Nicotinic Acetylcholine Receptors Flashcards
Nicotinic Acetylcholine Receptors (nAChRs)
Mediate neurotransmission at Neuromuscular junction and Autonomic ganglia.
Ganglionic nAChRs
Nicotinic receptor activation causes depolarization of the nerve cell.
-Ganglionic action potential is generated when excitatory postsynaptic potential (EPSP) threshold is reached at the post Ganglionic neuron.
True or False: Nicotinic agonist cause activation of both para- and sympathetic gangli.
True
The effects on the Cardiovascular System are Sympathomimetic
The effects on the GI and Urinary tract are Parasympathetic
True or False: All nAChR are subject to both depolarizing and non-depolarizing blockade.
True
What is a biphasic display in Nicotinic agents?
The effect of nicotine are going to depend on the dose.
Small dose: Stimulate
Large dose: A blockade is followed after the stimulation
Describe the two phases of depolarizing Blockade
Phase I: Continued presence of the agonist prevents electrical recovery of the postjunctional membrane.
Phase II (Desensitization): Continued agonist occupancy is associated with return of membrane voltage to the resting level but effect of agonist is desensitized.
True or False: Cigarette smoking is clearly the largest single preventable cause of illness and premature death in the US.
True
At low concentrations, which receptor of nicotine will have higher affinity?
Neuronal
How does Nicotine addiction occur?
Nicotine activates the release of dopamine in the mesolimbic system. However, chronic exposure leads to decrease the release of dopamine (desensitization)
What are the treatment for acute nicotine poisoning?
Atropine for ganglion stimulation
Diazepam for Central stimulation
What are approaches to help patients to stop smoking?
-Replacement Therapy
-Varenicline: a partial agonist of CNS nAChRs
-Bupropion: non-competitive antagonist of nAChRs.
Ganglionic Blocking agents
Nicotine and ACh can produce depolarizing Ganglionic block if amplified with a cholinesterase inhibitor.
What Ganglionic blocking drug was used to treat Tourette’s syndrome?
Mecamylamine: a non-selective and non-competitive antagonist of nAChRs.
What are Neuromuscular blocking agents used for?
Muscle relaxation
-Anesthetic or control muscle spasms.
What adverse effects is commonly cause by Tubocurarine, Mivacurium, Atracurium, and Succinylcholine?
Increase histamine release
-Depolarizing agents like succinylcholine can release K rapidly from intracellular sites.
How can we treat Neuromuscular Blocking agents adverse effects?
With AChE inhibitors but they will not reverse depolarizing neuromuscular blockade.
What are drug-drug interactions from Neuromuscular blocking agents?
-Halogenated anesthetics
-Aminoglycoside antibiotics
-Calcium Channel Blockers
-Cholinesterase inhibitors
Long acting competitive blocking agents
d-Tubocurarine: 80 minute duration. It produces histamine release and it’s an active compound of Curare.
Intermediate acting competitive blocking agents
Atracurium: 45 min duration y no se metabolizes en el hígado.
Atracurium and cisatracurium matabolism results in production of laudanosine (epileptogenic)
Which of the two produces lower concentrations of laudanosine? Atracurium or Cisatracurium
Cisatracurium
Short acting competitive blocking agents
Mivacurium: 15 a 21 min duration
Succinylcholine
Short acting (6-11 min) because of butyrylcholinesterase but persist in the neuromuscular junction because of their resistance to AChE.
Fastest onset and shortest duration of action of all muscle relaxants. Does not produce unconsciousness or anesthesia.
Succinylcholine Adverse Effects
-Hyperkalemia
-Malignant Hyperthermia
-Muscle soreness
Botox
Blocks ACh release at neuromuscular junctions
Botox treatments
-Ocular conditions
-Spasms
-Dystonias
-Cerebral palsy for children
-Reduce wrinkles (only temporary)
