NBME 16 help

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shubz123

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@plasmodium

Hopefully you can help me with this one
An investigator is conducting a study of Plasmodium infection in an experimental animal model. During the study, the animals are inoculated with various species of Plasmodium. A standard course of chloroquine is administered, and the effects of this treatment on hypnozoites in the liver are observed. After treatment, hypnozoites from which of the following two Plasmodium species are most likely to be viable?


falciparum+malariae
falciuparum+ovale
falciiparim+vivax
malaria + ovale
malarae + vivax
Vivax+ malariae (just noticed 2 of these choices are the same?)
Vivax + ovale
 
@plasmodium

Hopefully you can help me with this one
An investigator is conducting a study of Plasmodium infection in an experimental animal model. During the study, the animals are inoculated with various species of Plasmodium. A standard course of chloroquine is administered, and the effects of this treatment on hypnozoites in the liver are observed. After treatment, hypnozoites from which of the following two Plasmodium species are most likely to be viable?


falciparum+malariae
falciuparum+ovale
falciiparim+vivax
malaria + ovale
malarae + vivax
Vivax+ malariae (just noticed 2 of these choices are the same?)
Vivax + ovale

Chillax bro, this is straight outta FA.
 
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For the lady with a PE, I picked shunt instead of dead space. I'm unsure of the difference between shunt and dead space... this is what I've boiled it down to.

Dead space - ventilation is fine in the lung, but since there is a clot, no blood is getting there to get the O2 (perfusion problem, ventilation is fine)
Shunt - perfusion is fine but there is an airway blockage (ie I breathed in a peanut so it is a ventilation problem, but perfusion is fine)

Is this basically the difference?
 
Just to confirm... the old man with HTN living in a farm in central Cali who distills his own liquor, worked in hat factory, textile factory, smoker... comes in with gout - most likely cause of his gout is "drinking home-distilled liquor"? I think I got distracted and wondered if this guy somehow has bladder cancer (perhaps he was exposed to something at his factory + his smoking hx), and what the relationship of that would be to gout. But now I wonder if it's as simple as alcohol -> risk factor for gout.

Also, would love any input on that question with the sheep blood agar plate image. (Refresher: 70y F with eprsistent fever despite IV broad-spectrum abx 3 days post-operation. She has a central venous cathether and a well-healing surgical wound. Gram stain shows 4um elliptical purple budding org. Candida, Cryptococcus, Ecoli, Sporothrix schenckii, Staph aureus).

Thanks!!!

For the second question, why is it candida even though there are purple organisms on gram stain? are those just other random bacteria that happened to be cultured?
 
Lady has graves disease and gives birth to a kid who has stridor and asymmetric neck mass. What is the cause?

Is it just an enlarged thyroid? IgG from graves can cross placenta and stimulate the baby and give him graves too?
 
Lady has graves disease and gives birth to a kid who has stridor and asymmetric neck mass. What is the cause?

Is it just an enlarged thyroid? IgG from graves can cross placenta and stimulate the baby and give him graves too?

What were the options again?
 
For the second question, why is it candida even though there are purple organisms on gram stain? are those just other random bacteria that happened to be cultured?

Distractor. Also contamination of cultures isnt uncommon. key here is 1) persistent fever after broad spectrum abx, kinda pushes you away from bacterial cause and 2) budding organisms, points to fungal pathology 3) candida and cvc association is HY
 
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Stupid question but purple is gram positive or gram negative?

I always thought purple was positive and pink was negative but there was another question that used blue and pink (I guess blue is positive and pink is negative). Purple is in between blue and pink so...?

Purple positive, blue can also be positive, hell i remember an nbme q which organisms were black and u had to know they were gram +
 
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18mo M with lethargy for 3hrs unresponsive on arrival. 10mo ago had hypoglycemia and diarrhea followed by cardioresp arrest. PE reveals hepatomegaly. Decreased serum glucose, ketones, carnitine. Decreased urine ketones and presence of urine dicarboxylic acids. Pt responds with IV glucose. Medium chain TAGs administered for 6mos with normal serum glucose levels. Pt has what deficiency?

G6Phosphatase, HMG CoA lyase, Hormone sensitive lipase, LPL, Long chain acyl CoA DH, PEPCK

What are the "dicarboxylic acids" in this case?
 
I completely agree and that's what I was looking for in the choices, but unfortunately that was NOT one of the answer choices, so that can't be right. Anybody else have any ideas?Maybe macrophage activity goes down somehow... I don't know :-/
okay.It's an old post but i'd like to answer as so many will still come here.I think we all got the first two 1.Mucus production an secretion(up)2.Activity of cilia(down)In the third option they have asked about Alveolar macrophage FUNCTION which should be decreased (down) and not the NUMBER of macrophages that actually increases due to macrophage aggregation.That's creating the confusion here.
 
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just took this form 16 and scored 234. feel terrible. exam in just 6 weeks. don't know how will I cross 250 mark :(
 
the question with biopsy of scrotal testes. i know its klinefelter. but what does the picture show ? doesnt look like hyaline seminiferous tubules. or is it ?
 
the question with biopsy of scrotal testes. i know its klinefelter. but what does the picture show ? doesnt look like hyaline seminiferous tubules. or is it ?

It just looks like a bunch of fibrosis with no signs of normal spermatogonia. That made me think of Klinefelter's since Klinefelter's has testicular atrophy.
 
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How about the question about the newborn with the asymmetric neck mass who was born to the mother with untreated Graves disease? Enlarged thyroid would make sense given the history, but I feel like that would be a *symmetric* mass. I chose cystic hygroma, though I think that's probably wrong.
 
Also what about the question asking what causes the induration that occurs hours after a bee sting? The choices are:
decreased adhesion molecules on endothelial cells; decreased CRP; influx of macrophages producing cytokines; lysis of endothelial cells by complement; vasoconstriction.
 
Also what about the question asking what causes the induration that occurs hours after a bee sting? The choices are:
decreased adhesion molecules on endothelial cells; decreased CRP; influx of macrophages producing cytokines; lysis of endothelial cells by complement; vasoconstriction.
this one was tricky for me as well. its influx of macro producing cytokines
 
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How about the question about the newborn with the asymmetric neck mass who was born to the mother with untreated Graves disease? Enlarged thyroid would make sense given the history, but I feel like that would be a *symmetric* mass. I chose cystic hygroma, though I think that's probably wrong.
i went with enlarged thyroid. it just made more sense because the mother had graves. if it was a cystic hygroma they would describe the mass as compressible or transilluminating i guess
 
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the question about gastrinoma where you had to identify the parietal cells on a histo slide ?? how to work that one out ?

and the biostats question of lead foundry where you had to identify the control group?
 
the question about gastrinoma where you had to identify the parietal cells on a histo slide ?? how to work that one out ?

and the biostats question of lead foundry where you had to identify the control group?

Pathoma had talked about parietal cells having a bunch of Ps: Parietal, Proton pumps, Pink, Pernicious anemia. I remembered that and then just picked the pinkest cell on there.

And for the lead foundry question, they describe how they have a group of children whose parents worked at a lead foundry. So you can tell they are doing a cohort study (because they have chosen a group with an "exposure"). The control group has to be a similar group of children WITHOUT that exposure.
 
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18mo M with lethargy for 3hrs unresponsive on arrival. 10mo ago had hypoglycemia and diarrhea followed by cardioresp arrest. PE reveals hepatomegaly. Decreased serum glucose, ketones, carnitine. Decreased urine ketones and presence of urine dicarboxylic acids. Pt responds with IV glucose. Medium chain TAGs administered for 6mos with normal serum glucose levels. Pt has what deficiency?

G6Phosphatase, HMG CoA lyase, Hormone sensitive lipase, LPL, Long chain acyl CoA DH, PEPCK

What are the "dicarboxylic acids" in this case?

Dicarboxylic aciduria/acidemia/acidosis is pathognomic for MCAD/LCAD deficiency. It's where you have a defect in Beta oxidation in which there are acids on both sides of the fatty acid. Something like "COO-FA-OOC". Not too sure why exactly. My Kaplan teacher just briefly mentioned it then moved on.
 
I read through about 8 pages and didn't see too much info on these particular questions, if someone can help that'd be great.

1) 51 y/o man is a farmer and comes to doc 5 days after he cut his right foot while cleaning out his barn. 15 year h/o poorly controlled type 2 DM. T 101.3 F, P 105 bpm, BP 139/86. On PE, LE shows erythema up to mid-calf, edema, and exquisite tenderness of ankle and area around laceration. Leuk ct is 57,000/mm3. Response to patient injury?

A. Leukemoid rxn
B. Leukoclastic response (wrong)
C. Leukopenia
D. Leukoplakia
E. Leukotriene

I started thinking of leukemia since the WBC ct was so high, but quickly realized that has nothing to do with the question. Then wanted to choose A, but I remember reading somewhere that in Leukemoid reactions, the WBC count increases but never to more than a specific number (I think it was more than 1.5 or 2x the upper normal limit or something, I forgot). So I excluded it. Definitely not C or D, so between B and E I chose B. What is a leukoclastic response anyway?

2) 27 y/o nulligravid woman inability to conceive for 2 yrs. Menses occurred 3-4 month intervals since menarche at age 14. PE unremarkable. FSH/LH and estrogen normal. Which of the following is the best pharmacotherapy?

A. Clomiphene (I heard this is correct?)
B. Low dose estrogen
C. Medroxyprogesterone (wrong)
D. Metformin
E. Tamoxifen

I chose C because I figured maybe she has normal FSH/LH and estrogen but is lacking in progesterone so she can't conceive. And because of the progestin test, if she is given progesterone and she menstruates, it means she's lacking progesterone. So that's why I chose C. Now that I think about it C does sound wrong, but why is it A? I thought Clomiphene, a SERM, is used for PCOS, to remove the negative feedback estrogen has on the pituitary, and allow for increased LH/FSH to induce ovulation? This doesn't sound like a PCOS pt.

3) 4 month old boy with problem sending stuff out of ER to Golgi.

Is the answer "Dilated RER" due to things backing up in the RER since it cant send it to the Golgi?

4) The 20 y/o guy who binge drank all weekend and took Tylenol and had abd pain and headache on Monday morning.

I know the answer is that it's because alcohol induces P450 which breaks down tylenol into more NAPQI which is toxic, but I didn't choose that one specifically because I've learned that ACUTE ALCOHOL = inhibits p450, while CHRONIC ALCOHOL = stimulates P450. It seemed more like an acute alcohol ingestion so I instead picked E (Alcohol increased NADH:NAD ratio, which I know has nothing to do with tylenol OD but still picked it, thinking maybe we weren't talking about tylenol toxicity in the first place.)

5) Is rupture of an intervertbral disc and slipping or herniation the same meaning? I'm a weightlifter myself and am VERY familiar with this, but that one word made me not choose that answer. When I hear rupture, I think of fracture, and I thought that was an answer for osteoporosis (compression fracture). I instead chose "tearing the sciatic nerve"

6) 33 y/o man has 3 month h/o muscle weakness and cramping shortly after initiating exercise. PE normal, CK elevated, after forearm muscle exercises and measure venous lactate concentrations DO NOT increase compared with preexercise values. Deficiency of which enzyme?

A. Carnitine palmitoyl-transferase-1 (wrong)
B. Fumarase
C. Glucose-6-Phosphatase
D. Glycogen phosphorylase (was this it?)
E. Succinate dehydrognase

I was thinking McKardle disease, but doesn't that present in childhood? Usually a kid in school who can't keep up in gym class. Not sure what the answer is and why. What disease is this? I was thinking LCAT deficiency.

7) Differentiating between IDA and B-thal. I learned we could use the Mentzer index = MCV/RBC, <13 thal >13 IDA. Since in thal you have normal or elevated RBC counts compared to IDA. But they didn't give the RBC count. They also didn't give the RDW to differentiate (RDW high in IDA). Last clue is that in thal, the MCV ct is WAY lower than Hb (for example, MCV 59 but Hb 10.2). For this case I wasn't so sure if it's significantly lower or not, guess it wasn't. So was this just strict epidemiology knowing IDA is more common?

8) 10 y/o girl comes to eD 30 min after sudden onset progressive SOB. Had several similar episodes in past 3 months. Resp 24/min, Basically this was an asthma patient (even mentioned Charcot-Leyden crystals), and asked which substance is involvedi n pathogenesis of this disorder?

A. Elastase
B. H2O2
C. IFN-gamma
D. IL-10 (wrong)
E. Lactoferrin
F. Leukotriene C4.

I got down to D and F and went with D, because I'm 100% positive I've heard that people with asthma are somehow susceptible to increased humoral immunity and decreased cell-mediated immunity (due to increased IL-10 levels which inhibit cell-mediated immunity). I know leukotriene C4 is one of the mediators of the reaction but isn't D correct here too?

Thank you very much.
 
I read through about 8 pages and didn't see too much info on these particular questions, if someone can help that'd be great.

1) 51 y/o man is a farmer and comes to doc 5 days after he cut his right foot while cleaning out his barn. 15 year h/o poorly controlled type 2 DM. T 101.3 F, P 105 bpm, BP 139/86. On PE, LE shows erythema up to mid-calf, edema, and exquisite tenderness of ankle and area around laceration. Leuk ct is 57,000/mm3. Response to patient injury?

A. Leukemoid rxn
B. Leukoclastic response (wrong)
C. Leukopenia
D. Leukoplakia
E. Leukotriene

I started thinking of leukemia since the WBC ct was so high, but quickly realized that has nothing to do with the question. Then wanted to choose A, but I remember reading somewhere that in Leukemoid reactions, the WBC count increases but never to more than a specific number (I think it was more than 1.5 or 2x the upper normal limit or something, I forgot). So I excluded it. Definitely not C or D, so between B and E I chose B. What is a leukoclastic response anyway?

2) 27 y/o nulligravid woman inability to conceive for 2 yrs. Menses occurred 3-4 month intervals since menarche at age 14. PE unremarkable. FSH/LH and estrogen normal. Which of the following is the best pharmacotherapy?

A. Clomiphene (I heard this is correct?)
B. Low dose estrogen
C. Medroxyprogesterone (wrong)
D. Metformin
E. Tamoxifen

I chose C because I figured maybe she has normal FSH/LH and estrogen but is lacking in progesterone so she can't conceive. And because of the progestin test, if she is given progesterone and she menstruates, it means she's lacking progesterone. So that's why I chose C. Now that I think about it C does sound wrong, but why is it A? I thought Clomiphene, a SERM, is used for PCOS, to remove the negative feedback estrogen has on the pituitary, and allow for increased LH/FSH to induce ovulation? This doesn't sound like a PCOS pt.

3) 4 month old boy with problem sending stuff out of ER to Golgi.

Is the answer "Dilated RER" due to things backing up in the RER since it cant send it to the Golgi?

4) The 20 y/o guy who binge drank all weekend and took Tylenol and had abd pain and headache on Monday morning.

I know the answer is that it's because alcohol induces P450 which breaks down tylenol into more NAPQI which is toxic, but I didn't choose that one specifically because I've learned that ACUTE ALCOHOL = inhibits p450, while CHRONIC ALCOHOL = stimulates P450. It seemed more like an acute alcohol ingestion so I instead picked E (Alcohol increased NADH:NAD ratio, which I know has nothing to do with tylenol OD but still picked it, thinking maybe we weren't talking about tylenol toxicity in the first place.)

5) Is rupture of an intervertbral disc and slipping or herniation the same meaning? I'm a weightlifter myself and am VERY familiar with this, but that one word made me not choose that answer. When I hear rupture, I think of fracture, and I thought that was an answer for osteoporosis (compression fracture). I instead chose "tearing the sciatic nerve"

6) 33 y/o man has 3 month h/o muscle weakness and cramping shortly after initiating exercise. PE normal, CK elevated, after forearm muscle exercises and measure venous lactate concentrations DO NOT increase compared with preexercise values. Deficiency of which enzyme?

A. Carnitine palmitoyl-transferase-1 (wrong)
B. Fumarase
C. Glucose-6-Phosphatase
D. Glycogen phosphorylase (was this it?)
E. Succinate dehydrognase

I was thinking McKardle disease, but doesn't that present in childhood? Usually a kid in school who can't keep up in gym class. Not sure what the answer is and why. What disease is this? I was thinking LCAT deficiency.

7) Differentiating between IDA and B-thal. I learned we could use the Mentzer index = MCV/RBC, <13 thal >13 IDA. Since in thal you have normal or elevated RBC counts compared to IDA. But they didn't give the RBC count. They also didn't give the RDW to differentiate (RDW high in IDA). Last clue is that in thal, the MCV ct is WAY lower than Hb (for example, MCV 59 but Hb 10.2). For this case I wasn't so sure if it's significantly lower or not, guess it wasn't. So was this just strict epidemiology knowing IDA is more common?

8) 10 y/o girl comes to eD 30 min after sudden onset progressive SOB. Had several similar episodes in past 3 months. Resp 24/min, Basically this was an asthma patient (even mentioned Charcot-Leyden crystals), and asked which substance is involvedi n pathogenesis of this disorder?

A. Elastase
B. H2O2
C. IFN-gamma
D. IL-10 (wrong)
E. Lactoferrin
F. Leukotriene C4.

I got down to D and F and went with D, because I'm 100% positive I've heard that people with asthma are somehow susceptible to increased humoral immunity and decreased cell-mediated immunity (due to increased IL-10 levels which inhibit cell-mediated immunity). I know leukotriene C4 is one of the mediators of the reaction but isn't D correct here too?

Thank you very much.


to answer some of your questions..

1) This is a leukemoid reaction --> the patient has an infection which is the definition of leukemoid reaction listen to pathoma on WBC disorders and they explain the differences between leukemia and a normal leukemoid response to infection. Im not sure if leukoclastic response is a real thing but I would imagine it means damage due to increased wbc's i think an example is leucoclastic vasculitis where neutrophils damage vessels.

2) I think the patient might have had PCOS as all the listed treatment options are for PCOS but the only one to increases fertility is clomiphene

4) Acute Alcohol ingestion actually also acts as a mitochondrial poison and it inhibits glutathione synthesis. So i think maybe thats also why binge drinking can potentiate the toxicity of acetaminophen (depletion of glutathione)

5) I think the answer was rupture of an IV disc..when a patient had degenerative changes in the vertebral disc basically the disc is weakened and that can cause the nucleus pulposus to herniate out. Its basically the same thing when people say they "slipped a disc".

6) I think its McArdle Disease also b/c the lactate levels don't increase which is key b/c there is a skeletal decrees in glycogen phosphorylase that means the patient can't break glycogen down during exercise after serum glucose is used up, so there is no way to make energy and thus no lactic acid is produced. If you were tripped up on the older presentation apparently even though patients are usually symptomatic in the first decade of life they aren't usually diagnosed until the 3rd or 4th decade. I guess since the symptoms aren't so severe?

8) sorry I've never heard of IL-10 being involved in the pathogenesis of asthma. Type I hypersensitivity is not really th2 mediated. It is B cell mediated as far as the production of IgE, but that doesn't really directly related to IL-10. When I think of IL-10 I'm thinking of Th2 which is important for IgE switching of B cells in killing parasites so maybe thats what you were thinking of? Also IL-10 causes Th2 production to attenuate the immune response but we know that asthma is actually a mis-directed immune response, so I would stear away from that as an answer choice here. the question is asking what is most related to the mechanism of asthma its definitely the production of leukotrienes. Also they are specifying the delayed response (30 minutes later) which is directly due to leukotrienes and not so much the mast cells/ histamine release which is immediate.

Hope that helps!! not sure if I was right but that was my reasoning on those questions so let me know if I made a mistake
 
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to answer some of your questions..

1) This is a leukemoid reaction --> the patient has an infection which is the definition of leukemoid reaction listen to pathoma on WBC disorders and they explain the differences between leukemia and a normal leukemoid response to infection. Im not sure if leukoclastic response is a real thing but I would imagine it means damage due to increased wbc's i think an example is leucoclastic vasculitis where neutrophils damage vessels.

2) I think the patient might have had PCOS as all the listed treatment options are for PCOS but the only one to increases fertility is clomiphene

4) Acute Alcohol ingestion actually also acts as a mitochondrial poison and it inhibits glutathione synthesis. So i think maybe thats also why binge drinking can potentiate the toxicity of acetaminophen (depletion of glutathione)

5) I think the answer was rupture of an IV disc..when a patient had degenerative changes in the vertebral disc basically the disc is weakened and that can cause the nucleus pulposus to herniate out. Its basically the same thing when people say they "slipped a disc".

6) I think its McArdle Disease also b/c the lactate levels don't increase which is key b/c there is a skeletal decrees in glycogen phosphorylase that means the patient can't break glycogen down during exercise after serum glucose is used up, so there is no way to make energy and thus no lactic acid is produced. If you were tripped up on the older presentation apparently even though patients are usually symptomatic in the first decade of life they aren't usually diagnosed until the 3rd or 4th decade. I guess since the symptoms aren't so severe?

8) sorry I've never heard of IL-10 being involved in the pathogenesis of asthma. Type I hypersensitivity is not really th2 mediated. It is B cell mediated as far as the production of IgE, but that doesn't really directly related to IL-10. When I think of IL-10 I'm thinking of Th2 which is important for IgE switching of B cells in killing parasites so maybe thats what you were thinking of? Also IL-10 causes Th2 production to attenuate the immune response but we know that asthma is actually a mis-directed immune response, so I would stear away from that as an answer choice here. the question is asking what is most related to the mechanism of asthma its definitely the production of leukotrienes. Also they are specifying the delayed response (30 minutes later) which is directly due to leukotrienes and not so much the mast cells/ histamine release which is immediate.

Hope that helps!! not sure if I was right but that was my reasoning on those questions so let me know if I made a mistake

Thank you, yes that helped a lot. How about the Beta thal and IDA differentiation?

As for the IL-10 thing, I don't remember where but I remember hearing about it in some video. Yes IL-4 leads to increased IgE but I also heard that asthmatics tend to have more IL-10 than normal people which inhibits the CMI. But anyway, it clearly wasn't the best answer and I was thinking of something way more lower-yield than the higher yield simple stuff like the leukotrienes. I really hope I don't do that on the exam.
 
Thank you, yes that helped a lot. How about the Beta thal and IDA differentiation?

As for the IL-10 thing, I don't remember where but I remember hearing about it in some video. Yes IL-4 leads to increased IgE but I also heard that asthmatics tend to have more IL-10 than normal people which inhibits the CMI. But anyway, it clearly wasn't the best answer and I was thinking of something way more lower-yield than the higher yield simple stuff like the leukotrienes. I really hope I don't do that on the exam.


Yeah I definitely have the same problem and tend to overthink questions too but hopefully we get it out of the way before the real thing! Sorry I didn't answer that thalassemia question because I don't remember the question and don't have access to them. Do you remember any of the details of the question stem like clinical presentation? For example, age might be a factor and also did they show any images? Like I'm guessing it was distinguishing between beta thal minor and Iron Deficiency b/c beta thal major is really severe a few months after birth and they would probably have extra medullary hematopoiesis. Beta thal minor is basically asymptomatic and also they would have increased RBC's like you said. If they didn't give any info as far as family history or hemoglobin analysis like electrophoresis I would just go for most common which is Iron deficiency anemia.
 
Yeah I definitely have the same problem and tend to overthink questions too but hopefully we get it out of the way before the real thing! Sorry I didn't answer that thalassemia question because I don't remember the question and don't have access to them. Do you remember any of the details of the question stem like clinical presentation? For example, age might be a factor and also did they show any images? Like I'm guessing it was distinguishing between beta thal minor and Iron Deficiency b/c beta thal major is really severe a few months after birth and they would probably have extra medullary hematopoiesis. Beta thal minor is basically asymptomatic and also they would have increased RBC's like you said. If they didn't give any info as far as family history or hemoglobin analysis like electrophoresis I would just go for most common which is Iron deficiency anemia.

Here it is.

A 38 y/o woman comes for work physical. No history of serious illness. Takes no meds, vital signs normal. PE shows no abnormalities. Lab studies show:
Hb 8.5
Hct 25%
MCV 69
Leuks 5900
Retic 0.8%
Platelet ct 350,000

Diagnosis?

A. Aplastic anemia
B. Iron deficiency anemia
C. Sickle cell disease
D. B-thalassemia minor
E. Vit E (cobalamin) deficiency

Also, I forgot one more question if you can help. It had an image and was basically about a 16 y/o boy that dove into a 3 ft pool and got injured and couldn't move his right upper and lower extremities, and they showed a pic of a lumbar cord crosssection and had to determine where's the lesion. I chose G cuz for some reason I was thinking anterior motor horns (sounded like LMN lesion), but that isn't even the motor horn. I want to know what the right answer is. Is it E? I'm assuming E and F are the lateral corticospinal tracts, so it should be ipsilateral lateral corticospinal tract since it already decussated at the medulla, right?
 
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Here it is.

A 38 y/o woman comes for work physical. No history of serious illness. Takes no meds, vital signs normal. PE shows no abnormalities. Lab studies show:
Hb 8.5
Hct 25%
MCV 69
Leuks 5900
Retic 0.8%
Platelet ct 350,000

Diagnosis?

A. Aplastic anemia
B. Iron deficiency anemia
C. Sickle cell disease
D. B-thalassemia minor
E. Vit E (cobalamin) deficiency

Also, I forgot one more question if you can help. It had an image and was basically about a 16 y/o boy that dove into a 3 ft pool and got injured and couldn't move his right upper and lower extremities, and they showed a pic of a lumbar cord crosssection and had to determine where's the lesion. I chose G cuz for some reason I was thinking anterior motor horns (sounded like LMN lesion), but that isn't even the motor horn. I want to know what the right answer is. Is it E? I'm assuming E and F are the lateral corticospinal tracts, so it should be ipsilateral lateral corticospinal tract since it already decussated at the medulla, right?

http://i216.photobucket.com/albums/cc256/pyaarawala/Capture_zps9khfyfdd.png

So yeah basically I just put Iron deficiency anemia b/c they didn't give me a reason to pick B-thal minor and iron deficiency anemia is the most common cause of microcytic anemia in general. The only way to differentiate i think would be if they gave an Iron study or RDW (both normal in beta thal minor).

For the spinal lesion i also put G but now looking at it its definitely E b/c like you said its the lateral corticospinal tract and the tract comes down ipsilaterally from the cortex and then decussates at the pyramidal decussation of the medulla so then it would be on the contralateral side. Therefore if there is a lesion past the decussation you can't move the side ipsilateral to the lesion. Hope that helps! sorry i was kinda shaky on these 2 questions also so idk if i have the best explanations
 
So yeah basically I just put Iron deficiency anemia b/c they didn't give me a reason to pick B-thal minor and iron deficiency anemia is the most common cause of microcytic anemia in general. The only way to differentiate i think would be if they gave an Iron study or RDW (both normal in beta thal minor).

For the spinal lesion i also put G but now looking at it its definitely E b/c like you said its the lateral corticospinal tract and the tract comes down ipsilaterally from the cortex and then decussates at the pyramidal decussation of the medulla so then it would be on the contralateral side. Therefore if there is a lesion past the decussation you can't move the side ipsilateral to the lesion. Hope that helps! sorry i was kinda shaky on these 2 questions also so idk if i have the best explanations


Nope that's okay. Thank you!
 
A 9-year-old boy is brought to the physician by his mother because of a 1-year history of cough productive of mucoid sputum, wheezing, and shortness of breath with exertion. He has a history of recurrent upper respiratory tract and sinus infections since birth. He is at the 25th percentile for height and weight. The mother says that his younger sibling is beginning to develop similar problems. Physical examination shows mild clubbing of the fingers. Laboratory studies show markedly increased sweat chloride and sodium concentrations. A defect of which of the following in this patient’s bronchial epithelium is most likely causing these symptoms?
A)Adrenoreceptors
B)Membrane receptors
C)Nuclear receptors
D)Protein regulation
E) Protein structure

Okay admittedly I quickly answered this one when I saw membrane receptors. Obv the PT has CF. Yes, I understand that its due to a mutation in the 400th something Phe misfolding, leading to a structural problem, but is CFTR NOT a membrane receptor? That may be an extremely stupid q, but all this time it just seemed like it was.

It's a transmembrane transporter. Hence the name, Cystic Fibrosis Transmembrane regulator. It's not a membrane receptor the way a G protein is.
 
a 51 year old man with 3 month history of hepatitis B antigen negative polyarteritis nodosa has progressive proximal muscle weakness and myalgia. biopsy of involved muscle would most likely show which of the following?
a. central vacuolization with glycogen accumulation
b. central vacuolization with lipid accumulation
c. mitochondrail proliferation
d. mucopolysaccharide deposition
e. PAS positive intramyofibrillar vacuoles (wrong)
f. segmental ischemic necrosis.

Is it segmental ischemic necrosis since you're damaging the blood supply to the muscles?
 
Yup it's f: per uworld PAN causes segmental, transmural, necrotizing inflammation. (Fibrinoid necrosis)


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What is the deal with the questions that have "epigastric" sx and diaphoresis + orthostatic hypotension? What does that typically point to?
 
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.

I also got this wrong. I said 8%... 200/2500.

It's a somewhat fair question though because we don't know when the original 500 contracted chlamydia. Going forward [and I guess assuming those previously infected weren't treated ?...] look at it as 200 out of the remaining healthy 2,000 contracted it within the last year, so only they should be used for incidence.
 
Actually you are probably correct. Clonidine is down the line. I just thought since the diuretic didn't work, then centrally acting might be best. But just saw an article detailing hierarchy of pharmacologic intervention in diabetics with proteinuria: "The first line pharmacologic intervention should be an angiotensin converting enzyme inhibitor or angiotensin II type 1 receptor blocker in those with diabetes or non-diabetics with more than 200 mg protein/gram creatinine on a random urine sample. For non-diabetics with less than 200 mg protein/gram creatinine on a random urine sample, no specific first-line drug class is recommended. After initial dosing with an ACEi, ARB or other drug, a diuretic should be added to the regimen. Thereafter, beta-blockers, calcium channel blockers, apha blockers and alpha 2 agonists (e.g. clonidine) and finally vasodilators (e.g. minoxidil) should be added to achieve blood pressure goal. Combinations of ACEi and ARB are helpful in reducing proteinuria and may also lower blood pressure further in some some cases." http://www.ncbi.nlm.nih.gov/pubmed/16298269

ACE-i and ARBs for diabetic nephropathy are 5 different questions in uworld. they are first line. ive seen clonidine as second line for almost every possible vascular pathology
 
I also got this wrong. I said 8%... 200/2500.

It's a somewhat fair question though because we don't know when the original 500 contracted chlamydia. Going forward [and I guess assuming those previously infected weren't treated ?...] look at it as 200 out of the remaining healthy 2,000 contracted it within the last year, so only they should be used for incidence.
Yeah wasnt sure either. I put 8%. But, i think the 500 should be removed from the incidence. Incidence cannot be cumulative like that. Incidence would be misleading if it somehow incorporated people from different years/timepoints. So I'm guessing: 200/2000.

to MLD: read your definition of incidence again. 'total susceptible population'. those with the disease are excluded.
 
A horseshoe kidney is just a failure of the kidneys to develop into separate organs, and they are attached at one end to each other. This connection is what gets caught on the IMA. I believe the question was forcing you to infer why this would be a problem, and this is because the kidneys are much lower in the abdomen than they should be, the renal arteries are most likely to branch off the abdominal aorta at an abnormal place. Since the question was asking about a man with an abdominal aortic aneurysm undergoing repair, you'd definitely want to know the location of the renal arteries so you don't block their flow.


This was shockingly in uworld.
 
I don't remember the image specifically, but let's look at the clues.
Chemo: decreased immune function; neutropenic
CXR: lobar infiltrate
Histology: I'm guessing PAS has relevance here
All of this leads me to think a fungal infection, for which A would be correct.

Viral is typically not related to neutropenia and lobar infection.
Rheumatoid arthritis not suggested by given history.
Bacterial infection possible but the picture probably rules this in/out.

febrile neutropenia iirc. at risk for fungal and viral infections in particular. the thick PAS was hinting at a thick envelope. it was crypto.
 
A 27-year-old nulligravid woman comes to the physician because of the inability to concieve for 2 years. Menses have occurred at 3-4 month intervals since menarche at the age of 14 years. Physical and pelvic examinations show no abnormalities. Her serum FSH, LH and estrogen concentrations are within the reference ranges. Which of the following is the most appropriate pharmacotherapy for this patient?

A) Clomiphene
B) Low dose estrogen
C) Medroxyprogesterone
D) Metformin
E) Tamoxifen

I put B and it is wrong. What is the right answer?

What is the diagnosis? It's not PCOS because LH and other hormones are in range. So??

A) Clomiphene is used to treat infertility due to anovulation
 
The answer is 31. The percent of people who get the drug-resistant TB each year is 32/1000. Then since 32 people were taken away, you have 968 people left. So you multiply 968*(32/1000), giving you a number very close to 31. Honestly I feel like the math is pretty tricky on this one so you would probably want to estimate rather than doing all the division and multiplication.


HI :) thank you for this answer. May I ask, is this a probability question? Non-mutually exclusive? or is this an epidemiology question? thanks..
 
Don't remember the question from NBME 16, but from what purpledragon1 has written, its an incidence question (so epidemiology I suppose). What they want to test is that you're aware the denominator in the incidence equation are people at risk of the disease, ie people who already have the disease should be excluded.

@mymembernames I'm not sure why you even considered C neoformans. That should typically present with meningitis in an immunocompromised patient. What you have here is a patient with multiple IV lines and systemic inflammation. The more common cause of this should be staph, except the term budding clearly excludes it. That leaves candida. As far as I remember, the picture was atypical for candida, in that it showed neither germ tubes nor the typical mass of pseudohyphae, and thats what probably confused you.
 
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Also, C neoformans usual mode of entry is respiratory.
Most common catheter associated infections are staph, CoNS, enterococci, candida. They've clued you into this with the fever + the blood and catheter cultures both displaying the same organism.
 
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Don't remember the question from NBME 16, but from what purpledragon1 has written, its an incidence question (so epidemiology I suppose). What they want to test is that you're aware the denominator in the incidence equation are people at risk of the disease, ie people who already have the disease should be excluded.

@mymembernames I'm not sure why you even considered C neoformans. That should typically present with meningitis in an immunocompromised patient. What you have here is a patient with multiple IV lines and systemic inflammation. The more common cause of this should be staph, except the term budding clearly excludes it. That leaves candida. As far as I remember, the picture was atypical for candida, in that it showed neither germ tubes nor the typical mass of pseudohyphae, and thats what probably confused you.

Re the incidence question, I get that those who already have the disease should be excluded, but what I dont get is that, if it is an incidence question, why do we have to multiply the remaining cases (968) to the new cases??? Pls help, thanks a lot..
 
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Hey Guys

For the question 68 y/r lady who has severe abdominal pain post meal and they were asking for which artery is stenosed . ..I know that we determined the bruit to be coming from the SMA. I don't understand why because, i thought she had a gastric ulcer? which occurs in the lesser curvature of the duodenum? So why wouldn't it be right gastric?

Clarification on this would be great!
 
Hey Guys

For the question 68 y/r lady who has severe abdominal pain post meal and they were asking for which artery is stenosed . ..I know that we determined the bruit to be coming from the SMA. I don't understand why because, i thought she had a gastric ulcer? which occurs in the lesser curvature of the duodenum? So why wouldn't it be right gastric?

Clarification on this would be great!

This patients presentation was chronic mesenteric ischemia. Mechanism is similar to angina. After eating, there is increased energy requirement for the small bowel. Atherosclerosis of the SMA results in hypoperfusion to small bowel which results in her postprandial pain. Can be found on FA 2017 page 369.


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