NBME 13 discussion

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Are we allowed to talk about this topic? There's a NBME 12 discussion that has a lot of full questions posted but there are sticky posts that seem to say don't talk about the NBMEs. Thank you for any clarification!

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Hi,
I recently took my nbme 13 form .
That was the first ever nbme I took .
It was bad.
How do I improve my score in a month so I can take my exam?
When doing it I felt I knew most of the questions and was surprised to see the low score.
 
HI,
I could not find reply to one of the questions in nbme form 13.
Hoping that someone would know the right answer.
The question asked about the calcium sequestration with 5 graphs varying their frequencies.
Starting with the low frequency and ending with high.
I opted for the high frequency stimulation thinking that the free calcium is already in a bound state.
 
I have another question which I really dint get...
healthy woman ,with 24 hr nausea vomiting,smokes 1 pack, wine 4 glasses daily.
takes large doses of acetominophen .liver ast elevated.what effect does alchohol have?
a)decreased generation of napqi
b)increased glucoronidation
c)increased sulfation
d)increased glutathione stores
e)induction of cytochrome 450
 
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I have another question which I really dint get...
healthy woman ,with 24 hr nausea vomiting,smokes 1 pack, wine 4 glasses daily.
takes large doses of acetominophen .liver ast elevated.what effect does alchohol have?
a)decreased generation of napqi
b)increased glucoronidation
c)increased sulfation
d)increased glutathione stores
e)induction of cytochrome 450

I dont remember much of my NBME 13. It was the first one I took almost a month ago. I think it was induction of cytochrome 450? I think chronic alcoholism causes P450 induction.
 
Hi,
I recently took my nbme 13 form .
That was the first ever nbme I took .
It was bad.
How do I improve my score in a month so I can take my exam?
When doing it I felt I knew most of the questions and was surprised to see the low score.

Good morning and welcome to the forum. It can be quite frustrating seeing a low grade on the NBME exams, especially when putting hard work and effort into studying. I recommend, you click on the link below, and read the thread from starting at that page, to the end. Has good tips/points/recommendations on how to bring your score up. Good luck! :thumbup:

http://forums.studentdoctor.net/showthread.php?t=976815&page=40

HI,
I could not find reply to one of the questions in nbme form 13.
Hoping that someone would know the right answer.
The question asked about the calcium sequestration with 5 graphs varying their frequencies.
Starting with the low frequency and ending with high.
I opted for the high frequency stimulation thinking that the free calcium is already in a bound state.

iirc, it was the answer to the far left. would have to see the question/diagram again to tell you why i chose it, sorry.

I have another question which I really dint get...
healthy woman ,with 24 hr nausea vomiting,smokes 1 pack, wine 4 glasses daily.
takes large doses of acetominophen .liver ast elevated.what effect does alchohol have?
a)decreased generation of napqi
b)increased glucoronidation
c)increased sulfation
d)increased glutathione stores
e)induction of cytochrome 450

See what the poster above this post said. This is basic pharm 101. You need to know the inducers and inhibitors of the CYP450 family. It's a pretty important topic. Another example of this question is asked this way:

A 49 year old woman comes into your office, complaining of night sweats, weight loss, and fever. Doing a physical on her you conclude that she has TB. You start her on a drug regiment to control the TB. She returns to your office in 3 months later, and while performing her blood work, you find that she is pregnant. The patient is positive she's been taking her oral contraceptives, and begins to cry because she can't afford having a child right now. You notice her tears are of red/orange color. What happened?

- You started her on rifampin - which is a CYP450 inducer. It quickly metabolized the oral contraceptives, allowing her to get pregnant. You fix this by increasing the dosage of her oral contraceptives.
 
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ok I was confused if sulfation was involved in any way

Acetaminophen undergoes conjugation with sulfate and glucoronide... these are the good pathways that dont produce the toxic NAPQI, which is produced by P450 enzymes, which are induced by alcohol.
 
Anyone have any tips on how i could have reasoned through this one?

25 y/o woman with OSA, has some lipid abnormalities, which of the following drugs would cause steatorrhea and changes in lipid serum studies

atorvastatin
buproprion
orlistat
phentermine
sibutramine


I ruled out atovrastatin, buproprion and phentermine. Other than straight up knowledge, is there anything that should have driven me to choose orlistat instead of sibutramine?
 
Also, with loss of heterozygosity. The question with the p53, m and n being present in germline but only p53 and m being present in to tumor cells.

is loss of heterozygosity not the same thing as a point mutation in n
 
Anyone have any tips on how i could have reasoned through this one?

25 y/o woman with OSA, has some lipid abnormalities, which of the following drugs would cause steatorrhea and changes in lipid serum studies

atorvastatin
buproprion
orlistat
phentermine
sibutramine


I ruled out atovrastatin, buproprion and phentermine. Other than straight up knowledge, is there anything that should have driven me to choose orlistat instead of sibutramine?

I knew the side effect of orlistat was steatorrhea. I think I ruled out sibutramine because it ends in -amine, which probably means it has the properties of an SSRI which isn't known to cause steatorrhea.

Also, with loss of heterozygosity. The question with the p53, m and n being present in germline but only p53 and m being present in to tumor cells.

is loss of heterozygosity not the same thing as a point mutation in n

Someone earlier said that if you had a point mutation in the n allele, then you would still have the p53 allele in addition to the m allele. The question said the neoplastic cells only had the m allele.
 
37.
A 5-year-old girl is brought to the physician because of listlessness, fatigue, and dull pain in the right upper quadrant of the abdomen. Her height and weight are below the 25th percentile. Laboratory findings indicate that the content of her β-globin chain is 15% to 20% of normal. Sequencing of the β-globin gene shows a point mutation in a sequence 3′ to the coding region in which AATAAA is converted to AACAAA. Consequently, the amount of mRNA for β-globin is decreased to 10% of normal. Which of the following functions in mRNA synthesis and processing is most likely encoded by the sequence AATAAA?

a) capping with GTP
b) cleavage and polyadenlyation
c) silencing the promoter
d) splicing of the initial mRNA transcript in the nucleus
e) transport of the mRNA out of the nucleus



B. It's the polyadenylation sequence. Pg. 75 in FA.

Isn't the polyA tail on the 3' of the mRNA? so this would correspond with the 5' end of the DNA, right?

the question says that the mutation is in a sequence that is 3' to the coding region, which would mean upstream the coding sequence.

the polyadenylation signal (AAUAAA) should be 5' to the coding region right? this would correspond with the polyA tail being on the 3' side of the mRNA
 
Someone earlier said that if you had a point mutation in the n allele, then you would still have the p53 allele in addition to the m allele. The question said the neoplastic cells only had the m allele.

so loss of heterozygosity in general refers to the deletion of the entire allele?

like in terms of Rb. you have one germline mutation. when people say loss of heterozygosity, they mean that there is more than just a point mutation in the normal Rb, there are either multiple mutations or a general loss of the entire gene?

thanks!
 
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Isn't the polyA tail on the 3' of the mRNA? so this would correspond with the 5' end of the DNA, right?

the question says that the mutation is in a sequence that is 3' to the coding region, which would mean upstream the coding sequence.

the polyadenylation signal (AAUAAA) should be 5' to the coding region right? this would correspond with the polyA tail being on the 3' side of the mRNA

Polyadenylation is post-transcriptional modification.

Edit: I get what you're saying now. Let me think about that.

Edit 2: The wording is tricky. It says it found a point mutation in a sequence [that is] 3' to the coding region, so it is not actually in the coding region.
 
Anyone have any tips on how i could have reasoned through this one?

25 y/o woman with OSA, has some lipid abnormalities, which of the following drugs would cause steatorrhea and changes in lipid serum studies

atorvastatin
buproprion
orlistat
phentermine
sibutramine


I ruled out atovrastatin, buproprion and phentermine. Other than straight up knowledge, is there anything that should have driven me to choose orlistat instead of sibutramine?

What pharm source are you using? 3 out of 5 of those drugs are not in first aid
 
Polyadenylation is post-transcriptional modification.

Edit: I get what you're saying now. Let me think about that.

Edit 2: The wording is tricky. It says it found a point mutation in a sequence that is 3' to the coding region, so it is not actually in the coding region.

ahhh damn it is on the 3' region of the CODING strand, so not the template strand. That means it would also be in the 3' region of the mRNA.

that is why it has AA"T"AAA, because the coding strand has the same sequence as the mRNA, obviously with T instead of U

such as easy question I got wrong just because i thought about it too much
 
so loss of heterozygosity in general refers to the deletion of the entire allele?

like in terms of Rb. you have one germline mutation. when people say loss of heterozygosity, they mean that there is more than just a point mutation in the normal Rb, there are either multiple mutations or a general loss of the entire gene?

thanks!

Actually, that explanation doesn't really make sense now that I think about it. I just read it again on the first page of this thread. It's saying there are two alleles, m and n, that are closely linked to the p53 gene (so it's not a third p53 allele like someone was saying). Let me think about this one...
 
so loss of heterozygosity in general refers to the deletion of the entire allele?

like in terms of Rb. you have one germline mutation. when people say loss of heterozygosity, they mean that there is more than just a point mutation in the normal Rb, there are either multiple mutations or a general loss of the entire gene?

thanks!

The closest thing to an explanation I could find is this: http://en.wikipedia.org/wiki/Loss_of_heterozygosity#Detection

"Loss of heterozygosity can be identified in cancers by noting the presence of heterozygosity at a genetic locus in an organism's germline DNA, and the absence of heterozygosity at that locus in the cancer cells."

Absence of heterozygosity = m allele only, but I'm not sure why a point mutation in the n allele would be wrong other than the fact that it's too specific for what they're asking (i.e., a point mutation in the n allele could lead to a loss of heterozygosity, but that's not the best answer).
 
Yeah that makes sense I guess... going through my incorrects and a lot of what i missed, i had the right answer first and just changed it :(

but i really dont know what to do because i know i changed a lot of answers to the correct one too lol.

ALS - why does that cause loss of swallowing? i figured that swallowing would be mediated by the vagus nerve, and since ALS is a spinal cord issue, swallowing wouldn't be affected.
 
Anyone have any tips on how i could have reasoned through this one?

25 y/o woman with OSA, has some lipid abnormalities, which of the following drugs would cause steatorrhea and changes in lipid serum studies

atorvastatin
buproprion
orlistat
phentermine
sibutramine

One way youll never forget orlistat is to just look at one of the potential side effects... fecal leakage from unabsorbed fat... Not just going to the restroom and seeing fatty stools, I mean actual incontinence leaking fatty crap :eek: Btw, orlistat inhibits pancreatic lipases.
 
Yeah that makes sense I guess... going through my incorrects and a lot of what i missed, i had the right answer first and just changed it :(

but i really dont know what to do because i know i changed a lot of answers to the correct one too lol.

ALS - why does that cause loss of swallowing? i figured that swallowing would be mediated by the vagus nerve, and since ALS is a spinal cord issue, swallowing wouldn't be affected.

Cranial nerves that innervate muscles have alpha motor neurons with cell bodies residing in the cranial nerve nuclei. It's no different than a spinal nerve in that respect. With ALS you have destruction of alpha motor neurons and the descending corticospinal/corticobulbar tracts.
 
Cranial nerves that innervate muscles have alpha motor neurons with cell bodies residing in the cranial nerve nuclei. It's no different than a spinal nerve in that respect. With ALS you have destruction of alpha motor neurons and the descending corticospinal/corticobulbar tracts.

oh yeah taht was dumb of me...

i feel like they are trying to be overly tricky in their questions, but a lot of times they really aren't.
 
oh yeah taht was dumb of me...

i feel like they are trying to be overly tricky in their questions, but a lot of times they really aren't.

As a general philosophy - if you have First Aid level stuff down, then if you feel like they're trying to trick you're most likely over-thinking it. My take away from the exam and NBMEs was that most questions are presented in a straight forward manner. "Hard" or "WTF" questions come down to knowing the material or not.

This is not to say there's no place for test taking strategies, eliminating what you know isn't true, etc. But the NBME test writers are put into some known constraints. There must be one unambiguously right answer, patients must conform to epidemiological data (i.e. you're not gonna get female autism, most likely), and presentations are typical.
 
Just took NBME 13, and I thought it was easier compared to 15, but surprisingly I scored 250, with 20 mistakes. NBME 15 was 252 with 19 mistakes. SOOOOOO damn dissapointed!!! :mad: My exam is day after tomorrow, so you can see how it smashes your confidence down....Really bad idea to take an NBME just before the exam...:(

Anyway, the questions I got wrong. If someone knows the answers, please let me know. I tried to find the answers in the previous discussion, but its all jumbled up and I really don't have time to dig in for each of the question. Thanks

1. Antibody titer in a tumor? I selected B-Cell Lymphoma, but it was wrong. I am thinking its HPV, dont know why...

2.Genetic analysis show a missense mutation of Tyorosine kinase domain of TrKa gene. I selected "Formation of homodimer", but its wrong. The other option that I almost selected was "Phosphorylation of downstream growth factors in response to nerve growth factor". I thought this process happens AFTER the dimerization...WTF?

3.Cyt one..I rememberd Goljan's Cyt C = CO, CN ...but, its wrong!

4.Bevacizumab question. Why it doesn't launch an immune reaction. I selected "Agent containing the Murine antibody to VEGF"...I think it was "Humanized antibody"?

5.AATAAA mutation. I was stuck between polyadenylation or transport out of nucleus. I selected transport out of nucleus, and FREAKING **** IT WAS WRONG!!!:mad:

6.77 year old, vertebral column shown. First I was selecting IL1, but then I thought the one that is increased in OP is IL-6...so went with multiple myeloma, and voila, its wrong!

7.An electron microscopy pic of a NM junction. I selected MGravis, but its wrong. Dont even know what that picture is showing..

8.Now this is a complete nervewrecker...Epinephrine injection and they are studying B2 effects. I selected Lipolysis, but WTF!, its wrong. The only other B2 mediated is Uterine relaxation, so I guess that is the correct answer? But how? they both are B2 mediated.

9.Question about lettuce eating, and probability of diarhea. I got this wrong..1000 consumers of vegtebales, 800 ate tomotaes, 200 ate lettuce....total of 400 became ill; 80 of those ate tomotoes, and 40 ate lettuce.
I selected 40/400=0.1, but Wrong!

10. I hate muslces of the leg...from where does adductor of hip originate and insert on Femur. I selected Iliac crest...

11.A question of cancer, with 2 alleles linked to a Z locus near p53. M and N are present in germline, but only M is present in the tumor. I selection mutation of N...but its wrong..I think it was Loss of heterozygosity, but that doesnt make sense : M IS STILL PRESENT, loss of heterezygosity is when you loose both the allelles for p53. If one is still present, how can you have loss of heterozygosity? somone please explain this!

12. Acuter Intermittent Porphyria? I never thought it to be AD...I selected AR, but its wrong, so I guess its AD?

13.Another question of biostat i hate. Calculate annual mortality rate per 100,000. Annual incidence of the condition is 15/100,000; Case fatality rate is 40%;

14.Cushings, from pit adenoma. You are supposed to see Hyperplasia of cortex or Hypertrophy? I selected hypertrophy but its wrong...I thought Hyperplasia was only for Conn's?

15.This was a complete bummer! I was soooo damn sure of it. Where do u place the needle for thoracocentesis. I answered below the 9th rib on Midscapular line, but its wrong. But all the other answers would have punctured the pleura...

16.Autopsy of a brain..asked for cause of seizure disorder. I chose Herpes simplex...I ruled out Neonatal ischemic stroke, since she was having seizures for 25 years (she was 40)..that means it started at the age of 15...neonatal stroke would have caused seizures since the beginning....?

17.Resistant Klebsiella. What do you do to prevent its spread. I selected wear a mask. The other compelling answer was wash hands, but I assumed not everyone who comes to the room touches the patient, so wearing a mask is more important...?

18.70 year old, lower abdominal and back pain, radiates to lower extremity. Appears pale and cold sweat. Pule is high, BP is low, Weak pulses in lower extremity. Bruit over lower abdomen..Muscle stretch reflexes are normal..Diagnosis? I selected "Leaking left renal artery aneurysm"...?

19.Playing tennis, severe pain...Ruptured Achilles tendon...put a cast..six months later, the circumference is decreased compared to the other leg..I selected "Necrosis of muscle fibers"...

20. Finally, this one didn't make sense to me at all..Decreased nerve conduction velocity in nerves, with proximal/distal weakness in both upper and lower limb. Malfunction of what Ion channel? I selected "Neurotransmitter-gated Na channel", thinking it to be MGravis..

Thanks everyone,

Sigh...so sad now...I guess I'll just go out for a jogg :(

I know the correct answers to all of those, but I'm going to let someone else answer because you obviously didn't even try to browse this thread. You only got a 250? I'm disappointed in you.
 
Yeah I mean to be honest, I think with the position I am at, I would definitely be disappointed with a score someone else would be ecstatic with... but to be "SOOOOO DAMNNN DISAPPOINTED" at a 250... that is just poor form.

And instead of taking the time to type up all of those, you could have easily just searched this thread. copy and pasting each of those into google would also probably come up with the right answers
 
Hehe...thanks for the sarcasm...I am browsing it now, but I think some of them are not answered yet...Found answers for 5 of them...

Sorry, its just I've read that the NBME over predicts your score by 10 points, so you real score is like 10 points down, which is like 240..i was really aiming for a 260, and after intense studying for 2 weeks, you are at the same point...just throws your off..

Thanks anyways...
 
Hehe...thanks for the sarcasm...I am browsing it now, but I think some of them are not answered yet...Found answers for 5 of them...

Sorry, its just I've read that the NBME over predicts your score by 10 points, so you real score is like 10 points down, which is like 240..i was really aiming for a 260, and after intense studying for 2 weeks, you are at the same point...just throws your off..

Thanks anyways...

hmm ive heard NBME's are the best predictors. you might be thinking about UWSA?

i'd say you are in a good position to get a 250 man, don't stress to much about it!

and definitely post any questions that you realize aren't posted yet, or that you would like to talk more about!! :)
 
The stress of the exam is killing me, with every counting minute...its terrible!!!

Thanks for the push man...I will look around the discussion, and post the ones that are not posted yet...
 
Okay this one is killing me..

11.A question of cancer, with 2 alleles linked to a Z locus near p53. M and N are present in germline, but only M is present in the tumor. I selection mutation of N...but its wrong..I think it was Loss of heterozygosity,

But that doesnt make sense : M IS STILL PRESENT, loss of heterezygosity is when you loose BOTH the allelles for p53. If one is still present, how can you have loss of heterozygosity?
 
Also the thoracocentesis question doesn't make sense.

From Uworld, you puncture above a rib in the following locations:
Midclavicular:Between 5 and 7
MidAxillary: Between 7-9
Mid Scapular/Paravertebral :Between 9-11

None of the options satisfy this criteria. The one with "Above the 9th rib in Midscapular line" would puncture the lung...
 
Okay this one is killing me..

11.A question of cancer, with 2 alleles linked to a Z locus near p53. M and N are present in germline, but only M is present in the tumor. I selection mutation of N...but its wrong..I think it was Loss of heterozygosity,

But that doesnt make sense : M IS STILL PRESENT, loss of heterezygosity is when you loose BOTH the allelles for p53. If one is still present, how can you have loss of heterozygosity?

This is a pretty tough question which I don't understand either. My response above in post #419 is probably the closest you'll come to an explanation until someone more well-versed can come along and explain.

Also the thoracocentesis question doesn't make sense.

From Uworld, you puncture above a rib in the following locations:
Midclavicular:Between 5 and 7
MidAxillary: Between 7-9
Mid Scapular/Paravertebral :Between 9-11

None of the options satisfy this criteria. The one with "Above the 9th rib in Midscapular line" would puncture the lung...

It's definitely above the 9th rib in the midscapular line. You don't want to do one below the 9th rib because that is where the vessel bundle runs along the ribs. You always want to do it on top of the ribs as opposed to below, which is what the question was trying to get at.

Edit: also, the question was talking about an 82-year-old woman with dullness to percussion at the level of the 7th rib, which means the pleural effusion is probably at that level and below. You probably wouldn't hit the lungs past that point.
 
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I see his point though. I actually just got this UWorld question. UWorld clearly says that thoracocentesis should be performed between the 9th and 11th ribs at the paravertebral line (similar to the midscapular line, presumably). This is question 844 for reference.

Above the 9th rib doesn't technically fall within the range they recommend. Based on their recommendation, it seems as though above the 9th rib has a chance of piercing the lung.

Below the 9th rib would most likely not pierce the lung, but has a chance of injuring the vessel bundle.

Basing the answer on UWorld, you would have to choose which one would be safer, and so I can see how this question could be confusing.

Edit: based on your edit, I see why above the 9th would be the better choice. I just forgot what side the vessels were on, so I chose below lol.
 
I see his point though. I actually just got this UWorld question. UWorld clearly says that thoracocentesis should be performed between the 9th and 11th ribs at the paravertebral line (similar to the midscapular line, presumably). This is question 844 for reference.

Above the 9th rib doesn't technically fall within the range they recommend. Based on their recommendation, it seems as though above the 9th rib has a chance of piercing the lung.

Below the 9th rib would most likely not pierce the lung, but has a chance of injuring the vessel bundle.

Basing the answer on UWorld, you would have to choose which one would be safer, and so I can see how this question could be confusing.

Yeah, I definitely see the confusion, but I think you could rule out the other answer choices (all at 7th rib or above) and "above 9th rib" was the best one out of the two remaining choices. The paravertebral line is actually adjacent to the vertebrae as opposed to the midscapular line, so the lungs would be at a lower rib level at the paravertebral line. As you start moving laterally, the bottom of the lungs are at higher rib levels. I just went over this exact subject in Kaplan, and they actually recommended doing it at the 9th level above the ribs at the midclavicular line. It may actually be lower from the midscapular line, but the question also added that the dullness to percussion was at the level of the 7th rib, which is specific for that patient.
 
Ah....now I get this Loss of heterozygosity..

You see, we all have been thinking it the wrong way. Let me explain:

You have two alleles, linked tightly to the Z Point(which is an SNP-single nucleotide polymorphism - in short a marker).

M - p53 and N-p53 : You inherited two copies of it from the parents. One from either..This is HETEROZYGOUS.

When one is lost, for example N and only the M remains...Hence, you have LOST the HETERZYGOSITY....

I think the confusion arrives from the point that we assume p53 genes to be homozygous all the time. I.e. assuming both copies from the same parent. p53 should always be inherited in a heterozygoues fashion. When one is lost, there is LOSS OF HETEROZYGOSITY.

How do you fit the Knudson hypothesis? Simple. Knudson hypothesis says that both alleles of p53 have to be "disfunctional' i.e either mutated or lost. So conditions like Li-Fraumeni, you already are born with only 1 allele (i.e already loss of heterozygosity).

In the above case, the trick part of the whole question actually, is that the M allele is still present. So most of us automatically assumed it to be the normal allele. BUT, this M is mutated for the cancer to progress.....

In short, N was lost due to "Loss of heterozygosity" ; M is still present but is mutated! Hence = Cancer!!!

Hope it makes sense!!!
 
Ah....now I get this Loss of heterozygosity..

You see, we all have been thinking it the wrong way. Let me explain:

You have two alleles, linked tightly to the Z Point(which is an SNP-single nucleotide polymorphism - in short a marker).

M - p53 and N-p53 : You inherited two copies of it from the parents. One from either..This is HETEROZYGOUS.

When one is lost, for example N and only the M remains...Hence, you have LOST the HETERZYGOSITY....

I think the confusion arrives from the point that we assume p53 genes to be homozygous all the time. I.e. assuming both copies from the same parent. p53 should always be inherited in a heterozygoues fashion. When one is lost, there is LOSS OF HETEROZYGOSITY.

How do you fit the Knudson hypothesis? Simple. Knudson hypothesis says that both alleles of p53 have to be "disfunctional' i.e either mutated or lost. So conditions like Li-Fraumeni, you already are born with only 1 allele (i.e already loss of heterozygosity).

In the above case, the trick part of the whole question actually, is that the M allele is still present. So most of us automatically assumed it to be the normal allele. BUT, this M is mutated for the cancer to progress.....

In short, N was lost due to "Loss of heterozygosity" ; M is still present but is mutated! Hence = Cancer!!!

Hope it makes sense!!!

Great explanation. Thanks for this.
 
This also explains why the other answer "Mutation of allele n" is a wrong answer, since if that was the case, M would have been functional...

Again to clarify the concept:

Lost N due to Heterozygosity + Mutated M = Cancer!
 
You are more than welcome coolforschool.

I am having trouble finding explanation for these questions. All of the rest, I am okay with the explanations.

18.70 year old, lower abdominal and back pain, radiates to lower extremity. Appears pale and cold sweat. Pule is high, BP is low, Weak pulses in lower extremity. Bruit over lower abdomen..Muscle stretch reflexes are normal..Diagnosis? I selected "Leaking left renal artery aneurysm"...?

19.Playing tennis, severe pain...Ruptured Achilles tendon...put a cast..six months later, the circumference is decreased compared to the other leg..I selected "Necrosis of muscle fibers"...

20. Finally, this one didn't make sense to me at all..Decreased nerve conduction velocity in nerves, with proximal/distal weakness in both upper and lower limb. Malfunction of what Ion channel? I selected "Neurotransmitter-gated Na channel", thinking it to be MGravis..
 
You are more than welcome coolforschool.

I am having trouble finding explanation for these questions. All of the rest, I am okay with the explanations.

18.70 year old, lower abdominal and back pain, radiates to lower extremity. Appears pale and cold sweat. Pule is high, BP is low, Weak pulses in lower extremity. Bruit over lower abdomen..Muscle stretch reflexes are normal..Diagnosis? I selected "Leaking left renal artery aneurysm"...?

19.Playing tennis, severe pain...Ruptured Achilles tendon...put a cast..six months later, the circumference is decreased compared to the other leg..I selected "Necrosis of muscle fibers"...

20. Finally, this one didn't make sense to me at all..Decreased nerve conduction velocity in nerves, with proximal/distal weakness in both upper and lower limb. Malfunction of what Ion channel? I selected "Neurotransmitter-gated Na channel", thinking it to be MGravis..

18. Leaking abdominal aneurysm is the better answer. I can't really explain why but maybe it has something to do with radiation to the lower extremities (bilateral) instead of just to one side.

19. It's increased protein degradation from inactivity of his left leg muscles. Necrosis would imply something pathological.

20. I can't really explain this one well, but I got it right. It was voltage-gated Na+ channels. I think the tip-off was that the nerve conduction studies showed slowed conduction velocity, so it was measuring the nerve conduction (electrical activity) and not the NMJ (which is ACh-mediated).
 
You are more than welcome coolforschool.

I am having trouble finding explanation for these questions. All of the rest, I am okay with the explanations.

18.70 year old, lower abdominal and back pain, radiates to lower extremity. Appears pale and cold sweat. Pule is high, BP is low, Weak pulses in lower extremity. Bruit over lower abdomen..Muscle stretch reflexes are normal..Diagnosis? I selected "Leaking left renal artery aneurysm"...?

19.Playing tennis, severe pain...Ruptured Achilles tendon...put a cast..six months later, the circumference is decreased compared to the other leg..I selected "Necrosis of muscle fibers"...

20. Finally, this one didn't make sense to me at all..Decreased nerve conduction velocity in nerves, with proximal/distal weakness in both upper and lower limb. Malfunction of what Ion channel? I selected "Neurotransmitter-gated Na channel", thinking it to be MGravis..

for 20 - was there an answer choice that had "voltage-gated na channels" as an answer - if that's what it is, then that's the right answer...
 
But won't a decrease in conduction velocity also occur if there is a problem in NM junction? Or that will only lead to a decreased "End-plate potential" with no chance in conduction velocity.

Actually, come to think of it, how could they have framed the question to ask about the NM Na channels instead? Decreased conduction velocity? Or some other parameters?

Also, the patient with seizure+cystic space in the brain..That looks nothing like an AVM. I can tell its liqufactive necrosis, and I though it to be due to Herpes encephalitis. Also, an AVM wont start by the age of 15, symptoms would have presented much earlier...

Strange NBME questions.....
 
But won't a decrease in conduction velocity also occur if there is a problem in NM junction? Or that will only lead to a decreased "End-plate potential" with no chance in conduction velocity.

Actually, come to think of it, how could they have framed the question to ask about the NM Na channels instead? Decreased conduction velocity? Or some other parameters?

Also, the patient with seizure+cystic space in the brain..That looks nothing like an AVM. I can tell its liqufactive necrosis, and I though it to be due to Herpes encephalitis. Also, an AVM wont start by the age of 15, symptoms would have presented much earlier...

Strange NBME questions.....

yeah...i was thinking because in FA it talks about how schwann cells increase speed of conduction through nodes of ranvier due to a high concentration of sodium channels...obviously from pre-med 101 classes...we know that these are voltage-gated right...so that was my reasoning for going with "voltage gated sodium channels"

yeah that question, i had no idea...apparently the answer is AVM...still not sure what the actual diagnosis is from the question stem
 
I don't remember the Q but off the top of my head, avm+seizure could be sturge weber, especially if involved the meninges
 
But won't a decrease in conduction velocity also occur if there is a problem in NM junction? Or that will only lead to a decreased "End-plate potential" with no chance in conduction velocity.

Actually, come to think of it, how could they have framed the question to ask about the NM Na channels instead? Decreased conduction velocity? Or some other parameters?

Also, the patient with seizure+cystic space in the brain..That looks nothing like an AVM. I can tell its liqufactive necrosis, and I though it to be due to Herpes encephalitis. Also, an AVM wont start by the age of 15, symptoms would have presented much earlier...

Strange NBME questions.....

No. The nerve conduction would be fine (nothing wrong with the voltage-gated Na+ channels), so the NCV test would be normal. The thing that you would see in an NMJ problem is weak muscle contraction, but the nerve conduction upstream of that would be normal.

That is a classic picture of an AVM if you google it. AVMs are mostly found incidentally on autopsy, and they can be asymptomatic most of the time (Wikipedia that if you want to). The question stem described a classic case of AVM.
 
No. The nerve conduction would be fine (nothing wrong with the voltage-gated Na+ channels), so the NCV test would be normal. The thing that you would see in an NMJ problem is weak muscle contraction, but the nerve conduction upstream of that would be normal.

That is a classic picture of an AVM if you google it. AVMs are mostly found incidentally on autopsy, and they can be asymptomatic most of the time (Wikipedia that if you want to). The question stem described a classic case of AVM.

lame...seems like that AVM question was actually a pretty simple recall question....would you agree?
 
This is the one from NBME

2ztgbgj.jpg



This is a picture of an AVM from google:

311vyhi.jpg




Looks more like liquifactive necrosis, isnt it? But yeah, you are right...it was more of a recall question..The history was typical.
 
lame...seems like that AVM question was actually a pretty simple recall question....would you agree?

Yeah, I agree especially because of the other answer choices. I flagged that question and spent about 5 minutes trying to rule out hepatic encephalopathy and some other answer choice along with AVM. In the back of my mind, I knew it was AVM because I had seen that picture before during first year, but I ended up picking something else. Looked it up later and it was a classic description for AVM.
 
i know it's just an illustration...but cool is right...if we knew what it looked like, this should've been an easy point question

PE-AVM_Figure1a.jpg
 

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