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I'm just adding the page number from FA 2019 to this comment. FA 2019 page 625.
At the end of the fourth week, the yolk sac presents the appearance of a small pear-shaped opening (traditionally called the umbilical vesicle), into the digestive tube by a long narrow tube, the vitelline duct. (Wiki)
But why does it look completely detached from the fetus? I eliminated yolk sac first because of this
If you look reeeeeeeally closely, you'll see some signal between the yolk sac and the baby. Although you can't see the entire connection, they are connected.
Pt is roughly 8 weeks pregnant so and typically by 9th week, Amniotic cavity has expended to fill entire volume of Gestational sac. So the entire black part around the fetus is GS/AC.
and also by 7 week vitelline duct obliterates between umbillicus and yolk sac
What a weird question. I could definitely hear a fixed split heart sound. And it was loudest over the pulmonic valve too which makes it even more of a dirty question. But I guess what I was actually hearing was an S3 heart sound.
@the260guy I believe the splitting is being heard only during inspiration, making this normal physiologic splitting. Perhaps that's just my ears.
don't have adobe and couldn't download it, so I just chose whatever, but your explanation suddenly makes me feel dumb but grateful! Loving your tips! @benwhite_dotcom
@the260guy Have to agree with wutuwantbruv. I interpreted this as a physiological splitting, had the opportunity to hear it in a newborn as well.
Definitely S3. FA 2020 pg 287 "but can be normal in children, young adults, athletes, and pregnancy"
I swear to god it wasnt just during inspiration but what the hell do i know
Exactly!! it's an autosomal dominate disease!
Autosomal dominant diseases are variably expressive. Still, I think this was a badly written question (should have given us some family history).
Also, FA says that fractures may occur during the birthing process, which is what I believe they were going for. I don't believe these findings would be seen at birth with any of the other choices.
Yeah I thought I outsmarted NBME by selecting Rickets bc it said no family history ... guess I got played lol.
Could it be a sporadic cases? Spontaneous Mutation
This is a change in a gene that occurs without an obvious cause, in a family where there is no history of the particular gene mutation. OI is inherited as an autosomal dominant trait. Approximately 35% of cases have no family history and are called "sporadic" cases. In sporadic cases, OI is believed to result from a spontaneous new mutation.
Amboss says the severe subtypes (types II, III) of OI are usually due to a new (sporadic) mutation in COL1A1 or COL1A2, while patients with the mild forms (types I, IV) typically have a parent with the condition.
This has to do with Intention-to-treat analysis. Essentially, when participants are non-adherent but the data shouldn't be lost. They just undergo another statistical model to account for their changes.
Here is a nice video
Where does the question mention "intention-to-treat"?
They seem to be pretty obsessed with "intention-to-treat" it's been asked in one way or another in all the new NBMEs that I've done. (Haven't done 24 as yet)
They don't, intention-to-treat is just the best way to go about it @dr.xx
I agree with @notadoctor !!
i think if it were per protocol, both groups would be excluded, the ones that were inconsistent, the ones that dropped out, and the ones that switched. But answer choices only allow ITT or exclusion of one group.
Standard lab values are incorrect, way to go NBME.
I think they mean to put mm Hg. Normal CSF pressure is about 100-180 mm H20 which equates to about 8-15 mm Hg.
I lost a bit of time wondering about that ugh lol
I thought there must be an obstruction in the ventricles somewhere preventing csf from getting to the spine. so pressure is low in spinal tap but in the head it must be really high.
Pseudo tumor cerebri can have normal ICP. Who knew
Hi, mjmejora, MRI did not see anything abnormality, couldn't this mean that there was no obstruction in the ventricles?
Can't be 17α-hydroxylase because this would present with hypertension and some sort of ambiguous sexual presentation (males) or lack of secondary sexual development (females). Can't be 11β-hydroxylase because this would present with the opposite of the kid's presentation due to the production of 11-deoxycorticosterone (similar effects to aldosterone but not nearly as potent). The other two would not really make sense since there are increased levels of 17-hydroxyprogesterone.
Correct, you would not want to give fibrates to someone with recurrent pancreatitis since fibrates increase the risk of cholesterol gallstones due to inhibition of cholesterol 7α-hydroxylase.
FYI @gh889 can't follow your link w/o an NYIT username and password, unless there's a more tech-savvy way around that.. I appreciate the info, though. Niacin rx for familial hypertriglyceridemia w/ recurrent pancreatitis. Now I know..
Great points, very in depth knowledge taking place here. Also, familial hypertriglyceridemia (per FA 2019 pg 94) has hepatic overproduction of VLDL so picking this would have been the easiest answer (in retrospect)
@impostersyndrome1000 literally that's the ONE thing i remembered and i went YOLO lol cuz i was staring for a while
@gh889 I agree niacin is the answer, but even niacin causes increase in HDL.
As if getting to the drug wasnt tough enough, NBME puts two of its actions in the options! What a shit question
I forget where I saw (maybe UWorld), but I always thought increasing HDL is never really a primary form of lipid control. You want to lower the bad cholesterol etc. since increasing good cholesterol wont change LDL VLDL etc.