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This thread is lovely, thank you.

I have a few more questions.

The CREST syndrome question involving esophageal motility. Was the answer decreased LES and peristalsis? I was thinking CREST and achalasia were friends so I had the LES tone arrow up.

They are friends in the sense that you lose esophageal peristalsis in both, but CREST leads to lower sphincter tone (-> GERD) and achalasia leads to higher sphincter tone (-> bird beak)

Can anyone further explain why the answer to this was "homing": The question about mice melanoma that spreads everywhere, until you inject an antibody in the liver that protects the liver from the mets. I went with invasion. Fail.

Invasion = invasion through basement membrane. The antibody selectively prevents targeting to the liver (i.e. homing)

There was the young girl who clearly had albinism-like characteristics, neutropenia, but recurrent bacterial infections. I went with decreased NADPH oxidase but that was incorrect. I must be missing some association on this one...

Don't remember the question exactly, but sounds like Chediak-Higashi to me

Kid with either Becker/Duchenne had weak adduction, and weakness of an additional muscle that attaches where? Answer was previously listed as ischium. But I am terrible at anatomy from having a hardcore orthopod prodigy attack my cadaver (and not paying attention, clearly). Which muscle are they talking about? Thanks. I am terrible at anatomy.

I believe it's gluteus maximus

Gentamicin/aminoglycoside toxicity at the tubules. I went with collecting tubule. Was proximal correct?

In general, nephrotoxins target the PCT selectively in ATN

Doctor was trying to give a drug for cough suppression that would not cause constipation or addiction. I ended up going with tramodol because all of the others seemed addicting. Anyone know the correct answer for this one?

Dextromethorphan

Trucker sitting in car for 10 hours goes through with a V/Q scan. I am assuming he had a PE. I went with Decreased ventilation with normal perfusion. This was wrong.

Embolus blocks pulmonary artery -> decreased perfusion of that portion of the lung.. ventilation is intact

Any help would be great. I apologize for not posting the answer choices. UWorld has me conditioned not to try and print screen or copy anything.

Also, has anyone that has taken Step 1 have any advice on the most predictive test? I was scoring 240s on UWorld Assessments, the 150Q free practice test, and DIT's end of course exam. But my NBME scores these last couple days have been 230ish. Not a good sign close to exam day.

Thanks and good luck to all.
.
 
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Thank you! Just read the wiki for Dextro. I was thrown off because people use it recreationally but I see the research note at the bottom about its use as a codeine sub that is not addicting.
 
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Can anybody please help me with this question>> is it B??

a 23 y/o F come to the physican b/c of a 3wk hx of persistent cough that is worsened by the cold air in her drafty apt. She does not smoke, drink or use no medications, and has no history of asthma or chronic pulmonary disease. P/E shows no abnormalties. Short term cough suppressant tx is initiated with a drug that does not cause constipation and has a low potential for substance abuse. This dryg is most likely which of the following
A. Codeine
B.Dextromethorphan
c.hydromorphone ( wrong)
d. oxycodone
e. tramadol
 
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spyderracing32

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This thread is lovely, thank you.

I have a few more questions.

The CREST syndrome question involving esophageal motility. Was the answer decreased LES and peristalsis? I was thinking CREST and achalasia were friends so I had the LES tone arrow up.

Can anyone further explain why the answer to this was "homing": The question about mice melanoma that spreads everywhere, until you inject an antibody in the liver that protects the liver from the mets. I went with invasion. Fail.

There was the young girl who clearly had albinism-like characteristics, neutropenia, but recurrent bacterial infections. I went with decreased NADPH oxidase but that was incorrect. I must be missing some association on this one...

Kid with either Becker/Duchenne had weak adduction, and weakness of an additional muscle that attaches where? Answer was previously listed as ischium. But I am terrible at anatomy from having a hardcore orthopod prodigy attack my cadaver (and not paying attention, clearly). Which muscle are they talking about? Thanks. I am terrible at anatomy.

Gentamicin/aminoglycoside toxicity at the tubules. I went with collecting tubule. Was proximal correct?

Doctor was trying to give a drug for cough suppression that would not cause constipation or addiction. I ended up going with tramodol because all of the others seemed addicting. Anyone know the correct answer for this one?

Trucker sitting in car for 10 hours goes through with a V/Q scan. I am assuming he had a PE. I went with Decreased ventilation with normal perfusion. This was wrong.

Any help would be great. I apologize for not posting the answer choices. UWorld has me conditioned not to try and print screen or copy anything.

Also, has anyone that has taken Step 1 have any advice on the most predictive test? I was scoring 240s on UWorld Assessments, the 150Q free practice test, and DIT's end of course exam. But my NBME scores these last couple days have been 230ish. Not a good sign close to exam day.

Thanks and good luck to all.
CREST syndrome (and systemic sclerosis) both cause decreased lower esophageal sphincter tone. Thus you get GERD with these (which you wouldn't get with something that increased lower esophageal sphincter tone).

Regarding the homing question, my reasoning was that if it were preventing invasion, it would not affect solely the ability of neoplastic cells to invade the liver, but would presumably affect their ability to invade all over. I'm not sure if this is the correct reasoning because I've never read about it anywhere, but it made and still makes sense to me.

Girl w/ albinism and neutropenia is Chediak-Higashi. I think they also mentioned giant lysosomes or something to that effect. These are dead giveaways.

The anatomy one... no idea.

The aminoglycosides (and any other renal tubule toxicities) affect the proximal tubule to the greatest degree. The proximal tubule is the most metabolically active and is thus most susceptible to toxic insult.

I believe the anti-tussive you were looking for was dextromethorphan. Tramadol is a pretty classic opiate with all of the trimmings that go with it (abuse, dependence, etc.). You probably got tripped up because DXM has been in the media recently because kids are abusing it for a "legal" high, but I don't believe that it's habit forming (if I recall correctly it has a dissociative effect a la Ketamine or PCP which as far as I know do not result in dependence either).

For the trucker, you're going to see decreased perfusion. Ventilation (V) is how well you are able to blow off CO2 from within your alveoli. This is dependent on patent AIRWAYS. A pulmonary embolism blocks off perfusion (Q) of your pulmonary VASCULATURE. So you get a V/Q mismatch that approaches infinity because Q is ~0 (assuming you have a very large embolus that is totally occluding flow).

Regarding your scores, I've read pretty consistently that the UWSA overpredicts your score a little and that the free 150 are really easy (haven't taken them myself). So based on that, it seems your NBMEs are probably right about where they should be. I'd assume that 12 and 13 being the most recent are the most reflective of the actual exam and probably the most predictive, but I'm taking the real thing Friday, so really I'm just speculating.
 

ykmedicine

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Hey everyone,
I have a couple of questions that I need to verify answers for:

1. A 60yr old man who has weakness/light-headedness. His diet= fruits, veggies, whole grains, lean chicken and fish. 10 yr history of Hashimoto thyroiditis treated w/ thyroxine. He has pallow, increased methylmalonic acid and total homocysteine. He has megaloblastic anemia. What is the cause?

cystathion beta-synthasse deficiency (nope)
failure of IF production
Folic acid deficiency
Helicobacter pylor gastritis
Methylmalonyl-Coa Mutase deficiency (im guessing this is the answer?)

2. 10 yr old boy with type 1 diabetes is receiving insulin. One hour after his morning dose he becomes tremulous and diaphoretic and has tachycardia. Several hours later his symptoms resolve. What is the cause of the patients hyperglycemia?

activation of hepatic adenylyl cyclase (is this the answer?)
activation of muscle glycogen synthase
activation of muscle phosphorylase (why couldnt this be the answer?)
activation of muscle protein phosphatase (nope)
inhibition of hepatic protein kinase A

3. 15 yr old boy brought due to behavioral changes. Hes failing school. Pulse 110, rr 24/min, bp: 140/85. Pupillary dilation and diaphoresis. His affect is agitated and his thought process is confused. What is he intoxicated with?

Alcohol
amphetamine
amyl nitrate (is this it? Is he huffing glue?)
cannabis (nope)
heroine

4. Leading cause of death in women--> is it cardiovascular disease? I feel like I had a complete brain fart on this one.

Thanks in advance. :)
 
Feb 21, 2012
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Hey everyone,
I have a couple of questions that I need to verify answers for:

1. A 60yr old man who has weakness/light-headedness. His diet= fruits, veggies, whole grains, lean chicken and fish. 10 yr history of Hashimoto thyroiditis treated w/ thyroxine. He has pallow, increased methylmalonic acid and total homocysteine. He has megaloblastic anemia. What is the cause?

cystathion beta-synthasse deficiency (nope)
failure of IF production
Folic acid deficiency
Helicobacter pylor gastritis
Methylmalonyl-Coa Mutase deficiency (im guessing this is the answer?)

2. 10 yr old boy with type 1 diabetes is receiving insulin. One hour after his morning dose he becomes tremulous and diaphoretic and has tachycardia. Several hours later his symptoms resolve. What is the cause of the patients hyperglycemia?

activation of hepatic adenylyl cyclase (is this the answer?)
activation of muscle glycogen synthase
activation of muscle phosphorylase (why couldnt this be the answer?)
activation of muscle protein phosphatase (nope)
inhibition of hepatic protein kinase A

3. 15 yr old boy brought due to behavioral changes. Hes failing school. Pulse 110, rr 24/min, bp: 140/85. Pupillary dilation and diaphoresis. His affect is agitated and his thought process is confused. What is he intoxicated with?

Alcohol
amphetamine
amyl nitrate (is this it? Is he huffing glue?)
cannabis (nope)
heroine

4. Leading cause of death in women--> is it cardiovascular disease? I feel like I had a complete brain fart on this one.

Thanks in advance. :)
1: Intrinsic factor
2: A
3: Amphetamine ( his symptoms )
4: yes cardiovascular disease
 

ykmedicine

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thanks! For the first question, are we supposed to make the connection that since he has thyroiditis he is likely to have another autoimmune deficiency (i.e. pernicious anemia), or is there something that I am missing here?
 
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Dr McSexy

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thanks! For the first question, are we supposed to make the connection that since he has thyroiditis he is likely to have another autoimmune deficiency (i.e. pernicious anemia), or is there something that I am missing here?
Hashimoto's and pernicious anemia are both associated w/ the HLA DR5 subtype.
 
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lrkoehle

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I read the first few pages and found answers to most of my incorrects, but there were a couple I didn't see asked:

Section 4 #3
otherwise healthy 23 y/o female w/no menstrual period for 2 months. Regular 28 day cycle up to now. Pelvic exam shows blue-tinged vaginal mucosa. Uterus is somewhat soft in lower segment & about the size of an organge. Adnexa nontender; normal sized-ovaries. What is the most appropriate next step in diagnosis?
A) measure serum FSH
B) measure serum TSH
C) measure urine Beta-hCG
D) utrasound of pelvis
E) Enodmetrial biopsy

Not sure what I was missing on this one, but "blue-tinged vaginal mucosa" doesn't stick out to me as an indicator of anything...

Section 4 #18
40 y/o male brought to ED post-MVA. DOA. Hx of fever, headache, chills, and pain in RUQ 5 days ago. Histologic exam shows liver section w/disruption of normal hepatic lobule. Small shrunken hepatocytes w/intense eosinophilic cytoplasm, fragmented nuclear chromatin, & cytoplasmic bleb formations are noted. Which process is most likely occurring in the hepatocytes described?
A) apoptosis
B) Atrophy
C) Caseous necrosis
D) Coagulation necrosis
E) Dysplasia
F) Fatty change
G) Hetrophagy
H)Liquefaction necrosis
I) metaplasia

Again, not sure what I am not seeing on this, but I should Coag necrosis for sure. Apparently not...

Thanks in advance for the help. I got wrecked on the first part of the fourth section of this NBME...I missed 6 of the first 21 (almost half of my incorrects for the whole damn thing :mad:).
 

EaglesAllDay

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First one is beta hcg...blue tinged vagina is a sign of pregnancy

and the second one is apoptosis, classic features.
 
Jul 6, 2011
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I read the first few pages and found answers to most of my incorrects, but there were a couple I didn't see asked:

Section 4 #3
otherwise healthy 23 y/o female w/no menstrual period for 2 months. Regular 28 day cycle up to now. Pelvic exam shows blue-tinged vaginal mucosa. Uterus is somewhat soft in lower segment & about the size of an organge. Adnexa nontender; normal sized-ovaries. What is the most appropriate next step in diagnosis?
A) measure serum FSH
B) measure serum TSH
C) measure urine Beta-hCG
D) utrasound of pelvis
E) Enodmetrial biopsy

Not sure what I was missing on this one, but "blue-tinged vaginal mucosa" doesn't stick out to me as an indicator of anything...

I think this was mentioned on another page, but blue-tinged vagina = pregnant (google it for confirmation--you'll see lots of online pregnancy forums where people are complaining of the blue tinge to their vaginal mucosae haha). I've never heard of it before NBME 13 though.

Section 4 #18
40 y/o male brought to ED post-MVA. DOA. Hx of fever, headache, chills, and pain in RUQ 5 days ago. Histologic exam shows liver section w/disruption of normal hepatic lobule. Small shrunken hepatocytes w/intense eosinophilic cytoplasm, fragmented nuclear chromatin, & cytoplasmic bleb formations are noted. Which process is most likely occurring in the hepatocytes described?
A) apoptosis
B) Atrophy
C) Caseous necrosis
D) Coagulation necrosis
E) Dysplasia
F) Fatty change
G) Hetrophagy
H)Liquefaction necrosis
I) metaplasia

Again, not sure what I am not seeing on this, but I should Coag necrosis for sure. Apparently not...

the "intensely eosinophilic cytoplasm," "fragmented chromatin," and "blebs" are markers of apoptosis (Pathology chapter in FA). If you didn't know that I suppose you could also assume he's suffering from viral hepatitis, in which the hepatocyte damage is due to CD8+ cells --> apoptosis

Thanks in advance for the help. I got wrecked on the first part of the fourth section of this NBME...I missed 6 of the first 21 (almost half of my incorrects for the whole damn thing :mad:).
.
 
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lrkoehle

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First one is beta hcg...blue tinged vagina is a sign of pregnancy

and the second one is apoptosis, classic features.
Thanks guys. Not sure how I missed that apoptosis one. I just managed to convince myself that it had to have been from the car accident, which is of course stupid, since the pain started 5 days prior...oh well, like I said, my brain was not working on the first part of that 4th section.

I'm glad to know about the blue vagina thing...I actually chose check the beta-hcg answer initially, but talked myself out of it and decided that we should biopsy her...
 

spyderracing32

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First one is beta hcg...blue tinged vagina is a sign of pregnancy

and the second one is apoptosis, classic features.
You guys are totally whiffing on the concept with the blue vagina here; it really doesn't matter. The point is that the first step in the work-up of someone of reproductive age with amenorrhea is ALWAYS a pregnancy test (bHCG).
 

lrkoehle

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You guys are totally whiffing on the concept with the blue vagina here; it really doesn't matter. The point is that the first step in the work-up of someone of reproductive age with amenorrhea is ALWAYS a pregnancy test (bHCG).
That was my original reasoning for originally choosing pregnancy test, which I unfortunately talked myself out of...
 

spyderracing32

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THATS the connection I was missing! Thank you!
Could also go based on the fact that he has a megaloblastic anemia (B12 def), increased homocysteine (B12 def => non-functioning homocysteine methyltransferase), and elevated methylmalonic acid (B12 required for methylmalonyl-CoA mutase to function). Pernicious anemia was the only thing listed that caused a B12 def and fit all of those.

Cystathionine beta-synthase def fits the elevated homocysteine and nothing else.
Folate def fits the megaloblastic anemia and nothing else.
Methylmalonyl-CoA mutase def fits the elevated methylmalonate and nothing else.
B12 ties all three together. (Good to know the Hasimoto/Pernicious Anemia DR5 connection in addition too though.)
 
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spyderracing32

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That was my original reasoning for originally choosing pregnancy test, which I unfortunately talked myself out of...
Well, now you won't forget it! I'll bet you'll probably get a question on it too since it really is a basic tenet of forming a DDx, and you may or may not get a blue vagina associated with it, so better to know the concept!
 

bomgd3

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Can anyone else NOT tell which line is the central sulcus for #31 in section 4?
 

plee87

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question..

most appropriate pharmacotherapy for patient's infertility?
a. bromocriptine
b. clomiphene
c. DES
d. ethinyl estradiol
e. medroxyprogesterone
 

lrkoehle

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Can anyone else NOT tell which line is the central sulcus for #31 in section 4?
It's not perfect, but I was able to differentiate it.

question..

most appropriate pharmacotherapy for patient's infertility?
a. bromocriptine
b. clomiphene
c. DES
d. ethinyl estradiol
e. medroxyprogesterone
B. I think D & E would be found in OCP's, which is the opposite of what the patient wants. DES causes clear cell vag CA, so not good. DES was used to prevent spontaneous abortion originally, I believe. Bromocriptine is a ergot-alkaloid DA agonist used in Parkinson's (non-ergot alkaloid DA agonists like ropinorole & pramipexole are more commonly used now due to less side effects).
 
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batch5000

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Tobacco use definitely raises the rate of gastric adenocarcinoma. Cancer.org says: "Smoking increases stomach cancer risk, particularly for cancers of the upper portion of the stomach closest to the esophagus. The rate of stomach cancer is about doubled in smokers."

They don't put a % increase in cancer risk with nitrosamines. I guess it has to be more than doubled since the NBME says that "diet" is the correct answer but I haven't seen a source giving a definitive number. From the searches I've done it sounds like the dietary link to gastric adenocarcinoma is weaker than the smoking link. Wonder what's up with that?
I wouldn't exactly call Cancer.org an unbiased source. They will stop at nothing to blame tobacco for all sorts of cancer, despite the fact that people smoked tobacco for hundreds of years with no problems! Japanese people all smoke anyway and you don't exactly see a longevity problem there. Lay off of the smoked fish and you will be fine. In the mean time, I might enjoy myself an nice bedtime pipe of tobacco to help take the edge off. Cheers.
 

ijn

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Are you seriously defending smoking? And you're going to be a doctor. :(

Here's what UpToDate, another source of anti-smoking propaganda, says:

Smoking — Several studies have examined the relationship between tobacco smoking and gastric cancer. A meta-analysis of 40 studies estimated that the risk was increased by approximately 1.5 to 1.60-fold and was higher in men [34]. A subsequent prospective study from Europe found a similar magnitude of risk, which diminished after 10 years of smoking cessation [35]. Approximately 18 percent of gastric cancer cases were attributed to smoking. Another prospective study [36] found that, compared with nonsmokers, current smokers were at increased risk for cancer at gastric cardia (HR 2.9, 95% CI 1.7, 4.7), and gastric noncardia (HR 2.0, 95% CI 1.3, 3.2)
 
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batch5000

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Are you seriously defending smoking? And you're going to be a doctor. :(

Here's what UpToDate, another source of anti-smoking propaganda, says:
Wow. You sure are brainwashed. I bet you believe that vaccines cured Polio too? Even though it was clearly just renamed ALS. :sleep:
 
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1-38 y old woman 32 week gestation having fever nausea vomiting muscle ache fever 39c RR20 pulse 120 gram stain shown on a picture ?

a coryn urealyticum
b gardenella
c listeria mono
d rodococus equi
e staph

2- the woman with Rheumatoid Arthritis what pathological process affects her joint??

a bacterial necrosis
b caseous
c crystal formation
d necrotising vasculitis (wrong)
e pannus formation

3- female with progressive shortness of breath for 1 month pco2 70 po2 60 ph 7.33 decrease reduced
TV VC ERV and normal RV ?? is it maysthenia gravis??
 

frankyazz

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1-38 y old woman 32 week gestation having fever nausea vomiting muscle ache fever 39c RR20 pulse 120 gram stain shown on a picture ?

a coryn urealyticum
b gardenella
c listeria mono
d rodococus equi
e staph

2- the woman with Rheumatoid Arthritis what pathological process affects her joint??

a bacterial necrosis
b caseous
c crystal formation
d necrotising vasculitis (wrong)
e pannus formation

3- female with progressive shortness of breath for 1 month pco2 70 po2 60 ph 7.33 decrease reduced
TV VC ERV and normal RV ?? is it maysthenia gravis??
C
E
If I remember that question correctly it was mysthenia gravis. Acidosis with low A-a gradient, so something that affects respiratory center or diaphragm directly
 
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60 year old man with blisters and IGG in keratinocytes ??? is it anti desmosomes??

HIV positive with productive cough and they show a picture stain with silver has non productive cough?? it is not coccidiodes immitis

thaks guys
 
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C
E
If I remember that question correctly it was mysthenia gravis. Acidosis with low A-a gradient, so something that affects respiratory center or diaphragm directly
thanks but isn't listeria gram positive and infect through the GI???
 

hoodfigga1

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60 year old man with blisters and IGG in keratinocytes ??? is it anti desmosomes??

HIV positive with productive cough and they show a picture stain with silver has non productive cough?? it is not coccidiodes immitis

thaks guys
u have to be mroe specific for the first one, i believe both types of blistering diseases were on this test. the one that had blisters in the mouth was anti-desmosomes...

the hiv pneumonia with the picture was def PCP...ground glass, diffuse infiltrate, silver stain, etc...
 
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Hokay, here goes! Most of my questions have been answered, but I have a few lingering ones that I feel most people got automatically (so this shouldn't be too hard for you all!):

44) Young infertile couple. Girl's okay. Boy's got some issues. Sperm analysis shows low fructose (5% of nl). What's wrong with him?
a) adenohypophysis
b) bulbourethral glands
c) prostate (nope)
d) seminal vesicles
e) testes

F/u on the listeria question - I thought that listeria was an intracellular bug? I distinctly remember something called "actin rockets" from micro. That's why I went away from listeria -- the bug seemed to be extracellular in the pic. HALP!

F/u on the question re: the 2 mo old boy dying of meningitis despite antibiotics. Culture grows Mycobacterium tuberculosis. Two of his bros died of atypical mycobacterial infections. What's the immundef?
a) complement (nope, not listera... although they didn't mention MAC def... so perhaps?)
b) IFN-gamma receptor deficiency (yes? because it's M. tb, and that's a granulomatous response?)
c) leukocyte adhesion deficiency (nope; nothing about a stump)
d) x-linked agammaglobulinemia (I picked this one because they were all boys, and I link bacteria with humoral immunity. Why is this wrong?)



Also, if it makes people feel better: this exam sucked for me too, but I realized that it was more the curve than anything else. %age wise, I've been doing better, but the curve is what killed me. Stuff like that is out of my control, so best to just do the best YOU can and let the fates decide your score (literally!). Step 1 is just ONE of the things that go into residency apps, and there are plenty of places to shine that have little to do with curves. These are things I tell myself after I spend the whole day crying!!
 
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blah354

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Hokay, here goes! Most of my questions have been answered, but I have a few lingering ones that I feel most people got automatically (so this shouldn't be too hard for you all!):

44) Young infertile couple. Girl's okay. Boy's got some issues. Sperm analysis shows low fructose (5% of nl). What's wrong with him?
a) adenohypophysis
b) bulbourethral glands
c) prostate (nope)
d) seminal vesicles
e) testes

F/u on the listeria question - I thought that listeria was an intracellular bug? I distinctly remember something called "actin rockets" from micro. That's why I went away from listeria -- the bug seemed to be extracellular in the pic. HALP!

F/u on the question re: the 2 mo old boy dying of meningitis despite antibiotics. Culture grows Mycobacterium tuberculosis. Two of his bros died of atypical mycobacterial infections. What's the immundef?
a) complement (nope, not listera... although they didn't mention MAC def... so perhaps?)
b) IFN-gamma receptor deficiency (yes? because it's M. tb, and that's a granulomatous response?)
c) leukocyte adhesion deficiency (nope; nothing about a stump)
d) x-linked agammaglobulinemia (I picked this one because they were all boys, and I link bacteria with humoral immunity. Why is this wrong?)



Also, if it makes people feel better: this exam sucked for me too, but I realized that it was more the curve than anything else. %age wise, I've been doing better, but the curve is what killed me. Stuff like that is out of my control, so best to just do the best YOU can and let the fates decide your score (literally!). Step 1 is just ONE of the things that go into residency apps, and there are plenty of places to shine that have little to do with curves. These are things I tell myself after I spend the whole day crying!!
Hey ButterISMagical,
I believe the answer to the fructose/sperm question is seminal vesicles.
And the Listeria question, my reasoning was that the gram stain was dark (gram +) and Listeria affects pregnant people, babies, and old people.
And yes, I believe it's IFN gamma def (IFN gamma is impt for fighting M. tuberculosis)
Hope this helps!
 

FF430

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3-7) A 77-year-old woman dies in the hospital after a long illness. Her vertebral column, obtained at autopsy, is shown in the photograph. The process shown is most likely associated with an increase in which of the following?

A) Calcium
B) Estrogen
C) Interleukin-1 (IL-1)
D) Monoclonal immunoglobulin (INCORRECT)
E) Vitamin D

I thought it looked like MM b/c they say "in hospital with long illness" but can someone give a explanation as to what is going on with that picture...looked like a vertebral crush injury or something since the 2nd block of bone was squished.

3-49) A 48-y/o women comes to ED b/c of a 3-hr history of nausea and acute, sharp, right-sided lower abdominal pain that radiates to her back. She says the pain started 30 mins into her aerobics class and has increased in severity since then. PE shows enlarged right ovary. negative pregnancy test. Ultrasound confirms enlarged ovary, doppler ultrasound shows decreased flow. Which of the following structures is most likely affected in this patient?

a. mesometrium
b. oviduct
c. round ligament of the uterus (wrong)
d. suspensory ligament (right?)
e. transverse cervical ligament

Thank guys.
 

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thanks! For the first question, are we supposed to make the connection that since he has thyroiditis he is likely to have another autoimmune deficiency (i.e. pernicious anemia), or is there something that I am missing here?
B12 is the only thing that would explain both inc homocysteine & inc methyl malonic acid. no connection necessary
 

iCY

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3-7) A 77-year-old woman dies in the hospital after a long illness. Her vertebral column, obtained at autopsy, is shown in the photograph. The process shown is most likely associated with an increase in which of the following?

A) Calcium
B) Estrogen
C) Interleukin-1 (IL-1)
D) Monoclonal immunoglobulin (INCORRECT)
E) Vitamin D

I thought it looked like MM b/c they say "in hospital with long illness" but can someone give a explanation as to what is going on with that picture...looked like a vertebral crush injury or something since the 2nd block of bone was squished.

3-49) A 48-y/o women comes to ED b/c of a 3-hr history of nausea and acute, sharp, right-sided lower abdominal pain that radiates to her back. She says the pain started 30 mins into her aerobics class and has increased in severity since then. PE shows enlarged right ovary. negative pregnancy test. Ultrasound confirms enlarged ovary, doppler ultrasound shows decreased flow. Which of the following structures is most likely affected in this patient?

a. mesometrium
b. oviduct
c. round ligament of the uterus (wrong)
d. suspensory ligament (right?)
e. transverse cervical ligament

Thank guys.
i haven't seen the picture for the 1st one but i'm gonna assume she has osteoporosis. in which case IL-1 is also called osteoclast activating factor --> it activates osteoclasts leading to bone resportion & subsequent collapse of vertebra.

2nd one i would guess suspensory ligament of ovary b/c it contains the ovarian vessels...
 

iCY

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F/u on the listeria question - I thought that listeria was an intracellular bug? I distinctly remember something called "actin rockets" from micro. That's why I went away from listeria -- the bug seemed to be extracellular in the pic. HALP!
listeria = FACULTATIVE intracellular. it can survive both inside & outside
inside the cell = uses actin rockets
outside the cell = tumbling motility
 
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FF430

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Apr 20, 2008
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3-7) A 77-year-old woman dies in the hospital after a long illness. Her vertebral column, obtained at autopsy, is shown in the photograph. The process shown is most likely associated with an increase in which of the following?

A) Calcium
B) Estrogen
C) Interleukin-1 (IL-1)
D) Monoclonal immunoglobulin (INCORRECT)
E) Vitamin D

I thought it looked like MM b/c they say "in hospital with long illness" but can someone give a explanation as to what is going on with that picture...looked like a vertebral crush injury or something since the 2nd block of bone was squished.

3-49) A 48-y/o women comes to ED b/c of a 3-hr history of nausea and acute, sharp, right-sided lower abdominal pain that radiates to her back. She says the pain started 30 mins into her aerobics class and has increased in severity since then. PE shows enlarged right ovary. negative pregnancy test. Ultrasound confirms enlarged ovary, doppler ultrasound shows decreased flow. Which of the following structures is most likely affected in this patient?

a. mesometrium
b. oviduct
c. round ligament of the uterus (wrong)
d. suspensory ligament (right?)
e. transverse cervical ligament

Thank guys.
attached photograph.
 

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FF430

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sweet pics, thanks...do you know the mechanism behind IL-1 activation? Normally osteoblast activate osteoclast via RANK and MCSF in response to PTH. thanks.
 

Houmd

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Just wanted to say thanks to everyone on here, this is a quality thread and helped me out a bunch! You guys rock! Good luck to all of you! :thumbup:
 

darthmicrobius

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Nov 27, 2009
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Im having a realy hard time trying to figure out the answer to this one.... The question described a guy who had a bleeding ulcer and was hypovolemic and was given a transfusion..... I got the feeling he had acute tubular necrosis due to the prerenal azotemia and granular cast int he sediment and other lab values.... it said that two weeks later,the sediment cleared and renal functio was restored... what ould histo exam show at this time?

coag necorsis
collagen scar
granulation tissue
lymphocytic infiltrate and fibrogenesis (wrong)
regen tubular epithelial cells

any help wold be huge..... thanks
 

netminder

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Dec 18, 2007
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Somatosensory cortex is part of the parietal cortex, so I guess the first thing to look for is sensory loss and graphesthesia. Maybe the better way to look at it is in terms of large and small parietal strokes.

I think hemineglects are signs of a larger stroke while sensory losses are of a smaller stroke. If they were leading you towards a generalized parietal stroke I'd want to see at least one of the following 1) hemineglect 2) apraxias, 3) gerstmanns (finger agnosia, agrapha/alexia/left and right hand confusion), 4) inferior contralateral homonymous quadrantanopia.
Nice, ijn. Very nice explanation.
 

Ilovewater

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Apr 27, 2009
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I got this question wrong, and I'm not sure what the right answer is....

15 yo boy brought to the physician because of painless swelling in his left breast for 1 month. Physical exam shows mild facial acne, thickening of mustache hair on face, and the presence of axillary hair. The left breast appears mildly enlarged with a palpable breast bud; the right breast is normal with no gynecomastia. His genital are Tanner stage 3. Which of the following is the most appropriate initial statement by the physician?

A. Have you tried smoking marijuana recently? That has been known to cause breast enlargement.
B. Some teenagers experiment with their parents' prescription drugs, even birth control pills. Are you?
C. This is a common condition for teenage boys and should resolve in time.
D. This may be a sign of a chromosomal problem. We need to do some genetic testing.
E. This may be a sign of a more serious condition. We'll have to do more tests to be sure.

Thanks!
 

frankyazz

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Jun 23, 2010
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The answer is C. Some gyno is normal during puberty in males due to the hormones. Its somewhere in goljan, and he mentions it in lectures.. Its one of the three times where gyno is normal in males.
 
Apr 11, 2012
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hey everyone

1. I still can't get this one:
Transgenic mice with severe fasting hypoglycemia.
Glucagon -> no effect, epinephrine -> increase in glucose concentration. What's wrong?
I read earlier that the correct answer is "B. defect in glucagon receptor", if I'm not mistaken. But reasonably I could narrow answers only down to these ones: defective adenyl cyclase, G protein, protein kinase A.
First thing: I thought that glicagon doesn't have any specific, its own receptor (???), its receptor is Gs coupled receptor, so that's why I didn't go with B. Choosing among adenyl cyclase, G protein, protein kinase A - I got lost, because all of them are involved in Gs-receptor system and it could be defect in any of them. I decided that the reason why epinephrine worked is because it caused glucogenesis thru a1- Gq-coupled receptor that uses phospholipase C and protein kinase C rather than adenyl cyclase and protein kinase A. So I ended up guessing among adenyl cyclase, G protein, protein kinase A and of course I got this question incorrect.
Could someone be kind and explain me where I went wrong?

2. My "favorite" biostat:
Trial X statistical power is 0.8, Trial Y - 0.9.
What statement is correct regarding the likelihood of a type II error?
Since statist.power = 1 - b, type II error for trial X is 0.2, type II error for trial Y - 0.1. Am I right so far?
So the correct answer should be A. Type II error of trial X > type II error of trial Y ?

3. Again this one:
Patient with metastatic colon ca has maintained remission by taking Bevacizumab as a single agent. The ability to administer this agent despite it being a foreign protein is a result of which? The agent is:
A) Humanized Ab - CORRECT.
B) Variable region of murine Ab directed against VEDGF
C) B cell dysfunction
D) Immune suppression because of previous chemotherapy
E) T cell dysfunction
I found ijn's explanation here: "it's a humanized monoclonal antibody - meaning we recognize the Fc region as self. If it was horse Fc or something, like some antivenoms, then we could end up in anaphylaxis upon repeat administration", but I can't get. I chose D, thought that due to previous immunosuppression therapy there is no reaction on this drug as on foreign agent.

4. And why atrophy of muscles is caused by protein degradation? What initiates this degradation?

Thanks!
 

frankyazz

LECOM '14
Jun 23, 2010
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hey everyone

1. I still can't get this one:
Transgenic mice with severe fasting hypoglycemia.
Glucagon -> no effect, epinephrine -> increase in glucose concentration. What's wrong?
I read earlier that the correct answer is "B. defect in glucagon receptor", if I'm not mistaken. But reasonably I could narrow answers only down to these ones: defective adenyl cyclase, G protein, protein kinase A.
First thing: I thought that glicagon doesn't have any specific, its own receptor (???), its receptor is Gs coupled receptor, so that's why I didn't go with B. Choosing among adenyl cyclase, G protein, protein kinase A - I got lost, because all of them are involved in Gs-receptor system and it could be defect in any of them. I decided that the reason why epinephrine worked is because it caused glucogenesis thru a1- Gq-coupled receptor that uses phospholipase C and protein kinase C rather than adenyl cyclase and protein kinase A. So I ended up guessing among adenyl cyclase, G protein, protein kinase A and of course I got this question incorrect.
Could someone be kind and explain me where I went wrong?

2. My "favorite" biostat:
Trial X statistical power is 0.8, Trial Y - 0.9.
What statement is correct regarding the likelihood of a type II error?
Since statist.power = 1 - b, type II error for trial X is 0.2, type II error for trial Y - 0.1. Am I right so far?
So the correct answer should be A. Type II error of trial X > type II error of trial Y ?

3. Again this one:
Patient with metastatic colon ca has maintained remission by taking Bevacizumab as a single agent. The ability to administer this agent despite it being a foreign protein is a result of which? The agent is:
A) Humanized Ab - CORRECT.
B) Variable region of murine Ab directed against VEDGF
C) B cell dysfunction
D) Immune suppression because of previous chemotherapy
E) T cell dysfunction
I found ijn's explanation here: "it's a humanized monoclonal antibody - meaning we recognize the Fc region as self. If it was horse Fc or something, like some antivenoms, then we could end up in anaphylaxis upon repeat administration", but I can't get. I chose D, thought that due to previous immunosuppression therapy there is no reaction on this drug as on foreign agent.

4. And why atrophy of muscles is caused by protein degradation? What initiates this degradation?

Thanks!
It really sounds like you are over complicating things..
1) Yes there is a glucagon receptor.. every hormone needs a receptor, and every receptor acts through a certain mechanism.. for glucagon its Gs. There are not just random Gs receptors floating around for anything to bind to it. Knowing that AC, G protein, and PKA are all part of the same pathway should of led you to eliminate them.
2) The higher the power, the lower the possibility of having a type II error
3) Its a "mab"... these drugs are humanized Ab by definition
4)Use it or lose it.
 

heli0x

10+ Year Member
Aug 3, 2009
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i had one Q that hasnt been covered yet:

32 yo has had generalized band-like headaches and dizziness almost every day for the past 6 months. physical and CT of head are normal. Which of the following is more consistent with hypochondriasis rather than undifferentiated somatoform disorder
A. disproportionate fear of serious disease
B. frequent health care visits
C. past history of unexplained symptoms
D. persistence of symptoms longer than 6 months
E. presence of depressive symptoms
 
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