Pain medications (NSAIDs etc) Flashcards
NSAID indications
As needed for mild-moderate pain (e.g. dental, dysmenorrhoea)
Inflammation- MSK, RA, osteoarthritis, acute gout
NSAIDS MOA
Inhibits cyclo-oxygenase enzyme (COX) which inhibits the synthesis of prostaglandins from arachidonic acid
COX1 stimulates PGE synthesis (gastric mucosa, renal perfusion, inhibits clots)
COX-2: expressed in response to inflammatory stimuli. PGE which causes inflammation and pain
NSAIDs adverse reactions
- GI toxicity
- renal impairment
- increased CVS event (MI/stroke)
- hypersensitivity reactions
avoid in asthma, heart failure, liver failure, NSAID hypersensitivity, peptic ulcer disease, GI bleeding. meds such as anticoagulants, corticosteroids, aspirin
phospholipid -> aracodonic acid which gives
prostaglandin, thromboxane, leukotiene, PC
how are NSAID’s prescribed
taken orally (PO)
topical gels
suppositories
injectible preperations
regular treatment for at least 3 weeks is required.
acute pain: naproxen 250mg orally 6-8hrly as needed
ibuprofen 400mg
*if at risk of GI complications give PPI (lansaprozole 15mg daily)
types of NSAIDs
Ibuprofen
Naproxen
Etoricoxib
Paracetemol
first line analgesic for most forms of acute and phonic pain
antipyretic - can reduce fever and it’s associated symptoms (shivering)
MOA of paracetemol
poorly understod
weak inhibitor of COX- enzyme involved in prostaglandin metabolism
COX inhibition increases pain threshold and reduces PGE concentration
*weak anti inflammatory
paracetamol adverse effects
overdose- liver failure
metabolised by P45O enzyme into a toxic metabolite NAPQ (N-acetyl benzoquinonine? which is conjugated into glutathione. in a nOD this is saturated and NAPQI accumulates causing hepatocellular necrosis.
*treat with acetylcystine
paracetamol warnings
not indicated in liver toxicity, chronic excessive alcohol use, malnutrition, low body weight, severe hepatitisc imaprierment
important reactions of paracetemol
CYP inducers (phenytoin and carbamazepine) increase risk of NAPQI
how is paracetamol prescribed?
PO (orally)
IV infusion
rectal administration
0.5-1g every 4-6 hours
maximum of 4g daily
IV solution can be infused over 15 minutes or diluted in 0.9% saline chloride or 5% glucose solution before administation
regular/as required.
opioid examples
strong opioid:
morphine
oxycodone
weak opioid:
tramadol
codeine
dihydrocodeine
common indications for strong opioids
rapid relief of acute and severe pain including post-operative pain and pain associated with acute MI
relief of chronic pain (WHO ladder)
breathlessness (end of life care). breathlessness and anxiety in acute pulmonary oedema
strong opioids MOA
activation of opioid u receptors in the CNS (G couples receptors)reduces neuronal excitability and pain transmission
in the medulla, opioids blunt the response to hypoxia and hypercapnoea which reduces the rest drive and breathlessness.
reduces the sympathetic nervous system activity
(can reduce cardiac work and o2 demand)
adverse effect of opioids
respiratory depression (reduces respiratory drive) euphoria, detachement, neurological depression
activates the chemoreceptor trigger zone causing nausea and vomiting
pupillary constriction
large intestine - u receptor increases smooth muscle tone. reduces motility= constipation
skin= histamine= itching, urticaria, vasodilation, sweating
tolerance= dependence= withdrawal
important to consider age and GFR (do not give if GFR <50, give fentanyl insteaD)
strong opioid warning + reactions
! hepatic failure
! renal impairment
(opioids rely on the liver and kidneys for elimination)
! respiratory failure and reduced consciousness (sedation) . reverse with naloxone 400mg IV/subcut/IM
! biliary colic
do not give with other sedating drugs like antipsychotics, benzos, TCA’s
how are opioids prescribed
acute severe pain in high dependency areas
IV rapid effect
2-10mg initiall tailored to age and GFR
IM or SC
30mg PO 2-4 hrly 10mg IV (divide oral by 3 for IV dose)
chronic
oramorph 5mg orally every 4 hours
breakthoruh analgesia
immediate release morphien at a dose of 1/6th of the Toal daily dose.
features of opioid withdrawl
opposite of the clinical effect pain breathlessness increase anxiety pupils dilate skin is cool and dry with piloerection (cold turkey)
MOA of weak opioids
codeine and dihydrocodine are very weak opioids in their unmodified form. when they are metabolised by the liver they produce a relatively small amount of morphine (from codeine) or hydromorphine (from dihydrocodeine) which are stronger agonsit of opioid mu receptors.
tramadol is a synthetic analogue of codeine
tramadol MOA
synthetic analogue of codeine
moderate strength opioid
u receptor agonist
affects the serotonergic an adrenergic pathway where it is thought to act as a seretonin and noradrenaine reuptake inhibtor (SNRI)
adverse effect of weak opioids
nausea, constipation, dizziness, drowsiness
neurological and respiratory depression
caution with resp dsease renal impairment hepatic imapriment elderly tramadol lowers seizure threshold do not give with other sedsating drugs
how are weak opioids perscribed?
PO. regular / as required.
codeine / dihydrocodeine 30mg orally 4hrly
tramadol 50mg orally 4hrly (400mg max/day)
+ laxative e.g. senna
co/codamol means 8/500 so 8mg of codeine and 500mg of paracetemol.
co-dydramol 10/500mg contians 10mg of codeine, 500mg of paracetemol.
gabapentin and pregabalin indication (pain)
(focal epilepsy - not for absence or myoclonic seizures)
- first line for neuropathic pain including painful diabetic neuropathy. (trigeminal neuralgia= carbamezapine)
- GAD (pregabalin)
gabapentin and pregabalin MOA
related to GABA (the major inhibitory neurotransmitter in the brain)
bind to pre-synaptic voltage sensitive calcium channels which inhibits hthe release of excitatory neurotransmittors thus reuslting in a reduction of neuronal excitabiltiy. (in brain and perpiheralnerves)
gabapentin and pregabalin
- side effects
- warning
- contraindications
side effects- drowsy, dizzy, ataxia
warning- renal impairment (eliminated via kidneys)
enhanced when combined with sedating drugs
how are pregabalin/gabapentin perscribed?
start low dose and increase over days/weeks
lidocaine indication
1st choice local anaesthetic (catheterisation, minor procedures like suturing)
antiarrhythmic drug (VT) (uncommon)
alternative to lidocaine is Bupivacaine (8-16hrs) (lidocaine lasts 2-4 hrs)
lidocaine MOA
enters cells in it’s unchanged form then accepts a proton and becomes positively charged. once it’s inside the celll it blocks the voltage-gated SODIUM channels on the surface which prevents initiation and propogation of the action potentials in nerves and muscles.
in the heart it reduces duration of AP, slows conduction elocity and increases refractory period (Can terminate VT)
lidocaine side effects, warning and important reactions
side effects- stinging sensation during local adminisration.
neuro- drowsy, restless, tremor, fits
little cvs toxicity but overdose can cause hypotension and arrythmias
reduced CO
if given into plasma (toxicity) CVS arrhythmias, asystole, PEA (pulseless electrical activity), low CO and low BP
if CNS- seizres LOC
reverse with intralipid antidote. lidocaine is lipid soluable (that’s how it gets into the cell) so when you give intralipid it causes the LA to ‘sink’ into it
how is lidocaine prescribed?
minor procedure: 1% 10mg/mL of lidocaine hyrochloride
maximum dose is 200mg or 3mg/kg
for urinary catheterisation- gel with antiseptic agent such as chlorhexidine in pre-filled syringes (6-1mL)
PCA
patient controled analgesia
bolus dose is 1mg
lockout period is 5 min (after each dose they can’t have another one for five mins)
background (never give this)
fentanyl
only licenced in cancer pain
can give if not suitable for morphine (e.g if GFR <50)
does not work orally
same complicatoins as morphine
epidural
rectus sheath
errectar spina for rib frcure?
canhit CSF (dural headache)
can damage nerve route
can cause bleeding (epidural haematoma), compression of spinal cord= neuropathic pain.
- epidural abscess (fever, malaise, neuropathic pain, 5-10 days after the event)
