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It's so obscure of a test that wikipedia only has 4 sentences on it.
FA2020 added the Ham test to PNH I believe!
Whoops no sorry I am wrong. They did add something called the EMA test to spherocytosis though.
Ham test has been replaced by flow cytometry now. So fck off, NBME.
I remember it like this: PNH occurs at night due to mild respiratory acidosis (slower respiratory rate), which activates complement which destroys RBCs. The test is essentially doing the same thing, putting cells into an acidic environment -> dead RBCs.
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
But the question doesn't mention anything about which cyclin. How does this help?
@snripper I think the word choice of "mitotic cyclins" is suppose to show they wanted cyclin B which is produced in G2. This resource specifically refers to cyclin B with mitosis.
CDKs and different cyclins are expressed at different stages of the cell cycle: cyclin D (G1), cyclin E (G1/S), cyclin A (S), cyclin B (mitosis).
no pneumonia it is UTI
this is essentially urosepsis, one of the leading causes of sepsis
UTI -> Sepsis -> ARDS (exudative pathophysiology d/t increased pulmonary vasc permeability)
lmao I read it as upper respiratory tract infections, too.
Just rereading this question without the stress, i got it quickly! Could't believe i missed something as simple as this.
Can't believe I spent 5 minutes on this and still got it wrong lmao.
I was like, "it can't be 90% chance of missing an association, that's way too high." But I picked it nontheless...
Me four :-/
Slowly raising my hand as well
patient has malaria with obvious picture and clinic, i answered because only thing associated with liver was hypoglycemia
I was thinking that she is hypotensive which can cause an infarct of the pituitary (since pituitary is growing during pregnancy) and therefore she'd have secondary adrenal insufficiency.
Dumbasses unite lmao
me also :/ sitting there trying to figure it out during the test I thought I was so smart too - like "wow nbme, way to tie in micro and endocrine, not getting me though!" ... i was wrong.
No hepatosplenomegaly, ascites, or edema through me off. We that being said, I shied away from cirrhosis. I thought that he showed signed of depression, so I went with the thyroid. But who's to say he isn't injection anabolic steroids?!
The principle is you can get liver dysfunction without having HSM, ascites, etc. Liver disease is on a progressive spectrum.
He likely has hepatitis B/C given his history of intravenous drug use. I believe both can have liver dysfunction but may or may not have ascites, whereas the type of damage we would expect from alcohol that would match this presentation would also show ascites.
For Ascities u need to have portal HTN. Thats a must. (unless exudative cause like Malignancy)
For anyone who needs it; the FA photo is kinda burned into my mind for these questions. NBME has some weird infatuation with this clinical presentation.. FA (2019) Pg: 383 "Cirrhosis and Portal HTN".
@paulkarr the problem was that the FA image was burned into my mind so without no ascites or edema threw me off of cirrhosis.
cirrhosis doesn't present hepatomegaly, instead, the liver could be shrunken.
Cirrhosis (most likely due to alcoholism in this patient) leads to an increase in sex hormone binding globulin, causing a relative increase in estrogen compared to androgens. Cirrhosis doesn't always have to present with ascites and adema. I agree with @catch-22 that liver disease is a spectrum. This patient does not have ascites because his liver is still able to produce enough albumin to maintain oncotic pressure in the blood.
But why are there no bite cells? Question stem states that there is normal morphology? That's why I didn't pick accessory spleen
Bite cells are seen when splenic macrophages take "bites" out of hemoglobin precipitates in G6PD deficiency, which doesn't have to do with our question.
This patient had a splenectomy 3 months ago, 6 weeks later showed Howell-Jolly bodies (asplenia), and then today now has normal erythrocytes (spleen is working again somehow = accessory spleen)
@spow Bite cells are associated with G6PD deficiency, not ITP.
Main takeaway is the HJ bodies. They're seen pretty much whenever you have no spleen. So if they dissapear, that means another spleen-like structure has showed up
It can't be rotator cuff problems because abduction is normal up to 90 degrees.
Left atrial myxoma can mimic mitral stenosis (thus diastolic murmur)
RVOT obstruction would cause a systolic murmur that gets louder when standing, not diastolic.
RVOT obstruction = Hypertrophic Obstructive Cardiomyopathy which causes diastolic dysfunction (S3) not a systolic murmur.
To expand on this, the flushing/warmth/redness is due to release of PGD2 and PGE2 which is why taking an NSAID helps.
Doesn't acetaminophen inhibits COX 1-2, too? Why can't you use that instead of aspirin? Just wondering.
I had this same question too, and had it narrowed down to those two choices. Ended up going w/aspirin but it was sort of a coin toss. Still not sure why it's not acetaminophen.
I think the reason is that acetaminophen is inhibited peripherally and is mainly used to inhibit COX in the CNS
The worst side effect of Niacin is hepatotoxicity. Acetaminophen is famously known for hepatoxicity so aspirin is a better answer
Acetominophen is an antipyretic and analgesic, but it is not antiinflammatory, so it wouldn't be useful for Niacin induced flushing. (See sketchy pharm for NSAIDs)
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.
Pseudogynecomastia (False gynecomastia): this has nothing to do with puberty or hormones. Simple d/t the fast some guys have extra fat in chest area, making it look like they have breasts. The boy weight at 60 percentile while height at 50 percentile.
This makes sense, thanks!
I was able to break it down to diuretic or alcohol use and chose alcohol use under the assumption that the patient's serum Cl- levels were low (90; N = 95-105) since Cl- is also lost with vomiting. Im assuming that it was wrong for me to make the association between alcohol use and vomiting.
@dysdiadochokinesia I think we can rule out alcohol use by looking at our patient's history and demographic. A 16yo girl who is dieting and constantly studying probably isnt getting turnt because 1) alcohol has empty calories (defeats the point of dieting), 2) why would you try to study when you're drunk, 3) where will this 16yo in social isolation get alcohol
Laxatives would cause an anion gap metabolic acidosis due to loss of bicarbonate in the stool. You would see hypokalemia though as seen in this question.
it took me a lot of time choosing between laxatives and diuretics and at the end I choose diuretics. but I didn't realize that the only thing I had to do was check if were a anion gap or not.
Why would laxatives cause anion gap MA? Isn't it similar to diarrhea?
The above comments are incorrect. Diarrhea is a cause of normal-anion-gap metabolic acidosis (D in HARDASS from FA). Laxatives are wrong because they would lower HCO3- but in this scenario it is high. The low K+ and Cl- fits either case though.
Not sure why you're getting downvoted, but this makes sense to me.
Maybe because you're claiming that the fetus is Rh+ when it's not clearly stated? But take that away and your explanation still makes sense.
the question is not asking what to give to the mother.
it's asking what to give to the fetus.
Superior rectal comes from the inferior mesenteric vein which comes from the splenic vein --> portal veins
Thus, this dude had cirrhosis so it would "back-up" into the superior rectal vein.
FA 2018: p360
Superior rectal not superior mesenteric. Took me a minute
ugh am i ever gonna get these right EVER
why not the inferior mesenteric, since the superior rectal drains there
@titanesxvi think it is because question says direct which is why superior rectal
thomasburton, so are they asking what vessels do internal hemorrhoids directly drain into? The order is Superior rectal vein--> Inferior mesenteric vein--> portal vein.
Yes exactly, so they do eventually reach IMV but not 'directly'
Also worded poorly because the varicosities are connections between the superior rectal and the middle/inferior rectal veins of the systemic circulation. So the blood could be in both the superior rectal vein and the middle/inferior rectal vein as that is what a varicosity is.
You just gotta know indirect vs. direct hemorrhoids. In this case, it's an indirect hemorrhoid (superior rectal vein) because of the rectal bleeding.
@titanesxvi DrDoom explained it pretty well below: "Defining tributary: https://i.imgur.com/2zDxPbW.png Nice images make the term easier to recall. Smaller streams "pay tribute" to larger rivers (by flowing into them)"
The question asks "the most likely cause of the facial finding involving the lip in this patient..."
cleft lip = 'processes'
clef palate = 'shelves'
Don't let a dentist tell you whats up :(
I think Cleft palate could also be due to failure of fusion of lateral and medial nasal prominences.. but since the baby had lip involvement and the lateral nasals can be seen, I went with failure of Maxillary and medial nasal fusion. Someone correct me if im wrong.
@meningitis this is cleft lip, not cleft palate
If that's then thinking, then how would you differentiate between PT & PTT?
Why isn't "Decreased platelet count" correct? Aspirin does not decrease the platelet count, only inactivates platelets.
Because dicumarol does not decrease platelet count either.
@usmleuser007 Because the answer choice says decrease in PTT. If you take a heparin like drug then the PTT will increase. Drugs wont increase PTT (that would be procoagulant)
I think usmleuser007 and is3076 were working form the perspective of not knowing what dicumerol was. If you were unsure what dicumarol was, there really wasn't a way to get this correct, contrary to @seagull's comment. You can't really rule out any of these as possible options because aspirin doesn't do any of them.
yeah, it wouldn't work. We'll need to know with Dicumarol is.
Not true, the logic works. You gotta know what aspirin does at least, it interferes with COX1 irreversibly and inhibits platelet aggregation (kinda like an induced Glanzzman), all it does. PT, aPTT are functions of the coagulation cascade and the test itself is not an assessment of platelet function. Bleeding time/clotting time is an assessment of platelet function.
A- decreased plasma fibrinogen concentration- not impacted
B- decreased aPTT/partial- DECREASED, indicates you are hypercoaguable, not the case
C- decreased platelet count- aspirin does not destroy platelets
D- normal clotting time- no we established aspirin impacts clotting/bleeding time by preventing aggregation
E- prolonged PT- answer, aspirin does not impact the coagulation factor cascades in the test
FA P120-122. Immunosuppressants for RA are calcineurin inhibitor (cyclosporine and tacrolimus), 6MP, and TNFa inhibitors (adalimumab,infliximab, etanercept). It is important to distinguish that calcineurin inhibitors block t cell activation by preventing IL-2 transcription, not necessarily block IL-2 action. Sirolimus(rapamycin) blocks IL-2 action but it is used for kidney transplant rejection prophylaxis specifically.
in addition to the above responses, IL 1 antagonists (Anakinra) can be used to treat RA. Anakinra is a recombinant human IL 1 receptor anatagonist but less effective than other treatment modalities.
Prednisone is a glucocorticoid (which inhibits IL-2 synthesis) is already being used with no effect. So TNF-alpha is the next option.
DMARDs: methotrextate, sulfasalazine, hydroxychloroquine, leflunomide, TNF inhibitors, Anti- IL6 (Tocilizumab), JAK inhibitor (Tofacitinib), Rituximab.
You can use cyclosporine and tacrolimus to treat RA, but those aren't first line treatments. DMARDs are used the long term treatment of RA and methotrexate is often started first, and the other drugs are prescribed if methotrexate does not sufficiently control symptoms. None of the other choices listed are a part of DMARD therapy.
This question is likely not important for two reason:
They're both Trypansomastigotes, so of course they look almost the same.
You can differentiate these two species clinically as they have very little clinical similarity in patient presentation.
For these reasons there's little to no reason you would be expected to differentiate these two species by histology alone
Does Chagas have recurrent fever? Because that's what pointed me to African Sleeping Sickness.
The history of travel to the Amazon is what pointed me to Cruzi over Brucei but agree it's a tough distinction to make here. In the absence of that detail I would have probably picked Tsetse fly.
This was in pathoma, he said prostate cancer causes osteoblastic lesions and "the board examiners really want you to know that". also following the potential site of mets helps choose the answer
Also, osteosarcoma is less common in the elderly, more common in males <20 y/o (per F.A 2020)
Where do you guys learn that cooing starts at 2 months? It isn't in first aid or boards and beyond so this was an annoying question for me
@pg32 From being a parent! Otherwise little chance I'd remember all these milestones.
I'll get right on that @drshmoctor :). If only I could have a kid to memorize all these damn developmental milestones. That would make life easier haha.
Yeah, I don't see cooing anywhere.
thankfully a lot of my friends on insta keep posting pics/vids of their babies reaching milestones so im well updated lol
Mnemonic: "Coo at Two"
Someone please help me with this (always trips me up): PTH causes increased vit D production in kidney... are we assuming the increased PTH can't catch up with the kidney failure? Is it the level prior to PTH compensation that they want? D:
@paperbackwriter what it works for me ;;;; is find the first abnormality so CKD low calcitriol (no D vit) ---> is gonna increase PTH ---> the kidney are not working (chronic, they don't tell u recently- you can;t revert a CKD so the kidney never going to catch up) --> increase inorganic phosphorus.--> always start with the problem. I also use this for celiac and types of shocks. start with the problem, and trust yourself.
@miriamp3 thank you! I will try out your strategy next time!! :)
I thought renal insufficiency -> inability to reabsorb phosphate at PCT -> decreased phosphate?
stop being an ape. evolutionize!
as a creationist i'm offended
Also, Tarsal/Meibomian glands are found along the rims of the eyelid and produce meibum
So why is it apocrine? The dude is EXERCISING when playing football.
The question asks about "the characteristic odor" i.e. body odor coming from the APEocrine glands. The Eccrine glands secrete water and electrolytes.