homework question

[marcia888]

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Hello. I just found this forum. I'm a pre-pharmacy student. I hope you can help me with a homework question. Below the question is what I've figured out so far and my questions as I am having a hard time in my research drawing the conclusions they seem to want.

John was about to undergo abdominal surgery at Hillman's Hospital in Kansas. His anesthetist was Marie . . . affectionately known in town as Marie the Magnificent (for her great margaritas). Anyway, the night prior to John's surgery Marie threw a heck of a bash at her house and she and her friends were up all night imbibing libations and dancing. Upon arriving at the hospital Marie was surprised to learn that she had been put in charge of anesthesia for the day because the scheduled person was sick. Marie was sort of 'hung over' but decided to do the job anyway. She prepped for the surgery and then administered John his drug cocktail (IV administration) that included pancuronium. The surgical nurse soon noticed a dropped pulse Ox%, pallor, and cyanosis Marie panicked and without consultation of the physician, took the liberty of administering neostigmine; she did it without first giving atropine. Remarkably, she and the nurse were surprised about the tachycardia and hypertension just before John kicked off (died).
(a) What was the rationale for administering pancuronium prior to the surgery?
(b) Since it was administered IV - what precautions should have been taken?
(c) Why is the use of the drug contraindicated in asthmatics?
(d) Explain why John's Oxygen% dropped and why his skin color changed.
(e) Why did Marie think neostigmine would help? What would have been a good first course of action to take to prevent John from getting worse?
(f) Why was the neostigmine, without atropine first, an unsuccessful course of action?
(g) Why hypertension and tachycardia?

Here's what I've figured so far:
a) to relax the muscles
b) they should have checked for an athmasic condition and other conditions too such as dehydration, heart diesase, lung disease.
c) the muscle relaxant could cause relaxation in the trachea which would cause breathing difficulty.
d) He was having trouble breathing so his oxygen level dropped and he turned pale.
e) it reverses the effects of pancuronium. But I can't find what would have been a good course of action to prevent him from getting worse.
f) I have no idea. The words pancuronium, neostigmine and atropine are not mentioned in my textbook. And I've had no luck Googling for the answer.
g) His blood pressure and pulse went up as his heart tried harder to provide him with the oxygen he lacked from his breathing difficulties.


Thanks for your help

 

[jwk]

Hello. I just found this forum. I'm a pre-pharmacy student. I hope you can help me with a homework question. Below the question is what I've figured out so far and my questions as I am having a hard time in my research drawing the conclusions they seem to want.



Here's what I've figured so far:
a) to relax the muscles
b) they should have checked for an athmasic condition and other conditions too such as dehydration, heart diesase, lung disease.
c) the muscle relaxant could cause relaxation in the trachea which would cause breathing difficulty.
d) He was having trouble breathing so his oxygen level dropped and he turned pale.
e) it reverses the effects of pancuronium. But I can't find what would have been a good course of action to prevent him from getting worse.
f) I have no idea. The words pancuronium, neostigmine and atropine are not mentioned in my textbook. And I've had no luck Googling for the answer.
g) His blood pressure and pulse went up as his heart tried harder to provide him with the oxygen he lacked from his breathing difficulties.


Thanks for your help

Before someone gives you the answer, which would be pretty easy for anyone here, let me suggest you do a little more homework - look for some anesthesia textbooks - this is all Anesthesia 101. Not all answers are found on the internet - that's a shortcut, not real research.

 

[jetproppilot]

Hello. I just found this forum. I'm a pre-pharmacy student. I hope you can help me with a homework question. Below the question is what I've figured out so far and my questions as I am having a hard time in my research drawing the conclusions they seem to want.



Here's what I've figured so far:
a) to relax the muscles
b) they should have checked for an athmasic condition and other conditions too such as dehydration, heart diesase, lung disease.
c) the muscle relaxant could cause relaxation in the trachea which would cause breathing difficulty.
d) He was having trouble breathing so his oxygen level dropped and he turned pale.
e) it reverses the effects of pancuronium. But I can't find what would have been a good course of action to prevent him from getting worse.
f) I have no idea. The words pancuronium, neostigmine and atropine are not mentioned in my textbook. And I've had no luck Googling for the answer.
g) His blood pressure and pulse went up as his heart tried harder to provide him with the oxygen he lacked from his breathing difficulties.


Thanks for your help

OK folks, I'm gonna bite, although I really don't know why.

Pancuronium is an aminosteroidal, non-depolarizing, neuromuscular blocker molecularly similar to vecuronium, pipecuronium, and rocuronium.

(a) Noone would ever administer pancuronium properatively. Pancuronium causes paralysis by competing for, and displacing acetylcholine from nicotinic M receptors at the neuromuscular junction. Administering it as described in the question would constitute malpractice.
(b) The clinician shouldve waited to administer it until arriving in the OR and administering an induction agent prior to giving the pancuronium.
(c) Pancuronium causes histamine release (I think) so, in theory, should be used with caution in patients with airway hypersensitivity.
(d) John desaturated and turned cyanotic because he was administered a paralytic without concominant airway support. He stopped breathing, and noone breathed for him.
(e) Marie thought neostigmine would help because neostigmine inhibits the enzyme that hydrolyzes acetycholine, letting acetylcholine levels rise, which, given the right conditions, will displace pancuronium from the receptor it is occupying. Unfortunately neostigmine will not work for some time after administering pancuronium (45 min- 1 hour after an intubating dose) since too much pancuronium is still present and enough of it will not be displaced and the patient will remain paralyzed. To prevent John from getting worse, after realizing her mistake, she should've began aggressive bag-mask ventilation, and administered something for amnesia (i.e. midazolam)
(f) neostigmine given with or without atropine right after a big dose of pancuronium will not work. see (e).
Clinically, neostigmine may cause bradycardia dude to resultant acetylcholine concentration rise, so glycopyrollate is usually given to offset this. Atropine could theoretically be given for the same purpose, but its onset would precede neostigmine's. In practice glycopyrollate is used.
(g) Pancuronium's vagolytic effect causes tachycardia and sometimes a slight BP rise.

 

[jetproppilot]

OK folks, I'm gonna bite, although I really don't know why.

Pancuronium is an aminosteroidal, non-depolarizing, neuromuscular blocker molecularly similar to vecuronium, pipecuronium, and rocuronium.

(a) Noone would ever administer pancuronium properatively. Pancuronium causes paralysis by competing for, and displacing acetylcholine from nicotinic M receptors at the neuromuscular junction. Administering it as described in the question would constitute malpractice.
(b) The clinician shouldve waited to administer it until arriving in the OR and administering an induction agent prior to giving the pancuronium.
(c) Pancuronium causes histamine release (I think) so, in theory, should be used with caution in patients with airway hypersensitivity.
(d) John desaturated and turned cyanotic because he was administered a paralytic without concominant airway support. He stopped breathing, and noone breathed for him.
(e) Marie thought neostigmine would help because neostigmine inhibits the enzyme that hydrolyzes acetycholine, letting acetylcholine levels rise, which, given the right conditions, will displace pancuronium from the receptor it is occupying. Unfortunately neostigmine will not work for some time after administering pancuronium (45 min- 1 hour after an intubating dose) since too much pancuronium is still present and enough of it will not be displaced and the patient will remain paralyzed. To prevent John from getting worse, after realizing her mistake, she should've began aggressive bag-mask ventilation, and administered something for amnesia (i.e. midazolam)
(f) neostigmine given with or without atropine right after a big dose of pancuronium will not work. see (e).
Clinically, neostigmine may cause bradycardia dude to resultant acetylcholine concentration rise, so glycopyrollate is usually given to offset this. Atropine could theoretically be given for the same purpose, but its onset would precede neostigmine's. In practice glycopyrollate is used.
(g) Pancuronium's vagolytic effect causes tachycardia and sometimes a slight BP rise.

Are you sure this isnt Ashton?? I probably just got Punked...

 

[Gimlet]

Are you sure this isnt Ashton?? I probably just got Punked...

I think you might'a been...that whole bit about "Marie the Magnificent" being hungover was a little much. Whoever wrote that question has an interesting sense of humor. Seems like the question is pretty advanced for a PRE-Pharmacy student...what class is this for?