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Flashcards in Peters' Physiology Deck (28)
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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

2
Q

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

A

Nicotinic ACh receptors

3
Q

What subunits make up the nicotinic ACh receptor?

A

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

4
Q

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

A

One vesicle of ACh activating nictonic ACh receptors at the endplate

5
Q

What do many successive mepps produce?

A

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

6
Q

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

A

Voltage-gated sodium channels

7
Q

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

A

Acetylcholinesterase

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

9
Q

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

A

Carbamazepine

10
Q

Lambert-Eaton Myasthenic Syndrome is associated with muscle weakness and small cell carcinoma. 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)

11
Q

Which drugs increase ACh concn in the synaptic cleft?

A

Anticholinesterases (pyridostigimine)

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

13
Q

What are the 3 types of pain?

A

Nociceptive
Inflammatory
Pathological

14
Q

What is nociceptive pain?

A

Acute sensory; arises to limit further damage

15
Q

What is inflammatory pain?

A

Persistent; outlives initial injury but can heal over time

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