Lecture 18 Flashcards

(36 cards)

1
Q

What issues can Succinylcholine cause?

A
  • Potassium issues
  • prolonged paralysis in sick patients, stroke, spinal cord injuries, disuse, or neuromuscular disorders

Succinylcholine can lead to complications in various patient populations who have extrajunctional receptors (fetal receptors )

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

What are the components of the motor neuron?

A
  • Myelin on the axon
  • Nodes of Ranvier
  • Fast Na channels
  • Voltage gated potassium channels
  • Na/K ATPase Pumps
  • Leaky Ion channels
  • l type ca channels
    *P type ca Channels - primary
  • N Ach auto receptors - A3B2

These components are essential for the proper functioning of motor neurons.

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

At rest, what is the state of the activation and inactivation gates in a motor neuron?

A
  • Inactivation gate: open (H gate in fast Na channels) (f gate in slow ca channels)
  • Activation gate: closed (M gate in fast na channels). ( d gate in slow channels)

This configuration is crucial for maintaining the resting potential of the neuron.

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

What role do potassium channels play in the motor neuron?

A
  • Help with repolarization
  • Reset the cell after an action potential

Voltage-gated potassium channels are vital for the rapid repolarization of neurons.

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

What is the effect of hypocalcemia on motor neurons?

A
  • Less calcium occluding Na leak channels
  • Makes the cell more excitable
  • Can lead to Tetany if severe

Hypocalcemia affects the excitability of motor neurons significantly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are Trousseau’s sign and Chvostek’s sign indicative of?

A
  • Hypocalcemia

These signs are clinical indicators of low calcium levels in the body.

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

What mediates the release of acetylcholine vesicles?

A
  • Calcium

Calcium influx via Vg p type ca channels is crucial for the exocytosis of acetylcholine vesicles at the neuromuscular junction.

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

What are the two types of vesicles involved in acetylcholine release?

A
  • VP1 (reserve pool vesicles)
  • VP2 (ready release pool vesicles)

These vesicles play different roles in neurotransmitter release at the NMJ.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the primary influx channel for calcium in motor neurons?

A

P-Type Ca Channel

This channel is voltage-activated and essential for neurotransmitter release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the mechanism of Non-Depolarizing Muscle Relaxants (NDMR)?

A
  • Block neuromuscular transmission by binding to Nach receptors on the muscle
  • Block autoreceptors on the neuron

This mechanism reduces acetylcholine mobilization and affects muscle contraction.

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

What is the Train of Four (TOF) used for?

A
  • Gauge depth of muscular block
  • Verify NMJ integrity
  • Differentiate between depolarizing and non-depolarizing muscle relaxants

TOF monitoring is a critical tool in assessing neuromuscular function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the characteristic recovery pattern of a Non-Depolarizing Block?

A
  • Sequential reappearance of twitches
  • First twitch appears quickly, followed by more twitches
  • Twitches are often weak initially
    As the drug wears off the first twitch is stronger than the twitches to follow

This pattern indicates the gradual recovery of neuromuscular function.

Blocking of autoreceptors causes fade due to not being able to push vp1 to vp2 positions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the primary goal in treating Lambert-Eaton Myasthenic Syndrome (LEMS)?

A
  • Prolong the action potential in the neuron
  • TEA’s 3-4 diaminopyridine - ca+ mediated K channel blockers

Treatment includes:
1. Steroids - slow down immune system
2. Plasmapheresis - wash out antibodies
3. Remove lung tumors to stop production of antibodies

This approach allows more calcium influx and improves neurotransmitter release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the two main choline reuptake pathways in motor neurons?

A
  • Choline ATPase (High Affinity, Low Capacity)
  • Sodium-Choline Co-transporter (Low Affinity, High Capacity)

These pathways are essential for recycling choline in the motor neuron.

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

What is the difference in affected structures between LEMS and Myasthenia Gravis (MG)?

A
  • LEMS: Neuron (presynaptic cell)
  • MG: Muscle side of the synapse

This distinction is crucial for understanding the pathophysiology of each condition.

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

What are the classic symptoms of Myasthenia Gravis (MG)?

A
  • Droopy eyelids (ptosis)
  • Fatigue in small muscle groups
    Feel good early in day , get more tired at end of day

These symptoms are due to reduced functional receptors at the NMJ.

17
Q

What is the risk associated with using ca mediated potassium channel blockers in treating LEMS?

A
  • Can lead to dangerous arrhythmias

Potassium channels are vital for many bodily functions, and their non-specific blocking can have serious consequences.

18
Q

What does a T4/t1 ratio of less than 0.9 indicate?

A

Residual block

A ratio below 0.9 suggests that neuromuscular function is not fully recovered.

19
Q

In a Phase I Block with Succinylcholine, what is the expected T4/T1 ratio?

A

Close to 1.0 (100%)

This indicates no fade, although the height of all twitches is reduced.

20
Q

What happens in a Phase II Block with Succinylcholine?

A

Exhibits a fade pattern in the TOF

This resembles a non-depolarizing muscle relaxant block.

21
Q

What percentage of nAChRs are blocked when the 4th twitch disappears?

A

Approximately 75-80%

This indicates significant neuromuscular blockade.

22
Q

What is the first line of drugs for Myasthenia Gravis?

A

AChEi (acetylcholinesterase inhibitor)

These drugs increase the availability of acetylcholine at the neuromuscular junction.

23
Q

What is the role of the thymus gland in Myasthenia Gravis?

A

Dysfunction triggers antibody production

Antibodies block nACh-R, leading to neuromuscular impairment.

24
Q

What is the first symptom of Myasthenia Gravis?

A

Droopy eyelids towards the end of the day

Symptoms typically worsen throughout the day.

25
What is the effect of **scar tissue** on the neuromuscular junction (NMJ) in Myasthenia Gravis?
Reduces surface area for nACh-R ## Footnote This decreases the probability of generating an action potential.
26
What is the **clinical application** of neuromuscular monitoring?
To assess readiness for extubation ## Footnote Monitoring helps determine the function of the NMJ at the end of a procedure.
27
What does a **supramaximal stimulus** do in neuromuscular monitoring?
Recruits all motor neurons in the motor nerve ## Footnote Ensures a strong enough pulse to generate action potentials.
28
What happens to the **T4/T1 ratio** as non-depolarizing muscle relaxants wear off?
Increases ## Footnote A higher ratio indicates a reduction in neuromuscular blockade.
29
What is the **safety factor** in the context of the NMJ?
Large amount of nACh-R available ## Footnote Ensures reliable neuromuscular transmission despite some receptor blockade.
30
True or false: **Succinylcholine** interferes with autoreceptors.
FALSE ## Footnote Sux does opposite, actually facilitates the process of vesicle movement rather than inhibiting autoreceptors.
31
What is the effect of **AChEi** on acetylcholine in the synapse?
Prolongs the availability of ACh ## Footnote This increases the chance of neurotransmitter interaction with available receptors.
32
What is the **progression** of Myasthenia Gravis?
* Body creates antibodies * Antibodies block nACh-R * Immune system destroys receptors * Scar tissue forms ## Footnote This leads to a gradual decline in neuromuscular function.
33
What is the **duration of action** of non-depolarizing paralytics like Rocuronium?
Longer onset and longer to wear off ## Footnote This contrasts with depolarizing paralytics, which have rapid onset and offset.
34
What is the **first twitch** in a non-depolarizing drug TOF typically characterized by?
Strongest twitch ## Footnote The first twitch is usually the most robust before the drug effects diminish.
35
What is the **importance** of checking the **diaphragm** during neuromuscular monitoring?
Critical for maintaining airway function ## Footnote The diaphragm is essential for respiration, and its function must be assessed before extubation.
36
What are TEA drug class and what do they treat?
Ca mediated K channel blockers - treatment for LEMS block K channels from accepting intracellular ca - don’t open and don’t release K which allows for longer periods of time for calcium to be in cell allowing longer time to depolarize Example: 3-4 diamino pyridine High risk for arrhythmias due to cells being more positive - extra excited