Chapter 10 - Musculoskeletal Flashcards
Why do patients on methotrexate (for non malignant indications, e.g. Crohns, RA) take folic acid?
Methotrexate inhibits dihydrofolate reductase the enzyme responsible for reducing dihydrofolate to tetrahydrate folate (co factor in thymidylate synthesis - purines) this can result in various side effects (ab pain, diarrhoea, GI bleeding, malaise, nausea, visual disturbances are a few of many) due to affecting DNA synthesis.
Folic acid reduces the incidence of these.
Why would you refer a patient experiencing:
Sore throat, mouth ulcers, bruising
N+V, ab discomfort, dark urine
Breath shortness, dyspnoea, cough, fever
Respiratory effects including shortness of breath could be signs of pulmonary toxicity, referral needed if above and if pneumonitis suspected - discontinue
Liver issues such as cirrhosis
Could be signs of infection due to reduced immune response
Why can you use Colcichine in acute gout attacks in patients with heart failure?
It does not induce fluid retention.
*Can also be used in patients on anticoagulants as it doesn’t increase bleeding risk
Why would you preferentially recommend paracetamol over NSAIDs in the elderly?
Increased risk of GI ulceration in the elderly.
What patients groups would you use NSAIDs with caution?
Hypertension Oedema CVD risk factors Left ventricular dysfunction cardiac impairment Renal impairment?
Why would you choose NSAIDs over paracetamol in RA and advanced osteoarthritis?
As well as analgesic effects, regular full dosing gives anti-inflammatory action.
Why wait 3 weeks before switching to another NSAID?
Although pain relief occurs rapidly full anti-inflammatory effects can take 3 weeks, if no respond choose another (60% of patients will respond to any NSAID.
Naproxen and Tenoxicam have similar activity / tolerance, in what situation would you prefer Tenoxicam?
Tenoxicam has a longer half life so may be more of benefit in patients requiring once daily dosing (for example adherence issues)
Why would you avoid giving Aspirin with Cox2 selective inhibitors (Parecoxib, Etoricoxib, Celecoxib)
The benefit of reduced GI issues from use COX2 inhibitors is offset by the increased bleed risk/ GI ulceration from even low dose aspirin.
What NSAIDS are associated with highest CVD risk?
All the Cox2 (Parecoxib, Etoricoxib, Celecoxib), 150mg Diclofenac daily and over 2.4g Ibuprofen daily is associated with increased CVD risk (stroke and MI) especially if long term
What NSAIDs have increased GI side effects and should be used with caution in at risk groups?
Piroxicam (2nd line by specialist for RA, osteoarthritis, ankylosing spondylitis at under 20mg daily), ketoprofen, ketorolac
Why do we ask if a patient buying NSAID OTC if they have asthma?
NSAIDs are associated with asthma worsening (so could cause bronchospasm)
Why advise a patient on NSAIDs to limit alcohol intake to 2 units a day?
Increased risk of GI haemorrhage and also acute kidney damage is associated with NSAIDs and alcohol being combined.
Why would you use NSAIDs with caution in cardiac impairment and IBD?
These may worsen or exacerbate UC and Crohn’s disease and may lead to renal impairment affecting the heart.
Why would you counsel a patient taking NSAIDs for the first time to look out for signs of asthma (cough, bronchospasm), angioedema (flushing, red skin), urticaria (itching), rhinitis( runny nose)?
All these can be precipitated by taking an NSAID
Common side effects of NSAIDs?
Fluid retention
GI disturbances
Diarrhoea
Rashes
Why advise pregnant mothers to avoid NSAIDs in pregnancy (including topical)?
Increase risk of foetal ductus arteriosus closure in utero and possible persistent pulmonary hypertension following birth as well as possibly increase both the onset and duration of Labour
Why monitor renal function and electrolytes in renal failure?
Sodium and fluid retention can lead to reduced renal function and possibly failure.
Why should oral Piroxicam be restricted to use by an experienced specialist as a second line for osteoarthritis, RA and Ankylosing Spondylitis at a dose under 20mg and reviewed within 2 weeks?
Oral (not topical) Piroxicam has the aforementioned restrictions as it has a increased risk of SJS and other serious skin conditions like toxic epidermal necrolysis and GI side effects / bleeds.
A GI protectant may therefore be considered.
Why can Trimethroprin and proguanil/ pyrimethamine increase risk of side effects when taken with methotrexate?
Act via a similar mechanism - dihydrofolate reductase inhibition.
Why is it important to continually confirm a patients methotrexate dose, frequency, tablet strength and enquiry about health issues?
Due to risk of various toxicities, blood disorders presenting as sore throat, mouth ulcers, bruising. Liver toxicity presenting as NV, abdominal discomfort, dark urine. Respiratory toxicity presenting as SoB, dyspnoea, cough and fever.
GI toxicity first presenting as stomatitis
It is contraindicated in infection so signs of this require referral.
Why monitor FBC on methotrexate?
To check for clinically significant bone marrow suppression, in which the risk increases with age / renal impairment and if on Trimethropin
Why is contraception required for patients on methotrexate and for 3 months after course finished?
Should be avoided in pregnancy due to teratogenicity.
Why would a patient on methotrexate prescribed the following require possible intervention?
NSAIDs
PPIs
Retinoids
Trimethropin
Quinolones
Sulfamethoxazole/Sulfadiazine/Sulfadoxine
Others…
NSAIDs, retinoids Trimethropin, Penicillins, Quinolones all increase risk of toxicity so would be avoided (except NSAIDs in which dose monitoring and reduction appropriate)
PPIs reduce clearance so use with caution or avoid.
Sulfa’s increase exposure so use caution or avoid.
Caution in hepatotoxic, nephrotoxic, myelosuppressive or drugs that increase risk of thromboembolism.
