Welcome to whoissaad’s page.
Contributor score: 72
the question is asking about "adequate arterial supply"
The artery of the ductus deferens is USUALLY a branch of the SUPERIOR vesical artery, although it can branch from the inferior vesical artery in some individuals.
There is no guarentee. They are basically asking what a trigger is for her asthma recurrence. Smoking in this scenario can be the cause of this patients symptoms. Dont dwell to deep into the question.
could be pseudo tumor cereberi, ttt is also acetazolamide and is more common in female obese BMI 35KG/M
opening pressure could be normal in pseudo tumor cereberi
Hardy Wineberg equilibrium
square root 900 = 30
1/2 of all offspring will be carriers so 30*.5 = 15
simple as that
Though everything else fits, in order to diagnose RLS you need to actually have leg symptoms which aren't described here at all. I agree that MDD also requires a bit of a stretch bc not all of the diagnosis requirements are met which is annoying, but at least the core components are there (decreased energy, sleep disturbances, lack of concentration), whereas the core component of RLS isn't there at all. It's like wanting to diagnose someone with a migraine because they have irritability, decreased concentration, and a visual aura but the person never even said their head hurt. It's not a great question and I completely missed MDD as well, but I can kinda see now why it's MDD more so than any of the other choices so it's kind of a "but which is the BEST answer" scenario.
This is dumb but I remember FDP is needed for picking while FDS is need for scratching the superficial layer of the skin
@lsmarshall Flexor digitorum superficialis inserts at the middle phalanges to be more specific.
shittt I remember it like this D for distal P for profundus > Double Penetration. and I know the PIP flexion from the other Flexor digitorum, which is superficialis. Extensors are lumbricals. (Lengthen your fingers with Lumbricals)
'flexor digitorum profundus is profoundly long' is such a good mnemonic, thanks bro
Exactly my reasoning for not choosing collagen "synthesis"
dont overthink people, whether its an underproduction or overproduction of collagen, overproduction is still abnormal collagen synthesis. its abnormal to make an excessive amount of collagen 3 leading to a keloid
Made the same mistake
i thought exactly the same!! 2 cells looked like tear drop cells :/
I thought there were tear drop cells too. Seemed like it should be a metaplasia then. Oh well
I did the same, but looking at FA19 pg 423 it says "ineffective hematopoiesis --> defects in cell maturation of nonlymphoid lineage." You can get bilobed neutrophils, or if it progressed to AML you'd see auer rods. Nothing about tear drop cells. Then on pg 406 tear drop cells would be seen in myelofibrosis, and possibly thalassemias
I thought the same, but I think that would be myelofibrosis, not myelodysplastic. Hb is really high here too. Pretty tricky for them to put that there, easy knee jerk.
Interestingly enough, agnogenic myeloid metaplasia is the old name for myelofibrosis, with "agnogenic" being synonymous with "idiopathic." (or did everyone already know this)
@charcot The patient is young and doesn't have any risk factors for weak bones. Also, disc herniation is a common problem in the young. The disc gets fibrosed and stiff in the elderly so they have less chance for disc herniation.
So basically age was the key to answering this question.
you are genius! thank you! :)
I guess he is asking about integrate,,,,, where his should be integrated into host dna to get replicated .. triple therapy includes. 2drugs NRTIs and other one is integrate
@ususmle NRTIs would still inhibit DNA synthesis since they mess with the reverse transcriptase which is needed to make viral DNA.
@ususmle HIV triple therapy is 2 NRTIs/NNRTIs + 1 protease inhibitor. Plus, if her CD4+ cunt is already 60/mm, that shit is well integrated in her CD4 cells already, right?
I was confused because isn't HIV an RNA virus?
@brotherimodu yes and therefore it uses a reverse transcriptase
I also chose Gemfibrozil too because its the best TG lowering drug listed but I can see where there might be some red flags for this drug in the way they asked the question... 40 year old obese woman with some upper abdominal pain ..... HELLO GALL STONES which is a common adverse outcome of Fibrates.
Well I didn't wanna give a fat, forty, female, that smokes a fibrate. So a statin, for me, was the best next option.
Used same reasoning to choose statins. Fibrates are the main drug of choice for hypertriglyceridemia but given her symptoms, statins made more sense. Why do they do this to us...
what a tricky question! there are multiple factors should be taken in consideration.. she has triglyceridemia which put her in risk of pancreatitis, and most importantly atherosclerotic disease, and all of that would outweigh the risk of giving her gallstone.
Yeah I had statins selected initially because "statins are always the answer" but when I saw them stating first line "recently diagnosed with hyper TG" I figured this follow-up was purely to address that. So Fibrate is the best move.
http://medresearch.in/index.php/IJPR/article/view/782/1271 This explains a case in an infant. "Respiratory depression and coma after overdosage have been shown to be reversible by injection of naloxone . Owing to its structural similarity to opioid, loperamide toxicity can be reversed by using Nalaxone which is a specific opioid antagonist acts competitively at opioid receptors. Naloxone hydrochloride is usually given intravenously for a rapid onset of action which occurs within 2 minutes."
FA 2019: "Loperamide has poor CNS penetration" - so it still penetrates => can cause respiratory depression
Also maybe because the blood brain barrier in a baby is not developed as well as in an adult.
is it the same thing as antigenic variation?
No, antigenic variation involves genomic rearrangement
Phase variation can be thought of as MORE or LESS of something. An on/off switch. No DNA is being rearranged, just under or overexpressed in response to the environment.
This isn't in Zanki, Lightyear, or First Aid, and I don't remember ever learning about this in class. Thanks NBME! :D
Hellppp. pls why is it not decreased capillary oncotic pressure?
@ henoch280 Because there is no change in the levels of protein in the blood.
theoretically you could develop liver failure from the increase in central venous pressure (e.g. cardiac cirrhosis) and THEN you would develop a decrease in oncotic pressure.
Great explanation. Always found it hard to differentiate between ATN and AIN due to NSAID use. This made it clear. Thanks!
"occasionally writhes in pain" -- as a guy who has had a kidney stone, writhing in pain definitely hits the mark. Picture yourself knees on the ground, face on the couch, screaming incoherently while the paramedics are there because you can't control your own body movement and don't know if you're dying or whatnot from the canonball sized hole that (may or may not be) in your flank. Then imagine one of the paramedics is your premed study buddy. Never forget writhing and nephrolithiasis and premed study buddies. You will forever get this question correct in the future.
i swear to god ive done a similar question on the usmlerx qb and they answer was renal papillary necrosis. which is why i got it wrong :(
i also remember that uw ques which got me this ques wrong. i think in that ques,patient sibling or he himself had sickle cell
yes same question, both retinopathy and intraventricular hemmorage can occur due to high oxygen levels..
I mistakenly chose choroid plexus too, based on wiki seems this is most common cause of IVH in term infants: IVH in the preterm brain usually arises from the germinal matrix whereas IVH in the term infants originates from the choroid plexus. However, it is particularly common in premature infants or those of very low birth weight... Most intraventricular hemorrhages occur in the first 72 hours after birth. The risk is increased with use of extracorporeal membrane oxygenation in preterm infants.
choroid plexus is different than germinal amtrix
Extremely thorough answer holy shit thank u so much I hope you ACE Step 1
great answer assoplasty, I remember goljan talking about this in his endo lecture (dudes a flippin legend holy shit) but it kinda flew over my head! thanks for the break down!
you mean total amount of T4 is "not changed"?
2nd para last sentence.
@whoissaad, in a normal pregnancy total T4 is increased, but the free T4 will be normal and rest of T4 bound to TBG. If patient is hyperthyroid, total T4 would still be increased but the free T4 would now be increased as well.
To take it a step further, Goljan mentions that there are a myriad of things circulating in the body, often in a 1:2 ratio of free:bound, so in states like this you could acutally see disruption of this ratio as the body maintains its level of free hormone but further increases its level of bound hormone. Goljan also mentions that you'd see the opposite effect in the presence of steroids and nephrotic syndromes. So you could see decreased total T4 but normal free T4 because the bound amounts go down.
Amazing answer! THX
The above explanation is correct (disregarding the hard to read and unprofessional dialect) but just in case anyone was wondering:
chromatin-negative= Just a quick way of knowing it was a boy. The term applies to the nuclei of cells in normal males as well as those in individuals with certain chromosomal abnormalities
Turner syndrome patients are also chromatin negative as well though....
I didn't know a complication post-meningitis was lack of humor.
Ah, didn't read the last line. Yeah, that is taking it a bit far
yall are haters. this is the first explanation that has ever made sense to me
How does chormatin-negative indicate a normal cell? Isn't chormatin just condensed DNA?
According to this paper most individuals with Turner Syndrome are chromatin negative: "One of the initial laboratory procedures used to confirm or rule out this diagnosis involves a sex chromatin determination from a buccal smear. Cells from the lining of the mouth are stained for the presence or absence of X-chromatin or Barr bodies, which represent a portion of an inactivated X chromosome. The typical Turner’s syndrome patient, who has 45 chromosomes and only one sex chromosome (an X), has no Barr bodies and is, therefore, X-chromatin negative.
This abnormal X-chromatin negative finding in the majority of Turner’s syndrome females is similar to the result found in a normal male, who also has only one X chromosome, and differs from the X-chromatin positive condition observed in the normal female, who has two X chromosomes. Occasionally, the patient with features of Turner’s syndrome is found to be X-chromatin positive."
i really hate haters this is awesome!
to add to the above, free testosterone is aromatized to estrogen leading to breast development
Is the free testosterone not creating male internal or external gentalia because of the defect in androgen receptors?
Well then, I guess we should just forget about our old pals the Alpha-2 agonists.
Good call. I didn't even see that this was hypertensive emergency. Dumb on my part.
so yea clonidine would be used for hypertensive urgency, but this guy is over 180 (210) so they have to use something like hydralazine or nitroprusside both will increase cGMP
Drugs used to treat HTN emergency:
Hydralazine actually vasodilates arteries>veins and Nitroprusside vasodilates arteries = veins. Both increase cGMP.
Chancroid is described as an ulcer.. whilst in this question they mentioned "vesicles". Pretty much only herpes is vesicular
They mentioned ulcers too. I chose chancroid as well, couldn't find a clue to rule it out. Also thought "discharge" was pointing you towards a bacterial infection. But guess I'm wrong :)
I think NBME/USMLE writers make the assumption the patient is in America unless specified otherwise. Chancroid is not common in the US. If the question stem mentions a developing country, then chancroid can make your differential list.
for chancroid, there may be a mention of inguinal lymphadenopathy
Also with chancroid questions they want you to differentiate it between chancroid and syphilis, (eg. Painful vs. painless) and is usually described as a much larger ulcer that is painful (not vesicular as in this question)
Also believe that chancroid does not presents with systemic symptoms like in this vignette.
there is another clue, the man has diminished pulses in just one arm, which means that the left subclavian artery must be involved somehow, and an aortic dissection would be the best answer explaining this.
please why is there where a diastolic mumur?
@temmy Aortic dissection especially near the root of aorta can lead to dilatation of the aortic valves, which can lead to Aortic regurgitation (diastoic murmur at left sternal border)
Does anyone know why is this patient's tepmerature elevated?
@garibay92, not important for this question I think but cocaine can cause malignant hyperthermia
judging by his heart murmur, he probably has marfan syndrome. that's the only place where FA talks about dissecting aneurysm
he's only 28 - another clue for marfan?
did anyone else think it was weird his only sx was SOB? I always think of radiating pain as being a good clue for dissection
@almondbreeze his heart murmur is at the LSB (aortic regurg) and not consistent with MVP plus no other sx/indication of Marfan. I think the only association of RF you should think about in this question is the cocaine use and consequent HTN.
@turtlepenlight I agree. I chose another answer because I was like, there's no way this guy doesn't hurt if he's got a dissection.