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20 Cards in this Set
- Front
- Back
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Aminoglycosides (e.g. gentamicin)
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Antibiotics
prevent release of calcium Inhibit ACh presynaptically - “calcium release dependant mechanism” – need influx of Ca2+ to release vesicles |
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Tetracycline
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Antibiotic
binds and absorb calcium Inhibit ACh presynaptically - “calcium release dependant mechanism” – need influx of Ca2+ to release vesicles |
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Botulinum toxin (Clostridium botulinum)
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Botox
Neurotoxins Inhibit ACh presynaptically |
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Beta-bungarotoxin (Taiwanese banded krait)
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Neurotoxins
Inhibit ACh presynaptically |
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Nicotine
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Agonist AChR at NMJ
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Pancuronium
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NMJ blocking drugs
Onset: Medium Duration: Long Main side effects: Tachycardia Metabolism/elimination: Hepatic metabolism |
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Vecuronium
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NMJ blocking drugs
Onset: Medium Duration: Medium Main side effects: Few side effects Metabolism/elimination: Hepatic metabolism |
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Rocuronium
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NMJ blocking drugs
Onset: Fast Duration: Medium Main side effects: Tachycardia Metabolism/elimination: Unchanged in bile/urine |
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Atracurium
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NMJ blocking drugs
Competitive Antagonist (non-depolarising blockers) AChR at NMJ commonly used Onset: Medium Duration: Medium Main side effects: Hypotension/bronchospasm (histamine release) Metabolism/elimination:Ester hydrolysis/Hofmann elimination |
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Mivacurium
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NMJ blocking drugs
Onset: Fast Duration: Short Main side effects: Hypotension/bronchospasm (histamine release) Metabolism/elimination: Plasmacholinesterase |
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Suxamethonium
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NMJ blocking drugs
Agonist of nicotinic Ach receptors at NMJ Onset: Fast Duration: Short Main side effects: -Bradycardia (muscarinic agonist effect) -Cardiac dysrhythmias (increased plasma K+ concentration/hyperkalaemia) -Raised intraocular pressure (nicotinic agonist effect) -Postoperative myalgia (muscle fasciculation) -Malignant hyperthermia (Ryanodine receptor related) Metabolism/elimination: Plasmacholinesterase |
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Sugammadex
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selective relaxant binding agent (SRBA) – reverses effects of rocuronium and vecuronium
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Edrophonium
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Anticholinesterase drugs – increase excitability by increasing Ach availability at NMJ (decrease degradation)
Duration: Short Mechanism: Easily reversible |
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Neostigmine
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Anticholinesterase drugs – increase excitability by increasing Ach availability at NMJ (decrease degradation)
Duration: Medium Mechanism: Form carbamylated enzyme complex |
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Pyridostigmine
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Anticholinesterase drugs – increase excitability by increasing Ach availability at NMJ (decrease degradation)
Duration: Medium Mechanism: Form carbamylated enzyme complex |
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Dyflose
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Anticholinesterase drugs – increase excitability by increasing Ach availability at NMJ (decrease degradation)
Duration: Long Mechanism: Irreversible inhibition – phosphorylation is very stable |
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Parathion
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Anticholinesterase drugs – increase excitability by increasing Ach availability at NMJ (decrease degradation)
Duration: Long Mechanism: Irreversible inhibition – phosphorylation is very stable |
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Palidoxime
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used to coax off dyflos and parathion (insecticides)
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Nifedipine
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Promote smooth muscle relaxation by blocking calcium ion channels (DHPR)
Treat: smooth muscle hypertension, migraine, atherosclerosis |
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Dantrolene
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Spasmolytic drug acting as a muscle relaxant
Prevent Ca2+ release from SR (RYR) Treat (SR) muscle spasm in cerebral palsy, multiple sclerosis, used in surgery to prevent malignant hyperthermia in response to anaesthetic |
