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A&P Exam III > Neuromuscular physiology > Flashcards

Neuromuscular physiology Flashcards

1
Q

What is acetylcholine composed of

A

Acetyl+choline connected with an ester bond

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2
Q

Which side of the synapse is acetylcholinesterase usually located

A

Post synaptic
skeletal muscle side

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3
Q

What is synaptic fatigue

A

Temporary inability for neurons to release neurotransmitter.
Results from a depletion of synaptic vessicles

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4
Q

Where are P-type V-G calcium channels located

A

Neuron axons
and
purkinje fiber cells

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5
Q

Where are L-type Calcium channels located

A

All over body but predominantly in heart

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6
Q

Describe VP-1 and VP-2 in the pre-synaptic cell

A

VP-1 is a vessicle that is loaded with neurotransmitter and waiting to move up to the cell membrane
VP-2 is a vessicle that is up against the cell membrane and is ready to be signalled to be released into the synapse

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7
Q

What is choline acetyltransferase

A

The enzyme responsible for the synthesis of acetylcholine by connecting acetyl to choline

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8
Q

What is the job of leaky K+ and leaky Na+ channels

A

Regulating resting membrane potential (vrm)

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9
Q

How does Ca++ affect leaky Na+ channels

A

Free floating Ca+ likes to block leaky Na+ channels under normal conditions

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10
Q

How does a decrease in serum Ca++ affect leaky Na+ channels

A
  1. Less blocking of leaky Na+ channels
  2. Increase of Na+ floating in to cell
  3. Increased amount of AP’s
  4. Increased release of neurotransmitter
  5. Increased tetany
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11
Q

How does an increase in Ca++ or Mg++ affect the pre-synaptic cell

A

Reduces excitability of the cell, overall calming the system down

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12
Q

What happens after acetylcholinesterase cleaves ACh

A

After hydrolizing acetylcholine, the choline molecule is reabsorbed by the post-synaptic cell to be recycled and reused to make more acetylcholine

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13
Q

What is the A3B2 ACh-auto receptor

A

Involved in upregulation of acetylcholine in presynaptic cells.
Along with acetylcholine, opening of this channel results in a flow of Na+ and Ca++ into the cell
This flow of ions helps move VP-1 up to ready release position (VP-2)
Non-depolarizing agents will block this
Responsible for the change in heights of TOF response

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14
Q

What is the cause of malignant hyperthermia

A

Dysfunction of the Ryanodine Receptors on SR in skeletal muscle
Resulting in a continual release of Ca++ from the SR

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15
Q

What are symptoms of Malignant hyperthermia

A
  1. Severe muscle rigidity
  2. High body temp
  3. Spike in ETCO2
  4. Rapid HR/irregular rhythm
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16
Q

Treatments for malignant hyperthermia

A
  1. Remove volatile agent immediately
  2. Cool the patient
  3. Dantrolene
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17
Q

How does dantrolene work to treat malignant hyperthermia

A

Blocks RYR1 from releasing Ca++

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18
Q

What molecules flow throughan open ACh-receptor

A

Acetylcholine
Na+
Ca++
K+

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19
Q

What muscle moves the thumb midline

A

The adductor pollicis

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20
Q

How much current flows through the TOF

A

20-50mAmps

Maybe not correct

21
Q

How does the AP from a TOF differ from endogenous AP

A

AP from TOF only stimulates a small section of a nerve to ellicit a twitch

22
Q

What else can you do other than TOF to assess level of block

A

Shake them. “eyeball it” - J Schmidt PhD

23
Q

If you were to use continuous neuromuscular monitoring intraoperatively, how often would it typically stimulate the patient

A

Once every 10 seconds

24
Q

How many hz per second does the TOF operate at

A

2hz/2seconds

25
Q

What is double-burst stimulation

A

two High frequency stimulus with a short break inbetween

26
Q

How many hz are used by tetanic stimulation

A

100hz

27
Q

What is supermaximal stimuli

A

Stimulus that will recruit all of the motor units in the nerve we are shooting for

28
Q

If you wanted to measure quantitatively how much the adductor pollicis is responding to electrical stimulus, what could you use

A
  1. Pressure monitor under the thumb to measure physical movement
  2. Could put the stimulator and monitor directly on the exposed muscle (EMG)
29
Q

What are alternatives to the ulnar nerve for TOF stimulation

A
  1. Ophthalmic branch of facial nerve
  2. Peroneal nerve
  3. Posterior tibial nerve
30
Q

What is the TOF ratio

A

B(4th twitch)/A(1st twitch)

31
Q

Why do we have a fall off in twitches from 1st to 4th in non-depolarizing blocks

A

nACh autoreceptor (A3B2) on motor neuron, which helps to move VP-1 to VP-2, is blocked by non-depolarizing paralytics. Blocking this receptor slows the neurons ability to move its vessicles up into release ready position. So rapid concurrent depolarizations will quickly run out of neurotransmitter to release

32
Q

What is the TOF ratio target, and why

A

ratio of 0.90
At this point the patient is less likely to aspirate and likely can maintain own airway

33
Q

How can you determine diaphragm paralysis by observing adductor pollicis paralysis

A

The diaphragm requires a larger dose of paralytic to lose function
If we are waiting for paralysis to wear off during emergence, if the adductor pollicis has regained function, the diaphragm will have regained function already

34
Q

What is myasthenia gravis

A

Autoimmune disease, where the body forms antibodies to adult nACh receptors, destroying them over time and causing progressive weakness

35
Q

How does MG progress

A

Initially body will replace receptors, but eventually it cannot keep up with destruction.

36
Q

What are the three nACh receptors we talked about

A

Mature (adult)
Fetal
Neuronal (alpha 7)

37
Q

Myasthenia Gravis S/S

A
  1. Muscle weakness
  2. droopy eyelids
  3. Double vision
  4. Progression from small muscle weakness to larger muscle weakness
  5. Advanced disease results impaired swallowing and respiratory failure
38
Q

Myasethenia Gravis treatment

A
  1. AChesterase inhibitors
  2. Plasmapharesis
  3. Removal of thymus (thymus gland dysfunction can often trigger MG, but not always a fix)
39
Q

What can cause myasthenia gravis

A
  1. Thymus gland triggering or maintaining MG
  2. Thymus cancers or other various cancers may also play a role in MG trigger
40
Q

Myasthenia Gravis anesthetic considerations

A
  1. May be overly sensitive to non-depolarizing muscular blockers
  2. Inhalational anesthetic may be enough for paralysis
  3. May need increased dose of depolarizing muscular blockers
41
Q

What is Eaton Lambert myesthenic syndrome

A

Body forms antibodies to P-type calcium channels on peripheral motor neurons. These antibodies do not destroy the channels, they just block them.

42
Q

What are symptoms of ELMS

A
  1. Generalized weakness and fatigue
  2. Symptoms improve with activity (possibly because more auto receptors may open and contribute to more neurotransmitter release)
43
Q

What are treatments for ELMS

A
  1. 4,5 Quinopyridine (Blocks Ca++ activated K+ channel lengthening depolarization, increasing ACh release)
  2. TEA (tetraethyl ammonium) Generic potassium channel blockers (not safe, last resort)
  3. Plasmapheresis
44
Q

What is the tensilon test

A

Test designed to diagnose MG using electrostimulus and AChe-I (edrophonium)

45
Q

What is usually the source of ELMS

A

Lung cancers (produces endocrine and immune issues)

46
Q

ELMS anesthetic considerations

A
  1. Monitor airway
  2. AChe-i don’t have much effect
  3. More sensitive to paralytic agents
  4. Don’t use sux!
  5. Suggamedex is a better choice for rocuronium reversal
47
Q

What is suggamedex

A

Cyclic ring that is a sugar compound that can physically carry off rocuronium molecules

48
Q

What is a deadly AChe-i

A

Serin nerve gas

A&P Exam III (3 decks)

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