Class of 2017!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! !!!!!

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tatertots said:
i'd kill for your score! Haha o well. To each his own. :hungover:

though i kind of know what you mean. I come close but never reach my highest score from my 2nd test....
Click to expand...

+1
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GooseWing said:
Mo you're Aug 19 too right??
Which tests do you have left to take? I've got AAMC 8,9,10,11

Who else is Aug. 19?
Click to expand...

Yeah, I'm august 19. 8,9,10,11 left as well. I gotta figure out how to take the test though in the morning. I'm taking it a few hours later than my actual time, so I should try the whole "testing environment" thing soon. I just feel really sleepy in the morning, and I'm already going to bed at like 10 PM to get a good routine going.
 
mohad said:
Yeah, I'm august 19. 8,9,10,11 left as well. I gotta figure out how to take the test though in the morning. I'm taking it a few hours later than my actual time, so I should try the whole "testing environment" thing soon. I just feel really sleepy in the morning, and I'm already going to bed at like 10 PM to get a good routine going.
Click to expand...

Are you a morning person? The way I've been doing it may or may not work for you based on if you are or aren't.
I've been waking up at 5:30. Breakfast at 6 (with a cup of coffee). This gives time enough to relax and eat and wake up. I'll leave the house around 7-7:15 to arrive at the testing center 7:30-7:45.
I still have to drive to the place so that I know exactly where it is come test day. My mom says she wants to drive me though :D
 
GooseWing said:
Are you a morning person? The way I've been doing it may or may not work for you based on if you are or aren't.
I've been waking up at 5:30. Breakfast at 6 (with a cup of coffee). This gives time enough to relax and eat and wake up. I'll leave the house around 7-7:15 to arrive at the testing center 7:30-7:45.
I still have to drive to the place so that I know exactly where it is come test day. My mom says she wants to drive me though :D
Click to expand...

I have been trying to do this wake up early thing but its hard to actually get up at 6ish when you don't actually have an MCAT that morning =/
 
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GooseWing said:
Are you a morning person? The way I've been doing it may or may not work for you based on if you are or aren't.
I've been waking up at 5:30. Breakfast at 6 (with a cup of coffee). This gives time enough to relax and eat and wake up. I'll leave the house around 7-7:15 to arrive at the testing center 7:30-7:45.
I still have to drive to the place so that I know exactly where it is come test day. My mom says she wants to drive me though :D
Click to expand...

I've been waking up at 5 to eat, and then I just read to pass the time till 8 oclock, but when I start reading bio, I just get soooo woozy, and I close my eyes for "5 minutes". I tried doing something dumb like browsing the internet or watching something, and I stay awake, but my mind runs a bit slowly. I like doing something intellectually stimulating before an exam, but I just get tired from doing it.
 
Wow I'm jelly of all y'all's practice scores: I think I'm taking AAMC 7 tomorrow and in all likelihood I'll probably just drop four points again :(
Studying has been very slow lately ahhhhhh.

Any motivating songs for me, oh class of 2017ers?

Also, major props GooseWing and Mohad: those are some fiiiiine scores. I would, as StudyShy put it many a page ago, "kill my dog" for a 36 on my MCAT, hahaha. Not really. But maybe. :scared:

Poor Tashele...
 
ozzi22 said:
Ever since i watched that show, i now want to be a surgeon :love:
Click to expand...

:thumbdown:, ever since I watched Scrubs I DIDN'T want to be a surgeon. And it made me love endocrinology even more :love:

I TOTALLY DIAGNOSED THE WOMAN WITH POLYCYSTIC OVARIAN SYNDROME BEFORE ELLIOT DID. LIKE OMG. I totally paused the episode after J.D. presented the symptoms (amenorrhea and hirsutism, obese female patient), thought for a second, SCREAMED "POLYCYSTIC OVARIAN SYNDROME!!!!!", calmed myself, unpaused the episode, Elliot diagnosed the patient with said PCOS, and proceeded to feel validated as a human being. It's how I get the ladies.

Sorry for the epic nerd confession, hahaha. I guess I'm just... really into endocrinology...?
 
Kangaroo Paw said:
:thumbdown:, ever since I watched Scrubs I DIDN'T want to be a surgeon. And it made me love endocrinology even more :love:

I TOTALLY DIAGNOSED THE WOMAN WITH POLYCYSTIC OVARIAN SYNDROME BEFORE ELLIOT DID. LIKE OMG. I totally paused the episode after J.D. presented the symptoms (amenorrhea and hirsutism, obese female patient), thought for a second, SCREAMED "POLYCYSTIC OVARIAN SYNDROME!!!!!", calmed myself, unpaused the episode, Elliot diagnosed the patient with said PCOS, and proceeded to feel validated as a human being. It's how I get the ladies.

Sorry for the epic nerd confession, hahaha. I guess I'm just... really into endocrinology...?
Click to expand...

wow, i gotta be honest, i haven't quite seen anyone interested in endocrinology before. everyones wants to go into the so called ROAD specialties except for me :Dwell you know endo is competitive but still in you're reach if you work hard. more power to you bro :thumbup:
 
I don't miss the important tops.

minerva3121 said:
Okay so some 2017ers are upset I topped one of the pages in their thread (even though they started it by topping our pages!) Just be sure not to let them take the top once we reach 30K!
Click to expand...

hmmm.
 
ozzi22 said:
wow, i gotta be honest, i haven't quite seen anyone interested in endocrinology before. everyones wants to go into the so called ROAD specialties except for me :Dwell you know endo is competitive but still in you're reach if you work hard. more power to you bro :thumbup:
Click to expand...

Hahahaha thanks man! Really? I don't get how it's not more universally interesting: it includes some pretty bread-and-butter, staple diseases like diabetes, osteoporosis, and thyroid dysfunction. But yeah, I spent a whole summer working directly with endo patients and it was AMAZING.
 
This has to be a team effort :)


(also to add padding in case they try to cheat)
 
Tatertots said:
Can you teach me hormones. =( so many!
Click to expand...

Which ones be plaguin' ya, matey? I haven't really studied them properly yet, but I'm okay with some. Menstrual cycle's a huge weakness, otherwise I think I have a decent grasp.

Congrats on being happy with your practice score today, by the way, bro! Hopefully I'll be happy with my Tuesday/Wednesday score...
 
Deathstar said:
This has to be a team effort :)


(also to add padding in case they try to cheat)
Click to expand...

Let us know when they get close. We should all show up ^^

Deathstar said:
Why is no one in our class a mod.
Click to expand...

Go Go deathstar. :cool:

Kangaroo Paw said:
Which ones be plaguin' ya, matey? I haven't really studied them properly yet, but I'm okay with some. Menstrual cycle's a huge weakness, otherwise I think I have a decent grasp.

Congrats on being happy with your practice score today, by the way, bro! Hopefully I'll be happy with my Tuesday/Wednesday score...
Click to expand...

I have a handful of mnemonics to remember which ones are steroid/peptide/thyroid but I don't know what most of them do except the basic ones: Glucagon, Cortisol, Insulin, Parathyroid Hormone and Calcitonin. Any helpful hints for the other billion. -_-
 
Tatertots said:
Let us know when they get close. We should all show up ^^



Go Go deathstar. :cool:



I have a handful of mnemonics to remember which ones are steroid/peptide/thyroid but I don't know what most of them do except the basic ones: Glucagon, Cortisol, Insulin, Parathyroid Hormone and Calcitonin. Any helpful hints for the other billion. -_-
Click to expand...

Hmmm those are definitely good to know. I'd say ADH and aldosterone are two biggies, and I'd know the FLAT PEG mnemonic for the anterior pituitary. FLAT (FSH, LH, ACTH, TSH) are "tropic hormones", so they act on an organ which then releases something to effect change in the ultimate, target organ and PEG (Prolactin, Endorphins, and Growth Hormone) are "direct hormones", which bind directly to the target, affected organ. To make that make more sense, I guess I'll talk about a whole pathway? So Corticotropin Releasing Factor (CRF) is released from the hypothalamus into the hypophyseal portal system (bloodstream), swims on over to the anterior pituitary, binds, stimulates release of ACTH, ACTH swims waaaaaay over to the adrenal cortex, which releases cortisol, a glucocorticoid. The adrenal cortex ITSELF wasn't "changed" by the ACTH, to the ACTH is a tropic hormone. Then the cortisol does what it does (increased gluconeogenesis, decreased (?) protein synthesis, decreased inflammation/immunological response, and a bunch of other crap I really don't understand). The majority of the pituitary hormones work like that: 1) hypothalamus secretes its hormone (usually called a "releasing factor"-->2) pituitary secretes its hormone-->3) other crap happens!

Huh, I actually don't think I know which ones are steroid vs. peptide... I think estrogen, testosterone, glucocorticoids and mineralocorticoids are steroid and the rest except T3 and T4 are peptide?

But yeah, ADH and aldosterone: respond to the same thing, low blood volume (or high blood osmolarity, same thing), and act to increase blood volume by decreasing excretion of water and increasing reabsorption of it, but by very different pathways. ADH, secreted by the posterior pituitary (which is essentially just an extension of the hypothalamus that secretes oxytocin or ADH in response to action potentials from the hypothalamus), binds to the collecting ducts of the kidney tubule and makes the pores in the duct physically bigger, so that water flows out of the tubule and into the bloodstream (I don't know the exact mechanism by which this is done but I feel like that's totally unnecessary to know).

Aldosterone is a mineralocorticoid (so, a steroid hormone) released by the adrenal cortex in response to the renin-angiotensin pathway or ACTH bound to ACTH receptors on the adrenal cortex. Essentially, when blood volume is low (or, more specifically, blood pressure is low), renin is secreted by the juxtaglomerular apparatus (I think it's a part of the nephron right next to the glomerulus? hahaha), which converts inactive angiotensinogen into angiotensin I. Angiotensin I isn't really potent, so it pretty much just sits around, but ACE (Angiotensin Converting Enzyme) converts this active form of angiotensin into angiotensin II, which in and of itself is very potent and has a powerful vasoconstricting effect, leading to increased blood pressure. Angiotensin II binds to (receptors, I guess) on the adrenal cortex and releases aldosterone, which binds to Na+/K+ pumps in the collecting duct of the kidney tubule, changing their activity so that more Na+ leaves the tubule and is reabsorbed into the bloodstream, and so that K+ is pushed into the tubule (along with H+ protons), and excreted. Water follows the Na+ out of the tubule and into the bloodstream, so blood vessels experience increased blood pressure due to aldosterone's effects (in tandem with angiotensin II). Oh, just a cool note on ACE: ACE inhibitors are common ways to treat hypertension because angiotensin I pretty much does squat to increase blood pressure, so by not being able to be converted to angiotensin II--> aldosterone, the renin-angiotensin pathway is cut short and the patient experiences decreased blood pressure! ARB's are also common, they're antagonists to angiotensin II receptors.

Whew, sorry for the ridiculously long post, that was good to review for me. Totally suck at glucocorticoids so I should go look those up. Hope that helped a bit, tots!

Could someone go through the menstrual cycle, por favor? I'm having some trouble understanding it fully.

Merci!
 
GooseWing said:
How're you watching (Hopkins)??? Did you torrent it or buy it or what?
Click to expand...

Bumping my own question :)

Kangaroo Paw said:
Also, major props GooseWing and Mohad: those are some fiiiiine scores. I would, as StudyShy put it many a page ago, "kill my dog" for a 36 on my MCAT, hahaha. Not really. But maybe. :scared:
Click to expand...

Thanks KPaw!! I'm sure you'll do great. My senses say that a 4-point bump is in your future!
 
Kangaroo Paw said:
Hmmm those are definitely good to know. I'd say ADH and aldosterone are two biggies, and I'd know the FLAT PEG mnemonic for the anterior pituitary. FLAT (FSH, LH, ACTH, TSH) are "tropic hormones", so they act on an organ which then releases something to effect change in the ultimate, target organ and PEG (Prolactin, Endorphins, and Growth Hormone) are "direct hormones", which bind directly to the target, affected organ. To make that make more sense, I guess I'll talk about a whole pathway? So Corticotropin Releasing Factor (CRF) is released from the hypothalamus into the hypophyseal portal system (bloodstream), swims on over to the anterior pituitary, binds, stimulates release of ACTH, ACTH swims waaaaaay over to the adrenal cortex, which releases cortisol, a glucocorticoid. The adrenal cortex ITSELF wasn't "changed" by the ACTH, to the ACTH is a tropic hormone. Then the cortisol does what it does (increased gluconeogenesis, decreased (?) protein synthesis, decreased inflammation/immunological response, and a bunch of other crap I really don't understand). The majority of the pituitary hormones work like that: 1) hypothalamus secretes its hormone (usually called a "releasing factor"-->2) pituitary secretes its hormone-->3) other crap happens!

Huh, I actually don't think I know which ones are steroid vs. peptide... I think estrogen, testosterone, glucocorticoids and mineralocorticoids are steroid and the rest except T3 and T4 are peptide?

But yeah, ADH and aldosterone: respond to the same thing, low blood volume (or high blood osmolarity, same thing), and act to increase blood volume by decreasing excretion of water and increasing reabsorption of it, but by very different pathways. ADH, secreted by the posterior pituitary (which is essentially just an extension of the hypothalamus that secretes oxytocin or ADH in response to action potentials from the hypothalamus), binds to the collecting ducts of the kidney tubule and makes the pores in the duct physically bigger, so that water flows out of the tubule and into the bloodstream (I don't know the exact mechanism by which this is done but I feel like that's totally unnecessary to know).

Aldosterone is a mineralocorticoid (so, a steroid hormone) released by the adrenal cortex in response to the renin-angiotensin pathway or ACTH bound to ACTH receptors on the adrenal cortex. Essentially, when blood volume is low (or, more specifically, blood pressure is low), renin is secreted by the juxtaglomerular apparatus (I think it's a part of the nephron right next to the glomerulus? hahaha), which converts inactive angiotensinogen into angiotensin I. Angiotensin I isn't really potent, so it pretty much just sits around, but ACE (Angiotensin Converting Enzyme) converts this active form of angiotensin into angiotensin II, which in and of itself is very potent and has a powerful vasoconstricting effect, leading to increased blood pressure. Angiotensin II binds to (receptors, I guess) on the adrenal cortex and releases aldosterone, which binds to Na+/K+ pumps in the collecting duct of the kidney tubule, changing their activity so that more Na+ leaves the tubule and is reabsorbed into the bloodstream, and so that K+ is pushed into the tubule (along with H+ protons), and excreted. Water follows the Na+ out of the tubule and into the bloodstream, so blood vessels experience increased blood pressure due to aldosterone's effects (in tandem with angiotensin II). Oh, just a cool note on ACE: ACE inhibitors are common ways to treat hypertension because angiotensin I pretty much does squat to increase blood pressure, so by not being able to be converted to angiotensin II--> aldosterone, the renin-angiotensin pathway is cut short and the patient experiences decreased blood pressure! ARB's are also common, they're antagonists to angiotensin II receptors.

Whew, sorry for the ridiculously long post, that was good to review for me. Totally suck at glucocorticoids so I should go look those up. Hope that helped a bit, tots!

Could someone go through the menstrual cycle, por favor? I'm having some trouble understanding it fully.

Merci!
Click to expand...

Wow Thanks for the long explanation! You are amazing!

I don't have a lot of the menstrual cycle memorized since most of the time they tell you a lot in the passages but here are the details that I found important:

Follicular Phase
-LH/FSH
-Ends in Ovulation around day 14(?)

Luteal phase
- Estrogen/Progesterone
- Corpus Luteum develops in response

Thats all I know off the top of my head. I probably can recognize more. haha sorry that probably wasn't very helpful.
 
Kangaroo Paw said:
:thumbdown:, ever since I watched Scrubs I DIDN'T want to be a surgeon. And it made me love endocrinology even more :love:

I TOTALLY DIAGNOSED THE WOMAN WITH POLYCYSTIC OVARIAN SYNDROME BEFORE ELLIOT DID. LIKE OMG. I totally paused the episode after J.D. presented the symptoms (amenorrhea and hirsutism, obese female patient), thought for a second, SCREAMED "POLYCYSTIC OVARIAN SYNDROME!!!!!", calmed myself, unpaused the episode, Elliot diagnosed the patient with said PCOS, and proceeded to feel validated as a human being. It's how I get the ladies.

Sorry for the epic nerd confession, hahaha. I guess I'm just... really into endocrinology...?
Click to expand...

I freaking :love::love::love::love: Scrubs!
 
Kangaroo Paw said:
Hmmm those are definitely good to know. I'd say ADH and aldosterone are two biggies, and I'd know the FLAT PEG mnemonic for the anterior pituitary. FLAT (FSH, LH, ACTH, TSH) are "tropic hormones", so they act on an organ which then releases something to effect change in the ultimate, target organ and PEG (Prolactin, Endorphins, and Growth Hormone) are "direct hormones", which bind directly to the target, affected organ. To make that make more sense, I guess I'll talk about a whole pathway? So Corticotropin Releasing Factor (CRF) is released from the hypothalamus into the hypophyseal portal system (bloodstream), swims on over to the anterior pituitary, binds, stimulates release of ACTH, ACTH swims waaaaaay over to the adrenal cortex, which releases cortisol, a glucocorticoid. The adrenal cortex ITSELF wasn't "changed" by the ACTH, to the ACTH is a tropic hormone. Then the cortisol does what it does (increased gluconeogenesis, decreased (?) protein synthesis, decreased inflammation/immunological response, and a bunch of other crap I really don't understand). The majority of the pituitary hormones work like that: 1) hypothalamus secretes its hormone (usually called a "releasing factor"-->2) pituitary secretes its hormone-->3) other crap happens!

Huh, I actually don't think I know which ones are steroid vs. peptide... I think estrogen, testosterone, glucocorticoids and mineralocorticoids are steroid and the rest except T3 and T4 are peptide?

But yeah, ADH and aldosterone: respond to the same thing, low blood volume (or high blood osmolarity, same thing), and act to increase blood volume by decreasing excretion of water and increasing reabsorption of it, but by very different pathways. ADH, secreted by the posterior pituitary (which is essentially just an extension of the hypothalamus that secretes oxytocin or ADH in response to action potentials from the hypothalamus), binds to the collecting ducts of the kidney tubule and makes the pores in the duct physically bigger, so that water flows out of the tubule and into the bloodstream (I don't know the exact mechanism by which this is done but I feel like that's totally unnecessary to know).

Aldosterone is a mineralocorticoid (so, a steroid hormone) released by the adrenal cortex in response to the renin-angiotensin pathway or ACTH bound to ACTH receptors on the adrenal cortex. Essentially, when blood volume is low (or, more specifically, blood pressure is low), renin is secreted by the juxtaglomerular apparatus (I think it's a part of the nephron right next to the glomerulus? hahaha), which converts inactive angiotensinogen into angiotensin I. Angiotensin I isn't really potent, so it pretty much just sits around, but ACE (Angiotensin Converting Enzyme) converts this active form of angiotensin into angiotensin II, which in and of itself is very potent and has a powerful vasoconstricting effect, leading to increased blood pressure. Angiotensin II binds to (receptors, I guess) on the adrenal cortex and releases aldosterone, which binds to Na+/K+ pumps in the collecting duct of the kidney tubule, changing their activity so that more Na+ leaves the tubule and is reabsorbed into the bloodstream, and so that K+ is pushed into the tubule (along with H+ protons), and excreted. Water follows the Na+ out of the tubule and into the bloodstream, so blood vessels experience increased blood pressure due to aldosterone's effects (in tandem with angiotensin II). Oh, just a cool note on ACE: ACE inhibitors are common ways to treat hypertension because angiotensin I pretty much does squat to increase blood pressure, so by not being able to be converted to angiotensin II--> aldosterone, the renin-angiotensin pathway is cut short and the patient experiences decreased blood pressure! ARB's are also common, they're antagonists to angiotensin II receptors.

Whew, sorry for the ridiculously long post, that was good to review for me. Totally suck at glucocorticoids so I should go look those up. Hope that helped a bit, tots!

Could someone go through the menstrual cycle, por favor? I'm having some trouble understanding it fully.

Merci!
Click to expand...

Dang man, you've got this down!
 
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