Pharmacology Flashcards
Opiod receptors
MOR, DOR ad KOR type
they are found in the CNS, PAG, dorsal horn and peripheral tissues including GIT
Receptors are coupled with G protein, they inhibit the nerve by reducing intracellular cAMP or K+ efflux (hyperpolarisation) leading to reduction in neuronal excitability
Peripheral mechanism of opiods
hyperpolarisation of nerve, makes it less easily excitable and reduces pain transmission
Central mechanism of opioids
inhibit substance P release from 1st order neuron in dorsal horn, hyperpolarisation of 2nd order neurond
Supraspinal mechanism of opiods
euphoria- alters pain perception
and activation of descending pathways
Adverse reaction of opioids
drowsiness, repsiratory depression, bradycrdia, nausea, constipation,
Opiod receptor antagonists
Bind to receptors causing receptor to become non-functional and preventing agonists from interacting with same receptor
e.g. Naloxone- strong affinity for opioid receptors, it reverses opioid overdoses, used in cases of respiratory arrest in heroin overdoses.
Can buy agonist- antagonist preparations to offset side effects
NSAID mechanism of action and types
Normally, arachodonic acid becomes prostaglandins vis cyclo-oxygensae enzymes. NSAID blocks these enzymes
COX1-prostaglandins for homeostasis
COX2- prostaglandins for inflammation
Side effects of NSAIDs
GIT upset, rash, renal failure, hypertension
Paracetomal mechanism of action
inhibits prostaglandin synthesis centrally and modulates pain via serotongeric and cannabinoid receptors
Paracetamol side effects
less side effects than NSAIDs, taken in excess can lead to hepatoxicity
Pregabalin mechanism of action
reduce synpatic release of subsance P, glutamate and noreadrenalin. aka lyrica
Gabapentin mechanism of action
may activate GABA neurons or inhibit NMDA receptors
Carbbamezaepine mechanism of action
tegretol- firsst line therapy for trigeminal neuralgia. Promotes sodium efflux and delays rate of recovery of voltage gated sodium channels from inactivated state.
Tricyclic antidepressants mechanisms
e.g. amitryptiline. Blocks the pump on the presynaptic terminal responsible for serotonin and NA reuptake
Increased levels of these neurotransmitters = descending pain modulation
Corticosteroids
Steroid based= can enter cell
Bind to corticosteroid receptors in the nucleus and interact with DNA to alter gene expression
-Produce anti-inflammatory proteins (e.g. lipocortin, inhibits phospholipidase)
-Decreased production of inflammatory mediators and enzymes (e.g. less COX gene expression
Muscle relaxants
Stimulates GABA receptors in the spinal cord and also blocks release of substance P.
Local anaesthetic
Bind to receptors om membrane-bound channels and block influx of sodium= blocked transmission of pain signals to second order neuron
Anti-depressant side effects
nausea, impaired sexual function, dry mouth, fatigue, insomnia, drowsiness, blurred vision
Neuropathic pain recommendation
Offer a choice of amitriptyline, duloxetine, gabapentin or pregabalin as initial treatment for neuropathic pain
• Consider tramadol only if acute rescue therapy is needed.
• Consider capsaicin cream for people with localised neuropathic pain who wish to avoid, or who cannot tolerate, oral treatments.
Managment of acute LBP
- reassurance, exercise, education, non-pharmalogical
- NSAIDs with adjunct
- NSAIDs with weak opiods (e.g. codeine, tramadol, oxycodone) with adjunct
- NSAIDs + strong opiods (fentanyl, morphine)
- Local corticosteroid injection if very cute
Tramadol mechanism of action
Opiod receptor agonist + SSRI/ SNRI
Chronic LBP management
CBT, exercise, reassurane, NO OPIOIDS (opiod induced analgesia and tolerance) NO paraceetomal, NSAIDs short term, antidepressants
CRPS
hyperalgesia, allodynia, chnages in skin colour, blood supply, temperature, sweating, motor changes, changess in urine or other systems, affects widespread areas,
Diazepam
binds to benzodiazpam receptor > enhances GABA and chloride influx (hyperpolarisation)
