Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

A&P I 2024 > 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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What channels/pumps reset the Vᵣₘ of the cell?

A
  • Na⁺ K⁺ ATPase Pump
  • VG K⁺ Channels
  • Leaky K⁺ Channels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

CAT (or ChAT) Choline Acetyltransferase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

Ca⁺⁺

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

Leaky K⁺ channels
Leaky Na⁺ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which ion can block leaky Na⁺ channels?

A

Ca⁺⁺

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

Ca⁺⁺ and Mg⁺⁺

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What amperage is typically used by a peripheral nerve stimulator?

What amperage would be considered deadly?

A

20-50 mAmps

1 Amp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What electrical component “drives” the amps?

A

Voltage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

high amperage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What enzyme is capable of breaking down succinylcholine?

A

PlasmaCholinesterase (ButyrylCholinesterase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why isn’t Succinylcholine broken down by AChE?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the T½ of Succ?

A

47 sec, onset within 1 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

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

A

M and H

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is Succinylcholine’s effect on the PeriNMJ area?

A
  • More positive Vᵣₘ due to succinylcholine administration makes fast Na⁺ channels “stuck”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

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

A

↑ 0.5 mEq/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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 2024 (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions