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Introduction to Medical Sciences > Nerves and Muscles 4 > Flashcards

Nerves and Muscles 4 Flashcards

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USMLE® Step 1 flashcards
1
Q

What is a motor unit?

A

A motor unit consists of a motor neurone and all the muscle fibres it innervates. All the muscle fibres within a motor unit contract together when the motor neurone fires.

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2
Q

How does the number of muscle fibres in a motor unit affect the strength of contraction?

A

The greater the number of motor fibres in the motor unit, the greater the strength fo contraction. Finer movements utilise fewer muscle fibres stimulated.

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3
Q

What is the inherent time delay for contraction in neuromuscular transmission?>

A

0.5-1 ms

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4
Q

How is an impulse transmitted form the ventral horn to the muscle fibre?

A

The cell body of the motor neurone is found in the ventral horn of yeh spinal cord. The axon then sends the impulse through the ventral roots which innervate the appropriate muscles. The axon is myelinated as it passes through the CNS and the peripheral nerves in which they divide into thin and un-myelinated fibres. These fibres can then innervate individual motor fibres.

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5
Q

How can the ‘all or nothing’ principle be allied to muscle contraction?

A

A vesicle will either be released or not. The probability can be increased or decreased by altering calcium concentration.

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6
Q

What is the function of the basal lamina in the neuromuscular junction?

A

It is the site of acetylcholinesterase - this enzyme breaks down acetylcholine into acetate and choline.

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7
Q

What is the length of the neuromuscular junction?

A

50nm

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8
Q

What is the process of chemical synaptic transmission at the neuromuscular junction?

A
  1. The wave of depolarisation travels down the presynaptic neurone until it reaches the bouton.
  2. This causes the Calcium voltage gated ion channels to open and so it leads to the influx of calcium across the membrane.
  3. This causes docked and primed vesicles containing acetylcholine to fuse with the presynaptic membrane. This means reserved vesicles can move forward to take their place.
  4. Acetylcholine can then be released by exocytosis.
  5. Acetylcholine then diffuses across the synaptic cleft.
  6. Acetylcholine binds to the nicotinic receptors on the post-junctional membrane. This membrane has many folds to increase surface area.
  7. This binding causes sodium ion channels to open and so an influx of sodium.
  8. This depolarises the post-synaptic membrane and so transmitting the impulse to the muscle.
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9
Q

Why are vesicles docked?

A

This means as soon as there is an influx of calcium, the vesicles are already in the correct place to fuse with the presynaptic membrane and so acetylcholine can be released rapidly.

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10
Q

How is the probability of vesicles being released increased?

A

Increasing calcium concentration.

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11
Q

How can it be ensured the influx of calcium only causes vesicle release?

A

Calcium is restricted to micro domains

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12
Q

What is the structure of the nicotinic acetylcholine receptor?

A

It is made up of a 5 subunits - each subunit formed from 4 transmembrane domains. It has 2 alpha domains, 1 gamma domain, 1 beta domain and 1 sigma domain. Acetylcholine binds to the 2 alpha domains. 2 acetylcholine molecules are required to activate the receptor. The subunits depend on the species and the site of the receptor. The binding of acetylcholine to the receptor causes a conformational change in the structure of the protein enabling the pore to open and so an influx of sodium.

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13
Q

What is a miniature end plate potential?

A

One quantum = One synaptic vesicle. A MEPP is the depolarisation produced by a single quantum of acetylcholine. Without stimulation to the nerve, there are MEPP, causing the random release of acetylcholine from vesicles. They are approximately 0.5 mV. This is a random process. The MEPP can summate to form an end plate potential large enough to activate voltage gated channels in the membrane.

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14
Q

How many vesicles can Acetylcholine from one vesicle activate?

A

1000-2000 receptors

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15
Q

How many molecules of acetylcholine does a vesicle contain?

A

5000 - 10000

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16
Q

What happens to the products of the catabolism of acetylcholine?

A

They are recycled. Acetylcholine is broken down in acetate and choline. Acetate is taken into circulation. Choline is taken back into a nerve terminal. Choline is then packages in a vesicle. Choline is derived form the diet - this can then react with acetyl-coA, a product of the Kreb’s cycle, to form acetylcholine.

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17
Q

How is acetylcholine transported into vesicles?

A

Acetylcholine is coupled to a proton ani-port. This requires protons and energy.

18
Q

How are vesicles docked to the active zone.

A

Through docking proteins. v-Snare on the vesicle interacts with t-Snare on the membrane.

19
Q

How are reserve vesicles anchored near the active zone?

A

Through synapses. Synapsin anchors the vesicle to actin filaments. When the reserve vesicles take the place of vesicles in the active zone, synapsin is broken broken down and so the vesicles can move to fuse with the membrane.

20
Q

How is choline taken up into the nerve terminal?

A

Through co-transport with Na+.

21
Q

What are non-depolarising competitive nAChR antagonists?

Give an example.

A

These drugs bind to the nicotinic receptor in the same place as acetylcholine but do not cause the muscle to depolarise. An exmaple of this is Tubocuraine. At high does this drug however can also block pre-junctional Na+ channels, decreasing the release of acetylcholine.

22
Q

How is the mechanism of non-depolarising competitive nAChR antagonists reversed?

What is the clinical use?

A

Increasing the acetylcholine concentration. A common antidote is neostigmine (AChE inhibitor).

Clinically, these drugs are used in surgery; they are used alongside anaesthesia to produce paralysis. This can be to paralyse vocal cords, permit intubation of the trachea and to optimise the surgical field by inhibiting spontaneous ventilation.

23
Q

What is the time for onset of the result of non-depolarising competitive nAChR antagonists?
How long does their effect last?

A

Onset time: Greater than 5 minutes

Duration: 30 minutes

24
Q

What are depolarising nAChR agonists?

Give an example.

A

These drugs bind to the same site as acetylcholine on the receptor and stimulate the receptor to cause depolarisation of the sarcolemma.
An example of this is succinylcholine.

25
Q

What are the two phases of action of depolarising nAChR agonists?

A

Phase I: The membrane is depolarised by opening AChR channels causing a brief period of muscle twitching.

Phase II: These drugs are less easily broken down by acetylcholinesterase. As a result, they stay bound to the receptor for longer. Once the sarcolemma repolarises, acetylcholine cannot bind and so it leads to paralysis.

26
Q

What are the clinical uses of depolarising nAChR agonists?

A

They can be used in surgery. However they have to be given by IV. The duration of the effect is short-lived and only occurs whilst the drug is being give.

27
Q

Give examples of cholinesterase inhibitors?

A

Neostigmine and Edrophonium.

28
Q

What are clinical uses of cholinesterase inhibitors?

A

They can be used treat myasthenia graves (Neostigmine) and diagnose myasthenia graves (Edrophonium).
They can also be used in the treatment of glaucoma, postural tachycardia syndrome and an antidote to anticholinergic drugs.

29
Q

How does sarin work?

A

Sarin inhibits acetylcholinesterase enzymes. This means there is continual stimulation of the acetylcholine receptors. This leads to widespread dysfunction throughout the body. The muscles contract in powerful convulsions. This can lead to nausea, runny nose, watery eyes, drooling and constriction of the pulls. Loss of bowel and bladder control follows. Chest pains shortness of breath, collapse, seizure and death is the end result.

30
Q

Give other nerve agents.

A

VK and Novochok

31
Q

What is the common cause of death through nerve agents?

A

Asphyxia due to the inability to control muscles involved in breathing function. They are lethal in even very low concentrations - death will occur within 1 - 10 minutes after inhalation.

32
Q

What is an antidote for nerve agents?

A

Atropine

33
Q

How does Tetrodotoxin work?

A

Binds to Na+ channels to block activation.

34
Q

How does Tetanus and botulinum work?

A

Reduce the probability of neurotransmitter release by preventing vesicles binding to the pre-synaptic membrane. They interfere with the interaction between t-Snare and v-Snare reducing the probability of acetylcholine release.

35
Q

How does bungarotoxin work/

A

Similar to curare in that it is a non-depolarising nAChR antagonist.

36
Q

What is Lambert-Eaton Syndrome?

A

A rare autoimmune response which inhibits Ca2+ channels and thereby reduced EACh release. More than half of patients have small cell lung cancer. Antibodies are directed against the voltage gated calcium channels in the presynaptic terminal. This disease is usually observed in middle aged and older individuals.

37
Q

What is the treatment for Lembert-Eaton syndrome?

A
  • If there is an underlying malignancy- its treatment resolves the symptoms.
  • Use of immunosuppressant’s such as corticosteroids
  • Amifampridine –drug which blocks K+ channel so action potential duration is increased, so more ACh released.
38
Q

How is the electromyograph used to diagnose Lembert-Eaton Syndrome?

A

Apply electrical impulses to nerves and measuring the electrical response of the muscle. CMAP unusually small but incremental response to repetitive nerve stimulation.
If you keep stimulating, the EPSP build up. It build up - though initially small- as there is a initially reduced acetylcholine released. Continuous stimulation, means sufficient acetylcholine is released to cause normal muscle response

39
Q

What is Myasthenia Graves?

A

Autoimmune response against nAChR’s – NMJ less responsive to Ach. Since there are fewer AChR to bind, the end plate potentials (EPPs) are smaller.

40
Q

What are the symptoms of Myasthenia Gravis?

A 
Symptoms muscle weakness and fatigue. 
2 forms
1. effects extraocular muscles
2. generalised muscle weakness
Repetitive stimulation leads to decrease contractile strength weakness greatest at the end of the day or after exertion.
41
Q

What s the treatment of Myasthenia Graves?

A
  • Directed at enhancing transmission (anticholinesterase).
  • Immunosuppression (corticosteroids)
  • Some patients have a tumour of the thymus removal of which leads to improvement.

Introduction to Medical Sciences (43 decks)

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