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PN3312 > Pain > Flashcards

Pain Flashcards

1
Q

Define pain

A

An unpleasant sensory or emotional experience associated with actual or potential tissue damage - is subjective and personal

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2
Q

How is pain defined?

A
  1. Source - somatic, neurogenic, psychological
  2. Severity - assessed by clinician
  3. Quality - sharp, dull, aching
  4. Extent - localised or diffuse
  5. Duration - intermittent, acute, persistent, chronic
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3
Q

What is the function of pain?

A

To signal injury/inflammation to promote guarding/resting or learned avoidance

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4
Q

When can pain be pathological?

A

When it relates to an underlying malignancy and so has no utility

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5
Q

How is peripheral pain detected?

A

Through noicireceptors which have many subtypes e.g thermal, mechanical and ‘silent’ (only responsive after inflammation!) - DISTINCT NEURON TYPE

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6
Q

Describe the process of pain signalling due to damage of the skin

A
  • Noicireceptor firing projects through spinal cord to cortex
  • Inflammatory release of H+, K+, ATP, leukokines and prostoglandins causing sensitization
  • Release of substance P and histamine from mast cells cause further sensitization
  • Retrograde transport furthers sensitization
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7
Q

What are the fibres that transmit pain?

A

A delta fibres - sharp, shooting pain (first pain)

C fibres - dull, aching, burning pain (secondary pain)

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8
Q

What is the stucture of the A delta fibers?

A
  • Lightly myelinated
  • Small axons
  • Conduction of 5-30ms
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9
Q

What is the structure of the C fibers?

A
  • No myelination
  • Small diameter
  • slow conduction of 0.5-2ms
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10
Q

How can pain perception change following the initial pain?

A
  • Noicireceptors can fire more easily
  • “hyperalgesia” where pain becomes more painful
  • Allondynia- non-painful stimulus becomes painful
  • “silent” nocireceptors become actibe
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11
Q

What is the organisation of the spinal cord?

A
  • Dorsal and ventral roots
  • Sensory input goes to dorsal root
  • White matter are axon projections, grey matter are cell bodies
  • Divided into laminae 1-10 where 1 is dorsal
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12
Q

Where do noicireceptors project into the spinal cord?

A
  • A delta project to laminae 2-3
  • C fibres to laminae 1-2
  • Laminae 2 is important as it is where first and second pain converges (substantia gelatinosa)
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13
Q

How does the transmission of noicireceptor information differ to other sensory transmission?

A
  • Sends short projections rostrally and caudally in the zone of lissar ipsilaterally
  • Then synapse on to zone 2 (substantia gelatinosa) on to second order projection neurons which cross beneath the central canal and ascend contralaterally up the spinal cord (SPINOTHALAMIC TRACT)
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14
Q

Describe the neurochemistry of nocireceptors?

A
  • Release substance P early after injury and glutamate for a fast response at the dorsal horn peripheral laminae (shown with antibodies raised against it)
  • Substance P binds to post-synaptic tachykinin receptors (most importantly tachykinin1)
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15
Q

What is the ultrastructure of noiceptor neurons?

A

2 types of synaptic vesicle
- Large dense core vesicles (LDCV) contain peptides, require more Ca to be released and therefore more action potentials
- Small synaptic vesicles (SSV) contain glutamate
Therefore there is a co-release of substance P and glutamate

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16
Q

How does noiciceptive synapse release change?

A
  • Neurokinin A only released after sensitization

- NOS and NO are also upregulated during pain

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17
Q

What is ‘wind up’ dorsal pain?

A
  • Persistent repetitive activation of C-fibres causes response of dorsal horn to increase progressively
  • Dependent however on NMDA activation by glutamate
  • CENTRAL SENSITIZATION
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18
Q

What is gate control?

A
  • Mechanosensory stimulation can decrease sensation of pain
  • C fibres share tract with A alpha and A beta mechanosensory neurons which activate their own projection neurons and also inhibitory interneurons to the C fibres
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19
Q

What are the different classes of second order neurons within the spinothalamic tract?

A

Class I - thermal and mechanical stimuli
Class II - have a wide dynamic range
Class III - noiciceptive specific

20
Q

What is endogenous pain control?

A
  • Mitigates conflict between pain sensation and ability to escape
  • Done through PAG located in the midbrain which is activated during excessive pain and sends activation through raphe nuclei to dorsal horn
  • Releases enkephalin and endorphins which bind presyaptically to noiciceptors inhibiting Ca2+ and reducing AP length, and post synaptically to dorsal projection neurons to induce hyperpolarisation
21
Q

What are drugs that control pain referred to as?

A

Analgesics

22
Q

What are the classes of analgesics?

A
  1. Non-steroidal anti-inflammatory (aspirin)
  2. Morphine-like drugs (opiods)
  3. Local anaesthetics (lidocaine/benzocaine)
  4. Centrally acting non-opiod drugs e.g antidepressants and cannabinoids
    note: 95% constitute first 2 categories
23
Q

How was aspirin discovered?

A
  • Chewing on bark of salix alba had pain relieving properties - contains salicylic acid
  • Then synthesis in pure form of acetylsalicyclic acid called aspirin
24
Q

How does aspirin work?

A

Targets inflammatory components

  • Derived from arachidonic acid which is broken down by COX-1 constantly to produce housekeeping prostoglandins and COX-2 to produce inflammatory prostoglandins
  • Aspirin blocks COX-2 (but also a bit of COX-1 and reduces platelet aggregation)
25
Q

Why is ibuprofen more potent than aspirin?

A
  • Higher affinity for COX-2

- Less affinity for COX-1

26
Q

How do CNS acting analgesics (opiums) work?

A
  • Bind to endogenous opiod-like receptors - endorphins and enkephalin
  • These are usually released by local interneurons in the dorsal horn and from projections in the brainstem
27
Q

What are the properties of dimorphine (heroin)?

A
  • Converted into morephine in the body

- Lipid-souble so can pass through lipid membrane quickly

28
Q

What is codeine?

A
  • 20% as potent as morphine
  • Can be absorbed orally
  • Non addictive
29
Q

What is pethidine?

A
  • Can lead to dependency and euphoria
  • Used for labour as its short acting
  • However can cause drowsiness in newborn for several days
30
Q

What is fentanyl?

A
  • Short lasting opiod

- Used in patient controlled infusion systems to control pain

31
Q

What is methodone?

A
  • Used as a heroin substitute in recovering addicts

- Use S-enantiomer which is an antagonist at NMDARs

32
Q

What are the endogenous opiates?

A

Opioid peptides (endorphine) include beta-endorphin, met-enkephalin, leu-enkephalin and dynorphin

  • Widely distributed in the brain
  • In the spinal cord dynorphin is present mainly in interneurons, enkephalins also in interneurons and long descending projections
33
Q

What are the opioid receptor subtypes?

A
  • u opioid receptors thought to be responsible for most effects
  • delta receptors also contribute to to aanalgesia at the spinal levesl
  • All can activate AC which opens K channels and inhibits Ca channels
34
Q

What are neurosteroids?

A
  • Modulate GABAa recpetors which have many binding sites for different sunstances (bind to allosteric site)
  • Synthesized from peripherally derived progesterone/cholesterol in the neurons and glial cells
  • Only has effect when this and GABA binds to produce prolongation of inhibition
35
Q

What are endocannabinoids?

A

Lipids syntehsised from membrane phospholipids ‘on demand’ by neurons

36
Q

Give an example of an important endocannabinoid

A

Arandemide

  • Broken down by fatty acid amide hydrolase (FAAH)
  • Womean who doesn’t feel pain has mutation on FAAH gene therefore potential drug interest
37
Q

How do cone snails catch their prey?

A
  • Extend probasis with sting which causes paralysis in fish
  • Venom comes from bulb filled with peptides, this travels down the duct and is stored in the radular sac go be shot out by non-hydrostatic explosion
  • Tooth has barbs allowing fish to be retracted and eaten
38
Q

Why are the cone snails a target for pharmacology?

A

Each species has a venom containing 100s of neuropeptides, unique database for pharmacology

39
Q

How have the neuropeptides of the cone snail been classified?

A
  • Injecting isolated peptides into mice

- Each belongs to a super family based on which channel they affect and the number of cysteine residues

40
Q

What is the lighting cabal?

A

Cone snail uses delta-conotoxin blocking Na channels so fish cannot escape and also K channels to induce tetanic shock

41
Q

What is the motor cabal?

A

Uses alpha-conotoxin to block nAChRs and u-conotoxin to black Na channels

42
Q

What is zicotonide?

A
  • Used in the treatment of chronic pain
  • is a w-conotoxin MVIIA (targets Ca channels)
  • Synthetic version has identical structure
43
Q

How does zicotonide work?

A
  • Acts on Ca channels within dorsal horn
  • Rises in Ca levels usually triggers release of glutamate and substance P
  • Blocks N-type Ca channels to stop neurotransmitter release
    (note: these channels are also found at the NMJ and hippocampus)
44
Q

How is zicotonide administered?

A
  • Injected into cerebrospinal fluid into the brain as it is a large molecule
  • Must be placed carefully so that it does not spread too far
  • Only used as a last resort for chronic pain
45
Q

What are the side effects of zicotinide?

A
  • Diziness and confusion

- At high doses can lead to psychosis and depression

PN3312 (11 decks)

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