NSAIDs and opiates Flashcards
OVERVIEW
i) do NSAIDs or opiates account for more adverse drug reactions?
ii) give an indication for NSAIDS and opiates
iii) what is step 1,2,3 of the WHO analgesic ladder and give an example drug for each level
i) NSAIDs > account for 29.6%
opiates account for 6%
ii) NSAIDs > mild to mod MSK pain
opiates > mod to severe pain (visceral origin)
iii) Step 1 - non opioid + adjuvant analgesic (paracetamol or NSAID)
Step 2 - opioid for mild/mod pain + non opioid + adjuvant (codeine phosphate)
Step 3 - opioid for mod/severe pain + non opioid + adjuvant (morphine sulphate)
NSAIDS
i) how long can the effect take to work as an anti inflam? give three indications for its anti-inflam use
ii) which agents are important to use alongside long term NSAIDs?
iii) how long do they take to work as analgesics? name four inidics for analgesic use?
iv) why do NSAIDs work as anti pyretics?
v) how is aspirin used in CVD? explain how it works? give three indications
vi) what do NSAIDs principally affect? (3)
i) anti inflam - can take up to three weeks to work
- use in gout, seronegative arthritides (ankylosing spondylitis), RA, SLE
ii) need to give gastroprotection one when used long term eg omeprazole
iii) analgesics - effect after first dose but full dose after one week
- use in OA, RA, soft tissue rhum, back pain, minor trauma, headache, dysmennorea, dental pain, peri op pain, ureteric colic (parental)
iv) pyretics > inflam reactions rel IL-1 > PG release to CNS
- PG elevate hypothalamic set point for temp control > NSAIDs prevent this
v) aspirin in CVD - works as an anti plat agent > reduces plat aggregation and blood ability to clot
- use in unstable angina, NSTEMI, STEMI, TIA< ischaemic stroke, secondary prevention
vi) thromboxane A2, prostaglandin, prostacyclin
TYPES OF NSAID
i) which one is synth from acetyl salicyclic acid?
ii) what was developed as a safer alternative to aspirin and dervied from propionic acid?
iii) name three other NSAIDs
iv) name two NSAIDs with low gastric tox, med gastic tox and high gastric tox
v) what do all NSAIDs run the risk of? why?
i) aspirin
ii) ibuprofen
iii) celecoxib, diclofenac, naproxen
iv) low - ibuprofen, celecoxib
med - diclofenac, naproxen
high - ketoprofen, piroxicam, pheylbutazone
v) they can be pro-thrombotic as they affect prostacyclin (inhibits plat agg therefore inhibitng it can cause plat agg)
OPIOID CLASSIFICATION
i) what plant does it come from?
ii) name two naturally occ compounds?
iii) name two semi synthetic compounds
iv) name two synthetic compounds
i) papaver somniferum
ii) codiene and morphine
ii) buprenorphine, dihydrocodiene, diamorphine, naloxone, oxycodone
iii) alfentanil, fentanyl A, methadone, pethidine, tramadol
MECH OF ACTION OF NSAIDS
i) which COX enzyme is constituatively active and which is inducible?
ii) which COX enzyme is it undesirable to inhibit? which drug inhibits this one?
iii) which COX does ibuprofen inhibit? which one does aspirin mostly inhibit?
iv) which COX does celecoxib inhibit?
v) how does inhibiting COX allow therapeutic effects? what causes the side effects?
vi) what does PGI2 (prostaglandin) do? what does TXA2 (prostacyclin) do?
i) COX 1 is constit and COX 2 is inducible
ii) undesirable to inhibit COX 1 - selectively inhibited by aspirin (targets thomboxane A2)
iii) ibuprofen inhibits both COX1 and 2, aspirin mostly does COX1
iv) celecoxib inhibits COX2
v) inhib COX > inhib PG synth which is responsible for inflam and pain
- also protects gastric mucosa, supports renal func, supports plat func hence side effects
vi) PGI2 causes vasodilation and inhib of plat aggregation
TXA2 causes v constric and stim plat agg
CASE HISTORY
i) what would be the best analgesic for someone with a fracture but a PMH if AF (takes apixaban)?
ii) what must be checked before giving this analgesic?
i) morphine = gold standard opioid
ii) check renal function > if ok give a low dose
OPIOID CAUTIONS
i) what must always be considered?
ii) which population may need reduced doses?
iii) which organ function must be checked? why? (2)
iv) name three contra indications for opioids
v) name four side effects? what is it good to prescribe alongisde them? (3)
vi) name three symptoms of overdose? what is given?
vii) what is long term use classed as? what can this lead to? what should be done?
i) allergy
ii) elderly pop
iii) check renal function > excretion
check hepatic function > metabolism
iv) acute resp syndrome, comatose patient, head injury
v) confusion, dizzy, drowsy, constipation, euphoria, hallucination, naurea, resp dep with high dose
- good to prescribe naloxone, laxatives and anti emetic
vi) OD > coma, drowsy, pin point pupils, resp dep
vii) long term is >3 months use
- can cause dependence and addiction
- gradually taper dose to reduce risk of withdrawal
TREATMENT OF GOUT
i) what should not be given to someone with acute gout (first MTPJ joint) with PMH of gout?
ii) what drug can be used in an acute gout attack if the patient has heart disease?
iii) what is first line treatment? when may this be contraindicated?
iv) is aspirin used to treat gout? why?
v) what is not used in an acute attack?
i) thiazide diuretics as they affect uric acid secretion]
ii) colchicine - good in CVD as it does not induce sodium and water retention
iii) high dose NSAID + gastro protection
- contra indic if HF or HT > give colchicine
iv) dont use aspirin because it reduces uric acid excretion
v) allopurinol is not used in an acute attack
NSAID SIDE EFFECTS
i) name three common side effects
ii) name four less common SEs?
iii) what airway problem may NSAIDs cause? why?
i) GI discomfort, nausea, diarrhoea, oesophagitis, gastritis, renal impair
ii) upper GI bleed, peptic ulcer, fluid reten (renal probs), increased BP, hypersens rash, angioedema, bronchospasm, headache, CV event
iii) can cause bronchospasm as they inhibit COX and shunt arach acid metab > causes prod of asthma causing cysteinul leucotrienes (stop AA conversion to cycloox therefore all AA is converted to lipoxygenase > leucotriene prod)
CASE HX - DRUG INTERACTIONS
i) patient with AF, asthma and depression > which drug is contrainidcated alongside an NSAID in this patient?
ii) name four main drugs that interact with NSAIDs and why
iii) name three patient groups that are at risk of NSAID related GI compliations?
iv) name three patient groups at risk of CV or renal adverse effects?
v) name two other patient groups at risk of NSAID complications
i) dabigatran (DOACs and VKAs are contraindicated with NSAIDs)
ii) anticoags > inc risk of GI bleed
ACEi > inc GI bleed risk and anti coag effect
Digoxin > inc plasma conc of dig, inc risk of HF and decrease renal func
Anti hypertensives > antag of hypotensive effect
iii) history of GI ulcers, aged >65yrs, multiple NSAIDs, on interacting drugs eg anticoag, SSRIs
iv) pts >65yrs, estab CVD (HF), hypertension, renal/hepatic impair
v) asthma/hypersens reacs, coag defects, pregnant or breastfeeding
