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MSK > Neuromuscular junction > Flashcards

Neuromuscular junction Flashcards

1
Q

In the brain, there are 2 parts that are responsible for skeletal muscle movement. What are they and what do they do?

A

Primary motor cortex - Execute

Premotor cortex - Plan

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2
Q

Describe the path that upper motor neurons in the brain take to synapse on lower motor neurons (alpha motor neurons) in the spinal cord.

A
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3
Q

Describe the path taken for a motor neuron in the motor cortex of the brain to synapse on a lower motor neuron that innervates the face.

A
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4
Q

All lower motor neurons that innervate the face are also […] nerves

A

Cranial

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5
Q

What is the neurotransmitter that is released by motor neurons on muscle fibers?

A

Acetylcholine

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6
Q

Alpha motor neurons cause contraction of the […] muscle fiber

A

Extrafusal

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7
Q

Gamma motor neurons cause contraction of the […] muscle fibers

A

Intrafusal

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8
Q

What are the 2 types of receptors for acetylcholine?

A

Nicotonic

Muscarinic

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9
Q

[…] receptors are ligand-gated ion channels (ionotropic)

A

Nicotinic

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10
Q

[…] receptors are GPCRs (metabotropic)

A

Muscarinic

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11
Q
A
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12
Q

Describe how acetylcholine acts on Nicotinic receptors in the postsynaptic muscle cell to create an action potential in that cell.

A

Ach from presynaptic neuron binds to sites on Nicotinic receptor, causes shape change to open the ion channel, Na+ and K+ ions flood into the cell and generate an action potential in the muscle cell. That AP propagates along the membrane of the muscle cell. When reaches a DHP receptor, it stimulates a conformational change in the DHP receptor, which causes the DHP to remove an inhibitory portion (ryanodine) from the sarcoplasmic reticulum causing an efflux of Ca2+ into cytoplasm.

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13
Q

What is myasthenia gravis? Why isn’t this disease an immediate death sentence?

A
  • an autoimmune disease with Abs directed against the nicotinic receptor specifically on the muscle.
  • Not immediately deadly becuase there are many different types of Nicotinic receptors so they’re not all impacted equally by the Ab which is directed against a specific type of nicotinic receptor
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14
Q

What is lambert - eaton disease?

A

An autoimmune disease with Abs directed against the Ca2+ channel on the presynaptic neuron. Results in loss of ability to draw in Ca2+ and thus inability to release Ach onto postsynaptic cell.

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15
Q

What is issac’s syndrome?

A

Abs directed against the potassium channel in the presynaptic neuron. In normal function, these voltage gated channels open leading to the release of K+ to terminate an AP. If you don’t have these channels then you cannot stop the generation of APs so there is increased excitability and repeated discharge of the motor neuron.

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16
Q

What are the symptoms of myasthenia gravis?

A
  • Weakness of skeletal muscle
  • Usually begins with muscle of eyes
  • Ptosis (drooping eyelids)
  • Loss of coordination of movement of eyes
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17
Q

What are the symptoms of Lambert-Eaton disease?

A
  • Slowly progressing muscle weakness
  • Begins in extremeties and moves proximally
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18
Q

What are the symptoms of Issac’s syndrome?

A
  • Muscle stiffness
  • Continuous contractions
  • Muscle twitching
  • Cramping
  • Sweating
  • Delayed muscle relaxation
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19
Q

Describe how botulinum toxin affects neurons.

A

Botulinum toxin is taken up into the presynaptic neuron by binding of the heavy chain toxin to the botulinum neurotoxin receptor in the neuron. The light chain is then released and it binds to SNARE proteins in the neuron which normally help release Ach from the vescicles. Thus, botulinum prevents release of Ach and results in flaccid paralysis and inability to cause muscle contraction.

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20
Q

Describe how tetanus affects neurons.

A

It is taken up into the lower motor neuron and travels in a retrograde fashion up the LMN to the synapse in the spinal cord. It then is uptaken into inhibitory interneurons and prevents the release of GABA, which is an inhibitory neurotransmitter that normally regulates the firing rate of the LMN. Thus, it causes a lot more Ach to be released and results in spastic paralysis.

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21
Q

What affect does black widow spider venom have on neurons?

A

It contains a compound called alpha larotoxin which causes massive release of Ach and thus spastic paralysis.

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22
Q

Some pesticides and nerve gases, such as sarin, are cholinesterase inhibitors. What affect do these have on neurons?

A

Inhibition of cholinesterase –> more Ach around –> spastic paralysis –> a problem if it affects the diaphram –> can’t breathe

23
Q

Describe how the stretch reflex works.

A
24
Q

When testing the stretch reflex, a hyperactive response indicates a problem with what part of the reflex arc?

A

The upper motor neuron

25
Q

When testing the stretch reflex, a hypoactive response indicates a problem with what part of the reflex arc?

A

The lower motor neuron

26
Q

Autonomic Nervous System

  • What tissues does it innervate?
  • Does it involve ganglia?
  • Is it voluntary or involuntary movement?
  • What effects does it exert on tissues it controls?
A
  • Internal organs
  • Yes - peripheral autonomic ganglia that contain pre/postganglionic synapses. Postganglionic nerves are mostly unmyelinated.
  • Involuntary
  • Exerts both excitatory and inhibitory control over internal organs
27
Q

Somatic Nervous System

  • What tissues does it control?
  • Does it involve ganglia?
  • Is it voluntary or involuntary?
  • What effect does it have on target tissues?
A
  • Controls skeletal muscle
  • Does not involve ganglia, the motor neurons are all within the CNS and they are all myelinated.
  • Voluntary
  • Motor neurons are only excitatory. Any regulatory controls are in CNS.
28
Q

The nicotinicM and nicotinicN receptors are identical.

True/False

A

False - they are homologous but not identical

29
Q

Muscarinic Receptors

  • These receptors are all what type of receptor?
  • The odd numbered (M1, M3, M5) receptors follow what signaling pathway?
  • The even numbered (M2, M4) receptors follow what signaling pathway?
A
  • GPCRs
  • Gq –> stimulate PLC and ends up releasing Ca2+
  • Gi –> inhibits AC and produces Ca2+ via release of G_beta_gamma subunits
30
Q

Adrenergic Receptors

  • All adrenergic receptors are what type of receptor?
  • What are the 3 types of receptors?
  • What is the ligand that binds all these receptors?
A
  • GPCR
  • Alpha 1 (Gq) alpha 2 (Gi) , Beta1/2/3 (Gs)
  • Norepinephrine
31
Q

NicotinicM receptor is found in _______

NicotinicN receptor is found in _______

A

Skeletal muscle

ANS preganglionic neurons

32
Q
  • Edrophonium is an acetylcholinesterase inhibitor. Why does this help in the diagnosis of myasthenia gravis?
  • What else can it be used for?
A
  • In myasthenia gravis, a person has Abs against their own nicotinic receptors. This drug inhibits the degradation of acetylcholine, which prolongs its lifespan in the neuromuscular junction so that it can compete with the Abs for binding to the nicotinic receptors and reduce the effects of the disease.
  • Can be used to reverse the effects of post-operative competitive NMJ blocking drugs
33
Q

Succinylcholine is a neuromuscular blocking drug that is used in surgical procedures to produce ________ by binding to ______ receptors and causing _______ of the membrane

A

Flaccid paralysis

NM

Depolarization

34
Q

Alpha-turbocurarine is used in surgical procedures to produce ______ by binding to the ____ receptor and acting as a ______ of acetylcholine

A

flaccid paralysis

NM

competitive inhibitor

35
Q

Why do we use neuromuscular blocking drugs in surgery?

A
  • Maintain patient immobility
  • Reduce muscle contraction
  • Reduce amount of anesthesia needed in surgery
  • Facilitate mechanical ventilation and endotrachial procedures
  • Prevent bone fractures during electroconvulsive therapy
36
Q

Drugs that block the neuromuscular junction are paralytics and ARE NOT _____

A

anthesthesia or analgesics (they do not produce loss of consciousness or loss of pain)

37
Q

Describe the sequence of paralysis experienced when a neuromuscular blocking drug is administered?

A

Small rapildy moving muscles –> intercostal muscles –> diaphragm –> trunk / limbs

Recover in reverse

38
Q
  • Describe what happens once Ach binds to the nicotinic receptors on a muscle cell in skeletal muscle.
  • Describe what happens once Ach binds to the nicotinic receptors on a muscle cell in cardiac muscle.
A
  • Ach binds receptor –> Na+ and K+ rush in to generate an AP –> Voltage gated Na+ channels open flooding interior of cell with Na+ –> AP travels along sarcolemma into T-tubules where it stimulates conformational change in DHP receptor which also results in conformational change in RyR receptor which releases Ca2+ from sarcoplasmic reticulum –> Ca2+ used for muscle contraction –> Voltage gated Na+ channels close and voltage gated K+ channels open removing K+ from cell –> Na+/K+ pump works to restore RMP –> Cl- pump works to keep AP from depolarizing any part of sarcolemma except t-tubule
  • Same as above except when AP travels along sarcolemma it also stimulates the release of Ca2+ from intracellular vesicles that then bind to RyR to when DHP senses voltage to cause the release of Ca2+ from sarcoplasmic reticulum (calcium induced calcium release)
39
Q

What condition results if there is dysfunction of the Cl- channels in muscle cells?

A

Myotonia congenita

40
Q

What is myotonia congenita?

A

There is dysfunction of the Cl- channels so the sarcolemma is hyperexcitable and there is delayed relaxation of contracted muscle

41
Q

The voltage gated Na+ channel has 4 conformations.

  • Describe when the channel is in its inactivated state and how it returns to its resting conformation.
  • How is this channel related to the refractory period?
A
  • The channel is inactivated when the membrane reaches +30mV and is fully depolarized. Repolarization of the membrane causes it to return to its resting conformation.
  • The amount of time for the channel to go from inactivated back to its resting conformation is 1ms. This is the refractory period between APs.
42
Q
  • Succinylcholine is an _______ for nicotinic muscle receptors.
  • It binds NM receptors with _____ affinity compared to acetylcholine.
  • Succinylcholine is degraded by ______ in the ______
  • It is a _____ acting paralytic.
A
  • agonist
  • higher
  • cholinesterases; plasma
  • Short
43
Q
A
44
Q

Describe how succinylcholine (and other drugs like it) function as depolarizing blockers?

A

1) Ach (agonist) binds to NM receptors of skeletal muscle and cause depolarization –> open ion channels, influx Na+, depolarization
2) Succinylcholine binds to NM receptors with much higher affinity than Ach –> prevents Ach from binding and causes Na+ channels to be inactivated because the membrane cannot be repolarized –> causes widespread fasciculations (twitching)
3) Persistent block can continue after repolarization b/c if effect is prolonged enough the NM receptors can become desensitized (inactivated) and not respond to Ach

45
Q

Succinylcholine has a ____ duration and ____ onset

A

Short, rapid

46
Q

What are some of the adverse effects of Succinylcholine?

A
  • Postoperative myalgia (muscle pain) from fasciculations
  • Hyperkalemia (during prolonged depolarization, K+ can leave cell via leak channels, can be fatal in a person who is already hyperkalemic or sensitive to this –> burn patients, CKD)
  • Prolonged paralysis due to defective plasma cholinesterase that degrades succinylcholine (this is rare)
  • Bradycardia
  • Increased intraocular pressure
  • Malignant hyperthermia - rare, caused by uncontrolled release of Ca2+ from SR, due to autosomal dominant mutation of RyR in skeletal muscle
47
Q

Malignant hyperthermia is a potentially severe adverse event that can occur from use of succinylcholine. What drug is used to try and reverse the effects of malignant hyperthermia?

A

Dantrolene - it inhibits the RyR receptor preventing Ca2+ release. Also used in treatment of MS.

48
Q

Turbocurarine and other drugs of the curarine family are non-depolarizing blockers of the NMJ. What is their mechanism of action?

A

They are competitive antagonists of NM receptors. They bind to the same site as Ach.

49
Q

Competitive Blockers of NMJ

  • Competitive blockers of the NMJ have a _____ duration of action.
  • How are they degraded/eliminated?
  • What is a negative side effect of these drugs?
  • How is this side effect avoided?
A
  • longer (1-2 hours)
  • They are are eliminated unchanged in the urine
  • They can release histamine –> causing hypotension and tachycardia
  • Can conjucate the active part of the drug to steroid backbone –> does not cause histamine release
50
Q

What are some adverse effects of competitive blockers?

A
  • If the patient has a deficiency in plasma cholinesterase activity then it will take even longer to degrade these drugs if they are acted upon by these enzymes
  • Histamine release
  • Ganglionic blockade (older drugs not used anymore)
  • Renal and hepatic dysfunction - since these drugs undergo first pass metabolism and elimination, their degradation can be altered in patients with dysfunctions of renal and hepatic systems
51
Q
  • What are irreversible cholinesterase inhibitors?
  • Where are these compounds found?
A
  • They phosporylate a serine residue on the active site of the enzyme leading to permanent inactivation of the enzyme. This can cause constant muscle contraction/spasm and it can be lethal if it results in spasm of the diaphragm.
  • Insecticides and nerve gas
52
Q
  • What is 2-PAM?
  • What are its limitations?
A
  • 2-PAM reactivates a cholinesterase that has been inactivated by phosphorylation of the serine residue by breaking the phosphoryl group bond from the active site of the enzyme restoring its normal function.
  • Only able to reactivate enzyme if the phosphoryl bond has not strengthened –> therapeutic window is small –> used mostly by military
53
Q

Why is 2-PAM co-administered with atropine?

A

2-PAM has poor blood–brain barrier penetration, so it has little effect on centrally-mediated respiratory depression. Atropine can cross the blood-brain barrier and antagonizes the muscarinic effects of organophosphates in the CNS.

54
Q
A

MSK (38 decks)

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