range for 10-90% effectiveness on the adductor pollicis?

A

20ish-40ish mcg/kg

52
Q

Dose range for 10-90% effectiveness on the diaphragm?

A

40ish-100ish mcg/kg

53
Q

The diaphragm is what kind of muscle?

A

Skeletal muscle

54
Q

The motor neurons that control the diaphragm, where do they originate and what’s the nerve called? (vertebra #’s)

A

Phrenic nerve, C3-C5 (You must know this forever)

55
Q

If we break our neck and have a lesion above C3, what happens?

A

Cannot breathe on your own.

56
Q

As the drug is wearing off, your TOF generates 2/4 twitches. Is the diaphragm working?

A

it likely is. The diaphragm requires much higher doses so if the ulnar nerve isnt fully paralyzed then the diaphragm likely isnt.

57
Q

4th twitch disappears? %

A

75-80% nACHr’s blocked

58
Q

3rd twitch disappears? %

A

85% of nACHr’s blocked

59
Q

2nd twitch disappears? %

A

85-90% blocked

60
Q

All twitches disappear? %

A

90-95% blocked

61
Q

If a patient can reasonably lift their head, the nACHrs are what % blocked?

A

70%

62
Q

Stimulator settings #’s

A

50-80 mA (milliampures), this will be the supramaximal stimuli, and it varies per hospital.

63
Q

What does mA stand for?

A

Milliampures

64
Q

A high voltage battery can push

A

alot of current

65
Q

If you have a lesion/severed spinal cord at C4, what happens?

A

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
Q

Ways K+ gets out during depolarization in succinylcholine?

A

primarily leak channels, secondary voltage gated channels around NMJ, 3rd through ach receptors but this is very minimal.

67
Q

The succinylcholine will also allow what ion coming in? (other than sodium)

A

Calcium, causes minimal contraction but does allow calcium to leak in, only at NMJ.

68
Q

Fetal receptors on skeletal muscle with succiynlcholine, this allows more K+ to flow out, more Na+ to leak in, and more __________

A

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
Q

Ocular muscles in the eyes have ________

A

Several neurons controlling a single muscle, leads to lots of NMJs.

70
Q

If we hit ocular muscles with acetylcholine, what can happen?

A

They contract just enough to increase intraocular pressure.

71
Q

Depolarizing muscle block in ocular muscles side effects and why?

A

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
Q

GABA characteristics

A

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
Q

Glycine characteristics

A

important inhibitory NT in SPINAL CORD! Similar to GABA.

74
Q

2 most important inhibitory NTs in spinal cord?

A

GABA and Glycine

75
Q

Acetylcholine characteristics

A

Communication with skeletal muscles and smooth muscles.

76
Q

Acetlycholine in CNS characteristics

A

Within CNS, it increases awareness. More ACH in brain, more awake we are, and the more we are aware of our surroundings.

77
Q

If you have something that blocks ACH in our nervous system, it will

A

Cause drowsiness.

78
Q

Anticholinergics will cause us to

A

be drowsy i.e. benadryl via acetylcholine inhibition.

79
Q

Majority of awareness in CNS mediated through acetylcholine, is done through __________ receptors.

A

mACHr.

80
Q

If we have agents that block mACHr, it will

A

make us drowsy

81
Q

What common drug blocks mACHr? And what type of drug is it?

A

Benadryl, antihistamine/anticholinergics.

82
Q

Antihistamines are cross reactive with

A

mACHr. They’re very similar to CNS mACHr.

83
Q

Whats another side effect of benadryl since its anticholinergic?

A

Spike of heart rate due to inhibition of mACHr at the heart.

84
Q

How do we increase ACH at a central synapse?

A

Inhibit acetylcholinesterase.

85
Q

What types of drugs inhibit ach-esterase and make us more aware?

A

drugs that can cross BBB. -stigmines.

86
Q

If you want to wake a patient up and reverse paralytic, without waking them up, you would use a drug that:

A

is a acetylcholinesterase inhibitor that doesnt cross the BBB (if it crosses it would wake them up)

87
Q

What drugs do pt’s with alzheimers get?

A

Centrally acting acetylcholinesterase inhibitor to increase ach across the BBB

88
Q

Do stigmines cross BBB?

A

Yes.

89
Q

Side effects of inhibiting acetylcholinesterase across body?

A

-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
Q

Histamines

A

work similarly to ACH, more histamines in brain will result in more awareness.

91
Q

If we have drugs that block histamine receptors, we would expect

A

drowsiness

92
Q

Glutamate general characteristics

A

Stimulatory CNS NT that increases neuronal activity.

93
Q

Patients on meth will have an increased ________ due to what?

A

awareness; glutamate.T

94
Q

Too much glutamate will ________

A

Burn out brain cells and not be replaced.

95
Q

Are meth users more sensitive to pain?

A

Acutely, no… but after, yes.

96
Q

Dopamine

A

Pleasure/reward NT.

Can be a potent motor inhibitor

97
Q

Dopamine can inhibit:

A

Motor activity.

98
Q

If we have a difficult time producing enough dopamine, it results in:

A

an overactive nervous system

99
Q

Norepi in CNS

A

increases awareness/mood.

100
Q

Common antidepressants are:

A

norepi reuptake inhibitors. Those typically boost norepi in brain/spinal cord and increases awareness. A big chunk of older antidepressant drugs.

101
Q

Norepi reuptake inhibitors can be used for antidepressants but ALSO

A

chronic pain control.

102
Q

Large reduction in pH (more acidotic) results in

A

Reduction of CNS activity

103
Q

Large increase in pH (more alkalotic) results in

A

increased CNS activity.

104
Q

Why does increased/decreased pH result in alterations in CNS activity?

A

Everything to do with calcium levels

105
Q

Our body uses chemical reactions to control

A

acid-base issues

106
Q

How does the body buffer acids in the blood?

A

With bicarb. Combines bicarb with H+ (excess during acidosis) and produces carbonic acid (h2CO3)

107
Q

When carbonic acid dissociates, what does it become?

A

CO2 and H2O

108
Q

Carbonic acid formula

A

H2CO3

109
Q

Most significant plasma protein

A

albumin

110
Q

Albumin has a ton of ________ associated with it and they buffer _____.

A

Negative charges; positively charged things.

111
Q

What ions are attracted to albumin?

A

Ca++ and H+ due to its negative nature

112
Q

The amount of free calcium is dependent upon how many ________ we have hanging around.

A

Protons

113
Q

If we have lots of protons hanging around and hogging real estate of albumin, what happens to calcium?

A

Ends up freely circulating in the blood.

114
Q

Increased free calcium results in _________ CNS activity

A

Reduced

115
Q

A deficit of free calcium will result in __________ CNS activity.

A

Increased.

116
Q

Calcium will _________ CNS activity

A

inhibit

117
Q

If we get rid of all the H+, this allows calcium to

A

Bind to albumin, resulting in less free floating calcium. increased CNS.

118
Q

If someone hyperventilates, CO2 blows off and this will favor

A

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
Q

if someone hypoventilates, there will be an increase in CO2

A

Increased CO2 -> more protons binding to albumin -> more calcium in free blood -> results in more inhibited CNS activity.

120
Q

Chemical buffering in pH (chemical formulas he wrote on board)

A

H+ binds with HCO3- —> H2CO3 —> CO2 + H2O

A&P 1 (39 decks)

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