The Official StepI "Pimp each other" thread...

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Mike59

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Hey all,

To keep our brains well tuned for stepI in the upcoming months, who else is up for some quizzing while we're on SDN?

I'll start: (answers to follow)

1. Arthritis is characteristic of what stage of Lyme Disease?

2. Which autosomal trisomy is characterized by polydactyly, microphthalmia, umbilical hernia and cleft lip?

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MGoBlueDO said:
61 year old elderly gentleman presented to the ER with Bilateral Periorbital Hematoma. Patient was conscious and he was jumped in an alley.
Px: Normal Vital Signs, however the medical student noticed a few things on the CN exam: Pt had an absent gag reflex and loss of taste on the Posterior 1/3 of the tongue, had a hoarse voice and was drooling, the uvula was deviated to the left. and the patient also had weakness looking towards left and shrugging his shoulders. All other CN were WNL or is it GIB cause we were told that WNL means we never looked?

A.) Villaret Syndrome on the Left
B.) Vernet Syndrome on the Left
C.) Villaret Syndrome on the Right
D.) Vernet Syndrome on the Left

The answer here should actually be:

E.) I go to KCUMB and Friedlander teaches me pathology and his stuff is never on boards (trust me, I studied it).
 
Actually, this was taken from Dr. Stephens's Neuro notes not ERFs notes and BRS...they first one is Frey's Syndrome...I didn't know if there was any other name...I don't even know if they test on that esoteric stuff, I know some of those were on our exams this year and last year...
 
B. Jugular foramen syndrome on the right. This is where CN 9, 10, and 11 are closest together, and therefore most at risk for compressive symptoms.
 
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A patient is diagnosed with osteopetrosis develops ossification of the foramen ovale in his sphenoid bone. Which of the following nerve fibers will be damaged as a consequence of this stenosis?

A. GVA, GSA, SVE, GSE
B. GSA, SVE, GVE
C. SSA, GSA, GVE,
D. GSA, SVE
E. SVA, GSE, GVE, SVE
F. SVE, GVA
 
sorry to interrupt... do people actually get questions about GVA GSA SVE etc? i really see no point in these terms. i blew it off during both of my neuro sequences.
 
Standing Room Only - V1, V2, V3
So foramen ovale is V3, which does both GSA and motor (SVE?), and the front 2/3 of tongue (GVA), so answer D?
 
SVE is correct, you didn't need a question mark because V3 the mandibular portion of the trigeminal nerve is part of branchial arch 1.
 
ANSWER is B. the foramel ovale conveys the mandibular division of the trigeminal which carries GSA fiber to the anterior 2/3 of tongue and convey pain, temp, and tactile, proprioception from the mandibular dermatomal distribution. The foramen ovale also conveys the lesser petrosal nerve which is a branch of glossopharyngeal conveying the GVE preganglionic parasympathetic fibers to the otic ganglion in the infratemporal fossa and distributing from there to the parotid gland via the auriculotemporal nerve. So answer is B. GSA, SVE, and GVE.
 
doc05 said:
those are not the type of questions you'll see on step 1.
actually.... this is his question:
Mike59 said:
Which autosomal trisomy is characterized by polydactyly, microphthalmia, umbilical hernia and cleft lip?
and this is a question from Kaplan's USMLE Step 1 Practice Tests
A neonate presents with microphthalmia, cleft lip, micrognathia, polydactyly and mental ******ation. Which genetic abnormality would best explain the physical findings?

A) Cri-du-Chat syndrome
B) Klinefelter's syndrome
C) Trisomy 13
D) Trisomy 18
E) Trisomy 21
:rolleyes:
 
Just made a question, it is rather difficult though:

The parents of a 4 year-old boy are concerned about his bulging eyes and polyuria. Physical exam reveals pronounced exophthalmos and papilledema of the optic disc. He consumes three glasses of water during the exam. Urinalysis is remarkable for a urine osmolarity of 200 and low specific gravity. Imaging studies reveal several erosive bony masses, including one involving the posterior stalk of the pituitary. A biopsy of a lesion is positive for S-100 and CD1a, with cytoplasmic tennis-racket shaped (Birbeck) granules. Several months later, the lesions spontaneously regress.

This disorder was caused by a proliferation of which cell type?
A. Odontoblasts
B. Melanocytes
C. B cells
D. Osteocytes
E. Dendritic cells
F. Myeloid precursors
G. Neuroendocrine cells
H. T cells
 
s100 are neuroendocrine in origin

carrigallen said:
Just made a question, it is rather difficult though:

The parents of a 4 year-old boy are concerned about his bulging eyes and polyuria. Physical exam reveals pronounced exophthalmos and papilledema of the optic disc. He consumes three glasses of water during the exam. Urinalysis is remarkable for a urine osmolarity of 200 and low specific gravity. Imaging studies reveal several erosive bony masses, including one involving the posterior stalk of the pituitary. A biopsy of a lesion is positive for S-100 and CD1a, with cytoplasmic tennis-racket shaped (Birbeck) granules. Several months later, the lesions spontaneously regress.

This disorder was caused by a proliferation of which cell type?
A. Odontoblasts
B. Melanocytes
C. B cells
D. Osteocytes
E. Dendritic cells
F. Myeloid precursors
G. Neuroendocrine cells
H. T cells
 
caribsun said:
s100 are neuroendocrine in origin

Not necessarily. There are other cell types that are s100 as well.
Refer to First Aid, Robbins, or this abstract.

The question is still unanswered. =)
 
carrigallen said:
Just made a question, it is rather difficult though:

The parents of a 4 year-old boy are concerned about his bulging eyes and polyuria. Physical exam reveals pronounced exophthalmos and papilledema of the optic disc. He consumes three glasses of water during the exam. Urinalysis is remarkable for a urine osmolarity of 200 and low specific gravity. Imaging studies reveal several erosive bony masses, including one involving the posterior stalk of the pituitary. A biopsy of a lesion is positive for S-100 and CD1a, with cytoplasmic tennis-racket shaped (Birbeck) granules. Several months later, the lesions spontaneously regress.

This disorder was caused by a proliferation of which cell type?
A. Odontoblasts
B. Melanocytes
C. B cells
D. Osteocytes
E. Dendritic cells
F. Myeloid precursors
G. Neuroendocrine cells
H. T cells

E. Dendritic cells

Birbeck granules are the diagnostic feature equivalent to the Langerhan cell, which is an antigen-presenting cell like the dendritic cell. You can also see Birbeck granules in histiocytosis X (histiocytes are APCs).
 
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OK.....Birbeck granules means it's a form of histiocytosis X, so eosinophilic granuloma, Hand-Schuller-Christian disease and Letterer-Siwe Disease.

My guess would be Hand-Schuller-Christian disease because of the polydipsia, which would correspond with the diabetes insipidus that characterizes HSC disease. The histiocytosis syndrome is produced by proliferation of dendritic cells, which means the correct answer would be E.
 
Pox in a box said:
E. Dendritic cells

Birbeck granules are the diagnostic feature equivalent to the Langerhan cell, which is an antigen-presenting cell like the dendritic cell. You can also see Birbeck granules in histiocytosis X (histiocytes are APCs).
Dang it.....Pox posted the answer while I was typing out mine :(
 
~Congrats! I wrote an explanation too.

The correct answer is E. Multifocal unisystem Langerhans cell histiocytosis usually affects young children, who present with multiple erosive bony masses that sometimes expand into adjacent soft tissue. In about 50% of patients, involvement of the posterior pituitary stalk of the hypothalamus leads to diabetes insipidus. The combination of calvarial bone defects, diabetes insipidus, and exopththalmos is referred to as the Hand-Schuller-Christian triad. Many patients experience spontaneous regression; others can be treated successfully with chemotherapy. The tumor cells are derived from dendritic cells and express HLA-DR, S-100, and CD1a. The presence of Birbeck granules in the cytoplasm is characteristic of any of the Langerhans cell histiocytosis.

Cells of neural crest origin may stain positive for S-100 (A, B, D, E, G, H). However, only thymocytes (H) and dendritic cells (E) express CD1a, a class I MHC protein. Odontoblasts (A) may be found in a craniopharyngioma, which may also produce a posterior pituitary syndrome such as central diabetes insipidus. Although common in childhood, this disease would be unlikely to produce multiple lesions. A primary neoplasm of the pituitary (G) may produce compressive and dysfunctional symptoms, but is again unlikely to involve multiple sites. Pituitary involvement is distinctly uncommon in extranodal B or T cell lymphomas (C and H). A myeloid hyperplasia or hyperplasia (F) would be more likely to present with constitutional symptoms, such as splenomegaly or lymphadenopathy. A plasma cell myeloma (not included as an answer choice) may give rise to multiple erosive bony lesions, however it is an unlikely finding in children. Multiple osteoid neoplasms (D) may occur in the setting of Gardner syndrome, a hereditary polyposis syndrome. However, osteoid or osteosarcoid neoplasms do not contain immunological markers such as CD1a or Birbeck granules.
 
Yellowish low protein fluid is found in the lung pleura. There are occasional mesothelial cells. What's teh Dx?

a) heart failure
b) ARDS
c) adenocarcinoma
d) squamos cell carcinoma
e) sarcoidosis
 
omarsaleh66 said:
Yellowish low protein fluid is found in the lung pleura. There are occasional mesothelial cells. What's teh Dx?

a) heart failure
b) ARDS
c) adenocarcinoma
d) squamos cell carcinoma
e) sarcoidosis

Is it CHF with a pleural effusion that's leaking a transudate that's yellow? This is a good one Omar.
 
Heart failure b/c its the only transudative one and transudates have low protein (I think this is the right answer but I havn't looked over this in a while)
 
no its not heart failure. There are no RBCs in teh pleura, sorry just yellow transudate with an occasional mesothelial cell
 
omarsaleh66 said:
no its not heart failure. There are no RBCs in teh pleura, sorry just yellow transudate with an occasional mesothelial cell


Isn't that squamous cell ca with the mesothelial cells floating around (its been three years since I studied for step 1 so maybe that is a dumb answer...)
 
I'm sure you guys will nail this one:

name four big dx's with HLA-B27 associations

hint: fill in the acronym P.A.I.R.
 
omarsaleh66 said:
no its not heart failure. There are no RBCs in teh pleura, sorry just yellow transudate with an occasional mesothelial cell

I want to say it's SCC but I have no idea why I'm thinking that...it was initially my first instinct but I was thinking about the heart failure transudate and changed my mind.
 
macman said:
Isn't that squamous cell ca with the mesothelial cells floating around (its been three years since I studied for step 1 so maybe that is a dumb answer...)

hmm maybe, but thats not the answer I was trying to shoot for. my bad I should have take SCC out of the choices. the answer I was trying to get was adenocarcinoma. This cancer is usually in the periphery and is very hard to distinguish from mesothelioma once it is found in the periphery. Hence the presence of the occasional mesothelial cell. I got a question like this on my path shelf and thought it would be good for us who are prepping for step 1.


here is some more info on it for those who lust for knowledge:

Metastatic adenocarcinoma is often the major cause of malignant pleural effusions.
Distinguishing between adenocarcinoma and reactive mesothelial cells can be difficult cytologically, particularly in cases of long standing effusion where there may be some reactive mesothelial atypia.
A metastatic adenocarcinoma in a malignant effusion will often have two distinct cell populations - the adenocarcinoma cells and reactive mesothelial cells. Their proportions and architectural presentation will vary dependant on the case.

Features suggested a differential diagnosis of adenocarcinoma versus mesothelioma.

It was only through the use of immune markers on the cell block material that the lineage of the individual cell types became clear and the true nature of this malignancy identified. It should be noted that the dual cell populations identified cytologically were not observed in the surgical biopsy material. Preservation of architecture and morphological detail has been shown to be excellent in cell blocks, and this may have had some bearing on this result.

This case highlights the necessity of the preparation of cell blocks from effusion cytology specimens in cases where diagnosis is difficult.
 
macman said:
I'm sure you guys will nail this one:

name four big dx's with HLA-B27 associations

hint: fill in the acronym P.A.I.R.

Ankylosing Spondylitis
Ulcerative Colitis
Juvenile Rheumatoid Arthritis
Reiter's Syndrome
Psoriatic Arthritis
 
Pox in a box said:
Ankylosing Spondylitis
Ulcerative Colitis
Juvenile Rheumatoid Arthritis
Reiter's Syndrome
Psoriatic Arthritis


Oh yeah? get ready for the lightning round. Girl w Juvenile Rhematoid arthritis is postive for what antibody

a) Rheumatoid factor
b) ANA
c) centromere
d) topsoimerase
e) collagen
h) IgG
 
omarsaleh66 said:
Oh yeah? get ready for the lightning round. Girl w Juvenile Rhematoid arthritis is postive for what antibody

a) Rheumatoid factor
b) ANA
c) centromere
d) topsoimerase
e) collagen
h) IgG

If I recall, it's ANA for JRA but for rheumatoid arthritis, you'd pick IgG because that's what is making rheumatoid factor, which is diagnostic. In RA, you only find ANA in about 30%.
 
Pox in a box said:
You're thinking SLE based on what factor? That's she's a female?
based on i didn't read the question correctly :) thought it just said she had arthritic sx, not a dx of JRA. age (16) and sex (f) led me to jump the gun to SLE. still would have gotten the answer right though. haha.
 
Pox in a box said:
If I recall, it's ANA for JRA but for rheumatoid arthritis, you'd pick IgG because that's what is making rheumatoid factor, which is diagnostic. In RA, you only find ANA in about 30%.

for RA, you'd pick RF (assuming that it's not a 16 y/o girls also).
 
Pox in a box said:
Ankylosing Spondylitis
Ulcerative Colitis
Juvenile Rheumatoid Arthritis
Reiter's Syndrome
Psoriatic Arthritis


yes-good stuff: here's the acronym (which you more than fulfilled)

P- Psoriatic Arthritis
A- Ankylosing Spondylitis
I- Inflam Bowel ds. (i.e. UC)
R- Reiter's

Thanks and nice job.
 
Name the best physical exam sign for increased intracranial pressure (acutely)

(probably more for rotations than step 1-but take a crack at it)
 
macman said:
Name the best physical exam sign for increased intracranial pressure (acutely)

(probably more for rotations than step 1-but take a crack at it)

Note subtle changes in consciousness and if the patient reports a headache.
 
Pox in a box said:
Note subtle changes in consciousness and if the patient reports a headache.



1. "Note subtle changes in consciousness": way too non-specific, could be many things

2. "...if the patient reports a headache": symptom, not a sign, and see #1


Lets narrow it down, pt. had a SDH, is non-responsive, CT unit is 4 hours backlogged, other trauma present, intubated already, O2 sats dropping, you have your 'doctor' bag, time to figure out whether you rec. to neurosurg if you feel increased ICP is the primary problem.

what can you look for on PE???--for acute changes
 
macman said:
1. "Note subtle changes in consciousness": way too non-specific, could be many things

2. "...if the patient reports a headache": symptom, not a sign, and see #1


Lets narrow it down, pt. had a SDH, is non-responsive, CT unit is 4 hours backlogged, other trauma present, intubated already, O2 sats dropping, you have your 'doctor' bag, time to figure out whether you rec. to neurosurg if you feel increased ICP is the primary problem.

what can you look for on PE???--for acute changes

Watch the patient projectile vomit into a cup? Look for papilledema through an ophthalmoscope? Lumbar puncture? If the guy's crashing I might be concerned with the ABC's and worry about the ICP increase later.
 
Pox in a box said:
Watch the patient projectile vomit into a cup? Look for papilledema through an ophthalmoscope? Lumbar puncture? If the guy's crashing I might be concerned with the ABC's and worry about the ICP increase later.


papilledema is close, not good acutely, I think you are starting to avoid the original question :)

think physical exam
 
hydrocephalus will be mostly neuro signs..unless you intend a communicating hydrocephalus.
-Papilledema, lid lag
-Bulging Fontanelles if infant
-Proptosis/Exopthalmos (less so for acute though)
-Look for leaking CSF and Battle sign (if trauma)
-Kernig's sign
 
is "ask the patient if he has hydrocephalus" one of the options? if not i'm screwed.
 
macman said:
papilledema is close, not good acutely, I think you are starting to avoid the original question :)

think physical exam

Buddy, is your medical school teaching you some kind of physical exam that nobody else knows regarding increased cranial pressure? I don't have a doctor's bag but if I did it would contain a stethoscope, a penlight, and an ophtalmoscope at best. Now tell me you can do your "physical exam" with these objects...
 
here is one

Your hungry vegetarian friend goes to a chinese restaurant and loads up on lots of TOFU (almost all protein intake). 30 minutes later, he finds you in the corner of the library reviewing your physiology. He doesn't think you know your phys very well, so he proceeds to ask you the following after telling you what he had for lunch: "Which of the following best represents my insulin and glucagon levels in the serum right now"?

A. decrease insulin, increase glucagon
b. increase insulin, decrease glucagon
c. decrease insulin, decrease glucagon
d. increase insulin, increase glucagon
 
HiddenTruth said:
here is one

Your hungry vegetarian friend goes to a chinese restaurant and loads up on lots of TOFU (almost all protein intake). 30 minutes later, he finds you in the corner of the library reviewing your physiology. He doesn't think you know your phys very well, so he proceeds to ask you the following after telling you what he had for lunch: "Which of the following best represents my insulin and glucagon levels in the serum right now"?

A. decrease insulin, increase glucagon
b. increase insulin, decrease glucagon
c. decrease insulin, decrease glucagon
d. increase insulin, increase glucagon

Glucagon increases (gotta convert all that extra protein to sugar!)
So its either A or D.
Glucagon helps control insulin... there is no real trigger for insulin (not with the makeup of soy protein)... gotta go A.
 
Pox in a box said:
Buddy, is your medical school teaching you some kind of physical exam that nobody else knows regarding increased cranial pressure? I don't have a doctor's bag but if I did it would contain a stethoscope, a penlight, and an ophtalmoscope at best. Now tell me you can do your "physical exam" with these objects...


this was not a good question for this thread in retrospect-but you'll look like a stud on a neuro rotation if you know this

most specific sign on exam for increased ICP: lack of venous pulsations on fundoscopic exam. I learned this on my MGH neuro rotation.

sorry for the wacky question
 
Janders said:
Glucagon increases (gotta convert all that extra protein to sugar!)

Yea, and how are you going to take up that sugar you just made? Thus, BOTH insulin and glucagon go up.

However, if it was all carbs, only insulin would go up 30 mins later.
 
macman said:
this was not a good question for this thread in retrospect-but you'll look like a stud on a neuro rotation if you know this

most specific sign on exam for increased ICP: lack of venous pulsations on fundoscopic exam. I learned this on my MGH neuro rotation.

sorry for the wacky question

How do you see venous pulsations in the eye?
 
HiddenTruth said:
Yea, and how are you going to take up that sugar you just made? Thus, BOTH insulin and glucagon go up.

However, if it was all carbs, only insulin would go up 30 mins later.

Perhaps I was thinking through this too much. I was a bit to focused on Soy Protein's role as a insulin-leveler, due to its near-zero carb content, low GI value, and isoflavones (which reduce fat uptake of nutrients). Though it is high in arginine, usually, which can produce an insulin spike.

I'm still really not sure what a moderate amount of soy protein would do to an individual's insulin.

However, the take home point of a "high-protein" meal triggering both insulin and glucagon is a good one!
 
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