Official nbme 15 discussion

[abelabbot]

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

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[pvtbacon]

Can someone help me out with a question, I think im getting tripped up on PTH and its actions.
A question asks about a woman with decreased bone density on DEXA and it asks if the following variables increase or decrease.

Osteoblast Activity / Osteoclast Activity / Receptor Activator of Nucelear Factor kB Ligand (RANKL) concentration

So its osteoporsis so PTH is probably elevated correct?
Which means Osteoblast activity decreases, Oseoclast Increases, and RANKL increases as well right?

everything is normal in osteporosis. only thing decreased is bone mineral density

 

[CrouchingLiger]

Did this form have a question about NADH and ETOH metabolsm/ fatty liver change? If so, does anyone have/remember the gist of the question and want to explain?

I believe there was one with a histo picture of a alcoholic fatty liver asking what caused the droplets to form, is that what you're thinking of? I believe the answer to that had something to do with decreased fatty acid oxidation.

Can someone help me out with a question, I think im getting tripped up on PTH and its actions.
A question asks about a woman with decreased bone density on DEXA and it asks if the following variables increase or decrease.

Osteoblast Activity / Osteoclast Activity / Receptor Activator of Nucelear Factor kB Ligand (RANKL) concentration

So its osteoporsis so PTH is probably elevated correct?
Which means Osteoblast activity decreases, Oseoclast Increases, and RANKL increases as well right?

In osteoporosis the PTH isn't elevated, as pvtbacon said those lab values are all normal. But there is increased osteoclast activity due to increast RANKL. I don't remember what osteoblast activity is, but I want to agree with you in that it decreases (maybe no change? definitely doesn't increase).

 

[pvtbacon]

In postmenopausal women, the deficiency in estrogen results in decreased osteoprotegerin production by osteoblasts, which is a decoy of sorts for Rank-ligand. Normally rank ligand is produced by osteoblasts in response to PTH to trigger osteoclast activity.

Decreased estrogen -> increased rank ligand with no osteoprotegerin to block its effects -> increased osteoclast activity

For the purpose of that question though. Would assume decreased osteoblast activity, increased osteoclast activity and increased RANKL but probably not due to effects of PTH.

 

[Sugar87]

I have no idea why this question bugged me so much on nbme 15 but for the man who is 43 and is a stock broker who smoked marijuana up until he was 28 but nothing since then. He had diffuse wheezing and abdominal exam showed mild hepatomegaly. PFT's shows decreased FEV1 and decreased diffusing capacity. There was a chest x ray showing hyperinflation consistent with air trapping. Was it asthma, continuos marijuana use, diffuse idiopathic interstitial fibrosis, history of smoking marijuana sprayed with toxic herbacide or inherited protease deficiency?

I think i over thought this one

Gracias!

 

[pvtbacon]

I have no idea why this question bugged me so much on nbme 15 but for the man who is 43 and is a stock broker who smoked marijuana up until he was 28 but nothing since then. He had diffuse wheezing and abdominal exam showed mild hepatomegaly. PFT's shows decreased FEV1 and decreased diffusing capacity. There was a chest x ray showing hyperinflation consistent with air trapping. Was it asthma, continuos marijuana use, diffuse idiopathic interstitial fibrosis, history of smoking marijuana sprayed with toxic herbacide or inherited protease deficiency?

I think i over thought this one

Gracias!

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

 

[Pinkleton]

A 13-year-old boy is scheduled to receive chemotherapy for a leukemia that has the histologic features of malignent lymphocytes.
A) Activated cytolytic effector T lymphocytes in the circulation

E) T-lymphocyte thymocytes localized to the thymic cortex.

I put A, but apparently is E correct? I thought the cells in thymic cortex are double positive with CD 4 and 8. The stem says the cells don't have either

 

[shivakamini]

A 13-year-old boy is scheduled to receive chemotherapy for a leukemia that has the histologic features of malignent lymphocytes. T


A) Activated cytolytic effector T lymphocytes in the circulation
\\\
E) T-lymphocyte thymocytes localized to the thymic cortex.

I put A, but apparently is E correct? I thought the cells in thymic cortex are double positive with CD 4 and 8. The stem says the cells don't have either

Earliest thymocytes are double negative (CD4-/CD...they have to undergo TCR rearrangement first (Beta-selection, "...rearrangement of the T-lymphocyte receptor beta-chain gene D and J segments.") This occurs in the thymic cortex. Only after B-selection can thymocytes generate double positive CD4+/CD8+ cells, which then go on to choose their MHC class type (also in the cortex).

Detailed, yes. But the gist of it is this: Double negative --> TCR beta-selection --> Double positive --> MHC class typing....all occurs in the cortex.

 

[Pinkleton]

Stem described lupus and asked what you would find on blood smear. I narrowed it down to thrombocytopenia and multiple nucleated erythrocytes. I thought both can occur. Couldn't you have microangiopathic destruction of rbcs which would cause the marrow to put out immature rbcs?

Also:

Screening for splice variants of CD44v10. I put affinity column chromatography. Was it immunohistochemistry? Plz explain

 

[CrouchingLiger]

Stem described lupus and asked what you would find on blood smear. I narrowed it down to thrombocytopenia and multiple nucleated erythrocytes. I thought both can occur. Couldn't you have microangiopathic destruction of rbcs which would cause the marrow to put out immature rbcs?

Yeah, there would be immature RBC's, reticulocytes. But don't get that confused with nucleated RBCs. Reticulocytes don't have intact nuclei, what they do have is nuclear remnants, mostly in the form of rRNA fragments I believe.

 

[Pinkleton]

Yeah, there would be immature RBC's, reticulocytes. But don't get that confused with nucleated RBCs. Reticulocytes don't have intact nuclei, what they do have is nuclear remnants, mostly in the form of rRNA fragments I believe.

Oooh good call, thanks!

Also I edited my post to add another Q, if anyone wants to help out!

 

[Pinkleton]

Stem asked: inhibition of what causes the ductus arteriosus to close? I narrowed down to COX and LOX. I put LOX because that would shunt more AA to prostaglandin formation, which closes the PDA. Don't COX inhibitors keep the ductus open instead??

 

[pvtbacon]

Oooh good call, thanks!

Also I edited my post to add another Q, if anyone wants to help out!

Immunohistochemistry. They like to use monoclonal Ab with radiofluorescent tags to see where the variants are.

A similar procedure was done in this experiment if you look at the materials and methods section.

Can't link the paper since I had to access via school online library but it's by Liu, K, et al. Differential expression of CD44s and CD4v10 proteins and syndecan in normal and irradiated mouse epidermis. Histochem Cell Biol 1997:107;159-167

 

[pvtbacon]

Stem asked: inhibition of what causes the ductus arteriosus to close? I narrowed down to COX and LOX. I put LOX because that would shunt more AA to prostaglandin formation, which closes the PDA. Don't COX inhibitors keep the ductus open instead??

It's inhibition of COX. Indomethacin, a NSAID and a nonselective COX1 COX2 inhibitor is the preferred agent for closure of PDA

Alprostadil, a synthetic form of PGE1 is used to keep PDA open in cases like transposition of great vessels where right to left shunt is needed to keep baby alive until surgery can be performed

 

[Pamplemousse123]

I have no idea why this question bugged me so much on nbme 15 but for the man who is 43 and is a stock broker who smoked marijuana up until he was 28 but nothing since then. He had diffuse wheezing and abdominal exam showed mild hepatomegaly. PFT's shows decreased FEV1 and decreased diffusing capacity. There was a chest x ray showing hyperinflation consistent with air trapping. Was it asthma, continuos marijuana use, diffuse idiopathic interstitial fibrosis, history of smoking marijuana sprayed with toxic herbacide or inherited protease deficiency?

I think i over thought this one

Gracias!

Had a hard time on this one too. I knew it was a1at deficiency, but I was disturbed that they didn't mention "protease inhibitor" in that answer choice. Maybe a1at is a protease that cleaves a protease? Does anyone have any insight on this? Answer is inherited protease def btw.

 

[Sugar87]

Had a hard time on this one too. I knew it was a1at deficiency, but I was disturbed that they didn't mention "protease inhibitor" in that answer choice. Maybe a1at is a protease that cleaves a protease? Does anyone have any insight on this? Answer is inherited protease def btw.

Yea I went back and thought about it, I think thats what they were getting at. I guess technically a1at is the protease that keeps the bad proteases in check (elastase). Also, I should have known because the other answers didn't make sense lol.

 

[Pamplemousse123]

There was one question about the SITS muscle with a lady who had a hard time abducting her arm from 90deg abducted position giving a thumbs down appearance. The acro/coracoid process location made supraspinatus the answer choice, but I thought that supraspinatous abducts initially and then the deltoid takes over from 90deg and beyond. Can someone please explain this phenomenon? Thanks in advance.

 

[pvtbacon]

There was one question about the SITS muscle with a lady who had a hard time abducting her arm from 90deg abducted position giving a thumbs down appearance. The acro/coracoid process location made supraspinatus the answer choice, but I thought that supraspinatous abducts initially and then the deltoid takes over from 90deg and beyond. Can someone please explain this phenomenon? Thanks in advance.

The maneuver you are referring to is the known as the "empty can test". I have no idea how this works as the "full can test" where the patient gives a thumbs up is better for isolating the supraspinatus muscle. But you were correct to assume that the supraspinatus was the answer. As for the biomechanics, I'd have to defer to someone with a masters/phD in physiology

 

[Pinkleton]

There was one question about the SITS muscle with a lady who had a hard time abducting her arm from 90deg abducted position giving a thumbs down appearance. The acro/coracoid process location made supraspinatus the answer choice, but I thought that supraspinatous abducts initially and then the deltoid takes over from 90deg and beyond. Can someone please explain this phenomenon? Thanks in advance.

You are correct about the motion, but the questions is not asking that. You are told that range of motion is normal, which points toward rotator cuff injury. If the deltoid was injured the patient could not abduct to 90. Plus, at 90 degrees the supraspinatus is still contracted I believe. Regardless, I think putting it in this position simply serves to irritate the tendon running below the acromion

 

[goldenmug8]

Hey guys, I have a couple questions too:

1) The question about the women who was pregnent, had Marfan's syndrome, coarctation of the thoracic aorta, and had aortic regurgitation....question was what would increase the regurgitation? Answer: a) Dec vascular resistance 2) Hypovolemia 3) Increased cutaneous blood flow 4) Increased metabolic rate 5) Weight gain

2) The one about acetaminophen poisoning and liver toxicty, it asked what metabolites would change? The answers dealt with glucuronide conjugates, glutathione, NAD+, and NADH and asked which one decreased or increased

3) How do you have resistance to ampicillin but retain susceptibility to ceftriaxone?

Thanks!

 

[Legerdemain]

Hey guys, I have a couple questions too:

1) The question about the women who was pregnent, had Marfan's syndrome, coarctation of the thoracic aorta, and had aortic regurgitation....question was what would increase the regurgitation? Answer: a) Dec vascular resistance 2) Hypovolemia 3) Increased cutaneous blood flow 4) Increased metabolic rate 5) Weight gain I think the answer was HYPERvolemia (not hypovolemia) -- the idea being that increased blood volume would increase the pressure in the systemic circulation --> increased afterload --> increased AR

2) The one about acetaminophen poisoning and liver toxicty, it asked what metabolites would change? The answers dealt with glucuronide conjugates, glutathione, NAD+, and NADH and asked which one decreased or increased Decreased glutathione --> liver cannot protect itself against reactive metabolites (NAPQI in this case) --> liver damage

3) How do you have resistance to ampicillin but retain susceptibility to ceftriaxone? Ceftriaxone has R-groups that make it more resistant to B-lactamases than ampicillin

Thanks!

Here's what I remember.

 

[pvtbacon]

Hey guys, I have a couple questions too:

1) The question about the women who was pregnent, had Marfan's syndrome, coarctation of the thoracic aorta, and had aortic regurgitation....question was what would increase the regurgitation? Answer: a) Dec vascular resistance 2) Hypovolemia 3) Increased cutaneous blood flow 4) Increased metabolic rate 5) Weight gain

2) The one about acetaminophen poisoning and liver toxicty, it asked what metabolites would change? The answers dealt with glucuronide conjugates, glutathione, NAD+, and NADH and asked which one decreased or increased

3) How do you have resistance to ampicillin but retain susceptibility to ceftriaxone?

Thanks!

1) none of the answer choices make sense. Are you sure it wasn't hypervolemia?

2) Depletion of GSH by acetaminophen allows it to damage the liver

3) According to first aid 2013 p 178, cephalosporins are less susceptible to penicillinases

 

[goldenmug8]

Ah yes, I meant HYPERvolemia.

And now that I just relooked at FA about ampicillin, it says "penicillinase sensitive" NOT resistance. I should learn to read. and apparently type too.

Thanks guys!

 

[Pamplemousse123]

Hey guys,

Thanks for your help with my previous questions. I have two more:

1) There was one question with a 10 month old boy with a 10cm solid abdominal mass on the upper pole of kidney. Biopsy showed hypervascularity. What is it?

I chose Wilm's nephroblastoma but I remember there was also a mesoblastic nephroma...When I wikied it, I came across this as the ddx:

Mesoblastic nephroma (congenital): from birth to 1 year
Rhabdoid tumor: from 1 to 2 years of age
Clear cell sarcoma of kidney: from 2 to 3 years of age.
Wilm's tumor: over 3 years of age.

Why isnt the answer mesoblastic nephroma, then?

2) Also, about the question with an adenocarcinoma at the G-E junction with h pylori as the answer to chronic infection association, isn't the location of the adenocarcinoma atypical? I couldn't piece the information together as I learned that h pylori is protective against GERD and one would typically see intestinal metaplasia --> adenocarcinoma at the antrum and not the GE junction. I am definitely missing something here - would one see intestinal metaplasia at the GE junction with H pylori?

Thanks in advance!

 

[pvtbacon]

Hey guys,

Thanks for your help with my previous questions. I have two more:

1) There was one question with a 10 month old boy with a 10cm solid abdominal mass on the upper pole of kidney. Biopsy showed hypervascularity. What is it?

I chose Wilm's nephroblastoma but I remember there was also a mesoblastic nephroma...When I wikied it, I came across this as the ddx:

Mesoblastic nephroma (congenital): from birth to 1 year
Rhabdoid tumor: from 1 to 2 years of age
Clear cell sarcoma of kidney: from 2 to 3 years of age.
Wilm's tumor: over 3 years of age.

Why isnt the answer mesoblastic nephroma, then?

2) Also, about the question with an adenocarcinoma at the G-E junction with h pylori being the most important risk factor, isn't the location of the adenocarcinoma atypical? I couldn't piece the information together as I learned that h pylori is protective against GERD and one would typically see intestinal metaplasia --> adenocarcinoma at the antrum and not the GE junction. I am definitely missing something here - would one see intestinal metaplasia at the GE junction with H pylori?

Thanks in advance!

I picked mesoblastic nephroma because 10 months was way too young for Wilm's, though I can't say for sure which tumor is actually hypervascular and at the end of the pole. I've tried looking through radiology journals but couldn't find anything leading to a correct answer.

As for the adenocarcinoma at the GE junction, number one risk factor is Barrett's Esophagus, which has its own risk factors including: smoking, diet, pregnancy. I don't think H.Pylori has anything to do with GERD. Esophageal adeno is number 1 in the western world whereas squamous is most common elsewhere.

I often get the it mixed up with gastric adenocarcinoma, which occurs with chronic gastritis as a complication of h. pylori infection.

 

[cluelessnoob]

The question gives two pictures of hysterosalpingograms and asks why the woman was unable to conceive for 1 year. The choices were blockage of right fallopian tube/left fallopian tube/left and right blockage/rupture of left only/rupture of right only. Obviously the you need to look at the picture, but how do you tell from the picture?

 

[addo]

The question gives two pictures of hysterosalpingograms and asks why the woman was unable to conceive for 1 year. The choices were blockage of right fallopian tube/left fallopian tube/left and right blockage/rupture of left only/rupture of right only. Obviously the you need to look at the picture, but how do you tell from the picture?

it was blockage of both sides. One side looked slightly less blocked than the other one, but they were both blocked though.

 

[cluelessnoob]

it was blockage of both sides. One side looked slightly less blocked than the other one, but they were both blocked though.

how did you tell that? were they bigger than normal?

 

[eagles22]

The question gives two pictures of hysterosalpingograms and asks why the woman was unable to conceive for 1 year. The choices were blockage of right fallopian tube/left fallopian tube/left and right blockage/rupture of left only/rupture of right only. Obviously the you need to look at the picture, but how do you tell from the picture?

Think about fallopian tube anatomy. The don't connect directly to the ovary. There's a gap with access to the peritoneal cavity. If you inject dye into a normal tube, the dye should spill out. You didn't see that on either side, thus both tubes are blocked.

 

[Akr]

how did you tell that? were they bigger than normal?

This is normal (or at least not-blocked) hysterosalpingogram:

So if you can't visualize the fallopian tubes, think blockage...

 

[eagles22]

1. person had diarrhea from salmonella enterica and in 36 hrs within 36 hrs but persist in a milder form for several more days -- what is most likely to occur in this pt if treated with abx? anaphylaxis as a result of abx hypersensitivity, decreased risk of endocarditis, decreased risk for hemolytic uremic syndrome, establishment of a chronic carrier state in spleen, prolonged fecal excretion of the organism (this answer seemed weird to me - i guess the prolonged threw me off but im guessing that was correct?

2. the guy that smells of burnt almonds and is NONcynaotic is still tripping me up. It sounds like CO poisiong and I put hyperbaric oxygen but thats wrong! the other answers are: amyl nitrate, EPO, ethanol, physostigmine

3.would someone mind explaining the basics behind distinguishing incomplete penetrance from gondal moacism on a pedigree?

4. for the alcohol poisoning question and giving an antidote- the options were: blocks methanol in the GI tract and decreases its absorption, blocks tubular reabsorption and enhances urinary elimination of methanol, enhances metabolism of methanol by alcohol dehydrogenase and cytochrome p450 3A4, and inhibits alcohol dehydrogenase, blocking its conversion of methanol to foraldehyde

Gonadal mosaicism results from a mutation in the germline of a parent. Achondroplasia is a good example of this. It can result in the passage of an autosomal dominant condition from a non-affected parent to child. You'd see this trait develop and then a autosomal dominant pattern following.

Incomplete penetrance will follow a pattern in which some people have it some don't, but it doesn't match other genetic patterns. The thing is, everyone carries the gene and has the possibility to give it to their offspring. The chances that all those people had the same mutation in their germ cells is pretty low which leaves only incomplete penetrance.

 

[cluelessnoob]

ok thanks guys!

 

[coolforschool]

Does anyone have a good explanation for this one:

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

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

 

[pvtbacon]

Does anyone have a good explanation for this one:

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

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

There's a lot of debate on whether cancer follows depression or depression follows cancer. What's undebatable though is that there is a strong link between pancreatic cancer and depression.

"dysregulated immune response is supposed to be the causal link between depression and cancer. Animal models indicate that proinflammatory cytokines can elicit "depression-like" symptoms [12,45]. In pancreatic cancer patients indeed increased levels of several cytokines such as IL-6, IL-18 and TNF-alpha can be found. These factors may have impact on the hypothalamic-pituitary-adrenal (HPA) axis and the CRF (corticotropin-releasing factor). Some authors assume this pathway to be the cause for pathologic results in the dexamethason suppression test, in analogy to a paraneoplastic symptom. Elevated IL-6 plasma levels in particular seem to be associated with major depression in pancreatic cancer patients and tumor cells can influence production of serotonin receptor antibodies active in central nervous system [23,46-49]. "

You can read more on this if you like here: http://www.biomedcentral.com/1471-2407/10/569

 

[eagles22]

Does anyone have a good explanation for this one:

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

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

He's got a terminal diagnosis. It's logical to think he would be come depressed (also it's one of the stages of grieving). Plus if I remember correctly, the other options were all things that would show up sooner in life.

 

[computernerd225]

Just took this yesterday, scrolled through the thread and found it very helpful. For some reason I thought this test was easier than NBME 12 (took that last week, got a 210), got a 233 on NBME 15; maybe my knowledge base was just in tune with this particular test? I did finish the last week of DIT before I took 15 so maybe that helped.

Had a question that I couldn't find the answer/explanation to though, any help would be great:

30 y/o nulligravid woman, had recent weight gain, irregular periods, all levels of prolactin, TSH, FSH, and LH were normal. Positive progestin challenge test though (which indicates anovulation, I guess?)

Answer choices were:
Increased androgen production in adrenals (seems right, but doesn't PCOS have increased androgen production by the theca cells? Or am I too focused on PCOS and any increase in androgens can cause anovulation),
increased estrogen production in adipose,
increased gonadotropin in pituitary,
increased GnRH in hypothalamus,
increased progesterone in ovaries (picked this one because I was thinking PCOS, forgot that PCOS means NO progesterone)

 

[CrouchingLiger]

Just took this yesterday, scrolled through the thread and found it very helpful. For some reason I thought this test was easier than NBME 12 (took that last week, got a 210), got a 233 on NBME 15; maybe my knowledge base was just in tune with this particular test? I did finish the last week of DIT before I took 15 so maybe that helped.

Had a question that I couldn't find the answer/explanation to though, any help would be great:

30 y/o nulligravid woman, had recent weight gain, irregular periods, all levels of prolactin, TSH, FSH, and LH were normal. Positive progestin challenge test though (which indicates anovulation, I guess?)

Answer choices were:
Increased androgen production in adrenals (seems right, but doesn't PCOS have increased androgen production by the theca cells? Or am I too focused on PCOS and any increase in androgens can cause anovulation),
increased estrogen production in adipose,
increased gonadotropin in pituitary,
increased GnRH in hypothalamus,
increased progesterone in ovaries (picked this one because I was thinking PCOS, forgot that PCOS means NO progesterone)

One of the potential causes of PCOS is that excess adipose causes higher levels of estrogen, which may inhibit the LH surge to prevent ovulation. This is why PCOS is linked to obesity.

 

[pvtbacon]

Just took this yesterday, scrolled through the thread and found it very helpful. For some reason I thought this test was easier than NBME 12 (took that last week, got a 210), got a 233 on NBME 15; maybe my knowledge base was just in tune with this particular test? I did finish the last week of DIT before I took 15 so maybe that helped.

Had a question that I couldn't find the answer/explanation to though, any help would be great:

30 y/o nulligravid woman, had recent weight gain, irregular periods, all levels of prolactin, TSH, FSH, and LH were normal. Positive progestin challenge test though (which indicates anovulation, I guess?)

Answer choices were:
Increased androgen production in adrenals (seems right, but doesn't PCOS have increased androgen production by the theca cells? Or am I too focused on PCOS and any increase in androgens can cause anovulation),
increased estrogen production in adipose,
increased gonadotropin in pituitary,
increased GnRH in hypothalamus,
increased progesterone in ovaries (picked this one because I was thinking PCOS, forgot that PCOS means NO progesterone)

Nothing seems to hint at hirsutism, clitoromegaly, acne so I'd shy away from increased androgen.

PCOS would produce increase in LH relative to FSH 2:1 ratio. We don't see that here.

Id expct increased gnRH and gonadotropin to increase LH and FSH

none of these answer choices make sense if lab values were normal @_@

EDIT: I looked up the question and it seems that LH:FSH ratio was indeed 2:1 which points more towards PCOS. However, I'm having trouble settling on Increased estrogen in adipose tissue. I looked it up in UpToDate and it says that it is still unclear whether obesity is causative. And I'd also expect the increased production of weak estrones to induce negative feedback on GnRH production and thus lower LH and FSH . I'm gonna have to investigate this further

 

[coolforschool]

There's a lot of debate on whether cancer follows depression or depression follows cancer. What's undebatable though is that there is a strong link between pancreatic cancer and depression.

"dysregulated immune response is supposed to be the causal link between depression and cancer. Animal models indicate that proinflammatory cytokines can elicit "depression-like" symptoms [12,45]. In pancreatic cancer patients indeed increased levels of several cytokines such as IL-6, IL-18 and TNF-alpha can be found. These factors may have impact on the hypothalamic-pituitary-adrenal (HPA) axis and the CRF (corticotropin-releasing factor). Some authors assume this pathway to be the cause for pathologic results in the dexamethason suppression test, in analogy to a paraneoplastic symptom. Elevated IL-6 plasma levels in particular seem to be associated with major depression in pancreatic cancer patients and tumor cells can influence production of serotonin receptor antibodies active in central nervous system [23,46-49]. "

You can read more on this if you like here: http://www.biomedcentral.com/1471-2407/10/569

He's got a terminal diagnosis. It's logical to think he would be come depressed (also it's one of the stages of grieving). Plus if I remember correctly, the other options were all things that would show up sooner in life.

Thanks, guys. Thanks for that link. I guess I should've known what they were hinting at based on the other answer choices. I went like 5th order on that question to arrive at my wrong answer.

 

[computernerd225]

One of the potential causes of PCOS is that excess adipose causes higher levels of estrogen, which may inhibit the LH surge to prevent ovulation. This is why PCOS is linked to obesity.

The lab values are here:

Prolactin 15 ng/mL
Thyroid-stimulating hormone 2muU/mL
Follicle-stimulating hormone 10 mlu/mL
Luteinizing hormone 28 mlu/mL

I just don't see how the values would be in the normal range with excess estrogen. Wouldn't the negative feedback drive the FSH and LH levels down?

Also, FA says that PCOS has high LH, which inhibits the progesterone surge.

Am I overthinking that she has PCOS and maybe she's just obese, which would lead to increased estrogen -> preventing LH surge?

 

[pvtbacon]

The lab values are here:

Prolactin 15 ng/mL
Thyroid-stimulating hormone 2muU/mL
Follicle-stimulating hormone 10 mlu/mL
Luteinizing hormone 28 mlu/mL

I just don't see how the values would be in the normal range with excess estrogen. Wouldn't the negative feedback drive the FSH and LH levels down?

Also, FA says that PCOS has high LH, which inhibits the progesterone surge.

Am I overthinking that she has PCOS and maybe she's just obese, which would lead to increased estrogen -> preventing LH surge?

I am stuck in the same thought process. Hoping some endocrinology buff can clear things up. To be considered as PCOS, she needs to have signs of hyperandrogenism, and that isn't clear in the vignette. Sounds to me like she just has a lot of excess fat. But still, why doesn't excess estrogen change the levels of gonadotropin? Desensitization?

 

[eagles22]

I am stuck in the same thought process. Hoping some endocrinology buff can clear things up. To be considered as PCOS, she needs to have signs of hyperandrogenism, and that isn't clear in the vignette. Sounds to me like she just has a lot of excess fat. But still, why doesn't excess estrogen change the levels of gonadotropin? Desensitization?

The diagnostic criteria for PCOS is an/oligoovulation, androgen excess, and polycystic ovaries. I don't recall the stem including that. Anyways, FSH and LH were within range so the answer saying increased gonadotroph levels has to be wrong. I think she was obese so peripheral conversion of estrogens was the only answer that I thought could fit.

 

[CrouchingLiger]

Yeah sorry, ignore my last comment then since its not PCOS. I must've been remembering a Uworld question or something so I was going with your train of thought thinking its PCOS. I did pick estrone production in adipose tissue, but mostly because of her weight gain. Plus, you can rule out the other choices because don't fit the story:
Increased androgen production in adrenals. (no signs of hirsutism)
increased gonadotropin in pituitary, (this would cause elevated sex hormones)
increased GnRH in hypothalamus (this would also cause elevated hormones levels if pulsatile, or decreased if constant. But they were within normal limits).
increased progesterone in ovaries (this could only occur if there was ovulation)

Also, one other important thing that i forgot about before: positive progestin challenge test. What does this mean? Its a test where you administer progestin for about a week-10 days, and then when the progestin levels fall, menstruation should occur. This simulates the secretion of progestin by the corpus luteum in the second phase of the menstrual cycle. However, the only way that this test could result in a positive outcome is if the uterus was first exposed to high levels of estrogen to increase in thickness. Remember, progestin prevents further growth in endometrial thickness, instead causing it to increase secretory glands. After progestin levels fall, the glandular endometrium is no longer stimulated so the cells undergo apoptosis and start to shed. But if there was no increase in endometrial thickness to begin with, then there would be no excess cells to shed. This is the key to letting you know that this woman has excess estrogen levels, and then you can start picking the choice that results in excess estrogen that fits the rest of the scenario, such as having normal levels of FSH/LH.

Sorry if this isn't completely clear, i had looked it up after I took this exam so I'm just going from memory trying to explain this now. I hope it makes sense to someone.

 

[Akr]

Yeah thanks! The progestin challenge test was the only part that I didn't know, so I ignored that bit of info and forgot to look it up again later.

 

[pvtbacon]

Is Estrogen's role in negative feedback not important at all in this case?

 

[computernerd225]

Yeah sorry, ignore my last comment then since its not PCOS. I must've been remembering a Uworld question or something so I was going with your train of thought thinking its PCOS. I did pick estrone production in adipose tissue, but mostly because of her weight gain. Plus, you can rule out the other choices because don't fit the story:
Increased androgen production in adrenals. (no signs of hirsutism)
increased gonadotropin in pituitary, (this would cause elevated sex hormones)
increased GnRH in hypothalamus (this would also cause elevated hormones levels if pulsatile, or decreased if constant. But they were within normal limits).
increased progesterone in ovaries (this could only occur if there was ovulation)

Also, one other important thing that i forgot about before: positive progestin challenge test. What does this mean? Its a test where you administer progestin for about a week-10 days, and then when the progestin levels fall, menstruation should occur. This simulates the secretion of progestin by the corpus luteum in the second phase of the menstrual cycle. However, the only way that this test could result in a positive outcome is if the uterus was first exposed to high levels of estrogen to increase in thickness. Remember, progestin prevents further growth in endometrial thickness, instead causing it to increase secretory glands. After progestin levels fall, the glandular endometrium is no longer stimulated so the cells undergo apoptosis and start to shed. But if there was no increase in endometrial thickness to begin with, then there would be no excess cells to shed. This is the key to letting you know that this woman has excess estrogen levels, and then you can start picking the choice that results in excess estrogen that fits the rest of the scenario, such as having normal levels of FSH/LH.

Sorry if this isn't completely clear, i had looked it up after I took this exam so I'm just going from memory trying to explain this now. I hope it makes sense to someone.

Makes perfect sense, thanks a lot.

Only 11 more days until it's all over with...

 

[CrouchingLiger]

Is Estrogen's role in negative feedback not important at all in this case?

It has a role, I'm not sure if I can explain how too well but i'll try. Estrogen has different effects on but LH and FSH depending on its concentration. It can stimulate LH if it's at a slightly high level for sufficient time (which is how estrogen stimulates the LH surge), but if estrogen is at even higher levels then it will inhibit LH. I'm not too sure how it works for FSH, but I believe it's mostly inhibitory. The LH level in this woman is high (unless she was in the middle of the LH surge). This awkwardly high level is indicative that its being stimulated chronically by estrogen, but not actually suppresses the LH surge (which requires an initially low LH level in order to surge). Also, the FSH level is high-normal I believe, again unless she was in the middle of ovulation. Also, in this question, the LH:FSH ratio is fairly high, they should be close to equal at most points in the cycle. The higher ratio is again indicative of increased estrogen, since it will stimulate LH and inhibit FSH to some extent.

The changes of these levels during the cycle are what make interpreting the results of these kind of murky, so I try not to rely on them too much if I can help it. Also because I feel like I start thinking in circles when trying to interpret these, and it gets confusing fast. I hope I'm not making things even more confusing with these explanations.

 

[pvtbacon]

Thanks dude. I think I can put my mind to rest when you put it that way. I tried thinking through all the answer choices and none were really bulletproof but one was clearly better than the rest.

 

[zee620]

Anyone know the answer to the paraesophageal hernia one?

A 72 year old man comes to the physician bc of a 3 mo hx of progressive burning chest discomfort after meals. Xray of the chest and abdome show a paraesophageal hernia. Which of the following findings is most likely present in this patient (+ picture that didn't help me)

a. abnormal relation of the cardia to the lower end of the diaphgram -- not this one
b. displacement of the pylorus inferiorly
c. GE jxn that lies 2 vertebral levels above the diaphragm
d. protrusion of the fundus into the chest above the level of t10
e. right diaphragmatic hernia

 

[zee620]

What is the furuncle!?

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

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

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

 

[pvtbacon]

Anyone know the answer to the paraesophageal hernia one?

A 72 year old man comes to the physician bc of a 3 mo hx of progressive burning chest discomfort after meals. Xray of the chest and abdome show a paraesophageal hernia. Which of the following findings is most likely present in this patient (+ picture that didn't help me)

a. abnormal relation of the cardia to the lower end of the diaphgram -- not this one
b. displacement of the pylorus inferiorly
c. GE jxn that lies 2 vertebral levels above the diaphragm
d. protrusion of the fundus into the chest above the level of t10
e. right diaphragmatic hernia

I like D. Paraesophageal hernias usually just have the fundus sticking out through the diaphragm at the esophageal opening located at t10.

B wouldn't work because pylorus is already inferior to begin with and moving it down wouldn't have anything entering the chest cavity.

C. GE junction above the diaphragm might point more towards a sliding hiatal hernia

E. Diaphragmatic hernias usually present with loops of bowel in chest cavity.