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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[pvtbacon]

What is the furuncle!?

A food handler has a fresh furuncle on his face. He prepares meat loaf and lets it sit for 12 hrs at room temp before it's cooked at 350 for 1 hr. 8 of the 10 people who eat the meat loaf become ill within 4 hours. Which of the following sx is most likely?

a. blurred vision
b. dyspnea
c. paresthesias -- not this one
d. shock
e. vomiting

Is it just vomiting? I was thinking that there had to be a spore because he cooked it at 350 but maybe that's not right.

Just vomiting. Because they got sick within 4 hours, think of food poisoning via preformed exotoxin. Furuncle/boiil should make you think of a staph-like abscess because coagulase makes it very localized. Staph exotoxin causes vomiting and diarrhea.

 

[eagles22]

What is the furuncle!?

A food handler has a fresh furuncle on his face. He prepares meat loaf and lets it sit for 12 hrs at room temp before it's cooked at 350 for 1 hr. 8 of the 10 people who eat the meat loaf become ill within 4 hours. Which of the following sx is most likely?

a. blurred vision
b. dyspnea
c. paresthesias -- not this one
d. shock
e. vomiting

Is it just vomiting? I was thinking that there had to be a spore because he cooked it at 350 but maybe that's not right.

I think the key is that the onset of illness was 4 hours which generally indicates a pre-formed toxin. Normally, you'd see vomiting with this.

 

[zee620]

Thanks everyone! Seems like I made some silly mistakes.

 

[waitlist22]

This is probably going to be a really obvious answer but what was the one with the 17 year old boy, kidney removal that had a gross pic and looked dilated/cystic? Was it hydronephrosis?

 

[CrouchingLiger]

This is probably going to be a really obvious answer but what was the one with the 17 year old boy, kidney removal that had a gross pic and looked dilated/cystic? Was it hydronephrosis?

Yeah, that was a picture of a dilated renal pelvix and/or calyces. I thought they were cysts at first, but cysts would most often be in the cortices instead of the collecting system, and he's at an awkward age to present with either ADPKD or ARPKD. So yeah, hydronephrosis.

 

[medpack87]

Hey guys. I got 540/231 on this one. I dont know what went wrong. Anyway, I will finish DIT and then do my last NBME 7 and see how it goes, 11 days until my test.

It is incredible how easily we can miss easy stuff on these tests. At the beginning of the thread, people mentioned that question of a girl that presented with abdominal pain, and she had a tumor resection, and they showed the picture of the patholgy. There was some debate on whether it was hydatiform mole, or an ectopic pregnancy, and that the picture didnt help. I didnt have ir wrong, but I remember seeing a fully formed fetus inside that pathology piece, so it was obviously an ectopic.


Also, about the one with the patient that had GERD and had an imaging study, and they showed you the X-ray, the answer was obvious and could be deducted from looking at the picture, it shows the fundus going way up above the level of the diaphragm.

It was a tricky test indeed.

 

[medpack87]

Here are a couple:

1) About the boy that got bee stung. What is directly associated with the edema?
demargination of leukocytes, fibrin thrombi, gap formation between endohelial cells, vasoconstriction, vasodilation(wrong).

I read in this thread that it might be vasoconstriction?? And that Histmanine had something to do, but it wasnt explained fully. Can someone explain this better? I only have in my notes that edema is due to vasodilation and vascular permeability.

2) About a female patient that had 25 year history of multiple symptoms, a lot of physician visits and tests and had no clear dx. What is the most appropriate statement?
I went for the one asking for emotional trauma in childhood, which was wrong.

Any clear answer and explanation for this one? Other choices were to assess the worst symptom and schedule follow visits (didnt seem helpful at all to me, I mean, to assess 1 symptom and see what happens next after 25 yrs of being ill), look for porphyria, look for drug abuse, tell her she needs a psych evaluation (probably the worst answer).

Thanks

 

[Astarael]

Here are a couple:

1) About the boy that got bee stung. What is directly associated with the edema?
demargination of leukocytes, fibrin thrombi, gap formation between endohelial cells, vasoconstriction, vasodilation(wrong).

I read in this thread that it might be vasoconstriction?? And that Histmanine had something to do, but it wasnt explained fully. Can someone explain this better? I only have in my notes that edema is due to vasodilation and vascular permeability.

2) About a female patient that had 25 year history of multiple symptoms, a lot of physician visits and tests and had no clear dx. What is the most appropriate statement?
I went for the one asking for emotional trauma in childhood, which was wrong.

Any clear answer and explanation for this one? Other choices were to assess the worst symptom and schedule follow visits (didnt seem helpful at all to me, I mean, to assess 1 symptom and see what happens next after 25 yrs of being ill), look for porphyria, look for drug abuse, tell her she needs a psych evaluation (probably the worst answer).

Thanks

1) That's gap formation between the endothelial cells. The mediators that are released in acute inflammation cause both vasodilation and increased vascular permeability; the vascular permeability is increased by the endothelial cells contracting to allow space for things to move out of the vessel.

Vasodilation was wrong because you can vasodilate all you want and fluid won't leak out of the vessels-you need that increase in permeability to get edema.

2) Assess the worst symptom and schedule follow up visits. She had a lot of vague symptoms, if I recall correctly. I picked this answer because it seemed like she needed symptomatic relief more than a definitive diagnosis. Unfortunately I can't explain more than that.

 

[medpack87]

Thank you!

Any idea on what the answer to that question about the SF and NY virus strains and their resistance be? I marked M1/M2 and got it wrong. Anyone that remembers having it right and what their answer was? Or who else got it wrong and what their answer was? To start crossing out possibilities

 

[SLC]

Thank you!

Any idea on what the answer to that question about the SF and NY virus strains and their resistance be? I marked M1/M2 and got it wrong. Anyone that remembers having it right and what their answer was? Or who else got it wrong and what their answer was? To start crossing out possibilities

I got it right and I did so by looking at resistance values (I think) and noticing which ones were closest to SF and which ones were closest to NY.

I don't recall which one I chose but if you can pm me the specifics I'm sure I can give you a better explanation of how I reasoned through this one.

 

[Astarael]

Thank you!

Any idea on what the answer to that question about the SF and NY virus strains and their resistance be? I marked M1/M2 and got it wrong. Anyone that remembers having it right and what their answer was? Or who else got it wrong and what their answer was? To start crossing out possibilities

First, you look at the original strains. SF has high resistance, NY low resistance. Therefore, you know that the gene for resistance is something that SF possesses.

Now, quick review on recombination: if two genes are physically close to each other, they are less likely to recombine than if they are far apart. Therefore, if you're looking for a gene close to the resistance gene, you should look for the SF gene that shows up in the highly resistant strains.

Next, look at the highly resistant strains. You can do this by gestalt or by looking from the top down. You're looking for an SF gene that shows up *more frequently than it should* given random assortment in the highly resistant strains. Of the genes listed, the HA locus had the SF allele for all of the highly resistant strains. Since that's more frequent than expected, and was the most frequent out of any of the genes, it was the correct answer.

 

[medpack87]

First, you look at the original strains. SF has high resistance, NY low resistance. Therefore, you know that the gene for resistance is something that SF possesses.

Now, quick review on recombination: if two genes are physically close to each other, they are less likely to recombine than if they are far apart. Therefore, if you're looking for a gene close to the resistance gene, you should look for the SF gene that shows up in the highly resistant strains.

Next, look at the highly resistant strains. You can do this by gestalt or by looking from the top down. You're looking for an SF gene that shows up *more frequently than it should* given random assortment in the highly resistant strains. Of the genes listed, the HA locus had the SF allele for all of the highly resistant strains. Since that's more frequent than expected, and was the most frequent out of any of the genes, it was the correct answer.

Thank you, Im looking at it right now and it makes sense.

 

[MLT2MT2DO]

Thank you, Im looking at it right now and it makes sense.

Additionally the way I approached it "What gene that shows up with NY has the lowest ratio". I found this to be a much less muddled way of getting to the answer, though of course you end up with the same answer.

 

[MLT2MT2DO]

Have one I'm completely stumped on:

45 year old man chronic renal failure can not convert what to it's active form:

I put 24,25 (OH)2 since that is the inactive form of Vitamin D3...I'm confused as to how this is incorrect

 

[CrouchingLiger]

Have one I'm completely stumped on:

45 year old man chronic renal failure can not convert what to it's active form:

I put 24,25 (OH)2 since that is the inactive form of Vitamin D3...I'm confused as to how this is incorrect

That's the inactivated form of Vit. D, but that can longer be converted back into the active form of vitamin D. The precursor form of Vit. D is 25 (OH) D3, which is then hydroxylated at the 1 position to make 1, 25 (OH) D3 as the active form. If that initial 25 (OH)D3 is instead hydroxylated at the 24 position, it is inactive. This 24-hydryxylation occurs in the liver with excess Vit. D, wheras the activation with 1-hydroxylation occurs in the kidney in response to PTH.

 

[MLT2MT2DO]

That's the inactivated form of Vit. D, but that can longer be converted back into the active form of vitamin D. The precursor form of Vit. D is 25 (OH) D3, which is then hydroxylated at the 1 position to make 1, 25 (OH) D3 as the active form. If that initial 25 (OH)D3 is instead hydroxylated at the 24 position, it is inactive. This 24-hydryxylation occurs in the liver with excess Vit. D, wheras the activation with 1-hydroxylation occurs in the kidney in response to PTH.

Doh, thanks. Not really sure what I was thinking.

 

[blaqmamba]

A few questions:

1. The role of IkB in NF-kB signal transduction? I put Translocation to the nucleus after phosphorylation (figured NF-kB was a transcription factor anyways)


2. The lysosomal enzymes showing increased enzyme activity, and what is the mechanism? What the eff am I missing here?

3. Hodgkins disease 10 years ago, now AML. Why?

4. 50yo with hypokinesis of the posterior LV with increased activity. Why? Compression of the coronaries?

Man I feel like I got some of the difficult ones and missed the gimmies.

Also, I read online, as well as in another review book afterwards that cocaine can cause heart defects in the fetus...

 

[MLT2MT2DO]

A few questions:

1. The role of IkB in NF-kB signal transduction? I put Translocation to the nucleus after phosphorylation (figured NF-kB was a transcription factor anyways)

I got this correct but for the life of me can't remember what I put, the answer you put says that I-Kb would be translocated and not NF-kb...which is why I ruled this out.


2. The lysosomal enzymes showing increased enzyme activity, and what is the mechanism? What the eff am I missing here?

I cell disease, enzyme should get tagged to be exported by the golgi but don't they accumulate in the cell

3. Hodgkins disease 10 years ago, now AML. Why?

Myelogenous Leukemia is from a completely different line of WBCs. This is why I picked radiation instead of left over lymphoma cells

4. 50yo with hypokinesis of the posterior LV with increased activity. Why? Compression of the coronaries?

Right coronary artery artherosclerosis, right circulation predominant in ~80% of people, supplies the posterior LV.

Man I feel like I got some of the difficult ones and missed the gimmies.

Also, I read online, as well as in another review book afterwards that cocaine can cause heart defects in the fetus...

Placenta Abruptio is a big issue with cocaine

I too missed some easy ones though different ones

 

[CrouchingLiger]

A few more thoughts to add to the above:

A few questions:

1. The role of IkB in NF-kB signal transduction? I put Translocation to the nucleus after phosphorylation (figured NF-kB was a transcription factor anyways)

It was phosphorylation and dimerization of IkB to release NFkB (or something along those lines), because its the NFkB that will translocate into the nucleus as the transcription factor. IkB holds on to NFkB in the cytoplasm until it gets activated, releasing NFkB to be active. This is the general mechanism for several steroid pathways, which bind to cytosolic targets and then release a transcription factor to enter the nucleus.

2. The lysosomal enzymes showing increased enzyme activity, and what is the mechanism? What the eff am I missing here?

Lysosomal enzymes should get tagged with mannose-6-phosphate to be targetted to the lysosome, but when this is dysfunctional (as in I-cell disease), the lysosomal enzymes are instead secreted. Secreted lysosomal enzymes means that you'll find their activity elevated in the serum.

 

[blaqmamba]

wow. I-cell disease LOL
Thanks guys.

Also, for the angular gyrus, how is one to know that it is NOT Wernicke's but rather an angular gyrus lesion?

Lastly, does anyone remember the embryo one girl who was pregnant and what stage the embryo was at? Didn't show up on my feedback but can't remember what I put for the life of me

 

[MLT2MT2DO]

wow. I-cell disease LOL
Thanks guys.

Also, for the angular gyrus, how is one to know that it is NOT Wernicke's but rather an angular gyrus lesion?

Lastly, does anyone remember the embryo one girl who was pregnant and what stage the embryo was at? Didn't show up on my feedback but can't remember what I put for the life of me

Ummm..it was Wernicke's. At least I picked the superior/posterior temporal lobe location and got it correct.

I'm making a list of the questions I was going to ask and the embryo question is one I didn't get either, I'm curious as well.

 

[Astarael]

The embryo one was the beginning of week 4 (one week past when her menstrual period should have been). Neural plate was formed but not fully closed.

 

[blaqmamba]

Oh right it was that the neural plate was present but tube wasn't complete. I thought she was 20 days post intercourse?? or was it 28?
I always thought that it was the time from fertilization (ie when she had sex) which led me to my answer

 

[MLT2MT2DO]

I swear, if I was able to replace my embryo/genetics with ANY other discipline on my tests would be 10 points higher.

Questions I had:

1. Guy is hyperventilating, PCO2/PO2 relatively normal if not completely normal. AO2 % low, Venous O2 % low….I’m guessing this is anemia? What would one see with elevation?

2. Since when does a legion in the occipital area cause left/right hemaniopia, I always thought it would be contralateral eye scotoma w/ macular sparing.

3.Ammnioagenesis, I know this has been answered and is glutamine, can someone point me in the direction of where I can find an explanation or someone have an explanation for this?

4.Slip strand mispairing answer…why is this not just an insertion? It looks like it’s a random 2 base insertion that causes a shift frame mutation.

 

[CrouchingLiger]

I swear, if I was able to replace my embryo/genetics with ANY other discipline on my tests would be 10 points higher.

Questions I had:

1. Guy is hyperventilating, PCO2/PO2 relatively normal if not completely normal. AO2 % low, Venous O2 % low….I’m guessing this is anemia? What would one see with elevation?

At high elevations, the inspired air has a low PO2, leading to a low PO2 in the alveoli during respiration (maybe 70-80, instead of the normal 115 or so). Therefore, the PAO2 will also be low, because it will always be slightly lower than the PO2 in the alveoli, with an A-a gradient around 10-15. Also, the question had low O2 contents (not percents), right? Otherwise it wouldn't match with anemia. I don't remember it exactly anymore though.

2. Since when does a legion in the occipital area cause left/right hemaniopia, I always thought it would be contralateral eye scotoma w/ macular sparing.

If i'm understanding this right, since forever. Check out the image in First Aid 2013 p. 441 at the bottom. Occipital lobe lesions are lesions of the contralateral visual field of both eyes, usually with macular sparing.

3.Ammnioagenesis, I know this has been answered and is glutamine, can someone point me in the direction of where I can find an explanation or someone have an explanation for this?

Hopefully someone else can help, I don't remember the question and also don't know this stuff well enough to explain.

4.Slip strand mispairing answer…why is this not just an insertion? It looks like it’s a random 2 base insertion that causes a shift frame mutation.

What were the choices for this question? I don't remember that even being a choice, I thought I had ruled out the other options and went with slip strand mispairing.

hope this helps

 

[blaqmamba]

I swear, if I was able to replace my embryo/genetics with ANY other discipline on my tests would be 10 points higher.

Questions I had:

1. Guy is hyperventilating, PCO2/PO2 relatively normal if not completely normal. AO2 % low, Venous O2 % low….I'm guessing this is anemia? What would one see with elevation?
Yeah it was anemia. Because PO2 was normal you could rule out elevation; normal CO2 rules out hypo/hyperventilation; I forget the other ans choices but you know that O2 content was decreased with normal other stuff-->anemia. If anyone has more they can add

2. Since when does a legion in the occipital area cause left/right hemaniopia, I always thought it would be contralateral eye scotoma w/ macular sparing.
I forget the Q but I don't think they said anything about macular sparing being present/absent so maybe you read too much into it but you could rule out parietal/temporal because those are only the bottom/top and rule out optic nerve/chiasm if those were the other 2 choices for obvious reasons

3.Ammnioagenesis, I know this has been answered and is glutamine, can someone point me in the direction of where I can find an explanation or someone have an explanation for this?
Missed this and looking for more on it too

4.Slip strand mispairing answer…why is this not just an insertion? It looks like it's a random 2 base insertion that causes a shift frame mutation.

Same thought process as you on that last one. Anyone?

 

[Astarael]

Oh right it was that the neural plate was present but tube wasn't complete. I thought she was 20 days post intercourse?? or was it 28?
I always thought that it was the time from fertilization (ie when she had sex) which led me to my answer

I didn't calculate it from when she had sex, so I'm not sure what the exact number is. I calculated from when she should have ovulated and came up with three weeks/21 days, which means the embryo was just entering week 4.

 

[Astarael]

I swear, if I was able to replace my embryo/genetics with ANY other discipline on my tests would be 10 points higher.

Questions I had:

1. Guy is hyperventilating, PCO2/PO2 relatively normal if not completely normal. AO2 % low, Venous O2 % low….I'm guessing this is anemia? What would one see with elevation?

2. Since when does a legion in the occipital area cause left/right hemaniopia, I always thought it would be contralateral eye scotoma w/ macular sparing.

3.Ammnioagenesis, I know this has been answered and is glutamine, can someone point me in the direction of where I can find an explanation or someone have an explanation for this?

4.Slip strand mispairing answer…why is this not just an insertion? It looks like it's a random 2 base insertion that causes a shift frame mutation.

For number 2, I made the same mistake and assumed it couldn't be an occipital lesion since the macula wasn't spared. I went back and thought about it, and it turns out the macular sparing is specifically a feature of PCA ischemia. The occipital pole has several factors going for it that I don't totally understand that make it resistant to ischemic damage. A mass lesion in the occipital lobe would knock out the whole thing due to mass effect-there would be no sparing, because the sparing is a blood supply phenomenon.

That's not to say you couldn't get macular sparing with a mass lesion, it's just not required.

 

[MLT2MT2DO]

For number 2, I made the same mistake and assumed it couldn't be an occipital lesion since the macula wasn't spared. I went back and thought about it, and it turns out the macular sparing is specifically a feature of PCA ischemia. The occipital pole has several factors going for it that I don't totally understand that make it resistant to ischemic damage. A mass lesion in the occipital lobe would knock out the whole thing due to mass effect-there would be no sparing, because the sparing is a blood supply phenomenon.

That's not to say you couldn't get macular sparing with a mass lesion, it's just not required.

Yeah, regardless it was by far the best answer. If it doesn't fit into the nice neat package I always want it to fit in I start overthinking it

 

[waitlist22]

The answer choice for insertion was "transposon insertion". A transposon insertion would be much larger than one base pair but would also likely result in a frameshift mutation. What also leads to slipped strand is that it enters the same codon as the previous one, indicating that the strand slipped and it started re-transcribing one base pair early (i.e. the one it had just inserted).

A simple insertion would have been a much easier answer choice but since it wasn't there, strand slip was the only one that made since if I recall correctly. Let me know if that isn't clear and I can type a longer answer.

 

[blaqmamba]

The answer choice for insertion was "transposon insertion". A transposon insertion would be much larger than one base pair but would also likely result in a frameshift mutation. What also leads to slipped strand is that it enters the same codon as the previous one, indicating that the strand slipped and it started re-transcribing one base pair early (i.e. the one it had just inserted).

A simple insertion would have been a much easier answer choice but since it wasn't there, strand slip was the only one that made since if I recall correctly. Let me know if that isn't clear and I can type a longer answer.

I would be interested in a little more detail if you had the time to write something out

 

[waitlist22]

I'll do my best without being able to draw a diagram. As the strand is being synthesized bases are matched base for base. If the strand being synthesized slips it basically puts a loop in the DNA/RNA. The slipped loop is no longer matched up with its base pair match which essentially shortens the strand being synthesized and backs it up a few basepairs (usually around how many slipped). With multiple repeated bases in a row, DNA polymerase sees that the last few bases are still appropriately matched and continues on replicating but will mistakenly add an extra base because uses the same base twice on the parent strand. Here is my best attempt at a diagram:

AAAAAGGGGGTTTTCCCCCCCCCCCC
-------------------------------------------------------
TTTTTCCCCCCA GGGGGGG
----------------------A A
-----------------------A

So if the slip were to happen at this point, it would back the Gs up as if they were matched with the Ts and you would get extra bases added on as it continued synthesizing because the last few bases are still matched correctly and it doesn't sense that something is wrong. I realize this isn't the most scientific way of explaining and may not be the exact mechanism but is how I understand it. This is also the general mechanism by which you get the trinucleotide repeat expansion disorders. The strand slips but since it is repeats of the same 3 basepairs it re-matches up the slipped strand with the correct base pairs on the parent and carries on, adding the repeats. Some of the repeats will be looped out and not paired with the parent and so extra codons are added. Hope I didn't make you more confused than before?

 

[MLT2MT2DO]

The answer choice for insertion was "transposon insertion". A transposon insertion would be much larger than one base pair but would also likely result in a frameshift mutation. What also leads to slipped strand is that it enters the same codon as the previous one, indicating that the strand slipped and it started re-transcribing one base pair early (i.e. the one it had just inserted).

A simple insertion would have been a much easier answer choice but since it wasn't there, strand slip was the only one that made since if I recall correctly. Let me know if that isn't clear and I can type a longer answer.

Awesome explanation, thank you. Being weak in genetics I didn't know a transposon insertion had to be a bigger insertion, hence it was the easiest/most logical choice for my lack of knowledge. Damn a 15 on BS MCAT...if my test wasn't on Monday I'd pick your brain more.

 

[MLT2MT2DO]

Also, I really loved the more generous curve on this one compared to the others. I really didn't find this test any more/less difficult than 12/13 but the curve was a pleasant surprise.

 

[medpack87]

yea. I had almost the same number of total wrong answers than previous NBMEs, but my predicted went up 5-10 points. I do think it was a more difficult test, the curve proves that, and I had 2 DIT weeks on me when I took that NBME (I had 0 DIT weeks done when I took the preivous NBME).

 

[blaqmamba]

Can anyone confirm on the question with the serial blood counts - someone posted earlier that it was congenital neutropenia. If that's correct, can someone explain?

I felt it was a CMV infection (virus-->elevated lymphos)?

 

[medpack87]

That was a very tricky question. Lots of distractions within the question stem, plus lots of lab values. I got to the answer because I knew (luckily I have rotated in a neonatal ICU before), that the Hb of the neonate will have a physiologic decrease each day, because it starts to get diluted, but its normal, until it reaches a base value. Besides it didnt have any signs of hemolysis apart from the gradual Hc decrease (which is physiologic after all)

Then the total leukocyte count of the patient was incredibly increased (i cannot remember, but I think it was over 20,000, may be exaggerating though). So looking to the answer choices, none of them made sense, there were not any buzz words to relate to the answer choices presented. After much thinking and returning several times to check the question again, I decided to check the normal lab values that NBME gives you, and the % neutrophil count of that neonate was incredible low, even more because the total leukocyte was increased, so he was very deficient in neutrophils. And that was the only answer that made sense....

I dont even know what disease that neonate had exactly, because he seemed to have some kind of infection, but no idea what, all I know is that it had very low neutrophils, and that was an answer choice.

 

[Astarael]

Can anyone confirm on the question with the serial blood counts - someone posted earlier that it was congenital neutropenia. If that's correct, can someone explain?

I felt it was a CMV infection (virus-->elevated lymphos)?

I can confirm it. Best explanation I have is that the neutrophils were seriously low (like, less than 10% when they're supposed to be >50%). I'm not sure what the mechanism of lymphocyte proliferation is.

Edit: woops. Medpack beat me to it.

 

[MLT2MT2DO]

Can anyone confirm on the question with the serial blood counts - someone posted earlier that it was congenital neutropenia. If that's correct, can someone explain?

I felt it was a CMV infection (virus-->elevated lymphos)?

The child doesn't have a disease. This is a frequent and normal finding in newborns. The normal ranges for infants are different than adults. Most labs that have any volume of newborn labs come through will have different normal values for children younger than 2.

I'm not 100% sure that this has been explained "why" this happens but most theories are that at an early age children have >lymphocytes because the immune system is attempting to be primed. You can probably find a better explanation on Up to date.

Source: 5 years as a Medical lab Hematology Supervisor

 

[VivaLaVida]

Were the lymphocytes actually high? Leukocyte count was high which is normal for neonates I am pretty sure. I got the question correct so can't see the lab values anymore but I remember the neutrophil percent being ridiculously low...and the lymphocyte PERCENT beig ridiculously high... (Obviously since you have less neutrophils, lymphocytes would now make up a greater percentage of the WBC). I think lymphocytes just seemed high due to the relative scarcity of neutrophils.

 

[medpack87]

Were the lymphocytes actually high? Leukocyte count was high which is normal for neonates I am pretty sure. I got the question correct so can't see the lab values anymore but I remember the neutrophil percent being ridiculously low...and the lymphocyte PERCENT beig ridiculously high... (Obviously since you have less neutrophils, lymphocytes would now make up a greater percentage of the WBC). I think lymphocytes just seemed high due to the relative scarcity of neutrophils.

That seems to be the case. On this link you can check the question, I won't post the question directly here because of forum rules. But there it is, leukocytes are normal (for a neonate) and neutrophils are low, causing the lymphocytes to appear increased.

http://www.usmleforum.com/files/forum/2013/1/725793.php

 

[medpack87]

By the way, what was the answer on the Michelis Menten question. The one that involved guanine velocity? And how do you come up with that answer? I am really bad on these type of questions, it seems to be obvious, but I still dont know the answer.

 

[spartanmd2015]

took this mother of an exam yesterday. definitely felt more difficult than 13. After reading through all the posts, there were still a few questions I haven't seen the answers yet, and would really appreciate any input anyone has.
----

1. 60 y/o Man is brought to the ED because of generalized weakness for 6 hrs. Onset of Sx occured 2 hrs after he took 4 tablets (rather than usual 1 tablet) of medication that prevents angina pectoris. His pulse is 36/min, and blood pressure is 100/50 mmHg After the administration of isoproterenol, his pulse increases to 60/min. which of the following best describes MOA of this patient's usual chronic medication?
pretty sure I talked myself out of the correct answer. was this reversible, dose dependent?

A 37 y/o woman is brought to the ED after husband found her unconscious. Her temp is 98.6, pulse is 128/min, and BP is 70/40 mmHg. physical exam shows cool, pale extremities, jugular venous distention, faint peripheral pulses and crackles over the bottom two thirds of both lung fields. Heart sounds are normal and there are no murmurs. She withdraws to painful stimuli in all four extremities. This pt is likely experiencing what type of shock?
I think I was thrown by the pulm findings, with the crackles over the bottom 2/3 fields. This made me think anaphylactic due to an increase vascular permeability from histamine release. Now that I re-read it, this likely wouldn't fit due to the cold extremities, so would it be hypovolemia or cardiogenic? If anyone has any tips on how they approached this one, I'd really appreciate it.

I'll do my best to contribute to any of the other unanswered questions as well, and really appreciate the help. Thanks!

 

[spartanmd2015]

By the way, what was the answer on the Michelis Menten question. The one that involved guanine velocity? And how do you come up with that answer? I am really bad on these type of questions, it seems to be obvious, but I still dont know the answer.

(pg 226 of FA 2013) Km =1/2 Vmax. I don't remember the specifics of the question, but I definitely remember using that formula to solve the problem based on the table they provided. If this explanation is too vague, post more details of the problem up, and I can try to be more clear.

 

[OberynMartell]

Can someone explain about the question with the GERD guy who had "linear tears" in his esophagus and why it wouldn't be metoclopramide? Doesn't that indicate vomiting/Mallory Weiss? This is like the 5th time where I've been led astray by simple one liners like this. I assume they put that information in there for a reason, and you're supposed to catch it or you'll jump to the wrong conclusion. I had Omeprazole and then switched it when I thought about the linear tears.

I guess I'm starting to wonder what information you're supposed to pay attention to and which you aren't.

 

[Astarael]

took this mother of an exam yesterday. definitely felt more difficult than 13. After reading through all the posts, there were still a few questions I haven't seen the answers yet, and would really appreciate any input anyone has.
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1. 60 y/o Man is brought to the ED because of generalized weakness for 6 hrs. Onset of Sx occured 2 hrs after he took 4 tablets (rather than usual 1 tablet) of medication that prevents angina pectoris. His pulse is 36/min, and blood pressure is 100/50 mmHg After the administration of isoproterenol, his pulse increases to 60/min. which of the following best describes MOA of this patient's usual chronic medication?
pretty sure I talked myself out of the correct answer. was this reversible, dose dependent?

A 37 y/o woman is brought to the ED after husband found her unconscious. Her temp is 98.6, pulse is 128/min, and BP is 70/40 mmHg. physical exam shows cool, pale extremities, jugular venous distention, faint peripheral pulses and crackles over the bottom two thirds of both lung fields. Heart sounds are normal and there are no murmurs. She withdraws to painful stimuli in all four extremities. This pt is likely experiencing what type of shock?
I think I was thrown by the pulm findings, with the crackles over the bottom 2/3 fields. This made me think anaphylactic due to an increase vascular permeability from histamine release. Now that I re-read it, this likely wouldn't fit due to the cold extremities, so would it be hypovolemia or cardiogenic? If anyone has any tips on how they approached this one, I'd really appreciate it.

I'll do my best to contribute to any of the other unanswered questions as well, and really appreciate the help. Thanks!

1. Correct. If the effect can be overcome with isoproterenol, he was on a b-blocker; these are reversible.

2. Cold extremities rules out neurogenic and septic shock. That leaves you with cardiogenic, hypovolemic, and anaphylactic. I think I picked anaphylactic too, but you'd expect to see skin involvement (hives) and bronchospasm. That leaves you between cardiogenic and hypovolemic. The JVD and pulmonary edema are more consistent with cardiogenic, which I believe is the correct answer.

Can someone explain about the question with the GERD guy who had "linear tears" in his esophagus and why it wouldn't be metoclopramide? Doesn't that indicate vomiting/Mallory Weiss? This is like the 5th time where I've been led astray by simple one liners like this. I assume they put that information in there for a reason, and you're supposed to catch it or you'll jump to the wrong conclusion. I had Omeprazole and then switched it when I thought about the linear tears.

I guess I'm starting to wonder what information you're supposed to pay attention to and which you aren't.

I think the question said erosions, not tears; also, the guy had no risk factors for Mallory Weiss. Just simple old GERD.

 

[medpack87]

took this mother of an exam yesterday. definitely felt more difficult than 13. After reading through all the posts, there were still a few questions I haven't seen the answers yet, and would really appreciate any input anyone has.
----

1. 60 y/o Man is brought to the ED because of generalized weakness for 6 hrs. Onset of Sx occured 2 hrs after he took 4 tablets (rather than usual 1 tablet) of medication that prevents angina pectoris. His pulse is 36/min, and blood pressure is 100/50 mmHg After the administration of isoproterenol, his pulse increases to 60/min. which of the following best describes MOA of this patient's usual chronic medication?
pretty sure I talked myself out of the correct answer. was this reversible, dose dependent?

I think it was a cardioselective beta blocker. And the answer was straightforward, it is reversible because by administering isoproterenol, a b1 b2 agonist, you reversed the symptoms. And it is dose dependent because... well he overdosed on it.

A 37 y/o woman is brought to the ED after husband found her unconscious. Her temp is 98.6, pulse is 128/min, and BP is 70/40 mmHg. physical exam shows cool, pale extremities, jugular venous distention, faint peripheral pulses and crackles over the bottom two thirds of both lung fields. Heart sounds are normal and there are no murmurs. She withdraws to painful stimuli in all four extremities. This pt is likely experiencing what type of shock?
I think I was thrown by the pulm findings, with the crackles over the bottom 2/3 fields. This made me think anaphylactic due to an increase vascular permeability from histamine release. Now that I re-read it, this likely wouldn't fit due to the cold extremities, so would it be hypovolemia or cardiogenic? If anyone has any tips on how they approached this one, I'd really appreciate it.

It is a cardiogenic shock, basically the heart cannot pump blood, so her extremities are cold, and her BP is low. Then blood starts to build up on the right side leading to the jugular distention and the pulmonary edema,

I'll do my best to contribute to any of the other unanswered questions as well, and really appreciate the help. Thanks!

Can someone explain about the question with the GERD guy who had "linear tears" in his esophagus and why it wouldn't be metoclopramide? Doesn't that indicate vomiting/Mallory Weiss? This is like the 5th time where I've been led astray by simple one liners like this. I assume they put that information in there for a reason, and you're supposed to catch it or you'll jump to the wrong conclusion. I had Omeprazole and then switched it when I thought about the linear tears.

First line ttx for GERD is Omeprazole, if the question stem says or leads you to GERD, then Omeprazole is the answer. If it there is any history on vomiting, then it would be Mallory Weis. It is one of those questions where if you overthink it, you are going to lose time and probably answer incorrectly

I guess I'm starting to wonder what information you're supposed to pay attention to and which you aren't.

I hope that helps

 

[medpack87]

(pg 226 of FA 2013) Km =1/2 Vmax. I don't remember the specifics of the question, but I definitely remember using that formula to solve the problem based on the table they provided. If this explanation is too vague, post more details of the problem up, and I can try to be more clear.

Thank you. I think that leads me to the answer.

 

[as90]

Sorry, I haven't taken this yet but if anyone who has taken the real USMLE recently, do you suggest taking this one in addition to 12 and 7? Was this one more representative of the real test than the other ones?

I just wanted to get some feedback, because I'm planning on doing one before I finish DIT in order to determine if I should sit for the real exam. I have heard some people say that the real exam generally has longer question stems, is this the case for this one?

Thanks again

 

[birthdaycake]

does anyone know what tubular hydrostatic pressure refers to? i assumed that it was the same thing as glomerular hydrostatic pressure but apparently that's not the case, i'm now thinking it may refer to bowman's space/capsular hydrostatic pressure.

also it was mentioned earlier that the brain pic was an angular gyrus lesion.. but i looked that up and the symptoms of that are completely different (gerstmann syndrome) than wernickes. gerstmann is more to do with agraphia, acalculia. so if this was indeed wernicke's how come the lesion is not on the superior temporal gyrus?

also someone commented earlier that the diabetic wouldn't have any endogenous insulin secretion after 30 years, but most diabetic drugs require islet function to work like sulfonylureas so they still have some insulin secretion...did anyone get that question right? normal values for insulin secretion when fasting are 5 to 20