PHRM30002 EXAM STUDY GUIDE
What is pain? - Answer Unpleasant sensory and emotional experience that protects
subject from tissue damage.
If uncontrolled, can contribute to central and autonomic disturbances; anxiety,
depression, BP, HR
Acute pain and treatment - Answer Acute:
-typically defined as lasting less than 3 months
- somatic: sharp, localised pain
- visceral: dull ache, poorly localised
Treatment: depends on severity
1. Paracetamol
2. Paracetamol + Ibuprofen (NSAID) and/or oral opioid
3. Step 2 + increased dose of opioid or IV opioid or fentanyl
Chronic pain and treatment - Answer Chronic:
- Acute pain progresses to chronic when >3months
- Nociceptive: somatic or visceral
- Neuropathic: damage to nociceptive pathway (tumours/spinal cord
compression/phantom pain)
-Idiopathic: Unexplained (spinal, musculoskeletal (fibromyalgia), headache (migraines))
Neuropathic Pain - Answer - Damage to nociceptive pathway
- Tumour related; spinal cord compression; phantom pain; 'pins and needles'; tingling;
allodynia; sudomotor dysfunction
Nociceptive pain: - Answer Somatic
Superficial: no ANS effects; burning/stinging.
Deep: bones/muscle aches; dull ache; may have ANS effect
Visceral:
Deep tumours; dull and deep pain; nausea, vomiting
Idiopathic pain - Answer Unexplainable:
, Typically a manifestation of muscle aches or migraines:
fibromyalgia; migraines; IBS; myofascial pain
Mu opioid receptors - Answer Important for pain.
Agonists:
- beta-endorphins (endogenous)
- morphine
- codeine
- heroin
- methadone
- fentanyl
Can form homo or heterodimers, altering pharmacological properties & causing
response diversity
mu, delta, kappa receptors - Answer GPCRs:
Gi/o proteins
Gi-alpha:
1. Adenylyl cyclase reduced
2. cAMP reduced
3. Ca2+ reduced
beta-gamma:
1. K+ efflux ; Cl- influx
2. hyperpol post synaptically; NT release pre-synaptically
Opioid mechanism of action - Answer Activation of opioid receptors (Mu-1, Mu-2, Kappa,
Delta) inhibits presynaptic release of neurotransmitters. Postsynaptic hyper
polarization also occurs via increased K efflux and decreased Ca+ conductance into
cell.
Noxious stimulus of nociceptors - Answer capsaicin; noxious heat- activate TRPV1
receptors causing depolarisation --> NT release (SP and Glu)
Pain pathway: - Answer 1. Stimulus
2. Primary sens neuron ascends to dorsal horn
What is pain? - Answer Unpleasant sensory and emotional experience that protects
subject from tissue damage.
If uncontrolled, can contribute to central and autonomic disturbances; anxiety,
depression, BP, HR
Acute pain and treatment - Answer Acute:
-typically defined as lasting less than 3 months
- somatic: sharp, localised pain
- visceral: dull ache, poorly localised
Treatment: depends on severity
1. Paracetamol
2. Paracetamol + Ibuprofen (NSAID) and/or oral opioid
3. Step 2 + increased dose of opioid or IV opioid or fentanyl
Chronic pain and treatment - Answer Chronic:
- Acute pain progresses to chronic when >3months
- Nociceptive: somatic or visceral
- Neuropathic: damage to nociceptive pathway (tumours/spinal cord
compression/phantom pain)
-Idiopathic: Unexplained (spinal, musculoskeletal (fibromyalgia), headache (migraines))
Neuropathic Pain - Answer - Damage to nociceptive pathway
- Tumour related; spinal cord compression; phantom pain; 'pins and needles'; tingling;
allodynia; sudomotor dysfunction
Nociceptive pain: - Answer Somatic
Superficial: no ANS effects; burning/stinging.
Deep: bones/muscle aches; dull ache; may have ANS effect
Visceral:
Deep tumours; dull and deep pain; nausea, vomiting
Idiopathic pain - Answer Unexplainable:
, Typically a manifestation of muscle aches or migraines:
fibromyalgia; migraines; IBS; myofascial pain
Mu opioid receptors - Answer Important for pain.
Agonists:
- beta-endorphins (endogenous)
- morphine
- codeine
- heroin
- methadone
- fentanyl
Can form homo or heterodimers, altering pharmacological properties & causing
response diversity
mu, delta, kappa receptors - Answer GPCRs:
Gi/o proteins
Gi-alpha:
1. Adenylyl cyclase reduced
2. cAMP reduced
3. Ca2+ reduced
beta-gamma:
1. K+ efflux ; Cl- influx
2. hyperpol post synaptically; NT release pre-synaptically
Opioid mechanism of action - Answer Activation of opioid receptors (Mu-1, Mu-2, Kappa,
Delta) inhibits presynaptic release of neurotransmitters. Postsynaptic hyper
polarization also occurs via increased K efflux and decreased Ca+ conductance into
cell.
Noxious stimulus of nociceptors - Answer capsaicin; noxious heat- activate TRPV1
receptors causing depolarisation --> NT release (SP and Glu)
Pain pathway: - Answer 1. Stimulus
2. Primary sens neuron ascends to dorsal horn
