to snoo-finity ... and beyond!
Welcome to medschul's page.
Contributor score: 35
Felty syndrome, an extraarticular manifestation of RA. Symptoms include a triad of RA, splenomegaly and neutropenia. It's in FA, you just have to squint (look at the fine print under the RA vs OA table in the MSK section).
Incarcerated hernia. If the contents of the hernia become trapped in the weak point in the abdominal wall, it can obstruct the bowel, leading to severe pain, nausea, vomiting, and the inability to have a bowel movement or pass gas.
Like really? Why is he not in pain?
I thought that inguinal hernias were reducible?
could be a femoral hernia as they are more likely to cause incarceration. They do, however, present more often in females. (FA 2019- 364)
incarcerated, not strangulated, thus no pain as there's no serious tissue damage/ischemia. Incarcerated hernias may progress to strangulated in which case he would have pain
Under section, "complications"
You just have to know that POMC is a pro-protein that must be cleaved; not sure if there’s anything in the stem that would really have given it away.
Dunno if this helps, but it says "this protein" (singular) is the precursor of two different protein products. This must mean that the modification occurs after the protein is made, which means after transcription and splicing has already happened.
Also I believe mRNA refers to after the splicing already occurs. If the protein products are from the same mRNA then it can't be alternate splicing.
They're cleaved by tissue-specific proteases
Alternative splicing occurs with hnRNA not mRNA. You get mRNA from alternatively splicing the hnRNA. an mRNA can only make 1 type of protein.
Since the question says the 2 proteins comes from the same mRNA it cannot be alternative splice or post transcriptional mod. FA 2018 page 43 has a good illustration.
Why can it not be arterial hypertension?
I think Arterial HTN is referring to Pulmonary Artery HTN which would be present in LT HF in the long run with RT HF and edema. Pulm HTN would cause a backflow, and doesn't really answer the question "explain the patients Dyspnea". At least, that's how I saw it. Hope this helped.
the question has 2 murmurs, so does she have aortic stenosis too?
i guess it is not relevant since it asked for what is causing her SOB
I guess pulmonary HTN would happen in response to increased pressure after the edema happens, and would cause backflow (to the RV) over pulmonary edema.
There's a really great diagram in UWorld (QID 234) that explains what happens as a result of mitral stenosis. Very similar sounding to the patient in this question.
Would never have thought of that. Thanks
Excess carotene in what way? sorry if thats a stupid question
this is directly from Goljan
"Dietary β-carotenes and retinol esters are sources of retinol. β-carotenes are converted into retinol. (a) Increased β-carotenes in the diet cause the skin to turn yellow (hypercarotenemia). Sclera remains white, whereas in jaundice the sclera is yellow, which can be used to distinguish the two conditions. (c) Vitamin toxicity does not occur with an increase in serum carotene"
β-Carotenes are present in dark-green and yellow vegetables.
When I was a little kid, I like to eat oranges, like I could eat 10 oranges at once, and after a few days, I could tell that I turned yellow...
Mine would beg to differ >:O
Where would I have come across something like this (FA, Pathoma, or out of my S)?
I thought this bitch was a lipoma. Mother fucker
mf2 lipomas is fat. although fat may exist in liquid form, its still opaque, therefore negative transillumination. unlike ganglion cyst.
Only knew this because I have one that comes and goes...
How do we know the parents are not homozygous
Chances are they are not unless they had or are incestuous
Isn't the femoral nerve innervated by L2-4?
Would pheo have a normal resting BP though?
I was trying to justify these tricky questions but very true medschul.. It shouldn't have normal resting BP. Sometimes it seems these NBME always have a trick up their sleeve. Im getting paranoid lol
The reason why the patient probably has normal HTN is because Pheochromocytoma has symptoms that occurs in "spells" - they come and go. Apparently in that moment, when the physician is examining her, she doesn't have the HTN, but like @meningitis explained, so many adrenergic hormones around leads to double the vasoconstriction when the patient stands up.
Thank you @nala_ula for your contribution! Really filled in the gap Iwas missing.
No problem! Thank you for all your contributions throughout this page!
I thought the pheochromocytoma was getting squeezed during sitting and releasing the epinephrine then. kinda like how it can happen during manipulation during surgery. Got it right for sorta wrong reasons then oh well.
When she sits in the examination table there would be a normal activation of the sympathetic system from the stress of getting examined which is amplified by the pheo. Cheers.
UpToDate: Approximately one-half have paroxysmal hypertension; most of the rest have either primary hypertension (formerly called "essential" hypertension) or normal blood pressure.
My problem with this question is that a strawberry hemangioma should continue to grow until 5-8 yrs old so I did not see the answer choice "Continued enlargement as the child grows" would not be an acceptable answer as well.
It says what will happen over the next 5 years......so you literally answered your question. It will grow, and what will happen in 5 years is that it will go away
I still don't get that. Over the course of the next 5 years, it will 1. continue to enlarge as the child grows, and also 2. spontaneously involute. Both answers are literally correct.
I think the best way to answer this question was by process of elimination.
Haha I eliminated the answer by process of elimination.
I eliminated thiazides by process of elimination :(
Shit I eliminated thiazides because of elimination went with HTN thinking intercranial bleed effecting the pituitary
Wouldn't Fanconi syndrome also cause hypokalemia though?
Especially considering the fact that the DCT will be working in overdrive to compensate for lost solutes???
This question did not make sense to me at all. I knew it was Fanconi syndrome yet didn't select the obvious answer because it said "follow up examination 1 week after diagnosis". I thought it would already be in treatment... I searched (now) and it says that treatment is basically replenishing was is lost in the urine. So definitely the wording is like wtf to me
I was thinking since it affected the PCT that Na resorption would be affected as well? But I guess the other segments will pick up the slack?