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Otago HSFY chat - archive

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Carrington is awesome, and I'm glad I went there.

Really nice people.
Really nice food.
Good social events.
Got lots of people into med.

Other halls:

Really nice people.
Good social events.
A couple also get lots of people into med.

On the point of number of people getting into med though - while it's nice for me to have most of my friends from first year also in my med class, it does kind of mean I miss out on socialising with non-meddies (even more than I would otherwise). So, it's not necessarily a good or bad thing. And going to Carrington isn't going to increase your chances of getting into med or anything (the reason why Carrington gets lots of people in is because it attracts/selects for the kind of person who'll get into med).

So, conclusion:

Carrington is awesome. Come to Carrington and you'll love it. The other halls are all awesome. Go to any of them and you'll love it.

(The other halls don't have food as nice as Carrington food though. You should come to Carrington for the awesome food.)
 
I'm very confused about what we were supposed to get out of today's cells lecture (lecture 33). Could someone please clarify what we need to know? Thanks. :)
 
Hey can anyone help me with a question in the Hubs GLM booklet. It asks what happens when the Acetylcholinesterase is defective, and then cases where this defect occurs in humans. What happens to the person?

I was thinking that if the enzyme is defective Ach can't get degraded in the synaptic cleft so builds up and so when the next AP depolarizes the bouton then neurotransmitter can't be released into the cleft as it is already full, so the impulse can't get to the effector. Is that along the right track? And what does the next question mean, when does this happen in humans?

Thank-youuuu
 
hadfr504 said:
Hey can anyone help me with a question in the Hubs GLM booklet. It asks what happens when the Acetylcholinesterase is defective, and then cases where this defect occurs in humans. What happens to the person?

I was thinking that if the enzyme is defective Ach can't get degraded in the synaptic cleft so builds up and so when the next AP depolarizes the bouton then neurotransmitter can't be released into the cleft as it is already full, so the impulse can't get to the effector. Is that along the right track? And what does the next question mean, when does this happen in humans?

Thank-youuuu
Click to expand...

well, acetylcholinesterase is used to stop synaptic transmission, so if it is defective, it would lead to tetany of the muscle.

If this occurs in humans, it would cause muscle paralysis, as well as possibly asphyxiation if it occurred within the respiratory system.

does that help? (please correct me if I'm wrong)
 
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Hi guys :)

Did you all learn the contraction sequence of the heart? I was listening to the podcast, and I can't seem to workout whether he means that we can ignore it until HUBS192, or that we'll learn more in HUBS192, but this is still examinable when he talks about it... :/

[OFFTOPIC]I was procrastinating.... and then came up with a genuine question :D[/OFFTOPIC]
 
Nimbus2000 said:
Hi guys :)

Did you all learn the contraction sequence of the heart? I was listening to the podcast, and I can't seem to workout whether he means that we can ignore it until HUBS192, or that we'll learn more in HUBS192, but this is still examinable when he talks about it... :/

[OFFTOPIC]I was procrastinating.... and then came up with a genuine question :D[/OFFTOPIC]
Click to expand...

I would think the contraction sequence of the heart would come in Semester 2 as he didn't explain the whole process nor did he go into much detail.
 
jonathan810 said:
I would think the contraction sequence of the heart would come in Semester 2 as he didn't explain the whole process nor did he go into much detail.
Click to expand...

lol thanks :D but re-listen to it - the man seems to have a knack for writing nothing on the lecture slides, but yet endowing a trucketload of information... i'm not sure if all that he says is examinable or not :/

EDIT:
[OFFTOPIC] AAARGH. truckload/ bucketload... i'm not sure why I decided to mix those up :L [/OFFTOPIC]
 
Nimbus2000 said:
lol thanks :D but re-listen to it - the man seems to have a knack for writing nothing on the lecture slides, but yet endowing a trucketload of information... i'm not sure if all that he says is examinable or not :/
Click to expand...


I believe this is lecture 29? If so, the lecture objectives doesn't have anything regarding the contraction sequence in the heart, nor is there anything describing the contraction sequence in the essential readings. O.o?
 
Don't fret guys. It'd be downright bizarre for HUBS191 to question you about the contraction sequence of the heart when you're going to learn all about it in HUBS192.
 
greenglacier said:
Don't fret guys. It'd be downright bizarre for HUBS191 to question you about the contraction sequence of the heart when you're going to learn all about it in HUBS192.
Click to expand...

Thanks gg!

[MENTION=9540]juna[/MENTION], oh noo!!! dw, you'll find it easier to learn next semester i guess?
 
Oh lol... Guys, if something isn't even remotely related to the lecture objectives (or even the current module), you won't need to know it. You're doing what, endocrine? So stick to endocrine, leave cardio alone for now :p
 
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