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PAIN PHARMACOLOGY - Coggle Diagram
PAIN PHARMACOLOGY
Opioid Analgesics
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Opioids - general class of agents includes opiates, semi-synthetic derivatives of morphine/synthetic agents
Opium = greek for "juice", exudate from the incised opium poppy pod. contains in excess of 20 agents
Morphine, papaverine, noscapine & codeine used clinically
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CNS
- analgesia, euphoria/dysphoria, depression of cough reflex
- depression of respiratory centre, depression of vasomotor centre, stimulation of chemoreceptor trigger zone (vomiting), physical dependence/tolerance
PNS
- Reduced motility/increased tone of gastrointestinal tract, closet of GIT sphincters, reduced GIT/billary secretions, increased tone of detrusor & urethral sphincter etc.
Chronic pain
- pain lasting > 3-6 months
- 22% of primary care patients - almost 1 million Aust
- Detrimental effects:
- lost productivity
- decreased QOL/emotional well-being
- increased rates of comorbidities such as anxiety/depression
Nociceptive/inflammatory pain = osteoarthritis, cancer
Neuropathic pain:
- peripheral - diabetic peripheral neuropathy, lower back pain, AIDS, polyneuropathy, phantom limb pain
Central pain augmentation:
- fibromyalgia
- migraine
- IBS
- non-cardiac chest pain
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Chronic pain management
- chronic pain is multifaceted/requires individualised multimodal treatment
- pharmacologic - conventional, TCAs, Capsaicin
- non-pharmacological = cognitive, behavioural/rehab therapies
- mixed of therapy will be governed by pathophysioloy
- Glia recognise chemical signals from neurons
- release chemical signals that modulate communication between nerves
- this results in the adapations of painful sensations being exaggerated, touch being perceived as pain
- opiates increase this so in some people, opiate treatment can prolong neuropathic pain
- Work on drugs to adjust glial response
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TYPES OF PAIN
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C-fibre (sore, dull, aching, heavy)
temporal: long-lasting, pounding, throbbing, pulsing
spatial: diffuse
evaluative: annoying, miserable, intense, unbearable
receptive field: large
threshold: low
Anti-pyretic analgesics
- includes non-steroidal anti-inflammatory drugs (NSAID
- Mechanism of action - reducing the synthesis of prostaglandins (by inhibiting the enzyme cyclo-oxygenase, of COX)
- prostaglandins are inflammatory mediators and pain receptor 'stimulators'. Prostaglandins are released in the hypothalamus & produce fever or an increase in body temperature (i.e. hyper-pyrexia)
NSAIDS & Others:
- Diclofenac
- mefaclamic acid
- Aspirin
- Indomethacin
- Paracetamol
- Celecoxib
- For chronic pain (arthritis) pt put on one NSAID & then switched to another after 6 months
Tramadol
- relatively new analgesic
- not chemically related to opioids but acts like one
- has other effects (anti-depressant-like)
- gaining popularity/well received by pts.
Analgesia (suppression of the sensation of pain):
- spinal cord, thalamus, cerebral cortex
AND the reaction (emotional) to pain:
- limbic areas, cerebral cortex
Considerations for analgesia:
- effectiveness of agent
- duration of action
- duration of therapy
- drug interventions
- sensitivity of patient
- route of administration
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Management of pain
Pain (assessment, evaluation, individual parameters)
pain Severity
> Step 1 (1-3 mild) = non-opioid + non-pharmacological
> Step 2 (4-6 moderate) = non-opioid + weak opioid + non-pharmacological
>Step 3 (7-10 severe) = strong opioid + non-pharmacological
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Withdrawal syndrome
Start: Fear/anxiety
8-16 hours - nervousness, irritability, anxiety, runny nose, dilated pupils, poloerection
36 hrs - fasciculations, cramps, vomiting, diarrhoea, insomnia, hyperglycaemia
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PAIN RECEPTORS > SPINAL CORD > BRAIN STEM > LIMBIC SYSTEM (IDENTIFICATION OF PAIN) > THALAMUS > FRONTAL CORTEX (EXPERIENCE OF PAIN > SENSORY CEREBRAL CORTEX (LOCALISATION OF PAIN)