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4. BIOL257 > Pain > Flashcards

Pain Flashcards

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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:

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

axon reflex/ neurogenic inflammation: features

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

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

axon reflex causes release of:

A
  • neuropeptides (sub P) from afferent endings
25
Q

axon reflex/ neurogenic inflammation: sub P causes

A
  • vasodilation at site (redness)
  • mast cells -> histamine -> swelling of surrounding tissues (edema)
  • further stimulation/ sensitisation of nociceptors
26
Q

afferent pain pathways:

A
  • 2nd order neurons ascend to thalamus via lateral spinothalamic tract (ALS)
  • collaterals travel to reticular formation for ‘low level’ response
27
Q

convergence projection theory of referred pain:

A
  • 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
Q

pain transmission and pain perception: influenced by

A
  • past/ present experiences:
  • gate control theory of pain
  • descending pathways (eg. endogenous analgesia system)
  • sensitisation
29
Q

gate control theory of pain: what is it

A
  • transmission of pain signals to brain modulated by mechanical stimulation (rubbing skin around painful area) or electrical stimulation (TENS machine)
30
Q

gate control theory of pain: involves

A
  • 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
Q

gate control theory of pain: TENS

A
  • trans cutaneous electrical nerve stimulation
  • mimic stimulation of skin mechanoreceptors
  • targets large myelinated A beta fibres reducing C fibre transmission
32
Q

descending pain pathways:

A
  • 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
Q

endogenous analgesia:

A
  • 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
Q

endogenous analgesia: effect of endogenous opioids

A
  • presynaptic inhibition of sub P release from C fibres (primary pain afferent)
  • postsynaptic inhibition by generation of IPSPs in 2nd order neuron
35
Q

sensitisation:

A
  • 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
Q

sensitisation: hyperalgesia

A
  • abnormally heightened sensitivity to noxious stimuli
37
Q

sensitisation: allodynia

A

pain sensation responding to usually non-painful stimuli (touching, cooling/ heating)

38
Q

peripheral sensitisation: features

A
  • release of inflammatory mediators (NGF, bradykinin (BK), prostaglandins (PGE))
  • activate intracellular kinases (PKA, PKC)
39
Q

peripheral sensitisation: kinases cause

A
  • phosphorylate membrane receptors
  • decrease threshold of transducer channels
  • increase excitability of voltage gated Na channels (generate more APs)
  • hyperalgesia
  • allodynia
40
Q

eg. sunburn

A
  • release prostaglandin sensitises TRPV1 channel

- warm shower is painful following

41
Q

central peripheral sensitisation:

A
  • 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
Q

central sensitisation: immediate

A
  • glutamate activates AMPA and NMDA (postsynaptic membrane)
  • NMDA receptors activated (Mg expelled)
  • NMDA receptors allow Na influx (depolarisation) and Ca influx (kinase activation)
43
Q

central sensitisation: immediate - kinase activation leads to

A
  • 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
Q

central sensitisation: delayed/ late onset

A
  • 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
Q

central sensitisation: delayed/ late onset PGE2 effects

A
  • facilitate synaptic transmission
  • increase excitability of neurons
  • reduce inhibition by inhibitory interneurons
  • structural changes in synaptic connectivity
  • more pain
46
Q

analgesia: local anaesthetic eg

A
  • lidocaine
47
Q

analgesia: local anaesthetic lidocaine

A
  • blocks voltage gated sodium channels

- prevents firing of AP by nociceptive primary afferents

48
Q

analgesia: systemic analgesics eg

A
  • aspirin (acetylsalicylic acid)
  • opioids
  • NMDA antagonists/ Cox2 inhibitors
49
Q

analgesia: systemic analgesics aspirin

A
  • 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
Q

analgesia: systemic analgesics opioids

A

endogenous analgesia

51
Q

analgesia: systemic analgesics NMDA antagonists and Cox2 inhibitors

A

central sensitisation

4. BIOL257 (18 decks)

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