Karteikarten
Skeletal Neuromuscular Junction - James Hodge
Karten in diesem Stapel (53)
- 1What are the two sub categories of ACh receptorsNicotonic (nAChR)
Muscarinic (mAChR) - 2Where are mAChR found and how are they structured?postganglionic parasympathetic synapses; brain
- 3What are the two subtypes of nAChRs?Muscarinic (NMJ) and Neuronal
- 4Describe the structure of the NMJ nAChRPentameric. 2a subunits B, d, Y/E
- 5What is the structure of neuronal nAChRs?Pentameric. a2-10, B2-4
Usually 2(a3) 3(B4) - 6Where are neuronal nAChRs found in the PNS?Ganglionic synapses, adrenal medulla, presynaptic receptors at NMJ
- 7Where are neuronal nAChRs found in the CNS?Neurones in brain and spinal cord
- 8Where is the ligand binding site on the nAChR?a1 or a2
- 9Are nAChRs selective?No they allow Na+ to flow in and K+ to flow out
- 10What roughly is the RMP for nAChR usually?~60mV
- 11How do K+ and Na+ currents relate at rest through an nAChR?Na+>>K+
- 12Define endplate potential?Depolarisations of skeletal muscle fibres by the binding of neurotransmitters to the postsynaptic membrane in the NMJ
- 13What are the precursors to acetylcholine?Choline and Acetyl-CoA
- 14Which enzyme synthesises Acetylcholine?Choline acetyltransferase
- 15Which enzyme breaks down acetylcholineacetylcholinesterase
- 16What percentage of acetate and choline are recaptured?50%
- 17Which two drugs act presynaptically to prevent exocytosis?Botulinum and Tetanus Toxin
- 18Give an example of a non-depolarising blockerTubocurarine
- 19What effect on end plate current does a non-depolarising blocker have?End plate potential never reaches threshold for AP.
- 20What would you expect to see with inhibition of neuromuscular transmission?Flaccid Paralysis - muscle relaxation
- 21What would be the expected order of muscle relaxation?Eyes + small facial muscles
Limbs
Pharynx
Respiratory Muscles - 22What effect to non-depolarising blockers have on pain perception and consciousness?None.
- 23What are the benefits of non-depolarising blockers?Poor oral absorption (not taken across gut)
Quickly excreted
Don't cross the placenta - 24What is a common side effect in non-depolarising blockers?Histamine release.
- 25Give an example of a depolarising blockerSuxamethonium
- 26Explain the four stages1) nAChR activated
2)Fasciculations - lots of impulses when agonist first applied
3)Phase 1 block - Na+ channels desensitise
4)Phase 2 block - nAChR desensitise - 27Why is the desensitisation of nAChR a slow process?Secondary messengers
- 28What 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. - 29What effect does prolonged presence of an anticholinesterase cause?Build up of acetylcholine causes a depolarising block
- 30What are the two sites on acetycholinesterases?Esteric and anionic
- 31Which 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) - 32What are the main causes of myasenthia gravis?1) Genetic (mutation for nAChR receptor, or protein (rapsin) which takes nAChR to endplate)
2) Autoimmune disorder - 33What is the main underlying problem with myasthenia gravisToo low number of nAChR receptors - less transmission leads to muscle weakness
- 34What are the symptoms of myasthenia?Drooping eyelids muscle weakness
- 35How do you test for myasthenia gravis?Give Edrophonium - restores muscle strength rapidly
- 36What 3 anticholinesterases do you use to treat myasthenia gravis? Where do they act?Neostigmine
Physostigmine
Pyridostigmine
Act at NMJ - 37Which anticholinesterase would you give to reverse a non-depolarising block after surgery?Neostigmine
- 38Which two anticholinesterases can be used to treat alzheimers?Donepezil and Rivastigimine
(Can cross blood brain barrier) - 39Give an example of two organophosphates? Why are they so damaging to people?Malathion
Ecothiopate
Depolarising block is irreversible - 40Why does myasthenia gravis cause a rightward shift in a concentration response curve for a given amount of endogenous agonist?Loss of spare receptors
- 41Why 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
- 42Why is edrophonium short acting?Weak nucleophilic bonds
- 43Why are irreversible blocks irreversible?Covalent bond at serine
- 44What are the side effects of anticholinesterase intoxication at the:Begin
- 45EyeMitosis, blurred vision
- 46HeartBradycardia
- 47LungBronchoconstriction
- 48GI TractVomiting, diarrhoea
- 49GlandsSweating/Salvation
- 50NMJConvulsions, followed by flacid paralysis
- 51CNSAgitation followed by respiratory arrest
- 52How can you reverse/help the effects of anticholinesterase poisoning?Life support
Atropine (muscarinic agonist)
Cholinesterase reactivation (for iireversible anticholinesterase) - 53What 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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- Degree Neuropharmacology Karteikarten am Skeletal Neuromuscular Junction - James Hodge, erstellt von Anna mph am 14/12/2015.
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