clinical scenario Flashcards
(13 cards)
how does codine work?
its broken down 10% by the cyp2d6 enzyme in the liver into its active metabolite of morphine
morphine binds to the u-opioid receptor to inhibit cAMP synthesis from the breakdown of ATP, reducing the levels of cAMP leading to changes in gene expression and a decrease in the influx of Ca2+ ions, decreaseing neurotransmitter release by inhibiting the depolarisation of the cell
what can treat neuropathic pain?
gabapentin + pregabalin - binds to alpha subunit of the voltage gated Ca2+ channel
duloxetine - SSRI
amitryptiline - TCA antidepressant
capsican patches
what opioids arent broken down into active metabolites by CY2D6 enzyme?
hydromprphine
oxymorphine
morphine
tapendol
how do capsican patches work?
theyre derived from chilli peppers and bind to TRPV1 receptors on the neural membrane in TRPV1 nocioceptors
leads to mitochondrial dysfunction and increased Ca2+ release from the ER leading to breakdown of the cytoskeleton and interupting fast axonal transport of pain signals
resulting in deecreased pain perception and may cause inflammation at the administration site causing a burning sensation on the skin
how do topical rubefactants work and name an example?
movelat cream, this works with salasilic acid and mucopolysaccharide working together to provide moderate pain releif from inflammation under the surface
what is tapentadol?
its been shown to be effective in clinical studies for OA as it is able to treat both neuropathic and nocioceptive pain
its a synthetic opioid analgesic with a dual mode of action as a highly selective full agonist of the μ-opioid receptor and as a norepinephrine reuptake inhibitor, allowing the inc levels of NE to activate alpha2-adrenoceptors
its also a weak serotonin-reuptake inhbitor however this doesnt contribute to the analgesic effects of the drug
can also bind to kappa and delta opioid receptors but its actions are mainly mediated through the u-opioid receptor
how is tapentadol metabolised?
About 2% of tapentadol can also undergo CYP2D6-mediated hydroxylation to form Hydroxy tapentadol however none of its metabolites are active meaning that it wont contribute to any increased side effects
97% is metabolised by CYP450
what non-pharmacologic ways of pain management are there?
lifestyle changes such as diet and excersize
phycological councelling to help him deal with the pain better
what non-analgesics can he take to help?
corticosteroids like predisone or methylpredisone to reduce the swelling, however these shouldnt be taken long term due to the side effects
could be in injection form or cream form
NSAIDs - creams or gels applied to the affected area inhibit the inflammation by inhibiting the action of the COX enzymes, inhibiting the production of prostaglandins
what is the pharmacokenetics of ibuprofen?
1800–2400 mg/day can be prescribed to people with osteoarthritis and Ibuprofen is present in a free, unbound form in cerebrospinal fluid and is retained in the synovial fluid in the inflamed joints of arthritic patients . Ibuprofen has a wide therapeutic concentration range for its analgesic, antipyretic, and anti-inflammatory effects (~10–50 mg/l) and a relatively short plasma half-life (t1/2, ~ 1–3 h), necessitating frequent administration to maintain therapeutic plasma concentrations
the S enantiomer is mainly responsible for its analgesic effects and
whats the pharmacodynamics of ibuprofen?
ibuprofen non-selectively inhibits the activity of the COX1+2 enzymes, inhibiting the first committed step of prostanoid synthesis, the conversion of arachidonic acid from the phosphilipid membrane to prostaglandins, PGI2, PGE2, PGD2, PGF2alpha and thromboxane
the effects of PGE2 lead to pain, inflammation, fever and neoplasma
it also inhibits the effcts of NOS preventing the release of NO
what are the effects of codine toxicity?
respiritory depression
coma
loss of consiousness
breathing problems
cyanosis
risk of dependance
what are the nice reccomendations for ultrametabolisers and codine?
the reccomendation is that its contra-indicated for patients of any age known to be ultra-rapid metabolisers
