Autonomics III Flashcards
Classify each receptor by selectivity and frequency of utilization of cholinergic receptor inhibiting drugs. NN, NM, M1-5
NN - Non-selective rarely used, NM - Moderately selective often used, M1-5 - Very selective and often used
Name six muscarinic receptor inhibitors (Two groups and their respective uses
Dicyclomine, Tropicamide, Tolterodine (Tertiary amines for peripheral applications), Ipratropium, Tiotropium, (Quaternary amine for asthma), Benzotropine (Tertiary amine for Parkinson’s)
What is the mnemonic for atropine (and other muscarinic antagonists) overdose?
“Dry as a bone, blind as a bat, red as a beet, mad as a hatter”
Describe the reasons for the symptoms of muscarinic antagonist OD
Initially slight cardiac slowing due to the inhibition of the M2 autoreceptors along with dryness of the mouth (blockage of M3), and inhibition of sweating (sympathetic innervation), followed by dilation of the pupil (inhibit pupillary sphincter muscle) and rapid heart rate (Block M2 receptors on heart and therefore vagus can’t put the brake on the heart)
Why are ganglion-blocking drugs rarely used? What is an example?
They are non-specific (Both para and symp are blocked). Hexamethonium
What type of receptor is found at NMJ? What are drugs that target this receptor useful for?
NM; Muscle relaxants
What are the two types of medications used to block at NM at the NMJ?
Nondepolarizing blockers and Depolarizing blockers
Describe the mechanism of NM Nondepolarizing blockers. Give an example
Binding of antagonist to NM which keeps NM closed. Prevents depolarization. Tubocuarine
Describe the mechanism of NM Depolarizing blockers. Give an example
Super agonist binds to the receptor keeping it open causing continued depolarization and disallows for muscle cycling. Succinylcholine.
Clincial uses for NM inhibitors and toxicity
Tubocuarine results in flaccid paralysis - used for surgery w/o anesthesia, Succinylcholine - Quick onset and rapid hydrolysis - used for quick procedures (intubation). Toxicity: Respiratory paralysis
Cholinesterase inhibitors are good at reversing effects of…
Non-depolarizing NM blockers. Tubocurarine has no intrinsic activity. ACh can compete with it.
How does Botulinum Toxin A work? Where does it work? Use?
Degrade SNAP25 which stops the fusion of ACh with presynaptic nerve terminal. It works on the presynaptic nerve terminal of para and the presynaptic terminal of the NMJ.
