NBME 13 discussion

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

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Wanted to revive this thread as I just took the test so wanted to see if there were any recent exam takers who could help with this question:

it involved cyanide poisoning and a diagram showing which part of the electron transport chain would be blocked. The diagram showed cyt c being reduced (wrong), cyt c being oxidized (what I picked), and then a+a3 being oxidized (correct) answer by delivering their electrons to o2. Now, I know a few things here:

That cytochrome c oxidase is the target of cyanide.
That cyt c oxidase is "also know as" a+a3" oxidase.

However, if you know what question i'm talking about, it seems this a little more complex than first aid and other sources make it out to be. for the NBME's answer to be correct, there must be TWO reactions going on in the cytochrome c oxidase complex (complex IV). The actual oxidase of cyt c vai reduction to a+a3, and then the oxidation of a+a3. While I was away of both names of this complex, that doesnt actually help answer the question. Can anyone expand on how to break this question down about Complex IV...are there in fact two different parts to this enzyme, and not only did we have to know complex IV, but in fact WHICH REACTION WITHIN COMPLEX IV that cyanide blocked? (wtf)
 
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The answer is d) suspensory ligament. The ovarian artery is contained within the suspensory ligament which is a fold of peritoneum between the pelvic wall and the ovary. Twisting and turning movements like aerobics can cause the enlarged ovary to twist around the axis of the vessels and strangulate them.

The round ligament is the female equivalent of the the inguinal canal originating in the uterine horns and terminating in the labia majora, and it does not contain any vessels, certainly not those that supply the ovary.
 
thanks all for the reply...i found in one of my notes that a probable mechanism is due to hyperestrogenism --> increased SHBG (remember estrogen increases SHBG and TBG) --> decreased free testosterone --> leading to sexual dysfunction
yup thats correct
 
Can anyone help on this one?

A 20-yo comes to the physician because of cramping abdominal pain and diarrhea during the past 3 weeks; he has had a 4.5-kg (10-lb) weight loss during this period. The pain is exacerbated following meals. He went on a camping trip in upstate New York 3 weeks ago, swimming in the nearby lakes and hiking in the mountains. His vital signs are normal. Physical examination shows no abnormalities. Which of the following diagnostic tests is most likely to identify the causal organism of this patient's condition?

A) Culture of the stool for enteric bacterial pathogens
B) Electron microscopy of the stool for small round viruses
C) Microscopic examination of the stool for ova and parasites
D) Polymerase chain reaction test of the stool for Shiga toxin
E) Protoscopy and rectal biopsy

I think C is the correct answer but i am not sure why A is wrong. What parasite are they referring to?
 
Regarding the seizure question.

25year history would mean she was 15. GM is usually adults (and supratentorial)

HSV is temporal lobes...

I dont know what the other thing is

And AVM....sure why not?
Does anyone know why HSV encephalitis is incorrect? I thought i was putting two and two by thinking that since HSV encephalitis most commonly occurs in temporal lobe, which is the same location that seizures usually start, that should be the correct answer. But obviously that is not correct.
 
1. periosteum. anytime they ask about bone pain/regeneration, answer ir periosteum.

2. above 9th rib midscapular line not sure why this was right though becuase i thought you would hit the lung at that point.

3. PKD. they were a little vague, but a key was that they used CT to diagnose.

4. endothelium

5. anterior to sternocleidomastoid. weird way of asking it i thought, but its a branchial cleft cyst i believe.

6. phosphorylation

7. biofilm. they said antibiotics werent working. good sign it was bioflim, which is like a bunker for the bugs to hide in

8. uggg annoying one, but it was handwashing. my hint is if they ever ask how to prevent something and you dont know, put handwashing.

9. suppression. hes chosing to forget about it.

10. totally normal. for these questions, if you dont know the answer, i would always put its normal or dont treat. they're probably trying to see if you know the condition they are talking about will self resolve.
On number 4, i thought hemangioma was a derivative of mesoderm (like blood vessels?). But that choice was not given. How can hemangioma be endothelium? Is there an explanation for that, other than just something to know?
 
On number 4, i thought hemangioma was a derivative of mesoderm (like blood vessels?). But that choice was not given. How can hemangioma be endothelium? Is there an explanation for that, other than just something to know?
I think you're confusing endothelium and endoderm. Endothelium of blood vessels is a mesodermal derivative.
 
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thanks to all who are posting and helping answer questions. it is very helpful. have another one that i was pretty confused about.

an 18 year old man comes to the physician 6 hours after he twisted his ankle while playing football. Physical examination shows looseness of the lateral collateral ligament suggestive of a tear. Lack of which of the following components in the ligament will most likely healing of this inure.

blood vessels
collagen fibers
elasetic fibers
lymphatic vessels
nerves

I thought most joints and ligaments supporting them have poor blood flow to begin with, and thus receive most of their nutrition and oxygen from synovial fluid. Thus i thought collagen fibers would be the right answer, but it is not so... Does anyone have an explanation for this?
 
If the question is asking about the lack of components that will delay the healing, the answer is blood vessels. The poor supply is the reason for slow healing, not the lack of collagen.
 
1) Someone clear this up for me. Renin is released in response to a decrease in blood pressure, decreased sodium delivery to distal tubule, and due to increased sympathetic tone?So when patients have hypertension, there is increased blood pressure, however renin STILL gets released..Why the heck is that? does this have to do with the fact that "renin is released also due to increased sympathetic tone"? If anyone has a simple way of understanding this, please do share. I thought I knew enough about this subject to get uworld questions right but nbmes showed me I don't have a mastery of this concept.

2) Okay so the early DISTAL CONVOLUTED TUBULE actively reabsorbs SODIUM along with chloride. Its the diluting segment. In addition, LOW SODIUM DELIVERY TO DISTAL TUBULE CAN CAUSE RENIN RELEASE. so….my question is…if ANP causes an increase in gfr/brisk diureses/increase flow to nephron(as mentioned by colleagues on forums), and as a result, you decrease the time you have to reabsorb sodium, shouldn't the macula dense sense this as a DECREASE IN SODIUM AND THEREFORE INCREASE RENIN RELEASE?? I mean why the heck would the macula densa do the opposite and decrease its activity and decrease renin release
 
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a 50 yr old dude w type 2 diabetes(longstanding) comes to the doc cuz of several fainting episodes and fatigue during the past month. Man appears really ill(not sick). His temperature is 98.F, pulse is 94/min and respirations are 17/min and blood pressure is 155?95. Physical exam shows pallor..

then a bunch of values…low hemoglobin and hematocrit but increased mchc and mch…..increased creatinine…

anyways, why the heck is the answer erythropoietin? I got it right because nothing else made sense but please do explain
 
abel is the answer increased epo or decreased epo? if the answer is decreased epo it is because he has chronic kidney disease so he is not responding to his natural turnover in RBCs.
 
ok abel i found the Q. You left out the most important information in your post! NORMAL MCV. Also he is not REALLY ILL he is CHRONICALLY ILL. These words are there for a reason! Normal mcv means kidney is not making epo because the kidney is gorked, or it means he has anemia of chronic disease (i.e. chronically ill!). So the correct answer is epo because either he has ACD or CKD. The other labs illustrate that his bone marrow seems to be ok so it is a problem of not enough epo. Get on some sattar or goljan and review anemia! First thing you look at is MCV!!!

edit: also MCHC is normal. check units dawg.
 
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ok abel i found the Q. You left out the most important information in your post! NORMAL MCV. Also he is not REALLY ILL he is CHRONICALLY ILL. These words are there for a reason! Normal mcv means kidney is not making epo because the kidney is gorked, or it means he has anemia of chronic disease (i.e. chronically ill!). So the correct answer is epo because either he has ACD or CKD. The other labs illustrate that his bone marrow seems to be ok so it is a problem of not enough epo. Get on some sattar or goljan and review anemia! First thing you look at is MCV!!!

Erythropoietin is secreted secondary to when the kidney senses Low o2 content levels in the blood. Remember that o2 binding capacity to hb is a determinant of total o2 content in the blood, which = (o2 binding capacity to hb x % saturation of hb) + dissolved Po2. In this case, the patient has low hemoglobin, which means decreased o2 binding capacity to hb = decreased o2 content = erythropoietin secretion by the kidney to compensate for the loss. Another example of erythropoitetin secretion secondary to low o2 content would be living at high altitudes. Only this time the variable is not a decrease in o2 binding capacity but rather a decrease in Po2.
EazyE1907, 12 minutes agoReport
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A 22 yo woment comes to the physician 3 months after she noticed a painless slowly enlarging mass on the left side of her neck. PE shows a freely mobile soft cystic mass with a cutaneous surface opening. the physicial explain that it is from incomplete fusion during embryo development. which of the following is the most likely location of the opening of the duct leading to the mass of the pt?
a. ant. to the sternocleidomastoid muscle
b. midline of the neck
c. postauricular
d. pos. to the parotid gland
e. submental

What are characteristics that can tell you that this is a cervical cyst? In first AID I thought it says that if the mass is freely mobile mass--then it is going to be a thyroglossal cyst (midline of the neck).

Thanks for the help and explanation
 
A 22 yo woment comes to the physician 3 months after she noticed a painless slowly enlarging mass on the left side of her neck. PE shows a freely mobile soft cystic mass with a cutaneous surface opening. the physicial explain that it is from incomplete fusion during embryo development. which of the following is the most likely location of the opening of the duct leading to the mass of the pt?
a. ant. to the sternocleidomastoid muscle
b. midline of the neck
c. postauricular
d. pos. to the parotid gland
e. submental

What are characteristics that can tell you that this is a cervical cyst? In first AID I thought it says that if the mass is freely mobile mass--then it is going to be a thyroglossal cyst (midline of the neck).

Thanks for the help and explanation
This was tricky. However the question tells you the the mass is on the lateral neck. That is the first thing that led me away from thyroglossal duct cyst (TGD). TGD has the actual moveable mass in the midline.
They are asking you where the cutaneous duct opening is-a TGD doesn't have an opening to the surface. So that should push you away from TGD, and more toward cervical cyst.
 
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I thought it was F...that was wrong as well.

A 50 yo man comes to the physician because of a 2 mo history of pain in his wrists, changes in skin color, and progressive fatigue. His brother had DM2 and cirrhosis. PE shows bronze-colored skin, tenderness of the MCP joints in both hands, and hepatosplenomegaly. Serum studies show:
AST=100
ALT=110
Ferritin=1200
TIBC=200 (N=250-400)
Transferrin sat=80% (N=20-50)
Analysis of a liver bx specimen shows a markedly increase Fe concentration and cirrhosis. Which of the following is the most likely cause of the findings in this patient?
a). Increased EPO action
b). Increased intestinal Fe abs
c). Increased oral Fe intake
d). Decreased EPO
e). Decreased Fe excretion (wrong)
f). Decreased serum tranferrin concentration
 
A 40-year-old woman is brought to the emergency department 30 minutes after sustaining severe chest injuries in a motor vehicle collision. Despite appropriate treatment, she dies 1 hour later. She had a 25-year history of a well-controlled seizure disorder. A photograph of a coronal section of the brain obtained at autopsy is shown. Which of the following is the most likely cause of this patient's seizure disorder?

Glioblastoma multiforme
Herpes simplex encephalitis (wrong)
Mesial temporal sclerosis
Neonatal ischemic stroke
Vascular malformation

They showed a temporal lobe infarction so I thought it would be a herpes simplex encephalitis but that was wrong...was it just an SAH and thus a vascular malformation that just collapsed?
 
I've not taken NBME 13 but maybe I can help out.

First -- our body doesn't really have a good way to get rid of iron, which is why hemochromotosis is such a problem. Besides epithelial sloughing, you can't really get rid of it. This is a good thing, evolutionarily (how we developed), because it used to be a lot more difficult to get iron before you could buy a big steak every day at the grocery store, and so when we did obtain iron we wanted to hold onto every molecule of it.

Now, on to hemochromotosis. It doesn't mention anything about chronic blood transfusions, so I'm going to guess that this guy has primary hereditary hemochromotosis, which is a genetic mutation in the HFE gene HFE is thought to bind to Transferrin and accomidate iron transfer into the blood, which makes sense because when our iron low our transferrin is elevated (increased TIBC). The problem is hemochromotosis is the HFE doesn't really work properly anymore, and is stimulated without transferrin and your intestinal epithelial cells absorb as much iron as they can, even when it's not needed. There is also thought to be some issue with Hepcidin signaling from the liver but it doesn't sound like that is well understood.
 
Can someone help me with the nepritic question?

The one where it asked
Glomerular finding IM flouresence Deposits

and had various ones for each A/B/C/D

I didn't get it wrong but it raised a question I had that hasn't been addressed.

I read "hemoptysis" and "hematuria" and yadda yadda yadda and started thinking about Wegner's.... none of the answer choices lined up with Wegners... nothing about crescents or anything.

The question was going for Goodpastures which I finally conceded it was asking about considering none of the answer choices lined up with Wegners

OKAY so my question is; what would be differences between Goodpasture and Wegner? Correct me if I'm wrong, but both affect lungs and kidneys... all you had to go on in the question stem was pretty much the physical presentation of that. Do they present the same way and you just had to settle on one because Wegner histological findings weren't a choice? Or am I missing something
 
There will be no hematuria in Wegeners, only RPGN causing CKD. The description of Wegener's will usually include rhinitis, LRTI like symptoms associated with infiltrates and nodules in the lungs. This is all down to the underlying granulomatosis. There may also be vasculitic symptoms mentioned e.g. palpable purpuras. Many systems may be involved since it's a vasculitic disease.

With Goodpasture's disease, the antibody is directed to the basement membrane and tissue involvement is diffuse, so you will not have any nodules, etc. Haemoptysis and haematuria are the predominantly mentioned features in questions and there will be no vasculitic symptoms (although some generalised symptoms like fever, body ache could be present).

Both do affect the lung and the kidney. Both may be c-ANCA positive. Both are usually diagnosed with a kidney biopsy. In Wegener's you're looking for "leukocytoclastic vasculitis" and necrotizing granulomas. In Goodpasture's you need fluorescence to show GBM involvement.
 
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For the skiing question, I was a bit surprised about hypovolemia being the reason he's having orthostatic hypertension. I was taught acetazolamide isn't a very powerful diuretic and over time your body can compensate more distally for the sodium lost proximally. But that was definitely the answer, huh? oh well.
 
Both do affect the lung and the kidney. Both may be c-ANCA positive. Both are usually diagnosed with a kidney biopsy. In Wegener's you're looking for "leukocytoclastic vasculitis" and necrotizing granulomas. In Goodpasture's you need fluorescence to show GBM involvement.

wow... thank you so much!
 
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Can anybody explain the reasoning for IL-1 being the answer for the question of the mid 70 year old women with spinal compression fractures?

I chose monoclonal B cell as no other answer made sense. What mechanism is taking place that leads to increased IL-1 action in osteoporosis?
 
IL 1, IL6 and TNF are all downregulated by estrogen and upregulated when estrogen is lost. They directly activate osteoclast activity, especially IL1.
 
I thought it was F...that was wrong as well.

A 50 yo man comes to the physician because of a 2 mo history of pain in his wrists, changes in skin color, and progressive fatigue. His brother had DM2 and cirrhosis. PE shows bronze-colored skin, tenderness of the MCP joints in both hands, and hepatosplenomegaly. Serum studies show:
AST=100
ALT=110
Ferritin=1200
TIBC=200 (N=250-400)
Transferrin sat=80% (N=20-50)
Analysis of a liver bx specimen shows a markedly increase Fe concentration and cirrhosis. Which of the following is the most likely cause of the findings in this patient?
a). Increased EPO action
b). Increased intestinal Fe abs
c). Increased oral Fe intake
d). Decreased EPO
e). Decreased Fe excretion (wrong)
f). Decreased serum tranferrin concentration

B is the answer. You basically have a defect and absorb more Fe than you need.
 
It also helps to know the principles behind the physiological regulation of Fe and Cu by the body.

In the case of Fe, the enterocytes take up as much Fe as possible but export of Fe into the bloodstream is tightly controlled (ferroportin/hepcidin). Excess Fe in the enterocytes that do not enter the bloodstream is lost when the enterocytes are shed on a regular basis. Other than menstrual bleeding and this, the body basically has no other major mechanism of excreting Fe. So the big picture is, since there's no way for the body to excrete Fe, the only point of regulation is controlling uptake by the body. Hence, hemochromatosis is a defect of absorption into the bloodstream which causes Fe accumulation.

Cu however is a different story. The body normally has a large capacity to excrete Cu in bile. So the point of regulation physiologically is excretion in the biliary tract. Therefore, Wilson's disease is a defect of Cu excretion which causes Cu accumulation.

I believe a lot of this is covered in Pathoma though I forget where else I may have seen this.
 
Can anyone help on this one?

A 20-yo comes to the physician because of cramping abdominal pain and diarrhea during the past 3 weeks; he has had a 4.5-kg (10-lb) weight loss during this period. The pain is exacerbated following meals. He went on a camping trip in upstate New York 3 weeks ago, swimming in the nearby lakes and hiking in the mountains. His vital signs are normal. Physical examination shows no abnormalities. Which of the following diagnostic tests is most likely to identify the causal organism of this patient's condition?

A) Culture of the stool for enteric bacterial pathogens
B) Electron microscopy of the stool for small round viruses
C) Microscopic examination of the stool for ova and parasites
D) Polymerase chain reaction test of the stool for Shiga toxin
E) Protoscopy and rectal biopsy

I think C is the correct answer but i am not sure why A is wrong. What parasite are they referring to?


Here are the big buzz phrases "camping trip" and "swimming in near by lakes"--that just says Giardia- it resides in fresh waters and common in ppl going for hiking and so so...as the conditions are favourable for poor hygiene and feco-oral transmission would be eminent. Cheers. I know by now you are done with Step 1 but other folks would be happy to get fed.
 
a 50 yr old dude w type 2 diabetes(longstanding) comes to the doc cuz of several fainting episodes and fatigue during the past month. Man appears really ill(not sick). His temperature is 98.F, pulse is 94/min and respirations are 17/min and blood pressure is 155?95. Physical exam shows pallor..

then a bunch of values…low hemoglobin and hematocrit but increased mchc and mch…..increased creatinine…

anyways, why the heck is the answer erythropoietin? I got it right because nothing else made sense but please do explain

I think here is your best clue- Long Standing Type 2 DM- PLUS high BP and I remember there was given a high BUN/Creatinine, all suggesting Chronic Kidney Disease (CKD) secondary to long standing DM (leading cause for CKD). And the most important cause of Anaemia at the background of CKD is Erythropoietin (EPO) deficiency. EPO is produced in renal interstitial fibroblasts in close association with vasa rectae and tubular epithelial cells. So when DM damages the kidney---->NO EPO---->Anaemia. Treatment is with exogenous administration of EPO (injectables usually).
 
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I finished reading this forum- super nice. Thanks all. :claps:One question undiscussed tho,

6-wk-old neonate with persistent, non-bilous projectile vomiting. P/E- prominent peristalsis. what is the mechanism? I got it wrong but I know the answer is Hypertrophy of pyloric sphincter (typical for non-bilous and projectile vomiting at 6wks). But how do I reconcile "prominent peristalsis"?? doesn't that mean visible peristaltic small bowel loops? or does it just mean "hyper" bowel sounds? if it is the later one then the answer changes. Can you please help? thanks folks! in Advance!
 
I finished reading this forum- super nice. Thanks all. :claps:One question undiscussed tho,

6-wk-old neonate with persistent, non-bilous projectile vomiting. P/E- prominent peristalsis. what is the mechanism? I got it wrong but I know the answer is Hypertrophy of pyloric sphincter (typical for non-bilous and projectile vomiting at 6wks). But how do I reconcile "prominent peristalsis"?? doesn't that mean visible peristaltic small bowel loops? or does it just mean "hyper" bowel sounds? if it is the later one then the answer changes. Can you please help? thanks folks! in Advance!
Prominent peristalsis means you're able to see the peristalsis visibly on the skin of the abdomen. Pathoma explains this pretty well. Imagine the sphincter is closed but the smooth muscle is trying to push against a closed orifice.



Here's a video as well.
 
Prominent peristalsis means you're able to see the peristalsis visibly on the skin of the abdomen. Pathoma explains this pretty well. Imagine the sphincter is closed but the smooth muscle is trying to push against a closed orifice.



Here's a video as well.


Thanks for the video! I guess that is what ran in my mind when I was doing the exam. but that only led me to suspect an obstruction which is not as high as diaphragm (ruling out congenital defect of diaphragm) or even Gastro-duodenal junction (leaving out hypertrophy of the pylorus)...of which I can't be sure. When this happens usually there is obstruction within the small bowel loops, most commonly in the lower parts. So that leaves us with two options among the choices given (Aganglionosis of Large bowel, i.e.. Hirschsprung's, which came wrong for me, and Meconium Obstruction of Intestine ( which I thought is too late to to be recognised at 6wk of age)...in simple terms :wacky:...what is the answer?
 
Thanks for the video! I guess that is what ran in my mind when I was doing the exam. but that only led me to suspect an obstruction which is not as high as diaphragm (ruling out congenital defect of diaphragm) or even Gastro-duodenal junction (leaving out hypertrophy of the pylorus)...of which I can't be sure. When this happens usually there is obstruction within the small bowel loops, most commonly in the lower parts. So that leaves us with two options among the choices given (Aganglionosis of Large bowel, i.e.. Hirschsprung's, which came wrong for me, and Meconium Obstruction of Intestine ( which I thought is too late to to be recognised at 6wk of age)...in simple terms :wacky:...what is the answer?
The non-bilious vomiting should have tipped you off that the obstruction is somewhere between the stomach and duodenum, as if there is no bile then it has not reached the duodenum. The answer was a pyloric stenosis, which is due to hypertrophy of the pylorus muscle. Treatment is usually myotomy.
 
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The non-bilious vomiting should have tipped you off that the obstruction is somewhere between the stomach and duodenum, as if there is no bile then it has not reached the duodenum. The answer was a pyloric stenosis, which is due to hypertrophy of the pylorus muscle. Treatment is usually myotomy.

I figured it out later on tho but I wanted a good reason to believe before I could feel 100%. thanks :)
 
Q: 24 yo man comes to the physician with his wife because they have been unable to conceive for 3 years. The wife has been evaluated for infertility, and the test results were normal. Analysis of the man's semen shows normal numbers of living sperm but they are immotile. In addition to infertility, this man is most likely to have which of the following associated conditions?
A) cholelithiasis
B) coronary artery disease
C) fat malabsorption (wrong)
D) glomerulonephritis
E) sinusitis

I thought CF males had sperm but they were immotile, so I went with fat malabsorption. My next guess would be sinusitis? How do you go about distinguishing between the two? Or is it Kartagener? But they didn't give any other clues pointing toward that in the question....
 
Q: 24 yo man comes to the physician with his wife because they have been unable to conceive for 3 years. The wife has been evaluated for infertility, and the test results were normal. Analysis of the man's semen shows normal numbers of living sperm but they are immotile. In addition to infertility, this man is most likely to have which of the following associated conditions?
A) cholelithiasis
B) coronary artery disease
C) fat malabsorption (wrong)
D) glomerulonephritis
E) sinusitis

I thought CF males had sperm but they were immotile, so I went with fat malabsorption. My next guess would be sinusitis? How do you go about distinguishing between the two? Or is it Kartagener? But they didn't give any other clues pointing toward that in the question....
It's Kartageners. Immotile sperm is the clue. With CF there will be absence of the vas deferens.
 
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There might be a stream of questions coming from me, so bear with me, please! I don't see any mention on this thread of the question about the kid with rheumatic fever (migratory polyarthritis, febrile pharyngitis 2 weeks ago). Pericardial friction rub and quiet heart sounds are heard. ASO+ titers, no pathogens on culture. Greatest risk of death is from:
A) aortic stenosis (nope)
B) embolism
C) mitral insufficiency (wrong)
D) myocarditis
E) septic shock (nope)

I'm guessing it's myocarditis? I guess that would be a greater risk of death than mitral regurg/prolapse? Or is it embolism due to stasis in the L atrium?
 
There might be a stream of questions coming from me, so bear with me, please! I don't see any mention on this thread of the question about the kid with rheumatic fever (migratory polyarthritis, febrile pharyngitis 2 weeks ago). Pericardial friction rub and quiet heart sounds are heard. ASO+ titers, no pathogens on culture. Greatest risk of death is from:
A) aortic stenosis (nope)
B) embolism
C) mitral insufficiency (wrong)
D) myocarditis
E) septic shock (nope)

I'm guessing it's myocarditis? I guess that would be a greater risk of death than mitral regurg/prolapse? Or is it embolism due to stasis in the L atrium?
Myocarditis.
 
There might be a stream of questions coming from me, so bear with me, please! I don't see any mention on this thread of the question about the kid with rheumatic fever (migratory polyarthritis, febrile pharyngitis 2 weeks ago). Pericardial friction rub and quiet heart sounds are heard. ASO+ titers, no pathogens on culture. Greatest risk of death is from:
A) aortic stenosis (nope)
B) embolism
C) mitral insufficiency (wrong)
D) myocarditis
E) septic shock (nope)

I'm guessing it's myocarditis? I guess that would be a greater risk of death than mitral regurg/prolapse? Or is it embolism due to stasis in the L atrium?

Myocarditis. The valve pathology is more of a long term sequellae of rheumatic fever, while the myocarditis is part of the acute presentation (JONES criteria). I think the way the question was phrased was more along the lines of "Greatest risk of death AT THIS TIME is from," in which case, the myocarditis is what could possibly kill him right now. The septic shock is unlikely given that he cleared the infection, and rheumatic fever is caused by molecular mimicry, not an actual pathogen.

Either way, myocarditis is just a better answer, because it could clearly kill the patient. Valve changes (mitral insufficiency or aortic stenosis) usually require comorbidities to be lethal.
 
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Myocarditis. The valve pathology is more of a long term sequellae of rheumatic fever, while the myocarditis is part of the acute presentation (JONES criteria). I think the way the question was phrased was more along the lines of "Greatest risk of death AT THIS TIME is from," in which case, the myocarditis is what could possibly kill him right now. The septic shock is unlikely given that he cleared the infection, and rheumatic fever is caused by molecular mimicry, not an actual pathogen.

Either way, myocarditis is just a better answer, because it could clearly kill the patient. Valve changes (mitral insufficiency or aortic stenosis) usually require comorbidities to be lethal.

thank you! That makes complete sense. And I guess I kind of forgot about the friction rub oops
 
Hi all, so I just finished the nbme 13 and have some questions. There might be some redundancy from previous posts, but I would really appreciate your feedback.

1. An autopsy is done on a 46 yr old woman who died of adenocarcinoma of the colon. Exam of the neck show a 5 cm rounded mass next to the bifurcation of the carotid artery. A section of the mass is shown in the photomicrograph. Immunohistochemistry of the section is positive for synaptophysin, chromagranin and neuron-specific enolase. Electron microscopy shows numerous electron-dense, membrane-bound neurosecretory granules. Exam of the adrenal glands shows no masses. Which of the following is the most likely diagnosis?
upload_2016-2-28_10-27-24.png

A. metastatic colonic adenocarcinoma
B. metastatic squamous cell carcinoma of the larynx
C. papillary carcinoma of the thyroid gland
D. paraganglioma
E. parathyroid adenoma
--> + chromogranin, I was thinking carcinoid and went for A, but it's wrong.


2. A 33 yr old woman who is right-handed is brought to the physician b/c of a 3 day hx of progressive weakness and numbness of her arms and legs. Neurologic exam shows proximal and distal weakness of the upper and lower extremities. There is areflexia. Sensation to vibration and joint position is decreased in the fingers and toes. Nerve conduction studies show a slow conduction velocity in the median, ulnar, peroneal, and tibial nerves. These electrophysiologic findings most likely indicate impaired function of which of the following ion channel?

A. neurotransmitter gated Ca2+ channels
B. neurotransmitter gated K+ channels
C. neurotransmitter gated Na+ channels
D. voltage gated Ca2+ channels
E. voltage gated K+ channels
F. voltage gated Na+ channels
--> Arent these symptoms due to hypocalcemia??? I went for A and got it wrong, so is it D?
 
Hi all, so I just finished the nbme 13 and have some questions. There might be some redundancy from previous posts, but I would really appreciate your feedback.

1. An autopsy is done on a 46 yr old woman who died of adenocarcinoma of the colon. Exam of the neck show a 5 cm rounded mass next to the bifurcation of the carotid artery. A section of the mass is shown in the photomicrograph. Immunohistochemistry of the section is positive for synaptophysin, chromagranin and neuron-specific enolase. Electron microscopy shows numerous electron-dense, membrane-bound neurosecretory granules. Exam of the adrenal glands shows no masses. Which of the following is the most likely diagnosis?
View attachment 200826
A. metastatic colonic adenocarcinoma
B. metastatic squamous cell carcinoma of the larynx
C. papillary carcinoma of the thyroid gland
D. paraganglioma
E. parathyroid adenoma
--> + chromogranin, I was thinking carcinoid and went for A, but it's wrong.


2. A 33 yr old woman who is right-handed is brought to the physician b/c of a 3 day hx of progressive weakness and numbness of her arms and legs. Neurologic exam shows proximal and distal weakness of the upper and lower extremities. There is areflexia. Sensation to vibration and joint position is decreased in the fingers and toes. Nerve conduction studies show a slow conduction velocity in the median, ulnar, peroneal, and tibial nerves. These electrophysiologic findings most likely indicate impaired function of which of the following ion channel?

A. neurotransmitter gated Ca2+ channels
B. neurotransmitter gated K+ channels
C. neurotransmitter gated Na+ channels
D. voltage gated Ca2+ channels
E. voltage gated K+ channels
F. voltage gated Na+ channels
--> Arent these symptoms due to hypocalcemia??? I went for A and got it wrong, so is it D?


1 is D. bifurcation of common carotid is the key thing here . Paragang is a cluster of neuroendocrine cells also (aka synapto/chromogranin +)

2. I'm not sure about this one but I would have picked D Bc remember they are CALCIUM induced calcium receptors.


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Here are some more:

1. A 63 yr old woman comes to the physician b/c of a 2 month hx of a drooping left eyelid, intermittent pain of her Lt. eye, and an unusually large pupil. Her husband has told her that the eye appears to be "looking sideways." Ophthalmologic exam shows ptosis, lateral strabismus, and mydriasis of the Lt. eye. An MRI of the brain shows an aneurysm of the Lt. post. communicating artery. The function of which of the following muscles is most likely remain intact in this pt?

A. ciliary
B. inf. oblique
C. inf. rectus
D. pupillary constrictor
E. superior oblique
F. superior oblique
--> So the fact that the eye is looking sideway, I thought lateral rectus was intact, so I went for F since that does give you sideway movement.... Any clue?


2. A 5 yr old boy is brought to the physician by his mother b/c of progressive clumsiness and fatigue during the past 6 months. He says that his legs are tired. He was delivered at term after an uncomplicated pregnancy. He has met all developmental milestones, although there was some delay compared with other children his age. He is alert. He has difficulty rising from the chair; he uses his arms to push himself into a standing position. He is unable to jump with both feet together. Physical exam shows hypertrophy of the calf muscles. The pt most likely has weak hip adduction as a result of dysfunction of the muscle inserting onto the femur from which of the following locations?

A. anterior sacrum
B. iliac crest
C. iliac spine
D. ischium
E. lateral ilium


3. A 43 yr old man comes to the physician for a routine health maintenance exam. He is 170 cm tall and weighs 86 kg. BMI is 30. Physical exam and lab studies show no other abnormalities. He tells the physician, "My older brother just got diagnosed with diabetes. I don't want that to happen to me. What should I do?" Which of the following diets is most likely to be effective in decreasing this pt's risk for type 2 DM?

A. low calorie
B. low carbohydrate
C. low cholesterol
D. low protein
E. low sodium
--> I chose B and got it wrong. I have no clue....


4. A 52 yr old man comes to the physician b/c of a 3 month hx of epigastric abdominal pain. He also has had an unintentional 6.8 kg weight loss during this period. He has osteoarthritis treated with naproxen as needed. He immigrated to the USA from Japan 6 months ago. He eats mostly traditional Japanese food prepared by his wife. He has smoked 2 packs of cigarettes daily for 30 yrs and drinks three to four glasses of wine daily. He is 170 cm tall and now weighs 82 kg. BMI is 28. Physical exam shows epigastric tenderness. Upper gastrointestinal endoscopy shows a 4 cm ulcer in the stomach. Exam of a biopsy specimen of the lesion confirms adenocarcinoma. Which of the following is the strongest predisposing risk factor for this pt's condition?

A. alcohol use
B. diet
C. ethnicity
D. naproxen use
E. tobacco use
--> So I was debating between A and E and chose E. So is A the answer? Or perhaps C???


5. An executor of an estate consults with a physician concerning the terms of a will. The deceased woman was a philanthropist who was active in addressing disparities in health care. She designated that a large sum of her money be used to educate the public about the leading casue of death in women. The most appropriate use of this money would be a program addressing which of the following dz?

A. breast cancer
B. cardiovascular dz
C. cerebral infarction
D. cervical cancer
E. ovarian cancer
--> So I fell into the trap "women." Chose A and got it wrong. So it has to be B right?
 

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