pain/MSK Flashcards
NSAIDs
- examples? 3
- mechanism of action?
- ibuprofen
- naproxen
- diclofenac
Inhibits COX-2 (and a bit of COX-1)
- inhibits prostaglandins that cause pain
- breaks down gastric mucosa
- pro-thrombotic
- constrict afferent arteriole of renal glomeruli
Nb selective COX-2 inhibitors (eg etoricoxib) were developed to attempt to reduce adverse effects of NSAIDs
- but have increased risk of cardiovascular events…
NSAIDs
- examples?
- two groups of indications?
- ibuprofen
- naproxen
- diclofenac
1) ‘as needed’ for mild-moderate pain (as an alternative to paracetamol, but paracetamol preferred as fewer side effects)
2) regular treatment for pain related to inflammation (particularly MSK and rheumatological)
NSAIDs
- main groups of side effects? 3
- other adverse effects? 2
- which associated with least side effects?
- way of decreasing risk of side effects?
GI toxicity
- indigestion
- ulcers
- bleeds
Renal impairment
- dt constriction of afferent arterioles
CV thrombotic events
- increased risk
- hypersensitivity reaction (angioedema + bronchospasm)
- fluid retention
- ibuprofen least likely to have side effects
Prescribe a PPI
- elderly
- previous PUD
- long term use
- comorbidities
- on other drugs with GI effects
NSAIDs
- absolute contraindications? 4
- relative contraindications? 4
+ severe renal impairment
+ heart failure
+ liver failure
+ known NSAID hypersensitivity
- prior PUD
- GI bleeding
- cardiovascular disease
- renal impairment
Use safest NSAID for shortest possible time
NSAIDs
- interactions which increase risk of GI ulcers? 2
- interactions which increase risk of GI bleeding? 3
- interactions which increase risk of renal impairment? 2
GI ulcer risk
- aspirin
- corticosteroids
GI bleed risk
- anticoagulants
- SSRIs
- venlafaxine
Renal impairment
- ACEi
- diuretics
Nb also NSAIDs reduce therapeutic effects of antihypertensives + diuretics
NSAIDs
- when to take?
- commonest side effect?
- how long to take for acute pain?
- take with food
- indigestion (stop if get and see doc!!)
- take for max 10 days (see doc if pain continues)
weak opiods:
- examples? 3
- mechanism of action?
- main indication?
- tramadol
- codeine
- dihydrocodeine
metabolised in the liver to produce relatively small amounts of morphine
- opiod receptor agonist
nb tramadol is a synthetic analogue of codeine and slightly stronger and probably work on other neurotransmitter pathways as well
1) for mild-moderate pain, second line when paracetamol is insufficient (second rung of pain ladder)
weak opiods:
- examples? 3
- common side effects? 4
- effects of overdose? 2
- tramadol
- codeine
- dihydrocodeine
- constipation
- nausea
- dizziness
- drowsiness
neurological + respiratory depression in overdose
nb tramadol may cause less constipation + respiratory depression than other opiods
weak opiods:
- examples? 3
- relative contraindications for all? 4
- relative contraindication for tramadol? 1
- absolute contraindication for tramadol? 1
- tramadol
- codeine
- dihydrocodeine
- significant respiratory disease
- renal impairment
- hepatic impairment
- elderly
tramadol lowers seizure threshold
- ideally avoid in epilepsy
+ absolutely contraindicated in uncontrolled epilepsy
weak opiods:
- examples? 3
- interaction for all? 1
- interaction for tramadol? 1
- tramadol
- codeine
- dihydrocodeine
other sedating drugs
- antipsychotics
- benzodiazepines
- tricyclic antidepressants
tramadol: other drugs that lower seizure threshold:
- SSRIs
- tricyclic antidepressants
weak opiods:
- which route should codeine + dihydrocodeine NOT be given via?
- what should be prescribed alongside them for regular administration?
- what side effects to warn patients about?
IV (nb can give IM, normally in theatre)
- can give a severe reaction, similar to anaphylaxis, mediated by histamine but not an allergic reaction
- laxatives (normally a stimulant laxative, such as senna)
drowsy/confused
- avoid driving or operating heavy machinery if feel this!
strong opiods:
- examples? 2
- mechanism of action?
- morphine
- oxycodone
activation of opiod receptors
- reduce neuronal excitability + pain transmission
- in the medulla, blunt response to hypoxia + hypercapnoea, reducing resp drive + breathlessness
- reduce sympathetic response to pain, thus reduce cardiac activity + oxygen demand
nb oxycodone is synthetic analogue of morphine
strong opiods:
- examples? 2
- two indications for pain relief?
- two other indications?
- morphine
- oxycodone
1) rapid relief of acute severe pain (incl post-op pain + acute MI)
2) relief of chronic pain (where paracetamol, NSAIDs + weak opiates are insufficient) - rung 3 of WHO pain ladder
3) relief of breathlessness in end-of-life care
4) relieve breathlessness + anxiety in acute pulm oedema
- alongside oxygen, furosemide + nitrates
strong opiods:
- examples? 2
- common side effects? 7
- symptoms of withdrawal reaction, if dependent? 5
- morphine
- oxycodone
- respiratory depression
- euphoria + detachment (neurological depression in high doses)
- nausea + vomiting
- pupillary constriction (edinger-westphal nucleus)
- constipation
- itching/urticarial/vasodilation + sweating (dt histamine release)
- tolerance + dependence (prolonged use)
opposite effects to clinical use:
- anxiety
- pain
- breathlessness
- dilated pupils
- cool + dry skin with piloerection (‘cold turkey’)
strong opiods:
- examples? 2
- relative contraindications? 5
- oxycodone
- morphine
- hepatic failure
- renal failure
- resp failure (generally only give if palliative)
- elderly
- biliary colic (as may cause spasm of sphincter of odi -> more pain)
strong opiods:
- examples? 2
- relative contraindication? (3 examples)
- morphine
- oxycodone
other sedating drugs
- antipsychotics
- benzodiazepines
- tricyclic antidepressants
strong opiods:
- what to co-prescribe when first prescribing?
- what else to co-prescribe?
- what to warn patients about?
- antiemetic (eg metoclopramide)
- laxative (eg senna)
- not to drive or operate heavy machinery if feel drowsy or confused
nb warn patients that may have to increase dose as body becomes tolerant but not to be alarmed
also, if for long term relief often prescribe modified release tablets and then oramorph for breakthrough pain
paracetamol:
- mechanism of action?
- main indications? 2
poorly understood
- weak COX-2 inhibitor (so less side effects than NSAIDs, though doesn’t seem to have same anti-inflammatory effects)
- probably another mechanism of action too
1) first line analgesic (rung 1 of WHO analgesia ladder)
2) antipyretic (reduces fever + associated symptoms - eg shivering)
paracetamol:
- side effects?
- effects of overdose?
- mechanism of overdose?
- treatment for overdose? (incl drug name)
few side effects
acute liver failure
normally metabolised by cytochrome P450 enzymes to a toxic metabolite (N-acetyl-p-benzoquinone imine - aka NAPQI)
- this is norm conjugated with glutathione (makes safe) before excretion
- in overdose, this elimination pathway is saturated + NAPQI accumulation -> hepatocellular necrosis
a glutathione precursor (acetylcysteine)
paracetamol:
- relative contraindications? 4 (incl reasons)
dose should be reduced in people at increased risk of liver toxicity
eg increased NAPQI production
- chronic excessive alcohol use
eg reduced glutathione stores
- malnutrition
- low body weight (<50kg)
- severe liver impairment
nb this is especially important when drug is given IV
paracetamol:
- drugs which shouldn’t be given after overdose?
cytochrome P450 INDUCERS
- eg phenytoin + carbamazepine
as these will increase the rate of NAPQI production + thus increase risk of liver toxicity
paracetamol:
- what to always make clear to patients?
- what should patients NOT take when on paracetamol?
- exactly how often to take it and what maximum daily dose is!
- check ingredients of OTC cold + flu remedies etc to ensure not accidently overdosing
- similar issue with co-codamol
xanthine oxidase inhibitors:
- main example?
- mechanism of action?
- main indications? 3
allopurinol
xanthine oxidase normally metabolises xanthine (produced from purines) to uric acid
- allopurinol inhibits this enzyme -> lower plasma uric acid concentrations
- therefore reducing precipitation of uric acid in the joints or kidneys
1) prevent acute attacks of gout
2) prevent uric acid + calcium oxalate renal stones
3) to prevent hyperuricaemia + tumour lysis syndrome associated with shemotherapy
xanthine oxidase inhibitors:
- main example?
- most common side effect?
- serious adverse effect?
- effect on acute attack of gout?
allopurinol
- skin rash (may be mild or rarely start of more serious reaction…)
hypersensitivity syndrome
- steven-johnson syndrome or toxic epidermal necrolysis
starting allopurinol can trigger or worsen an acute attack of gout
