finally got around to reviewing my nbme 15, from reading through this thread to find the answers, all

I can say
is dang a lot of you all over think things. Just focus on the most obvious answer based on the facts in first aid
and don't freak yourselves out, if your spending more like like 15 seconds of "hard thinking" and its not a
calculation or one of the up/down arrow problems, your probably just talking yourself out of the right answer.
Which of the following best explains why deoxygenated blood can carry more carbon dioxide for a given
Pco2 than oxygenated blood?
A- Deoxyhemoglobin does not bind to 2,3-bisphosphoglycerate as efficiently as oxyhemoglobin
B- Deoxyhemoglobin has a lower capacity to form carbamino compounds than oxyhemoglobin
C- Deoxyhemoglobin has a lower pKa than oxyhemoglobin
D- Deoxyhemoglobin is a better buffer of hydrogen ions than oxyhemoglobin
E- Oxygen and carbon dioxide compete for the same binding site in hemoglobin
F- Oxyhemoglobin binds nitric oxide with a higher affinity than deoxyhemoglobin

For the first question, it is asking about the Haldane effect regarding deoxyhemoglobin's higher affinity
for H+ than oxyhemoglobin.
The mechanism here is very interesting and important for Step 1. Remember this equation:
CO2 + H2O --> H2CO3 --> H+ + HCO3As a result, the majoring of CO2 in the blood exists as bicarb. [nb: lab results often use Bicarb and
CO2 interchangeably for this very reason]
The Haldane effect basically says that dHgb is a better proton acceptor than OHgb. When hgb is in the
tissues releasing O2, it becomes a better proton acceptor and starts pulling protons out of the blood.
Per Le Chatlier's, that equation above will shift to the right and convert more and more CO2 to
bicarbonate ion.
Therefore, D is the correct answer.
For #2, this is HUGE concept and if it doesn't show up on your Step 1, will definitely show up on your
psychiatry shelf, internal medicine shelf, and Step 2 CK. It's totally fair game for step 1 also. The BIG
CONCEPT is this:
Terminal diseases tend to make people depressed.
So it's not just pancreatic cancer, but any disease will do it. Metastatic melanoma, ESRD, etc. Anything
terminal and scary can and will often lead to major depression. Receiving a terminal diagnosis is a
major risk factor for suicide as well.
They will typically not ask this question so obviously as above. They will give you the same vignette,
but end with this:
.... In addition to chemotherapy and radiation, which of the following medications would be most
appropriate to start in this patient?
a) atenolol
b) Oxybutinin
c) citalopram
d) donepezil
e) propranolol
So, basically the same question as above, but adding in you need to pick the antidepressant (C) from
the bunch of other non-indicated drugs.

Oh man, let me think... Genetics is so tied in with cell and molecular biology! There's so much high yield
stuff that it's hard to narrow down. Certainly all the stuff in FA is fair game. I would say it's important to
have a strong conceptual knowledge because they will try and write questions that make you think beyond
what's in FA.
I would pay particular attention to the clinical aspects of genetics. For a given disease, knowing what kind of
genetics tests you would want to use, and even how to interpret them. They will definitely through some
electrophoresis gels at you or a microarray or a FISH and expect you to interpret the information. Certainly
know all the genetics-related diseases - all the cancers, CF, SC, etc.
I'll have to think -- the more I type, the more I feel like i'm not helping much. I'll have to think and get back
to you with some better thoughts. Do you have any more specific questions? Genetics is just a HUGE topic!

youngdoc260 - 05/15/15 20:05

The #1 thing you MUST do when answering behavioral science question is this:
Figure out what the learning objective of the question is.
Before you can answer the question, you must figure out what the "real" question is. A lot of people
struggle with the ethical and behavioral questions because they think they can get the right answer
just by gut instinct. Unfortunately, this doesn't always work. You need to have a method. Start by
figuring out the objective.
Once you know the objective, answering the question gets easier.

youngdoc260 - 05/16/15 05:15

"Majority of behavioral science questions are common sense" is exactly what I mean by people trying
to rely on gut instinct for these questions. Often, the answer that feels correct is wrong, so you've got
to have a strategy for answering these.
I'm intrigued by the differences in how medical ethics and similar topics are taught overseas. If it's not
too broad a question, would you mind sharing some examples?

It can be difficult. Pheos tends to have sort of a cyclical pattern in that the symptoms come and go; thyrotox
it depends on the etiology. That's pretty vague though and the truth is they have quite a bit of overlap. On
an exam, I would look for any of the classic thyroid stigmata -- proptosis, etc. For pheo, I would look for
tachycardia/headache/extreme hypertension, especially that comes and goes.
For the exam, they would have to give you some additional information. IF they asked you what labs you'd
want, you would want TSH and free T4. If they gave you normal thyroid studies and no other clue to the
etiology, then you would want serum or urine metanephrines or imaging. Remember a favorite of board
examiners: if you see no tumors on the adrenal glands themselves, where would you be most likely to find a
pheo? At the bifurcation of the aorta (Organ of Zuckerkandl).

Thanks, that helps.

and Pheos can occur anywhere along the sympathetic chain. correct? I will definitely keep bifurcation of
aorta in mind.

HUMAN PLACENTA LACTOGEN

youngdoc260 - 05/07/15 21:51

It's produced by the placenta -- specially the syncytiotrophoblast. It's similar to GH though much
weaker. It's main function is to increase the supply of nutrients to the placenta. It does this by being
kind of an anti-insulin. By decreasing insulin sensitivity, the mother has increase blood glucose levels
which then give the fetus more glucose. It also mobilizes fatty acids for mom's energy, thus leaving
more glucose for the fetus.
I can think of a few ways examiners might want to ask about this:
1) Easy question: where is it made? (syncytiotrophoblast)
2) HPL as the mechanism of maternal gestational diabetes -- decreased insulin sensitivity and increase
blood glucose --> gestation diabetes if too much. This is probably the most likely question. I would
give you vignette showing elevated glucose tolerance test in a pregnant woman and ask which
hormone was most likely elevated.
3) Asking about it in conjunction with other placental hormones like HCG, progesterone, etc. I could
envision one of those arrows questions here.
Thanks!
The more I think about it, HPL makes a better distractor than anything else.
That's definitely one thing I noticed on the steps and shelves -- they loved to include at least one answer
choice that was something I had never heard of. The result was that I never felt 100% confident about my
answers because there was always that one weird answer choice I couldn't be sure of. HPL would work really
well as one of those!
For future testers, I would know about it, but be careful about picking it unless you've got good reasons.
.

1.

IkB keeps NFkB sequestered in cytoplasm in inactive form. During activation of the pathway IkB are
phosphorylated by kinases and NFkB is released, which then goes to nucleus and activates
transcription of certain proteins.
Ans would be.. release of NFkB after phosphorylation.

littleturtle - 03/15/16 12:47

Ok lets make this MEPP clear......it stands for miniature end plate potential
It is formed by leakage of acetylcholine vesicles in the synaptic cleft.......

In order to produce an action potential u need to have a summation of MEPP to reach threshold level
for an End Plate Potential to occur.
But in this case the patient has botulisum so what u will see very low MEPP leaking into the cleft plus
the response to Ach is going to be like a normal muscle but not enough to produce an EPP like in a
normal muscle.
Your EPP in this experimental case case is dependent on yur concentration of Ach + yur EPP that the
muscle has.
The most important in this quest is to appreciate that botulism does not affect the end plate on the
muscle so it will be same as normal.
No problem me the under average student learning here too :)
But logically if u have botulism yur EPP has to decrease coz u releasing less Ach....right so we are left
with choice A-D
Now, its not a post synaptic problem so response to Ach should be the same as control so the answer is
B.