Skeletal Neuromuscular Junction - James Hodge

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Degree Neuropharmacology Fichas sobre Skeletal Neuromuscular Junction - James Hodge, creado por Anna mph el 14/12/2015.
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Pregunta Respuesta
What are the two sub categories of ACh receptors Nicotonic (nAChR) Muscarinic (mAChR)
Where are mAChR found and how are they structured? postganglionic parasympathetic synapses; brain
What are the two subtypes of nAChRs? Muscarinic (NMJ) and Neuronal
Describe the structure of the NMJ nAChR Pentameric. 2a subunits B, d, Y/E
What is the structure of neuronal nAChRs? Pentameric. a2-10, B2-4 Usually 2(a3) 3(B4)
Where are neuronal nAChRs found in the PNS? Ganglionic synapses, adrenal medulla, presynaptic receptors at NMJ
Where are neuronal nAChRs found in the CNS? Neurones in brain and spinal cord
Where is the ligand binding site on the nAChR? a1 or a2
Are nAChRs selective? No they allow Na+ to flow in and K+ to flow out
What roughly is the RMP for nAChR usually? ~60mV
How do K+ and Na+ currents relate at rest through an nAChR? Na+>>K+
Define endplate potential? Depolarisations of skeletal muscle fibres by the binding of neurotransmitters to the postsynaptic membrane in the NMJ
What are the precursors to acetylcholine? Choline and Acetyl-CoA
Which enzyme synthesises Acetylcholine? Choline acetyltransferase
Which enzyme breaks down acetylcholine acetylcholinesterase
What percentage of acetate and choline are recaptured? 50%
Which two drugs act presynaptically to prevent exocytosis? Botulinum and Tetanus Toxin
Give an example of a non-depolarising blocker Tubocurarine
What effect on end plate current does a non-depolarising blocker have? End plate potential never reaches threshold for AP.
What would you expect to see with inhibition of neuromuscular transmission? Flaccid Paralysis - muscle relaxation
What would be the expected order of muscle relaxation? Eyes + small facial muscles Limbs Pharynx Respiratory Muscles
What effect to non-depolarising blockers have on pain perception and consciousness? None.
What are the benefits of non-depolarising blockers? Poor oral absorption (not taken across gut) Quickly excreted Don't cross the placenta
What is a common side effect in non-depolarising blockers? Histamine release.
Give an example of a depolarising blocker Suxamethonium
Explain the four stages 1) nAChR activated 2)Fasciculations - lots of impulses when agonist first applied 3)Phase 1 block - Na+ channels desensitise 4)Phase 2 block - nAChR desensitise
Why is the desensitisation of nAChR a slow process? Secondary messengers
What are the four key differences in depolarising v. non-depolarinsing drugs? (fasciculations, post-op,reversibility) 1) Depolarising drugs cause fasciculations 2) Depolarising drugs often cause post operative pain 3) Depolarising block, suxamethonium is hydrolysed by plasma cholinesterase 4)Non-depolarising block is reversible by anticholinesterase drugs.
What effect does prolonged presence of an anticholinesterase cause? Build up of acetylcholine causes a depolarising block
What are the two sites on acetycholinesterases? Esteric and anionic
Which part of the acetycholine molecule is attracted to which part of the acetycholinesterase? Acetate (CH3COO) bonds to esteric site (Hydolysed to CH3COOH) Choline (With N+ binds to anionic site)
What are the main causes of myasenthia gravis? 1) Genetic (mutation for nAChR receptor, or protein (rapsin) which takes nAChR to endplate) 2) Autoimmune disorder
What is the main underlying problem with myasthenia gravis Too low number of nAChR receptors - less transmission leads to muscle weakness
What are the symptoms of myasthenia? Drooping eyelids muscle weakness
How do you test for myasthenia gravis? Give Edrophonium - restores muscle strength rapidly
What 3 anticholinesterases do you use to treat myasthenia gravis? Where do they act? Neostigmine Physostigmine Pyridostigmine Act at NMJ
Which anticholinesterase would you give to reverse a non-depolarising block after surgery? Neostigmine
Which two anticholinesterases can be used to treat alzheimers? Donepezil and Rivastigimine (Can cross blood brain barrier)
Give an example of two organophosphates? Why are they so damaging to people? Malathion Ecothiopate Depolarising block is irreversible
Why does myasthenia gravis cause a rightward shift in a concentration response curve for a given amount of endogenous agonist? Loss of spare receptors
Why do medium lasting anticholinesterases last longer than short duration? Bind more strongly to active site, hydrogen bond with serine from carbamyl, glut binds with N+ groups
Why is edrophonium short acting? Weak nucleophilic bonds
Why are irreversible blocks irreversible? Covalent bond at serine
What are the side effects of anticholinesterase intoxication at the: Begin
Eye Mitosis, blurred vision
Heart Bradycardia
Lung Bronchoconstriction
GI Tract Vomiting, diarrhoea
Glands Sweating/Salvation
NMJ Convulsions, followed by flacid paralysis
CNS Agitation followed by respiratory arrest
How can you reverse/help the effects of anticholinesterase poisoning? Life support Atropine (muscarinic agonist) Cholinesterase reactivation (for iireversible anticholinesterase)
What drug can you use to combat the effects of irreversible anticholinesterases? Pralidoxime, phosphate group/bond gets attracted to N+ group on pralidoxime. Unblocks acetylcholinesterase
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