NBME 13 discussion

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Are we allowed to talk about this topic? There's a NBME 12 discussion that has a lot of full questions posted but there are sticky posts that seem to say don't talk about the NBMEs. Thank you for any clarification!

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Just one more thing to clarify. Correct me if my concept is wrong..I have enumerated them for better explanation

1-Polyadenylation SIGNAL is present at the end of every gene, i.e at the 5' end of the Template strand (corresponding to the 3' end of the Coding strand) .
2-And thereby its also present on the 3' end of the mRNA (i.e its transcribed)
3-Its sequence is AATAAA (and AAUAAA for mRNA) with respect to 'CODING STRAND'.
4-There are no anticodons for it, but this signal is somehow interpreted in the nucleus to add 200 Adenine resides at the 3'end of the mRNA
5-And I assume that the stop codon(AUG,UAA,UAG) for the gene is supposed to be BEFORE this signal on the template strand(i.e 5'end), and this signifies the ribosome to detach. [i.e the stop codons are transcribed but not translated]

Hence, to rephrase the question, if there is a point mutation in a sequence 3' to the coding region in which AATAAA is converted to AACAAA there will be a decrease in mRNA amount. In short, mutation in 3'end of coding strand->mutation in 3' end of mRNA

The polyadenylation signal won't be recognized, and polyadenylation won't take place..the mRNA transcript hence can't exist the nucleus. I.e the first error will be no polyadenylation, and the 2nd consequence will be inability to exit the nucleus.

Did I get this right?

6. Also, one more confusing thing. I know how translation stops (by ribosome coming across a Stop codon). How does DNA transcription or DNA replication stop at the end of a gene?
 
42 year old man presents with 4 week history of muscle pain. Patient started simvastatin 2 months ago and gemfibrozil 4 weeks ago. The patient's myalgia is due to which of the following effects gemfibrozil has on simvastatin?

A- Decreased bioavailability
B- Increased absorption
C- Inhibition of cytochrome p450
D- Inhibition of hepatic glycosylation
E- Inhibiton of hepatic sulfation

"There are several theories explaining the increased risk of muscle toxicity
when statins and fibrates are combined. These include additive effects of statins and
fibrates on skeletal muscle resulting in the increased risk, displaced protein binding (all
statins are highly protein bound), and finally, inhibition of a recently recognized mode of
statin metabolism via glucuronidation. Gemfibrozil and fenofibrate both undergo
glucuronide-mediated metabolism. In two in-vitro studies using human and dog
hepatocytes, the glucuronide mediated-metabolism of atorvastatin acid, simvastatin acid,
cerivastatin acid and rosuvastatin acid were all inhibited by gemfibrozil."

http://www.pbm.va.gov/Safety Reports/87ry38statin-fibrate-Final.pdf

It's competitive inhibition of phase II conjugation, of which you should pick from sulfation or glucuronidation (not glycosylation).

Acetaminophen also undergoes sulfation and glucuronidation. CYP450 2E1 will conjugate it into toxic NAPQI too at high concentration (treat with glutathion / NACysteine)


I got this one right on my test and i put, C. inhibition of P-450. this was also addressed earlier in the thread. not sure why about fibrates though. statins are metabolized via P-450 so this makes sense.
 
Great explanation. Thanks for this.

yeah i agree, that was very helpful. for some reason i thought it was referring to there being 3 alleles. the p53 gene, m allele (of a random gene) and n allele (of a random gene). i thought it was referring to how all of the genes were linked together (ie on the same chromosome). didn't realize they meant the m and n allele were two different p53 alleles.

man its scary though, if you ever asked me if i would miss a question on the loss of heterozygosity concept, i would have bet money that i had it down lol.

Yeah, I agree especially because of the other answer choices. I flagged that question and spent about 5 minutes trying to rule out hepatic encephalopathy and some other answer choice along with AVM. In the back of my mind, I knew it was AVM because I had seen that picture before during first year, but I ended up picking something else. Looked it up later and it was a classic description for AVM.

it is in the temporal lobe though right? i went back to look at that question and other than the picture, don't see any hints of it being an AVM, other than the picture itself.

i guess unless hsv encephalitis wouldn't normally cause seizures... i assumed it could, but if it can't, that should have been another tip off
 
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1: Intrinsic factor
2: A
3: Amphetamine ( his symptoms )
4: yes cardiovascular disease

3: is incorrect. the answer is not amphetamines, it is heroin. i got it right on my test. here is a basic concept to keep in mind when doing these types of questions....

withdrawal: presentation with opposite signs of whatever the drug is. the baby is now out of the womb, no longer exposed to opioids that the mom was taking. therefore you get a rebound type effect where you present with the opposite symptoms of opium. irritable, frantic, overreacting to stimuli around him and easily started. i.e. no longer chilled out like he would be on opioids. give that baby a tinge opium!

only in overdose-esque situations do you see symptoms of the actual drug.

simple concept, keep it in mind. it works everytime.

for reference, the question was:
1-21: A male newborn was delivered at 38 weeks gestation following an uncomplicated pregancy. 12 hours later, he begins sucking frantically and crying inconsolably. He overreacts to stimuli around him and has a marked startle response. Symptoms slowly resolve over the next 2-3 weeks. The most likely explanation for these symptoms is maternal use of which of the following substances during pregnancy?
a)alcohol
b)heroin
c)LSD
d)marijuana
e)psilocybin
 
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it is in the temporal lobe though right? i went back to look at that question and other than the picture, don't see any hints of it being an AVM, other than the picture itself.

i guess unless hsv encephalitis wouldn't normally cause seizures... i assumed it could, but if it can't, that should have been another tip off

Yeah, the picture was a dead giveaway (DEAAAD GIVEAWAY!), but Wikipedia says that AVM is usually asymptomatic OR causes a huge list of symptoms, but it is usually found incidentally on autopsy, which was exactly what happened according to the question stem. AVM was the best answer. I accidentally wrote "hepatic encephalopathy" instead of HSV encephalitis in my response. I think I was in another thread before typing that haha. HSV encephalitis does cause seizures, and that's why I couldn't rule it out at first. I picked something else. I think it was liquefactive necrosis or ischemic necrosis or something.
 
6. Also, one more confusing thing. I know how translation stops (by ribosome coming across a Stop codon). How does DNA transcription or DNA replication stop at the end of a gene?

for transcription:

prokaryotes - there's two ways. a rho dependent and a rho independent mechanism. for rho dependent you have the rho factor (rf). when the new RNA is made from transcription, it comes and binds to the RNA. it moves up the RNA to where the rna polymerase has stopped, and knocks it off the tracks.

in rho independent, once the RNA has been made, towards the end you get a GC rich region, which is in the shape of a stem-loop structure. after this there are 6-8 (iirc) U residues. these two features help push the new rna made from the dna.


eukaryotes - i assumed that once the capping, splicing, and poly-adenylation is added, it just gets pushed out, and starts translation. i don't think there's really any stopping point when it comes to eukaryotic transcription...maybe somebody could correct me
 
for transcription:

prokaryotes - there's two ways. a rho dependent and a rho independent mechanism. for rho dependent you have the rho factor (rf). when the new RNA is made from transcription, it comes and binds to the RNA. it moves up the RNA to where the rna polymerase has stopped, and knocks it off the tracks.

in rho independent, once the RNA has been made, towards the end you get a GC rich region, which is in the shape of a stem-loop structure. after this there are 6-8 (iirc) U residues. these two features help push the new rna made from the dna.


eukaryotes - i assumed that once the capping, splicing, and poly-adenylation is added, it just gets pushed out, and starts translation. i don't think there's really any stopping point when it comes to eukaryotic transcription...maybe somebody could correct me

Haha holy crap, you just brought me back to my undergrad days with that rho factor BS. Good times.
 
Can someone explain the question about metastatic melanoma that is somehow selectively blocked from metastasizing to the liver?

people on here say the answer is "homing" but i dont even know what that means.

i chose invasion. if you have an antibody to the liver cell surface receptor that the metastatic cells would normally bind to, you would prevent invasion of those cells into the liver. obviously this is wrong, but this is how i thought about it.
 
3: is incorrect. the answer is not amphetamines, it is heroin. i got it right on my test. here is a basic concept to keep in mind when doing these types of questions....

withdrawal: presentation with opposite signs of whatever the drug is. the baby is now out of the womb, no longer exposed to opioids that the mom was taking. therefore you get a rebound type effect where you present with the opposite symptoms of opium. irritable, frantic, overreacting to stimuli around him and easily started. i.e. no longer chilled out like he would be on opioids. give that baby a tinge opium!

only in overdose-esque situations do you see symptoms of the actual drug.

simple concept, keep it in mind. it works everytime.

for reference, the question was:
1-21: A male newborn was delivered at 38 weeks gestation following an uncomplicated pregancy. 12 hours later, he begins sucking frantically and crying inconsolably. He overreacts to stimuli around him and has a marked startle response. Symptoms slowly resolve over the next 2-3 weeks. The most likely explanation for these symptoms is maternal use of which of the following substances during pregnancy?
a)alcohol
b)heroin
c)LSD
d)marijuana
e)psilocybin

i guess i just didn't know that opioid withdrawal presented with a marked startle response, overreaction to stimuli, etc.

the only opioid withdrawal symptoms i know are related to "cold turkey" and "flu-like symptoms"

any other hints on how to have reasoned this out?

EDIT: if there really isn't any other way, i definitely understand. marijauna also presents with irritability which is why i was confused. i also even considered that it might be that the newborn is still somehow intoxicated from marijuana and that the "sucking frantically" could be related to an increased appetite? lol
 
Basically, homing means where a tumor will go and 'plant' itself. That is the 'seed and soil theory'. I.e tumors go to 'specific' sites because of some specific receptor/tissue interaction, and then they implant there. I like to think it this way : tumors are very picky! They go to some organs, not all, depending on the receptor type they like.

So, if you blocked the receptors of liver, they are unable to bind to it, and hence implant. Its not invasion, since if they are able to metastatize, by definition, they are already invading. Also, if you somehow prevented invasion, there won't be any metastasis to any sites. But we know from the question that it did metastatize to the other 2 organs.

Although I don't completely agree with the 'seed and soil' theory, it helps to explain this phenomenon at least...
 
Also, what about the paint thinner question? i randomly guessed alcohol dehydrogenase, but have no idea what is found in paint thinner...
 
Basically, homing means where a tumor will go and 'plant' itself. That is the 'seed and soil theory'. I.e tumors go to 'specific' sites because of some specific receptor/tissue interaction, and then they implant there. I like to think it this way : tumors are very picky! They go to some organs, not all, depending on the receptor type they like.

So, if you blocked the receptors of liver, they are unable to bind to it, and hence implant. Its not invasion, since if they are able to metastatize, by definition, they are already invading. Also, if you somehow prevented invasion, there won't be any metastasis to any sites. But we know from the question that it did metastatize to the other 2 organs.

Although I don't completely agree with the 'seed and soil' theory, it helps to explain this phenomenon at least...

wow thanks for the explanation! you seem like you really know your stuff, i'm sure you will do great :)
 
Paint thinner have Methanol. This guy was going blind. Remember "I drunk MEself blind...."

Basically, the problem is not methanol. Its metabolism of Methanol. For any alcohol this is the path:

Alcohol----(Alcohol Dehydrogenase)----->Aldehyde-----(Aldehyde dehydrogenase)------>Acetate

The brackets show the respected enzyme catalyzing the reaction.

In the case of Methanol:

Methanol----(Alcohol Dehydrogenase)--->Formaldehde----(Aldehyde Dehydrogenase)---->Formic acid

I.e you are making forlmaldehyde in your liver! The same chemical use to preserve cadavers!!!!! So that is the main culprit. Hence, you block alchohol dehydrogenase, by FOMIPEZOL...

Forgot to mention: The same logic applies for using Fomipezol for Ethylene Glycol poisoning. In that case, the culprit is Oxalate, which causes Renal failure
 
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Also, what about the paint thinner question? i randomly guessed alcohol dehydrogenase, but have no idea what is found in paint thinner...

Methanol I think. Poor people around here sometimes ingest it by mixing it up with other alcohols because its cheap and easily available, that way you get more bang for your buck. If you dont mix it with enough ethanol, you'll get methanol toxicity.
 
i guess i just didn't know that opioid withdrawal presented with a marked startle response, overreaction to stimuli, etc.

the only opioid withdrawal symptoms i know are related to "cold turkey" and "flu-like symptoms"

any other hints on how to have reasoned this out?

EDIT: if there really isn't any other way, i definitely understand. marijauna also presents with irritability which is why i was confused. i also even considered that it might be that the newborn is still somehow intoxicated from marijuana and that the "sucking frantically" could be related to an increased appetite? lol
hint on how to reason it out, firstly, look at the logic i explained about withdrawal v. overdose. whenever one is in withdrawal, they are experiencing the opposite of the symptoms. you don't need to know exactly how withdrawal from a drug is presented (they could present the symptoms in a variety of ways, dont be fooled. think it out). you need to know what the drug does, then think of the person experiencing the opposite. if you need to, write out the effects of a drug then next to each symptom, write down the opposite.

secondly, think of real life situations. have you ever heard of a baby having really bad effects from marijuana? have you ever seen a friend or someone who smoked marijuana have those types of effects when they weren't taking the drug? yes okay, maybe a little irritable, but it's known that there is no actual physical dependence on marijuana, just a mental one. also, i've found that marijuana is usually never the answer to these drug questions if the symptoms are intense/severe. marijuana is a relatively mild drug compared to the rest (euphoria, giggling, increased appetite, slowing of time, anxiety, dry mouth).
 
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Opioids hit Gi coupled receptors. This lowers NE levels (explains miosis). Your body upregulates adrenergic receptors in response. Take opioids away, you have sympathetic overload. That's the rationale for giving clonidine to ease withdrawal
 
i thought opioids hit mu receptors- open K+ channels, close Ca+ and then you get decreased synaptic transmission. are those Gi coupled receptors? edit: just looked it up, i guess they are kind of. couldn't figure out how to delete my comment though.

definitely spot on with the up regulation of adrenergic receptors.
 
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Phew. Just got done reading the thread. Overall not too bad, although my score didn't go up a whole lot, I felt like the questions I missed were just simple trivia that I'll have in my short term memory by the 10th.

One question that's been bugging me, and I brought this up in the complicated concepts thread but now I've finally run into a question about it. Why in the world does MPO deficiency has milder symptoms than CGD? It seems like the HOCl is what kills the bacteria (at least in the First Aid respiratory burst diagram), which is the big loss in MPO deficiency.

Does the superoxide radical and/or hydrogen peroxide also kill bacteria along the way? If so, that FA diagram is mad confusing.
 
Phew. Just got done reading the thread. Overall not too bad, although my score didn't go up a whole lot, I felt like the questions I missed were just simple trivia that I'll have in my short term memory by the 10th.

One question that's been bugging me, and I brought this up in the complicated concepts thread but now I've finally run into a question about it. Why in the world does MPO deficiency has milder symptoms than CGD? It seems like the HOCl is what kills the bacteria (at least in the First Aid respiratory burst diagram), which is the big loss in MPO deficiency.

Does the superoxide radical and/or hydrogen peroxide also kill bacteria along the way? If so, that FA diagram is mad confusing.

Myloperoxidase uses H2O2 from the NADPH oxidase reaction to produce HOCl. Theres definitely plenty of killing power from H2O2 and production of other radicals, so the killing deficiency that results from CGD would be greater.
 
3: is incorrect. the answer is not amphetamines, it is heroin. i got it right on my test. here is a basic concept to keep in mind when doing these types of questions....

withdrawal: presentation with opposite signs of whatever the drug is. the baby is now out of the womb, no longer exposed to opioids that the mom was taking. therefore you get a rebound type effect where you present with the opposite symptoms of opium. irritable, frantic, overreacting to stimuli around him and easily started. i.e. no longer chilled out like he would be on opioids. give that baby a tinge opium!

only in overdose-esque situations do you see symptoms of the actual drug.

simple concept, keep it in mind. it works everytime.

for reference, the question was:
1-21: A male newborn was delivered at 38 weeks gestation following an uncomplicated pregancy. 12 hours later, he begins sucking frantically and crying inconsolably. He overreacts to stimuli around him and has a marked startle response. Symptoms slowly resolve over the next 2-3 weeks. The most likely explanation for these symptoms is maternal use of which of the following substances during pregnancy?
a)alcohol
b)heroin
c)LSD
d)marijuana
e)psilocybin

you're talking about a different question.
 
A 52-year-old man comes to the physician because of a 3-month history of epigastric abdominal pain; he also has had an unintentional 6.8-kg (15-lb) weight loss during this period. He has osteoarthritis treated with naproxen as needed. He has immigrated to the UsA from Japan 6 months ago. He eats mostly traditional Japanese food prepared by his wife. He has smoked 2 packs of cigarettes daily for 30 years and drinks three to four glasses of wine daily. He is 170 cm (5 ft 7 in) tall and now weighs 82 kg (180 lb); BMI is 28 kg/m^2. Physical examination shows epigastric tenderness. Upper gastrointestinal endoscopy shows a 4-cm ulcer in the stomach. Examination of a biopsy specimen of the lesion confirms adenocarcinoma. Which of the following is the strongest predisposing risk factor for the patient's condition?
A. Alcohol use
B. Diet
C. Ethnicity
D. Naproxen
E. Tobacco use

I want to talk about this question again. I looked at some of the posts in this thread and they said B. But nitroso compound would cause squamous carcinoma right? Wouldn't it tobacco use then?

edit: I looked it up, smoked foods do cause adenocarcinoma.. but how on earth are we supposed to know that smoked foods are a greater risk factor than smoking (which is always the greatest risk factor in everything lol)

i 100% completely agree with where you're coming from. i thought B, C, and E are all good answer choices for potential risk factors for the adenocarcinoma. even looking in pathoma he just lists that these are the potential risk factors, but never specifies that one is more superior than the other.

This is what Goljan has to say about it...

53wuuww.png
 
I also had this one wrong. marked smoking. The answer seems to be diet. They are both very good answers, and in my opinion, a very cruel way to ask for it, since the guy has all of the above.

But I guess they just wanted to test the fact that japanese people have very high incidence of gastric carcinoma, and it is not because they are japanese, but because of their very special diet. So even if the guy is in USA, he only has 6 months living there, and he keeps eating traditional japanese foods, So that its his greatest risk. If he came from older generations of japanese immigrants in the USA, or if he avoided japanese traditional food, then diet would not be the highest risk factor.

an article talking about japanese food intake, risk of gastric carcinoma, and how it decreases when they immigrate.
http://pmj.bmj.com/content/81/957/419.full
 
A 52-year-old man comes to the physician because of a 3-month history of epigastric abdominal pain; he also has had an unintentional 6.8-kg (15-lb) weight loss during this period. He has osteoarthritis treated with naproxen as needed. He has immigrated to the UsA from Japan 6 months ago. He eats mostly traditional Japanese food prepared by his wife. He has smoked 2 packs of cigarettes daily for 30 years and drinks three to four glasses of wine daily. He is 170 cm (5 ft 7 in) tall and now weighs 82 kg (180 lb); BMI is 28 kg/m^2. Physical examination shows epigastric tenderness. Upper gastrointestinal endoscopy shows a 4-cm ulcer in the stomach. Examination of a biopsy specimen of the lesion confirms adenocarcinoma. Which of the following is the strongest predisposing risk factor for the patient's condition?
A. Alcohol use
B. Diet
C. Ethnicity
D. Naproxen
E. Tobacco use

I want to talk about this question again. I looked at some of the posts in this thread and they said B. But nitroso compound would cause squamous carcinoma right? Wouldn't it tobacco use then?

edit: I looked it up, smoked foods do cause adenocarcinoma.. but how on earth are we supposed to know that smoked foods are a greater risk factor than smoking (which is always the greatest risk factor in everything lol)

edit2: i had it written in my notes that nitroso compounds (smoked foods, right?) cause SCC. i got that from Uworld question ID 122... this would especially make it seem liek the answer is tobacco use

I think you might be confusing gastric cancer and esophageal cancer. For boards purposes, gastric cancer is almost always adenocarcinoma. Esophageal cancer, however, can be adenocarcinoma or squamous cell carcinoma. The risk factors for gastric cancer (H. pylori, nitrosamines, chronic gastritis, Type A blood, etc) all refer to adenocarcinoma. If you see a Japanese male with stomach cancer, it's most likely going to be adenocarcinoma, with smoked foods as a risk factor.

On the other hand, the risk factors for esophageal cancer vary depending on adenocarcinoma or squamous cell carcinoma.
The major risk factors for squamous cell carcinoma of the esophagus include smoking (most important), alcohol, and nitrosamines (this is probably what you were thinking about). Other risk factors include achalasia, Zenker's diverticuli, esophageal webs, and hot liquids (i.e. tea).
The major risk factors of adenocarcinoma are GERD & Barrett's esophagus. Other risk factors include obesity & chewing tobacco.
 
I think you might be confusing gastric cancer and esophageal cancer. For boards purposes, gastric cancer is almost always adenocarcinoma. Esophageal cancer, however, can be adenocarcinoma or squamous cell carcinoma. The risk factors for gastric cancer (H. pylori, nitrosamines, chronic gastritis, Type A blood, etc) all refer to adenocarcinoma. If you see a Japanese male with stomach cancer, it's most likely going to be adenocarcinoma, with smoked foods as a risk factor.

On the other hand, the risk factors for esophageal cancer vary depending on adenocarcinoma or squamous cell carcinoma.
The major risk factors for squamous cell carcinoma of the esophagus include smoking (most important), alcohol, and nitrosamines (this is probably what you were thinking about). Other risk factors include achalasia, Zenker's diverticuli, esophageal webs, and hot liquids (i.e. tea).
The major risk factors of adenocarcinoma are GERD & Barrett's esophagus. Other risk factors include obesity & chewing tobacco.

oh wow yeah you are right. is smoking a risk factor for gastric adenocarcinoma?

also, is it the "epigastric" pain that would make you think stomach instead of esophagous?
 
oh wow yeah you are right. is smoking a risk factor for gastric adenocarcinoma?

also, is it the "epigastric" pain that would make you think stomach instead of esophagous?

As far as I know smoking is not a major risk factor for gastic adenocarcinoma.
The question stem tells you they found "a 4-cm ulcer in the stomach," so you don't really need to worry about epgastric pain. But yes, epigastric pain would make you lean more towards gastric cancer than esophageal. For esophageal cancer you want to think more along the lines of dysphagia, hematemesis, and weight loss, though pain is definitely part of it as well.
 
I can't remember off the top of my head, but there was a question asking about what happens when taking HIV protease inhibitors, and the answer was that the virus will "lack a mature core". Here's the thing- I thought the protease cleaves gp160 into its 2 active envelope proteins for attachment and fusion. There was an answer choice that read "In the presence of a protease inhibitor, the virus cannot bind to host cells" which seems like the exact mechanism of protease inhibitors, yet for some reason was "less" correct, I guess. Anybody remember that one/able to explain why?
 
I can't remember off the top of my head, but there was a question asking about what happens when taking HIV protease inhibitors, and the answer was that the virus will "lack a mature core". Here's the thing- I thought the protease cleaves gp160 into its 2 active envelope proteins for attachment and fusion. There was an answer choice that read "In the presence of a protease inhibitor, the virus cannot bind to host cells" which seems like the exact mechanism of protease inhibitors, yet for some reason was "less" correct, I guess. Anybody remember that one/able to explain why?

I do not remember the question, but I guess it is because the protease is more important for capsid and core structures which are mainly proteins. While the gp molecules are glycoproteins, and other HIV drug's mechanism of action would better explain an effect on the gp molecules, like the fusion inhbitors.

I do not have a direct answer for your question though, but it is true that a lot of questions have more than 1 answer, but 1 fits better.
 
Ah yes. You can also see in the question stem, they ask, how would you know it would be working SPECIFICALLY as a protease inhibitor. So lack of mature core is the most appropriate answer
 
So....apparently the answer for the first question is Ovarian Ligament? How does that work? The ovarian ligament attaches to the fundus of the uterus and is no where near the cervix, nor does it continue posterior? I feel like this is really simple and I can't wrap my head around it...
 
I know an answer to this has been posted, but I was hoping on a clarification. I chose A at first as well (correct answer), but I changed it to E. If there's a blood flow obstruction, ventilation/perfusion ratio approaches affinity, so if embolus was in lower lung, they'd be a increased V/Q ratio at the base compared to the apex. Normally, the apex has a higher V/Q ratio then the base, b/c the high alveolar pressure in the apex is higher then the arterial pressure, which impedes blood flow. This is the reason I changed my answer from A, because I thought "absence of perfusion in some areas that are ventilated" is a normal finding at the apex of the lung.


A 63-year-old man comes to the emergency department 30 minutes after the sudden onset of right-sided chest pain and shortness of breath that began after a 10-hour drive in his truck. The pain is more severe with inspiration. He does not smoke cigarettes. His pulse is 110/min, and respirations are 32/min. The lungs are clear to auscultation. Which of the following findings is most likely on ventilation-perfusion lung scans?
A) Absence of perfusion in some areas that are ventilated
B) Absence of ventilation in some areas that are perfused
C) Absence of ventilation-perfusion mismatching
D) Decreased perfusion gradient from the apices to the bases of the lungs
E) Increased ventilation-perfusion ratios at lung bases compared with those at the apices

The whole lung is normally perfused. A good rule of thumb is if you have 2 options that seem right and option 1 is a-->b such as a clot causing decrease in perfusion rather than a-->b-->c(in certain spots)--> d, then you're better of choosing option 1. Also, it said most likely, not which is possible. You way over thought this one.
 
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I know an answer to this has been posted, but I was hoping on a clarification. I chose A at first as well (correct answer), but I changed it to E. If there's a blood flow obstruction, ventilation/perfusion ratio approaches affinity, so if embolus was in lower lung, they'd be a increased V/Q ratio at the base compared to the apex. Normally, the apex has a higher V/Q ratio then the base, b/c the high alveolar pressure in the apex is higher then the arterial pressure, which impedes blood flow. This is the reason I changed my answer from A, because I thought "absence of perfusion in some areas that are ventilated" is a normal finding at the apex of the lung.


A 63-year-old man comes to the emergency department 30 minutes after the sudden onset of right-sided chest pain and shortness of breath that began after a 10-hour drive in his truck. The pain is more severe with inspiration. He does not smoke cigarettes. His pulse is 110/min, and respirations are 32/min. The lungs are clear to auscultation. Which of the following findings is most likely on ventilation-perfusion lung scans?
A) Absence of perfusion in some areas that are ventilated
B) Absence of ventilation in some areas that are perfused
C) Absence of ventilation-perfusion mismatching
D) Decreased perfusion gradient from the apices to the bases of the lungs
E) Increased ventilation-perfusion ratios at lung bases compared with those at the apices
You also can't assume that the entire bottom of both lungs has had a PE, which would be what choice E is saying. In fact, the PE would most likely be in just one lung (right or left), whereas the other lung would have normal V/Q ratios, so that's why you can eliminate choice E. And to reiterate what was just said, even though the top of the lung has a lower V/Q ratio, there still is a good amount of ventilation there. The ventilation is relatively uniform through the whole lung, its more the amount of blood flow that changes from top to bottom in a healthy lung.
 
I didn't like the question talking about pulmonary embolism and what happens with ventilation-perfusion. THe answer was ventilating areas of no perfusion, but isn't there a compensatory reaction here where the ventilation will decrease? Kinda tricky for no reason.
 
Maybe overall ventilation would decrease, but you would still get some ventilation to the areas where perfusion is completely blocked by the embolus.

But yeah I hate almost all step 1 questions. It feels like they all have one or two things that are confusing so you always feel like you are guessing.
 
Actually, during a PE, ventilation will increase. At least that is how I get it, since the arterial BG will show respiratory alkalosis. I can't remember what i chose for that question, but answer A seems to be the most accurate.
 
Is this NBME known to be notoriously difficult? I took NBME 12 two weeks ago and got a 252 and then took this one today and got a 252. I'm happy with the score regardless but just seems like I wasted my time for the past 2 weeks if I'm not making any progress haha.

Also I have a friend who scored the same as me on NBME 12 and scored a 260 on NBME 7. I thought all of the NBME's were supposed to be curved so that your score stays roughly the same. The only reason I could possibly see the earlier ones being easier is because they've been around for longer so I would assume that a lot of the study material (FA, pathoma, etc) has included the topics on that exam in their material. Glad to see what others think of this.
 
32 yo woman unable to conceive. Husband's fine. Regular 28 day menses, BP 110/70, normal pelvic and abdominal exams, normal hormone levels. First choice for infertility?

Bromocriptine
Clomiphene
Diethylstilbesterol
Ethinyl estradiol
Medroxyprogesterone

Bromocriptine - doubt she has prolactinoma bc she has normal menses
Clomiphene – stimulates ovulation, but she has normal menses, which almost always means she's ovulating, right?
DES causes clear cell adenocarcinoma in female fetuses, so I don’t wanna give that
Medroxyprogesterone this decreases LH surge, preventing ovulation?
Ethinyl estradiol isn’t this in OCPs?
 
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32 yo woman unable to conceive. Husband's fine. Regular 28 day menses, BP 110/70, normal pelvic and abdominal exams, normal hormone levels. First choice for infertility?

Bromocriptine
Clomiphene
Diethylstilbesterol
Ethinyl estradiol
Medroxyprogesterone

Bromocriptine - doubt she has prolactinoma bc she has normal menses
Clomiphene – stimulates ovulation, but she has normal menses, which almost always means she's ovulating, right?
DES causes clear cell adenocarcinoma in female fetuses, so I don’t wanna give that
Medroxyprogesterone this decreases LH surge, preventing ovulation?
Ethinyl estradiol isn’t this in OCPs?


I missed that same question and I remember reading somewhere (Kaplan I think) that often times when people have regular mensus but can't get pregnant it's because they aren't producing enough progesterone to maintain the hCG and progesterone or something so you should supplement with progesterone so I put progesterone. I also assumed that because she had 28 day cycles that she was ovulating regularly and no benefit in clomiphene but I guess clomiphene is the right answer :confused:
 
I missed that same question and I remember reading somewhere (Kaplan I think) that often times when people have regular mensus but can't get pregnant it's because they aren't producing enough progesterone to maintain the hCG and progesterone or something so you should supplement with progesterone so I put progesterone. I also assumed that because she had 28 day cycles that she was ovulating regularly and no benefit in clomiphene but I guess clomiphene is the right answer :confused:

Here is what I have in my notes:

Hypogonadotrophic anovulation: Use GnRH (like Leuprolide).
Normogonadrophic anovulation: Use Clompihene (bloks negative feedback on the pituitary and will lead to increased FSH and LH).

I think this woman has normogonadotrophic anovulation, because she has normal menses. So use clomiphene.

Besides, among the other answers, DES and bromocriptine can be easily excluded, and I've never seen any of the other drugs being used for increasing fertility, as a matter of fact, they all sound like drugs that you would use as contraceptive pills.
 
Thanks! Nice to see a Lima person on here. I lived in Miraflores for a month and loved it, Lima's a great city.
 
Infant born at 38 weeks starts sucking frantically and inconsolably crying at 12 hours. Heightened startle reflex, over-responsive to stimuli. Symptoms resolve in 2-3 weeks. What was mom abusing?

Alcohol
LSD
Heroin
Marijuana
Psilocybin (???)
 
Infant born at 38 weeks starts sucking frantically and inconsolably crying at 12 hours. Heightened startle reflex, over-responsive to stimuli. Symptoms resolve in 2-3 weeks. What was mom abusing?

Alcohol
LSD
Heroin
Marijuana
Psilocybin (???)

It's heroin. Baby is born addicted and then is in withdrawal bc symptoms begin at 12 hours and is hyperactive which would happen after withdrawing from a depressant.
 
Question on the 6 yo presenting with Tanner stage 2, and asked what percentile he would be if left untreated. Not even sure what disease they are trying to get at...assume his height/etc would be higher than normal? Any help would be awesome!
 
Question on the 6 yo presenting with Tanner stage 2, and asked what percentile he would be if left untreated. Not even sure what disease they are trying to get at...assume his height/etc would be higher than normal? Any help would be awesome!

Shorter. Precocious puberty (inc sex hormones) causes the growth plates to fuse early.
 
Homing explains the tendency of the site of metastasis of tumors. Too often, anatomical relationship and lymphatic drainage does not explain the metastatic site of tumors. One of the most well known examples is the tendency of lung cancer to metastasize to the adrenal glands.

The mechanism underlying homing is explained by expression of adhesion factors and chemokines. If these factors are blocked or inhibited, then it may be possible to prevent metastasis, as it is shown in the experimental study given in the question stem.
 
Is there a NBME 7 Discussion thread like this one?
I searched but could not find a dedicated thread for NBME 7 like this one.
Thanks
 

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