NBME 16 help

[shubz123]

Hi all,

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[sjonies88]

Thanks for your help! I tend to think of an asterixus/high ammonia type of picture for hepatic encephalopathy…can you clarify the link between hepatic encephalopathy and cerebral edema for me?
Thanks again

 

[hello2]

The pyramidal decussation takes place at the caudal medulla, hence I said that CST lesion in the spinal cord is for all practical purposes always ipsilateral. The mechanism of injury in most spinal flexion/extension injuries (diving, whiplash, falling on one's head from a ladder) is injury to the cervical cord because it is contained in the most mobile part of the spine. You don't need histology here, you need gross anatomy to identify various sections, which is pretty important in neuroanatomy. The brainstem is usually identified by the presence of the various nuclei, peduncles and the the dorsal location of the spinal canal (apart from the distinctive shape of certain levels). The spinal cord can be identified by the expansion of the central grey matter especially at the cervical and lumbar levels, and the typical formation of posterior and anterior horns with a more central spinal canal. For it to be upper and lower motor deficit, you're right it has to be high up, i.e. between C1-c5 (after which the brachial plexus begins and some nerves branch off). A medullary lesion is highly unlikely due to mechanical injury. Vascular lesions or even mass effect will affect more than just the corticospinal tract in the medulla, and such signs will be mentioned (especially on the exam). Here is a link that you might find helpful with regards to gross neuroanatomy.

Thanks for this thorough explanation; very helpful

 

[hello2]

Thanks for your help! I tend to think of an asterixus/high ammonia type of picture for hepatic encephalopathy…can you clarify the link between hepatic encephalopathy and cerebral edema for me?
Thanks again

Good point. I couldn't find a solid connection on wiki, but I found an article with a couple of theories (link and abstract below). In any case, hepatic encephalopathy and cerebral edema are two SEPARATE diagnostic criteria for Reye's (in varying stages), even though the former probably directly or indirectly leads to the latter.
http://www.ncbi.nlm.nih.gov/pubmed/18688582

"Cerebral edema is a potential life-threatening complication in patients with acute liver failure who progress to grade III/IV encephalopathy. The incidence is variably reported but appears to be most prevalent in those patients with hyperacute liver failure as opposed to subacute forms of liver failure. In those patients who are deemed at risk of cerebral edema and raised intracranial pressure, insertion of an intra-cranial pressure monitoring device may be considered to optimize treatment and interventions. The pathogenesis of cerebral edema in this setting remains controversial, although recent work suggests a pivotal role for arterial ammonia, whose effects appear to be potentiated by the presence of systemic inflammation. Recent work has also suggested the import of free radical formation occurring at a mitochondrial level as being the potential mediator of cellular dysfunction as opposed to ammonia per se. Treatment of such patients requires a multi-disciplinary approach incorporating both hepatology and critical care. In a significant proportion of such cases, consideration of liver transplantation may be required. Treatment should be focused at optimizing liver function and regenerative capacity and minimizing the inflammatory milieu. Controlled studies are lacking and much of the management has been extrapolated from neurocritical care. Sustained elevation of intracranial pressure may be responsive to mannitol or hypertonic saline bolus, and in those with hyperemia indomethacin has been reported as beneficial in case series. Recently, interest has developed into the use of cooling in the management of patients with acute liver failure and raised intracranial pressure. Animal studies support this treatment option as do case series, although randomized trials are still awaited."

 

[hello2]

4) Do you form immunity against chlamydia? I didn't think you did. There was a stats question where you screened freshman girls for chlamydia and 500 out of 2500 tested positive. Then a year later you tested them again and there were an additional 200 positives, and it then wants you to find the incidence. I thought you would divide 200/2500 as it's a year later and one of the original 500 girls could have been infected again. The correct answer is 200/2000 as you subtract the original 500 girls from the population, so I'm assuming there is immunity? And even if you do have immunity, there are multiple types of chlamydia (D-K), so what if an original girl was infected with D strain and then a year later with F strain? This question seems flawed to me.

What if the girls weren't treated after being screened? I haven't seen the question so I don't know what it says exactly.

Treatment would be a key factor to consider. You are correct in thinking that immunity would rule out those previously infected, but so would chronic infection (when considering a "positive test" for chlamydia trachomatis in general, not for the various serovars):
"Chlamydiae have the ability to establish long-term associations with host cells. When an infected host cell is starved for various nutrients such as amino acids (for example, tryptophan),[13]iron, or vitamins, this has a negative consequence for Chlamydiae since the organism is dependent on the host cell for these nutrients. Long-term cohort studies indicate that approximately 50% of those infected clear within a year, 80% within two years, and 90% within three years.[14]"
http://en.wikipedia.org/wiki/Chlamydia_infection

So technically, according to Dr. Wiki, the answer would be approximately 200/(2000+250). I don't recall if that was an option, but if it was, then I would be happy to have gotten it wrong Also, I really hope that the "epidemiologist mind" behind this question is not concerned about infection with different serovars, because that would also be a very interesting twist. I appreciate you bringing these points up though, because they cover some important concepts that could be used in questions on the real deal!
And not to keep beating this dead horse, but did the question specifically state that "an ADDITIONAL 200" were infected? If so, then this would automatically rule out the original 500 for calculation purposes, I guess. And by the way, I did get this question wrong, which is why I'm so adamant about it, lol.

 

[Handinhand]

It does say that an additional 200 were infected, but that should mean you remove the original 500. The correct answer was 200/2000, and I don't agree with this.

Incidence is new cases per defined time period / total susceptible population. If the 200 additional cases occurred within the same year, then it would be 700/2500. The question said that this was a year later though, so you're beginning with the same 2500 girls again. Whether they are immune should not matter, as there are other serotypes to be infected with, and I don't think it's correct to take those 500 original girls out of the equation because they could be reinfected with chlamydia.

 

[notbobtrustme]

It does say that an additional 200 were infected, but that should mean you remove the original 500. The correct answer was 200/2000, and I don't agree with this.

Incidence is new cases per defined time period / total susceptible population. If the 200 additional cases occurred within the same year, then it would be 700/2500. The question said that this was a year later though, so you're beginning with the same 2500 girls again. Whether they are immune should not matter, as there are other serotypes to be infected with, and I don't think it's correct to take those 500 original girls out of the equation because they could be reinfected with chlamydia.

no I agree, but we gotta think how they want us to calculate incidence. I took the question at face value. They got tested, never got treated and aren't at risk for reinfection. 200/2000. It's a dumb question but that's how 50% of these NBMEs end up being.

 

[afschlatter]

Answers in quote.

I just took NBME 16 and I got this golgi trafficking question wrong by picking D (increased smooth endoplasmic reticulum) I think that its C, due to backing up of proteins in the RER -> dilation - problem with COPII. What do you think?

 

[sjonies88]

Good point. I couldn't find a solid connection on wiki, but I found an article with a couple of theories (link and abstract below). In any case, hepatic encephalopathy and cerebral edema are two SEPARATE diagnostic criteria for Reye's (in varying stages), even though the former probably directly or indirectly leads to the latter.
http://www.ncbi.nlm.nih.gov/pubmed/18688582

"Cerebral edema is a potential life-threatening complication in patients with acute liver failure who progress to grade III/IV encephalopathy. The incidence is variably reported but appears to be most prevalent in those patients with hyperacute liver failure as opposed to subacute forms of liver failure. In those patients who are deemed at risk of cerebral edema and raised intracranial pressure, insertion of an intra-cranial pressure monitoring device may be considered to optimize treatment and interventions. The pathogenesis of cerebral edema in this setting remains controversial, although recent work suggests a pivotal role for arterial ammonia, whose effects appear to be potentiated by the presence of systemic inflammation. Recent work has also suggested the import of free radical formation occurring at a mitochondrial level as being the potential mediator of cellular dysfunction as opposed to ammonia per se. Treatment of such patients requires a multi-disciplinary approach incorporating both hepatology and critical care. In a significant proportion of such cases, consideration of liver transplantation may be required. Treatment should be focused at optimizing liver function and regenerative capacity and minimizing the inflammatory milieu. Controlled studies are lacking and much of the management has been extrapolated from neurocritical care. Sustained elevation of intracranial pressure may be responsive to mannitol or hypertonic saline bolus, and in those with hyperemia indomethacin has been reported as beneficial in case series. Recently, interest has developed into the use of cooling in the management of patients with acute liver failure and raised intracranial pressure. Animal studies support this treatment option as do case series, although randomized trials are still awaited."

thanks! makes sense - thanks for looking that up

 

[sjonies88]

I just took NBME 16 and I got this golgi trafficking question wrong by picking D (increased smooth endoplasmic reticulum) I think that its C, due to backing up of proteins in the RER -> dilation - problem with COPII. What do you think?

i put dilated and it didn't show up as wrong on my expanded feedback!

 

[THH]

For those who don't mind posting it, what was your # of incorrects and predicted 3 digit score?

 

[hello2]

It does say that an additional 200 were infected, but that should mean you remove the original 500. The correct answer was 200/2000, and I don't agree with this.

Incidence is new cases per defined time period / total susceptible population. If the 200 additional cases occurred within the same year, then it would be 700/2500. The question said that this was a year later though, so you're beginning with the same 2500 girls again. Whether they are immune should not matter, as there are other serotypes to be infected with, and I don't think it's correct to take those 500 original girls out of the equation because they could be reinfected with chlamydia.

Yea bad question, but nevertheless, I need to understand something: would getting infected with a different serotype of Chlamydia be the same as getting infected with antigenically shifted Influenza A? I know that shift causes resistance to treatment, whereas different serotypes are usually susceptible to the same treatment (at least for chlamydia, but not sure about other organisms), so then people who get infected with one strain of influenza A are still susceptible to re-infection with another strain that would require different treatment (i.e. a new vaccine), and therefore would be considered among the population of 'new infections' for calculation of incidence. But people who are chronically infected with chlamydia (different serotypes) would probably not be considered 'newly infected'. Just want to clarify this. Have yet to see an incidence question related to antigenic shift...probably because its not as big a deal as I'm making it, or something, I dunno

 

[Handinhand]

For those who don't mind posting it, what was your # of incorrects and predicted 3 digit score?

13 wrong, 3 digit score of 660 which correlates to a 262.

 

[1dayatatime]

can someone please help me settle this? test in <1 week now.

1. went through this forum and usmleforums and couldn't find a thorough or RIGHT answer on the q about the vocal cord position during swallowing, immed after laryngeal irritation, and coughing. i put closed open open and it was wrong but yet that's what the other forum said was right. someone on this thread wrote that they'd be CLOSED after laryngeal irritation, that doesn't make sense to me b/c wouldn't that trap the food in the wrong tube?

2. 20 yr old man that has been heavily drinking all weekend and took three doses of acetaminophen mon. morning at the onset of a severe headache. Increased risk of liver injury b/c of which of the following actions of ethanol?
(chronic alcohol is a p450 inducer but acute alcohol is a inhibitor and he seems like he binged so wtf...)

C. increased bioavailabily of acetaminophen
D.induction of p450 that activate acetaminophen to a hepatotoxic metabolite
E. Met. acidosis due to increased ratio of Nadh/Nad ratio.

3. 15 yr old female ingested Vit D in a suicide attempt. Follow up 1 month later show Ca [C] 10.4 (slightly elevated) What is the mechanism of increased Ca.

A. Decreased Excretion of Ca from GIT
B.Decreased osteoclast activity in bone
C.Increased absorption of ca in GIT
D.Increased 1 Hydroxylase activity in kidney
E.Increased Ostoblast activity in bone

ok so online forums say C which is kinda like duh, that's the MOA of vit d but i don't get why this would still be true a whole month later...wouldn't calcitonin have kicked in? How did you guys know that it was just basically asking the MOA of vit d and not get tripped up on the "1 month" thing?

Thanks in advance guys!!

 

[Handinhand]

can someone please help me settle this? test in <1 week now.

1. went through this forum and usmleforums and couldn't find a thorough or RIGHT answer on the q about the vocal cord position during swallowing, immed after laryngeal irritation, and coughing. i put closed open open and it was wrong but yet that's what the other forum said was right. someone on this thread wrote that they'd be CLOSED after laryngeal irritation, that doesn't make sense to me b/c wouldn't that trap the food in the wrong tube?

2. 20 yr old man that has been heavily drinking all weekend and took three doses of acetaminophen mon. morning at the onset of a severe headache. Increased risk of liver injury b/c of which of the following actions of ethanol?
(chronic alcohol is a p450 inducer but acute alcohol is a inhibitor and he seems like he binged so wtf...)

C. increased bioavailabily of acetaminophen
D.induction of p450 that activate acetaminophen to a hepatotoxic metabolite
E. Met. acidosis due to increased ratio of Nadh/Nad ratio.

3. 15 yr old female ingested Vit D in a suicide attempt. Follow up 1 month later show Ca [C] 10.4 (slightly elevated) What is the mechanism of increased Ca.

A. Decreased Excretion of Ca from GIT
B.Decreased osteoclast activity in bone
C.Increased absorption of ca in GIT
D.Increased 1 Hydroxylase activity in kidney
E.Increased Ostoblast activity in bone

ok so online forums say C which is kinda like duh, that's the MOA of vit d but i don't get why this would still be true a whole month later...wouldn't calcitonin have kicked in? How did you guys know that it was just basically asking the MOA of vit d and not get tripped up on the "1 month" thing?

Thanks in advance guys!!

1) It's a reflex. If something irritates your larynx, it's going to reflex spasm and close to prevent further material from entering the airway, and then you forcefully cough to expel the foreign object that's in your airway.

2) I too thought this question was BS. I put it induced because that's the only thing that makes sense, but I agree, first aid says that acute alcohol use is an inhibitor or p450s. Meh.

3) Remember that vitamin D supplements are inactivated, so you're still relying on your liver, and then your kidney (with activation via PTH -- key step) to turn it into 1,25-dihydroxy. If her parathyroids are working properly, you shouldn't see more than a slight elevation in Ca++ even with excess vitamin D. Beyond all that though, it was basically asking you what the mechanism is through which vitamin D increases Ca++ levels.

 

[4thQTHailMary]

I know it doesn't meet the criteria for chronic alcohol use, but I assumed that they wanted us to know that chronic use of alcohol induces the p450 metabolism of acetaminophen. I agree, poor question amongst many other poor questions. Just the name of the game with the NBME.

 

[1dayatatime]

Thank you guys and gl tomorrow Diggidy!

 

[AlmostAnMD]

I think I'm missing something on one of the questions here

The one with the drug experiment where you have blood pressure before and after drug injection
angiotensin II
Drug X
angiotensin II + Drug X

options are aldosterone receptor antagonist
angiotensin II converting enzyme inhibitor (wrong)
angiontensinogen inhibitor
partial agonist at angiotensin II receptors
renin inhibitor

I guess I'm just not seeing something. Why would my choice be wrong? The blood pressure went up a little bit...was it a partial agonist?

 

[notbobtrustme]

they inject both ATII and Drug X. even if drug X was an ACE-I, you are bypassing the block by putting ATII directly into the bloodstream. Hence, partial agonist because the site of action is the ATII receptor.

 

[AlmostAnMD]

Ooohhhhh I figured it was something simple I was missing >_> thanks!

 

[mt10eers2016]

I know it doesn't meet the criteria for chronic alcohol use, but I assumed that they wanted us to know that chronic use of alcohol induces the p450 metabolism of acetaminophen. I agree, poor question amongst many other poor questions. Just the name of the game with the NBME.

They may be looking for knowledge that when you are currently drunk/drinking CYP metabolism of other drugs is inhibited but after drinking, like in this question, the CYP system is induced to handle the large volumes of alcohol that were ingested. With an induced CYP system APAP gets metabolized to NAPQUI and thus can cause hepatic damage.

 

[step1murder]

Answers in quote.

3-12; I was thinking along the same lines and I chose D- increased SER and it was wrong

 

[Apoplexy__]

3-12; I was thinking along the same lines and I chose D- increased SER and it was wrong

Not sure what to say about this. Someone else replied to this post of mine you're quoting, but then another person said they put what I said and didn't have it in their incorrects. It's been too long since I took the NBME to really recall anything about the answer choices anymore, sorry.

 

[masterwolfie]

Gender is better than smoking, I guess. I put gender and it wasn't in my incorrects. I'm assuming you annotated the smoking risk factor thing from a UWorld Q, and I think that list of risk factors in UWorld is referring to risk factors among women.

Unfortunately, it's just one of those "this is a better answer than that" things, even if they're both very good.

Ah, I see - I should be more careful/specific when I annotate. Thanks, bruh!

 

[rcdamania]

Man who develops a temperature after running a 10-km race. The man temperature is going to return back to normal due to which of the following mechanisms?
a. central vasodialation
b. evap of sweat
c. increased minute ventilation
d. increased muscle tone
e. peripheral arteriolar vasoconstriction
f. peripheral venous vasoconstriction

 

[whotheheckcares]

......

 

[Apoplexy__]

Classic osteoporosis, so gender.

So gender, much wow, very doge.

Man who develops a temperature after running a 10-km race. The man temperature is going to return back to normal due to which of the following mechanisms?
a. central vasodialation
b. evap of sweat
c. increased minute ventilation
d. increased muscle tone
e. peripheral arteriolar vasoconstriction
f. peripheral venous vasoconstriction

Evap of sweat. Your only other consideration would be peripheral vessel vasodilation (dilating your SVC isn't going to change heat dissipation), but you see how they made sure that wasn't an option. Ventilation would only minorly contribute, and muscle tone is irrelevant.

Incidentally, I got this on my COMLEX real deal.

 

[Enzymes]

Dumb question, but there was a question where a blood in the stool test was going to replace colonscopy in order to detect colon cancer, but the doctor had a problem with doing that test. Is it because it has low sensitivity for detecting colon cancer? I put low specificity, just because I thought that many things can cause bleeding. But at the same time, it might not be very sensitive. Anyone know the answer to this one?

 

[Renaissance Man]

I kind of feel like this question stunk, but what is the biggest risk factor for pancreatic adenocarcinoma? Everywhere I look either just states all of the risk factors or gives conflicting info. I put down diabetes (which is wrong), so I am guessing it has to be smoking? Other choices were obesity, gallstone disease, and hypercalcemia. Thanks!

 

[Enzymes]

I kind of feel like this question stunk, but what is the biggest risk factor for pancreatic adenocarcinoma? Everywhere I look either just states all of the risk factors or gives conflicting info. I put down diabetes (which is wrong), so I am guessing it has to be smoking? Other choices were obesity, gallstone disease, and hypercalcemia. Thanks!

Yes smoking. Big time risk factor.

Smoking increases the risk of: larynx, pharynx, lung, renal/urothelial, cervical, and pancreas.

 

[scrappylemur]

Dumb question, but there was a question where a blood in the stool test was going to replace colonscopy in order to detect colon cancer, but the doctor had a problem with doing that test. Is it because it has low sensitivity for detecting colon cancer? I put low specificity, just because I thought that many things can cause bleeding. But at the same time, it might not be very sensitive. Anyone know the answer to this one?

The answer was sensitivity.

When concerned with cancer, you want the INITIAL TEST you give to have a high sensitivity. In other words, if the patient has cancer, a very serious disease, you want the test to have a high percent chance of catching it (the definition of sensitivity). A test with high sensitivity is good for RULING OUT a certain disease; if the test is negative, the patient very likely does not have a certain disease. FOBT is a bad test for screening for colon cancer because colon cancer can quite often occur without any bleeding, meaning the test is not very sensitive at catching it.

On the flip side, specificity is a good CONFIRMATORY TEST, for RULING IN cancer/disease. Since initial screening test have a high sensitivity to begin with (they catch a lot a people with disease because the threshold is lower), they naturally also catch a lot of false positives. To eliminate these, you want to give the high specificity test, where there is a higher threshold, making it more likely that any positive test is a true positive (meaning they really have the disease), and not a false positive.

 

[wonderbread12]

2) An animal study is conducted to assess the effects of smoking on pulmonary defense and maintenance mechanisms. For 1 week, normal
male rats are exposed to levels of cigarette smoke comparable to those encountered by humans who smoke cigarettes. Results of
pulmonary testing are compared with baseline levels obtained the week before the smoke exposure. Which of the following sets of changes
is most likely to be observed? Is everything low? smoking impairs mucocilliary clearance I know that much..

Mucus Production and Secretion up/down

Alveolar Macrophage Function up/down

Activity of Airway Cilia up/down


numero 2. should definitely be

Mucus Production and Secretion up

in response to cigarette smoke, combustible fumes and etc mucus production always increases. Just think of the reid index in chronic bronchitis, the submucosal mucous glands increase in size in response to cigarette smoke because they are secreting more mucous in order to clear all those nasty inhaled carcinogens

Alveolar Macrophage Function up

the inhaled carcinogens from cigarette smoke damage the lining of the alveoli. in response to this alveolar macrophages aggregate to clear up the mess

Activity of Airway Cilia down

this one should be easy. carcinogens in cigarette smoke destroy cilia cells lining the airway.

Listen to Dr. Sattar's lecture starting with obstructive pulmonary diseases. he explains all this really well. hope this helped

So up/down/up (mucus, cilia, macrophage) is not an option....someone suggested that it is all down but no one confirmed...do you (or anyone else) know what the correct ways the arrows should be going? Thanks!

***EDIT ...looks like it's supposed to be mucus up and cilia & macrophages both down

Can anyone explain? guess i am confused that the initially wouldn't the cilia and macrophages be going nuts to try and clear whatever the cigarette smoke is causing to accumulate?

 

[EazyE1907]

I googled it and really couldn't find anything relevant. Of the 2 research articles i skimmed they both say macrophages increase as well. The only other thing i found was that carcinogens inhibit macrophage ability to interact with TLR's and elicit a proper cell-mediated response against infection which would then lead to an increase risk of pneumonia/viral resp infections. So the only thing i can think of is that if they can't do, the macrophages will undergo apoptosis. So it would end up being mucous UP....cilia DOWN, as i explained above, and macrophages DOWN. this question is ******ed if that is the answer tho. Anyways, thats all i got man.

 

[thehundredthone]

Again, there's a discussion about macrophage function being diminished on page 4.

 

[elyswim]

I'm confused on this as well as Pathoma states that the cause of emphysema in smokers is because the macrophages cause inflammation of the lung tissue leading to destruction of the walls of the alveoli.

So up/down/up (mucus, cilia, macrophage) is not an option....someone suggested that it is all down but no one confirmed...do you (or anyone else) know what the correct ways the arrows should be going? Thanks!

***EDIT ...looks like it's supposed to be mucus up and cilia & macrophages both down

Can anyone explain? guess i am confused that the initially wouldn't the cilia and macrophages be going nuts to try and clear whatever the cigarette smoke is causing to accumulate?

 

[Bancrofti]

2) Are you sure you copied the wording of this question down right? The disease prevalence in heterozygous females would be zero because it's XR, not XD, but if you mean what is the diseased allele prevalence, then the carrier frequency would be 2pq, where p~1 because q=1E-5 (1/100,000) and p+q=1. So 2 x 1 x 1E-5 = 2E-5 = 1/50,000 = B.

Is there anyone who could explain this again? Or Phloston if you're still lurking these threads. Trying to do my last minute cramming before Friday and my brain does not want to comprehend this.

 

[thehundredthone]

What was the gist of the question? It has been removed from the OP.

 

[Bancrofti]

What was the gist of the question? It has been removed from the OP.

Basically it was an X-linked recessive disease. The frequency of the disease in males is 1/100,000. Question then asked what the frequency of heterozygous females was.

 

[thehundredthone]

Right. Since this is XR, the prevalence of affected males gives you q for the male population. This because males can only either be p or q (their Y chromosome is noncontributory). Remember that this same allele, however, also exists in the general population, and so q is the same even for females. In XR disorders, the frequency genotype of the male is equal to the diseased allele prevalence.

Now for females, the allele distribution is (p+q)^2 since females can be homozygous or heterozygous. So we have p^2 as homozygous dominant, q^2 as homozygous recessive (exceedingly rare) and 2pq as heterozygous.

The assumption we make is that given the rarity of the disease, p>>q, and p~1.

So with p~1 and q=1/100000, the heterozygous frequency becomes 2pq = 2/100000 = 1/50000.

If you want to look at it with very fuzzy logic, think of it this way. Homozygous recessive females are too rare to be considered in our equation (think about it, if a single diseased allele appears at a frequency of 1/100000, then the chance of both, by probability is the square of that number, which for all practical purposes is ~0). Hence all diseased males can be thought to have been born of heterozygous mothers. Given that the mother has 50% chance of passing down her recessive gene, there must be twice as many mothers, i.e. 1/50000. I strongly urge that you understand it based on the Hardy Weinberg equilibrium though.

The difference between XR and AR is that in AR diseases, the diseased frequency is q^2 even in males.

 

[Bancrofti]

Right. Since this is XR, the prevalence of affected males gives you q for the male population. This because males can only either be p or q (their Y chromosome is noncontributory). Remember that this same allele, however, also exists in the general population, and so q is the same even for females. In XR disorders, the frequency genotype of the male is equal to the diseased allele prevalence.

Now for females, the allele distribution is (p+q)^2 since females can be homozygous or heterozygous. So we have p^2 as homozygous dominant, q^2 as homozygous recessive (exceedingly rare) and 2pq as heterozygous.

The assumption we make is that given the rarity of the disease, p>>q, and p~1.

So with p~1 and q=1/100000, the heterozygous frequency becomes 2pq = 2/100000 = 1/50000.

If you want to look at it with very fuzzy logic, think of it this way. Homozygous recessive females are too rare to be considered in our equation (think about it, if a single diseased allele appears at a frequency of 1/100000, then the chance of both, by probability is the square of that number, which for all practical purposes is ~0). Hence all diseased males can be thought to have been born of heterozygous mothers. Given that the mother has 50% chance of passing down her recessive gene, there must be twice as many mothers, i.e. 1/50000. I strongly urge that you understand it based on the Hardy Weinberg equilibrium though.

The difference between XR and AR is that in AR diseases, the diseased frequency is q^2 even in males.

Thanks! When I haven't done genetics for a while, which is about every time I have to use this equation, I always forget how to properly apply the fact that "something" is essentially = 0 and something is essentially = 1. Great explanation, thanks again.

 

[ashokaramani]

I just took NBME 16 and I got this golgi trafficking question wrong by picking D (increased smooth endoplasmic reticulum) I think that its C, due to backing up of proteins in the RER -> dilation - problem with COPII. What do you think?
I cell disease is dilation so C is correct for this this question

 

[ashokaramani]

Answers in quote!

thanks. very good explaination

 

[SBR249]

Schizoaffective requires mood symptoms, there is none (patient doesn't really tick any of the SIGECAPS of depression nor does he have manic symptoms) in this patient so D is definitely out. Delusional disorder is not only ruled out because it's less than a month but also because delusional disorder is usually one fixed delusion with relatively intact function and reasoning otherwise. This patient has more symptoms than that and definitely is not at normal level of function. The patient has delusions (the voices) and possible hallucinations (the intruders), he also has disorganized behavior and the symptoms are less than a month in duration so it satisfies the criteria for brief psychotic disorder. The answer is B.

The way I look at brief psychotic disorder, schizophreniform disorder, and schizophrenia is that it's the exact same symptoms for all three except the duration of symptoms.

<1mo = brief psychosis
1-6mo = schizophreniform
>6mo = schizophrenia

The whole stress thing is really not that important. If anything, the presence of an identifiable stress would lead me to think about adjustment disorder in the context of mood symptoms or possibly acute stress disorder/PTSD though the symptoms would have to be more severe.

 

[egc2012]

Answers in quote.

Sorry if I'm missing something obvious, but could you explain how 3-12 is increased SER? Thanks in advance

 

[Montana]

I think I'm missing something on one of the questions here

The one with the drug experiment where you have blood pressure before and after drug injection
angiotensin II
Drug X
angiotensin II + Drug X

options are aldosterone receptor antagonist
angiotensin II converting enzyme inhibitor (wrong)
angiontensinogen inhibitor
partial agonist at angiotensin II receptors
renin inhibitor

I guess I'm just not seeing something. Why would my choice be wrong? The blood pressure went up a little bit...was it a partial agonist?

you are forgetting important information. u did the experiment and measure blood pressure before and after giving the drug. Drug X alone has an increase in blood pressure (ACEI does not have this effect). so it must be an agonist. when you use angiotensin + drug x pressure increases but not as much. wich means its probably drug x is probably a partial agonist. remember a partial agonist in the presence of a full agoinst works as an antagonist

 

[AlmostAnMD]

You may be correct

on the other hand, I took step 1 back in June and got a 239 on it, which I was quite happy with, and no longer care But hopefully you're helping out someone else who has trouble with that question.

 

[Montana]

You may be correct

on the other hand, I took step 1 back in June and got a 239 on it, which I was quite happy with, and no longer care But hopefully you're helping out someone else who has trouble with that question.

yeah did not see your post was dated in June. i took my nbme 16 this week so was goin trhu the answers. im glad you did great. best of luck

 

[T@k∂šhî]

It's A. Cant explain it well though.

Choice A
Nitrous oxide
- Has low blood and lipid solubility and thus:
- Fast Induction & Low Potency

Isoflurane
- ↑ Lipid and Blood solubility and thus:
- Slow Induction & High Potency

Blood
- ↑ Blood solubility = ↑ Blood/Gas partition coefficient = ↑ solubility = ↑ Gas required to saturate blood =
Slower onset of action.

*** Blood/Gas Partition Coefficient = Blood Solubility Indicator ***

 

[T@k∂šhî]

Hi everyone, all the comments have been super helpful so far! I have a few Q of my own.

1) Young man with left flank pain radiating to groin; tenderness in left flank and LLQ abdomen; mildly hypoactive bowel sounds and negative occult blood in stool.

I know the answer was speculated briefly above, but I was wondering if anyone knows the answer for sure. I narrowed it down to ureteral calculus and renal infarction (other choices being colon cancer, diverticulitis, epididymitis, torsion of testis - which none of this sounded like).

2) Old man who came in with difficulty sleeping since his wife's death 8 months ago. Wakes up early, cries thinking about her, etc; but still enjoys life with grandkids, remains active in community, etc. No suicidal ideation. Initial action?

Regular appt's to monitor patient
Neuropsych test
Sleep study
Antidepressant

Is it the first one? This patient doesn't quite sound like he has major depressive disorder...

3) Question about a man who has bullous pemphigoid: production of autoantibodies against which structure is causing sx?

Bullous pemphigoid antigen
Collagen type 7
Cystokeratin
Desmoplakin
Plakoglobin

Is the answer really obvious as "bullous pemphigoid antigen"? I thought collagen VII, desmoplakin, and plakoglobin were also components of desmosomes.

4) Middle aged man with 2 months of diarrhea and abd pain that's relieved temporarily with eating and antacids. Serum gastrin is 500 (normal 100) and gastric acid secretion is 80 (6-40). Most definitive treatment to decrease risk of complications?

Low protein diet
Antibiotics
Antihistamine
Section the vagus n to stomach
Surgically remove suspected tumor

I thought it was gastric ulcer caused by H pylori, but antibiotics wasn't correct

An 83-year-old man comes to the physician because of a 3-day history of painful blisters on his torso...
Histopathologic examination of a biopsy specimen from the affected area shows:
****subepidermal blister****
Production of autoantibodies directed against which of the following structures best explains the findings in this patient?
Choice A
A) Bullous pemphigoid antigen
- Sub-Epidermal Blisters
- Hemidesmosomes
- Epidermal basement membrane
- Spares Oral Mucosa
B) Collagen Type VII
- Epidermolysis bullosa acquisita
C) Cytokeratin
- Participate in maintaining the structural integrity of cells
D) Desmoplakin
- Paraneoplastic pemphigus antigen
E) Plakoglobin
- Pemphigus vulgaris antigen
- Supra-Basal Blisters
- Desmosomes
- Affects Oral Mucosa
- Plakoglobin binding by human Desmoglein 3 & 1

 

[ok]

just a question
if there is a pdf with all QA combined for #16?
thank you

 

[Wolverine2410]

I don't think anybody has answered 1-33 yet. I got it right, and I think it's Charcot-Marie-Tooth disease (defective production of myelin and associated with scoliosis, foot deformities -- it says high or flat arches in FA, but I remember learning "hammer toes" as a buzzword). I can't remember what the exact answer options are, but I put down something to do with defective myelin (probably the Schwann cells that you mentioned).

Also, maybe this is a basic/obvious question because nobody seems to have asked about it yet, but I can't figure out the woman with anemia:

2-14: 38 yo woman comes to physician for pre-employment exam; she has no history of serious illness; she takes no meds; her vitals are normal; PE shows no abnormalities
Lab studies show: Hb 8.2, Hct 25%, MCV 69, leukocytes 5900, retic 0.8%, platelets 350K

Most likely DX = ?
Aplastic anemia
Iron-deficiency
Sickle cell
B-thal minor
B12 deficiency

So I was between iron deficiency and B-thal minor, and went with B-thal because people are usually asymptomatic and it was wrong; what am I missing here??

Patients with B-thal minor are asymptomatic AND lab tests are normal