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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
So glad it helped!
very well put, thank you
this explanation was on par with Dr. Sattar IMO
Just to add on to this: FA2020 pg. 297. CHALK (Calcium, H+, Adenosine, Lactate, K+) is known to vasodilate muscles during exercise as well as regulate sympathetic tone of arteries at rest
I got this question wrong myself, but the second I looked at the vignette when reviewing, I noticed metaplasia as a hint toward dysplasia as well
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
Great explanation, thanks. Does anyone know why this patient is anemic though? Is there some link between hyperparathyroidism and anemia I am missing?
*Patient erythryocytes = 3million/mm3 (normal 3.5 - 5.5)
So I understand why parathyroid can be the right answer, but why couldn't kidney be correct? This is just my overthinking things, but renal cell carcinoma can present with PTHrp leading to hypercalcemia
Lol, I way overthought that question
In Type 1 DM, the glucagon response to hypoglycemia is not functional and these individuals are reliant on the epinephrine-stimulated hepatic glycogenolysis. I recall this by remembering you can administer glucagon to these patients if they're having a hypoglycemic episode. They can respond to it, but they aren't releasing it.
How did you eliminate thyroxine? As it also plays a role in lipolysis. I was thrown off my the low blood pressure and therefore did not select epinephrine. Why would they still have a low blood pressure?
^ they have low blood pressure because DKA causes a lot of dehydration (vomiting, diuresis due to osmotically active glucose in urine) so low BP
Thyroxine I eliminated because remember that thyroxine is unique in that it functions similar to a steroid hormone and acts in the nucleus to upregulate expression of many genes. I figured hormone-sensitive lipase needs to be activated, not stimulated to upregulate expression, so I thought about EPI and beta-3 stimulation.
I figured since he has low BP/dehydrated, his body would try to maintain cardiac output by increasing sympathetic tone (releasing epinephrine). In hypovolemic shock, systemic vascular resistance is up because of this compensation.
also thyroxine works like a steroid hormone meaning it takes a while to cause its effect
That'd be cool if it were called "epinephrine sensitive lipase"
you're definitely not alone lol
And its not in FA, so fuck it IMO
I guessed it because the names sounded similar :D
I also guessed because both words start with "glu")))
same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle.
Not a clue. This was so random.
this made me feel a lot better.
also, no fucking clue
My immediate thought after reading this was "why would i know this and how does this make me a better doctor?"
Generally speaking Glutamine is often used to aminate things. Think brain nitrogen metabolism. You know that F-6-P isn't an amine, and that Glucosamine is, so Glutamine isn't an unrealistic guess.
yea, I mature 30k anki cards to see this bs
I literally shouted wtf in quiet library at this question.
Lol def didn't know it. Looks like I'm not going to be a competent doctor because I don't know the hexosamine pathway lol
Is it biochemistry? Then I do not know it.
I Ctrl+F'd glucosamine in FA and it's not even there lol
i definitely guessed, for some reason got it down to arginine and glutamine
I did not
Narrowed it down to Arginine and Glutamine figuring the Nitrogen would have to come from one of these two but of course I picked the wrong one. Classic.
+1 no idea!
Ahhh yes the classic Glucosamine from fructose 6-phosphate question....Missed this question harder than the Misoprostol missed swing
no idea. i could only safely eliminate carbamoyl phosphate because that's urea cycle
just adding in to say, nope.
Lol I didn't either. I think this is just critical thinking though. The amine has to come from somewhere. Glutamine/glutamate is known to transfer amines at the least
Isn't the round ligament of the uterus inferior to the ovary? Why would that not want to be preserved as well?
It is inferior, but I think it comes down to what the question is trying to ask. To me I was stuck on that fact as well, but it came down to "what has a significant function and therefore needs to be protected?". The round ligament doesn't have any arteries and whatnot, whereas damaging the ureter has significant consequences. With that, the question seemed to be hinting at "ureter"