analgesia Flashcards
what is an analgesic
an agent that alleviates pain without causing loss of consciousness
what is a narcotic analgesic
aka an opioid analgesic which is a class of compounds that can act upon opioid receptors to block the preception of pain or modify the emotional response to pain
what is a non-narcotic analgesia
a compound that achieves analgesia without acting upon opioid receptors
what is an anti-inflammatory agent
a compound that supresses the inflammatory response
what is a steroidal agent
chemically related to the steroid hormone cortisol, referred to as corticosteroids
what is a nonsteroidal agent
NSAID
what is an adjunctive agent
used to potentiate the effects of analgesics or manage associated issues
where are opioid receptors located
everywhere
what is the effect of opioids at the supraspinal level
indices euphoria and can alter the perception of pain by activating descending neural pathways that inhibit nociceptive transmission in the dorsal horn
what are the potential disadvantages of opioid analgesics
addiction, sedation, constipation, hallucination
what is the drug used to reverse opioid overdose
narcan (naloxone)
how to NSAIDS work
they inhibit the COX enzymes to reduce prostaglandin synthesis and therefore reduce the inflammation which is causing pain
cox 1 is responsible for synthesising prostaglandins for
homeostatic functions
cox 2 is responsible for synthesising prostaglandins for
inflammation
non selective cox inhibitors include
aspirin, ibuprofen, naproxen, diclofenac
what are the adverse effects of nonselective nsaids
gi upset, skin rashes
overuse can lead to HTN and renal failure
aspirin specific adverse effects include
directly toxic to the gastric mucosa, reyes syndrome, and tinnitus (associated with aspirin overdose)
what are some common selective cox 2 inhibitors
celebrex, meloxicam
what is the mechanism of paracetamol
poorly undersood but - it inhibits prostaglandin synthesis centrally rather than peripherally, indirectly interfering with COX activity by changing peroxide concentration
it also influences pain modulation pathways - serotonergic neurons, cannabinoid receptors
in excess, paracetamol is
hepatotoxic
who should be cautious when taking paracetamol
alcoholics - increased rate of conversion of paracetamol to its toxic metabolite
children
Low BMI
how do local anaesthetics work
by blocking sodium channels - and decreasing the release of excitatory neurotransmitters, decreasing the ability of the action potential to cross the synapse - meaning no action potential is travelling up the neuron
how do anti-epileptics (anticonvulsants) reduce neuropathic pain
by acting like GABA which is the major CNS inhibitory naurotransmitter, which downregulates pain by acting on the calcium channels (which decreases the ability of the action potential to cross the synapse)
how do cannabinoids reduce pain
AEA and 2ag are synthesised in the post synaptic neuron, they they travel backwards towards the cb1 receptors and take out calcium channels (which decreases the ability of the action potential to cross the synapse)
how do antidepressants work to reduce pain
serotonin and noradrenaline are inhibitory, an inhibitor to their reuptake will allow 5HT and NA to stay in the synaptic cleft for longer, keeping inhibitory neurotransmitters at a surplus over substance P, not allowing for the activation of the second order neuron
if depression is present alongside pain, it can also help with the emotional perception of pain
how to opioids work to reduce pain
periphery - opioid receptors are on free nerve endings - transduction is effected by blocking calcium channels on the presynaptic (first order) neuron and by causing a potassium efflux on the postsynaptic (second order) neuron
dorsal horn - they will decrease transmission as well - by blocking calcium channels on the presynaptic (first order) neuron and by causing a potassium efflux on the postsynaptic (second order) neuron
supraspinal brainstem (PAG) - causing increased descending pain modulation
brain - decreasing pain perception
why are opioids very effective at modulating pain
they act upon all levels (periphery, dorsal horn, midbrain, brain)
why are opioids highly addictive
they produce eurphoria,
the more you take the more opioid receptors you create + it decreases your ability to make your own endogenous opioids
how do cortocoseroids work to reduce pain
by mimicking cortisol which is responsible for releasing sugar in times of stress and supressing the immune system.
they act in the nucleus of the cell and dictate what the cell will synthesise, once it is at the DNA it tells the cell to synthesise lipocortin that will inhibit phospholipase A2 which tells the cell to downregulate inflammatory protein production, therefore having antiinflamatory affects, and affecting transduction and then also transmission
what is the difference between an NSAID and corticosteroids
nsaids wil prevent cox producing prostaglandins, where as a SAID will directlt target the nucleus and change gene expression
how does ketamine work to reduce pain
by acting as an antagonist on NMDA receptors and preventing glutamate from binding, which decreases pain as glutamate is excitatory to pain modulation in the CNS, stopping the pain signal from getting to where it was meant to go.
