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4. BIOL257 > Pain > Flashcards

Pain Flashcards

(51 cards)

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1
Q

types of pain

A
  • neuropathic

- nociceptive

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2
Q

neuropathic pain: define

A
  • pain initiated by primary lesion or disease in PNS or CNS
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3
Q

nociceptive pain: define

A
  • non/inflammatory response to noxious stimulus
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4
Q

neuropathic pain: eg

A
  • pinching of nerves (sciatica)
  • nerve trauma
  • infection
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5
Q

nociceptive pain: features

A
  • protective mechanism for awareness tissue damage occurring/ may happen

may be accompanied by:

  • reflexive withdrawal from stimulus
  • autonomic response (increase BP)
  • emotional responses (fear, anxiety)
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6
Q

nociceptive pain: for pain transmission

A
  • ascending pathways
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7
Q

nociceptive pain: for pain modulation

A
  • descending pathways
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8
Q

nociceptors: types of free nerve endings and for?

A
  • mechano (intense physical)
  • thermo (intense hot/cold)
  • chemo (noxious endogenous/ exogenous chemicals, inflammatory mediators)
  • polymodal (intense mechanical, thermal, chemical)
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9
Q

nociceptors: free nerve endings found

A
  • skin
  • mm, joints
  • internal organs
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10
Q

nociceptors: vs non-nociceptive receptors

A
  • no spontaneous/ background firing of APs
  • relatively large receptive fields
  • slow adapting/ non
  • high threshold
  • sensitised by intense/ prolonged stimulation
  • glutamate and substance P onto 2˚ neurons
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11
Q

non-nociceptors bs nociceptors:

A
  • spontaneous firing (resting level of AP generation)
  • low threshold (high sensitivity)
  • small/ large receptive fields
  • fast/ slow adapting
  • mostly release glutamate
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12
Q

nociceptors: fibre types name

A
  • A delta

- C fibres

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13
Q

nociceptors: fibre types features

A
  • A fast (mechanical/ thermal pain receptors) - myelinated
  • C slow (polymodal receptors) - non-myelinated
  • differences in conduction velocity generate ‘double pain’ sensation
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14
Q

nociceptors: cutaneous mechanical

A
  • first pain after mechanical injury
  • A delta fibre
  • pricking, stabbing
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15
Q

nociceptors: cutaneous thermal

A
  • fast pain via A delta fibres
  • intense thermal stimuli (>45˚ and <10˚)
  • temperature sensitive TRP ion channels
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16
Q

nociceptors: cutaneous polymodal

A
  • second pain
  • thin C type fibre
  • slow burning, throbbing
  • slow/ no adaptation
  • intense mechanical/ thermal/ specific chemical (capsaicin, H+)
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17
Q

nociceptors: cutaneous polymodal- substances released responding to tissue damage

A

mechanical:
- K, H+, ATP, acetylcholine, substance P

damaged blood v: bradykinin

mast cells: nerve growth factor, histamine

damaged blood platelets: serotonin

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18
Q

nociceptors: visceral

A
  • free nerve endings
  • mechano and chemo
  • pain diffuses and difficult to locate
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19
Q

nociceptors: visceral eg

A
  • excessive distention of organ
  • infection in digestive/ renal
  • cancer
  • (lack of blood supply)
  • inflammation
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20
Q

tissue damage causes release of substances:

A
  • ATP
  • H+ ions
  • K+ ions
  • prostaglandins
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21
Q

substances released in tissue damage act:

Study These Flashcards
A
  • directly on ion channels
  • bind to metabotropic receptors (G proteins, 2˚ messengers)
  • depolarise nociceptors
22
Q

axon reflex/ neurogenic inflammation: features

Study These Flashcards
A
  • depolarisation of nociceptor primary afferent endings
  • generator potential spreads to trigger zone generating APs that:
  • spread centrally to synapse w 2nd order = pain signal in spinal cord
  • spread peripherally (antidromically) along sensory endings = axon reflex
23
Q

axon reflex is very few eg of

Study These Flashcards
A
  • neural reflex not involving at least one neuron in CNS
24
Q

axon reflex causes release of:

Study These Flashcards
A
  • neuropeptides (sub P) from afferent endings
25
axon reflex/ neurogenic inflammation: sub P causes
- vasodilation at site (redness) - mast cells -> histamine -> swelling of surrounding tissues (edema) - further stimulation/ sensitisation of nociceptors
26
afferent pain pathways:
- 2nd order neurons ascend to thalamus via lateral spinothalamic tract (ALS) - collaterals travel to reticular formation for 'low level' response
27
convergence projection theory of referred pain:
- visceral sensory afferents run in same n bundle as somatic sensory afferents - also share some 2ndary neurons in spinothalamic pathway - severe visceral pain referred to dermatome
28
pain transmission and pain perception: influenced by
- past/ present experiences: - gate control theory of pain - descending pathways (eg. endogenous analgesia system) - sensitisation
29
gate control theory of pain: what is it
- transmission of pain signals to brain modulated by mechanical stimulation (rubbing skin around painful area) or electrical stimulation (TENS machine)
30
gate control theory of pain: involves
- A beta fibre collaterals from cutaneous mechanoreceptors excite inhibitory interneurons (GABAergic/ glycinergic) in spinal cord/ brainstem - suppress transmission of pain signals (delivered by C fibres) inhibiting 2nd order neurons)
31
gate control theory of pain: TENS
- trans cutaneous electrical nerve stimulation - mimic stimulation of skin mechanoreceptors - targets large myelinated A beta fibres reducing C fibre transmission
32
descending pain pathways:
- limbic system involved in affective (mood) aspects of pain (fear, sleep, hunger, temp) - limbic system sends efferent fibres to spinal cord affecting balance of activity in dorsal horn - inhibitory efferents (release noradrenaline/ serotonin) inhibition - reduce pain - excitatory efferents (release serotonin) facilitation - enhance pain
33
endogenous analgesia:
- response to stressful situations -> suppress transmission of pain signals - descending pathways from midbrain periaqueductal grey matter via medulla to spinal cord - release endogenous opioids (enkephalin) onto synapse btw primary nociceptor afferents
34
endogenous analgesia: effect of endogenous opioids
- presynaptic inhibition of sub P release from C fibres (primary pain afferent) - postsynaptic inhibition by generation of IPSPs in 2nd order neuron
35
sensitisation:
- inflammation/ tissue damage causes sensitisation - in periphery (receptor endings) - in CNS (at synapse w 2nd order neurons) - increase sensitivity (Vm closer to threshold for AP) lower threshold to pain
36
sensitisation: hyperalgesia
- abnormally heightened sensitivity to noxious stimuli
37
sensitisation: allodynia
pain sensation responding to usually non-painful stimuli (touching, cooling/ heating)
38
peripheral sensitisation: features
- release of inflammatory mediators (NGF, bradykinin (BK), prostaglandins (PGE)) - activate intracellular kinases (PKA, PKC)
39
peripheral sensitisation: kinases cause
- phosphorylate membrane receptors - decrease threshold of transducer channels - increase excitability of voltage gated Na channels (generate more APs) - hyperalgesia - allodynia
40
eg. sunburn
- release prostaglandin sensitises TRPV1 channel | - warm shower is painful following
41
central peripheral sensitisation:
- prolonged pain (inflammation)/ brief intense pain trigger changes in CNS resemble underlying peripheral sensitisation - prolonged/ intense release of glutamate from primary nociceptor afferent n terminals onto dendrites of 2ndary afferent n in response cell increasingly excitable - allodynia - hyperalgesia - 2ndary hyperalgesia (spread of sensitivity to non-injured areas)
42
central sensitisation: immediate
- glutamate activates AMPA and NMDA (postsynaptic membrane) - NMDA receptors activated (Mg expelled) - NMDA receptors allow Na influx (depolarisation) and Ca influx (kinase activation)
43
central sensitisation: immediate - kinase activation leads to
- phosphorylation of NMDA receptor proteins - insert more NMDA receptors in membrane - NMDA receptors stay open longer - increased excitability of 2ndary afferent neurons - more pain
44
central sensitisation: delayed/ late onset
- neuroactive substances release by inflammatory cells into CSF - eg. cytokines like IL - 1beta - IL 1beta promotes activity of Cox2 - Cox 2 generates prostaglandin E2
45
central sensitisation: delayed/ late onset PGE2 effects
- facilitate synaptic transmission - increase excitability of neurons - reduce inhibition by inhibitory interneurons - structural changes in synaptic connectivity - more pain
46
analgesia: local anaesthetic eg
- lidocaine
47
analgesia: local anaesthetic lidocaine
- blocks voltage gated sodium channels | - prevents firing of AP by nociceptive primary afferents
48
analgesia: systemic analgesics eg
- aspirin (acetylsalicylic acid) - opioids - NMDA antagonists/ Cox2 inhibitors
49
analgesia: systemic analgesics aspirin
- arachidonic acid released by cellular damage converted to prostaglandins and cytokines - prostaglandin blocks K from nociceptors - enhance depolarisation in response to stimulus (more AP) - aspirin blocks converse - reduce firing by nociceptors
50
analgesia: systemic analgesics opioids
endogenous analgesia
51
analgesia: systemic analgesics NMDA antagonists and Cox2 inhibitors
central sensitisation

4. BIOL257 (18 decks)

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