Welcome to soph’s page.
Contributor score: 62
This makes sense, but I was thrown off by the "normal-appearing" b/c wouldn't AIS pts not have pubic hair?
They just say it's a normal appearing 17 year old girl; not that the external genitalia are normal appearing.
If they were measuring risk shouldn't it be a cohort study though? By looking at first aid..
They both can determine risk. Key here is the time efficiency of case-control studies when compared to cohort.
Case-control only determines odds ratio which is not calculating risk. In rare diseases the odds ratio can be used as an estimate of the risk ratio however.
The smiley face got to me more than it should have. Preciate you.
I agree. I was hesitating between the two choices. I still think cohort study is better regarding the "risk". I hope this kind of questions wont pop out on the real thing.
I think key here was they were measuring risk though
I also chose cohort, since it is comparing a given exposure.
I was also thinking retrospective cohort study - just as time efficient, can look at risk, and the Q stem said the cancer was common, and I think of case-control for rare conditions. It's like they forgot a cohort study could be retrospective.
The classic example they always give for why not to do retrospective cohort is because patients who have whatever disease your testing for are more likely to remember all their risk factor exposures than a normal person that doesn't have any disease. Of course in this case I'm sure the people running the study would be the ones who figure out how much arsenic was in the water but this also would be very time consuming to figure out for each individual person in the study. Thus a case-control study where you look at a group of people with >50 arsenic exposure and a group <5 arsenic exposure and simply see who has cancer and who doesn't would be easier and take less time.
Yes! Allergic/anaphylactic blood transfusion reaction is within minutes to 2-3 hours.
(pg 114 of the 2019 FA has a list of them ordered by time)
(also allergy / anaphylactic presents with more skin findings (urticaria, pruritus)
The time through me off too. I though ABO mismatch since it occured around an hour. I thought TRALI would take a little longer.
Guys anaphylactic reaction to whole blood doesnt occur much except for selective IgA defi. so look out for prev history of mucosal infection. And it can have all feature of type 1 HS inclding bronchospasm.
I saw hypotension and though anaphylaxis........ -.-
Chest Xray showed "bilateral diffuse airspace disease". This is much more indicative of TRALI than anaphylaxis which would have wheezing and possibly respiratory arrest but no actual damage to the lungs. Additionally there was no urticaria or pruritus one would expect to see with anaphylaxis.
I just dont understand how that is the cause of his altered state of consciousness. Why wouldnt altered affinity of oxygen from HbA1c be correct? A1C has a higher affinity for oxygen so wouldnt that be a better reason for him being unconscious?
HbA1c is more of a chronic process. It is a snapshot of three months. Also, people can have elevated A1c without much impact on their mental status. Other organs are affected sooner and to a greater degree than the brain. DKA is an acute issue.
Can somebody please explain why 'Inability of neurons to perform glycolysis' is wrong?
Probably because they're sustained on ketones.
@snafull glucose is very high in the blood, why would neurons not be able to use it?
@snafull maybe u are confusing bc DK tissues are unable to use the high glucose as it is unable to enter cells but I dont think thats the case in the neurons?
I thought the high amount of glucose in the blood (osmotic pressure), sucks out the water from the cells. But you also pee out all that glucose and water goes with it. That's why you have to drink and pee a lot..
Neurons are not dependent on insulin, so they are not affected by utilization of glucose (only GLUT4 receptors in the muscle and adipose tissue are insulin dependent)
@titanesxvi You really enlightened me!
I don't make the connection of what titanesxvi said to the question - can someone explain?
@mutteringly it explains why the answer choice "inability of neurons to perform glycolysis" is wrong
Synaptobrevin is a SNARE protein. Why they couldn’t just give us SNARE I’ll never know.
Cause they're dicks, and they watched sketchy to make sure our buzzwords were removed from the exam
Oh and they read FA and did UW to make sure its not in there either
This toxin binds to the presynaptic membrane of the neuromuscular junction and is internalized and transported retroaxonally to the spinal cord. Enzymatically, tetanus toxin is a zinc metalloprotease that cleaves the protein synaptobrevin, an integral neurovesicle protein involved in membrane fusion. Without membrane fusion, the release of inhibitory neurotransmitters glycine and GABA is blocked. -rx questions!
So out of curiosity I checked out B) N-Acetylneuraminic acid
It's sialic acid
shocked they haven't started calling a "farmworker" a "drudge" <-- word I pulled from thesaurus.
"You shouldn't memorize buzzwords. You gotta learn how to think."
Lemme pick another random ass word that doesn't have anything to do with critical thinking skills and use it instead.
Just as an FYI, there are multiple "SNARE" Proteins. Syntaxin, SNAP 25, Synaptobrevin (VAMP). From google it looks like Tetanospasmin cleaves Synaptobrevin (VAMP). Botulism toxin has multiple serotypes that target any of the SNARE proteins.
Here's one fact I won't forget: Step 1 testwriters are incels
its not an ACH-E inhib because he doesnt have dumbell signs
I'm not even mad I got this wrong
I think the distribution half-life and elimination half-life was saying that by the time you checked, it had fully distributed (10 half-lifes) and had not been cleared yet (super long half-life)
1000ug= 1mg and 1g=1000000ug
so then 4ug/ml * 1g/ 1000000ug= 0.000004 g/ml
0.000004g/ml * 1000ml/L= 0.004 g/L
80mg*1g/1000mg= 0.08 g
vd= 0.08g/ 0.04g/l =20L
Or, like a normal human, convert 4ug/mL into mg/L ... which is 4 mg/L. 80mg/4mg/L is 20L.
I hate NBME... I thought these stupid conversions were over after undergrad. Nope.
You do 1000000000s of these a day if you do any type of labwork o.O You just get used to it eventually
OR another allele has a diff type of mutation because CF is done by like hundreds of diff type of mutation. SO the 70 types that we screened covered one type from one parent but not another that was inherited from other parent.
I put D thinking there was a mutation in another protein that interacts with CFTR....thus u dont have CF but some disease with similar phenotype. Is this wrong bc its simply not the case ??
@charcot_bouchard I think that makes more sense if I understand what you're saying- Probably had a mutation only in 1 of 2 of the same alleles in the analysis but had another mutation in 2 of 2 alleles at a different location not included in the analysis, right?
CF is a rare disease , and the possibility to have a mutated gene plus a gene that its not belong to 70 most common cf mutations is extremely rare
@soph i picked D too but now looking back, the panel had 70 of the most common CFTR gene mutations so it is unlikely that they didn't already check a gene that codes for a protein that interacts with CFTR? that's the only way i can rationalize it. its bad writing ultimately
I also picked D, but there are over 1700 different mutations for CF and it's too hard to test for them all - the panel in the question tested for the 70 most common. As others mentioned, CF is an autosomal recessive disease, so there must be another mutated allele here for the child to present with the disease. It's more likely, and I imagine not uncommon, that the mutation is not in the panel. As for D, I suppose the best reasoning I can come up for it is that nothing like that exists - what protein interacts with ONE mutated CFTR allele in that it results in the same phenotype as CF, a disorder that requires TWO mutated alleles? I have never heard of such a thing, whereas I have definitely heard of A being the case.
Hey thanks for finding the image! Do you know why the answer can’t be Chloroquine resistance? I was b/w that and formation of hypnozoites.
I think it's just that Schuffner stippling and hypnozoites are both specific to vivax and ovale species. These species could be chloroquine resistant or sensitive, but if you have Schuffner stippling or hypnozoites, you can definitively say that it's either vivax or ovale.
Species with hypnozoites is not called chloroquine resistant. Chloroquine-resistant species means trophozoite/schizont cant be killed by chloroquine. We dont have enough info to decide whether the spp in the q is resistant/sensitive. But we do know he moved from Honduras to USA 1 year ago.
UW: in africa most malaria species are resistant to chloroquine. he is from hondruas
Can anyone explain the 1-week history of fever? Ruled out vivax and ovale due to 48 hr cycles. Or did they just throw that in as an unspecific symptom.
unspecific symptom probably
how I know that is an infection by vivax/ovale ? if there's nothing that says about tertian fever?
While it COULD be Chloroquine resistant, its not likely.
This patient is likely infected with Vivax or ovale (not Falciparium) why?
1. Honduras (Falcip would be Africa)
2. Sx 1 year later (Liver form Vivax or OVale)
3. As many mentioned, Schuffer bodies
Falciparium tends to be the species resistant to Chloroquine.
Typically, Chloroquine is given for Vivax & Ovale (typically with something else- Atovaquone, Dapsone etc) to cover Liver
Falciparium (no Liver form) is generally Chloroquine resistant (B) and therefore covered with Atovaquone/Proguanil. You do need 8-14 days of tx after coming for Falcip bc it can remain in the Liver for a few days (just not a dormant hypno form).
To cover the "week of fever" question- its re-emergence of her sx. They probably just did not want to say cyclic to make it trickier.
Looks like it's been touched on, but you could answer this solely based on the fact that it's been one year since living in Honduras. While it MAY be chloroquine resistant, it IS dormant. Test taking skills would be to choose the answer you can't argue with
Yeah haha I had the same conundrum.
If she's breathing deep as she breathes fast, then oxygen is still reaching the alveoli , so arterial pO2 would not be effected.
lmao i'm so freaking dumb i thought she was having alcohol withdrawals because it was relieved by alcohol
Maybe Po2 is unaffected bc its perfusion (blood) limited not difusion limited (under normal circumstances).
PErioral tingling- due to transient hypocalcemia induced by resp alkalosis.
I believe CO2 diffuses ~20x faster than O2, so increases in her respiratory rate have more effect on her PCO2 than her PO2
adding onto Charcot_bouchards comment, I found this:
Respiratory alkalosis secondary to hyperventilation is probably the most common cause of acute ionised hypocalcaemia. Binding between calcium and protein is enhanced when serum pH increases, resulting in decreased ionised calcium. Respiratory alkalosis can induce secondary hypocalcaemia that may cause cardiac arrhythmias, conduction abnormalities and various somatic symptoms such as paraesthesia, PErioral numbness, hyperreflexia, convulsive disorders, muscle spasm and tetany.