Welcome to angelaq11's page.
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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
prefer “patients with hx of substance abuse” over more conveniently typed but less redemptive “drug addict”
I don't see why switching her to oral pain meds when she is ready would be incorrect. Clearly she is worried about being on the pain meds, I feel making a proclamation that she has a low risk of addiction would be profiling just because she doesn't have a history.
The opioid epidemic also affects people who didn't have a previous history of drug abuse. Just a thought, not trying to push any buttons. Maybe I am thinking to hard about this, but I don't see the clear A vs B line for this question.
@sugaplum I thought the exact same thing as you and chose the acetaminophen answer accordingly. I maintain that I am correct, my score be damned!
I had a similar question on UW and the explanation stated that the correct answer choice was the only one that addressed the patient's concern and answered her question. The rest were just alternative treatments, so they were incorrect.
But I too answered with oral pain meds.
couldn't agree more with you all. I chose acetaminophen because opioid abuse is NO joke. The crisis is still going strong because of answers like this...
I ruled out oral acetaminophen because they described in great detail the severity of her injuries, and indicated that she wasn't even fully conscious/aware when she asked this question about opioids. Rather than expose her to more pain, and possibly worsen her long-term pain prognosis, by switching to acetaminophen too early, in this case it makes sense to keep her comfortable because she's very seriously injured and not even fully lucid. It's kind to reassure her in this case.
I appreciate all of the passion for the opioid crisis, and the wording of the answer is definitely not ideal. However, PAIN is also very real, and there is no way acetaminophen alone would cut it in a case like this, not "as soon as she can take medications orally." Maybe I'm lucky to have 6 months in clinicals before STEP or had a mom who just went through urgent spine surgery for breast cancer mets, but there is a time and place for opioids and this is clearly one of them. Thank you for coming to my ted talk.
I agree with anastomoses, cmon guys have you ever had serious pain? oral acetaminophen is NOT enough for that type of pain.
I r/o oral acetaminophen b/c she's post-op for major GI surgeries so you might want to avoid PO meds for a while
As argument against the oral acetaminophen answer choice, it says "switch the patient to oral acetaminophen boldas soon as she can take the medication orallybold" This means you're just waiting for her swallowing inability from the facial fracture surgery to come back, which might not have much to do with her pain, and so it seems somewhat arbitrary.
Maybe logically/clinically A is true, but this seems like a "patient communication" question to me and I could NEVER imagine A being a good way to phrase this point IRL.
THANK YOU! here I was thinking I was the only one. I chose the incompetent physician xD
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.
Though let's everyone be real, if the patient is poor, they are muuuuch less likely to have access to legal means for a malpractice suit. If only the USMLE cared enough to test us on social determinants of health...
Based on the correct answer choice, the person is now in metabolic acidosis with respiratory compensation.
The correct answer choice is as listed above (all decreased). Note that whether metabolic acidosis is combined with primary respiratory alkalosis, which is an important teaching point I’ve argued the question writers are probably getting at, or even if just simple respiratory compensation for metabolic acidosis–both can have the same arrows. In this case, it’s not respiratory compensation. In ASA overdose, the respiratory alkalosis actually happens first. Ultimately, the metabolic acidosis dominates and the pH is almost always low. This mixed primary acid/base response to ASA toxicity is highly testable.
How long till the respiratory alkalosis turns into a metabolic/mixed picture?
@ali 12 hours is a good number to memorize but it can definitely happen much earlier.
From what I understand, the metabolic acidosis only presents 12h post ingestion, while she is only 3h. What do you think?
@yoav, It can definitely happen earlier. It’s more of a by 12 hours (not only beginning then).
I'm beginning to think that they don't actually care about how many hours lapse after the ingestion, but if we actually know the unique acid-base disturbance. I chose the wrong one, again because I was foolishly thinking about those 12 hours postintoxication
I think this is good rule of thmb in USMLE "a Right answer may or may not tick all the correct things but will NEVER have a wrong thing in it". So the ans choice we all chose has Bicarb inc. But this will never happen. at 3 hour we should have pure resp alkalosis with normal bicarb (as per uw). Or in this case decreased due to neutralization by organic salicylic acid. In Aspirin poisoning bicarb will nver increase.
Another important point- they probably gave her RR (30) to indicate that she is hyperventilating==> LOW CO2
I totally hated this Q! I almost completely overlooked the "no tonsillar tissue", and thank God I didn't because that's the clue that made me change my answer. I had CGD (yeah, I know, S. pneumoniae not catalase +), but it said that he had muuultiple infections since birth. And I took to heart that "since birth" thing, because, isn't Bruton supposed to present with infections from around 6moa? I hope I don't screw this up next week
I believe it's that this muscle everts the foot + runs over the lateral malleolus
.. But the phrasing on the question is odd
I didn't actually know this one. I just ruled out everything except the fibularis muscles, and then to be quite honest, I think I had never heard before of the tertius one, so...I chose brevis.
@angelaq11 same here :D
Exactly. I know there are papers saying there is some conversion of T3 to T4 but I try to keep it simple and think of it as once you break it apart (T4->T3), you cant put it back together. Only thyroglobin etc can put another I on it, so any T3 cant become T4 because you need it to be done in thyroid.
I honestly don't know about this, but the way I reasoned this was: she is taking a whole lot of T3, so on top of already having hypothyroidism, she is just making things worse, so TSH is going to be decreased because of feedback inhibition, and hence T4 (Which is the main one produced by the thyroid) is also going to be decreased. I think the high T3 is the exogenous T3.
Sorry about the format, it came out wrong but I hope his helps.
looks good to me!
According to FA2019, stage 2 ends at 11, stage 3 starts 11.5-13, and stage 4 starts at 13-15, where did you get your info from?
You can change it to ENDS at 11, ENDS at 13, ENDS at 14... I simply have it as a range just like you stated in a couple of them. The importance is in how the kid presents because he/she will have some things mature but others not, the age will vary in questions.
stage 3 breast mound is for females not males btw
see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females
this is just too funny, I LOVE it! xD
While this is impressive, this doesn't help with answering the question.
why not membrane receptor?
delF508 is a 3 base pair deletion of phenylalanine at amino acid position 508. Mutation causes impaired post-translational processing of CFTR (improper folding) which rough ER detects. Sends mutant misfolded CFTR to the proteasome for degradation, preventing it from reaching cell surface. So problem is not malfunctioning CFTR channels in the surface; problem is complete absence of CFTR on cell surface (since they keep getting misfolded and sent to proteasome to be trashed). Source of primary problem: error in protein structure
@Is3076 because the CFTR is a channel not a receptor.
FA 2019 p. 60
@a1913 is correct- as for @angelaq11, you can still have a receptor that also functions as a channel as they are not mutually exclusive. An example of this is the nAChR found on postsynaptic NMJ neurons. This is a non-selective, ligand-gated, ionotropic receptor that functions as a channel once its ligand (i.e., ACh) has bound to the active site to induce conformational change. Similarly on the same realm: CFTR is an ionotropic receptor that concurrently functions as a Cl- channel once its ligands (ie. 2 ATP) is bound to open the channel and enable Cl- flux.
This question in particular is asking for the underlying pathophysiologic mechanism for cystic fibrosis, which boils down to an issue with the primary structure of a protein resulting in its misfolding and subsequent sequestration/degradation.
I get Parvo has tropism for RBC precursors, but wouldn’t it take 120 days to manifest?
RBCs don’t just spill out of the bone marrow every 4 months on the dot. Erythropoesis is a constant process. If you get a parvo virus on “Day 1” then the RBCs that were synthesized 120 days before “Day 1” will need to be replaced. They can’t be because of parvovirus. This leads to symptomatic anemia within 5 days because the RBCs that were synthesized 125-120 days before the infection are not being replaced.
@gainsgutsglory @keycompany It seems unlikely that “1 week” of illness can explain such a large drop in Hb. It seems more likely that parvo begins to destroy erythroid precursors LONG BEFORE it manifests clinically as “red cheeks, rash, fever,” etc. Might be overkill to do the math, but back-of-the-envelope: 7 days of 120 day lifespan -> represents ~6 percent of RBC mass. Seems unlikely that failure to replenish 6 percent of total RBC mass would result in the Hb drop observed.
He can drop from 11 to 10 hgb easily
Apologies if this is completely left-field, but I didn't think this was Parvovirus. Parvo would affect face. Notably, patient has fever and THEN rash, which is more indicative of Roseola. Thoughts??
@is2076 check my comment to @hello I thought the same thing for a sec too :)
also i think you guys are thinking of hb in adults in this q it says hb is 10g/dL(N=11-15) so it's not relatively insanely low
@Is3076 I completely agree with @hyperfukus and I think that thinking of Roseola isn't crazy, but remember that usually with Roseola you get from 3-5 days of high fever, THEN fever is completely gone accompanied by a rash. This question says that the patient has a history of 4 days of rash and 7 days of fever, but never mentioned that the fever subsided before the appearance of the rash. And Roseola is not supposed to present with anemia.
@Is3076 another point is that malar rash refers to the butterfly rash on the cheeks that is commonly seen in lupus, so the face is NOT spared.
Honestly y'all lmao
First line...RED CHEEKS AND RASH
Malar Erythema --- Hello?
Rash - Eventually it may extend to the arms, trunk, thighs and buttocks, where the rash has a pink, lacy, slightly raised appearance
Hemoglobin is 1 g/dL below normal.
This is Parvo B19 -- SLAPPED CHEEK.
I swear man, y'all make this easy nonsence. WAY to hard.
because metaplasia would be a transformation of the normal architecture of the respiratory epithelium to one that does not belong there, in response to chronic irritation. This woman had pneumococcal pneumonia that was correctly (and I dare say promptly) treated, so she suffered an acute rather than a chronic insult.
because metaplasia isn't how the normal healing/regeneration response happens in the alveoli. the type 2 pneumocytes serve as stem cells/precursors to both type 1 and 2 pneumocytes so the regeneration is not metaplasia.
This is a cohort study! (Since it involves splitting people into "groups"; group = cohort.) But the stem asks what "best describes" the design. So, yes, it's a cohort study but a more precise ("more specific") description is Open-label. In other words, "Open-label clinical trial" is a type of cohort study, and, in this case, "Open-label" is a more precise description of what is described in the stem.
It is a cohort, just as @drdoom said, but it isn't an "Observational" one.
It's actually not a cohort study, imo. In a cohort you find people with an exposure and see if they develop some outcome. In this experiment, people were RANDOMLY ASSIGNED to the different exposures. That doesn't happen in cohorts.
It may be a cohort in that these people are in groups, but for the purposes of Step 1, I don't think we will deal with typical "Cohort" studies in which participants are randomly assigned.
Thanks for the explanation! Do you know why Mg would not be a potential answer? Phosphate also accumulates in those with undialyzed renal failure, so I was thinking that maybe magnesium as a divalent cation would complex with PO3 (in a mechanism similar to Ca).
From the little bit of research I just did (because I didn't learn anything about dialysis at my medical school), ESRD can be associated with either low or high Mg levels, so the dialysate can cause either increased or decreased Mg levels depending on the patient's serum content, therefore I don't think based on this question, would could determine if removal of dialysis would lead to elevated or decreased magnesium. The end of the first article seems to favor ESRD leading to hypermagnesemia, so if that's the case, then removal of dialysis would cause Mg to increase as well.
https://www.karger.com/Article/FullText/452725 and https://www.karger.com/Article/FullText/485212
why is it that we aren't learning this stuff and they r just throwing it on step there's barely a blurb in FA about ckd/eskd
does uremia potentially have to do with this?
ESRD and not getting dialysis -> he is uremic -> met acidosis -> dec bic
@medulla this is the best and simplest explanation. I got it wrong and chose Mg, wish I had made that connection.
to all my public school peeps out there (and not the nice public schools in rich areas, the real public schools)... we made it!
Thankfully I was taught how to convert units, but let me tell you that I was SO lost on this one. It's USELESS to know how to do it if you (I, I mean I) don't know the damn formula xD. Obviously got this one wrong, but it's good to know that if it ever comes up again (and I know it won't) I already know it.
How do you know the gracile fasciculus is damage?!?!
which parte of the image its damage?, the pink? or black?
the pink park yes
i still don't see where the damage is lol! FML
i finally figured it out lol that was a slow moment i hope im not this slow on step yikes!
@hyperfukus I had the same problem at first, marked it and then came back. If you remember, in the spinal cord the white matter and gray matter are "reversed" compared to the brain. That said, if the butterfly shaped region (ie, the gray matter) is colored (in this case) lilac and the rest (ie, white matter) is blackish, the only thing that is actually abnormal, is the region where the dorsal columns are, because it stains just like the normal gray matter. After that, you have to think about which fasciculus is damaged, the gracilis or the cuneatus. The gracilis is medial while the cuneatus is lateral (picture someone with glued legs and open arms). Hope this helped
Gracilus Fasciculus = Graceful legs
tripped me up cause I didn't know the names :(
omg, same here! I thought, well, I don't know of any duct that connects the pancreas to the liver, so...2nd part of the duodenum it is :'( :'(