Doing a second residency: am I nuts?

[aaronjw]

honestly are you actually ok right now? This stream of consciousness text is hard to follow.

 

Not sure this is the word I'd use in this context lol

[apache]

dude im fine... here: google raj sherman, and imagine way worse for a year

 

honestly are you actually ok right now? This stream of consciousness text is hard to follow.

[futureGP]

I have realized that I am not very thrilled about my job. I don't identify with it, and I cannot see myself doing it for long periods of time.

 

I am going to be an attending in a very short time frame. If afterwards I work for a year (if I can find work) I can apply for one of those bonded labor positions to get into a career I feel is rewarding, with the caveat that I work in a small community somewhere.

 

The thing is, I'm in my mid-thirties now. If I go this route - work a year, then go into another residency, then do the ubiquitous fellowship- I'm going to be older than forty before I actually start my career. Add five years to that before I have the freedom to settle down in a place of my choosing (which may very well be the community I work in during those years) and I'm basically pre-andropause before I start being a doctor with any personal autonomy.

 

I started medical school in my mid-twenties.

 

It'll have taken 21 years, from med school to being done, if I go this way. Six of those years would be a total complete waste of time.

 

This sounds like the most hairbrained scheme I could come up with. But the truth is I get no satisfaction from my work. None. I'm numb to it.

 

Would anyone here do it? Or am I just nuts, and should suck it up, work hard, fast and early, and retire soon after I start and go explore other non-medical things?

 

hey brooksbane

 

if ur not getting satisfaction from work, maybe u can try pursuing other interests outside of work?

 

at ur age it'll def be a long road again if you decide to do another residency (which might come with a ROS contract since u already did 1 residency)

 

then u'll truly be an uber-resident know-all

 

:S idk just brainstorming

[apache]

sorry bud... you know that cortisol caused 5ht2a abd 5ht2c downregulation, hence the lack of inhibition, blockade, primarily of the latter, via down regulation (remember, clonazepam temporarily works via 5ht1a temporarily upregulation of 5ht2a) or antagonist... basically i express low d2... i can't get bipolar, or schizophrenia... short succinct, and totally just showed whatever you spent 3 classes in psych learning, yeah... i try not to be a bit of an elitist, but seriously, they're not incoherant, they're true, but unlike the person who made the first report, i don't need to have a meeting on my songs funeral, to be intimidated, ahve my family life ruined... i'm sorry, politics, and medical agencies can be corrupt... google the alberta doctor who suspected the water was causing caner, david schwann... and please, google, the neurobio, because behavioral assessment will soon be a relic, and you'll see im right on... and well, i know i'm better than psych clinicians, i don't care, i dont need to tell people, i'm tired of feeling ashamed of the lack of quality around something i was interested in... that's ok, though, you'd be crazy to work as hard as me, even surg residents ... 110, yeah, ive done more... and dont tell me about mental illness, serious, you just look bad, appreciate the concern though, cheers

 

I really have to wonder if muse is having a manic bipolar episode right now. should last 7-10 days right? if these long bumbling posts stop in a little while, I guess we'll have our answer

 

ETA: these posts started becoming incoherent on Jan 10th, so let's see what happens around Jan 20th.

[thebouque]

How do you know that you express low D2?

[NLengr]

i try not to be a bit of an elitist, but seriously, they're not incoherant...

 

Really? Cause to me(and many others) they're basically unreadable. Which is a bit of a shame because sometimes there are some good thinking points in there.

[rogerroger]

sorry bud... you know that cortisol caused 5ht2a abd 5ht2c downregulation, hence the lack of inhibition, blockade, primarily of the latter, via down regulation (remember, clonazepam temporarily works via 5ht1a temporarily upregulation of 5ht2a) or antagonist... basically i express low d2... i can't get bipolar, or schizophrenia... short succinct, and totally just showed whatever you spent 3 classes in psych learning, yeah... i try not to be a bit of an elitist, but seriously, they're not incoherant, they're true, but unlike the person who made the first report, i don't need to have a meeting on my songs funeral, to be intimidated, ahve my family life ruined... i'm sorry, politics, and medical agencies can be corrupt... google the alberta doctor who suspected the water was causing caner, david schwann... and please, google, the neurobio, because behavioral assessment will soon be a relic, and you'll see im right on... and well, i know i'm better than psych clinicians, i don't care, i dont need to tell people, i'm tired of feeling ashamed of the lack of quality around something i was interested in... that's ok, though, you'd be crazy to work as hard as me, even surg residents ... 110, yeah, ive done more... and dont tell me about mental illness, serious, you just look bad, appreciate the concern though, cheers

 

 

I second what others are saying. Your posts are rambling rubbish. Sorry, maybe harsh but read that above and honestly tell me I'm wrong. If you have some sort of thought you aren't making it even remotely clear.

 

Poor punctuation, poor sentence structure, few to no paragraphs, no main theme or point can readily be identified. You switch from random rambling topic to another rambling topic mid sentence. Whatever you are or are not "expressing" it isn't coherent English.

[apache]

sort of how aripirazole or nefazadone works the prior targeting 5ht2a and c as antagonists... or how buspirones 5ht1a agonism in the raphne upregulates my downregulated 5ht2a receptors, clonazepam actually does the same thing via the medial raphne, both do, but clonazepams the only really effective agents because those 5ht2a inhibitory interneurons synapse onto gaba receptors in v5 of the occipital cortex... yeah, you can look up all about the recprical density and density and or binding of 5ht2a and c and the inverse binding to d2... its sort of like, everywhere, that 900 page text i posted, the one that talks about comt polymorphisms which break down some dopamine into 5ht2aa... causing the agressive adhd phenotype via over agonism of 5ht2a downreg from the continious agonism, how amphetamines are worse because of the maob effect, reuptake blocking effects and effect of increasing binding... compared to methylphenidate which does nothing in the cleft, just proures dat1 near teh end of the neuron and causes increased release, hense the increased effectiveness in the odd/violant subtype... the val/val... tbh, i dont feel like wasting time explaining, so you get the incoherant paraphrasing, just read that textbook i posted, its like on every 3rd page, and it's only around 900 pages, or read 4-500 articles a textbook on neurochem... of course i sound incoherant, the only person that gets it is the guys in the psychology dept who do psychopharm research... but if i explained in textbook grammar and what not i would go ovr the word count 5 posts over, which i do on pm all the time, but yeah, i've got stuff to do, and i's not intended as an insult, so i dont have 3 hours kicking round...

 

the 400 hours of research into my visual disorder, was sort of to see, and help all the people i chatted with whose neuros told them it was in their head... oh, sorry, adhd, getting back on track, it's caused by down-regulation of 5ht2a, by immunomodulatory psychotropic agents, that polymorphism and the downregulation due to the repeated overstimulation, it causes blood flow variations too, ortical spreading inhibition in the migrain aura side... and well, there only yeah, lets say a lot of studies that show that 5ht2a, which is coregulated with 5ht2c, metabotropic, regulator of rna expression, blah blah blah... differntial gender effects of the phenotypes and the exclusive 4 scizophrenic/bipolar members of my moms side (of 12, the other 8 are male, lucky me), also my lack of addictiveness to cigarettes... oh, my dad had me old too.... so ****, you know, being over the max dose of amphetamines, shouldnt really calm me down either... like yeah, especially over years, youd think id go ape **** by now eh, yeah no, i feel more tired on them actually (less hyperkinetic i guess)... im just joking around now, but seriously, with my genetic load, proven aeteology in every possible way, rad henry abraham, hes only been dong the vision thing for 30 years... and, well, i wont say my dose, but its rediculous, as in people go manic on maob inhibior effexor (only maob at high doses) and it's snri effect... i think im good, but thanks... and i didnt give enough depth, really read the book, seriously i can't put it down.

 

 

How do you know that you express low D2?

[thebouque]

sort of how aripirazole or nefazadone works the prior targeting 5ht2a and c as antagonists... or how buspirones 5ht1a agonism in the raphne upregulates my downregulated 5ht2a receptors, clonazepam actually does the same thing via the medial raphne, both do, but clonazepams the only really effective agents because those 5ht2a inhibitory interneurons synapse onto gaba receptors in v5 of the occipital cortex... yeah, you can look up all about the recprical density and density and or binding of 5ht2a and c and the inverse binding to d2... its sort of like, everywhere, that 900 page text i posted, the one that talks about comt polymorphisms which break down some dopamine into 5ht2aa... causing the agressive adhd phenotype via over agonism of 5ht2a downreg from the continious agonism, how amphetamines are worse because of the maob effect, reuptake blocking effects and effect of increasing binding... compared to methylphenidate which does nothing in the cleft, just proures dat1 near teh end of the neuron and causes increased release, hense the increased effectiveness in the odd/violant subtype... the val/val... tbh, i dont feel like wasting time explaining, so you get the incoherant paraphrasing, just read that textbook i posted, its like on every 3rd page, and it's only around 900 pages, or read 4-500 articles a textbook on neurochem... of course i sound incoherant, the only person that gets it is the guys in the psychology dept who do psychopharm research... but if i explained in textbook grammar and what not i would go ovr the word count 5 posts over, which i do on pm all the time, but yeah, i've got stuff to do, and i's not intended as an insult, so i dont have 3 hours kicking round...

 

the 400 hours of research into my visual disorder, was sort of to see, and help all the people i chatted with whose neuros told them it was in their head... oh, sorry, adhd, getting back on track, it's caused by down-regulation of 5ht2a, by immunomodulatory psychotropic agents, that polymorphism and the downregulation due to the repeated overstimulation, it causes blood flow variations too, ortical spreading inhibition in the migrain aura side... and well, there only yeah, lets say a lot of studies that show that 5ht2a, which is coregulated with 5ht2c, metabotropic, regulator of rna expression, blah blah blah... differntial gender effects of the phenotypes and the exclusive 4 scizophrenic/bipolar members of my moms side (of 12, the other 8 are male, lucky me), also my lack of addictiveness to cigarettes... oh, my dad had me old too.... so ****, you know, being over the max dose of amphetamines, shouldnt really calm me down either... like yeah, especially over years, youd think id go ape **** by now eh, yeah no, i feel more tired on them actually (less hyperkinetic i guess)... im just joking around now, but seriously, with my genetic load, proven aeteology in every possible way, rad henry abraham, hes only been dong the vision thing for 30 years... and, well, i wont say my dose, but its rediculous, as in people go manic on maob inhibior effexor (only maob at high doses) and it's snri effect... i think im good, but thanks... and i didnt give enough depth, really read the book, seriously i can't put it down.

 

It's raphe not raphne. I still think your D2 levels are normal unless you're on some kind of antipsychotics.

[tooty]

any new developments in this brooks?

[justletmein]

No offence muse, but your posts are often very long blocks of run on sentences slathered in ellipses. You are a good fella but I would wager that few people would want to read those posts, even if they have good points in them. It's your choice, but I bet you would generate more discussion if you made things a bit more brief.

 

agree x 100 000 000 000

[apache]

i said binding and/or density... oi, and sorry for that, im a terrible speller, yeah, i need to avoid the run on's, tend to happen when i get over-emotional about topics... then i tend to logic leap, cause i realize that the whole explanation would be 2 hrs, and then say **** it... lets go with short cuts

 

hehe, i do generate quite a bit of discussion when i dont discuss trashing psych and what not, but that's not my intention

 

and with the antipsychs, do you mean abnormally high, or downregulated from prolonged use... just kidding, seriously, read some of my lighter commentary, it's way more palatable, i promise

 

It's raphe not raphne. I still think your D2 levels are normal unless you're on some kind of antipsychotics.

[apache]

lol, yeah it's strange, the more chill the topic... as in non-flashback inducing of awful experiences which have shaped a real intense passion about a few topics... which are most things, honestly, that i notice diff people tend to read, then things become short, no logic leaps, rambling, and i even use paragraphs... so, my apologies for this thread... in general, and i hope u find what ur looking for

 

No offence muse, but your posts are often very long blocks of run on sentences slathered in ellipses. You are a good fella but I would wager that few people would want to read those posts, even if they have good points in them. It's your choice, but I bet you would generate more discussion if you made things a bit more brief.

[cdnmaple]

This sounds like the most hairbrained scheme I could come up with. But the truth is I get no satisfaction from my work. None. I'm numb to it.

 

Would anyone here do it? Or am I just nuts, and should suck it up, work hard, fast and early, and retire soon after I start and go explore other non-medical things?

 

Well. I'm doing it. Crazy, yes, but I would be crazier not to. The day I made the decision I had the best sleep in ages... total relief. Don't know if I will be successful yet, but I can only hope.

 

That said, if you're still in residency/fellowship, I hope this isn't just burnout. I know plenty who have come through that phase and come out the attending end and realized it wasn't so bad. Then, there's people like me... I didn't think it was going to be insurmountable, until I was done residency.

[steve999]

The thing is, I'm in my mid-thirties now. If I go this route - work a year, then go into another residency, then do the ubiquitous fellowship- I'm going to be older than forty before I actually start my career. Add five years to that before I have the freedom to settle down in a place of my choosing (which may very well be the community I work in during those years) and I'm basically pre-andropause before I start being a doctor with any personal autonomy.

[Talon01]

if you do switch, part way through a residents or start a completely new one, do you start back at the PGY1 pay scale as per whatever province you're in?

[A-Stark]

I don't know about starting a new one, but it will depend on the contact for switching. In my contract, if you were to switch after PGY1, you get paid as a PGY2 regardless of the level you're transferring into.