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
what does allopurinol and febuxostat target
xanthine oxidase
26
why is allopurinol not commenced during acute episodes
Rapid reduction in uric acid level may result in exacerbation of gout
27
side effects of allopurinol
Rash (vasculitis) commoner in elderly and in renal impairment, therefore use lower doses
28
who gets febuxostat
those who cannot tolerate allopurinol i.e. those with renal impairment
29
examples of uricosurics
Probenecid Sulphinpyrazone Azapropazone Benzbromarone
30
what rheumatogical diseases are steroids used in
CTD PMR/GCA Vasculitis RA
31
metabolic effects of steroids
Salt and water retention Increased gluconeogenesis Increased hepatic glycogen deposition Increased protein breakdown
32
side effects of steroids
``` 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
how can corticosteroids toxicity be reduced
Use lowest possible dose for as short a time as possible Consider steroid sparing agents Osteoporosis prophylaxis Watch cardiovascular risk factors