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Neuromuscular Blocking Agents
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- Опубліковано 6 сер 2024
- A basic introduction into the Neuromuscular Junction, Neuromuscular Blocking Agents (NMBAs) and Reversal Agents. This video is part 2 of 3 and focuses on Neuromuscular blocking agents, their basic interaction in the Neuromuscular Junction, and how it produces temporary muscle paralysis when administered to a patient.
Learn more at the Xavant University at www. university.xavant.com. #eliminateRNB2025
Wow this was so easy to understand! You literally made medicine so much more interesting 🔥
Glad you liked it!
Blessing this is amazing
This was such a great explanation! Thank you.
honestly very well made and explained
In depolarizing one why did the sodium gates remain opened and if sodium influx takes place then intracellular membrane potential will be positive so how did the persistent depolarisation will take place
While in non depolarizing one you told that drug will block the binding of ach along with closing of sodium gates
Very helpful, thank a lot
Cu respect din Romania Domnul Isus sa va binecuvanteze Amin
Great video!
Thanks a lot 🥺💗
Very helpful
Hello! SRNA here! We are currently learning that one of the mechanisms behind the decreasing amplitude in TOF twitches has to do with the NDMR blocking a n-ACh-R auto-receptor on the motor neuron. This blocking inhibits the movement of VP1 ACh vesicles to VP2 position thereby decreasing the amount of ACh released with each impulse. Here in the video it is saying that the NDMR is blocking ChT (Choline transporter) and blocking the uptake of choline into the cell, thereby decreasing the actual production of ACh. Just wondering if you can tell me which is correct or maybe it is a combination of the two?
Great, ty
thank you
Was part 3 ever made? I cannot find the video about the antidotes.
Sooooo great!
BEST❣️
Depolarizing nmb's are the agonist bind with receptor and sodium channel gets open and sodium influx take place.Intra cellular charge become possitive.Then how skeletal muscle relaxation take place. Ach also depolarize cell. How its happen?
Suxamethonium is a compount of two acetylcholine molecules joined back-to-back which causes a prolonged depolarisation of the neuromuscular junction to a membrane potential above which action potential cannot be triggered. Normal neural transmission of action potential through indigenous acetylcholine stores does not happen hence an initial depolarisation (usually manifested by fasciculations) then followed by paralysis.
Thank u
Why depolarizing neuromuscular agent act on post synaptic and
Non depolarizing act on pre synaptic
👏🏻👏🏻👏🏻