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 +0  (nbme21#25)

ok but why is blue nevi wrong? i thought q asks lession in both exposed and unexposed areas.


 +0  (nbme21#6)

all the other options pt would have uterus, ovaries. turners they wouldnt look normal and they would have atrophic ovaries.


 +1  (nbme24#1)

I think key here is they are investigating the hypothesis of ammount of arsenicin water increases RISK of cancer.... best way to measure risk is case control.

nbmehelp  If they were measuring risk shouldn't it be a cohort study though? By looking at first aid..
270onstep1  They both can determine risk. Key here is the time efficiency of case-control studies when compared to cohort.

 +0  (nbme24#42)

"Nuclear laminin dissasembles + reform nuclear envelope during mitosis. They are helpfull for structure and transcriptional regulation in cell nucleus." -OSMOSIS


 +0  (nbme24#42)

"Nuclear laminin dissasembles + reform nuclear envelope during mitosis. They are helpfull for structure and transcriptional regulation in cell nucleus." -OSMOSIS


 +2  (nbme21#34)

its bc this are the only 2 muscles on the orbital floor google orbital floor muscles in google images https://www.google.com/search?q=orbital+muscles&tbm=isch#imgrc=NNOONaLRFuEP1M:


 +0  (nbme23#1)

Toto the dog (tinea can be spread through animals) was with the Three little munchkins, the Tinea tin man and with the wizard wearing turbin in the dermaophyte forest :)


 +10  (nbme23#40)

you need to know diff bt negative pressure ventilation (which is normal ventilation) and positive presssure ventilation (which is mechanical ventilation). In negative pressrue ventilation the diaphragm contracts making a - intrapleural pressure which allows alveoli to expand. in positive ventilation (the pt diaphragm is not contracting thus not expanding chest cavitiy and not creating the - pressure) the machine is creating positive pressure inside alveoli so so alveoli expands. :)


 +2  (nbme23#4)

pt with progressive muscle weakness--> resp muscles not working --> decrease oxygen consumption. no oxygen= no aerobic metabolism --> increase venous lactate, also you keep doing anaerobic glycolysis since you cant go to TCA --> increase energy production via glycolysis :)





Subcomments ...

submitted by catch-22(18),

I woud do a retrospective cohort here. I don't think this question is correct and provides too little information to get the correct answer. "Time efficient" is the operant word here but they simply didn't consider that retrospective cohort would be a better design here as long as the variables are coded.

sherry  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. +1  
soph  I think key here was they were measuring risk though +  
yex  I also chose cohort, since it is comparing a given exposure. +  


submitted by mousie(83),

Is 45 minutes too long to be anaphylactic and would the absence of rash (urticaria, pruritus) RO anaphylactic?

hayayah  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) +3  
hayayah  (also allergy / anaphylactic presents with more skin findings (urticaria, pruritus) +1  
seagull  The time through me off too. I though ABO mismatch since it occured around an hour. I thought TRALI would take a little longer. +4  
charcot_bouchard  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. +2  
soph  I saw hypotension and though anaphylaxis........ -.- +  
usmile1  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. +  


submitted by vshummy(54),

So the best i could find was in First Aid 2019 pg 346 under Diabetic Ketoacidosis. The hyperglycemia and hyperkalemia cause an osmotic diuresis so the entire body gets depleted of fluids. Hence why part of the treatment for DKA is IV fluids. You might even rely on that piece of information alone to answer this question, that DKA is treated with IV fluids.

fulminant_life  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? +3  
toupvote  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. +1  
snafull  Can somebody please explain why 'Inability of neurons to perform glycolysis' is wrong? +1  
johnson  Probably because they're sustained on ketones. +1  
doodimoodi  @snafull glucose is very high in the blood, why would neurons not be able to use it? +1  
soph  @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? +  
drmomo  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909073/ states its primarily due to acidosis along wth hyperosmolarity. so most relevant answer here would be dehydration +  


submitted by lsmarshall(199),

Synaptobrevin is the target of tetanospasmin (tetanus toxin); muscle spasms are characteristic. Only other answer you might consider is Acetylcholinesterase since he is a farmer and buzzwords often carry us to the promised land... but symptoms of a cholinergic storm are absent.

vshummy  Synaptobrevin is a SNARE protein. Why they couldn’t just give us SNARE I’ll never know. +14  
yotsubato  Cause they're dicks, and they watched sketchy to make sure our buzzwords were removed from the exam +10  
yotsubato  Oh and they read FA and did UW to make sure its not in there either +9  
soph  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! +1  


They’re giving a lot of confusing extra information here, maybe to trip us up. They just want volume of distribution, simple as that.

Vd = [drug administered] ÷ [plasma drug concentration]

First convert it all to g/L because this is how the answer will be:

administered: 80 mg = 0.08 g plasma concentration: 4 ug/ml = 0.004 g/L

Thus,

Vd = 0.08 grams ÷ 0.004 g/L = 20 L

Clearance of drug is not a huge factor because the half life is so long that the drug is distributing before significant clearance occurs.

gonyyong  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) +4  
soph  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 +  


submitted by colonelred_(48),

The analysis only showed a mutation in one allele. CF is an autosomal recessive disease: the disease only manifests if there are mutations in both alleles of the CFTR gene.

If you still have 1 functional copy of the CFTR gene, you can still make the CFTR protein (the chloride channel/transporter), hence your body won’t have any issues.

This is analogous to tumor suppressor genes like Rb: so long as one of the alleles you have is functional, you can make enough of the protein to “make up” for the defective allele. If both get knocked out (Rb-/-), you lose the protection provided by the gene because now you make no protein at all.

The only thing that made sense for this question was the fact that the other allele was not included in the analysis.

charcot_bouchard  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. +4  
soph  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 ?? +  
nbmehelp  @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? +  
fallot4logy  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 +  


submitted by jejunumjedi(15),

The blood smear depicts Schuffner stippling. Found the exact image on the web with explanation:

http://spot.pcc.edu/~jvolpe/b/bi234/lec/2_parasites/images/P._vivax.htm

doctorboomboom  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. +1  
jejunumjedi  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. +1  
sherry  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. +1  
soph  UW: in africa most malaria species are resistant to chloroquine. he is from hondruas +  
randios  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. +  


submitted by seagull(432),

This is a panic attack. Hyperventilation drops pCO2 leading to a respiratory alkalosis. po2 is relatively unaffected (don't ask me how?)

sympathetikey  Yeah haha I had the same conundrum. +  
sajaqua1  If she's breathing deep as she breathes fast, then oxygen is still reaching the alveoli , so arterial pO2 would not be effected. +3  
imnotarobotbut  lmao i'm so freaking dumb i thought she was having alcohol withdrawals because it was relieved by alcohol +  
soph  Maybe Po2 is unaffected bc its perfusion (blood) limited not difusion limited (under normal circumstances). +  
charcot_bouchard  PErioral tingling- due to transient hypocalcemia induced by resp alkalosis. +