Pharmacology Flashcards

1
Q

function and examples of NSAIDS

A

anti-inflammatory + Analegesic

e.g. Ibuprofen, Naproxen, Diclofenac

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2
Q

mode of action of NSAIDs

A

target cyclooxygenase-2, an enzyme responsible for inflammation and pain

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3
Q

how can the risk of peptic ulcers in NSAIDs be reduced

A

Targeting COX-2 selectively

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4
Q

side effects of NSAIDS

A
Dyspepsia
Oesophagitis
Gastritis
Peptic Ulcer
Small/large bowel ulceration
Renal impairment
Increased cardiovascular events (Cox 2 inhibitors + others)
Fluid retention
Wheeze
Rash
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5
Q

function of DMARDs

A

anti-inflammatory with no direct analgesic effect
improve standard lab tests of inflammation e.g. ESR CRP
Reduce rate of joint damage
slow acting - weeks to months

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6
Q

what is the first choice DMARD in most patients

A

Methotrexate

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7
Q

what drug is a folate antagonist

A

Methotrexate

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8
Q

side effects of methotrexate

A
Leucopenia / thrombocytopenia 
Hepatitis / cirrhosis (alcohol intake must be limited)
Pneumonitis
Rash / mouth ulcers
Nausea / diarrhoea
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9
Q

what needs monitored in methotrexate

A

FBC

LFTs

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10
Q

can methotrexate be given in pregnancy

A

no
it is teratogenic
must be stopped in male and females at least 3 months before conception

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11
Q

what are side effects of sulfasalazine

A
Nausea
Rash / mouth ulcers
Neutropenia
Hepatitis
Reversible oligozoospermia
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12
Q

what needs to be monitored in sulfasalazine

A

FBC

LFTs

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13
Q

Hydroxychloroquine can be used to prevent joint damage - true or false

A

false
has no effect on joint damage
used in CTDs e.g. SLE, Sjogren’s syndrome, RA

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14
Q

side effects of Hydroxychloroquine

A

retinopathy

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15
Q

what are other less common DMARDS and their side effects

A

Sodium aurothiomalate (gold) given IM. Adverse effects – bone marrow suppression, glomerulonephritis, rash , mouth ulcers. Monitor FBC plus urine for proteinuria.

Penicillamine oral, adverse effects as for IM gold

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16
Q

what are anti-TNF drugs

A

Etanercept
Adalimumab
Certolizumab
Infliximab

17
Q

what is the comparison of anti-TNF to DMARDs

A

About 1.5 times as effective as standard DMARDs
More effective in combination with DMARDs
~£10,000 per annum
Majority given by sub-cutaneous injection

18
Q

what can anti-tnf be used in

A

RA
Psoriatic arthritis
AS

19
Q

adverse effects of Anti-TNF

A

Major risk of infection (esp TB)
Question over risk of malignancy (esp skin cancer)
Contraindicated in certain situations e.g. pulmonary fibrosis, heart failure

20
Q

criteria for anti-TNF treatment

A

high disease activity score

use of previous standard DMARDs

21
Q

examples of other biologics (not anti-TNF)

A

Rituximab - monoclonal antibody against B (CD20) lymphocytes
Tocilizumab – inhibits Interleukin 6
Abatacept - CTLA-4 Ig -blocks full activation of T lymphocytes
Ustekinumab – Inhibits IL12 and IL23

22
Q

what is the treatment of acute episode of gout

A

Colchicine (can cause diarrhoea and vomiting)
NSAIDs
Steroids

23
Q

gout prophylaxis treatment

A

Urate lowering:

  • allopurinol
  • febuxostat
  • uricosurics
24
Q

what is the process of making uric acid in the body

A
Purine 
>>>>
Xanthine
>>>> Xanthine oxidase
Uric acid
25
Q

what does allopurinol and febuxostat target

A

xanthine oxidase

26
Q

why is allopurinol not commenced during acute episodes

A

Rapid reduction in uric acid level may result in exacerbation of gout

27
Q

side effects of allopurinol

A

Rash (vasculitis) commoner in elderly and in renal impairment, therefore use lower doses

28
Q

who gets febuxostat

A

those who cannot tolerate allopurinol i.e. those with renal impairment

29
Q

examples of uricosurics

A

Probenecid
Sulphinpyrazone
Azapropazone
Benzbromarone

30
Q

what rheumatogical diseases are steroids used in

A

CTD
PMR/GCA
Vasculitis
RA

31
Q

metabolic effects of steroids

A

Salt and water retention
Increased gluconeogenesis
Increased hepatic glycogen deposition
Increased protein breakdown

32
Q

side effects of steroids

A
Weight gain - centripetal obesity
Muscle wasting
Skin atrophy
Osteoporosis
Diabetes
Hypertension
Cataract
Glaucoma
Fluid retention
Adrenal Suppression
Immunosuppression
Avascular necrosis of the femoral head
33
Q

how can corticosteroids toxicity be reduced

A

Use lowest possible dose for as short a time as possible
Consider steroid sparing agents
Osteoporosis prophylaxis
Watch cardiovascular risk factors