Biggest adjustment from intern year in IM to PGY-2 Neurology?

[95439]

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I was wondering if anyone had any thoughts/insight regarding the transition from PGY-1 (Internal Medicine) to PGY-2 Neurology? Is PGY-2 essentially an intern year all over again because you're starting fresh in a new specialty? (I really really hope so.. 😳/ ). Any words of wisdom would be greatly appreciated in regards to preparation etc!!

Thanks as always,
bblue

 

[danielmd06]

Yup, it was about the same in terms of expectations from my experience.

The big difference is that you may not have an entire team of fellow residents on-call with you (including an in-house senior to bounce things off of). I actually found the PGY-2 year to be much more difficult in terms of call strain and work load, but easier because I loved the subject matter.

 

[95439]

Yup, it was about the same in terms of expectations from my experience.

The big difference is that you may not have an entire team of fellow residents on-call with you (including an in-house senior to bounce things off of). I actually found the PGY-2 year to be much more difficult in terms of call strain and work load, but easier because I loved the subject matter.

Call strain and workload doesn't scare me...being the hospital's whipping boy does. Your response is actually good news!

 

[typhoonegator]

It is going to vary a lot program to program, but you will not be relied on as an independent thinker from the start, as you might be as a PGY-2 IM resident (at least on some rotations). That is both good and bad, because for a lot of things, you are now fully capable of working things out on your own, and it can get frustrating to be put back on a leash. On the flip side, you aren't going to know much detailed neurology when you show up, so it is good to be able to take a more passive stance for at least part of another year. You'll gradually start taking more responsibility, and before you know it you'll be running your plan by your senior rather than calling for orders/advice. It's a really cool progression.

I totally second the sentiment that while just as hard or harder than PGY-1 year, it goes down a lot more easily because a) it is what you want to do with your life, b) you can see a direct application to each teaching point and case, and c) fewer FTT admits.

 

[95439]

It is going to vary a lot program to program, but you will not be relied on as an independent thinker from the start, as you might be as a PGY-2 IM resident (at least on some rotations). That is both good and bad, because for a lot of things, you are now fully capable of working things out on your own, and it can get frustrating to be put back on a leash. On the flip side, you aren't going to know much detailed neurology when you show up, so it is good to be able to take a more passive stance for at least part of another year. You'll gradually start taking more responsibility, and before you know it you'll be running your plan by your senior rather than calling for orders/advice. It's a really cool progression.

I totally second the sentiment that while just as hard or harder than PGY-1 year, it goes down a lot more easily because a) it is what you want to do with your life, b) you can see a direct application to each teaching point and case, and c) fewer FTT admits.

The first 6 months of intern year, I studied hard and really dedicated myself to IM. But honestly, it has become hard as the year comes to an end to see the point of learning extensively about the signs/symptoms of CHF, COPD etc. I'm looking forward to memorizing info relevant to my future patients at this point.
Sooo...I'll just ask, what are "FTT admits"? I'll assume failure to thrive lol

 

[danielmd06]

The first 6 months of intern year, I studied hard and really dedicated myself to IM. But honestly, it has become hard as the year comes to an end to see the point of learning extensively about the signs/symptoms of CHF, COPD etc. I'm looking forward to memorizing info relevant to my future patients at this point.
Sooo...I'll just ask, what are "FTT admits"? I'll assume failure to thrive lol

FTT = failure to thrive.

Oh, and you might be surprised at how valuable knowledge on CHF and COPD turn out if you wind up in Sleep Medicine...you never know where the winds will blow you and studying is almost invariably time well spent. Good luck with the rest of the year, though. You're almost there.

 

[95439]

FTT = failure to thrive.

Oh, and you might be surprised at how valuable knowledge on CHF and COPD turn out if you wind up in Sleep Medicine...you never know where the winds will blow you and studying is almost invariably time well spent. Good luck with the rest of the year, though. You're almost there.

Thanks Danielmd06. You and TN have provided alot of helpful info on here and it's greatly appreciated!
I can see how CO2 retention can relate to sleep studies in COPD, but aside from BiPap, I'm not sure how CHF can effect it. Is it mainly the effects of hypoxia/orthopnea/PND? Am I starting a new thread?

 

[danielmd06]

Thanks Danielmd06. You and TN have provided alot of helpful info on here and it's greatly appreciated!
I can see how CO2 retention can relate to sleep studies in COPD, but aside from BiPap, I'm not sure how CHF can effect it. Is it mainly the effects of hypoxia/orthopnea/PND? Am I starting a new thread?

No problem. CHF is seriously linked to OSA and central sleep apnea.

 

[95439]

No problem. CHF is seriously linked to OSA and central sleep apnea.

CHF -> Chronic Hypoxic state -> eventual suppression of central respiratory drive? If that's the case why aren't more patients with longstanding CHF hypercapneic?

 

[danielmd06]

CHF -> Chronic Hypoxic state -> eventual suppression of central respiratory drive? If that's the case why aren't more patients with longstanding CHF hypercapneic?

They don't really know why central apneas occur with CHF, but one theory is the combination of long circulatory time (courtesy of impaired cardiac function) to the peripheral and central chemoreceptors at the carotid bifurcation and brainstem.

By the time the breathing patterns ramp up (hyperpnea phase) and adjust to an increased CO2 load (from the perspective of the *behind-the-ball* receptors), enough CO2 has been blown off to drive systemic CO2 levels way below what is required to reach the hypercapnic respiratory drive levels (which are higher in sleep anyway) and you get hypopeas or frank apneas. Then those selfsame hyopneas result in increased CO2 levels which creep higher than you'd normally see because once again the receptors are slow to detect the change until they've hit a suprathreshold point. And the whole cycle repeats. It's not a state of perpetual hypercapnia.

Chronic hypercapnia is more something you see with hypoventilating patients. In the sleep world...this would include obesity hypoventilation syndrome.

 

[95439]

They don't really know why central apneas occur with CHF, but one theory is the combination of long circulatory time (courtesy of impaired cardiac function) to the peripheral and central chemoreceptors at the carotid bifurcation and brainstem.

By the time the breathing patterns ramp up (hyperpnea phase) and adjust to an increased CO2 load (from the perspective of the *behind-the-ball* receptors), enough CO2 has been blown off to drive systemic CO2 levels way below what is required to reach the hypercapnic respiratory drive levels (which are higher in sleep anyway) and you get hypopeas or frank apneas. Then those selfsame hyopneas result in increased CO2 levels which creep higher than you'd normally see because once again the receptors are slow to detect the change until they've hit a suprathreshold point. And the whole cycle repeats. It's not a state of perpetual hypercapnia.

Chronic hypercapnia is more something you see with hypoventilating patients. In the sleep world...this would include obesity hypoventilation syndrome.

Had to read it twice but it does make sense. Thanks DanielMD. (I don't think anyone else wanted to hear about 2nd year anticipatory anxiety anyway lol)

 

[sarcoid]

They don't really know why central apneas occur with CHF, but one theory is the combination of long circulatory time (courtesy of impaired cardiac function) to the peripheral and central chemoreceptors at the carotid bifurcation and brainstem.

By the time the breathing patterns ramp up (hyperpnea phase) and adjust to an increased CO2 load (from the perspective of the *behind-the-ball* receptors), enough CO2 has been blown off to drive systemic CO2 levels way below what is required to reach the hypercapnic respiratory drive levels (which are higher in sleep anyway) and you get hypopeas or frank apneas. Then those selfsame hyopneas result in increased CO2 levels which creep higher than you'd normally see because once again the receptors are slow to detect the change until they've hit a suprathreshold point. And the whole cycle repeats. It's not a state of perpetual hypercapnia.

Chronic hypercapnia is more something you see with hypoventilating patients. In the sleep world...this would include obesity hypoventilation syndrome.

That is way more Interesting to me than doing USMLE world questions. Thanks!