Week 3 Part 2 Flashcards

1
Q

What is the implications of Hyperalgesia?

A

Tissue damage

Adaptive Change in nociceptors “amplification”

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2
Q

What is the implication of Allodynia?

A

Damage to the nervous system

Pathophysiological change in sensory coding “switching”

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3
Q

Primary Hyperalgesia

A

At the site of injury

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4
Q

Secondary Hyperalgesia

A

More distant site

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5
Q

What happens in the distal oesophagus?

A

Sensitisation of proximal site to acid

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6
Q

What is referred Hyperalgesia?

A

Felt at a site distant from the site of origin
More pronounced in subcutaneous tissue than in skin
Related to duration and intensity of episodes of visceral pain

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7
Q

What are examples of central sensitisation?

A

Allodynia
Hyperalgesia
Secondary Hyperalgesia
Referred Hyperalgesia

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8
Q

What is example of peripheral sensitisation?

A

Hyperalgesia

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9
Q

Secondary Hyperalgesia

A

Sensitisation of the dorsal neurons

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10
Q

What is normal sensitive - normal threshold of pain?

A

30-40ml of Mercury

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11
Q

Hypersensitive patients

A

15/20ml of Mercury

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12
Q

What is peripheral sensitisation?

A

Increased sensitivity to an afferent nerve stimuli
Occurs after there has been an injury or cell damage to area and produce a flare response to nociceptors producing lots of neuropeptides

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13
Q

What are the different types of mediators?

A

Tissue (epithelial and stromal for support)
Blood supply
Immune cells

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14
Q

What are examples of classical mediators ?

A
Bradykinin 
Prostaglandin 
ATP/Adenosine
5-HT
Histamine
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15
Q

What are examples of immune mediators?

A

Cytokines
Chemokines
Processes
Protease activated receptors

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16
Q

Gain of system

A

Sensitisation

Form protective reflexes

17
Q

How will we sensitise or stimulate these nerves?

A

Enhance the activity in the channels that depolarise the ending
Reduce the activity in the channels that hyperpolarise the ending

Dial up activities in TRP
Dial down activities in KTP channels

18
Q

What happens during tissue injury?

A

Mediators released from certain cells
Activate GPCR
Stimulus transduction mechanism
Modulate the activity in those translucent channels

19
Q

What is an agonist of TRP A one channel?

A

AITC

Inward current - response desensitises repeated application

20
Q

What is TREK-1 and TRAAK activated by?

A

Arachidonic scid

21
Q

What is Trek-1 inhibited by?

A

Gq and Gd coupled GPCRs I.e PGE2

22
Q

What switches on and enhances current in KTP channels?

A

AA

23
Q

What is the function of prostaglandin?

A

Sensitise nociceptors

24
Q

What happens in the presence of PGE2?

A

Reduce the current mediator through KTP channel

25
Q

How can we modulate the activity in transducer channels?

A

Amplify gain in sensory nerve endings
Tune the response to initial activation through transducer channels
Several subtypes - voltage hated channels Nav1.9 on one side and low voltage activated Cav 3,2 channels on other

26
Q

What is the function of transducer channels?

A

Move calcium into nerve endings

27
Q

What is NAv1.9?

A

Sensitisation to inflammatory mediators

28
Q

What has no effect on Nav1.9 current?

A

CAMP

29
Q

What is Kv 7.x inhibited by?

A

Inflammatory mediators

30
Q

What gives brisk activation of sensory nerves?

A

Beta

Block it with TTX

31
Q

Implication of ruthenium red

A

Block the enhancement of TNF alpha

32
Q

How do we promote excitation?

A

Dialling up activity in transducer channels

33
Q

What are examples of inhibitory GPCR?

A

Opioids/endocannabinoids
Somatostatin/galanin
MGluR/P2Y
Gi/o coupled - decreased CAMP

34
Q

What is helping keep our sensory nerves in check?

A

Releasing certain tone of endogenous opioids