Official nbme 15 discussion

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abelabbot

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

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does anyone know what tubular hydrostatic pressure refers to? i assumed that it was the same thing as glomerular hydrostatic pressure but apparently that's not the case, i'm now thinking it may refer to bowman's space/capsular hydrostatic pressure.

also it was mentioned earlier that the brain pic was an angular gyrus lesion.. but i looked that up and the symptoms of that are completely different (gerstmann syndrome) than wernickes. gerstmann is more to do with agraphia, acalculia. so if this was indeed wernicke's how come the lesion is not on the superior temporal gyrus?

also someone commented earlier that the diabetic wouldn't have any endogenous insulin secretion after 30 years, but most diabetic drugs require islet function to work like sulfonylureas so they still have some insulin secretion...did anyone get that question right? normal values for insulin secretion when fasting are 5 to 20

I don't recall the first question you're asking

The lesion IS on the superior temporal gyrus. Just google "wernicke's" and look at an image.
The lady was using insulin (pretty sure it said Insulin not other drugs)...the answer is 1. She has long standing diabetes after 30 years you would expect the beta cells to be filled with amyloid, they would not be working. Even if they weren't filled with amyloid they'd be atrophied because of INSULIN use, instead of a drug that works on beta cells (like sulfonylureas).
 
I don't recall the first question you're asking

The lesion IS on the superior temporal gyrus. Just google "wernicke's" and look at an image.
The lady was using insulin (pretty sure it said Insulin not other drugs)...the answer is 1. She has long standing diabetes after 30 years you would expect the beta cells to be filled with amyloid, they would not be working. Even if they weren't filled with amyloid they'd be atrophied because of INSULIN use, instead of a drug that works on beta cells (like sulfonylureas).
aaah excellent call on the atrophy/amyloid issue, didn't occur to me.. and thanks for confirming it was indeed superior temporal gyrus.

the filtration pressure referred to bilateral hydronephrosis, which i'm guessing refers to ureteral obstruction, which would produce an increase in hydrostatic pressure in bowman's space. however that was not an answer choice. the other answer choice referred to changes in the glomerular, tubular, and interstitial hydrostatic and oncotic pressure.

i thought interstitial= bowman's space
glomerular= GC
tubular=??
 
aaah excellent call on the atrophy/amyloid issue, didn't occur to me.. and thanks for confirming it was indeed superior temporal gyrus.

the filtration pressure referred to bilateral hydronephrosis, which i'm guessing refers to ureteral obstruction, which would produce an increase in hydrostatic pressure in bowman's space. however that was not an answer choice. the other answer choice referred to changes in the glomerular, tubular, and interstitial hydrostatic and oncotic pressure.

i thought interstitial= bowman's space
glomerular= GC
tubular=??

Interstitial is between the tubules/nephron segments. Don't recall the question but it interstitial pressure shouldn't have really any impact on filtration fraction/GFR/hydrostatic or oncotic pressure. In this case I believe they are using tubular to indicate Bowman's space as increased tubular pressure/hydrostatic pressure (from hydronephrosis) will also increase the hydrostatic pressure in Bowman's capsule leading to a decreased GFR and FF.
 
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finally got around to reviewing my nbme 15, from reading through this thread to find the answers, all I can say is dang a lot of you all over think things. Just focus on the most obvious answer based on the facts in first aid and don't freak yourselves out, if your spending more like like 15 seconds of "hard thinking" and its not a calculation or one of the up/down arrow problems, your probably just talking yourself out of the right answer.
 
does anyone know what tubular hydrostatic pressure refers to? i assumed that it was the same thing as glomerular hydrostatic pressure but apparently that's not the case, i'm now thinking it may refer to bowman's space/capsular hydrostatic pressure.

also it was mentioned earlier that the brain pic was an angular gyrus lesion.. but i looked that up and the symptoms of that are completely different (gerstmann syndrome) than wernickes. gerstmann is more to do with agraphia, acalculia. so if this was indeed wernicke's how come the lesion is not on the superior temporal gyrus?

also someone commented earlier that the diabetic wouldn't have any endogenous insulin secretion after 30 years, but most diabetic drugs require islet function to work like sulfonylureas so they still have some insulin secretion...did anyone get that question right? normal values for insulin secretion when fasting are 5 to 20

I do not remember the question you are talking about, but i think that, glomerular hydrostatic pressure refers to the pressure that is in the glomerulus made up of the afferent arteriole, and efferent arteriole. So increasing glomerular hydrostatic pressure, means that there is a higher glomerular filtration rate. That would occur, for example, when you dilate the afferent arteriole and constrict the efferent. On the other side you have the capsular hydrostatic pressure, that is the pressure that is inside the bowman's capsule and then the tubules, and therefore, opposite to the glomerular hydrostatic pressure.
urinar15.jpg


Check that img. Hope that clears out your doubt.


The brain image question, I got it wrong also. In my opinion, the question stem was classic for Wernicke's aphasia, and none of the arrows were pointing exactly at Wernicke's area. I chose the one closest to the superior temporal lobe. For me, the answer looked like it was the arrow pointing to the arcuate fasciculus, which makes no sense to me because that would lead to a conductive aphasia, but oh well... that was the answer, its confirmed.
In the img below, the area numbered (4) is the arcuate fasciculus, in the test image the correct answer was pointing here according to me. :mad:
clip_image002_0001.jpg



For your third question, in the long run, DM2 patients will become insulin dependent, basically, their pancreas are done producing insulin, and now the pt requires insulin for survival. HIstologically, the pancreas would be filled with amyloid. That is why, we do not use the classic nomenclature for diabetes, which was insulin dependent diabetics (DM1) and insulin independent diabetics (DM2), because we have improved so much the life expectancy of the "insulin independent diabetics" that they eventually become insulin dependent. The answer for that one was like 1 I think, they didn't have any insulin left.
 
finally got around to reviewing my nbme 15, from reading through this thread to find the answers, all I can say is dang a lot of you all over think things. Just focus on the most obvious answer based on the facts in first aid and don't freak yourselves out, if your spending more like like 15 seconds of "hard thinking" and its not a calculation or one of the up/down arrow problems, your probably just talking yourself out of the right answer.

That sir is... the truth.
 
Interstitial is between the tubules/nephron segments. Don't recall the question but it interstitial pressure shouldn't have really any impact on filtration fraction/GFR/hydrostatic or oncotic pressure. In this case I believe they are using tubular to indicate Bowman's space as increased tubular pressure/hydrostatic pressure (from hydronephrosis) will also increase the hydrostatic pressure in Bowman's capsule leading to a decreased GFR and FF.

I do not remember the question you are talking about, but i think that, glomerular hydrostatic pressure refers to the pressure that is in the glomerulus made up of the afferent arteriole, and efferent arteriole. So increasing glomerular hydrostatic pressure, means that there is a higher glomerular filtration rate. That would occur, for example, when you dilate the afferent arteriole and constrict the efferent. On the other side you have the capsular hydrostatic pressure, that is the pressure that is inside the bowman's capsule and then the tubules, and therefore, opposite to the glomerular hydrostatic pressure.
urinar15.jpg


Check that img. Hope that clears out your doubt.


The brain image question, I got it wrong also. In my opinion, the question stem was classic for Wernicke's aphasia, and none of the arrows were pointing exactly at Wernicke's area. I chose the one closest to the superior temporal lobe. For me, the answer looked like it was the arrow pointing to the arcuate fasciculus, which makes no sense to me because that would lead to a conductive aphasia, but oh well... that was the answer, its confirmed.
In the img below, the area numbered (4) is the arcuate fasciculus, in the test image the correct answer was pointing here according to me. :mad:
clip_image002_0001.jpg



For your third question, in the long run, DM2 patients will become insulin dependent, basically, their pancreas are done producing insulin, and now the pt requires insulin for survival. HIstologically, the pancreas would be filled with amyloid. That is why, we do not use the classic nomenclature for diabetes, which was insulin dependent diabetics (DM1) and insulin independent diabetics (DM2), because we have improved so much the life expectancy of the "insulin independent diabetics" that they eventually become insulin dependent. The answer for that one was like 1 I think, they didn't have any insulin left.

okay i think i finally get it lol!
i just have to remember that tubular pressure contributes to bowman's space pressure.. and to choose very carefully locations on the brain :)
 
What is the genetic term for when a patient simply does not get the autosomal dominant allele from the parent?

The pedigree one, I figured it was an AD trait, pt had a 50/50 chance of getting the disease but she didn't. Instead of choosing incomplete penetrance, i just assumed that the proper word was germline mosaicism, since the germline of the parent will presumably be a mosaic of sperm with some having the mutation and some not having it.
 
What is the genetic term for when a patient simply does not get the autosomal dominant allele from the parent?

The pedigree one, I figured it was an AD trait, pt had a 50/50 chance of getting the disease but she didn't. Instead of choosing incomplete penetrance, i just assumed that the proper word was germline mosaicism, since the germline of the parent will presumably be a mosaic of sperm with some having the mutation and some not having it.

Think germline mosaicism if you see a pedigree and no one above a certain person has the disease but progeny of that person do. I think you were thinking that the person in question didn't get the AD allele but then developed a germline mutation which caused her kids to have it, but that's probably less likely than if the disease had incomplete penetrance (where the person still has the AD allele, but the phenotype just doesn't show up).
 
What was the one about a girl who has continued heavy blood loss one half hour after delivery? What hormone would you give her? I think the choices were estrogen, progesterone, oxytocin, prolactin, and maybe something else.

And what is the issue here? I was completely lost with this one.
 
I have seen diabetic neuropathy** (edited) described as a burning pain and as a needle-like sharp pain (I think). I chose the latter because the question says that hot water makes it feel better, and I just thought it would be odd of heat would make burning pain better lol.
 
With the question about the ADHD kids and treatment allocation, is the right answer stratification?

I thought stratification would more so describe how the data is analyzed? I just put simple random assignment, because even though the groups were split up into guys and girls, I figure that determining which boys gets the treatment would be done by random assignment (and this is what treatment allocation refers to, right)?
 
Can someone explain the deoxyhemoglobin being a better buffer for H+ than oxyhemoglobin for me?

This is what I know

1) O2 in the blood causes H+ dissociate from hemoglobin
2) H+ combines with HCO3 to form CO2 + H2O
3) CO2 leaves RBC in exchange for Chloride

So deoxyhemoglobin would bind to H+ better, so that would presumably decrease CO2 in the blood because more would be used to form bicarbonate, right?



Ohhh maybe I got it. Is it because the blood can only hold so much CO2, most of it needs to be in the form of bicarbonate. Deoxygenated hemoglobin is bound to more H+, which drives the reaction to form more HCO3 and decrease the amount of CO2. This allows the blood to hold even more CO2.

Thanks for the clarification!
 
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Can someone explain the seizure one to me?

I put tonic clonic, because although it started on the right side, the question stem eventually says the patient had repetitive lip smacking and picking movement of the hands.

Since hands is plural, this is presumably on both sides of the body and no longer a partial seizure, right? And to add to it, the stem describes the patient as extending and stiffening the arm to, which seems to describe tonic-clonic. Thanks!
 
What was the one about a girl who has continued heavy blood loss one half hour after delivery? What hormone would you give her? I think the choices were estrogen, progesterone, oxytocin, prolactin, and maybe something else.

And what is the issue here? I was completely lost with this one.
oxytocin. causes contraction of uterus and stops bleeding
 
oh cool. so it wasn't some condition or disease or anything, just extra bleeding that needs to be stopped? i didn't know if it was placenta accreta or something haha
it could have been. I was actually thinking that as well but i guess it wasnt relevant.
 
Just got done with the real deal, and had 3 questions word for word from NBME 15. All 3 were ones I'd missed last week and had the opportunity to pick apart.

Take these tests very seriously folks!
 
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oh cool. so it wasn't some condition or disease or anything, just extra bleeding that needs to be stopped? i didn't know if it was placenta accreta or something haha

On a more clinical tone, and to help you remember better this issue, during parturition, after the baby comes out, an oxytocin infusion is started on the woman to help her uterus contract, lose the placenta, and to prevent further bleeding. This is done always, as protocol.
 
Some of the behavioral science stuff tripped me up on this test, can someone help me understand these?

1) 39 year old woman comes to the physician, and essentially has somatization disorder. What is the most appropriate statement by the physician?
I put "Tell me about any emotional trauma you may have experienced during childhood", but was the answer "Your symptoms could be caused by stress; I would like you to undergo a psychiatric examination"? Is that not just passing her off to another doctor?

2) 28 year old woman comes in with hypoglycemia, doctor suspects surreptitious use of insulin. Which is the most appropriate action?

I put "Confront the patient about the physician's suspicion", but was the answer "Determine the C-peptide concentration in the latest blood specimen drawn"? Do you not need to get the patient's permission for additional tests run on her blood?

3) A study is conducted to evaluate effectiveness of cough meds in children, results were obtained by surveys completed by the parents about their kid's cough at baseline and 1 day after receiving therapy. Which was the most significant limitation to the internal validity of this study?

I put "Subjective nature of the survey instrument", don't know what else it could've been.


Thanks in advance
 
1) I don't remember what the exact answer was, maybe something about tell me the most pressing issue so we can tackle that? But the one you chose assume she had emotional trauma without her ever mentioning it, which is why thats wrong.

2) I was choosing between those two as well, I ended up choosing C-peptide.Since it said latest drawn blood specimen, that shoudl take care of your concern about needing to run additional tests. Also I questioned the word "confront" (even though a previous behavioral question required you to confront the athlete about steroid use)

3) I got this wrong, it was lack of blinding between groups. Something about the difference between external and internal validity. Hopefully someone can elaborate.
 
Can someone explain the seizure one to me?

I put tonic clonic, because although it started on the right side, the question stem eventually says the patient had repetitive lip smacking and picking movement of the hands.

Since hands is plural, this is presumably on both sides of the body and no longer a partial seizure, right? And to add to it, the stem describes the patient as extending and stiffening the arm to, which seems to describe tonic-clonic. Thanks!

The patient clearly loses consciousness, making it a complex type seizure. But all of the brain isnt firing, so its just partial. The generalized ones, like the tonic clonic affects all of the body.

These partial complex are common in children, and they can have automated movements, like lip smacking, hand flapping, sometimes even walking.
 
1) I don't remember what the exact answer was, maybe something about tell me the most pressing issue so we can tackle that? But the one you chose assume she had emotional trauma without her ever mentioning it, which is why thats wrong.
Yeah, the answer for that one was to schedule further appointments to assess the symptom that bothered her the most, or something among those lines. I got it wrong also, I went for the emotional trauma one.

2) I was choosing between those two as well, I ended up choosing C-peptide.Since it said latest drawn blood specimen, that shoudl take care of your concern about needing to run additional tests. Also I questioned the word "confront" (even though a previous behavioral question required you to confront the athlete about steroid use)
Yes, C-peptide was the answer, you already have her blood, so you might as well run it.


3) I got this wrong, it was lack of blinding between groups. Something about the difference between external and internal validity. Hopefully someone can elaborate.
All of the answers presented here would cause bias, I think this question was very difficult because all of them were right. But the strongest 2 choices were that the measuring tool was too subjective, and the lack of blinding. Not having parents blinded on whether they were receiving dextrometorphan or just nothing would cause the greatest bias. Just imagine, a physician comes to you, hands over a questionnaire about how bad was your child's cough and gives you nothing, and next to you is another study subject receiving the same questionnaire but also getting some dextrometorphan for their child. Biased. You need to give them a placebo, without them knowing it.



Hard test.
 
The patient clearly loses consciousness, making it a complex type seizure. But all of the brain isnt firing, so its just partial. The generalized ones, like the tonic clonic affects all of the body.

These partial complex are common in children, and they can have automated movements, like lip smacking, hand flapping, sometimes even walking.

thank you! would you say this is a good basis for the types of seizures?

- Simple partial - one side of the body, automated movements
- Complex partial - one side of the body, automated movements, changes in consciousness
- Tonic clonic - limb extension, then rhythmic movements of extremities
- Myoclonic - no extension/rigidity involved, just rhythmic movements
- Abscence - blank stare
- Status epilepticus - lasting 30 minutes or something

thanks!
 
Yeah, the answer for that one was to schedule further appointments to assess the symptom that bothered her the most, or something among those lines. I got it wrong also, I went for the emotional trauma one..

i thought the answer to this one was the undergoing psychiatric exam?

isn't assessing one complaint at a time kind of like rationing/limiting resources for a patient?
 
Yes. That looks like a good summary of it. There are many other details, but not high yield. I would recommend watching some youtube videos to get an idea of how each of them present. That clinical vignette they gave in this NBME is very classic.
 
i thought the answer to this one was the undergoing psychiatric exam?

isn't assessing one complaint at a time kind of like rationing/limiting resources for a patient?

That is what I thought when I crossed it out, but earlier on the thread they said that was the correct answer. No good explanation though.
 
i thought the answer to this one was the undergoing psychiatric exam?

isn't assessing one complaint at a time kind of like rationing/limiting resources for a patient?

i think its just something with somatiziation disorder. since they have so many problems that don't seem to have any cause, its best to just handle the worst problem first. we also learned in lecture that frequent follow up visits are important to get the problem under control.
 
Anyone help me with this one?

A 37-year-old woman is brought to the emergency department after her husband found her unconscious. Her temperature is 36°C (96.8°F), pulse is 128/min, and blood pressure is 70/40 mm Hg. Physical examination shows cool, pale extremities, jugular venous distention, faint peripheral pulses, and crackles over the bottom two thirds of both lung fields. Heart sounds are normal, and there are no murmurs. She withdraws to painful stimuli in all four extremities. This patient is most likely experiencing which of the following types of shock?

A) Anaphylactic
B) Cardiogenic
C) Hypovolemic
D) Neurogenic
E) Septic

I put D. I would have put B except that they said normal heart sounds, C except that I didn't know why there would be JVD and lung crackles and don't anaphylactic and septic have warm extremities?

Thanks!
 
The answer is B.

The normal heart sounds confused me too. Everything else pointed towards cardiogenic, so I chose that, but I really don't understand this at all.

I think neurogenic shock is when all vascular tone is gone so you get massive vasodilation. In this case, I don't think you would get JVD.
 
Thanks. Yeah.. odd question, I didn't feel like there was any great answer, I guess cardiogenic was the "best" answer haha
 
Think I already know the answer to this one but not sure:

A 25 yr old woman--- comes with general malaise and facial rash for 1 week. she has a10 yr H/O episodes of pleurisy and arthritic painin peripheral joints. P/E shows an malar reash that does not involve nasolabial folds. results of cardiolipin ab, anti-dsDNA and anti-Sm ab assays are positive. which of the foll hemat abnormalities is most likely in this patient?

a--HUS
b--macrocytic anemia
c--multiple nucleated RBCs
c--rouleax formations
d--thrombocytopenia

I put c, now thinking d?
 
She has SLE, and in SLE you can get autoantibodies against both RBCs and platelets, so its thrombocytopenia.

You labeled C twice so I'm not sure what you meant by D lol.
 
7 month old girl with decreased femoral pulses and a systolic murmur in the interscalpular region and the low overall BP?. I know this was coarctation, but what was up with the murmur?

WTF was up with the ethics question where the chick comes in with a million complaints? People said the answer to this is to go for the most distressing symptom and move on from there. But it seems to just go against all other ethics questions I've answered. Like it seems should address her psychological problem lol.

What is the lifestyle change for a duodenal ulcer? Smoking? Is that in first aid?
 
JP - I think that answer was smoking. Not sure about First Aid.

I wanted to confirm one of my incorrects.

Previously healthy 35 y/o hypoxemia from barbiturates. I believe the answer is
D. PO2 50, PCO2 80, A-a 10.

Thanks.
 
Major depressive disorder. I believe the patient age also factors in. If you really think about it, all the other choices dont make sense.

Havent seen it on any USMLE review book or course, so it is very low yield, but I know because of my clinical experience that patients that have a history of stroke are at great risk of major depressive disorder, specially if they dont recover fully, you know, they have a part of their body paralyzed.

You can read about it here:
http://en.wikipedia.org/wiki/Post_stroke_depression
 
JP - I think that answer was smoking. Not sure about First Aid.

I wanted to confirm one of my incorrects.

Previously healthy 35 y/o hypoxemia from barbiturates. I believe the answer is
D. PO2 50, PCO2 80, A-a 10.

Thanks.

I do not remember all the answer choices, but the A-a gradient had to be normal, his PaO2 low and PCO02 high.
 
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!

Essentially getting at precocious puberty (dont give a cause) just want you to know that initially the height will be above normal (75th percentile) and there growth plates will fuse earlier leading to a shorter person than normal (25th percentile) as an adult.



Couple questions for you guys!

1. The old woman with the Ca around 8 and really really high PTH-muscle pain exacrbated by activity-any idea. I put primary hyperPTH but that was wrong.

2. Vignette of a albino (white skin, hair, blue eyes) child-asks what the number of melanocytes and melanin would be, I assume its decreased melanocytes and normal melanin?

3. Right wrist injury, not a fracture in 15 y/o. Point tenderness to palpation of radial aspect between abductor pollicis longus and extensor brevis tendons-asks for sequelae. Put subluxation of trapezium, wrong. Could it be damage to median N.?

4. 18 y/o trys suicide w/ 100 ASA tablets-two days later you find blood in stool, her Hb conc is 12, what else would you expect to find abnormal?
I put platelet count, but that was incorrect.

5. newborn with esophagela atresia, what germ layer is the origin of the cells filling the lumen? Endoderm? I suck at embryo

Thanks guys
 
Essentially getting at precocious puberty (dont give a cause) just want you to know that initially the height will be above normal (75th percentile) and there growth plates will fuse earlier leading to a shorter person than normal (25th percentile) as an adult.



Couple questions for you guys!

1. The old woman with the Ca around 8 and really really high PTH-muscle pain exacrbated by activity-any idea. I put primary hyperPTH but that was wrong.

2. Vignette of a albino (white skin, hair, blue eyes) child-asks what the number of melanocytes and melanin would be, I assume its decreased melanocytes and normal melanin?

3. Right wrist injury, not a fracture in 15 y/o. Point tenderness to palpation of radial aspect between abductor pollicis longus and extensor brevis tendons-asks for sequelae. Put subluxation of trapezium, wrong. Could it be damage to median N.?

4. 18 y/o trys suicide w/ 100 ASA tablets-two days later you find blood in stool, her Hb conc is 12, what else would you expect to find abnormal?
I put platelet count, but that was incorrect.

5. newborn with esophagela atresia, what germ layer is the origin of the cells filling the lumen? Endoderm? I suck at embryo

Thanks guys

1. If the patient has high PTH and low Ca then it cannot be primary hyperparathyroidism. It has to be secondary to something. I do not remember the question to tell what was the cause.

2. In albinos there are normal melanocytes and decreased production of melanin. As opposed to vitiligo where there is destruction of melanocytes.

3. Cannot remember, but I think it was median nerve dmg.

4. cannot remember the other answer choices.

5. Yes, endoderm is the right answer.
 
1. If the patient has high PTH and low Ca then it cannot be primary hyperparathyroidism. It has to be secondary to something. I do not remember the question to tell what was the cause.

2. In albinos there are normal melanocytes and decreased production of melanin. As opposed to vitiligo where there is destruction of melanocytes.

3. Cannot remember, but I think it was median nerve dmg.

4. cannot remember the other answer choices.

5. Yes, endoderm is the right answer.

Thanks dude, totally miffed the albino Question-I new that

Yeah I had between median and the subluxation and went with the incorrect answer I guess

The others were like increased PT, Increased Bleeding time, decreased platlets etc.. tough question I though

The other answer choices for the old lady were like osteomalacia, and metastatic breast cancer I believe with some other stuff thrown in
 
Thanks dude, totally miffed the albino Question-I new that

Yeah I had between median and the subluxation and went with the incorrect answer I guess

The others were like increased PT, Increased Bleeding time, decreased platlets etc.. tough question I though

The other answer choices for the old lady were like osteomalacia, and metastatic breast cancer I believe with some other stuff thrown in

The aspirin overdose one, I think it might be increased PT. It is the first thing that starts failing during liver damage. The liver cannot produce coagulation factors and the PT increases.
 
Why not just post up some of the answers for a few of the question, so we can help you answer them. For the albinism, remember the metabolic pathway involving tyrosine, where you need copper for it, and it can lead to albinism.
 
I didn't like the colon cancer question which showed the picture of the liver. I remember Pathoma talking about the cancers that spread by hematogenous route, and colon cancer isn't one of them. Chose "direct extension" for that, and got it wrong. :(
 
I didn't like the colon cancer question which showed the picture of the liver. I remember Pathoma talking about the cancers that spread by hematogenous route, and colon cancer isn't one of them. Chose "direct extension" for that, and got it wrong. :(

Ive never read pathoma, but that seems wrong. Colon cancer will almost always metastasize to liver through the portal circulation.
 
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Think I already know the answer to this one but not sure:

A 25 yr old woman--- comes with general malaise and facial rash for 1 week. she has a10 yr H/O episodes of pleurisy and arthritic painin peripheral joints. P/E shows an malar reash that does not involve nasolabial folds. results of cardiolipin ab, anti-dsDNA and anti-Sm ab assays are positive. which of the foll hemat abnormalities is most likely in this patient?

a--HUS
b--macrocytic anemia
c--multiple nucleated RBCs
c--rouleax formations
d--thrombocytopenia

I put c, now thinking d?

Can somebody help me out and tell me where i went wrong, I answered macrocytic anemia for this one because I was thinking that she had pernicious anemia. My reasoning was:
1) if a person has one autoimmune disease they're likely to have others( ie: anti-parietal cell antibodies)
2) the question said that the patient had a "ten year history" of symptoms leading to think that all the stored b12 has been depleted by this time, I was thinking maybe she got the anti- parietal cell antibodies sometime early during the 10 years and that then lead to a depletion of the b12...
After looking it up in pathoma it said that both anemia and thrombocytopenia can occur in SLE (pg. 18 B-8). I'm just really confused how it can be possible to pick btw the two answer choices.
Maybe I over thought this question... Picked thrombocytopenia at first then told myself that macrocytic anemia was a better answer for the above reasons.
Sorry in advance if this is an uber dumb question....
 
Can somebody help me out and tell me where i went wrong, I answered macrocytic anemia for this one because I was thinking that she had pernicious anemia. My reasoning was:
1) if a person has one autoimmune disease they're likely to have others( ie: anti-parietal cell antibodies)
2) the question said that the patient had a "ten year history" of symptoms leading to think that all the stored b12 has been depleted by this time, I was thinking maybe she got the anti- parietal cell antibodies sometime early during the 10 years and that then lead to a depletion of the b12...
After looking it up in pathoma it said that both anemia and thrombocytopenia can occur in SLE (pg. 18 B-8). I'm just really confused how it can be possible to pick btw the two answer choices.
Maybe I over thought this question... Picked thrombocytopenia at first then told myself that macrocytic anemia was a better answer for the above reasons.
Sorry in advance if this is an uber dumb question....

I honestly think you over thought this. Everything in the question points to classic SLE (female of child bearing age, pleuritic chest pain, joint pain, malar rash), and even confirms it for you with the antibodies present. one of the causes of secondary ITP in adults is SLE, so answer to this is D.
 
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