Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

physiology 3 > 1 - physiology of pain > Flashcards

1 - physiology of pain Flashcards

1
Q

allodynia

A

sensitization. - abnormal response to touch

caused by lesion or trauma to nerve or CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

hyperalgesia

A

sensitisation - enhanced sensitisation to noxious stimuli following injury

normal response to injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

somatogenic pain

A

pain with a physiological. cause

- localised in the body tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

2 types of somatogenic pain

A

a) nociceptive pain - picked up by a pain receptor and sent to the brain
b) neuropathic pain - damage to sensory nuerons along the pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

nueropathic pain

A

caused by damage at some point along the pathway of transmission eg. spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

nociceptive pain

A

starts at painreceptor andmessage sent to the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

pschyogenic pain

A

no known physical cause but processing of sensitive information in CNS is disturbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

examples pf nociceptive pain

A

postoperative pain
mechanical lower back pain
arthritis
exercise and sports injuries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

neuropathicpain examples

A 
CRPS (complex regional pain syndrome)
trigeminal neuralgia 
central post-stroke pain 
distal polyneuropathy (diabtic, HIV) 
neuropathic lower back pain 
postherpetic neuralgia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

mechanical pain

A

prickingm stabbing, pinching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

thermal pain

A

burning, freezing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

chemical pain

A

aching, stinging, soreness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

fast pain

A 
sharp and well localised
transmitted by myelinated axons 
glutamate neurotransmitter 
- extremely rapid acting 
- very short duration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

slow pain

A 
dull aching sensation
transmitted by unmyelinated axons 
substance P neurotransmitter 
- slower acting 
-long duration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

visceral pain

A

very poorly localised (lacks tactile afferents)

referred pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

fast pain is transmitted by

A

myelinated axons

glutamate neurotransmitter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

slow pain is transmitted by

A 
unmyelinated axons (C fibres)
substance P neurotransmitters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

TRP channels

A

transient receptor potential channels
temperature sensitiveion channels
excitatory Na+/Ca2+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

cold receptors

A

TRPM8 channels

- firing rate increases as temp decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

hot receptors

A

TRPV1/3 channels

firing rate increases as temp increases

21
Q

freezing or burning can excite

A

any nocioceptor

22
Q

damage can excite

A

any nocioceptor

23
Q

specific mechanical nocioceptors

A

receptors with stretch gated ion channels
Na+/Ca2+ channels - excitatory
excited by strong pressure, pinch or squeezing
high threshold
mediate pain from skeletal muscle or viscera due to excessive stretch or contractile force

24
Q

exogenous chemicals that can penetrate the skin

A

acid, alkali, organic molecules

capsaicin, mustard oil

25
Q

intracellular molecules released by cell injury

A

cations (K+, H+)
peptides, neurotransmitters
prostaglandins, histamine, bradykinin

26
Q

things that chemical nociceptors respond to

A
  • exogenous chemicals that penetrate skin
  • intracellular molecules released by cell injury
  • pathological substances released by diseased tissue
  • toxins - from microorganisms,insect bites, venom
27
Q

polymodal nociceptors

A

receptive to all other painful stimuli

  • C fibres - unmyelinated free nerve endings
  • release glutamate and/or substance P
  • respond to head, cold, pinch and chemical stimuli
  • express multiple receptors
28
Q

chemicals causing sensitisation - sensitising soup

A 
H+ 
norepinephrine
bradykinin 
histamine 
K+ 
prostanoids 
purines 
interleukins 
tumor necrosis factor 
serotonin 
neuropeptides 
leukotrienes
29
Q

what does sensitising soup do

A

turns a nociceptor from having a high threshold to. a low threshold

30
Q

neospinothalamic tract

A

fast, sharp
only has 2 synapses
myelinated sensory neuron, synapses at the spinal cord, up the anterolateral pathway to the thalamus, synapses and then goes to the cortex

31
Q

branching in neospinothalamic tract

A

nearly no branching

32
Q

somatosensory cortex gives

A

localisation

33
Q

insular cortex gives

A

intensity of pain

34
Q

anterior cingulate cortex

A

pain emotional reaction

35
Q

hypothalamus and limbic cortex gives

A

body physical response to pain

subjective memory of pain

36
Q

role of the efferent analgesic system

A

inhibition of afferent pain signals

37
Q

pain afferents stimulate neurons in

A

periaqueductal grey region (PAG)
locus coeruleus (pons)
nucleus raphne magnus

38
Q

neurons stimulated by pain afferents activate

A

descending anti-nociceptive pathways

transmitted through the spinal cord to the dorsal horn

39
Q

anti-nocciceptive pathwyas

A

release neurotransmitters

cause analgesia

40
Q

which neurotransmitters are released by anti-nociceptive pathways

A

serotonin, noradrenaline
enkephalins, endorphins

inhibit or block transmission of nocicceptive signals

41
Q

gate-control theory

A

neurons will talk to and suppress each other
inhibitory interneurons prevent non-damaging pain from getting through.
always active
when there is only a low level of action potentials, pain doesn’t transmit eg. don’t feel pain just from sitting on a chair

42
Q

gate control when there is s strong pain stimulus

A

the nociceptive inhibits the inhibition interneuron

the fibres override the internuerons inhibition, pain is able to travel to the brain

43
Q

confusion of the nervous system

A

‘rub it better’
lateral inhibtion from sensory fibres activate inhibitory interneurones
if both pain stimulus and non pain stimulus arrive at the same time, there will be partial inhibition of pain transmission

44
Q

opiates

A

act centrally by inhibiting neurotransmission of afferent neurons

45
Q

a2-adrenergic agonists

A

ie. clondine
act centrally
stimulate endogenous anti-nociceptive neurones

46
Q

local aneasthetics

A

block action potential conduction in nociceptive nerve fibres
cation channel blockers
lidocaine

47
Q

anti-inflammatory drugs + aspirin

A

can reduce hyperalgesia and allodynia

blocks prostaglandin production

48
Q

congenital analgaesia

A

hereditary sensory neuropathy (sensation is inhibited)
specific to pain
- nociceptive stimuli are not produced, processed and/or integrated

49
Q

causes of congenital analgesia

A
  • increased anti-nociceptive pathways activity - high endorphins
  • SCN9A (a nociceptive specific Na channel) mutations
  • PRDM12 (a gene essential for nociceptor neurone development) mutations

physiology 3 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions