Official nbme 15 discussion

[abelabbot]

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

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[watchmenaenae]

A 60 year old woman comes to physician because of a 6 month history of knee and hips pain due to osteoarthritis. The physician recommends her ibuprofen. The patient refuses and asks for glucosamine. What's the best response?
A "glucosamine hasn't been studied well enough for me to recommend it".

B "glucosamine side effects aren't listed. It maybe more dangerous than we realize"

C"ibu has been proven effective for your condition"

D"what have you heard about using glucosamine to treat osteoarthritis?"

E " why did you come to me if you don't want to take what I recommend?"

F" you should really see a naturopathic Doctor"

I chose "C" that was wrong can anyone explain what's right and why? Thanks


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[walakin25]

the answer is D. basic idea here is initiating a discussion which usually starts off with exploration of patient knowledge, what he/she has heard or read about. i didn't think about this question any further and apologize if this answer isnt comprehensive, behavioral is one of my weaknesses.

Edit: can somebody explain what slipped-strand mispairing is. I have read what others have posted on this thread but Im not getting my head around it.

 

[chillaxbro]

Does anyone have a good explanation for this one:

A 54yo man has abd. pain for 2 months and weight loss. He's jaundiced, and basically has a mass in the head of the pancreas that has extended into the stomach and biliary system. He's most at risk for: major depressive disorder.

Are they saying he is at risk for major depression as a result of the cancer diagnosis? I haven't really ever come across any review material that covers this, but I vaguely remember the idea from class.

Is the answer really MDD? That's a bull**** question

I was thinking along the lines of heptaic failure -> hyperammnonianainaenamia -> encephalopathy -> memory impairment/personality change.

 

[Postictal Raiden]

Is the answer really MDD? That's a bull**** question

I was thinking along the lines of heptaic failure -> hyperammnonianainaenamia -> encephalopathy -> memory impairment/personality change.

I chose memory impairment for this question and apparently I got it wrong. Frustrating.

 

[chillaxbro]

I chose memory impairment for this question and apparently I got it wrong. Frustrating.

Same here... just took this exam today and I'm going over the answers I got wrong right now

 

[chillaxbro]

Guy gets salmonella enterica and his symptoms resolves to a milder form after 36 hours. If he took antibiotics, which of the following is most likely to occur?

a. anaphylaxis as a result of antibiotic hypersensitivity (Chose this one and it's wrong)
b. decreased risk of endocarditis - salmonella doesnt cause endocarditis
c. decreased risk for hemolytic uremic syndrome - HUS I think of e. coli - never heard of salmonella doing this
d. establishment of carrier state in spleen - why would antibiotics cause a carrier state? also never heard of carrier state in spleen... maybe gallbladder
e. prolonged fecal excretion of organism - why would taking antibiotics make it longer?

...I chose A because I eliminated all the other ones for the reasons listed above. What's the answer?

 

[Postictal Raiden]

Guy gets salmonella enterica and his symptoms resolves to a milder form after 36 hours. If he took antibiotics, which of the following is most likely to occur?

a. anaphylaxis as a result of antibiotic hypersensitivity (Chose this one and it's wrong)
b. decreased risk of endocarditis - salmonella doesnt cause endocarditis
c. decreased risk for hemolytic uremic syndrome - HUS I think of e. coli - never heard of salmonella doing this
d. establishment of carrier state in spleen - why would antibiotics cause a carrier state? also never heard of carrier state in spleen... maybe gallbladder
e. prolonged fecal excretion of organism - why would taking antibiotics make it longer?

...I chose A because I eliminated all the other ones for the reasons listed above. What's the answer?

I chose E and I think it's the correct response because I don't see that I got the question wrong. I did it by POE. Maybe it's because Salmonella invades M cells of Peyer patch in ileum, so treating with antibiotics would cause it to be slowly shed from these cells into the lumen of intestines?

 

[Postictal Raiden]

Same here... just took this exam today and I'm going over the answers I got wrong right now

If you don't mind me asking, how did you do?

 

[chillaxbro]

If you don't mind me asking, how did you do?

234... no improvement from last week

 

[Postictal Raiden]

234... no improvement from last week

That's really good! How far is your test?

 

[chillaxbro]

That's really good! How far is your test?

15 days!! Omg not even done with Uworld first pass or FA first pass yet...

 

[Postictal Raiden]

15 days!! Omg not even done with Uworld first pass or FA first pass yet...

You are golden as is, imo. However, you still have time to improve. Best of luck!

 

[walakin25]

15 days!! Omg not even done with Uworld first pass or FA first pass yet...

@chillaxbro im not a super high scorer for SDN standards but i can tell you the best thing you can do these last few days is hit FA and UW hard. I would personally hit FA mostly and maybe do one last NBME within next 5 days, then pure reading/understanding as much as possible till test day.. goodluck

 

[Guero]

Putting my money on the inherited protease deficiecy. Air trapping, decreased FEV1, and decreased diffusion capacity due to reduced surface area make me think of COPD but since he hasn't smoked any tobacco, would expect inherited alpha 1 antitrypsin deficiency. Makes sense with the hepatomegaly too. Can do a PAS stain and look for eosinophilic inclusions

Alpha-1 anti-trypsin (A1AT) is a serpine protease inhibitor, more specifically in this setting, an irreversible inhibitor of elastase, a protease. Some have argued that A1AT is a protease itself, a "good protease" cancelling out a "bad protease." But A1AT's mechanism of action functions via conformational change to (1) irreversibly bind and thus inhibit elastase, forming a complex thereby (2) facilitating its degradation. The A1AT has no direct proteolytic action. Thus, an A1AT deficiency is a protease inhibitor deficiency that results in protease overabundance & hyperactivity. (Source: Carrell RW, Lomas DA. Alpha1-antitrypsin deficiency--a model for conformational diseases. N Engl J Med. 2002;346(1):45.)

Update: I sent the NBME a message about this to see if they'd consider reviewing it...They agreed very quickly. I'll post the outcome later. (Be cautious about the copyright policy you agreed to when taking the exam, especially now that this question will be under review.)

 

[AshNiffler]

Is the answer really MDD? That's a bull**** question

I was thinking along the lines of heptaic failure -> hyperammnonianainaenamia -> encephalopathy -> memory impairment/personality change.

I've been doing Rx for the past couple of weeks so this took a second, one of the risk factors for major depression is a serious illness.

I actually found 15 easier to reason through than 13 for some reason, I took them 2 weeks apart after doing half of the RX qbank.

 

[OrthoRehab33]

Alpha-1 anti-trypsin (A1AT) is a serpine protease inhibitor, more specifically in this setting, an irreversible inhibitor of elastase, a protease. Some have argued that A1AT is a protease itself, a "good protease" cancelling out a "bad protease." But A1AT's mechanism of action functions via conformational change to (1) irreversibly bind and thus inhibit elastase, forming a complex thereby (2) facilitating its degradation. The A1AT has no direct proteolytic action. Thus, an A1AT deficiency is a protease inhibitor deficiency that results in protease overabundance & hyperactivity. (Source: Carrell RW, Lomas DA. Alpha1-antitrypsin deficiency--a model for conformational diseases. N Engl J Med. 2002;346(1):45.)

Update: I sent the NBME a message about this to see if they'd consider reviewing it...They agreed very quickly. I'll post the outcome later. (Be cautious about the copyright policy you agreed to when taking the exam, especially now that this question will be under review.)

any update on this? I just took 15 today and got this wrong- I was really confused by this simply because it said protease deficiency and I've always considered it to be a protease inhibitor deficiency...but I feel like I should probably aire on the side that, "they are not tricking me" I feel like that's where I miss most questions.
I missed the renal ammoniogenesis question- because I thought if that process was impaired you couldnt use glutamine to generate ammonia. I'm still a little confused over this
UW states: Acidosis stimulates renal ammoniagenesis, where renal tubular cells metabolize glutamine to glutamate, generating ammonium that is excreted in the urine, so I thought if this process was impaired you couldnt metabolism glutamine to glutamate

 

[OrthoRehab33]

43yo man with 10yr history of alcoholism has jaundice. He takes 2 extra strength acetaminophen every 4-6hrs for the past 3 days. He has increased prothrombin time and increased AST activity. Alternation in which metabolites within hepatocytes is a/w his illness?
- I choose increased NADH due to his alcoholism apparently that's not what they we're going for. Some people thought decreased glutathione but that wasn't right either- the answer supposedly is "decreased NAD+"---does anyone understand this? I mean I know his NADH/NAD ratio should be increased but then I feel like increased NADH should be right too.

 

[gobigorgohome22]

43yo man with 10yr history of alcoholism has jaundice. He takes 2 extra strength acetaminophen every 4-6hrs for the past 3 days. He has increased prothrombin time and increased AST activity. Alternation in which metabolites within hepatocytes is a/w his illness?
- I choose increased NADH due to his alcoholism apparently that's not what they we're going for. Some people thought decreased glutathione but that wasn't right either- the answer supposedly is "decreased NAD+"---does anyone understand this? I mean I know his NADH/NAD ratio should be increased but then I feel like increased NADH should be right too.

You're right about the increased NADH/NAD ratio but main reason for it has to do with not enough NAD+ being around to continue glycolysis, not that there is too much NADH. If you could somehow inject NADH into the cell, you wouldnt see the symptoms. BUT if you could selectively take away NAD+, you would.

 

[OrthoRehab33]

You're right about the increased NADH/NAD ratio but main reason for it has to do with not enough NAD+ being around to continue glycolysis, not that there is too much NADH. If you could somehow inject NADH into the cell, you wouldnt see the symptoms. BUT if you could selectively take away NAD+, you would.

This makes sense, I literally just reviewed this a few days ago but I want to make sure I get this down. The increased NADH shunts oxaloacetate (OA) to make malate this means there's no OA to combine with Acetyl CoA so that gets shunted to make Fatty acids generating Malonyl CoA which inhibits fatty acid oxidation. I thought this was the mechanism responsible for alcoholic fatty liver

 

[Guero]

any update on this? I just took 15 today and got this wrong- I was really confused by this simply because it said protease deficiency and I've always considered it to be a protease inhibitor deficiency...but I feel like I should probably aire on the side that, "they are not tricking me" I feel like that's where I miss most questions.
. . .

No, but the fact they've not yet replied with a simple "it's correct," is rather promising. I think if they stay behind their original choice, they're considering A1AT a protease. Because in retrospect, after rereading my message to them and realizing much of my argument hinged on my use of "lack of proteolytic activity," not all proteases are proteolytic. Still, based on the functional and structural biology, I don't see it as a "protein processor" either, much like a similar question from another NBME test that reworded the best answer to "protein processing" to describe the end result of pol gene translation (e.g., ligases, integrases, etc). That was a tricky little bastard.

I'll post an update as soon as the NBME committee responds, promise.



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[Guero]

No, but the fact they've not yet replied with a simple "it's correct," is rather promising. I think if they stay behind their original choice, they're considering A1AT a protease. Because in retrospect, after rereading my message to them and realizing much of my argument hinged on my use of "lack of proteolytic activity," not all proteases are proteolytic. Still, based on the functional and structural biology, I don't see it as a "protein processor" either, much like a similar question from another NBME test that reworded the best answer to "protein processing" to describe the end result of pol gene translation (e.g., ligases, integrases, etc). That was a tricky little bastard.

I'll post an update as soon as the NBME committee responds, promise.



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I'm saddened by their answer to this inquiry:

"Here is the response that they have provided to your question: Long-term cannabis smoking has not been found to be associated with measures of pulmonary function or airflow obstruction. As an example, a longitudinal study of 5,115 people over a 20-year period found that occasional and low, cumulative cannabis use was not associated with reduced pulmonary function (forced expiratory volume and forced vital capacity) [http://www.uptodate.com/contents/ca...is-and-long-term-medical-effects/abstract/34]."

EDIT (my reply to NBME): I thanked them for their time and effort despite leaving us somewhat in the dark. Since the primary question and challenge remains unaddressed, regarding abundant literature qualifying ATA1 deficiency as a protease inhibitor deficiency resulting a protease abundance; I'll presume "deficiency" in this case refers broadly to a "defect" in protease physiology moving forward. @Hunterthekidd Sorry the outcome wasn't as clear as I'd hoped. Good luck everyone. I tried.

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[Donald Kimball]

43yo man with 10yr history of alcoholism has jaundice. He takes 2 extra strength acetaminophen every 4-6hrs for the past 3 days. He has increased prothrombin time and increased AST activity. Alternation in which metabolites within hepatocytes is a/w his illness?
- I choose increased NADH due to his alcoholism apparently that's not what they we're going for. Some people thought decreased glutathione but that wasn't right either- the answer supposedly is "decreased NAD+"---does anyone understand this? I mean I know his NADH/NAD ratio should be increased but then I feel like increased NADH should be right too.

A little late, but acetaminophen toxicity depletes hepatic glutathione reserves. So, the answer is reduced glutathione. My reasoning at the time was that we give acetylcysteine to regenerate glutathione, so that must be the problem. Expanded feedback, and I can guarantee I got that question right.

 

[StuartLiu]

It is really interesting between Smashingdude's answer and my answer.

Smashingdude was 252/19 incorrect, I took it today and was 241/25 incorrect.
However, out of the 16 incorrect questions Smashingdude posted, I got 14 of them correct.

I've graduated in 2008, and had been practicing internal medicine since then.
Maybe this is the reason?

Just took NBME 15. 252/19 incorrect. I was hoping for 260, but I made some silly mistakes...Anyway, on to questions:

1. Whats the risk of fetus if the mom is on Cocaine? I chose Heart Defect, but it was wrong.

2. Anyone managed to do the NY/SF question? I sure crapped my pants when I saw it I have the data for it, so if anyone wants to solve it, let me know. Cant post it here, copyright problems I guess.

3. Concentration of Insulin in DM2 . This was a silly mistake, it suppose to be high, ..I wanna know if it is 40 or 80.

4. I think this one we know from the above discussion..OGP poisoing, first thing after Airway securing is Atropine, not Pralidoxime.

5.Unpasterized cheese, Gram+ cocobacilli. I chose Bacillus cerues, but wrong. I missed the point that it was recovered from Blood. Options are: Camplybacter, Clostridium, Listeria, Ecoli, Salmonella, Staph, Vibrio, Yersinia.

6.Study, for Dextromethorphan use and cough. what limited the validity? I chose "Study location limited to emergency department", but this was wrong. Other options were Limited number of participants; Marginal statistical significance; Lack of blinding between groups; Subjective nature of the study(but this is wrong, in another thread)

7.Pharmacotherapy for GERD. I chose metoclopramide over Omeprazole, but this was obviously wrong. I was thinking metoclopromide will increase the LES tone, and prevent reflux, but apparently its wrong. So the answer has to be omeprazole then. Other options were Cimetidine, sucralfate, Calcium carbonate,

8. Again, another nutcracker, and I feel like an idiot. Down, with symtoms of leukemia. What is seen on BM? I chose Megaloblastosis, since the child is less than 5 year old and is increased risk for M7, but this is wrong. Its sure Excess Lymphoblasts. I guess the distinction of the risk for Down in terms of age is a minor detail, not relavent (i.e. Less than 5 = Risk of M7 , More than 5 year old = Risk of ALL)

9. Huge heart shown. Hx of HTN. I chose Infarct, since there was a red mark under the LV ventricle. But, its wrong. I think it was hypertrophy. The size of the heart is 650g.

10. Kid at 2 month, decreasing Hb/Ht. 3 columns for his CBC at 24hours/1week/1month. I chose congenital CMV infection, wrong again!

11. This was a bummer, since I was so sure its right. Patient has hypokinesia of LV post wall on increasing activity on stress echo. Reason for this finding? I chose "Increased myocardial oxygen consumption". Crap! I think it was "Increased LV end diastolic pressure"

12. Another crapy question. Got shot in abdomen, patient requires decreasing dose of Warfarin 6 weeks later. I chose "Septic shock caused by Ecoli", but wrong!

13. Patient, cries after loss of sister, and then has a headache. I chose "abnormal grief response". I think its "normal emotional response"

14. Female Hx of fever, Lower quadrant pain, Leukocytosis, Increase hcg . Pic shows a cavity, lookling like a mole. I chose "Hydatiform mole", but I think it was Choriocarcinoma, since the entire wall was invaded. Or was it Ectopic?

15. Function of IkB in NF-KB. I know this now, its "Release NFkB after undergoing phosphorylation"

The other 4 were my silly mistakes. G+ve messed up, Teratoma is a Germ cell tumor, not Sex chord etc.

Aright, let me know what you guys answered. If you want to know an answer to some question, let me know and I'll try to remember my response.

Thanks.

 

[-EuroDoc-]

Soooo, what is the right answer for this one?

2) 64 year old man with 2 month progressive shortness of breath, 98.6 F temperature, 30/min respirations, bp 125/80, clubbing of fingers, total lung capacity decreased, chest x ray shows a coarse reticular pattern. Most likely cause of these findings?

A)constriction of the terminal bronchioles

B)destruction of the alveolar walls

C)increased fibrosis in the intersittium

D) increased mucus secretion in the bronchioles

E) loss of elastic support to the walls of the bronchioles

 

[PowerDan]

its a tough question

 

[aspiringmd1015]

-the tanner stage question about the 3 year old boy with precocious puberty and delayed height growth, how did you guys get to the answer? i had no idea

-18 month old boy with scid, which type of blood to give him?
if he has scid he cant develop any reaction towards it, so why give irradiated blood? cant we give him any typ eof blood?

-couple had two children with osteogenesis imperfeta, analysis shows the 42 y/o father has /10 sperm with the mutation, i believe the answer is germline mosaicism, but why?

-investigator testing his hypothesis over cd44 splice variants correlates with aggressive disease progression and risk of relaspse in pt's with hodgkin's, especially if variant cd44v10 is expresed, he plans to retrospectively screen fresh frozen tissue and biopsy specimens from documented hogdkin patients, which method would be effective ins creening the archives? I chose Northern Blot bc i thought htey were looking for splice variants but i believe the answer is immunohistochemistry. WHY?

 

[MedBrah 19]

please help with this one

A 45 year old pt with ulcer in anterior superior fondus of stomach has acute pain in left upper quadrant and left shoulder x4 hours. PE shows rigid abdomen. Perforation of stomach wall by ulcer is suspected. Irritation of which of the following by gastric contents explains the left shoulder pain?

Diaphram
Duodenum
Gallbladder
Liver
Pancreas (I chose this and was marked wrong)
Spleen

Regarding this, how can you differentiate between Diaphragm and Spleen? Aren't they describing the Kehr sign perfectly?

 

[Jay2910]

1) So there's this question on 32 year old man who is brought to the ED in coma. Drug overdose suspected. They then go on to ask what are his pH, pO2, pCo2 and HCO3- . . . .I put the answer: His respiration: 8/min

7.40(pH) pO2=80mmHg pCo2=70mmHg HCO3-=42

Do you guys know what is the right answer for this? I thought because he's not breathing as much, he should be alkalotic right? and the way to be alkalotic is to have either high bicarb or low, pCO2 .. .. in this question I didn't see either?

I would definitely appreciate all the help, as I have an exam in few days

37) There was this other question of: 70 yo guy w/ hx of weight loss, abdominal pain . . .Stool shows increased excretion of neutral fat and muscle fiber. They ask like what we give him

How do you differentiated between azathioprine, and pancreatic enzymes? Isn't azathioprine given for IBD? Which is what he has?



What is the difference between saying that deoxyhemoglobin has lower pKa than oxyhemoglobin vs. "Deoxyhemoglobin is better buffer of hydrogen ions than oxyhemoglobin"?


I have a lot of questions on this NBME, and I have my exam in few days . .. .so I plan to be on this thread frequently . .. .and I would definitely appreciate y'all's help!

 

[Rahas]

I don't remember the question at all, but going by what you say, if its ALL -> lymphoblasts, and if its AML -> myeloblasts. Megaloblasts are what you see in B12 / folate deficiency (megaloblastic anemia with hypersegmented neutrophils).

 

[AGSC.MD]

43yo man with 10yr history of alcoholism has jaundice. He takes 2 extra strength acetaminophen every 4-6hrs for the past 3 days. He has increased prothrombin time and increased AST activity. Alternation in which metabolites within hepatocytes is a/w his illness?
- I choose increased NADH due to his alcoholism apparently that's not what they we're going for. Some people thought decreased glutathione but that wasn't right either- the answer supposedly is "decreased NAD+"---does anyone understand this? I mean I know his NADH/NAD ratio should be increased but then I feel like increased NADH should be right too.

Hi there! I just took the NBME 15 yesterday and picked “ decreased NAD+” … and got it wrong. The correct answer is In fact “ decreased glutathione”

Now I’m really confused with why !
Appreciate the help!