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This question is a little bit BS, in that there is nothing in the stem at all to make you infer this specifically. What the question is trying to ask is what factors cause malpractice suits in general. While professional incompetence is a cause, people love to discuss (and the boards love to test) poor physician communication and lack of empathy as root causes.

angelaq11  THANK YOU! here I was thinking I was the only one. I chose the incompetent physician xD +5  
arcanumm  I was on the fence here, but what led me to the correct answer is simply that a question based on an incompetent physician has really no teaching point for our purposes. +  


submitted by yotsubato(519),

Was it just me, or did "age at onset in years" appear RIGHT above the number of patients, rather than the mean. Which confused me for a good 3 minutes.

fulminant_life  Definitely was the same for me. I was so confused for like 5 mins +7  
d_holles  dude i almost didn't get the question bc of this ... i thought the age of onset was the actual age of onset (36) +4  
mellowpenguins  Are you serious. NBME strikes again with shitty formatting. +4  
yex  OMG!! Now I just realized that. Super confused and also thought onset of age was 36. :-/ +4  
monkey  what is 36 supposed to be? +  
thomasburton  Think the number of people in that group +1  
paulkarr  Yup...was looking at it for a good 3 min before just doing the "fuck it..it's gotta be 99" +  
arcanumm  Age of Onset is the Title of the table, which I didn't figure out until after exam was over. What terrible formatting. +  


submitted by seagull(714),

i'm still convinced this is irritable bowel syndrome. Change my mind.

mousie  haha I picked this too bc she's 44.... isn't celiac something that would present much younger?? but I don't think IBS would cause an iron deficiency anemia is the hint they were trying to give us. +  
sympathetikey  If it was IBS, they would have mentioned something about them having abdominal pain, different stool frequency, and then relief after defecation, me thinks. +1  
aknemu  I was between celiac sprue and IBS but what pushed me towards celiac's was a few things: 1. The Iron deficency anemia (I think that would be unlikely in IBS) 2. Steatorrhea (which would also be unlikley in IBS) 3. Osteopenia- I was think vitamin D deficency 4. Lack of a psychiatric history +5  
catch-22  IBS is a diagnosis of exclusion. If you haven't excluded Celiac (and this can't be excluded based on epidemiology alone), you can't diagnose IBS. +9  
arcanumm  I think you may have confused it with IBD, IBS would not present like this. +  


submitted by seagull(714),

"why don't you stop what you're doing because it's ridiculous". --actual answer

sympathetikey  Mam--mam. Put down the egg, mam. +7  
woodenspooninmymouth  I spent sometime in Guatemala last year, and someone told me that the egg thing is uncommon. What is common is giving their children a small gold bracelet. The bracelet is supposed to prevent the evil eye, dunno how. +1  
arcanumm  I think this is a terrible question, but "not a lot" of evidence to support what she was doing is what I had picked. I realize now that is a lie which must be why it is wrong: there is NO evidence to support it. +  


Patient has polycythemia vera, as evidenced by erythrocytosis, granulocytosis, and headaches & diziness. EPO is decreased due to erythrocytosis. Decreased LAP would indicate CML, not PV.

btl_nyc  I thought this was CML. What am I missing that would say CML over PV? +2  
btl_nyc  Nvm, RBCs go down in CML, but everything goes up in PV. +7  
arcanumm  Tricked me. I knew right away that it was PV, but I thought PV would crowd out normal cell creation (e.g. decrease platelets). So apparently crowding out normal cells is just a quality of AML/CML? +  
drzed  More AML. Remember Sattar always stresses that all the myeloproliferative disorders are expansions of ALL lineages, ESPECIALLY "xx" (depends on which one, for CML it'll be granulocytes, for PV it'll be RBCs etc). They're called MYELOproliferative because all the myeloid linages go up, but one will be increased more than the rest. In this case, it is the RBCs. +  


submitted by guillo12(31),

The subscapularis muscle is very important for the Internal rotation of the humerus. The internal rotation supports the upper arm during abduction and adduction.

There are some band exercises that can help you strength the Subscapularis muscle... 1. Internal Rotation - uses medial internal rotation 2. External Rotation - uses lateral external rotation 3. Front Row - You have you hand up in front of you and with your arm extended pull back the band. 4. Side Row - You're side to the band with your hand facing the hip, pull down toward your body. (ADDUCTION)

THIS IS NOT A FAIR QUESTION NBME!!!

arcanumm  I got this wrong too, but I think the exercise of internal rotation makes sense because it will isolate the muscle (without assistance by teres minor for adduction). +3  
tiredofstudying  The subscapularis assists in medial (internal) rotation and adduction, but the teres minor also assists in adduction, so the best choice to isolate the subscapularis would be internal (medial) rotation. Choice E +  
thotcandy  @tiredofstudying teres major also internally rotates so it wouldn't really be isolated either. I guess Tmajor isn't relevant cuz it's not a SITS muscle? Still a stupid question. +  


submitted by youssefa(57),

Pathoma: - Lymphocytes are the most sensitive cells to whole body radiation - Granulocytes (Mainly neutrophils) are particularly very sensitive to chemotherapeutic alkylating agents (requiring G-CSF shortly after)

arcanumm  Always think of NEUTROPENIA when chemotherapy is treating rapidly dividing cells (a small fever is an ER visit for these patients). +4  


submitted by welpdedelp(137),

30* 0.15. Think about it, there is x flow with an oxygen concentration of y--so to find out the delivery you just multiply them together.

yotsubato  One of those questions too simple to believe its actually the right answer +17  
mimi21  Right, I was like this is too simple lol ! im not sure if this is also a good tip but I tend to look at the units they are asking for and double check my math to make sure I end up with them. +5  
osgood-schlatter  what equation is it exactly? +  
arcanumm  Literally did not even conceptualize this question, just looked at the units. +  


submitted by cocoxaurus(44),

Per UWORLD- Adenocarcinoma is associated w/ lung scarring related to granulomatous disease, old COPD (chronic) and damage due to recurrent pneumonia.

arcanumm  Here i was thinking i was being clever by not being tricked by distractors when metastasis is more common... +1  


submitted by defalty98(3),

Why are we complicating things? Change in the bases will destroy the palindromic sequence required for any restriction endonuclease to work. Methylation is the only option that makes sense.

arcanumm  This makes sense have reading what your comment. I overlooked this and just assumed the GATC was a mutation that allowed the restriction enzyme to work on the mutant only. +1  
arcanumm  it makes even more sense when looking at "numerous small fragments." Methylation is truly the obvious answer here in retrospect. +1  
bgiri  DNAse can also cause a change in base by breaking down dna at the GATC sequence? +  
almondbreeze  @bgiri Had the same reasoning - according to wiki, DNase catalyzes the hydrolytic cleavage of phosphodiester linkages in the DNA backbone, thus degrading DNA. +  


submitted by defalty98(3),

Why are we complicating things? Change in the bases will destroy the palindromic sequence required for any restriction endonuclease to work. Methylation is the only option that makes sense.

arcanumm  This makes sense have reading what your comment. I overlooked this and just assumed the GATC was a mutation that allowed the restriction enzyme to work on the mutant only. +1  
arcanumm  it makes even more sense when looking at "numerous small fragments." Methylation is truly the obvious answer here in retrospect. +1  
bgiri  DNAse can also cause a change in base by breaking down dna at the GATC sequence? +  
almondbreeze  @bgiri Had the same reasoning - according to wiki, DNase catalyzes the hydrolytic cleavage of phosphodiester linkages in the DNA backbone, thus degrading DNA. +  


submitted by yotsubato(519),

Murmur that is louder with reduced venous return => Hypertrophic cardiomyopathy

HOCM is due to mutations encoding sarcomeres such as myosin binding protein C and beta myosin heavy chain.

btl_nyc  So I thought this was Marfan's because the murmur from HOCM is at the left sternal border, but Marfan's is a defect in fibrillin, not in collagen. +1  
arcanumm  To help rule out Marfran's, it is stated that there are "no history of major medical illness," which I wouldn't expect them to put if there was a syndrome going on. (they also tend to give body habitus descriptors at least) +  


submitted by keycompany(183),

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5290806/

Osler Sign is a low-sensitivity, low-specficity finding of Mockenberg Arteriolosclerosis (MA) characterized by "a palpable although pulseless, radial artery while the BP cuff is inflated above systolic pressure".

It is possible that either: a) The low-specificity of this test means it is also applicable to atherosclerosis (not just MA) b) The NBME incorrectly implies that MA is interchangable with atherosclerosis.

bubbles  This was my reasoning, too. I thought this was Mockenberg for sure +  
hello  I don't think think it's a type. According to 2 other comments: "It's atherosclerosis because it said “radial artery is NON-pulsatile BUT REMAINS PALPABLE even as the cuff is inflated”--> normally, you can’t feel the artery when the cuff is overinflated b/c overindlation occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!): "If if something were to not be palpable then it would have to collapse -- atheroclerosis prevents this vessel collapse." +8  
arcanumm  I agree, I just reasoned that atherosclerosis would not be thicker when the lumen is blocked. I don't think they were going for Mockenberg at all. +  
arcanumm  would be thicker +  
drzed  Atherosclerosis isn't common in the radial artery though... it's common in the abdominal aorta + coronary, popliteal, and carotid arteries. I am not going to assume a guy has radial artery atherosclerosis when he is in his 80s without a dyslipidemia syndrome over monckeberg calcification! +  


submitted by keycompany(183),

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5290806/

Osler Sign is a low-sensitivity, low-specficity finding of Mockenberg Arteriolosclerosis (MA) characterized by "a palpable although pulseless, radial artery while the BP cuff is inflated above systolic pressure".

It is possible that either: a) The low-specificity of this test means it is also applicable to atherosclerosis (not just MA) b) The NBME incorrectly implies that MA is interchangable with atherosclerosis.

bubbles  This was my reasoning, too. I thought this was Mockenberg for sure +  
hello  I don't think think it's a type. According to 2 other comments: "It's atherosclerosis because it said “radial artery is NON-pulsatile BUT REMAINS PALPABLE even as the cuff is inflated”--> normally, you can’t feel the artery when the cuff is overinflated b/c overindlation occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!): "If if something were to not be palpable then it would have to collapse -- atheroclerosis prevents this vessel collapse." +8  
arcanumm  I agree, I just reasoned that atherosclerosis would not be thicker when the lumen is blocked. I don't think they were going for Mockenberg at all. +  
arcanumm  would be thicker +  
drzed  Atherosclerosis isn't common in the radial artery though... it's common in the abdominal aorta + coronary, popliteal, and carotid arteries. I am not going to assume a guy has radial artery atherosclerosis when he is in his 80s without a dyslipidemia syndrome over monckeberg calcification! +  


submitted by jooceman739(15),

Retinoblastoma:

The physician said the boy is unlikely to develop any other neoplasms, so he doesn't have the inherited Rb mutation.

In this case, he has the sporadic retinoblastoma. Sporadic retinoblastoma requires two somatic mutations of Rb in the same retinal cell.

Just as a side note: Inherited retinoblastomas tend to be bilateral. Sporadic are unilateral.

carls14  aren't retinal cells a type of somatic cell? Why not is the mutation not considered in the somatic cell of the child? +4  
omerta  Although this mutation would be considered somatic, I believe the question is just asking you to be specific as to which cells. If you answered "somatic cells of the child," that's quite broad and could apply to almost anything. +6  
kernicterusthefrog  I had the same struggle and thought process. +1  
eacv  There is a Uworld qx that explain this in detail> ID: 863 +2  
arcanumm  I read the answer options too fast so got this wrong. It is a somatic cell type, but somatic in general implies a higher risk for developing other cancers. The hint here is that the physician stated he is unlikely to develop any other neoplasms, so it is a specific double hit mutation in the retina. +2  
almondbreeze  wouldn't she have any possibility of developing osteosarcoma as well? :( +  
almondbreeze  did some reading and it seems like osteosarcoma only occurs in familial retinoblastoma with RB mutation +