Chapter 10 - Musculoskeletal Flashcards

1
Q

Why do patients on methotrexate (for non malignant indications, e.g. Crohns, RA) take folic acid?

A

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.

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2
Q

Why would you refer a patient experiencing:
Sore throat, mouth ulcers, bruising

N+V, ab discomfort, dark urine

Breath shortness, dyspnoea, cough, fever

A

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

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3
Q

Why can you use Colcichine in acute gout attacks in patients with heart failure?

A

It does not induce fluid retention.

*Can also be used in patients on anticoagulants as it doesn’t increase bleeding risk

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4
Q

Why would you preferentially recommend paracetamol over NSAIDs in the elderly?

A

Increased risk of GI ulceration in the elderly.

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5
Q

What patients groups would you use NSAIDs with caution?

A
Hypertension
Oedema
CVD risk factors
Left ventricular dysfunction
cardiac impairment 
Renal impairment?
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6
Q

Why would you choose NSAIDs over paracetamol in RA and advanced osteoarthritis?

A

As well as analgesic effects, regular full dosing gives anti-inflammatory action.

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7
Q

Why wait 3 weeks before switching to another NSAID?

A

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.

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8
Q

Naproxen and Tenoxicam have similar activity / tolerance, in what situation would you prefer Tenoxicam?

A

Tenoxicam has a longer half life so may be more of benefit in patients requiring once daily dosing (for example adherence issues)

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9
Q

Why would you avoid giving Aspirin with Cox2 selective inhibitors (Parecoxib, Etoricoxib, Celecoxib)

A

The benefit of reduced GI issues from use COX2 inhibitors is offset by the increased bleed risk/ GI ulceration from even low dose aspirin.

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10
Q

What NSAIDS are associated with highest CVD risk?

A

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

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11
Q

What NSAIDs have increased GI side effects and should be used with caution in at risk groups?

A

Piroxicam (2nd line by specialist for RA, osteoarthritis, ankylosing spondylitis at under 20mg daily), ketoprofen, ketorolac

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12
Q

Why do we ask if a patient buying NSAID OTC if they have asthma?

A

NSAIDs are associated with asthma worsening (so could cause bronchospasm)

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13
Q

Why advise a patient on NSAIDs to limit alcohol intake to 2 units a day?

A

Increased risk of GI haemorrhage and also acute kidney damage is associated with NSAIDs and alcohol being combined.

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14
Q

Why would you use NSAIDs with caution in cardiac impairment and IBD?

A

These may worsen or exacerbate UC and Crohn’s disease and may lead to renal impairment affecting the heart.

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15
Q

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)?

A

All these can be precipitated by taking an NSAID

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16
Q

Common side effects of NSAIDs?

A

Fluid retention
GI disturbances
Diarrhoea
Rashes

17
Q

Why advise pregnant mothers to avoid NSAIDs in pregnancy (including topical)?

A

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

18
Q

Why monitor renal function and electrolytes in renal failure?

A

Sodium and fluid retention can lead to reduced renal function and possibly failure.

19
Q

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?

A

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.

20
Q

Why can Trimethroprin and proguanil/ pyrimethamine increase risk of side effects when taken with methotrexate?

A

Act via a similar mechanism - dihydrofolate reductase inhibition.

21
Q

Why is it important to continually confirm a patients methotrexate dose, frequency, tablet strength and enquiry about health issues?

A

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.

22
Q

Why monitor FBC on methotrexate?

A

To check for clinically significant bone marrow suppression, in which the risk increases with age / renal impairment and if on Trimethropin

23
Q

Why is contraception required for patients on methotrexate and for 3 months after course finished?

A

Should be avoided in pregnancy due to teratogenicity.

24
Q

Why would a patient on methotrexate prescribed the following require possible intervention?
NSAIDs
PPIs
Retinoids
Trimethropin
Quinolones
Sulfamethoxazole/Sulfadiazine/Sulfadoxine

Others…

A

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.

25
Q

Why be wary of long term opioid use?

A

Risk of hyperalgesia which will require therapy change or introduction of ketamine, alpha2 agonists or COX2 inhibitors

26
Q

Why are opioids contraindicated in acute respiratory depression and cautioned in asthma?

A

The mew receptors mediate respiratory depression so when activated reduce sensitivity to plasma CO2 and inhibit respiratory rhythm generation. It should be avoided in acute asthma attack and COPD.

Opioids also cause histamine release leading to itching, bradycardia, hypotension and importantly BRONCHOCONSTRICTION.

27
Q

Why might you need 5HT3 antagonists, antihistamines, droperidrol or Prochlorperazine, especially initially, in opioid use?

A

Nausea and vomiting due to opioid action on chemoreceptor trigger zone in medulla.

28
Q

Why are opiates contraindicated in biliary disease?

A

Opioids cause biliary sphincter contraction and gall bladder contraction

increase risk of gallstones (increased amylase and lipase) in biliary colic so avoid

29
Q

Why does morphine need dose reduction in liver and renal impairment?

A

In liver metabolised primarily by glucoronide conjugation and impaired function may cause a coma.

In renal the 3/6 metabolites are excreted.

30
Q

Why is Pethidine the opioid of choice in pregnancy?

A

Does not cause uterine contractions (though be wary of inhalation pneumonia and gastric stasis).

Other opioids should be used due to low conjugation ability of neonates so can lead to respiratory depression and potentially withdrawal.

31
Q

What do you monitor in infants of breastfeeding mothers on opiates?

A

Drowsiness
Weight
Developmental milestones.

32
Q

Why avoid alcohol in extended release morphines?

A

Causes rapid release

33
Q

Why would you be concerned if a Fentanyl patient presented with: breathing difficulties, marked drowsiness, confusion, dizziness, impaired speech?

A

Potential overdose, patch to be removed and medical attention sought.

34
Q

Why would you be vigilant administrating Naloxone to buprenorphine, methadone and pentazocine?

A

Both Buprenorphine and Pentazocine are partial agonists so may not have full effect.

Both Buprenorphine and Methadone are long acting and repeated dosing of Naloxone May be required.