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2MBChB Musculoskeletal > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What are the functions of non-steroidal anti-inflammatory drugs (NSAIDs)?

A

Anti-inflammatory.

Analgesic.

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2
Q

Give examples of NSAIDs?

A

Ibuprofen.

Naproxen.

Diclofenac.

Indometacin.

Etodolac.

Celecoxib (Cox 2 inhibitor).

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3
Q

What are the indications in rheumatology for prescribing NSAIDs?

A

Inflammatory arthritis.

Mechanical musculoskeletal pain.

Pleuritic/pericardial pain.

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4
Q

What are the adverse effects of NSAIDs?

A

Dyspepsia.

Oesophagitis.

Gastritis.

Peptic ulcer.

Small/large bower ulceration.

Renal impairment.

Increased cardiovascular events.

Fluid retention.

Wheeze.

Rash.

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5
Q

When do you aim to start patients with inflammatory arthritis on DMARDs?

A

Within 3 months of symptom onset.

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6
Q

How long does it take for a DMARD to take effect?

A

Slow-acting.

Takes about 6 weeks to work.

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7
Q

What effect do DMARDs give?

A

Pure anti-inflammatory with NO direct analgesic effect.

Reduce rate of damage to joints.

Improve standard lab tests of inflammation e.g. ESR, CRP.

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8
Q

What are the commonly used DMARDs?

A

Methotrexate.

Sulphasalazine.

Leflunomide.

Hydroxychloroquine.

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9
Q

How can methotrexate be administered?

A

Orally, subcutaneously.

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10
Q

What conditions can methotrexate be used to treat?

A

Rheumatoid arthritis.

Psoriatic arthritis.

Connective tissue disease.

Vasculitis.

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11
Q

Can methotrexate be used in pregnancy?

A

No it is teratogenic and must be stopped for 3 months before trying to conceive in both male and female patients.

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12
Q

What are the adverse effects of methotrexate?

A

Leukopenia/thrombocytopenia.

Hepatitis/cirrhosis - alcohol intake must be limited.

Pneumonitis.

Rash/mouth ulcers.

Nausea/diarrhoea.

Needs monitoring of FBC and LFTs.

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13
Q

Can leflunomide be used in pregnancy?

A

No, it is teratogenic.

Tend to be avoided in female patients of child-bearing age as it has a very long half-life and requires a washout.

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14
Q

What are the adverse effect of sulfasalazine?

A

Nausea.

Rash/mouth ulcers.

Neutropenia.

Hepatitis.

Reversible oligozoospermia.

Monitoring of FBC and LFTs.

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15
Q

What are the side effects of leflunomide?

A

Leukopenia/thrombocytopenia.

Hepatitis/cirrhosis - alcohol intake must be limited.

Pneumonitis.

Rash/mouth ulcers.

Nausea/diarrhoea.

Needs monitoring of FBC and LFTs.

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16
Q

Which DMARD can be used in pregnancy?

A

Sulphasalazine.

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17
Q

What are the effects of hydroxychloroquine?

A

No effect on joint damage.

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18
Q

Which conditions would you prescribe hydroxychloroquine to?

A

Used in connective tissue diseases such as SLE (helps skin, joints and general malaise), Sjogren’s and rheumatoid arthritis.

Given to all patients with SLE.

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19
Q

What are biologic therapies?

A

Drugs designed to target specific aspects of the immune system found to be implicated in inflammatory conditions.

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20
Q

What are the current targets of biologic therapies?

A

Tumour necrosis factor (TNF).

CD20 B cells.

IL-6.

IL-17, 12 and 23.

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21
Q

Which drug is more effective, DMARDs or biologics?

A

Biologics are found to be 1.5 times more effective than DMARDs, but not all patients need them.

22
Q

What conditions is anti-TNF therapy given to?

A

Rheumatoid arthritis.

Psoriatic arthritis.

Ankylosing spondylitis.

23
Q

Give examples of anti-TNF therapies?

A

Etanercept.

Adalimumab.

Certolizumab.

Infliximab.

Golimumab.

Biosimilars: Benepali.

24
Q

When would you put a patient on biologic therapy?

A

Somebody must have a DAS28 score >5.1 whilst on 2 DMARDs.

25
Q

What are the main adverse effects of anti-TNF therapy?

A

Risk of infection - reactivation of latent TB.

Risk of malignancy - skin cancer.

Contraindicated in certain situations - pulmonary fibrosis, heart failure.

26
Q

What medications are given to treat an acute episode of gout?

A

Colchicine (diarrhoea common side effect).

NSAIDs.

Steroids (either oral or IM).

27
Q

What treatments are given as prophylaxis in gout?

A

Allopurinol.

Febuxostat.

Uricosurics - not normally used anymore.

28
Q

What is allopurinol?

A

Xanthine oxidase inhibitor.

29
Q

How is allopurinol prescribed?

A

Needs to be increased gradually in steps to make sure uric acid levels are below a threshold of 360micromol/L because rapid reduction in uric acid level may result in exacerbation of gout.

Interacts with azathioprine -> irreversible bone marrow suppression.

30
Q

If a patient is on allopurinol prophylactically and has an acute flare, do you stop the allopurinol?

A

No.

31
Q

What are the side effects of allopurinol?

A

Rash (vasculitis) - commoner in elderly and in renal impairment (use lower doses).

Azathioprine interaction.

Marrow aplasia - rare.

32
Q

What is febuxostat?

A

Xanthin oxidase inhibitor.

33
Q

Which patients would you consider giving febuxostat to?

A

Those who cannot tolerate allopurinol.

Those with renal impairment.

Caution in patients with ischaemic heart disease.

34
Q

What are the indications of corticosteroids in rheumatology?

A

Connective tissue disease.

Polymyalgia rheumatica/giant cell arteritis.

Vasculitis.

Rheumatoid arthritis.

35
Q

What are the adverse effects of corticosteroids?

A

Weight gain - centripetal obesity (only an issue in high dose over a prolonged time period).

Muscle wasting.

Skin atrophy.

Osteoporosis.

Diabetes.

Hypertension.

Cataract.

Glaucoma.

Fluid retention.

Adrenal suppression.

Immunosuppression.

Avascular necrosis of the femoral head.

36
Q

How can the toxicity of corticosteroids be reduced?

A

Use the lowest possible dose for as short a time as possible.

Consider steroid-sparing agents.

Osteoporosis prophylaxis.

Watch for cardiovascular risk factors.

37
Q

What innervates skeletal muscle?

A

Motorneurons with myelinated axons.

38
Q

What neurotransmitter and receptor do the motorneurons that innervate skeletal muscle release and act upno?

A

Acetylcholine.

Nicotinic acetylcholine receptors.

39
Q

What are the key features found at a skeletal neuromuscular junction?

A

Terminal bouton (and surrounding Schwann cell).

Synaptic vesicles.

Synaptic cleft.

Endplate region of the muscle cell membrane (sarcolemma) thrown into a series of junctional folds.

Synaptic vesicles containing ACh.

Nicotinic ACh receptors located at regions of the junctional folds.

40
Q

What process occurs at each of the numbered points?

A
41
Q

How does choline get into the synaptic terminal?

A

Choline is transported into the terminal by the choline transporter (symport with Na+).

42
Q

Where is acetylcholine synthesised and how it this done?

A

Acetylcholine is synthesised in the cytosol from choline and acetyl coenzyme A (acetyl CoA – supplied by mitochondria) by the enzyme choline acetyltransferase (ChAT, or CAT).

43
Q

How does acetylcholine get from the cytosol of the synaptic terminal into vesicles?

A

Vesicular acetylcholine transporter.

44
Q

How is acetylcholine released into the synaptic cleft?

A

Arrival of the action potential at the terminal causes depolarization and the opening of voltage-activated Ca2+ channels, allowing Ca2+ entry to the terminal.

Ca2+ causes vesicles ‘docked’ at active zones to fuse with the presynaptic membrane (exocytosis) – ACh diffuses into the synaptic cleft to activate post-synaptic nicotinic ACh receptors in the endplate region.

45
Q

How is endplate potential generated?

A

ACh binds to NAChR on the muscle endplate.

Channel opens -> Na+ influx & K+ efflux.

Driving force for Na+ is greater than that for K+ causing a depolarisation known as endplate potential.

46
Q

How does an action potential in skeletal muscle bring about contraction?

A

Action potential propagates over the surface membrane (sarcolemma) of skeletal muscle fibre and enters transverse (T) tubules (invaginations of the sarcolemma that dip deeply into the muscle cell).

T-tubules are in close apposition to the sarcoplasmic reticulum (SR, Ca2+ store).

Action potential arriving at the T-tubule triggers release of Ca2+ from the SR which in turn causes contraction by interacting with troponin associated with the myofibrils.

47
Q

What breaks down excess acetylcholine in the synaptic cleft and what does it break it into?

A

Acetylcholinesterase.

Choline and acetate.

48
Q

What part of synaptic transmission goes wrong in Neuromyotonia?

A

Antibodies are formed against the voltage-activated K+ channels in motorneurons -> disrupt function resulting in hyperexcitability.

49
Q

What part of synaptic transmission goes wrong in Lambert-Eaton Myasthenic Syndrome?

A

Antibodies form against the voltage-activated Ca2+ channels in the motor neuron terminal -> reduced Ca2+ entry in response to depolarisation -> reduced vascular release of ACh.

Reduced Ca2+ conductance presynaptically -> decreased release of ACh -> muscle weakness.

50
Q

What part of synaptic transmission goes wrong in Myasthenia Gravis?

A

Antibodies form against nicotinic ACh receptors in the endplate -> reduction in the number of functional channels -> reduction in amplitude of endplate potentials.

Reduced numbers of nAChRs ->muscle weakness.

51
Q

What part of synaptic transmission goes wrong when botulinum toxin enters the body?

A

Enters presynaptic nerve terminal to irreversibly, enzymatically modify proteins involved in the docking of vesicles containing ACh -> preventing exocytosis.

Failure of ACh release -> paralysis.

52
Q

What part of synaptic transmission goes wrong when curare-like compounds enter the body?

A

Interfere with the postsynaptic action of ACh by acting as competitive antagonists of the nAChR -> reduced amplitude of the endplate potential to below threshold for muscle fibre action potential generation.

2MBChB Musculoskeletal (17 decks)

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