Cholinergics & Adrenergics Biology Flashcards
Muscarinic receptors bind to:
ACh, NE
Nicotinic receptors bind to
nicotine, ACh
What time of receptors are Nicotinic receptors? Muscarinic?
Na/K channels - activates and then deactivates. Muscarinic - GPCR - continual effect.
How would you treat cholinergic poisoning?
atropine (muscarinic antagonist)
How would you treat organophosphate poisoning?
pralidoxime
Why would you get paradoxical bradycardia with muscarinic receptor activation?
M receptor activation - get hypotension due to NO-mediated vasodilation, but also get paradoxical bradycardia because there are M receptors on the SA node.
What is the cholinergic syndrome?
DUMBBELSS Diarrhea Urination Miosis Bronchorrea/Bronchoconstriction Bradycardia Emesis Lacrimation Salivation Sweating
What 3 enzymes terminate ACh signaling?
True, Pseudo (blood), and RBC AChE
What are direct M. agonists?
pilocarpine (carbachol), methacoline, and bethanecol
What are indirect M agonists?
AChE inhibitors that increase ACh: Edrophoniium, Neostigmine, Pyridostigmine, Echothiophate
What happens with over-activation of N receptors? (5 things)
1) initial depolarizations, which lead to muscle fasciculations/spasms
2) prolonged occupancy of the receptor with ligand –> paradoxical flaccid paralysis
3) activation of mesolimbic reward system/dopamine secretion
4) net K efflux from muscle –> hyperkalemia + cardiac effects (arrhythmias)
What are short, intermediate, and long-acting cholinesterase inhibitors? What do they do?
potentiates ACh by preventing its degradation
short: edrophonium
Intermediate: neostigmine, physostigmine
long: echothiophate
What happens if you OD on ACh?
1) respiratory suppression due to paralysis of the diaphragm + intercostals (due to nicotinic activation)
* respiratory support is IMPT*
2) increase bronchial secretions/bronchoconstriction (due to nicotinic activation)
What are carbamates?
intermediate acting cholinesterase inhibitors (neostigmine, physostigmine)
What are organophosphates?
long acting cholinesterase inhibitors (echothiophate)
How do you treat organophosphate AChE poisoning? How do you treat carbamate AChE poisoning?
Organophosphate Poisoning: muscarinic blockers (atropine, pralidoxime).
Carbamate poisoning: muscarinic blocker, but NOT NOT PRALIDOXIME (long-acting organophosphate), since it makes it worse.
What is a depolarizing block? Non-depolarizing block?
How would you treat a depolarizing block? Non-depolarizing block?
depolarizing block: inhibitor that binds to the receptor and causes depolarization, followed by receptor desensitization phase that results in receptor inactivation. Reverses with TIME, which allows the ChE to clear the ACh.
nondepolarizing block: inhibitor that binds to the receptor but does not depolarize the motor end plate. Reverses with neostygmine (ChE inhibitor)
An M receptor-antagonist results in these two major effects:
1) blocking parasympathetic transmission
2) sweat glands/CNS activity
What is an inverse agonist?
an agonist that produces an inhibitory effect by shifting the receptor equilibrium from active –> inactive
What is atropine?
muscarinic blocker (M1, M2, M3) - causes UNOPPOSED sympathetic effects: anti-DUMBBELSS
What is ipratropium usually packaged with?
Ipratropium is an inhaled muscarinic blocker and it usually causes bronchodilation.
It is usually packaged with albuterol, which inhibits bronchoconstriction.
What should you worry about for patients who lack plasma ChE? How would you treat these patients if they were accidentally given a loaded dose of succinylcholine?
Succinylcholine (depolarizing nicotinic receptor antagonist) will hang around a lot longer, and will cause flaccid paralysis for a lot longer and will require RESPIRATORY support.
What is tubocuarine? How do you reverse its effects?
its a Nm receptor antagonist. reverse with Neostygmine (AChE inhibitor to increase ACh levels to compete out with the tubocuarine)
What is an example of a non-specific anti-cholinergic?
Botulinum Toxin Type A - prevents docking of ACh vesicles at the cell membrane. Results in flaccid paralysis @ NMJ junctions and atropine effects at M junctions.
