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A&P I (Fall 2022) > Skeletal Muscle Physiology pt.2 (Exam III) > Flashcards

Skeletal Muscle Physiology pt.2 (Exam III) Flashcards

1
Q

What role does Ca⁺⁺ play at the neuromuscular junction?

A

Ca⁺⁺ release from an action potential causes secretory vesicles to move towards and bind with cell membrane.

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2
Q

What channels/pumps reset the Vᵣₘ of the cell?

A
  • Na⁺ K⁺ ATPase Pump
  • VG K⁺ Channels
  • Leaky K⁺ Channels
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3
Q

What presynaptic enzyme combines choline and acetyl-CoA to from Acetylcholine?

A

CAT (or ChAT) Choline Acetyltransferase

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4
Q

Differentiate VP1 (Vesicular Pool 1) and VP2 (Vesicular Pool 2) vesicles.

A
  • VP1 Vesicles are “waiting” to merge with pre-synaptic membrane.
  • VP2 vesicles have attached to pre-synaptic membrane and are ready to fuse and exocytose their neurotransmitter.
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5
Q

What ion causes VP1 vesicles to “become” VP2 vesicles?

A

Ca⁺⁺

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6
Q

What two types of Ca⁺⁺ channels are found in motor neurons?
What are the differences?

A
  • L-Type VG Ca⁺⁺ Channels: Found everywhere, especially the heart. open up quickly.
  • P-Type VG Ca⁺⁺ Channels: Found in axons of motor system only.
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7
Q

Which two channels help regulate the general “excitability” of a cell?

A

Leaky K⁺ channels
Leaky Na⁺ channels

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8
Q

Which ion can block leaky Na⁺ channels?

A

Ca⁺⁺

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9
Q

What would be the cellular response to decreased levels of serum Ca⁺⁺? What is the mechanism of this response?

A
  • ↓ serum Ca⁺⁺ = less blockage of leaky Na⁺ channels = ↑ pNa⁺ = ↑ excitability.
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10
Q

Hypocalcemia does what to general cell excitability?
Which two “signs” point towards hypocalcemia?

A

↑ cell excitability
Trousseau’s sign and Chvostek’s sign.

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11
Q

Elevated levels of which two ions would help decrease excitability at the NMJ?

A

Ca⁺⁺ and Mg⁺⁺

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12
Q

What was one cause of synaptic fatigue, discussed in lecture, focusing on the presynaptic cell?

A

The inability of ACh to reach the NMJ because of VP1 vesicles not moving up to become VP2 vesicles.

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13
Q

What nerve is traditionally stimulated with a peripheral nerve stimulator?
What muscle twitches due to this stimulation?
What is the purpose of this?

A
  • Ulnar nerve
  • Adductor Pollicis
  • Qualitative Neuromuscular assessment determining the degree of paralysis (aka number of blocked nACh receptors)
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14
Q

How does a peripheral nerve stimulator produce a muscular twitch?

A

The nerve stimulator (through e⁻ flow) makes the outside of the cell ( - ), effectively depolarizing the nerve.

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15
Q

What amperage is typically used by a peripheral nerve stimulator?

What amperage would be considered deadly?

A

20-50 mAmps

1 Amp

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16
Q

What electrical component “drives” the amps?

A

Voltage

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17
Q

What is more dangerous comparatively, high amperage or high voltage?

A

high amperage

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18
Q

Describe single twitch stimulation vs TOF (Train-of-Four) stimulation?

A
  • Single Twitch = 1 stimulation per given time (say 10sec)
  • TOF = 2 stimulations per second for 2 seconds (4 total)
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19
Q

When would it be possible to contract skeleton muscle despite “paralysis”?

A

Through direct electrical current to the muscles causing depolarization at PostNMJ area. (ex. direct electrical stimulation of muscle despite succ blocking depolarization at NMJ proper).

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20
Q

How can EMG (Electromyography) be used to diagnose neuromuscular problems?

A

EMG can diagnose neuromuscular diseases by determining if electrical issue is at NMJ (and thus a neuro issue) or the wider muscle belly (and thus a widespread muscle issue)

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21
Q

What other areas besides the adductor pollicis can be assessed using peripheral nerve stimulation?

A
  • Ophthalmic branch of facial nerve (Orbicularis Oris)
  • Peroneal nerve
  • Posterior Tibial nerve
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22
Q

What is occurring for both A and B in the figure below?

A

Single Twitch Stimulation for:
A. Non-Depolarizing NMJ blocker
B. Depolarizing NMJ blocker

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23
Q

What enzyme is capable of breaking down succinylcholine?

A

PlasmaCholinesterase (ButyrylCholinesterase)

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24
Q

Why isn’t Succinylcholine broken down by AChE?

A

Succ has an Acetate-methyl linkage (rather than an ester bond).

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25
Q

What is the T½ of Succ?

A

47 sec, onset within 1 min

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26
Q

What areas of the muscle cell are usually affected by Succ depolarization? What areas are not affected?

A
  • NMJ and Perijunctional area = affected
  • Postjunctional area = unaffected
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27
Q

Repolarization of the cell is required to reset the ___ gate and thus re-open the _____ gate.

A

M and H

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28
Q

What is Succinylcholine’s effect on the PeriNMJ area?

A
  • More positive Vᵣₘ due to succinylcholine administration makes fast Na⁺ channels “stuck”
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29
Q

Administration of Succinylcholine usually results in how much of an increase in potassium levels?

A

↑ 0.5 mEq/L

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30
Q

What occurs to adult nACh receptors when theres a loss of basal resting tone?

A

The body adds more fetal nACh receptors and adds them along the entire muscle belly (NMJ, perijunctional area, and postjunctional area.)

31
Q

How does a fetal nACh receptor differ from an adult nACh receptor?

A

Fetal nACh receptors have a gamma (γ) subunit that replaces the epsilon (ε) subunit of the adult nACh receptor.

32
Q

When does the body replace adult nACh receptors with fetal nACh receptors?

A

Large Scale Denervation such as:
- strokes
- spinal cord injuries

33
Q

What characterizes a high conductance receptor?

A

↑ ↑ ↑ Na⁺ influx for a short period of time. (adult nACh receptors)

34
Q

What characterizes a low conductance receptor?

A

↓ Na⁺ influx but open for a much longer period of time. (fetal nACh receptors)

35
Q

Is the net movement of Na⁺ greater in fetal nACh or adult nACh receptors?

A

Fetal nACh receptors (due to being open so much longer)

36
Q

What is a massive risk factor for succinylcholine administration aside from hyperkalemia and ESRD?

A

States of Denervation: stroke, spinal cord injury, late stage MS, etc.

37
Q

How quickly would you see development of fetal nACh receptors post stroke?

A

12 hours post stroke onset.

38
Q

Why is succinylcholine contraindicated in conditions of increased intraocular pressure (IOP)?
What conditions mentioned in lecture cause IOP?

A
  • Superficial eye muscles have multiple neuron innervation. Succ causes extensive contractions because of this and greatly ↑ IOP.
  • Glaucoma, head-down position, eye injury, retinopathy, intracranial hypertension, etc.
39
Q

Increased permeability of Na⁺ will lead to increased permeability of what other ion (in skeletal muscle tissue)?

A

K⁺

40
Q

Why is succinylcholine administration in someone with fetal nACh receptors dangerous?

A

Fetal nACh receptors are usually developed all along the muscle, not just at the NMJ. Succ will attach to all of these and cause a massive influx of Na⁺ and massive efflux of K⁺.

41
Q

Why is the first twitch the strongest in a TOF (Train-Of-Four) assessment of a non-depolarizing block’s effectiveness?

A

Autoreceptor Inhibition

(needs verification) and better explanation.

42
Q

How is nACh receptor inhibition quantitatively analyzed?
What metric is used to determine that enough paralytic has worn off to adequately decrease risk of aspiration?

A
  • TOF B/A ratio using the nerve stimulator with EMG.
  • B/A ratio = 0.9
43
Q

What is the B/A ratio in TOF monitoring?

A

B = magnitude of twitch #4
A = magnitude of twitch #1

44
Q

Does TOF quantitative monitoring show the same results whether a depolarizing and non-depolarizing blocker is administered?

A

No.
- Non-Depolarizing = variable B/A ratio due to autoreceptor inhibition.
- Depolarizing = 1:1 B/A ratio

45
Q

What ion can feed back into the pre-synaptic cell and cause the release of more neurotransmitter from their vesicles?
What receptor is used for this process?

A

Ca⁺⁺
α₃β₂ subunit ACh receptor.

46
Q

What drug blocks the α₃β₂nACh receptor? What is the result?

A

Non-Depolarizing Blockers. By blocking this receptor, NMB’s exhibit autoreceptor inhibition and block ACh from vesicular ready-release pool.

47
Q

Why does the diaphragm have more resiliency than the adductor pollicis or other smaller peripheral muscles?

A
  1. Bigger NMJ’s
  2. ↑ receptor sites
  3. ↑ resiliency
48
Q

At what number of blocked nACh-receptors would we expect to see all twitches (using a nerve stimulator) disappear?

A

90-95% nACh - receptors blocked

49
Q

At what number of blocked nACh-receptors would we expect to see the 4th twitch (using a nerve stimulator) disappear?

A

75-80% nACh - receptors blocked

50
Q

At what number of blocked nACh-receptors would we expect to see the 4th twitch (using a nerve stimulator) disappear?

A

75-80% nACh - receptors blocked

51
Q

What ACh receptor is utilized by the ANS for signaling?
What is unique about this receptors structure?
What is unique about this receptor and various pathophysiologies?

A
  • Neuronal nicotinic ACh Receptor
  • 5 α-7 subunits
  • This receptor is not affected by paralytics or NMJ system diseases.
52
Q

What is a one sentence summary of the pathophysiology of Myasthenia Gravis?

A

Progressive loss of adult nACh receptors due to autoimmune reaction where antibodies attach to α-subunits of the receptor and target it for destruction.

53
Q

What signs/symptoms appear first for myasthenia gravis?
What signs/symptoms appear later?
What is eventually deadly?

A

1st: loss of control of small central muscles
- droopy eyelids or double vision from loss of eye muscle strength.
2nd: generalized fatigue and weakness in large muscle sets.
Death: eventual loss of airway (diaphragm) and swallowing muscles.

54
Q

Why do myasthenia gravis symptoms tend to worsen towards the end of the day?

A

When one runs out of ready-release ACh (particularly in older people)

55
Q

What 3 general treatments exist for myasthenia gravis and how do they work?

A
  1. AChE Inhibitors = ↑ circulating ACh
  2. Plasmapheresis = removal of antibodies
  3. Thymus Removal = stunts immune system response, can even be curative occasionally.
56
Q

What anesthesia considerations exist for myasthenia gravis patients?

A
  1. Myasthenia Gravis patients are more sensitive to NMB’s. (Use less Roc more isoflurane)
  2. Myasthenia Gravis patients are less sensitive to Succinylcholine. ( ↑ dose needed)
57
Q

What is the Tensilon Test used to diagnose?
How does the test work?

A
  • Myasthenia Gravis
  • Elicit twitch response (or muscle strength) then administer AChE Inhibitor. If twitch response (or muscle strength) improves then Myasthenia Gravis is diagnosed.
58
Q

If a patient with myasthenia gravis was paralyzed with rocuronium, could it be reversed with a -stigmine? What drug would be used?

A

No, already on an AChE Inhibitor for myasthenia gravis. Would need Sugammadex instead.

59
Q

What should be known about Sugammadex (structure & MOA)?

A

Sugar complex Ring structure that is given IV to bind to rocuronium and pull it out of circulation.

60
Q

What is the pathophysiology of Eaton-Lambert Myasthenic Syndrome (ELMS) ?

A

Autoimmune disorder where antibodies attach to and stop the utilization of P-Type Ca⁺⁺ Channels.

61
Q

Between P-type Ca⁺⁺ channels and L-type, which is more important in neuron signaling?

A

P-Type Ca⁺⁺ Channels

62
Q

What should be known about the location of signs/symptoms of ELMS?
What causes improvement of symptoms? Why?

A
  • Marked increase in effect on peripheral muscles vs central muscles (weakness/fatigue)
  • ↑ activity improves symptoms. This is due to increased recruitment of the α₃β₂ subunit ACh receptor.
63
Q

What is the usual underlying cause of Eaton-Lambert Myasthenic Syndrome (ELMS)?

A

Lung cancer.

64
Q

What two drugs can be used to treat ELMS and what is their mechanism of action?

A
  1. 4-Aminopyridine: blocks Ca⁺⁺ activated K⁺ channel = ↑ time in depolarized state = ↑ ACh.
  2. Tetra-ethyl-Ammonium: K⁺ Channel blocker.

Essentially, both block pK⁺ in the neuron.

65
Q

What four treatment options are there for ELMS?

A
  1. 4-Aminopyridine
  2. TEA (Tetra-ethyl-Ammonium)
  3. Plasmapheresis
  4. Root cause treatment (usually treating lung cancer)
66
Q

What drug is a last resort treatment for ELMS?

A

Tetra-ethyl-ammonium (TEA) very dangerous, last resort kind of drug.

67
Q

What anesthetic considerations should be given to a patient that has ELMS?

A
  1. AChE Inhibitors don’t work as well (use roc and Sug)
  2. No Succinylcholine.
68
Q

What’s the pathophysiology of Malignant Hyperthermia?

A
  1. Abnormal response to inhaled anesthetics.
  2. RyR1 dysfunction where continuous Ca⁺⁺ is released from stores causing total body contractions.
  3. Full body contractions ↑ temperature excessively.
69
Q

How should Malignant hyperthermia be treated?

A
  1. Removal of volatile anesthetic
  2. Dantrolene
  3. Cool patient down
70
Q

What is Dantrolene’s mechanism of action?

A

Dantrolene blocks RyR1 receptors preventing flood of Ca⁺⁺ out of the sarcoplasmic reticulum.

71
Q

Is malignant hyperthermia inheritable?

A

Yes, through inherited RyR1 gene mutation

72
Q

What is the 1st sign/symptom of malignant hyperthermia?

A

↑ EtCO₂

73
Q

What does IV Mg⁺⁺ administration do (in general)?
What pregnancy related condition can be treated by Mg⁺⁺ infusion?
Mg⁺⁺ makes reversal of what drug more difficult?

A
  • Decreases excitability of cells
  • Ecclampsia
  • Paralytics

A&P I (Fall 2022) (17 decks)

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