Official nbme 15 discussion

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abelabbot

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

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Clarify please.

Not sure if I read it right or if it was how they phrased it or maybe I straight up confused myself... but I thought what they meant was actually increasing the INFLUX of sodium. I was thinking that driving more sodium into the cell would work the Na+/Ca2+ exchanger and force Ca2+ out (like a normal elimination of Ca2+) -> inhibiting contraction. As opposed to thinking of it like digoxin and letting Na+ ACCUMULATE inside.

If that even makes sense... :thumbdown:

Also, 3) by itself doesn't make sense. The question referred to "a substance". Myosin binding sites being covered.... so what? How does that relate to the problem?
i felt this is one of those questions where we've gotta only concentrate on what exactly is bein asked.. they only mentioned that some substance decreases intracellular contraction and asked which of the options explains the end result (i.e. inhibition of contraction).. this was my approach to the question.. hope it makes sense..
 
My score went down from NBME 13 to 15 (took 2 weeks apart). Found 15 tougher overall, more experiment type questions, more "murky" answers. Probably more representative of the actual Step 1. Score fell 4 points. Not a major dropoff but a good reality check.

Did you guys also have a question that straight just asked for the average of ten different ages? I re-read it so many times thinking they were trying to trick us somehow but in the end I guess that's all they wanted lol.

And then there was ridiculous experiment thing with botulism and end plate potentials and Ach, I had no idea what was going on.

havent taken 15 yet, but just by looking in FA, we know that botulinum toxin prevents Ach from being released into the synaptic cleft, i guess from there you could extrapolate that EPP goes down...
 
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Is anyone's NBME15 score out of whack with how they've been doing on previous tests? Granted, I've only taken the UWSAs right now and I expected to dip (since everyone says the UWSAs overshoot), but I went from 244, 262, on the UWSAs then 238 here. I look at my performance and most of the bars are above the average and then I look here and lots of the questions I had trouble with I seem to have gotten right (according to discussion in this thread). Should have bought the expanded pack or whatever, because now I have no clue what I did wrong. :(

This one was crap. Should have bought 12 or 13 or something. Plan to take one more in about 3 days or so... any recommendations? Hoping not to deflate my morale by taking it, lol... test in 7 days.

My NBME 15, finished about 2 hours before my actual exam, was within 2 points of my real score.

If you have a wild swing in your score, you need to normalize your studying habits and become less anxious. My UWSA and NBME were very close to each other.
 
Q1. 6 year girl with known renal tubular acidosis with "a defect in renal ammoniagenesis suspected". The question is "the source of ammonia production in THIS patient".

Would someone like to discuss this? I know the answer for this is glutamine but I have my doubts. Glutamine is deaminated by glutaminase in the kidney to produce glutamate + NH3. The ammonia is then used to buffer protons for acid excretion. Now in context to this question there is a "defect in renal ammoniagenesis" so I'm thinking defective glutaminase. How can glutamine serve to be the source of ammonia then? "Glutamate" would have been a much better answer I reckon.

Q2. 50 year old man with fatigue. pO2=96 mm Hg, pCO2=30 mm Hg, arterial O2 'content' is significantly low and so is mixed venous O2 content. The answer is obviously anemia as the oxygen content is low inspite of fairly normal pO2. Can someone explain the low pCO2? Or are they just playfully messing with our already traumatized brains?

Over-thinking cost me these two. I hope the questions could be a bit more accurate and a bit less redundant in the real exam. I didn't like this NBME so much.
 
I didnt understand the question with the r value (r= -0.25). They were asking what the correlation was between body fat and lung capacity. I thought a positive r value meant there is more of a correlation...i said that there was no correlation between the two but that was wrong.
 
I didnt understand the question with the r value (r= -0.25). They were asking what the correlation was between body fat and lung capacity. I thought a positive r value meant there is more of a correlation...i said that there was no correlation between the two but that was wrong.

its like this man. R= correlation +ve r means positive correlation. You'd see something go up on a graph along with something else. ie: more one value means more of another eg: more body % and higher insulin levels. ↑ and ↑ relationship (or ↓ and ↓)

-ve r means a negative correlation. Like one value goes up, and the other goes down on a graph. Like amount of miles jogged everyday, and incidence of heart disease. ↑ and ↓ (or ↓ and ↑)

This form was annoying as hell. haha. I hated that mean question. I was like wtf, ain't nobody got time for that, still got a 680 (264), but yeah, form seems to have this "hey here's a normal presentation....OR IS IT? mwa hahahahaha. The clock is ticking little man, choose and go" thing about it. Also I saw that influenza SF NY question and I said "**** you" marked it immediately and did it at the end.

Annoying ass form. If this is representative of the actual step I can see why people go crazy after 3 weeks waiting for the result. I could barely wait the 3 seconds after I clicked done.
 
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its like this man. R= correlation +ve r means positive correlation. You'd see something go up on a graph along with something else. ie: more one value means more of another eg: more body % and higher insulin levels. ↑ and ↑ relationship (or ↓ and ↓)

-ve r means a negative correlation. Like one value goes up, and the other goes down on a graph. Like amount of miles jogged everyday, and incidence of heart disease. ↑ and ↓ (or ↓ and ↑)

This form was annoying as hell. haha. I hated that mean question. I was like wtf, ain't nobody got time for that, still got a 680 (264), but yeah, form seems to have this "hey here's a normal presentation....OR IS IT? mwa hahahahaha. The clock is ticking little man, choose and go" thing about it. Also I saw that influenza SF NY question and I said "**** you" marked it immediately and did it at the end.

Annoying ass form. If this is representative of the actual step I can see why people go crazy after 3 weeks waiting for the result. I could barely wait the 3 seconds after I clicked done.

ah okay, now the R value question makes sense, thanks! Also, how do you do the SF NY influenza question? I know it was covered earlier and someone explained it simply as the ratios, but how do you figure that out?
 
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I also wanted to ask if anyone has nbme 15 offline. My exam is in a week and i wanted to review it inside out because all my friends who took the step said it was really really similar
hi, i was wondering if you were able to find this..i would also really like to review my mistakes on this and go through the entire exam. if you were able to get it could i please get it from you. thank you!
 
where do you find these exams i keep hearing people discuss? exam 11, 12, 15, etc. i tried searching for them but all my searches bring me back to forums discussing them
 
where do you find these exams i keep hearing people discuss? exam 11, 12, 15, etc. i tried searching for them but all my searches bring me back to forums discussing them
Nbme.org .... U have to start your own account .. Then buy the exam u want


Sent from my iPhone using Tapatalk 2
 
Can anyone answer these please?

Q . Adenocarcinoma at GE junction - chronic infection of which of the pathogens causes this - clonorchis, CMV,Entameoba, H pylori, M tuberculosis.

Q. A old woman with DM type 2 for 30 years, the patient is most likely to have an endogenous fasting serum insulin concentration closest to? (n =5-20 ) - 1 , 10, 20, 40 ,80

Q. A daughter brinds her 84 yr old mom with dementia, who has lost 9 lbs in 3 months who refuses to eat but is relaxed and cooperative during examination . daughter is tearful, stressed and what interventions is most appropriate ? - get started on feeding tube ; get started on TPN ; disccus stresses of patient care with the daughter and provide info regarding assistance; reassure that weight loss isnt problem cuz she is still overweight ; reassure daughter and tell her that weight loss is common in elderly.

Thanks !!
 
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Reviving this thread....Have a couple of questions that could use some clarification!

For the question on the pregnancy with passing of tissue with obvious fetus and D&C showing chorionic villi with focal edema and trophoblastic proliferation, is the answer partial mole? I put placental site trophoblastic tumor, but I'm not even sure what that is. I didn't put partial mole cause I thought it was only fetal parts, not an "obvious fetus". If someone could explain, that'd be great! :D

What's the consensus on the barium swallow with the paraesophageal hernia question? Is it that the fundus protrudes into chest above lvl of T10?

For the man with the blindness in his left eye with pale, opaque fundus and brith red fovea centralis and a dense scotoma of entire visual field of left eye, the question asks what happens to the right pupil with left eye illumination, is the answer no constriction b/c retinal ganglion cells in L eye have been destroyed? (I put no constriction b/c ciliary nerve dmg but I guess the red fovea centralis should point me to an abnormality with the ganglion cells?)
 
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Also...for the referred L shoulder pain question with the perforation of the stomach by an ulcer question, is it diaphragm? I put spleen cause I thought it usually referred to the shoulder. Does diaphragm pain also refer there? That seems like the only logical thing than can be irritated by stomach acid.
 
A few more questions...

In the one w/ the sudden complete L eye blindness, why do the retinal ganglion cells die? What was the underlying pathology?

28 y/o male w/ fatigue, weakness, weight loss, 6mo of dry cough + CP, smoker. b/l hilar adenopathy + paratracheal node enlargement, noncaseating granulomas. biggest RF? i said employment (carpenter)... was the ans race? sarcoidosis?

loop diuretics → contraction alkalosis?

man w/ alcohol binge w/ severe abd pain. dies, autopsy shows pink picture of mesenteric adipose. what was the cause?
panc enzymes on adipose tissue
acute alc hep (no)
acute ruptured appendicitis
direct effect of EtOH on adipose
malnutrition

67 y/o man w/ 2 days of droopy right eyelid, double vision. eye is fixed in the out position, dilated. Cause?
-aneurysm of PCoM
-compression of sup cerv ganglion (no)
-trochlear n damage
-occlusion of scleral venus sinus
-tumor of optic n

woman w/ pheo and picture of the layers of the adrenal gland. can someone orient me to these layers??

Thanks!
 
Also, 1 more thing. The question w/ the woman who had a Ca of 8 and a v high PTH level... the answer was primary hyperparathyroidism. This drives me crazy, because she should have secondary hyperparathyroidism! (excess PTH having no effect → Ca doesn't elevate). Primary should be high Ca, high PTH. Any thoughts??
 
A few more questions...

In the one w/ the sudden complete L eye blindness, why do the retinal ganglion cells die? What was the underlying pathology?
Central retinal artery occlusion. Hint is bright red spot at fovea (cherry red spot)

28 y/o male w/ fatigue, weakness, weight loss, 6mo of dry cough + CP, smoker. b/l hilar adenopathy + paratracheal node enlargement, noncaseating granulomas. biggest RF? i said employment (carpenter)... was the ans race? sarcoidosis?

Sarcoidosis so Race

loop diuretics → contraction alkalosis?

Yes, Via ATII

man w/ alcohol binge w/ severe abd pain. dies, autopsy shows pink picture of mesenteric adipose. what was the cause?
panc enzymes on adipose tissue
acute alc hep (no)
acute ruptured appendicitis
direct effect of EtOH on adipose
malnutrition

Pancreatic enzymes of adipose tissue. Fat necrosis

67 y/o man w/ 2 days of droopy right eyelid, double vision. eye is fixed in the out position, dilated. Cause?
-aneurysm of PCoM
-compression of sup cerv ganglion (no)
-trochlear n damage
-occlusion of scleral venus sinus
-tumor of optic n

Aneurysm of Posterior communicating artery affecting CN III

woman w/ pheo and picture of the layers of the adrenal gland. can someone orient me to these layers??

From top to bot, Capsule, Glomerulosa, Fasiculata, Reticularis, Medulla. Go for the deepest layer

http://www.histology-world.com/photomicrographs/adrenallabel.jpg


Thanks!
 
Also, 1 more thing. The question w/ the woman who had a Ca of 8 and a v high PTH level... the answer was primary hyperparathyroidism. This drives me crazy, because she should have secondary hyperparathyroidism! (excess PTH having no effect → Ca doesn't elevate). Primary should be high Ca, high PTH. Any thoughts??

Answer was osteomalacia
 
Can anyone explain the answers to these?

1) 32y M with epigastric cramping episodes that wake him up at night and is sometimes relieved by antacids. He smokes and drinks coffee regularly. He has H pylori and is given abx for that. Which of the following lifestyle changes will most likely decrease recurrence of these symptoms? Decrease smoking

I realize that "quit smoking" is generally a good answer, but I'm having a hard time seeing how that's specific to this case. Is smoking tied to recurring H pylori infections or something? Won't antibiotic treatment for H pylori fix the problem?

2) Man who has a language problem post-stroke (fluent speech but with grammatical errors, substitutions... can't repeat words or understand other verbal commands).

I know this stirred up a debate on previous pages but I wasn't sure what the consensus was. So IS this Wernicke's aphasia? It's just that in the diagram they provide it's an arrow that seems to point to angular/supramarginal gyrus?

3) 18 year old athlete with 2cm soft mounds of tissue beneath areola bilaterally. No evidence of obesity, very muscular, BMI 29. Tanner stage 5.

I gathered that the answer appears to be steroid use. But how does anabolic steroid lead to gynecomastia?

I picked "measure serum testosterone" wondering if excess testosterone was being converted peripherally to estrogen (though I guess this guy has minimal peripheral fat)... Could this happen?

Also, I got tripped up by "gynecomastia in boys" question more than once now :-/ is the bottom line that during puberty (Tanner stage 2-4; age 9-14), gynecomastia is usually normal in boys?

4) Boy with leukemia, where neoplastic cells do NOT express: CD4, CD8, surface IgM, surface IgG, cytoplasmic IgM, u-heavy chain, cytoplasmic IgG, g-heavy chain. Leukemic cells express class I MHC molecules and show rearrangement of the T-lymphocyte receptor b-chain gene D and J segments. Normal counterpart of these malignant lymphocytes?
· Activated cytolytic effector T lymphocytes in circulation
· Mature IgM-secreting B lymphocytes in the LN
· Mature Ig-secreting plasma cells in the LN
· Pre-B lymphocyte progenitor of mature B lymphocytes in the BM
· T-lymphocyte thymocytes localized to the thymic cortex

I don't even know where to begin on this one.

Thanks in advance!
 
Can anyone explain the answers to these?

1) 32y M with epigastric cramping episodes that wake him up at night and is sometimes relieved by antacids. He smokes and drinks coffee regularly. He has H pylori and is given abx for that. Which of the following lifestyle changes will most likely decrease recurrence of these symptoms? Decrease smoking

I realize that "quit smoking" is generally a good answer, but I'm having a hard time seeing how that's specific to this case. Is smoking tied to recurring H pylori infections or something? Won't antibiotic treatment for H pylori fix the problem?

2) Man who has a language problem post-stroke (fluent speech but with grammatical errors, substitutions... can't repeat words or understand other verbal commands).

I know this stirred up a debate on previous pages but I wasn't sure what the consensus was. So IS this Wernicke's aphasia? It's just that in the diagram they provide it's an arrow that seems to point to angular/supramarginal gyrus?

3) 18 year old athlete with 2cm soft mounds of tissue beneath areola bilaterally. No evidence of obesity, very muscular, BMI 29. Tanner stage 5.

I gathered that the answer appears to be steroid use. But how does anabolic steroid lead to gynecomastia?

I picked "measure serum testosterone" wondering if excess testosterone was being converted peripherally to estrogen (though I guess this guy has minimal peripheral fat)... Could this happen?

Also, I got tripped up by "gynecomastia in boys" question more than once now :-/ is the bottom line that during puberty (Tanner stage 2-4; age 9-14), gynecomastia is usually normal in boys?

4) Boy with leukemia, where neoplastic cells do NOT express: CD4, CD8, surface IgM, surface IgG, cytoplasmic IgM, u-heavy chain, cytoplasmic IgG, g-heavy chain. Leukemic cells express class I MHC molecules and show rearrangement of the T-lymphocyte receptor b-chain gene D and J segments. Normal counterpart of these malignant lymphocytes?
· Activated cytolytic effector T lymphocytes in circulation
· Mature IgM-secreting B lymphocytes in the LN
· Mature Ig-secreting plasma cells in the LN
· Pre-B lymphocyte progenitor of mature B lymphocytes in the BM
· T-lymphocyte thymocytes localized to the thymic cortex

I don't even know where to begin on this one.

Thanks in advance!

1. Asking about lifestyle change for GERD.
-Smoking is a lifestyle change adding ABs is not

2. Wernickes. I mixed up my anterior-posterior orientation and got this wrong. Just find where the somatosensory cortex is and the answer should be posterior to most inferior portion of somatosensory cortex.

3. Exogenous steroids leads to peripheral conversion to estrogen regardless of their obesity.

4. T-cell thymocytes in thymic cortex.
-The cells are T-cell in origin because they have t-cell receptors so can't be B-cells so cross out B & C & D.
-Cytotoxic T-cells are CD8+, these cells are not, cross out A.
-Answer is E because immature T-cells in thymic cortex are CD4- and CD8-. They have not undergone positive/negative selection yet to become either CD4+ or CD8+.
-Also, MHC I is expressed in all nucleated cells.
 
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Thanks!

The reason I mentioned gynecomastia in boys is because that was supposed to be "normal" in another NBME exam because apparently teenage boys commonly have gynecomastia during puberty... but anyway, can you then expand on why the answer choice "measure serum testosterone" isn't the right answer over "ask about history of anabolic steroid use"?
 
Thanks!

The reason I mentioned gynecomastia in boys is because that was supposed to be "normal" in another NBME exam because apparently teenage boys commonly have gynecomastia during puberty... but anyway, can you then expand on why the answer choice "measure serum testosterone" isn't the right answer over "ask about history of anabolic steroid use"?

Gynecomastia is definitely normal in boys as they go through puberty. I don't remember the exact question, but what led me away from thinking it was normal gynecomastia were a couple things. First, it was bilateral. The gynecomastia experienced by teenage boys is more commonly unilateral, and that's how I've seen it present in every question where "it's normal" was the answer. Second, it mentioned his muscles being incredibly developed (or something similar), pointing towards steroid usage.

I can't recall 100%, but I think he was also 18, right? That was also an indicator that he's most likely done with puberty, further decreasing the possibility that gynecomastia occurred through normal means.

As for which answer to pick, sorry I can't be of more help here. I'm pretty sure using steroids diminishes SHBG, so perhaps that would mess up the testosterone measurement? Either way, the reason I chose asking about history of steroid usage was that it seemed more appropriate to ask the patient about it rather than just order a test. But perhaps I was approaching that from too much of a behavioral science viewpoint, and there's a better explanation.
 
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All the physical descriptors of the pt (BMI 29, no body fat/all muscle) was pointing towards exogenous steroids and he admitted he was embarrassed/seeking explanation for it, which sort of gives you an opening to ask about steroid use. This didn't apply to the lady injecting insulin for some reason. Was 'confront' too much of a forward answer? I figured the multiple blood sugar checks and glucose tolerance tests were given to help us rule out insulinoma, but were you supposed to do labs in that case?
 
This didn't apply to the lady injecting insulin for some reason. Was 'confront' too much of a forward answer? I figured the multiple blood sugar checks and glucose tolerance tests were given to help us rule out insulinoma, but were you supposed to do labs in that case?

Yeah, I found "confront" came across as a bit too strong of a word in that scenario. Plus, the football player brought up his concern about the gynecomastia, so the conversation had already been initiated. But I think the main thing I liked about the C-peptide answer was that it said to determine C-peptide in the most recent blood sample taken, which seemed to indicate that the blood was already available for you to test, meaning you wouldn't have to actually perform another procedure on the patient.
 
Yeah, I found "confront" came across as a bit too strong of a word in that scenario. Plus, the football player brought up his concern about the gynecomastia, so the conversation had already been initiated. But I think the main thing I liked about the C-peptide answer was that it said to determine C-peptide in the most recent blood sample taken, which seemed to indicate that the blood was already available for you to test, meaning you wouldn't have to actually perform another procedure on the patient.
I think with the insulin question, the point is two-fold. First, if exogenous insulin is used, c-peptide is low, period, since pro-insulin cleavage generates c-peptie, and exogenous insulin is not a prodrug. Second, they have to specify exogenous insulin here, and not a sulfonylurea since that will elevate c-peptide via normal insulin release.
 
1)And plz d one with ...the effect of valporic acid on histone deacetylase( polyadenylation,translation,transcription,mRna splicing,&post translational processs)

2)what will a mass in the head of a pancreas,with extension to stomach and biliary system, affect wrt behaviuoral science (memory loss,personality change,bipolar,schizophreniform,major deprssive disorder)
3)The guanine / velocity question? not familiar with dat..
 
Combed through and don't think these have been asked.

4-47: Girl awaiting renal transplant who misses her dialysis appointments; the answers were review criteria for remaining on the list (maybe a little...aggressive...I picked this and it was wrong), more time to talk with physician (probably this?), and other things that were obviously wrong.

2-13: Man with pulsatile periumbilical mass; guarding and rigidity on abdominal exam; poorly controlled HTN; the question was what else would be associated with his presentation and the answers were ankle brachial indices w/in normal limits, aortic regurg, asymmetric radial pulses, BP readings higher in L upper extremity than right, and decreased femoral pulses

I chose the mismatched BP readings b/c I was thinking aortic dissection (he clearly has a AAA) and that's what it says in FA, but not sure.
 
Also...for the referred L shoulder pain question with the perforation of the stomach by an ulcer question, is it diaphragm? I put spleen cause I thought it usually referred to the shoulder. Does diaphragm pain also refer there? That seems like the only logical thing than can be irritated by stomach acid.

Did anyone figure this out? I'm unsure of the answer
 
7 month old girl with decreased femoral pulses and a systolic murmur in the interscalpular region and the low overall BP?. I know this was coarctation, but what was up with the murmur?
Can someone explain the coarc thing? Why wasn't it PDA?
 
Can someone explain the coarc thing? Why wasn't it PDA?
See my post in http://forums.studentdoctor.net/threads/coarc-vs-pda.1070020/

Also, the interscapular murmur in coarctation is due to the coarctation. There is possibly an eponym which I cannot remember.

Combed through and don't think these have been asked.

2-13: Man with pulsatile periumbilical mass; guarding and rigidity on abdominal exam; poorly controlled HTN; the question was what else would be associated with his presentation and the answers were ankle brachial indices w/in normal limits, aortic regurg, asymmetric radial pulses, BP readings higher in L upper extremity than right, and decreased femoral pulses
I chose the mismatched BP readings b/c I was thinking aortic dissection (he clearly has a AAA) and that's what it says in FA, but not sure.
It's actually a ruptured AAA not a dissection, hence it's a wrong mismatch, because an AAA is beyond the subclavian whereas a dissection can involve one subclavian. I haven't seen the answer choices but decreased femoral pulses would be correct out of those choices, given that blood is possibly accumulating in the abdomen.

Did anyone figure this out? I'm unsure of the answer
Diaphragmatic irritation by the stomach contents. The diaphragm is what refers to either shoulder, not the liver/gallbladder and spleen themselves.
 
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Combed through and don't think these have been asked.

4-47: Girl awaiting renal transplant who misses her dialysis appointments; the answers were review criteria for remaining on the list (maybe a little...aggressive...I picked this and it was wrong), more time to talk with physician (probably this?), and other things that were obviously wrong.

2-13: Man with pulsatile periumbilical mass; guarding and rigidity on abdominal exam; poorly controlled HTN; the question was what else would be associated with his presentation and the answers were ankle brachial indices w/in normal limits, aortic regurg, asymmetric radial pulses, BP readings higher in L upper extremity than right, and decreased femoral pulses

I chose the mismatched BP readings b/c I was thinking aortic dissection (he clearly has a AAA) and that's what it says in FA, but not sure.

4-47 was more time to talk with physician.

I've scanned all of the comments and have not noticed a few questions that I missed:

1. 75 yo lady with enlarging lesion on her face that is 1.5-cm, brown-black, mottled, scaly lesion with irregular borders. Biopsy shows atypical melanocytes spread along the basilar layer of the epidermis. Cause? Answers were: acanthosis nigricans, actinic keratosis, compound nevis, lentigo maligna, and seborrheic keratosis

2. 3yo in old house with stomach pain, normocytic hypochromic anemia, increased 5-aminolevulinic acid, and lead 50ug/dl (normal<10). What enzyme has decreased activity? Answers: ferrochelatase, porphobilinogen deaminase, protoporphyrinogen IX oxidase, uroporphyrinogen III, uroporphyrinogen decarboxylase.

Lead poisoning, right? So, ferrochelatase and ALA dehydratase should be deficient.. would ferrochelatase could a buildup of 5-aminolevulinic acid? I feel like I'm missing the obvious here.

3. 51yo man with Wegener's. Which indicates an exacerbation? Answers: glucosuria, hematuria, hypokalemia, hyponatremia, increased GFR.

Thanks!
 
4-47 was more time to talk with physician.

I've scanned all of the comments and have not noticed a few questions that I missed:

1. 75 yo lady with enlarging lesion on her face that is 1.5-cm, brown-black, mottled, scaly lesion with irregular borders. Biopsy shows atypical melanocytes spread along the basilar layer of the epidermis. Cause? Answers were: acanthosis nigricans, actinic keratosis, compound nevis, lentigo maligna, and seborrheic keratosis

This is classic melanoma. Asymmetry, borders, color, diameter, and evolution are all there in the stem. The question is just figuring out which one is melanoma: It's lentigo maligna, which if I recall correctly is melanoma that spreads at the dermal-epidermal junction. It has a great prognosis if removed early.

2. 3yo in old house with stomach pain, normocytic hypochromic anemia, increased 5-aminolevulinic acid, and lead 50ug/dl (normal<10). What enzyme has decreased activity? Answers: ferrochelatase, porphobilinogen deaminase, protoporphyrinogen IX oxidase, uroporphyrinogen III, uroporphyrinogen decarboxylase.

Lead poisoning, right? So, ferrochelatase and ALA dehydratase should be deficient.. would ferrochelatase could a buildup of 5-aminolevulinic acid? I feel like I'm missing the obvious here.

All they asked is which enzyme has decreased activity, and lead inhibits ferrochelatase. Should have been a slam dunk given your knowledge base.

3. 51yo man with Wegener's. Which indicates an exacerbation? Answers: glucosuria, hematuria, hypokalemia, hyponatremia, increased GFR.

Thanks!

I believe I said hematuria and got it right. Wegener's causes a nephritic syndrome.
 
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4-47 was more time to talk with physician.

I've scanned all of the comments and have not noticed a few questions that I missed:

1. 75 yo lady with enlarging lesion on her face that is 1.5-cm, brown-black, mottled, scaly lesion with irregular borders. Biopsy shows atypical melanocytes spread along the basilar layer of the epidermis. Cause? Answers were: acanthosis nigricans, actinic keratosis, compound nevis, lentigo maligna, and seborrheic keratosis

2. 3yo in old house with stomach pain, normocytic hypochromic anemia, increased 5-aminolevulinic acid, and lead 50ug/dl (normal<10). What enzyme has decreased activity? Answers: ferrochelatase, porphobilinogen deaminase, protoporphyrinogen IX oxidase, uroporphyrinogen III, uroporphyrinogen decarboxylase.

Lead poisoning, right? So, ferrochelatase and ALA dehydratase should be deficient.. would ferrochelatase could a buildup of 5-aminolevulinic acid? I feel like I'm missing the obvious here.

3. 51yo man with Wegener's. Which indicates an exacerbation? Answers: glucosuria, hematuria, hypokalemia, hyponatremia, increased GFR.

Thanks!

1. They left out the "melanoma" from lentigo maligna melanoma, which may have tripped some people up. It's Lentigo Maligna Melanoma here.

2. Lead poisoning. Ferrochelatase and ALA dehydratase are deficient, yes. The lack of ALA dehydratase causes a buildup of ALA. Really all there is to that one.

3. Hematuria; that signals renal involvement (rapidly proliferative glomerulonephritis. In most any disease process, renal involvement pretty much means **** just got real.
 
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I have a few questions:

- The 65 year old with the DEXA showing decreased bone density. What is the activity of the Osteoblasts, osteoclasts and RANK? I thought this was osteoperosis, but then shouldn't everything be normal? You had to either say increased or decreased activity, so I wasn't sure what to choose.

-The teenager getting a BM transplant with the cells with no CD4/8 and other markers. Is this just thymic immature T cells that don't yet express CD4/8? I misread the question, I thought it wanted to know the paired cell if it was MHC 1 positive, so I picked the CD8+ T cell.

- The woman with a lifes worth of medical problems with no confirmed diagnosis - obvious Somatiform disorder. I know the general rule on Step 1 is to never refer to another provider, but this is listed as a psychiatric illness, so shouldn't some kind of psych workup be done? I just felt like if you agree to see her monthly and address complaints that aren't real you aren't actually addressing the underlying psychiatric illness.

- The ADHD study -- what is the treatment allocation? I figured it would just be random assignment and you're either placed into the new experimental program or the old standard program.

Lastly; since this has been out for over a year now, how have people found this correlated with their actual Step 1? I just took this and didn't do as well as I would have liked -- thought it was pretty tough (like UWorld questions, but without the generous curve). I got a 254 with 17 wrong, definitely not terrible just a little lower than expectations, and much lower than the 265 I got less than a week ago ago on UWorld SA2.
 
I have a few questions:

- The 65 year old with the DEXA showing decreased bone density. What is the activity of the Osteoblasts, osteoclasts and RANK? I thought this was osteoperosis, but then shouldn't everything be normal? You had to either say increased or decreased activity, so I wasn't sure what to choose.

I'm pretty sure that there's decreased osteoblast activity. Not 100% sure about the other things. Lab values should be normal.

-The teenager getting a BM transplant with the cells with no CD4/8 and other markers. Is this just thymic immature T cells that don't yet express CD4/8? I misread the question, I thought it wanted to know the paired cell if it was MHC 1 positive, so I picked the CD8+ T cell.

Can't answer this without seeing the question.

- The woman with a lifes worth of medical problems with no confirmed diagnosis - obvious Somatiform disorder. I know the general rule on Step 1 is to never refer to another provider, but this is listed as a psychiatric illness, so shouldn't some kind of psych workup be done? I just felt like if you agree to see her monthly and address complaints that aren't real you aren't actually addressing the underlying psychiatric illness.

See her monthly - Her illness won't go away. However, somatization patients need a firm provider who is willing to see them for their complaints but also remain reasonably rigid. You don't want to make it so that she won't come back, but you also want to make sure that she's not draining your resources or anyone else's unnecessarily.

- The ADHD study -- what is the treatment allocation? I figured it would just be random assignment and you're either placed into the new experimental program or the old standard program.

They've already separated them into boys and girls, which is by definition a type of stratification, from what I understand. Awful question.

Lastly; since this has been out for over a year now, how have people found this correlated with their actual Step 1? I just took this and didn't do as well as I would have liked -- thought it was pretty tough (like UWorld questions, but without the generous curve). I got a 254 with 17 wrong, definitely not terrible just a little lower than expectations, and much lower than the 265 I got less than a week ago ago on UWorld SA2.

This is the best I can give you:

http://www.reddit.com/r/medicalschool/comments/255fp7/step_1_practice_test_correlations_update/
 
A daughter brinds her 84 yr old mom with dementia, who has lost 9 lbs in 3 months who refuses to eat but is relaxed and cooperative during examination . daughter is tearful, stressed and what interventions is most appropriate ? - get started on feeding tube ; get started on TPN ; disccus stresses of patient care with the daughter and provide info regarding assistance; reassure that weight loss isnt problem cuz she is still overweight ; reassure daughter and tell her that weight loss is common in elderly.
 
Yes, it was. This patient has dementia, and although you can admit her and give her a feeding tube, the problem isn't going to go away. The best option here is to console the distraught daughter who's taking care of her mother and give her options for assistance, since her mom's condition is only going to worsen.
 
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There was also a question about a man getting struck on the lateral side of his leg. On physical exam, he can't dorsiflex foot but inversion and eversion of foot is normal. I got the answer right because I picked the answer (deep fibular nerve is damaged) but isn't EVERSION(just like dorsiflexion) also affected in deep fibular nerve damage?
 
There was also a question about a man getting struck on the lateral side of his leg. On physical exam, he can't dorsiflex foot but inversion and eversion of foot is normal. I got the answer right because I picked the answer (deep fibular nerve is damaged) but isn't EVERSION(just like dorsiflexion) also affected in deep fibular nerve damage?

No. The common peroneal nerve innervates both motions, but once they split into deep and superficial they separate these actions. The superficial peroneal innervates the fibularis longus and brevis, which are you everters as well as dorsoflexion. The deep goes on to innervate the tibialis anterior, which is responsible for the inversion.
 
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A man on hydrochlorothiazide gets light-headed and dizzy when he stands up to quickly. Which of following sets of changes (up or down arrows) best characterizes changes in the cardiovascular system as man goes from supine to standing?
Venous Return -- up or down
Carotid Sinus Baroreceptor activity -- up or down
Cerebral blood flow -- up or down


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


Can someone please give me the right answer plus explanation?

Venous return is down. He stood up and the blood went to his feet.

Carotid sinus baroreceptor activity is down - There's less blood there, so there's less pressure. Remember that you can also stimulate baroreceptor activity by massaging (putting pressure on) the carotid.

Cerebral blood flow is down - the blood can't get back to the heart (see venous return), so the heart can't pump it through the cerebral circulation.
 
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