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Year 3 Drug > MSK/Pain > Flashcards

MSK/Pain Flashcards

1
Q

what does NSAIDs stand for

A

Non-sterioidal anti-inflammatories

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2
Q

example for NSAIDs

A

Diclofenac, Naproxen (oral/topical), Ibuprofen, Etoricoxib

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3
Q

how does NSAIDs work

A

inhibit the prostaglandin synthesis by reducing cyclooxygenase (COX) mainly COX 2

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4
Q

what are the 2 isoforms of cyclooxygenase

A

COX 1 - constitutive form (always there) - stimulate prostaglandin synthesis which is essential to preserve integrity of gastric mucosa, maintain renal perfusion (by dilating afferent glomerular arterioles) and inhibit thrombus formation at the vascular endothelium

COX 2 - inducible form - expressed in response to inflammatory stimuli - stimulate production of prostaglandin which cause inflammation and pain

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5
Q

indication for NSAIDs

A

midl-moderate pain as required (alternative for paracetamol)

regular treatment for pain related to inflammation particularly of the MSK eg RA, severe OA

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6
Q

contra-indication for NSAIDs

A 
severe renal impairment 
HF 
LF
peptic ulcer disease 
GI bleeding 
cardiovascular disease 
renal impairment
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7
Q

where is NSAIDs eliminated from the body

A

liver

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8
Q

Side effect of NSAIDs

A

GI toxicity
renal impairment
inc risk of CV events
fluid retention

different NSAIDs have different side effects - non-selective COX 2 inhibitor have a greater risk than selective for CV event

Non-selective NSAIDs - lowest CV risks are ibuprofen and naproxen

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9
Q

interaction of NSAIDs

A

many drugs can cause increase adverse effect of NSAIDs

GI ulceration - low-dose aspirin, corticosteroid
GI bleeding - anticoagulants, SSRIs, venlafaxine (SSNRI)
renal impairment - ACE inhibitors, diuretics
in risk of bleeding - warfarin, reduce the therapeutic effects of antihypertensives and diuretics

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10
Q

how should pt take NSAIDs

A

with meals ideally with PPIs

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11
Q

what is an example of weak opioids

A

tramadol, codeine, dihydrocodeine

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12
Q

how does weak opioids work

A

so weak opioids like codeine and dihydrocodeine is metabolised in the liver and produce a small amount of morphine or dihydromorphine

they are agonist of opioid mu receptors

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13
Q

who might find codeine and dihydrocodeine ineffective ?

A

10% of white caucasians

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14
Q

what has been described as moderate opioids

A

tramadol which is a synthetic analogue of codeine

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15
Q

how does tramadol work

A

same as codeine but also work on serotonergic and adrenergic pathway and act as a serotonin and noradrenaline reuptake inhibitor

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16
Q

how does opioid mu receptor work

A

activation of this receptor in the CNS will reduce neuronal excitability and plain transmission

in medulla, reduce the response of hypoxia and hypercapnoea reducing the respiratory drive and breathlessness

by relieving pain, breathlessness and associated anxiety, opioids reduce sympathetic nervous system (fight or flight) activities

this in turn reduces the cardiac work and oxygen deman as well as relieving symptoms

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17
Q

what are examples of strong opioids

A

morphine (natural) and oxycodone (synthetic)

18
Q

indication for opioids

A
  • acute severe pain (post-op, MI pain)
  • chronic pain - the highest in the analgesia ladder
  • for relief of breathlessness in the context of end-of-life care
  • relieve breathlessness and anxiety in acute pulmonary oedema
19
Q

contra-indication of opioids

A

mos t opioids rely on liver and kidney for elimination so doses should be recued in HepF and RenF and in elderly

do not give opioids in resp filure except under seniro guidance

avoid opioids in biliary colic - may cause spasm of sphincter of ODDi

20
Q

side-effect of opioids

A

resp depression (reducing resp drive)
may cause euphoria (excitment) and detachment and in high doses, neurological depression
trigger CTZ - nausea and vomiting
pupillary constriction (due to stimulation)
reduce motility - constipation (activation of opioids mu receptors
skin - may cause histamine release - itching, urticaria, vasodilation and sweating
continue use lead to tolerance and dependance and withdrawal reaction

21
Q

where is opioids eliminated in the body

A

liver and kidney

22
Q

interaction of opioids

A

should not be used with other sedative drugs eg antipsychotics, benzodiazepines, tricyclic antidepressants)

23
Q

pt info on opioids ?

A

constipation is v. common - take with laxative and good hydration

24
Q

what is the class name for opioids

A

opiate

25
Q

what is the class name for paracetamol

A

paracetamol

26
Q

indication for paracetamol

A

first-line analgesia for most form of acute and chronic pain

also a antipyretic which reduced fever

27
Q

MOA for paracetamol

A

poorly understood

weak inhibitor for COX 2
also a weak anti-inflammatory

28
Q

interaction for paracetamol

A

should be reduced in ppl with liver failure
avoid use with P450 cytochrome inducer eg phenytoin
inc rate of production of NSAIDs and risk of liver failure

29
Q

contra-indication for paracetamol

A

should be reduced in ppl with inc risk of liver failure (either due to NAPQI - toxic substance which is almost de-toxicify by liver - eg in chronic excessive alcohol use or reduced glutathione stores eg in malnutrition, severe hepatic impairment)

30
Q

side-effect of paracetamol

A

v.safe and few side-effect

overdose - liver failure (after LF, NAPQI conc inc and accumulate and cause hepatocellular necrosis)

31
Q

where is paracetamol eliminated

A

liver

32
Q

pt info for paracetamol

A

importance of taking it 6 hourly not before otherwise overdose

other drug also contain paracetamol so need to watch out for that

33
Q

example of an xanthine oxidase inhibitor

A

allopurinol

34
Q

main indication for allopurinol

A

prevent acute attack of gout
prevent uric acid and calcium oxalate renal stones
prevent hyperuricaemia and tumour lysis syndrome associated with chemo

35
Q

MOA for xanthine oxidase inhibitors, allopurinol

A

xanthine oxidase metabolises xanthine (produced from purines) to uric acid

inhibition of xanthine oxidase lowers plasma uric acid conc and reduces precipitation of uric acid in joint and kidney

36
Q

contra-indication for allopurinol

A

should not be started during an acute attack of gout but can continue if a pt is already established on it to avoid sudden fluctuations in serum uric acid levels

dose should be reduced in pt with severe renal impairment or hepatic impairment

37
Q

where is allopurinol metabolised and eliminated

A

metabolised in liver and eliminated in kidney

38
Q

side effects of allopurinol

A

common - skin rashes which maybe mild or severe which can indicate for Stevens-Johnson Syndrome or toxic epidermal necrolysis

start can trigger or worsen an acute attack of gout

39
Q

interaction of allopurinol

A

interaction with cytotoxic drugs such as mercaptopurine and pro-drug azathioprine as they require xanthine oxidase for metabolism - allopurinol inhibits their metabolism and inc risk of toxicity

with amoxicillin - inc risk of skin rash
with ACEs or thiazides - inc risk of hypersensitivity reaction

40
Q

pt info for allopurinol

A

advise pt to seek medical advice if they develop a rash

Year 3 Drug (12 decks)

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