Peters' Physiology Flashcards

1
Q

With regards to the alpha motor neurone and innervation of skeletal muscle fibres, where is the ACh receptor concentrated?

A

At the endplate region of the muscle fibre

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2
Q

Which receptors are located at the endplate of the muscle fibre?

A

Nicotinic ACh receptors

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3
Q

What subunits make up the nicotinic ACh receptor?

A

2x alpha1
1x beta1
1x delta
1x epsilon

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4
Q

What generates a miniature endplate potential (mepp) at muscle fibres?

A

One vesicle of ACh activating nictonic ACh receptors at the endplate

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5
Q

What do many successive mepps produce?

A

Graded epp which, if above threshold, triggers an action potential that will initiate contractions

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6
Q

Once threshold epp is achieved, which channels open to cause an action potential to be fired?

A

Voltage-gated sodium channels - these also allow for the action potential to propagate down the muscle fibre

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7
Q

Which enzyme hydrolyses ACh at the endplate to terminate neuromuscular transmission?

A

Acetylcholinesterase

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8
Q

Neuromyotonia involves muscle twitches, stiffness, cramps and slow relaxation. How does it arise?

A

Antibodies produced against K channels in the motor neurone, resulting in repeated firing/hyperexcitation

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9
Q

Which drug blocks Na channels and may be useful in neuromyotonia?

A

Carbamazepine - an anticonvulsant that blocks voltage activated sodium channels

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10
Q

Lambert-Eaton Myasthenic Syndrome is associated with muscle weakness and small cell carcinoma of the lung. How does it arise?

A

Antibodies produced against Ca channels causing reduced Ca entry and thus reduced ACh vesicle release (which is needed to initiate muscle contraction)

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11
Q

Which drugs increase ACh concn in the synaptic cleft?

A

Anticholinesterases (pyridostigimine)

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12
Q

Myasthenia gravis involves muscle weakness during activity. How does it arise?

A

Antibodies produced againsts nicotinic ACh receptors, causing reduced amplitude of epp and less AP generation

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13
Q

What are the 3 types of pain?

A

Nociceptive
Inflammatory
Pathological

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14
Q

What is nociceptive pain?

A

Acute sensory; arises to limit further damage

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15
Q

What is inflammatory pain?

A

Persistent; outlives initial injury but can heal over time

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16
Q

Which receptors are activated in the presence of noxious stimuli?

A

Nociceptors (sensory afferents)

17
Q

Nociceptive pain requires threshold to be achieved to activate nociceptors. True/False?

A

True

18
Q

Give an example of heightened pain sensitivity in inflammatory pain

A

Touching an inflamed joint would be sorer than touching the joint when it is not inflamed

19
Q

What is pathological pain?

A

Abnormal nervous system function causes normal stimuli to be felt as noxious

20
Q

What are the 2 main subtypes of nociceptors?

A

A-delta-fibres

C-fibres

21
Q

What is the difference between A-delta-fibres and C-fibres?

A

A-delta-fibres mediate initial/fast pain; C-fibres mediate the second/aftermath pain

22
Q

C-fibres conduct faster than A-delta-fibres. True/False?

A

False

A-delta-fibres conduct faster

23
Q

Peptidergic polymodal nociceptors are a subset of C-fibres. What are their efferent function?

A

Release pro-inflammatory mediators from peripheral terminals; contribute to neurogenic inflammation

24
Q

Peptidergic polymodal nociceptors are a subset of C-fibres. What are their afferent function?

A

Transmit nociceptive stimuli to the CNS via glutamate and peptides

25
Q

Axon of primary afferents terminate centrally in the dorsal horn of the spinal cord in various laminae of Rexed. Where do A-delta-fibres and C-fibres terminate?

A

Laminae I, II

also V for A-delta-fibres

26
Q

Second order neurones ascend the spinal cord in a system comprised of which two tracts?

A

Spinoreticular

Spinothalamic

27
Q

What is the spinothalamic tract concerned with?

A

Pain perception - where it is, how bad is it

28
Q

What is the spinoreticular tract concerned with?

A

Autonomic/emotional response - fear of pain, what can I do to stop it

29
Q

What is skeletal muscle innervated by?

A

fast conducting alpha motor neurones with myelinated axos and cell bodies in the spinal cord or brain stem

30
Q

What are the key steps in neuromuscular transmission

A

synthesis of ACh in cytoplasm of bouton, uptake of ACh in synpatic vesicles, Ca2+ dependant release of ACh into synpatic cleft by exocytosis, brief activation of nicotinic ACh receptors by reverse binding of ACh then rapid termination of transmitter action by ACE within synaptic cleft

31
Q

What does each vesicle of ACh contain?

A

a quantum of neurotransmitter

32
Q

What does the botulinum toxin do?

A

Extremely potent exotoxin - acts at motor neurone terminals to irreversibly inhibit ACh release

enters presynaptic nerve terminal to enzymatically modify proteins involved in the docking of vesicles containing ACh - preventing exocytosis

33
Q

What do curate-like compounds do?

A

Interfere with postsynaptic action of ACE by acting as competitive antagonists of the nicotinic ACh receptor - reduce amplitude of the end plate potential