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Symposium > Pain > Flashcards

Pain Flashcards

1
Q

What are classifications of pain?

A 
Duration= acute/chronic
Pathophysiology= neuropathic/nociceptive
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2
Q

What is nociceptive pain?

A
  • Regulated by opioidergic system -Acute nociceptive pain subsides when damage resolves
  • Chronic pain persists may lead to neuropathic/mixed pain
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3
Q

Describe the analgesic ladder

A
  1. Non-opioid (NSAIDs, aspirin)
  2. Opioid for mild-moderate pain & non-opioid (Codeine, tramadol)
  3. Opioid for moderate-severe pain & non-opioid, freedom from cancer pain (morphine, methadone)
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4
Q

What is the mechanism of action for non-opioids for acute pain?

A
  • NSAIDs/COX-2 inhibitors act peripherally
  • Paracetamol has central activity
  • Efficacy in acute pain management & control of nociceptive pain
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5
Q

What is the mechanism of action for opioids for acute pain?

A
  • Activate endogenous analgesic system
  • Stimulate receptors in limbic system to eliminate pain
  • Affects descending pathway modulating pain perception
  • Acts at 2 sites
  • Presynaptically pain signal transmission is inhibited
  • Postsynaptic membrane hyperpolarised, decreasing the probability of ap generation
  • Main efficacy in nociceptive pain
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6
Q

What is the mode of action and any side effects for NSAIDs?

A 
MA= inhibition of cyclooxygenase, prostaglandin synthesis decreases
-SE= GI irritation/bleeding, renal toxicity, drug interactions, CV effects
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7
Q

What is the mode of action and any side effects for paracetamol?

A 
MA= Inhibition of central prostaglandin synthesis
SE= risk of toxic liver damage
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8
Q

What are side effects of opioids?

A
  • Nausea
  • Vomiting
  • Constipation
  • Dizziness/vertigo
  • Somnolence
  • Dry skin/pruritus
  • Respiratory depression & hypoxia
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9
Q

What is epidural analgesia used for?

A

-Postop: thoracic, abdo, lower limb surgery, labour, chronic

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10
Q

What are the benefits of epidural analgesia?

A
  • High quality pain relief
  • Improved pulmonary function
  • Reduced sepsis & chest infection
  • Reduced cardiac morbidity
  • Reduced vascular graft failure
  • Reduced incidence of DVT
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11
Q

When is a celiac plexus block used?

A
  • Pancreatic carcinoma

- Upper abdominal neoplasia

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12
Q

Describe neuropathic pain

A
  • Spont pain &hypersensitivity associated with damage/lesion of NS
  • Intense pain accompanied b other pain phenomena
  • Persistent & recurrent
  • Associated with severe comorbidity & poor QOL
  • post herpetic neuralgia, pain after CVA, post-op, painful diabetic neuropathy, trigeminal neuralgia
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13
Q

What features suggest neuropathic pain?

A
  • Pain different from everyday pain
  • Pain in area of sensory loss
  • Paroxysmal/spontaneous pain
  • Allodynia (pain from non painful stimuli)
  • Hyperalgesia (inc pain in response to painful stimuli)
  • Dysaesthesias (unpleasant abnormal sensations)
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14
Q

What drug therapy is there for neuropathic pain?

A

-NSAIDs
-Antidepressants
-Anticonvulsants
-Opioids
-Membrane stabilising drugs
Topical drugs

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15
Q

What is the mechanism of action and side effects of antidepressants?

A 
MA= Inhibition of neuronal reuptake of noradrenaline & serotonin
SE= Dry mouth, insomnia, inc appetite, constipation, abnormal heart rate/rhythm, somnolence
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16
Q

What is the mechanism of action and side effects of anticonvulsants?

A 
MA= Gabapentin: binds to presynaptic voltage-dependent Ca channels, pregabalin: interacts with special N-type Ca channels, Carbamazepine: blocks Na+, Ca2+ channels
SE= sedation, dizziness, ataxia, nausea, weight gain, peripheral oedema
17
Q

What are the types of nociceptors?

A
  • Unmyelinated C fibres

- thinly myelinated Ad fibres

18
Q

What modalities do nociceptors respond to?

A
  • Mechanical
  • Thermal
  • Chemical (histamine)
19
Q

What neurotransmitter is released by pain afferents?

A

Glutamate

20
Q

Neurons in the dorsal horn express what neuropeptide?

A

Substance P receptor (NK1) and project to the thalamus

21
Q

What can hyperalgesia be?

A
  • Spontaneous pain
  • Reduced threshold for pain
  • Increased intensity of painful stimuli
22
Q

Describe first & second pain

A

1st=Fast, A-delta fibres, sharp/ pricking, rapid, easily localised, short time, mechanical/thermal
2nd=Slow, C-fibres, dull ache/ burning, poorly localised, persistent, polymodal, slow onset

23
Q

Where are nociceptors found?

A
  • Periphery as free nerve endings

- Branched, unmyelinated in dermis

24
Q

How does hyperalgesia occur?

A

1) Tissue damage/inflammation
2) Release of prostaglandins, bradykinin, histamine
3) Sensitize peripheral nociceptors that express heterogenous receptors/ion channels
4) Transmission of impulses via A-delta & C sensory afferents to dorsal horn
5) Projection to brain via ascending pathways
6) Experience sensory/emotional hyperalgesia

25
Q

Give the sub modality, position and fibre type of thermoreceptive & nociceptive afferents

A
  • Warm= C, deep epidermis
  • Cold=A-delta, deep epidermis
  • Nociceptive= either C or A-delt, superficial epidermis
26
Q

Where do nociceptive fibres have their cell bodies?

A
  • Dorsal root ganglion
  • Travel up/down in zone of lissauer
  • Innervates substantia gelatinosa
27
Q

Describe the components of the ascending pain pathway

A
  • Lateral spinothalamic tract
  • Spinoreticulothalamic tract
  • Anterior spinothalamic tract (to RF and periaqueductal grey matter)
  • Contralateral pathway at the level of the spinal cord
28
Q

What occurs in a unilateral spinal cord injury/lesion?

A
  • Brown sequard syndrome
  • Dissociated sensory loss
  • Loss of pain on opposite side
  • Loss of sensory on the same side
29
Q

What does the VPM & VPL of the thalamus innervate?

A 
VPM= face
VPL= rest of body

Symposium (17 decks)

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