Information includes:
- Name and class of medication
- Indications for use
- Mechanism of action
- Side effects and interactions
- Route of administration
MUSCULOSKELETAL DRUGS
Name Class Clinical Indications Receptor Action Mechanism of Action Adverse Effects and Administration + PK
Interactions
Skeletal muscle relaxation Binds to an allosteric site on ACh receptors on the motor end plate of the neuro-muscular
Malignant hyperthermia
during intubation, mechanical Non-competitive ACh junction. This initially causes activation of the receptor but after a short time, prevents new
Suxamethonium Depolarising Muscle pain IV
ventilation and surgical receptor agonist ACh from binding and therefore inhibits muscle contraction causing relaxation.
Hyperkalaemia
procedures
Neuromuscular
Blockers
Skeletal muscle relaxation Binds to ACh receptors on the motor end plate of the neuromuscular junction. This prevents
Seizures
Atracurium during intubation, mechanical Competitive ACh receptor ACh from binding and eliciting an action potential therefore decreasing skeletal muscle
Non-depolarising IV
Pancuronium ventilation and surgical antagonist contraction and therefore causing relaxation.
Bronchospasm
procedures
Myasthenia gravis Inhibits acetylcholinesterase which would usually break down ACh in the synaptic cleft of
Acetylcholinesterase the neuromuscular junction. By preventing this breakdown, more ACh remains in the cleft Cholinergic crisis leading to
Parasympathomimetics Neostigmine ACHE inhibitor IV
To reverse effects of muscle inhibitor causing increased stimulation of nicotinic ACh receptors, therefore increasing muscle tone. respiratory failure
relaxants
Pain and inflammation
Irreversible, non-selective
Aspirin Inhibits COX1 and COX2 enzymes (preference for COX1). This blocks the production of Oral
COX inhibitor
Myocardial infarction PGH2, a precursor for all prostaglandins and prostacyclins produced in the arachidonic acid
pathway. Reduction in these molecules leads to decreased inflammation and an analgesic GI ulcers
effect. Asthma exacerbation
Ibuprofen Hypersensitivity
Naproxen Reversible, non-selective Meloxicam has a preference for inhibiting COX2. Oral
Diclofenac COX inhibitor
NSAIDS NSAID
Meloxicam Aspirin binds irreversibly and has extra anti-thrombotic effects.
Pain
Inflammation Selectively inhibits COX2 enzymes. This blocks the production of PGH2, a precursor for all
prostaglandins and prostacyclins produced in the arachidonic acid pathway. Reduction in
Reversible, selective Exacerbation of asthma
Celecoxib these molecules leads to decreased inflammation and an analgesic effect. It is important to Oral
COX2 inhibitor Hypersensitivity
note that unlike COX1, COX2 is only present during inflammation.
Inhibits COX1, COX2 and COX3 enzymes only in the central nervous system and not in
Reversible, non-selective, peripheral tissues. This blocks the production of PGH2, a precursor for all prostaglandins Hepatotoxicity in overdose
Analgesics Paracetamol Analgesic Pain Oral
indirect COX inhibitor and prostacyclins produced in the arachidonic acid pathway. Reduction in these molecules Nephrotoxicity in long term use
leads to decreased pain.
Moderate to severe Binds to and inhibits TNF𝛂 which is a cytokine involved in recruitment of white blood cells to Local skin irritation
rheumatoid arthritis sites of inflammation within the body. It also amplifies the immune response and is seen in Subcutaneous injection 2x a
Etanercept many autoimmune diseases. By inhibiting this, the autoimmune response is dampened. week
Infliximab Anti-TNF𝛂 Psoriatic arthritis TNF𝛂 Inhibitor Headache
Slow IV infusion
GI disturbance
Ankylosing spondylitis
Converted to teriflunomide. In the mitochondria, it inhibits dihydroorotate dehydrogenase Alopecia
which in turn inhibits pyrimidine synthesis for T-cells. This stops T-cell proliferation, therefore
Anti T-cell Specialist treatment of Pyrimidine synthesis
Leflunomide damping the autoimmune response. Increased liver enzymes Oral
proliferation rheumatoid arthritis inhibitor
Rash
Competitively antagonises interleukin-1 which is a key cytokine in the pathogenesis of Immune deficiency
Anakinra Anti-rheumatic Rheumatoid arthritis IL-1 antagonist rheumatoid arthritis. By inhibiting IL-1 , cartilage degradation and bone reabsorption is Subcutaneous injection
slowed down. Neutropenia
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