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► Med - Anatomy & Physiology > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is an unpleasant sensory and emotional experience, associated with actual tissue damage or described in terms of such damage?

A

Pain

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2
Q

What are the three classifications of pain?

A
  1. Nociceptive pain - adaptive
  2. Inflammatory pain - adaptive
  3. Pathological pain - maladaptive
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3
Q

What does nociceptive pain begin with?

A

activation of nociceptors

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4
Q

What are specific peripheraly primary sensory afferent neurones normally activated preferentially by intense stimuli that are noxious?

A

Nociceptors

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5
Q

What does depolarisation due to noxious stimulus elicit?

A

Action potentials that propagate to the CNS

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6
Q

Nociceptors are first order neurones that relay information to second order neurones in the CNS by what?

A

Chemical synaptic transmission

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7
Q

What type of pain serves as an early warning system to detect and minimise contact with damaging stimuli?

A

Nociceptive pain

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8
Q

What threshold is nociceptive pain?

A

High - provoked only by intense stimuli that activate nociceptors

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9
Q

What does nociceptive pain initiate?

A

A withdrawal reflex

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10
Q

What pain is activated by the immune system in injury or infection?

A

Inflammatory pain

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11
Q

What does inflammatory pain response cause?

A

Pain hypersensitivity (heightened sensitivity to noxious stimuli) and allodynia (innocuous stimuli now elicit pain)

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12
Q

What threshold is inflammatory pain?

A

Low

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13
Q

What type of pain assists in healing of damaged body part i.e. discourages contact and movement?

A

Inflammatory pain

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14
Q

What type of pain has no protective function?

A

Pathological pain

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15
Q

What does pathological pain result from?

A

Abnormal nervous system function - may be neuropathic, or dysfunctional

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16
Q

What threshold of pain is pathological pain?

A

Low

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17
Q

What is dysfunctional pain?

A

No neural lesion, inflammation but positive symptoms

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18
Q

What does congenital insensitivity to pain due to?

A

Loss of function mutations (missense, in frame, deletions) in the gene SCN9A that encodes a particular voltage-activated Na+ channel that is highly expressed in nociceptive neurones

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19
Q

What are nociceptors comprised of?

A

Agamma and Cfibres

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20
Q

What type of nociceptors are mechanical/thermal nociceptors that are thinely myelinated - respond to noxious mechanial and thermal stimuli and mediate first pain?

A

Alpha-fibres

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21
Q

What type of nociceptors are unmyelinated (have a faster conduction velocity) - collectively respond to all noxious stimuli (polymodal) and mediate second, or slow pain?

A

C-fibres

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22
Q

Name a membrer of the transient receptor potential family which is activated by noxious heat?

A

TRPV1

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23
Q

In chemical stimuli for activation of terminal polymodal nociceptors: what are the chemical channels and what are they activated by?

A
  1. H+ activates acid sensing ion channels
  2. ATP activates P2X nad P2Y receptors
  3. Bradykinin activates B2 receptors
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24
Q

In pain, what opens ion channels (cation selective) in nerve terminals to elicit a depolarising receptor potential?

A

Stimulus (mechanical, thermal or chemical)

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25
Q

In pain the amplitude of generator potential is graded and proportional to what?

A

Stimulus intensity

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26
Q

What, which is a subset of c-fibres, have afferent and efferent functions?

A

Peptidergic polymodal nociceptors

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27
Q

How does peptigergic polymodal nociceptors function afferently?

A

Transmit nociceptive information to the CNS via release of glutamate and peptides (substance P, neurokinin A) within the dorsal horn

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28
Q

How does peptigergic polymodal nicoceptors function efferently?

A

Release proinflammatory mediators [e.g. calcitonin gene-related peptide (CGRP), substance P] from peripheral terminals - contributes to neurogenic inflammation

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29
Q

What does noxious stimulation in the long term increasing spinal excitability contribute to?

A

Hyperalgesia and allodynia

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30
Q

What is the first stage in the outline of neurogenic inflammation?

A

Peptides (SP and CGRP) released from free nerve ending of peptidergic nociceptor due to tissue damage, or inflammatory mediators

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31
Q

In neurogenic inflammation - after peptides SP and CGRP have been released, what does SP cause (three things)?

A
  1. Vasodilation and extravasation of plasma proteins (promotes formation of bradykinin and prostaglandins)
  2. Release of histamine from mast cells
  3. Sensitises surrounding nociceptors
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32
Q

In neurogenic inflammation - after peptides SP and CGRP have been released, what does CGRP cause?

A

Induces vasodilation

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33
Q

What is the final stage in neurogenic inflammation?

A

Primary and secondary hyperalgesia and allodynia ensue

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34
Q

In relation to neurotransmission between the primary afferent and second order neurone in the dorsal horn: what are the four steps occuring at terminal of primary afferent?

A
  1. Action potential
  2. Opening of voltage gated calcium channels
  3. Calcium influx
  4. Glutamate release
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35
Q

In relation to neurotransmission between the primary afferent and second order neurone in the dorsal horn: what are the four steps occuring at the projection neurone in dorsal horn?

A
  1. Activation of glutamate receptors
  2. Membrane depolarisation
  3. Opening of voltage gated sodium channels
  4. Action potential
36
Q

In relation to neurotransmission between the primary afferent and second order neurone in the dorsal horn: what is the primary transmitter?

A

Glutamate

37
Q

In relation to neurotransmission between the primary afferent and second order neurone in the dorsal horn: how does glutamate produce a fast e.p.s.p and neural excitation?

A

By activating primarily postsynaptic AMPA receptors with NMDA receptor participation

38
Q

In relation to neurotransmission between the primary afferent and second order neurone in the dorsal horn: what substances also participate in high frequency stimulation to cause a slow and prolonged e.p.s.p that facilitates activation of NMDA receptors by relieving voltage-dependent block by magnesium?

A

Peptides - substance P and CGRP

39
Q

Where are primary afferent cell bodies located?

A

In the dorsal root ganglia

40
Q

Where do axon terminates centrally?

A

In the dorsal horn of the spinal cord in various laminae of Rexed

41
Q

Where do nociceptive C and Agamma fibres mostly terminate?

A

Superficially in laminae I and II (and also V for Agamma-fibres)

42
Q

What do nociceptive specific cells synapse only with?

A

C and Agamma fibres

43
Q

Cells that receive input from only Abeta-fibres are what?

A

Proprioceptive

44
Q

What do wide dynamic range (WDR) neurones receive input from?

A

All three types of fibre and thus respond to a wide range of stimuli

45
Q

Second order neurones ascent the spinal cord in the anterolateral system comprising mainly of what?

A 
Spinothalamic tract (STT)
Spinoreticular tract (SRT)
46
Q

In the STT: Projection neurones originating from lamina I (fast fibre Aδ pain) terminate where?

A

In the posterior nucleus of the thalamus

47
Q

In the STT: Projection neurones originating from lamina V (WDR neurones) terminate where?

A

In posterior and ventroposterior nucleus of the thalamus

48
Q

In the SRT: what is largely transmitted?

A

Slow C-fibre pain

49
Q

In the SRT: extensive connections with what are made in the brainstem?

A

With reticular nuclei in the brainstem [e.g. periaqueductal grey (PAG) and parabrachial nucleus (PBN)]

50
Q

What anterolateral spinal cord system is involved in autonomic responses to pain, arousal, emotional responses and fear of pain?

A

SRT

51
Q

What does the motor neurone axon divide into near the muscle?

A

Unmyelinated branches

52
Q

Action potentials arising in the muscle cell body are conducted via the axon to boutons causing the realse of what?>

A

Transmitter acetylcholine

53
Q

Where does presynaptic terminal (bouton) synapse at?

A

The endplate region of skeletal muscle fibre

54
Q

What are four key features of skeletal neuromuscular junction?

A
  1. Terminal bouton (and surrounding schwann cell
  2. Synaptic vesicles
  3. The synaptic cleft
  4. Endplate region
55
Q

In the skeletal neuromuscular jiunction - what cluster at the active zones?

A

Synaptic vesicles containing ACh awaiting release

56
Q

In the skeletal neuromuscular junction - where are ACh receptors located?

A

At regions of the junctional folds that face the active zones

57
Q

During the pre-synaptic process of the skeletal neuromuscular junction - how is choline transported into the terminal?

A

By choli ne transporter (symport with Na+)

58
Q

During the pre-synaptic process of the skeletal neuromuscular junction - what happens after choline enters the cytosol?

A

ACh is synthesised from choline and acetyl coenzyme A (supplied by mitochondria) by the enzyme choline acetyltransferase (CAT)

59
Q

During the pre-synaptic process of the skeletal neuromuscular junction - what happens when ACh has been made?

A

It is concentrated in vesicles by the vesicular ACh transporter

60
Q

During the pre-synaptic process of the skeletal neuromuscular junction - what happens once ACh has been concentrated in vesicles?

A

Arrival of action potential at terminal causing depolarisation and the opening of voltage-gated calcium channels allowing ca entry to terminal

61
Q

During the pre-synaptic process of the skeletal neuromuscular junction - what happens when calcium has entered terminal?

A

It causes vesicles docked at active zones to fuse with presynaptic membrane - ACh diffuses into synaptic cleft to activate post-synaptic nicotinic ACh receptors in endplate region.

62
Q

In relation to the post-synaptic process of skeletal neuromuscular junction - how are nicotinic ACh receptors assembled?

A

As a pentamer of glycoprotein subunits [(a1)2B1Gd], that surround a central, cation selective pore

63
Q

In relation to the post-synaptic process of skeletal neuromuscular junction - how does the pore inside the pentamer glycoprotein open and close?

A

closed in absence of ACh but open when two molecules of ACh bind to exterior of receptor

64
Q

In relation to the post-synaptic process of skeletal neuromuscular junction - what is the open channel permeable to?

A

Equally permeable to Na and K

65
Q

In relation to the post-synaptic process of skeletal neuromuscular junction - what enters and exits when the gate is open?

A

Na enters and K exits

66
Q

In relation to the post-synaptic process of skeletal neuromuscular junction - how is end plate potential generated?

A

Driving force for Na is greater than K at resting membrane potential

67
Q

What does each neuromuscular junction vesicle contain?

A

A quantum of neurotransmitter

68
Q

During the post-synaptic process of skeletal neuromuscular junction - what does an e.p.p that exceeds threshold trigger?

A

An all or none propagated action potential that initiates contraction

69
Q

During the post-synaptic process of skeletal neuromuscular junction - what does the e.p.p trigger the opening of?

A

Voltage-activated Na channels causing a muscle action potential

70
Q

On a muscle fibre - what allows the e.p.p to propagate from the end plate over the length of the fibre?

A

The adjacent voltage gated sodium channels

71
Q

How does rapid termination of neuromuscular transmission occur?

A

Hydrolysis of ACh by acetylcholinesterase (AChE), an enzyme associated with the end plate membrane

72
Q

Once AChE has hydrolysed ACh to choline and acetate, what happens to the two products?

A

Choline taken up by choline transporter

Acetate diffuses from the synaptic cleft

73
Q

What is another name for neuromyotonia?

A

Isaac’s syndrome

74
Q

What condition has symptoms of multiple disorders of skeletal muscle function including cramps, stiffness, slow relaxation *(myotonia) and muscle twitches?

A

Neuromyotonia

75
Q

What is the drug treatment for neuromyotonia?

A

Anti-convulsants - carbamazepine, phnytoin which block voltage-gated sodium channels

76
Q

What condition is characterised by muscle weakness in the limbs , bery rare and assocaited with small cell carcinoma of the lung?

A

Lambert-Eaton Myasthenic Syndrome

77
Q

What condition has an autoimmune origin: antibodies against voltage-activated calcium channels in the motor neurone terminal resulting in reduced ca entry in response to depolarisation and hence reduced vesicular relase of ACh?

A

LEMS

78
Q

What is the drug treatment for Lambert-Eaton Myasthenic Syndrome?

A

Anticholinesterases (pyridostigmine) and potassium channel blockers (3,4-diaminopyridine) which increases concentration of ACh in synaptic cleft

79
Q

What disease is characterised by progressively increasing muscle weakness during periods of activity. Often weakness of the eye and eyelid muscles is a presenting feature?

A

Myasthenia Gravis

80
Q

What condition has an autoimmune origin: antibodies against nicotinic ACh recepotrs in the endplate result in reduction in the number of functional channels and hence the amplitude of the e.p.p

A

Myasthenia gravis

81
Q

What is the drug treatment for Myasthenia Gravus?

A

Anticholinesterases (edrophonium for diagnosis, pyridostigmine for long term treatment) and a variety of immunosuppressants (azathioprine)

82
Q

What condition has an extremely potent exotoxin (related to tetanus and diptheria toxins) that act as motor neuron terminals to irreversibly inhibit ACh release?

A

Botulinum toxin

83
Q

What toxin enters presynaptic nerve terminal to enzymatically modify proteins involved in the docking of vesicles containing ACh?

A

Botulinum toxin

84
Q

What interfere with the postsynaptic action of ACh by acting as competitive antagonists of the nicotinic ACh receptor (vecuronium, atracurium)?

A

Curare-like compounds

85
Q

What do curare-like compounds do?

A

Reduce the amplitude of the endplate potential to below the threshold for muscle fibre action potential generation

► Med - Anatomy & Physiology (130 decks)

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