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Flashcards in Pain Deck (29):

What are classifications of pain?

Duration= acute/chronic
Pathophysiology= neuropathic/nociceptive


What is nociceptive pain?

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


Describe the analgesic ladder

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


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

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


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

-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


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

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


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

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


What are side effects of opioids?

-Dry skin/pruritus
-Respiratory depression & hypoxia


What is epidural analgesia used for?

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


What are the benefits of epidural analgesia?

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


When is a celiac plexus block used?

-Pancreatic carcinoma
-Upper abdominal neoplasia


Describe neuropathic pain

-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


What features suggest neuropathic pain?

-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)


What drug therapy is there for neuropathic pain?

-Membrane stabilising drugs
Topical drugs


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

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


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

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


What are the types of nociceptors?

-Unmyelinated C fibres
-thinly myelinated Ad fibres


What modalities do nociceptors respond to?

-Chemical (histamine)


What neurotransmitter is released by pain afferents?



Neurons in the dorsal horn express what neuropeptide?

Substance P receptor (NK1) and project to the thalamus


What can hyperalgesia be?

-Spontaneous pain
-Reduced threshold for pain
-Increased intensity of painful stimuli


Describe first & second pain

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


Where are nociceptors found?

-Periphery as free nerve endings
-Branched, unmyelinated in dermis


How does hyperalgesia occur?

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


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

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


Where do nociceptive fibres have their cell bodies?

-Dorsal root ganglion
-Travel up/down in zone of lissauer
-Innervates substantia gelatinosa


Describe the components of the ascending pain pathway

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


What occurs in a unilateral spinal cord injury/lesion?

-Brown sequard syndrome
-Dissociated sensory loss
-Loss of pain on opposite side
-Loss of sensory on the same side


What does the VPM & VPL of the thalamus innervate?

VPM= face
VPL= rest of body