NBME 12 discussion

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titan25

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1 v max 1 enzyme is 300 and 2 nd 30 compare the Km values

km1 is 10 times km 2
km1 is 1/10 km2
we cant compare


2 upregulation of which protects from ARDS is IL 10

3 which anti hypertensive restores back potassium other k sparing

4 a 14 years old brougt to physian because mostly sleeping withdrawn and complaining of abdomen pain 3 weeks , what history will u take first...should we recretion drug history....options school history , devlopmental, family history

5 a drug given in two patients obese and normal given same doses graph ploted with conc on y axis and time on x , slope of normal person is greater
compared to normal person drug x in obese has

greater VD/ lower bioavailability / higher clearance/ shorter absorption

6 pedigree given four genrations AD 1st genration gene seq 4 5 6 changes to 156 cause...is it recombination

7 cytoplasmic enzyme mutated at 127 alanine replaced by serine why reduction of enzyme activity

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Qs 7) After cholecystectomy , pt has swelling and redness of great toe ?? also past H/o of great toe swelling ???

The question mentions a man with fever after cholecystecomy. Past medical history shows a 2 year intermittent case of toe pain, which worsened after the surgery. Physical examination shows redness and swelling of the same toe. The question is asking what caused the joint findings?
Removal of the gallbladder means this man won't have proper food digestion anymore. I can only suspect the meal he ingested is competing for the same excretion site in the kidney as uric acid (Ans: Urate Crystals). Resulting in a decreased secretion of uric acid, exacerbating his Gout Toe.
 
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Been awhile I think the answer is (C).
If there's a clot in the Pulmonary Artery, the pressure would be higher in the Right Ventricle. Therefore removing the clot, would lower the pressure in the Right Ventricle.

Thank you for responding and helping.

Had pondered, that if there was a block in the conduit for transmitting blood to the left atrium, there is less blood reaching the same ( although collateral circulation can compensate) and when the clot is lysed, the path is cleared for the conduction of blood and perhaps an increase in the volume in Lt atrium. :oops:

alza689
 
Thank you for responding and helping.

Had pondered, that if there was a block in the conduit for transmitting blood to the left atrium, there is less blood reaching the same ( although collateral circulation can compensate) and when the clot is lysed, the path is cleared for the conduction of blood and perhaps an increase in the volume in Lt atrium. :oops:

alza689

We can actually figure this out using Change in P = Q x R
Pressure gradient is what drives flow.
Resistance (R) is inversely proportional to radius of lumen.

So let's look at Flow (Q) in the RV to PA.
The clot is in the PA. Therefore the the radius is decreased. So Resistance would be increased. Increased Resistance will decrease Flow (Q), the Change in Pressure will be increased as well.
Busting the Clot will increase the radius, decrease Resistance, increase flow (Q), and Pressure is decreased.
 
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We can actually figure this out using Change in P = Q x R
Pressure gradient is what drives flow.
Resistance (R) is inversely proportional to radius of lumen.

So let's look at Flow (Q) in the RV to PA.
The clot is in the PA. Therefore the the radius is decreased. So Resistance would be increased. Increased Resistance will decrease Flow (Q), the Change in Pressure will be increased as well.
Busting the Clot will increase the radius, decrease Resistance, increase flow (Q), and Pressure is decreased.
Oh! Thank you very much ZGX for the response and am greately indebted to you. This question was had me pondering a while in the test, took some time to respond as the choices were equally appealing to select. any how thank you for helping me out.
 
Just checked my expanded feedback.
The answer is Choice (A). Chronic release of GnRH will result in a inhibitory function. No FSH and LH means no Testosterone. The lack of testosterone means no DHT, which acts on the prostate.
oh! thank you again ZGX for you help, it was vital for surviving. Much indebted to you for these helps. But frankly, kaplan notes does not provide any explanation regarding the mechanism of development of prostrate cancer, as the explanation in Kaplan notes are very concised and one worded and does not co-relate that testosterone being the culprit for this cancer. Merely PSA is increased in this pathology is all that is given. USMLE world does provide some information regarding continuous infusion of GnRH will Decrease LH and FSH but no co-relation regarding prostrate cancer and testostrone nor does FA provide any hint. Have I missed any other vital books or notes that such answers are provided?? Wherefrom this piece of information was deduced regarding testosterone and prostrate caner???

Thank you very much.
alza689
 
^^ I believe the question is referring to the drug 'leuprolide'.

Leuprolide is a GnRH analog, and if given continuously it will result in initially an increase in FSH and LH (and testosterone), but eventually the GnRH receptors downregulate, and testosterone levels fall.
*Leuprolide can also be used in infertility, however here the use is pulsatile*

Alternately, 'flutamide' can also be used, which is an androgen receptor blocker.

Note with flutamide FSH and LH values will be high (due to decreased negative feedback)
With leuprolide FSH and LH levels will be low (due to GnRH receptor downregulation).

Also.. flutamide and leuprolide are often used together in conjunction, with flutamide given first to counteract the initial testosterone surge with leuprolide.

Off the top of my head.. kaplan pharm videos (with lionel raymon) discuss this very well, also conrad fisher in kaplan physio endocrine talked about this.
 
^^ I believe the question is referring to the drug 'leuprolide'.

Leuprolide is a GnRH analog, and if given continuously it will result in initially an increase in FSH and LH (and testosterone), but eventually the GnRH receptors downregulate, and testosterone levels fall.
*Leuprolide can also be used in infertility, however here the use is pulsatile*

Alternately, 'flutamide' can also be used, which is an androgen receptor blocker.

Note with flutamide FSH and LH values will be high (due to decreased negative feedback)
With leuprolide FSH and LH levels will be low (due to GnRH receptor downregulation).

Also.. flutamide and leuprolide are often used together in conjunction, with flutamide given first to counteract the initial testosterone surge with leuprolide.

Off the top of my head.. kaplan pharm videos (with lionel raymon) discuss this very well, also conrad fisher in kaplan physio endocrine talked about this.

Yes, Indeed. There were one worded sentences about the actions of these on receptors but co-relation of testosterone and prostatic cancer I believe were not discussed in the notes nor in the video when I had viewed it three years back..But that was the vital connector to deduce the answer.

Thank you
alza689
 
Yes, Indeed. There were one worded sentences about the actions of these on receptors but co-relation of testosterone and prostatic cancer I believe were not discussed in the notes nor in the video when I had viewed it three years back..But that was the vital connector to deduce the answer.

Thank you
alza689


I am not sure if you're asking something or just saying it wasn't in kaplan. All what I typed above was what I learned from kaplan videos.
 
I am not sure if you're asking something or just saying it wasn't in kaplan. All what I typed above was what I learned from kaplan videos.

Co relation of testosterone and prostrate cancer were not discussed in the video nor notes, am quite certain since I took 3- 4 hours to view each video jotting down all possible examples as once the videos are seen, they do not allow us to view a second time since the number of students were several, until the rotation ceases.This I do not merely state as I took considerable time to evaluate even if there were any hidden concepts lurking.
 
Co relation of testosterone and prostrate cancer were not discussed in the video nor notes, am quite certain since I took 3- 4 hours to view each video jotting down all possible examples as once the videos are seen, they do not allow us to view a second time since the number of students were several, until the rotation ceases.This I do not merely state as I took considerable time to evaluate even if there were any hidden concepts lurking.


lol.. if you can find flutamide/leuprolide in your notes, then it was discussed. The sole purpose of these drugs is to help prostate cancer patients. And their mechanism of action relies on the basic principle that prostate cancers can be androgen sensitive.

Conrad fischer (in kaplan physio) specifically spent 4-5 minutes hammering on (in his usual crazy way) about a person who was given leuprolide first, and developed leg paralysis; the reason being the tumor grew due to the initial testosterone surge, and he should've been given flutamide first.

I didn't watch the path kaplan videos, so I cant speak on if it was mentioned there.

I don't know what else to tell you. Anyway.. who cares, you know the mechanism now right?
 
lol.. if you can find flutamide/leuprolide in your notes, then it was discussed. The sole purpose of these drugs is to help prostate cancer patients. And their mechanism of action relies on the basic principle that prostate cancers can be androgen sensitive.

Conrad fischer (in kaplan physio) specifically spent 4-5 minutes hammering on (in his usual crazy way) about a person who was given leuprolide first, and developed leg paralysis; the reason being the tumor grew due to the initial testosterone surge, and he should've been given flutamide first.

I didn't watch the path kaplan videos, so I cant speak on if it was mentioned there.

I don't know what else to tell you. Anyway.. who cares, you know the mechanism now right?

I think these two drugs Leuprolide/ flutamide comes in Pharmacology endocrine section. During which I had taken considerable pain jotting down almost all wordings by pausing the cassette 20 - 30 times, dont remember the co-relation of testosterone and prostrate cancer being explained. Perhaps newer Kaplan tapes may have included these extra piece of information. I do not remember the teachers name. there was a mention would have included the same in the jotted notes.
 
1. D
I'm guessing the patient has Hereditary Spherocytosis. The differential diagnosis between this and G6PD deficiency can be done through the blood smear (small red blood cells lacking the central pallor vs Heinz bodies).

2. D
The patient most likely has portal hypertension. The only veins that belong to the portal system are the Short Gastric (Short Gastric Veins from the Fundus of the stomach drain in the Splenic Vein. The Portal Vein is formed from Superior Mesenteric Vein and Splenic Vein)

Thank you Dr Tom gr for the for the help. The first question I had an inclination for beta thalssemia peripheral figure shows microcytes and the bottom of the figure indicates some pallor in the RBC's.Although target cells or basophilic stipulling were not found, thought I missed some point in the question stem.

the second question I had no idea of the concept had marked the answer due to the location of the arrow.Thanks any how for the help.

alza689
 
Thank you Dr Tom gr for the for the help. The first question I had an inclination for beta thalssemia peripheral figure shows microcytes and the bottom of the figure indicates some pallor in the RBC's.Although target cells or basophilic stipulling were not found, thought I missed some point in the question stem.

the second question I had no idea of the concept had marked the answer due to the location of the arrow.Thanks any how for the help.

alza689

Beta thalassemia never manifest at birth because the predominant hemoglobin is still HbF. The patient had jaundice at birth so this diagnosis is excluded.
 
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Thank you Dr Tom gr for the for the help. The first question I had an inclination for beta thalssemia peripheral figure shows microcytes and the bottom of the figure indicates some pallor in the RBC's.Although target cells or basophilic stipulling were not found, thought I missed some point in the question stem.
alza689

funny question
I realized just looking at the peripheral blood smear you can just go with hereditary spherocytosis
Notice the lack of central pallor and how round they look.
 
Beta thalassemia never manifest at birth because the predominant hemoglobin is still HbF. The patient had jaundice at birth so this diagnosis is excluded.
Forgive me for the delayed response, Was away from the computer for a few days. My sincere gratitude for the help and explanation. I thought Sickle cell disease was salvaged in infancy due to high fetal Hb. Glad to hear that Thalassemia was also redeemed similarly. Thank you once again

alza689
 
Forgive me for the delayed response, Was away from the computer for a few days. My sincere gratitude for the help and explanation. I thought Sickle cell disease was salvaged in infancy due to high fetal Hb. Glad to hear that Thalassemia was also redeemed similarly. Thank you once again

alza689

On the topic of β-Thalassemia you should really know the importance of the amount of generated HbF, HbA2, HbA in relation to β-trait and β-major - this topic is HY
 
hi all ,
this is my first post here so hi for all again .
im IMG preparing for usmle step 1 and ill take my exam at march 14 .
i took nbme 11 2 weeks ago and got 167\200 which correspond to 540\231 .
i took nbme 12 yesterday and got 162\200 correspond t 500\221 , i really disappointed and my confidence steep down somekind , is there any advice for ethical and patient doctor relationship to study from that i got 10 wrong qs at nbme 12 .
i studied behavioral science from kaplan notes , i read first aid 3 times till now and did uworld qbank 2 time ( my average at u world was 64 at firs time and it become at 90's+ at 2nd time ).
so is it a problem to be weak at ethical , patient-doctor relationship and the experimental qs or at the real exam there are less qs than what i saw at nbme 12 .
i found uworld qs is harder that u need to think more but the question language and the way they ask is clear but the nbme's qs was more odd in the qs style and language even they r easier but their language make the question harder .
so for the ones whom take the exam they found the exam is closer in style and language for uworld or nbmes .
ill try to post some wrong questions at the following post asking for ur help in answering them if u dont mind .
 
I found this explanation to be very helpful.

Btw, the answer is A. The Km cannot be predicted based solely on the value of Vmax.

Some of the people, including, myself have taken the exam online with the extended feedback and we confirmed that neither B, C, nor D is the correct answer.

KM = 1/2Vmax (That's wrong!!!)

Well, that's kind of difficult to explain in a few words, but it's much simpler if you look at the following graph:

http://www.mystrica.com/images/uploaded/lactase Km.jpg

If you take a look at the image, you can see a blue curve with the kinects of an enzyme in a normal state. Also, you have a red curve with the same enzyme with a competitive inhibitor. Obviously, the blue and the red curves have the same Vmax as you can see from the graph, and because they're basically the same enzyme with the red curve being with the addition of a competitive inhibitors. However, what happens to the Km? They're different!! You can see the Km of the red curve is bigger than the Km of the blue curve. This graph easily proves that Km = 1/2Vmax assumption is false!!!

In contrast, if you're still not convinced you can take a look at the gray curve in the same image, with the same enzyme, but with a competitive inhibitor and compare with the blue curve and see that they clearly have different Vmax, but, wait, they have the same Km? Wow..

So, in summary, there's clearly no numerical relationship between Km and Vmax, since they measure different independent aspects of the enzyme!!
 
hi all ,
this is my first post here so hi for all again .
im IMG preparing for usmle step 1 and ill take my exam at march 14 .
i took nbme 11 2 weeks ago and got 167\200 which correspond to 540\231 .
i took nbme 12 yesterday and got 162\200 correspond t 500\221 , i really disappointed and my confidence steep down somekind , is there any advice for ethical and patient doctor relationship to study from that i got 10 wrong qs at nbme 12 .
i studied behavioral science from kaplan notes , i read first aid 3 times till now and did uworld qbank 2 time ( my average at u world was 64 at firs time and it become at 90's+ at 2nd time ).
so is it a problem to be weak at ethical , patient-doctor relationship and the experimental qs or at the real exam there are less qs than what i saw at nbme 12 .
i found uworld qs is harder that u need to think more but the question language and the way they ask is clear but the nbme's qs was more odd in the qs style and language even they r easier but their language make the question harder .
so for the ones whom take the exam they found the exam is closer in style and language for uworld or nbmes .
ill try to post some wrong questions at the following post asking for ur help in answering them if u dont mind .

Merging with NBME thread.
 
This is for the three-test battery...

ans. C. 85%


in each test, there's 0.5 % chance of not having a normal result.....and there are 3 tests

0.5x 3=0.15...(not having a normal result of all 3 tests)

and we are looking for the one that is normal

so 1.00- 0.15=0.85 or 85% (normal result)
 
The most likely cause of this patient's current symptoms is a decrease in which of the following?

ans. C. duodenal pH

- decrease in ph denatures pancreatic enzymes
- pancreatic enzymes need to be in a basic state in order it to function. Acid is bad for the pancreatic enzymes.
- a patient with chronic pancreatitis, who develops a fatty diarrhea, due to malabsorption. i assume that the secretin secretion is also impaired, which normally increase the duodenal ph, for the pancreatic enzymes to work. since there is no option for "decrease pancreatic enzymes", the answer decrease duodenal ph comes closest to it
 
ans. B. G --> A at position 246

I found this explanation to be very helpful!

"B" (Splice Site mutation)


Position 1 and position 2049 are not part of the "Beta globin gene (154 - 1577)"

so option A and D are out.

-position 246 and 672 , both are located within the Beta globin gene. So, let’s narrow down between B or C.

-Beta-Thalassemia have "POINT Mutation" in

either "SPLICE Site" (* as at position 246 where the first Intron start)

or "Non-sense mutation" introducing a STOP Codon (but this is not the case here)



NOTE that: (EXONS are in Bold Capital letters)

154--[EXON1]--245_*246--[Intron1]--*375_376--[EXON2]--598_*599--[Intron2]--*1448

149--[EXON 3]--1577


* are the Splice Sites and site at position 246 if get mutated, it will cause Beta-Thalassemia
 
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47.
A 3-day-old female newborn is brought to the physician because of yellow eyes for 1 day. The newborn was delivered at term after an uncomplicated pregnancy. The newborn and her mother are both blood group A, Rh-positive. Physical examination shows scleral and facial icterus. Her serum total bilirubin concentration is 6 mg/dL with a direct component of 0.5 mg/dL. Serum AST and ALT activities are within the reference ranges. A direct antiglobulin (Coombs) test result is negative. Which of the following is the most likely cause of the jaundice in this newborn?

A
)
Biliary atresia

B
)
Galactose 1-phosphate uridylyltransferase deficiency

C
)
Glucose 6-phosphatase deficiency

D
)
Immune hemolysis

E
)
UDP glucuronosyltransferase deficiency

F
)
Viral hepatitis
Your answer is indicated by the filled-in circle.
cant understand this question ..........need help
:confused:
 
47.
A 3-day-old female newborn is brought to the physician because of yellow eyes for 1 day. The newborn was delivered at term after an uncomplicated pregnancy. The newborn and her mother are both blood group A, Rh-positive. Physical examination shows scleral and facial icterus. Her serum total bilirubin concentration is 6 mg/dL with a direct component of 0.5 mg/dL. Serum AST and ALT activities are within the reference ranges. A direct antiglobulin (Coombs) test result is negative. Which of the following is the most likely cause of the jaundice in this newborn?

A
)
Biliary atresia

B
)
Galactose 1-phosphate uridylyltransferase deficiency

C
)
Glucose 6-phosphatase deficiency

D
)
Immune hemolysis

E
)
UDP glucuronosyltransferase deficiency

F
)
Viral hepatitis
Your answer is indicated by the filled-in circle.
cant understand this question ..........need help
:confused:

E.

physiological jaundice of the newborn - newborn's liver enzymes are not mature yet, hence the increase in unconjugated bilirubin.
 
hey guys good afternoon...i just finished taking the exam...what was the overall consensus for the exam? i thought the exam was kinda on par with the level of difficulty with nbme 11. i got the same score on both of them, which is unfortunate.

however, 11 had more topics of my strengths whereas 12 had more of my areas of weakness (ie acid/base). exam is coming up very soon...and still need to do 13, 15, and the free 150 questions...
 
20 yo man who recently immigrated to US from Mexico comes to the physician bc of a 3 day history of painful ulcer on his penis. It's 0.5cm, non-indurated, tender ulcer on the shaft of the penis. Culture shows it grows on chocolate agar, oxidase-positive, g- bacillus, that expresses beta-lactamases. what is it?

a. chlamydia trachomatis
b. haemophilus ducreyi
c. klebsiella (calymmatobacterium) granulomatis
d. neisseria gonorrhea
e. treponema pallidum


i chose neisseria, because the last sentence describes the growth of NG, however i can see that since the question talks about a tender ulcer, it probably can't be D. it can't be E either, since syphilis causes a painless ulcer, correct? i guess that means the answer is B?

anybody confirm?
 
20 yo man who recently immigrated to US from Mexico comes to the physician bc of a 3 day history of painful ulcer on his penis. It's 0.5cm, non-indurated, tender ulcer on the shaft of the penis. Culture shows it grows on chocolate agar, oxidase-positive, g- bacillus, that expresses beta-lactamases. what is it?

a. chlamydia trachomatis
b. haemophilus ducreyi
c. klebsiella (calymmatobacterium) granulomatis
d. neisseria gonorrhea
e. treponema pallidum


i chose neisseria, because the last sentence describes the growth of NG, however i can see that since the question talks about a tender ulcer, it probably can't be D. it can't be E either, since syphilis causes a painless ulcer, correct? i guess that means the answer is B?

anybody confirm?

I chose H. ducreyi and it didn't show up on my extended feedback, so I guess that's correct.
 
20 yo man who recently immigrated to US from Mexico comes to the physician bc of a 3 day history of painful ulcer on his penis. It's 0.5cm, non-indurated, tender ulcer on the shaft of the penis. Culture shows it grows on chocolate agar, oxidase-positive, g- bacillus, that expresses beta-lactamases. what is it?

a. chlamydia trachomatis
b. haemophilus ducreyi
c. klebsiella (calymmatobacterium) granulomatis
d. neisseria gonorrhea
e. treponema pallidum


i chose neisseria, because the last sentence describes the growth of NG, however i can see that since the question talks about a tender ulcer, it probably can't be D. it can't be E either, since syphilis causes a painless ulcer, correct? i guess that means the answer is B?

anybody confirm?

Also I think the fact that the question says that it's a G- bacillus eliminates Neisseria, which is a G - coccus.
 
I chose H. ducreyi and it didn't show up on my extended feedback, so I guess that's correct.

Also I think the fact that the question says that it's a G- bacillus eliminates Neisseria, which is a G - coccus.

and the fact it grows on chocolate agar and a bacillus makes it haemophilus

yup, im an idiot...only realized what i chose after i made the post...FML
 
I don't really know what you guys are discussing, but I saw a few pages back in this thread that mebendazole was the correct answer to a test given in 2012. It may be correct technically but the drug has been completely unavailable in the US since 2011, and no one seems to know why. I was searching for it and came across this thread. I was prescribed the drug, but it's just not available. TEVA made it and was the only company that did make it for the US and just stopped.

I wonder if that invalidated the question that was being talked about.
 
20 yo man who recently immigrated to US from Mexico comes to the physician bc of a 3 day history of painful ulcer on his penis. It's 0.5cm, non-indurated, tender ulcer on the shaft of the penis. Culture shows it grows on chocolate agar, oxidase-positive, g- bacillus, that expresses beta-lactamases. what is it?

a. chlamydia trachomatis
b. haemophilus ducreyi
c. klebsiella (calymmatobacterium) granulomatis
d. neisseria gonorrhea
e. treponema pallidum


i chose neisseria, because the last sentence describes the growth of NG, however i can see that since the question talks about a tender ulcer, it probably can't be D. it can't be E either, since syphilis causes a painless ulcer, correct? i guess that means the answer is B?

anybody confirm?

What eliminates K. granulomatis? I know it's wrong but still not following why. Haemophilus species are coccobacilli and I've gotten questions wrong in the past because the explanation said something along the lines "Haemophilus is a coccobacillus, not a bacillus". Can anybody clarify the bacilli/coccobacilli distinction?

I know that they have different morphologies, but it'd be nice if somebody can explain how the question writers choose to use those terms.

Next question (if you guys can't tell, I'm updating this post as I go through answers):

65 y/o woman with TIA's and cannot tolerate aspirin. What is the best stroke prophylaxis for her?

Dipyridamole = wrong
Clopidogrel = correct

From first aid under dipyridamole: "prevention of stroke or TIAs (combined with aspirin)"
When they said "cannot tolerate aspirin", I was expecting GI side effects, but I guess that's not the case and there's something else I'm missing. Either that, or dipyridamole requires aspirin to become activated? The mechanism of dipyridamole doesn't seem to have anything to do with COX so I couldn't imagine it worsening an ulcer or whatever. It seems like this patient is ideal for dipyridamole. What side effect am I overlooking? Renal? Something else? Ugh, science why do you do this?


One last question- does anybody remember something about the mechanism of Reye's syndrome? I completely guessed and must have gotten it right unfortunately because now I have no idea what the answer is. I've searched far and wide for an explanation and every single source says something along the lines of "pathogenesis is unclear except for aspirin and viruses".
 
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What eliminates K. granulomatis? I know it's wrong but still not following why. Haemophilus species are coccobacilli and I've gotten questions wrong in the past because the explanation said something along the lines "Haemophilus is a coccobacillus, not a bacillus". Can anybody clarify the bacilli/coccobacilli distinction?

I know that they have different morphologies, but it'd be nice if somebody can explain how the question writers choose to use those terms.

Next question (if you guys can't tell, I'm updating this post as I go through answers):

65 y/o woman with TIA's and cannot tolerate aspirin. What is the best stroke prophylaxis for her?

Dipyridamole = wrong
Clopidogrel = correct

From first aid under dipyridamole: "prevention of stroke or TIAs (combined with aspirin)"
When they said "cannot tolerate aspirin", I was expecting GI side effects, but I guess that's not the case and there's something else I'm missing. Either that, or dipyridamole requires aspirin to become activated? The mechanism of dipyridamole doesn't seem to have anything to do with COX so I couldn't imagine it worsening an ulcer or whatever. It seems like this patient is ideal for dipyridamole. What side effect am I overlooking? Renal? Something else? Ugh, science why do you do this?


One last question- does anybody remember something about the mechanism of Reye's syndrome? I completely guessed and must have gotten it right unfortunately because now I have no idea what the answer is. I've searched far and wide for an explanation and every single source says something along the lines of "pathogenesis is unclear except for aspirin and viruses".

From my weak understanding, chocolate agar is only Haemophilus and Neiserria species. The selective agar for this would be Thayer-Martin which selects for the Neisseria. Also from the great flow chart in first aid, we divide gram negatives into Cocci (neiserria), Coccoid (rods that are almost cocci - Haemophilus and Bordetella), Rods (subdivided based on lactose fermenting and fast or slow).

SO TL;DR coccoid are the short rods - haemophil and bordetella while bacilli are the long rods (Kleb, ecoli, enterobacter, serratia, salmonella, shigella, pseudomonas, h. pylori)
 
51 YO woman comes to physician because of firm lump in her neck for 5 months; she also tires easily. Exam shows modest symmetric enlargement of thyroid gland. T4 is 1.8 ug/dL (low). Which of the following serum findings is most likely in this patient?

A) Decrreased TSH concentration - obvi wrong
B) Decreased TRH concnetration - obvi wrong
C) Increased TBG concentration
D) Presence of antithyroid peroxidase antibodies

E) Presence of thyroid-stimulating antibodies - obvi wrong

Answer is D but why is TBG not increased since T4 is decreased, so it would have less T4 to bind.Much like in Fe deficiency, TIBC will increase if Fe decreases (though i know that's a bit different with the intracellular stores and everything)

Thanks in advance
 
51 YO woman comes to physician because of firm lump in her neck for 5 months; she also tires easily. Exam shows modest symmetric enlargement of thyroid gland. T4 is 1.8 ug/dL (low). Which of the following serum findings is most likely in this patient?

A) Decrreased TSH concentration - obvi wrong
B) Decreased TRH concnetration - obvi wrong
C) Increased TBG concentration
D) Presence of antithyroid peroxidase antibodies

E) Presence of thyroid-stimulating antibodies - obvi wrong

Answer is D but why is TBG not increased since T4 is decreased, so it would have less T4 to bind.Much like in Fe deficiency, TIBC will increase if Fe decreases (though i know that's a bit different with the intracellular stores and everything)

Thanks in advance

TIBC represents a kind of "potential" binding capacity, so if iron is low you're going to ramp up the avidity for iron in the blood. TBG, however, is an actual protein concentration measurement. So if T4 is low, the actual amount of TBG in the blood will be low.
 
Hello everyone. My nerve totally failed with NBME 12, I got 510/224. i even went down a couple of points from NBME 11 and 13, but it is all my fault, since I went a little lazy the last week, and just limited myself to finishing bioethics and checking my past NBME wrong answers (which didnt help at all, lol).

So, lets keep this rolling for the 2013 people, yay! :p

I don't really know what you guys are discussing, but I saw a few pages back in this thread that mebendazole was the correct answer to a test given in 2012. It may be correct technically but the drug has been completely unavailable in the US since 2011, and no one seems to know why. I was searching for it and came across this thread. I was prescribed the drug, but it's just not available. TEVA made it and was the only company that did make it for the US and just stopped.

I wonder if that invalidated the question that was being talked about.

Dont know if its available in the US, but i remember mebendazole being mentioned in the Kaplan videos for ttx of parasites such as the one presented in that question. We also still use it widely in developing countries for most parasitic infections. The answer choices basically narrowed down between a fungal and a parasitic infection. Mebendazole was the correct choice

Answer is D but why is TBG not increased since T4 is decreased, so it would have less T4 to bind.Much like in Fe deficiency, TIBC will increase if Fe decreases (though i know that's a bit different with the intracellular stores and everything)

Thanks in advance

Maybe you are thinking that TBG means total binding globulin or something like that like TIBC which means Total Iron Binding Capacity. TBG just means Thyroid binding globulin. People that chose that answer were thinking about the woman taking estrogens, and thought about the mechanism of estrogen increasing TBG and therefore less free T4 present in pregnant women.

From first aid under dipyridamole: "prevention of stroke or TIAs (combined with aspirin)"
When they said "cannot tolerate aspirin", I was expecting GI side effects, but I guess that's not the case and there's something else I'm missing. Either that, or dipyridamole requires aspirin to become activated? The mechanism of dipyridamole doesn't seem to have anything to do with COX so I couldn't imagine it worsening an ulcer or whatever. It seems like this patient is ideal for dipyridamole. What side effect am I overlooking? Renal? Something else? Ugh, science why do you do this?
You need to be aware that some people are allergic to aspirin, with serious adverse effects, such as dangerous bronchospasms (i think asthma is a contraindication for aspirin) so they cannot receive attack dosage when an MI is suspected, that is why you carry with you your backup clopidogrel which binds to ADP and blocks platelet aggregation. You can also give Ticlopidine in cases of aspirin allergy, but that carries the risk of severe neutropenia.

One last question- does anybody remember something about the mechanism of Reye's syndrome? I completely guessed and must have gotten it right unfortunately because now I have no idea what the answer is. I've searched far and wide for an explanation and every single source says something along the lines of "pathogenesis is unclear except for aspirin and viruses".
i cannot recall, nor find the exact mechanism in my notes, but it had to do with hepatic mitochondrial b-oxidation inhibition, and the pathology clasically associated with it is microvesicular fatty changes.

Hope that helps. I just finished reading this whole thread, i'll be checking my NBME extended format and come up with a few q's of my own. :)
 
Anyone have an explanation on the question about the boy that had decreased appetite, abdominal pains and sleeps constantly for the past 3 weeks? Someone back there answered that it was to ask for suicidal ideation, but didnt give a thorough explanation. I think 3 weeks is too little to think about major depressive disorder, didnt give any other buzz word symptoms depression, and the abdominal pain and fatigue made me think of lead poisoning. The question asks for "what is more critical for the physician?", is that why I should ask for suicidal ideation? what about the abdominal pain?

The answer choices were:
developmental history
family history of affective disorders
orientation on space, time and person
school history (marked this one and got it wrong, because I was thinking about lead poisoning, maybe he would be failing at school or something)
suicidal ideation or attempts
 
Anyone have an explanation on the question about the boy that had decreased appetite, abdominal pains and sleeps constantly for the past 3 weeks? Someone back there answered that it was to ask for suicidal ideation, but didnt give a thorough explanation. I think 3 weeks is too little to think about major depressive disorder, didnt give any other buzz word symptoms depression, and the abdominal pain and fatigue made me think of lead poisoning. The question asks for "what is more critical for the physician?", is that why I should ask for suicidal ideation? what about the abdominal pain?

The answer choices were:
developmental history
family history of affective disorders
orientation on space, time and person
school history (marked this one and got it wrong, because I was thinking about lead poisoning, maybe he would be failing at school or something)
suicidal ideation or attempts

Suicidal ideation was the answer. He has s/s of depression.

- decreased appetite
- look at the time interval x > 2 weeks. major depressive order can be made if the s/s last longer than 2 weeks.
- i recall that he was also sleeping a lot as well, correct
- all of the clues in the question stem pointed towards him being depressed.

There's a question in NBME 5, similar to this...
 
Right, it has to be at least 2 weeks. i dont know why i was thinking about needing like 6 months. I just realized I was thinking about the time interval for schizophrenia. damn.
 
Right, it has to be at least 2 weeks. i dont know why i was thinking about needing like 6 months. I just realized I was thinking about the time interval for schizophrenia. damn.

yup...here's the question from nbme 5...highlight the text if you want to read it...wasn't sure if you had done the exam or not. basically the same principal applies...:)


**nbme 5 spoiler - highlight text below to read the question**

#1: A 62-year-old man comes to the physician with a 3-month history of fatigue and depression. He lives alone and has been drinking more (up to 6 mixed alcoholic drinks daily) since his wife of 40 years died 6 months ago. He says, "Yeah, I know I've been drinking a lot lately, but I'm so down in the dumps there's nothing else I want to do. I miss her so much. " Which of the following responses by the physician is most appropriate?

a) "Anybody in your circumstance would be depressed. Time will help you overcome the loss of your wife."
b) "Drinking isn't going to bring your wife back. You need to get on with your life and put this sad experience behind you."
c) "I know you have been through a lot recently. Have things been so bad recently that you have thought about killing yourself."
d) "I'd like to start you on some medication for depression. It sometimes takes a few weeks to work."
e) "You seem to be developing an alcohol problem. You need to quit drinking. I can refer you to the local chapter of Alcoholics Anonymous."
 
This questions hasnt been posted before:

A question about 7 people and serum creatinine concentration values ordered in a table. The question asked, what would happen with the median, the mode and the mean if the last person (the one with the highest creatinine value) was removed.

I marked that the median would be unchanged, the mode decreases, and mean decreases. Any input on this one?
 
This questions hasnt been posted before:

A question about 7 people and serum creatinine concentration values ordered in a table. The question asked, what would happen with the median, the mode and the mean if the last person (the one with the highest creatinine value) was removed.

I marked that the median would be unchanged, the mode decreases, and mean decreases. Any input on this one?

lol, i also got that question wrong too...i know i chose one of the top two answers...can't remember if it was A or B...i want to say the latter...is that what you chose?
 
yup...here's the question from nbme 5...highlight the text if you want to read it...wasn't sure if you had done the exam or not. basically the same principal applies...:)

I havent taken NBME 5 and I dont plan on taking it. The answer there must be to start him on antidepressants right? The picture is much more clear on that question than on the one on NBME12. Thanks for the heads-up. And cool way to warn about spoilers and preventing them. :cool:
 
I havent taken NBME 5 and I dont plan on taking it. The answer there must be to start him on antidepressants right? The picture is much more clear on that question than on the one on NBME12. Thanks for the heads-up. And cool way to warn about spoilers and preventing them. :cool:

negative. the patient is in a state of grieving since it's less than x < 1 year, however he has the s/s of depression which you were able to conclude. however it's asking what's the best response to this, so asking about suicide and how he feels is the more appropriate answer?

were you born in peru? is english your 2nd language? im only asking because i've noticed that we can come up with a diagnosis or make associations, but ******ed response questions like this give me a really difficult time when the question arises.
 
lol, i also got that question wrong too...i know i chose one of the top two answers...can't remember if it was A or B...i want to say the latter...is that what you chose?

No, I chose E. There were A-H answer choices. lol
 
negative. the patient is in a state of grieving since it's less than x < 1 year, however he has the s/s of depression which you were able to conclude. however it's asking what's the best response to this, so asking about suicide and how he feels is the more appropriate answer?

were you born in peru? is english your 2nd language? im only asking because i've noticed that we can come up with a diagnosis or make associations, but ******ed response questions like this give me a really difficult time when the question arises.

damn. I need to check this out. Yes, I am from Peru, and English is my second language, and its true that when reading the question, (even aloud), it just feels wrong. This is ridiculous, I have asked this to real patients in my own practice (in spanish of course), but I seem unable to even think about it when presented in English.
 
damn. I need to check this out. Yes, I am from Peru, and English is my second language, and its true that when reading the question, (even aloud), it just feels wrong. This is ridiculous, I have asked this to real patients in my own practice (in spanish of course), but I seem unable to even think about it when presented in English.

yeah it sucks...i hate getting these questions wrong. i hope i get easy response questions on my exam...

- patient has child present in room but pt doesn't speak english, what do you do...
- pt with child and the child is speaking for the pt...what do you do...
- etc etc

cant think of the other easy ones right now lol
 
This questions hasnt been posted before:

A question about 7 people and serum creatinine concentration values ordered in a table. The question asked, what would happen with the median, the mode and the mean if the last person (the one with the highest creatinine value) was removed.

I marked that the median would be unchanged, the mode decreases, and mean decreases. Any input on this one?

The mode is the value that occurs most frequently. There were two of the same numbers in the set, not including the last number that was taken out, so mode is the same. Removing the last number removed a larger value so the mean (average) would decrease and the median would decrease (you can actually calculate it and see).
 
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