Pharmacology Flashcards

1
Q

What is the function of paracetamol?

A

pure analgesic with little anti-inflam action

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2
Q

What is step 1 in the pain pathway?

A

non-opiod +/- adjuvant

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3
Q

What is sstep 2 in the pain pathway?

A

weak opiod =/-non-opioid +/- adjuvant

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4
Q

What is step 3 in the pain pathway?

A

strong opioid +/- non-opioid +/- adjuvant

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5
Q

What is the first line NSAID in Tayside?

A

naproxen

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6
Q

What are the indications for NSAIDs?

A

inflammatory arthritis; mecahnical MSK pain; pleuritic/pericardia lpain

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7
Q

What are the GI SE of NSAIDs?

A

dyspepsia; oesophagitis; gastritis; peptic ulcer; small/large bowel ulceration

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8
Q

What are the other SE of NSAIDs?

A

renal impairment; increased CVS events; fliud retention; wheeze (exacerbation of asthma); rash

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9
Q

What are COX-2 inhibitors?

A

NSAIDs which selectively target Cyclooxygenase-2 which is an enzyme responsible for inlfam and pain

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10
Q

What the benefits and risks of COX-2 inhibitors?

A

reuces the risk of peptic ulceration but increases CVS risk

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11
Q

What are the actions of DMARDs?

A

pure anti-inflammatory with no direct analgesice effect; reduce rate of joint damage

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12
Q

What is the aim for DMARD therapy in RA patients?

A

to start therapy within 3 months of symptom onset

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13
Q

What are the commonly used DMARDs?

A

methotrexate; sulphasalazine; leflunomide; hydroxycholoquien

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14
Q

What is the mode of action of methotrexate?

A

folate antagonist

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15
Q

What are the 2 routes of administration for methotrxate?

A

orally and subcut

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16
Q

What diseases is methotrexate used to treat?

A

RA; psoriatic arthritis; connective tissue disease; vasculitis

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17
Q

What are the SE of methotrexate?

A

leucopenia/thrombocytopenia; hepatitis/ cirrhosis; penumonitis; rash/mouth ulcers; nausea/diarrhoea

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18
Q

When must methotrexate be stopped?

A

teratogenic- so must be stopped in BOTH males and females at least 3 moths before conception

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19
Q

Why is methotrexate used more frequently then sulfasalazine when both are first line?

A

methotrexate works quicker and is better tolerated

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20
Q

Why is started RA patients on DMARDs ASAP imprtoant?

A

theres only a limited time to reduce inflam before joint function cannot be recovered

21
Q

How can the SE of methotrexate be modified?

A

changing the mode of action: PO/ injection

22
Q

How long after stopping leflunomide can patients get pregnnat?

A

at least 2 years

23
Q

What are the adverse effects of sulfasalzine

A

nausea; rash/mouth ulcers; neutropenia; hepatitis; reversible oligozoospermia

24
Q

What is the very serious skin condition that can be caused by sulfasalazine?

A

Stevens-Johnson syndrom

25
Q

What is HCQ used for?

A

connective tissue disease such as SLE; Sjogrens and RA

26
Q

What is the action of HCQ?

A

no effect on joint damage?

27
Q

What is the SE of HCQ?

A

retinopathy

28
Q

Name an anti-TNF drug?

A

inflixumab

29
Q

What is the benefit of biologics compared to DMARDs?

A

1.5x more effective than DMARDs

30
Q

When are biologics used in patients with RA?

A

when they have a high disease activity score and have already used methotrexate

31
Q

What are anti-TNFs licensed for?

A

RA; psoriatic arthritis and ank.spon

32
Q

How are anti-TNFs give?

A

subcut

33
Q

What are hte SE of anti-TNFs?

A

risk of infection; increase risk of skin cancer; exacerbate heart failure

34
Q

What must be screened for before commencing anti-TNF therapy?

A

TB

35
Q

What is the action of secukinimab?

A

inhibits IL17

36
Q

What is rituximab?

A

monocolonal antibody against B cells

37
Q

How is gout treated actuely?

A

colchicine; NSAIDs; steroids either oral or IM

38
Q

What is the common SE of colchicine?

A

diarrhoea

39
Q

What are hte urate lowering drugs availbale?

A

allopurinol; febuxostat; uricosurics

40
Q

What are the actions of allopurinol and febuxostat?

A

block xanthine oxidase whic hconverts xanthine to uric acid

41
Q

Why must allopurinol not be started during an acute attack of gout?

A

may result in an exacerbation of gout due to the rapid reduction in uric acid level

42
Q

When is the rash caused by allopurinol made more likely?

A

in the elderly and in renal impairment

43
Q

What is the serious SE of allopurinol?

A

marrow aplasia

44
Q

What drug must never be used at the same time as allopurinol?

A

azathioprine

45
Q

When is febuxostat used?

A

in patients who cannot tolerate allopurinol

46
Q

In what patients should febuxostat be used caustiously?

A

in those with IHD

47
Q

What diseases are steroids indicated for?

A

connective tissue disease; PMR/ GCA; vasculitis; RA

48
Q

What are the SE of steroids?

A

weight gain- centripetal obesity; muscle wasting; skin atrophy; osteoporosis; diabetes; HT; cataracts; glaucoma; fluid retention; adrenal suppression; immunosuppression; avascular necrosis of femoral head

49
Q

How is allopurinol treatment started/managed?

A

6 weeks after acute flare; blood urate levels and PMHx asked about; allopurinol started and after 6 weeks urate levels checked again and dose changed; continues til urate levels are below 360mcg/L