Official nbme 15 discussion

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abelabbot

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A new NBME 15 is out! Here is the official discussion page. How did you guys feel about this nbme?

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I think you guys are just over thinking this. DKA, too much glucose in the blood correct, that isn't getting taken up. Glucokinase is inducible, hence why it has a high Vmax, by insulin. This was the logic that I used, and in addition going back to my previous argument, all the other enzymes listed would only make the situation worse since they would lead to an increase glucose levels in the blood.
.

OK , Glukokinase is affected positively by Insulin .
I know that as a fact working in ICU with Ketoacidosis patients .

Second reason is that Glukokinase mutation is responsible for MODY ( mature onsetT DM of the young) . And this is also a fact .
 
Hi guys, was wondering if I could get some help on some of the questions. A brief EXPLANATION would be great too if you have one.

Before I post though, I briefly read some of the above posts and thought I'd contribute:
- I got the Down Syndrome with ALL wrong too. I put MEGALOBLASTOSIS because of pathoma. But note that Megaloblastosis DOES NOT refer to Megakaryoblastic Leukemia, it refers to large RBC's (MCV>100). So I guess pathoma isn't wrong in this case.

- saw someone post that the anal lesion with a picture was SCC of the anus, but its actually external hemorrhoids (painful and doesn't bleed). Maybe someone already corrected this.

My questions:

Lymphocyte neoplasm DOES NOT express: CD4, CD8, surface igM, surface IgG, cytoplasmic IgM and mu-heavy chains, cytoplasmic IgG, and gamma-heavy chains. It DOES express class I MHC and show rearrangement of the T-lymphocyte receptor beta-chain gene D and J segments. Which is the normal counterpart?
a. Activated cytolytic effector T lymphocytes in circulation
b. Mature IgM-secreting B lympchotes in LN
c. Mature Immunoglovulin secreting plasma cells in LN
d. Pre-B lymphocyte progenitor of mature B lymphobytes in the BM
e. T-lymphocyte thyocytes localized to the thymic cortex
This is a double negative immature T cell that localizes to the thymic cortex

Kid presents with congestive heart failure due to a VSD. After fixing the VSD, what changes will be seen in the following:
- Left Ventricular P
- Right Ventricular P
- Left Atrial P
LV pressure increases, RV pressure decreases, and LA pressure decreases. The left to right shunt from LV to RV is driving the pressure in the LV down, and since the RV is getting an increased volume of blood the pressure in the RV is greater. This increased volume is then transmitted through the LA. The pressure doesnt drop until the LV when it all repeats again
-
 
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Pls help :
1.The question of the 25 yrs old man participating in the muscle function study ..3 columns were put with : epp-Amplitude , mepp- Amplitude and response in mV to Ach .
Based on the normal values the question asked about the muscle Bx specimen in Acute botulism
I answered A which was wrong .

I am not good in experiment questions ... .

6.During the experiment of muscle contraction intracellular Ca is decreased after a substance is adm .The question asks WHY contraction is inhibited in this case .
I answered E which was wrong .
Somebody with a better idea ?

Much appreciated .

In the question about end plate potential it gave an epp in response to a normal release of acetylcholine. I believe it said a normal epp gave a concentration of 10 micromolar of ach. a mini end plate potential consists of random release of ach that does not amount to more than 1 micromolar, and it said the voltage response was 1mv for every 1 micromolar of ach... if I recall correctly. So then it asked what would happen in the presence of botulism- Botulism would block epp, but would have no effect on mepp (because these are random discahrges of ach) or voltage difference in response to a given amount of ach.
 
look at that muscle study question...because i know for a fact there was another option that had the value of 1 as the answer choice for Ach on the far right hand side...can you just post up a link to the question?

OK ,So the muscle study question :
Normal muscle epp Amplitude 10, mepp Amplitude 1 , Response in (mV) to ASch 1 .

The answeres options we are looking at are :

epp amplitude 1 , mepp Amplitude 1 ,Response in( mV) to Ach 1
or

epp Amplitude 15 , mepp Amplitude 1 , Response in (mV) to Ach 1 .

Which one do we chose after Botulinum administration ?
I can not do more explicite due to copyright ...

Thanks a lot .
 
OK ,So the muscle study question :
Normal muscle epp Amplitude 10, mepp Amplitude 1 , Response in (mV) to ASch 1 .

The answeres options we are looking at are :

epp amplitude 1 , mepp Amplitude 1 ,Response in( mV) to Ach 1
or

epp Amplitude 15 , mepp Amplitude 1 , Response in (mV) to Ach 1 .

Which one do we chose after Botulinum administration ?
I can not do more explicite due to copyright ...

Thanks a lot .

Its the first one. botulism blocks ach release, but it has no effect on mepp because these are normal random quantum fluctuations of ach in the synapse. Like wise botulism, blocking ach release has no effect on voltage difference response. The voltage difference is dependent on other factors such as membrane potential and ion concentrations.
 
.

OK , Glukokinase is affected positively by Insulin .
I know that as a fact working in ICU with Ketoacidosis patients .

Second reason is that Glukokinase mutation is responsible for MODY ( mature onsetT DM of the young) . And this is also a fact .

makes much sense... thanks
 
Its the first one. botulism blocks ach release, but it has no effect on mepp because these are normal random quantum fluctuations of ach in the synapse. Like wise botulism, blocking ach release has no effect on voltage difference response. The voltage difference is dependent on other factors such as membrane potential and ion concentrations.

Thanks man .
I got it .
 
I forget the answers to the other 2. So someone else can chime in

4. Woman has history of altered consciousness. She stops talking in mid-sentence, turns her head to the right, and extends and stiffens her right upper extremity. She has a blank look and does not respond to any questions. She then has some repetitive lip smacking and picking movement of the hands. Episodes lasts 30secs. She slowly returns to he normal state during the next 4-5min. What type of seizure is it?
- Absence
- Complex partial
- Generalized tonic clonic
- Simple partial motor
- Simple partial sensory
Put Tonic clonic just cause I saw the stiffness, followed by a repetitive movement. Is this wrong because its not the entire body/extremities? Is the answer Complex partial? Didn't know it would switch from stiffness to clonus like that.

Complex Partial is the answer. The key here is NO Loss of consciousness and the automatisms after the seizure

MedicineMike, thanks for your response, But for the above question, there IS loss of consciousness right? since she "wouldn't respond" and has a blank look. Also, isnt the definition of COMPLEX partial seizure = loss of consciousness (vs simple partial = maintain consciousness). Thanks!
 
Any thoughts with this investigation question on H . Pylori .
I got wrong this one .
Thanks a lot
 
There was a question about a premature baby with respiratory distress and it asked which of the following parameters would INCREASE?
alveoli radii
lung complience
lung elastic recoil
pleural pressure
surfactant secretion

Obviously it is not surfactant secretion, lung elastic recoil, and I didnt think it was pleural pressure. I was between lung complience and alveoli radii. I put lung complience which was wrong. So is it alveoi radii? I know the radius of some alveoli increases, but at the same time other alveoli collapse...
 
There was a question about a premature baby with respiratory distress and it asked which of the following parameters would INCREASE?
alveoli radii
lung complience
lung elastic recoil
pleural pressure
surfactant secretion

Obviously it is not surfactant secretion, lung elastic recoil, and I didnt think it was pleural pressure. I was between lung complience and alveoli radii. I put lung complience which was wrong. So is it alveoi radii? I know the radius of some alveoli increases, but at the same time other alveoli collapse...

I think I had lung elastic recoil and i didn't get it wrong...
 
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I think that question is just gearing you towards ARDS of a newborn ---> hyaline membrane ---> restrictive

not saying that your answer is wrong, but the way I thought about it was

ARDS due to decreased surfactant--> Increase tension --> alveoli want to collapse (P =2T/r) P = collapsing pressure
 
hmm thats interesting. any idea on the mechanism?

not saying that your answer is wrong, but the way I thought about it was

ARDS due to decreased surfactant--> Increase tension --> alveoli want to collapse (P =2T/r) P = collapsing pressure

I agree with you actually, but looking at those answer choices is what made me gear towards Restrictive
 
I think I had lung elastic recoil and i didn't get it wrong...

There are at least 3 processes in RDS .

1.Increased lung recoil and decreased lung compliance .
The intra pleural pressure will be more NEGATIVE .Will be more difficult to inflate the lungs .

2.Atelectasis . There is a tendency for the alveoli to collapse .Once they are collapsed cannot be re inflated . So the radius of the alveoli does not increase , but decrease .The sigmoid curve of gas exchange will be pushed to the right .

3.Pulmonary edema . The deficiency in the surfactant increases recoil , a negative intra thoracic pressure is required to maintain a lung volume .Practically, if we intubate these patients the oxygenation is not going to improve too much , we need to give them synthetic surfactant over the tube

The conclusion of all these is that the recoil is increased and I am pretty sure this is the answer .
 
what was the personality behavior of the one patient? i wrote narcissistic...but that obviously was wrong...

was it antisocial? reviewed the personality disorders, and it seems to be the one that fits.
 
what was the personality behavior of the one patient? i wrote narcissistic...but that obviously was wrong...

was it antisocial? reviewed the personality disorders, and it seems to be the one that fits.

What was the gist of the presentation?
 
What was the gist of the presentation?

AnVN4eb.png
 
Yup I answered antisocial and it wasn't marked wrong for me! I think the "feeling jobs were beneath his ability" throws you towards narcissistic, but the whole no regard for authority sways the answer more towards antisocial.
 
Yup I answered antisocial and it wasn't marked wrong for me! I think the "feeling jobs were beneath his ability" throws you towards narcissistic, but the whole no regard for authority sways the answer more towards antisocial.

yeah but mainly because i forgot that antisocial personality disorder =/= antisocial as we usually hear it as in the non-medical setting..lol

can't lose these points on behavioral questions. i feel these are easy gimme-points...even got the question about ADHD wrong...talked about open, assessed, stratification - which is what i chose.
 
It's okay, we all have those moments when we misread, or just make silly mistakes. I think being well fed, rested and relaxed will help us avoid those during the exam--or at least that's what I'm hoping for!
 
Alright, my two questions:
Woman comes in who obviously has somatization disorder. What's the question that you want to ask her?
Is it: "I'd like to assess the symptom causing you the most distress and schedule a monthly follow up appointment."?

The other one was the phenylalanine hydroxylase one. The PH gene was homozygous for a point mutation in intron 12 (GT->AT) that causes skipping of exon 12. What causes the skipping of exon 12?
a- alternative polyadenylation site
b- deletion of 5' untranslated region
c- expansion of trinucleotide repeat
d- gene duplication
e- nonhomologous recombination
f- not it
g-RNA splice error
h- X inactivation
 
Alright, my two questions:
Woman comes in who obviously has somatization disorder. What's the question that you want to ask her?
Is it: "I'd like to assess the symptom causing you the most distress and schedule a monthly follow up appointment."?

The other one was the phenylalanine hydroxylase one. The PH gene was homozygous for a point mutation in intron 12 (GT->AT) that causes skipping of exon 12. What causes the skipping of exon 12?
a- alternative polyadenylation site
b- deletion of 5' untranslated region
c- expansion of trinucleotide repeat
d- gene duplication
e- nonhomologous recombination
f- not it
g-RNA splice error
h- X inactivation

and i also got the top one wrong
 
Alright, my two questions:
Woman comes in who obviously has somatization disorder. What's the question that you want to ask her?
Is it: "I'd like to assess the symptom causing you the most distress and schedule a monthly follow up appointment."?

yup...i recall that one of the answers was blatantly wrong, which was the last option...you never refer them to another physician...if you list the other choices...i can tell you why they're wrong

edit: how do you go about solving that 2nd question...hate questions pertaining to molecular techniques...
 
yup...i recall that one of the answers was blatantly wrong, which was the last option...you never refer them to another physician...if you list the other choices...i can tell you why they're wrong

edit: how do you go about solving that 2nd question...hate questions pertaining to molecular techniques...

Introns are taken out using snRNPs specific to certain splice sequences. RNA splicing is really the only association with intron/exon problems.
 
Phew this one was tough. Going over it now so I'll surely have a few questions coming up (and I'm trying to search the thread to make sure I don't repeat questions... bear with me people). The first one is about the autosomal dominant pedigree that skips the mother. On a different NBME, I literally saw the exact same pedigree and it was variable expressivity. Not the case on this one... I'm guessing it was incomplete penetrance (both were answer choices on both questions).

The variable expressivity was in reference to NF1 while this question was about Hereditary Telangiectasia. Do we just have to memorize which diseases are which and accept the fact that the pedigrees can look the same?
 
Phew this one was tough. Going over it now so I'll surely have a few questions coming up (and I'm trying to search the thread to make sure I don't repeat questions... bear with me people). The first one is about the autosomal dominant pedigree that skips the mother. On a different NBME, I literally saw the exact same pedigree and it was variable expressivity. Not the case on this one... I'm guessing it was incomplete penetrance (both were answer choices on both questions).

The variable expressivity was in reference to NF1 while this question was about Hereditary Telangiectasia. Do we just have to memorize which diseases are which and accept the fact that the pedigrees can look the same?

On NBME 11, the disease wasn't present in the first generation. If I remember correctly, in this pedigree it skipped a generation. That's a much stronger case for incomplete penetrance.
 
Tx of lady with exposure to radioactive I?
Levothyroxine
Liothyronine
Propylthiouracil
Methimazole (my choice - wrong)
Potassium Iodine

I was thinking this or PTU to prevent the organification and formation of radioactive Thyroid hormone. Maybe PTU was right I don't know. Am I missing something here?
 
Tx of lady with exposure to radioactive I?
Levothyroxine
Liothyronine
Propylthiouracil
Methimazole (my choice - wrong)
Potassium Iodine

I was thinking this or PTU to prevent the organification and formation of radioactive Thyroid hormone. Maybe PTU was right I don't know. Am I missing something here?

It was Potassium Iodine. It will compete with the 125I, so less of the radioactive iodide will be taken up by the thyroid cells.
 
Tx of lady with exposure to radioactive I?
Levothyroxine
Liothyronine
Propylthiouracil
Methimazole (my choice - wrong)
Potassium Iodine

I was thinking this or PTU to prevent the organification and formation of radioactive Thyroid hormone. Maybe PTU was right I don't know. Am I missing something here?

Iodine. You need to compete with the radioactive iodine for absorption. Once you've absorbed the radioactive isotope, you're going to use it eventually, regardless of PTU etc.
 
Nice, thanks guys! So essentially it works in a somewhat similar fashion to the anions (perchlorate and -technate) since they comp inhibit the Na/I symporter?

I ask because I want to understand the concept completely. If perchlorate was a choice and KIodine wasn't it would be the correct answer also right?
 
Nice, thanks guys! So essentially it works in a somewhat similar fashion to the anions (perchlorate and -technate) since they comp inhibit the Na/I symporter?

I ask because I want to understand the concept completely. If perchlorate was a choice and KIodine wasn't it would be the correct answer also right?

Yep.
 
Female with non-foul, non-fishy STD with frothy yellow green discharge from the vagina with red spots on cervix and motile organisms with flagella. How do you treat?

IM Pen G
IV Ceftriaxone and oral doxy
Metronidazole
or an antifungal?

I couldn't figure out if what organism they were asking here
 
Female with non-foul, non-fishy STD with frothy yellow green discharge from the vagina with red spots on cervix and motile organisms with flagella. How do you treat?

IM Pen G
IV Ceftriaxone and oral doxy
Metronidazole
or an antifungal?

I couldn't figure out if what organism they were asking here
Metronidazole. It's Trichomonas vaginalis.
 
yup...i recall that one of the answers was blatantly wrong, which was the last option...you never refer them to another physician...if you list the other choices...i can tell you why they're wrong

edit: how do you go about solving that 2nd question...hate questions pertaining to molecular techniques...
Hah, I put that last option. And yes I feel bad about it.

The only other one it possibly could have been was, "Tell me about any childhood trauma you may have experienced." But that seemed silly. For the other two, one was related to testing for porphyria, and the other one was accusing her of malingering.
 
Phew this one was tough. Going over it now so I'll surely have a few questions coming up (and I'm trying to search the thread to make sure I don't repeat questions... bear with me people). The first one is about the autosomal dominant pedigree that skips the mother. On a different NBME, I literally saw the exact same pedigree and it was variable expressivity. Not the case on this one... I'm guessing it was incomplete penetrance (both were answer choices on both questions).

The variable expressivity was in reference to NF1 while this question was about Hereditary Telangiectasia. Do we just have to memorize which diseases are which and accept the fact that the pedigrees can look the same?

what'd you think about this exam? did you already go through 11, 12, and 13...
 
Introns are taken out using snRNPs specific to certain splice sequences. RNA splicing is really the only association with intron/exon problems.

actually i was thinking of the wrong question...i apologize...it was the one that had the options of northern, southern, pcr, etc etc...im pretty sure i wrote northern...but ended up being wrong...fml
 
what'd you think about this exam? did you already go through 11, 12, and 13...

I can only compare it to 12 and the one our school gave us (which was incredibly easy), but I thought this was way harder than 12. Got the exact same score in the end but missed 4 more questions.

I'm ok with it because on this one I didn't make any stupid mistakes... each of the ones I got wrong were straight up things I either never learned or the question was written poorly, so at least my testing skills have improved if my general knowledge hasn't :shrug:
 
I can only compare it to 12 and the one our school gave us (which was incredibly easy), but I thought this was way harder than 12. Got the exact same score in the end but missed 4 more questions.

I'm ok with it because on this one I didn't make any stupid mistakes... each of the ones I got wrong were straight up things I either never learned or the question was written poorly, so at least my testing skills have improved if my general knowledge hasn't :shrug:

yeah this one was kinda hard...i didnt know colorectal carcinoma metastasizes via hematogenously...i only thought it was the ones mentioned in pathoma...

even that other question that had the frameshift mutation...an additional C is inserted...but none of the answer choices made sense...got that wrong

got the NY/SF question wrong, but got the botulisum question right...

i hope the step isn't as difficult as 15...

edit: imo, 11 = 12 > 13 >> 15 from easiest to difficult...emphasis on the two >'s from 13 to 15...lol...i'd say 13 is only a fraction/tad bit harder than 11 and 12
 
yeah this one was kinda hard...i didnt know colorectal carcinoma metastasizes via hematogenously...i only thought it was the ones mentioned in pathoma...

even that other question that had the frameshift mutation...an additional C is inserted...but none of the answer choices made sense...got that wrong

got the NY/SF question wrong, but got the botulisum question right...

i hope the step isn't as difficult as 15...

edit: imo, 11 = 12 > 13 >> 15 from easiest to difficult...emphasis on the two >'s from 13 to 15...lol...i'd say 13 is only a fraction/tad bit harder than 11 and 12

Yea... there's a C insertion but "insertion" was the wrong answer apparently? Or did I mix it up with a different question?

I've heard the actual test is way harder but people also generally do way better than they expected based on how they felt after the test. Have faith in the curve.
 
Okay, let's see what I can contribute... Just read the whole thread (that was exhausting but good work guys). One quick note:

3. A man on hydrochlorothiazide gets light-headed and dizzy when he stands up to quickly. Which of following sets of changes (up or down arrows) best characterizes changes in the cardiovascular system as man goes from supine to standing?
Venous Return -- up or down
Carotid Sinus Baroreceptor activity -- up or down
Cerebral blood flow -- up or down

Venous return down, cerebral blood flow down, and I want to say carotid sinus baroreceptor activity down (I got it right so I cant see it)... Keep in mind the baroreceptors send out inhibitory signals so it's the opposite of what you'd expect. They sense a drop in BP, and then they decrease their inhibitory signals in order to allow your sympathetic nervous system to increase your heart rate. It's kind of like that tricky thyroid hormone question... even though the end result is increased sympathetic activity, the direct effect (whenever it says "direct" I've learned to anticipate a trick) is via decreased inhibition from the baroreceptors. Sorry that that's complicated... let me know if I got it twisted.


Now I'm gonna go over my wrong answers, so stay tuned for some of my questions.
 
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I'm trying to look up the answers to save you guys time and you can either agree/disagree with what I find. If I have no effing clue, then I'll list the answer choices. Aaaaand go!

--Half hour after uncomplicated vaginal delivery, mother is still bleeding/hypotensive. What treatment would be "helpful"? (Thought that was a funny word selection)
A) androgen
B) estrogen
C) progesterone
D) Prolactin
E) Oxytocin

--The 4 day old male with respiratory depression, periauricular skin tags, micrognathia, mandibular cleft, etc.... Is that supposed to be Treacher Collins?

--3 year old girl with Mycobacterium avium infection with normal immunoglobulins... It seems to be IL-12 receptor deficiency but that's not an answer choice. The next best thing is IFN-gamma receptor which may have the same effect? Either way it looks like a macrophage problem.

--Back to the H. pylori (you guys already mentioned it), but the pain improves with food. That makes me think duodenal ulcer, and I always thought the pain was relieved by food because it gets a bunch of bicarb when you eat to neutralize the acid. Does it not work like this? Then again, H. pylori alkalinizes the stomach so who knows. I think the answer was smoking cessation. :confused:

--Guy who lives with cats and avoids people... but apparently that's not avoidant. What am I missing?

--Endocarditis after root canal... Is it strep mitis? Goes to show if it's not in first aid I haven't learned it.

K that's all for now. Thanks everybody, keep up the good work!
 
A person going for surgery under gen anesthesia. He is out after only 3-5 breaths of inhalational anesthetic. Which of the following properties of the anesthetic is the most likely explanation for the rapid onset of action?

was trying top decide between Low blood solubility and low MAC.

Correct me if I am wrong but low blood solubility= high lipid solubility= low MAC right?

Am I missing something... I read FA saying low blood sol = fast induction but I'm just wondering if low MAC alludes to the same thing
 
the root canal question is strep mitis.... Its in first aid. its part of the viridans/mutans group of strep i think. Reason they can cause endo is their ability to break down dextran and cause adherance.
 
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