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Comments ...

 +1  (nbme18#11)

A 3-week old male with a firm mass in near where the stomach should be. Seems like pyloric stenosis. From First Aid:

  • Occurs at 2-6 weeks old with non-bilious vomitting
  • first born males
  • no mention of a syndrome, sequence, or other associations

Just a stand alone defect

j123  I was thinking it was annular pancreas. The question stem said vomiting after feeding since birth" whereas pyloric stenosis usually doesn't present until usually week 4 or so. I think annular pancreas presents very similar to the question stem and may also show a mobile mass in the same area? Not fully sure about the mobile mass part (since their description does sound like pyloric stenosis for that one). Either way, still "single primary developmental defect" as the answer +4
utap2001  Sequence describes the pattern of multiple anomalies that occurs when a single primary defect in early morphogenesis produces multiple abnormalities through a cascading process of secondary and tertiary errors in morphogenesis [17]. When evaluating a child with multiple anomalies, it is extremely important from the standpoint of recurrence risk counseling to differentiate between multiple anomalies secondary to a single localized error in morphogenesis (a sequence) and a multiple malformation syndrome. In a sequence, recurrence risk counseling for the multiple anomalies depends entirely on the recurrence risk for the initiating, localized error. The words malformation, deformation, disruption, and dysplasia sequence are used if the nature of the initiating error in morphogenesis is known. +1
utap2001  VATER syndrome refers to several birth defects that frequently occur in conjunction with one another. The letters stand for the areas of the body impacted by these defects: Vertebrae Anus Trachea Esophagus Renal (or kidneys) +

 +0  (nbme18#46)

Question is asking what increases coronary blood flow? Adenosine and Nitric oxide (NO). Other local metabolites (minor) are CO2 and low O2.

lokotriene  FA2020 p297 +

 +11  (nbme18#36)

If you knew that basement membrane disruption prevents restoration of normal tissue (repeat from another NBME), then you missed this because you didn't know what "preclude" means.

Missing questions I miss due to lack of vocab and grammar, you love to see it

cbreland  Say a prayer for me +
drdoom  you can include. you can exclude. or you can altogether preclude. +1
drdoom  all these words, along with “claudication”, share the same Latin root: clud = claud (to shut) +
dhpainte22  Missed it for the same reason :( +1
hamdiabdeen  Can someone explain why basement membrane is correct answer as opposed to capillaries or Type I pneumocytes? +
dremosq  Pathoma pg 4. Irreversible cellular injury.. The HALLMARK of irreversible injury is membrane damage. +

 +2  (nbme18#21)

She has DKA, due to the ketones in her blood

  • Type of increased Anion Gap metabolic acidosis (MU D PILES), meaning that HCO3- is decreased (all met. acidosis have decreased HCO3-)
  • Breathing fast to get rid of acid --> decreased Pco2

 +2  (nbme19#0)

Siblings have a 25% chance of inheriting the same HLA markers

There is also: + 50% chance of being haplo-identical (share one haplotype) + 25% chance of having no HLA in common

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628004/

NBME loves this question for some reason





Subcomments ...

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dhlOesSa-ottrgco si olas nkwno as ohapityissp of hte ibilta ltecb.eru ’stI deu to chnocri iirrtts/tsnrasieo at hte inistrnoe of the pllaatre endont on hte talibi tre.becul ’sIt alcilscsaly esen ni eregsante ngdio ertepieitv vrisuogo yticavit gn,unnri( n.mupijg) hTe dhrgaaipor msrnasdotete accliss regnoamfnaitt fo teh itliab lbretuec c(ihhw tsi’n casenersy ot rziongece ot tge het sntuoieq trc.ecor)

cbreland  Very tender irl, from experience +  


submitted by b1ackcoffee(44),

Any good material for this and lymph node drainage in general? Is this common knowledge or low yield stuff?

cbreland  Got it with process of elimination, seems very low yield +  


submitted by b1ackcoffee(44),

confused why this is not autonomic dysfunction or hyponatremia due to sweating and why is this orthostatic hypotension?

mamed  Not sure if this is correct thinking but how I got this right was: 1. She is hypovolemic 2. Likely retaining salt so water follows (ADH or just renal dynamics in general). This is how I ruled our hypokalemia and hyponatremia 3. If she is hyponatremic b/c sweating then why wouldn't she also be hypokalemic? so both have to wrong because both can't be right 4. Volume depletion ==> orthostatic hypotension +1  
blah  I thought that orthostatic hypotension was more of a chronic condition, but I fooled myself into believing that. +  
cbreland  I completely read over the initial BP measurement and picked the wrong answer (mostly b/c of that). Test in 4 days lets get it! +3  


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ihTs is a dab isq.unoet Pleltate agggrieoant tmei negbi anol,rm ok ifen I nca ese att.h tuB FVW ielstzbsai tfroca 8 and u'dyo ees an enraesci in TTP sir(tf inel txen to WFV ni tisFr id).A yWh si hiret PTT no?amlr

a1_antitrypsin  Totally agree, and they give you a slight increase in PT instead +  
mambaforstep  yeah but if they gave you an increase in PTT then Hemophilia A could have been a valid answer choice. so they prob showed a nl PTT to differentiate vWF dz from hemophlia A +  
drpee  VWD only sometimes presents with a slightly increased PTT. Don't let those anki facts steer you wrong... Plus all the other answers make no sense. Afibrinogenemia? That means literally no fibrinogin (PT and PTT would be infinitely increased). Hemophelia? Or vitamin K deficiency? Those are coagulation factor disorders so they would present with deep bleeding and large bruising. (Unlike platelet disorders, including VWD, which present with mucosal bleeding, petechiae, and heavy menses). VWD is actually the ONLY one that makes sense. +5  
cbreland  I get why it's not afibrinogenemia (which is what I picked), but still don't understand how VWD is right. You have normal PTT and normal platelet aggregation (both of which should be abnormal). Is the only thing leading us to VWD is it being a primary bleeding issue? Again, my answer made no sense, but VWD in this context, seems way out there +  
osteopathnproud  I agree with you @cbreland once I noticed I had to bend lab values for any answer choice then in my head most of them were possible. I took a step back and answer with the most common bleeding disorder, vW disease. Funny thing is when I retook it to check my answers, I had time to overthink and got it wrong. +  
aakb  the anki facts never steer you wrong! my zanki cards say "Low vWF in von Willebrand disease impairs platelet {{c1::adhesion}}" (Gp1B binds to vWF) not platelet aggregation (GpIIbIIIa binds to fibrinogen). additionally it says you can have either a normal or increase PTT. in this case the PT is not increased. It is decreased a little, which I assume is fine esp w an INR of 1.0 +  
lebabs  Shut up +  


submitted by claptain(21),
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I 'dton enrantddus htis it.qeuosn Thye teueqa st-craterrusai to amne feteacfd by hte ela.ell We ownk ehr throme is a acrierr seauebc seh ash edlavtee .CK thaT seman hte aptitne ahs a %50 cacenh to eb a rrcreia senic 'hess faelem. mdRnao -ovctiXanitian etnods' mtater enhw kiagltn oaubt eirrarc tsusta cebsuae btho elalsle ehav a nehcca ot egt dspsea o.n odnmRa X tvaatioiinnc is ylon manitoptr fro mgeeidrnint ehrhwte she wlil dveoepl yopmms.st

I gesus ihts is ywh het netuqsoi asw nhowrt to?u lssUne Im' gsniism egm.snohit

claptain  Nvm, this question played me. I realize that E is the only possible choice. Both A and B would be 25% chances, not 50% chances, and you cannot assume whether she is or is not a carrier without genetic analysis (choices C and D). That leaves only E. +5  
beansbeansbeans  Wait I agree with your first comment, can you explain what made you change your mind and understand this? +  
yerpderp  They are referring to x inactivation in the daughter which would mean she could be a carrier but we cant tell. +1  
cbreland  so her mom is a carrier because she doesn't have complete symptoms like the brother and uncle?? I guess I thought it was all of nothing with duchenne +  
cbreland  Damn, her mom is 50. Duchenne patients don't live that long... nvm dumb on my part, should have made the connection +  
j44n  her mom cant have the full blown disease because its an XLR disease. I think we had to narrow this down by process of elimination +  


submitted by claptain(21),
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I d'ont dsnuarnetd ihts suoqtein. yehT teqaeu iurearcsrsta-t ot mean eftedafc by het lae.ell eW nwko her emotrh si a aercrri acesbue ehs sha evtledea .CK htaT amsne het ipttane ahs a %50 nacehc ot be a raircer escni ess'h .ealfem dRaonm tn-icviaXoatni otedns' ermtta wenh gatinkl baotu airrecr uastst esuecab otbh eeallsl haev a heccan ot egt sapsed .on oRamdn X nciantivoiat is olyn opnairtmt fro idernmgetni hewtehr she will oepvedl om.sytsmp

I ugsse tshi si wyh the neuistoq swa torwnh o?ut sUnles I'm issmgni nesmothig.

claptain  Nvm, this question played me. I realize that E is the only possible choice. Both A and B would be 25% chances, not 50% chances, and you cannot assume whether she is or is not a carrier without genetic analysis (choices C and D). That leaves only E. +5  
beansbeansbeans  Wait I agree with your first comment, can you explain what made you change your mind and understand this? +  
yerpderp  They are referring to x inactivation in the daughter which would mean she could be a carrier but we cant tell. +1  
cbreland  so her mom is a carrier because she doesn't have complete symptoms like the brother and uncle?? I guess I thought it was all of nothing with duchenne +  
cbreland  Damn, her mom is 50. Duchenne patients don't live that long... nvm dumb on my part, should have made the connection +  
j44n  her mom cant have the full blown disease because its an XLR disease. I think we had to narrow this down by process of elimination +  


submitted by lpp06(30),

Treated with a thiazide diuretic for HTN with measured hypokalemia, hypotension and decreased Hgb

Thiazide increases Na+ delivery to collecting ducts, increases K+ secretion, causing hypokalemia - which will lead to muscle weakness.

Low blood pressure may be sign of volume depletion from the diuretic

Low Hgb/Anemia due to chronic alcohol abuse (macrocytic, non-megaloblastic anemia)

ootscoot  Does anyone know why she would be presenting NOW after being on the thiazide for 10 years? +6  
nnasser33  This question was frustrating because it is clear that she is volume depleted given her orthostatic BP presentation, which could be caused by both the Thiazide and alcohol use (suppression of ADH release). You can certainly say her presentation is the result of an "adverse drug effect" but how can you completely rule out orthostatic hypotension and dehydration as possible answers? +2  
cbreland  Orthostatic hypotension would refer to a significant decrease in blood pressure when standing. Her BP is low sitting and standing +1  
cbreland  @nnasser33 I was stuck between the two answers as well, but I remembered a similar question on another NBME related to that explanation ^ +  
mmizell  Her BP also only dropped by 6 systolic/1 diastolic from sitting to standing. Orthostatic hypotension is defined as a drop >20/10. +4  
helenwei  I also think with dehydration her Hct would be higher +1  


submitted by lpp06(30),

Treated with a thiazide diuretic for HTN with measured hypokalemia, hypotension and decreased Hgb

Thiazide increases Na+ delivery to collecting ducts, increases K+ secretion, causing hypokalemia - which will lead to muscle weakness.

Low blood pressure may be sign of volume depletion from the diuretic

Low Hgb/Anemia due to chronic alcohol abuse (macrocytic, non-megaloblastic anemia)

ootscoot  Does anyone know why she would be presenting NOW after being on the thiazide for 10 years? +6  
nnasser33  This question was frustrating because it is clear that she is volume depleted given her orthostatic BP presentation, which could be caused by both the Thiazide and alcohol use (suppression of ADH release). You can certainly say her presentation is the result of an "adverse drug effect" but how can you completely rule out orthostatic hypotension and dehydration as possible answers? +2  
cbreland  Orthostatic hypotension would refer to a significant decrease in blood pressure when standing. Her BP is low sitting and standing +1  
cbreland  @nnasser33 I was stuck between the two answers as well, but I remembered a similar question on another NBME related to that explanation ^ +  
mmizell  Her BP also only dropped by 6 systolic/1 diastolic from sitting to standing. Orthostatic hypotension is defined as a drop >20/10. +4  
helenwei  I also think with dehydration her Hct would be higher +1  


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iThs eutniqos si knisag rof het vrcauasl ypplsu fo hte prdyorihaat sl.nagd thTa oudwl eb the rfieorni dyhrito e,iserrat ihwhc reais romf eth leroachrcvyti .rkutn

weenathon  I originally chose vein because I was thinking maybe the hormone release couldn't be carried to the body anymore, but looking back the working of "moderate hemorrhaging" and vessels requiring ligation is what implies it's an artery. Just throwing that out there in case you thought like I did. +4  
cheesetouch  if you were clueless like me (well I knew artery but..), picking one with 'thyro' in the name when discussing a thyroid surgery is a good guess :) +6  
cbreland  I'm really out here picking one of the answers with vein +  


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Farglei X si a CGG tdcnoeuiteilr eaterp xoeinpasn dedosrir iwhh(c keli os’nugiHttnn si a etst i.ra)oftev ehT rlnetmaa cunle si hte tihn to eht lki-endX r.ciineathen uiel-kmtisA ahovriseb and ytevirllea lagre hdae are ;nomcom raleg licteests olyn aearpp erfat .bptyure

cbreland  Also repeat expansions will get worse with each generation. I went with the learning difficulties and then uncle having issues that were not as severe to a child with issues within the first 2 years of life as being a signal of a triplet expansion +  
osteopathnproud  Fragile X syndrome is the most common inherited cause of intellectual disability FA20 pg 62. I just saw intellectual disability plus heritable = fragile X syndrome. +1  


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ehT ssanapiifnrtu nad retes oirnm rea eibseplorns for tleanrxe oto.artin tBoh het itasnnsairupf and saaputprnisus cesmlus era evnandtier by a rurasapsuclpa .vnere

cbreland  Rotator cuff muscles: Supraspinatus, infraspinatus, teres minor, subscapularis (SITS), their movement is AEEI --> Abduction (first 15), external rotation, external rotation, and internal rotation, respectively. Someone threw out SITS AEEI on another nbmeanswers thread so I'm using it here. Hope this helps +1  


submitted by diabetes(28),

if we know that dorsal coloumn ascending is medial and decussate in medulla and ascend contralaterally then we will choose c

cbreland  I was struggling with if the UMN would have crossed yet, but from what I remember, the cortospinal tract crosses at the bottom of the medulla. Also the CN XII has ipsilateral lesions ("Tongue licks the lesion") so that helped think through this problem. +  


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As wla,say it’s atmosl eetrtb to onreig eth srcueitp henw ssblopi.e hisT lanemntge hsa a pipect erlc,u iwchh we nkow is eaudsc dieyamtonprel yb .H yoprli net.iocfin H. irpyol opscduer rstoaeesp adn rtiluyacplra eeas,ur hiwch alwlo it ot snereaic teh Hp of ist caoll rvnoitnmeen yb gaivnlce arue toni an,mimoa iwhch si cotxi ot agtsrci o.ascum ehT iuperct eomstsdtnare H ilpo,yr hichw are dtvneie whit ilsver .iagnitsn

joonam  Hey bro, thank you so much for your contributions on these free 120 questions. Your advice on test taking strategies for step 1 have been very helpful. +21  
luciana  "Elaborated enzymes by H. pylori may also contribute directly to epithelial cell injury. Ammonia produced through urease activity may be toxic to gastric epithelial cells. H. pylori protease and lipase degrade gastric mucus and disrupt the phospholipid-rich layer at the apical epithelial cell surface, allowing for cell injury from back diffusion of gastric acid." https://www.ncbi.nlm.nih.gov/pubmed/9394757 +2  
luciana  I got tricked :( Thought the damage was due to destruction of local somatostatin cells with increased gastrin and acid production... but this is actually the mechanism of duodenal ulcers development related to H. pylori But makes sense, so thats how the somatostatin producing cells are destroyed lol +4  
drpee  "Hyperacidity and gastric ulcer development" is also sort of true, but this is hinting at the mechanism for DUODENAL ulcer development from H Pylori. Irritation in the stomach leads to G Cell hyperplasia, increasing acid secrection which causes downstream ulceration. +5  
itsalwayslupus  Did anyone else pick the hyperacidity answer just because the correct answer had "local tissue destruction" in it? I figured that H. Pylori was non-invasive, so would not directly damage the tissue it is localized too +5  
cbreland  @itsalwayslupus exact same thoughts over here +  


submitted by anechakfspb(36),

Just a rant - i hate this f*cking picture it's been on 3 NBMEs now and every time I've gotten it wrong.

cbreland  And it's a different answer every time +6  


submitted by usmile1(109),

Like t123 said, I think the key to this question was to rule out the other answer choices as they would not have normal stool. I found this article that essentially breaks down GI disorders in diabetes into gastroparesis and intestinal enteropathy. These complications and their symptoms are often caused by abnormal GI motility, which is a consequence of diabetic autonomic neuropathy involving the GI tract.

Intestinal enteropathy in patients with diabetes may present as diarrhea, constipation, or fecal incontinence. The prevalence of diarrhea in patients with diabetes is between 4 and 22 percent.4,5 Impaired motility in the small bowel can lead to stasis syndrome, which can result in diarrhea. In addition, hypermotility caused by decreased sympathetic inhibition, pancreatic insufficiency, steatorrhea, and malabsorption of bile salts can further contribute to diarrhea. Abnormal internal and external anal sphincter function caused by neuropathy can lead to fecal incontinence. When evaluating a patient with diabetes who has diarrhea, drug-related causes (e.g., metformin [Glucophage], lactulose) should be considered.

https://www.aafp.org/afp/2008/0615/p1697.html

cbreland  I agree, felt like all the other choices would have something odd in the stool studies +  
jurrutia  Orthostatic hypertension implies sympathetic dysfunction. Loss of sympathetic input causes dishinibition of intestinal motility. +  


This lady had preterm premature rupture of membranes. She had a genital tract infection, which is a risk factor for PPROM.

From Uptodate: Many of the microorganisms that colonize the lower genital tract have the capacity to produce phospholipases, which can stimulate the production of prostaglandins and thereby lead to the onset of uterine contractions. In addition, the host's immune response to bacterial invasion of the endocervix and/or fetal membranes leads to the production of multiple inflammatory mediators that can cause localized weakening of the fetal membranes and result in PPROM.

alimd  did you pay fucking $30? +1  
cheesetouch  some institutions give students UpToDate access +3  
cbreland  I knew that misoprostol (PGE1) can be used for abortions by forcing uterine contractions, so I figured the answer had something to do with prostaglandins +3  
rthavranek  I knew prostaglandins increased uterine contraction, but I also thought PGE2 caused cervical ripening and since there was a closed cervix, I eliminated that choice. I had no idea what was going on so I just picked oxytocin since that would increase uterine tone without dilation, though my reasoning seems to be incorrect +2  
utap2001  Great, the above message deserve $30. +  
notyasupreme  I think also it said that the fetus releases oxytocin and steroids, which I guess is stupid wording that makes it not right. Anyways, fuck the curve on NBME 18 :) +2  
okokok1  if anyone didn't know what "PPROM" stood for it is: Preterm Premature Rupture Of Membranes" +2  
aakb  I was between the prostaglandin answer and stressed fetal production and release of oxytocin and the reason I didn't pick oxytocin was if the cervical os is closed (membranes ruptured 32 hrs ago and contractions been going on for 12) and there's no effacement, it didn't seem like that baby actually wanted to come out so I thought that's not what's happening here. Plus mom has a fever so inflamed maternal decidua seemed to fit. +  
helppls  If there was an increase in Pgs why did she not have a ripened cervix? +  


submitted by niboonsh(355),
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NiteCcrnOc - cssrttiONC treecinlv

iErnceCCt - EsCdapnC rletivnce dens)apx(

jmangels  Also, he's an endurance athlete. It would most likely be a physiological adaptation. "Volume overload-induced cardiac hypertrophy is known as eccentric hypertrophy. In endurance training, the volume load is a predominant factor; therefore, the endurance-trained heart develops eccentric hypertrophy" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2300466/ +2  
cbreland  Also, the patient has nothing wrong with him, no symptoms, so the other options are a no go +  


submitted by azibird(177),

Costanzo Physiology 6th E p456

Regulation of Vitamin D Synthesis Whether the renal cells produce 1,25- dihydroxycholecalciferol (the active metabolite) or 24,25-dihydroxycholecalciferol (the inactive metabolite) depends on the “status” of Ca2+ in the body. When Ca2+ is sufficient, with an adequate dietary intake of Ca2+ and normal or increased plasma Ca2+ concentration, the inactive metabolite is preferentially synthesized because there is no need for more Ca2+. When Ca2+ is insufficient, with a low dietary intake of Ca2+ and decreased plasma Ca2+ concentration, the active metabolite is preferentially synthesized to ensure that additional Ca2+ will be absorbed from the gastrointestinal tract.

cbreland  Constanzo is the best resource, change my mind +  
tekkenman101  If you want quick info: https://step1.medbullets.com/endocrine/109010/vitamin-d +  


submitted by adong(97),
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Iesdecran ureeprss si ni eth anBmow pscea NO(T eht urgrellmao eiicplsa)ral so het lnyo ayolpohgt seiltd htat ulwdo scuae kcwaabrd dibul up of ueprsser si HPB

peyerpatchkids6  Does anyone know why its not diabetes? +  
michaelshain2  because the NBME said so, obvs! +  
cbreland  Diabetes would have non-enzymatic glycosylation causing increased GFR and hyperfiltation. The stem is referring to increased back pressure (Inc hydrostatic at bowmans space) which alludes to decreased GFR +1  


submitted by breis(50),
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I ma ton %010 no shti bieng cercr,to utb I lrefybi rebrmeem a strahcyPiits asngyi atth eht taenpit sha ot be szeerui eefr orf 6 nmtsoh uimnimm nda predeerrf ot aevh on uizeser ithnwi hte ltsa 3 yreas to be t.ypmictaosam oD htiw ttha nmoaifiront tawh uyo l.iwl tbu orf drsBoa: 3 yera.s

suckitnbme  Question stem also implies that the patient has been driving already. "has not had any collisions while driving his personal motor vehicle". +15  
cbreland  Also 10 years is a really long time. Just didn't seem like a good answer +  


submitted by sympathetikey(1349),
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nPsoer ybropalb hsa brlreitIa wloeB Sredmy.on sgs,erlaedR it sesme leik erhy'et yntrig ot terta ossmpymt wthi na odoipi tlari-ahindaer ilke opamdl.eire

cbreland  "intermittent" made me think IBS as well +  


submitted by hello(311),

This patient has been taking HAART therapy and subsequently develops resistance mutations. The therapeutic purpose of HAART therapy is to target reverse transcriptase and protease enzymes. Since the patient is taking HAART therapy and subsequently developed viral resistance, we know the resistance has developed due to mutations in the genes that encode reverse transcriptase and protease.

cbreland  "High viral load" made me think that the main issue was rev transcriptase inhibitor being messed up. Picked the only answer with that as an option +  
pfebo  Adding to Hello comment, it is a pol gene mutation. +  


submitted by anechakfspb(36),

This is describing hereditary hemorrhagic telangiectasia (FA 2019 p. 312). It is also known as Osler-Weber-Rendu syndrome. It is an autosomal dominant disorder of blood vessels. Findings include blanching lesions (telangiectasias) on skin and mucous membranes, recurrent epistaxis, skin discolorations, AV malformations, GI bleeding, and hematuria.

cbreland  Wow, I was completely lost on this one, thanks! +17  


submitted by cheesetouch(131),

Teratogens are most susceptible to give damage in 3-8th weeks (embryonic period - organogenesis) of pregnancy. FA p 596 (2018); teratogens section

cbreland  as @azibird stated below, the neural tube starts to form at the 3rd week and completely forms by the 4th week. Valproic acid can cause NTD, affecting their formation in weeks 3-4. +1  


submitted by anechakfspb(36),

I personally picked two groups with similar sample size, can someone explain how they answered this question? Thank you!

tnc  I was very close to picking that as well. However, I ended not going with it because I can just control how many in each groups without picking at random. I would only think about picking at random if I don't want any bias in putting people on one side or another based off certain characteristics. Hence, picking at random would probably by chance put equal similar characteristics on each sides, rather than how many on each side. I hope that makes sense. +2  
cbreland  I agree, I feel like randomization is better for balancing characteristics and potential confounders because it would be hard to take in any and all differences in people when hand picking the groups. +1  


submitted by breis(50),
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psoaileC si a peornti hatt cinsoftun sa a caoftcro orf creanitcpa e,islpa hwit hichw ti rsfmo a cteriihmotisoc c.pomexl tI lsao bnsid ot eht es-tlblia ervodec rgycyilctarlloe enctfiare shtu galinwlo eth zyemen to cornha elifst to het aitpiedlr-w teicfnrae.

cbreland  Lipase (active) and procolipase (inactive) are both secreted by the pancreas. Lipase is inactivated by bile salts in the intestines. Colipase (once activated by trypsin) is able prevent the interaction of bile salts and lipase. End result being that lipase is doesn't have to worry about bile salts if colipase is around +2  
s039p811  To add onto this, I had picked Phospholipase A2, but that's used for phospholipid hydrolysis and not triglyceride hydrolysis specifically. +  


submitted by cheesetouch(131),

Even though following people ahead for 3 years may seem like a prospective cohort, that is minor and the study design with randomly assigned experimental and control groups is still a randomized clinical trial

cbreland  To add to this, a study would be observational, nothing is being assigned/added to the patients. This is too organized into groups/treatments to be a study +4  


submitted by baja_blast(104),

I'm skeptical of this being Toxic Shock Syndrome, as the rash in TSS is usually described as being similar to that of a severe sunburn and, besides fever, there are no other associated TSS symptoms (hypotension, shock, vomiting, abnormal LFTs, etc). Moreover, questions about TSS usually mention nasal packing or a left-in tampon, both of which are absent in this three year old boy. You can read about TSS in FA 2019 on p. 135.

I think it's more likely that this is Bullous Impetigo, which is mentioned briefly on FA 2019 p. 470 as being caused by S. Aureus.

Either way, both are caused by S. Aureus so even if you thought this was TSS you should still get the right answer here.

cbreland  I agree with this explanation. Thought that they would make us decide between S aureus and GAS (bullous v. non-bullous impetigo) but seems like they went easy on us +1  
jer040512  It sounded more like Scalded Skin Syndrome to me. I saw this in Amboss and thought i'd post it here. "SSSS belongs to the spectrum of diseases mediated by specific staphylococcal toxins, which also includes bullous impetigo, toxic shock syndrome (TSS), and Staphylococcus aureus food poisoning. Unlike TSS, SSSS does not have systemic manifestations (e.g., liver, kidney, bone marrow, and CNS involvement)!" +1  
jer040512  It sounded more like Staph Scalded Skin Syndrome to me. Here's what i found on AMBOSS. SSSS belongs to the spectrum of diseases mediated by specific staphylococcal toxins, which also includes bullous impetigo, toxic shock syndrome (TSS), and Staphylococcus aureus food poisoning. Unlike TSS, SSSS does not have systemic manifestations (e.g., liver, kidney, bone marrow, and CNS involvement)! +  
jer040512  It sounded more like Scalded Skin Syndrome to me. I saw this in Amboss and thought i'd post it here. "SSSS belongs to the spectrum of diseases mediated by specific staphylococcal toxins, which also includes bullous impetigo, toxic shock syndrome (TSS), and Staphylococcus aureus food poisoning." +  
jer040512  I thought this was Scalded Skin Syndrome. Here's what I got from AMBOSS. SSSS belongs to the spectrum of diseases mediated by specific staphylococcal toxins, which also includes bullous impetigo, toxic shock syndrome (TSS), and Staphylococcus aureus food poisoning. Unlike TSS, SSSS does not have systemic manifestations (e.g., liver, kidney, bone marrow, and CNS involvement)! +  


submitted by lowyield(24),

I was stuck on this one for a long time but maybe my super round about way will help someone?

you know this person has chronic bronchitis (especially cause they have cyanosis which is blue bloater vs pink puffer of emphysema). The distinguishment of pink vs blue is b/c in emphysema you have destruction of both the alveoli with the associated vasculature. Therefore there is no V/Q mismatch (pink). But in chronic bronchitis the damage is further up from the alveoli. All the other answers were in the alveoli so that's how I chose pseudostratified columnar epithelial cells.

Or maybe i'm just dum as hell and this level of overthinking is why i'm losing points on other questions

cbreland  I think this is high yield +  


submitted by cbreland(79),

If you knew that basement membrane disruption prevents restoration of normal tissue (repeat from another NBME), then you missed this because you didn't know what "preclude" means.

Missing questions I miss due to lack of vocab and grammar, you love to see it

cbreland  Say a prayer for me +  
drdoom  you can include. you can exclude. or you can altogether preclude. +1  
drdoom  all these words, along with “claudication”, share the same Latin root: clud = claud (to shut) +  
dhpainte22  Missed it for the same reason :( +1  
hamdiabdeen  Can someone explain why basement membrane is correct answer as opposed to capillaries or Type I pneumocytes? +  
dremosq  Pathoma pg 4. Irreversible cellular injury.. The HALLMARK of irreversible injury is membrane damage. +  


submitted by nwinkelmann(292),
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AF 2109 paeg .803 otsM mconom ceasu fo prmicauayer/t srciiridtpae si eamudss ot eb vlir.a

cbreland  Primary made me think that it couldn't be acquired from virus/bug +  


submitted by match95(49),
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nIlhade inseetatchs thta eahv olw laboogsd: oiapritnt leb/fifootcdocein itloslbiyu isvoedsl ni obdlo emor .leysia er,Tfeeohr ethre si LSSE ags eeendd ot eratstua bldoo -- aka raefts trnasaouti fo olob.d hiTs eslad ot asrtef rousttaain fo in.abr

dltr; low olbtuslyii t;&--g afsert tseno t&;--g rsftea yvceorre

pelparente  great answer; just to add to it. Lipid solubility determines potency, not onset/offset (that is determined by blood solubility as stated above). The more lipid soluble the more potent the drug. The more lipid soluble the drug the higher the oil:gas partition (directly proportional to potency) and the lower the MAC (inversely proportional to potency). Source: Boards and Beyond General Anesthesia Neurology +5  
cbreland  I really went down a rabbit hole on this one... Convinced myself that it had something to do with mask v. IV anesthesia even though I haven't seen/heard that anywhere. Taking step in a week🙏🏼 +  
jer040512  I thought a low blood:gas partition coefficient meant that it has a low solubility and therefore DOESN'T dissolve in the blood that easily. +2  
dhpainte22  Think onset/offset is about blood solubility and potency of drug higher with higher lipid solubility so low blood gas coefficient has faster onset and recovery. +  
jurrutia  Just to drill point home further: consider halothane, high lipid solubility (so high potency) and high blood solubility (slow onset). If you want fast onset, low solubility is the key. +1  


submitted by azibird(177),

Follow-up vs support group?

The only thing that saved me was the ancient Step 1 adage: "Never refer!"

Especially when the answer to another question in the same exam was "Encourage the patient to participate in a support group for persons with her condition"

I mean REALLY! The only difference is that they used the word "encourage" instead of refer. Exact same answer.

cbreland  Note to self: Never refer, even when that seems like the better answer +  


submitted by apurva(73),

THIS IS KAPOSI's SARCOMA ==> give antineoplastic

"THIS IS JUST TO LENGTHEN THIS ANSWER, NEVER EVER PAY THIS SITE, EDUCATION SHOULD BE FREE FOR ALL!"

michaelshain2  It's unfortunate that I had to pay in order to get these answer explanations. They aren't as informative/thorough on freenbme :/ +3  
jamaicabliz  So annoyed, I thought it was asking us to recognize that it could also be Bacillary Angiomatosis from Bartonella, which also presents in the immunocompromised... So any different study materials stress the importance of differentiating them, given they look very similar. +2  
drdoom  @apurva tell that to my loan officer!😝😂😂 +  
cbreland  Between this and bacillary angiomatosis, I think it came down to Kaposi being more likely with a HIV patient and also the lesions being purple +  
jsanmiguel415  It says that "in addition to treatment with highly active antiretroviral therapy" which makes me think this is HHV-8 -> Kaposi sarcoma. Bartonella is bacterial and would be treated with azithro + doxy +  


between macrophages and neutrophils; neutrohpils are more acute. here is long standing :)

azibird  Is there anything else to it? I was thinking neutrophils because they could be filled with diplococci in gonorrhea. +4  
nbmeanswersownersucks  I think if they wanted neutrophils they would've had to mention something about maybe pus or white discharge but since this is chronic and scarred, its unlikely neutrophils would be present i.e. no longer an active infection +3  
cbreland  Can't believe this was that simple... +4  


submitted by sympathetikey(1349),
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A lscec,yeto aols onknw sa a psrpoalde ,aldberd si a dicamle niocotnid ni chwhi a saownm' rdalbde esbglu into reh n.iavag moSe aym evha no moytmps.s tOher yam ahev etolurb anigsrtt i,urontina ryurani nencinct,oeni ro enrfqtue niiaon.tur inatlciCpmoso yma luendci crrnretue rnyauri tcrta nfieonctis nad uayrirn inner.etot

/kpckeeiCipds.oa:/.i/tywgeittno/elsrwhi

cbreland  How would you rule out uterine prolapse? +  
baja_blast  With a Uterine Prolapse you would see the uterus move down, into the vagina. With Cystocele you have the finding described in the question; bulge of anterior vaginal wall (which borders the bladder) into the vagina. Here's a pic to help illustrate: https://www.health.harvard.edu/media/content/images/cr/205345.jpg +  


submitted by azibird(177),

What is going on here? The mother is not the patient, why are we exploring this further when the son is completely normal? I get it that we would say this if the patient were concerned, but he's not and he's normal so why don't we just tell her that everything is normal? Exploring further will probably make the patient feel worse.

drdoom  Another way to read the stem is like this: “Assume you will make a statement that assures mom that boy is fine. What other statement do you want to make?” Since we’re *already* assuring mom, the best next thing is to ask an open-ended question. There’s a reason for this. As a physician, you really don’t want to say more than what you are (1) sure of or (2) obliged to. “Accept him as he is” = judgy. “He’s not going to get any taller” = you don’t know this for sure. +4  
cbreland  I had it down between the correct answer and "your son is average". Picked the wrong one. As stated by @drdoom, the stem says you have already reassured that everything is fine. It would be a good time to get extra info from mom instead of say the same thing over again. Really the question gave us the answer (I still picked wrong, but we'll do better on test day!) +1  


submitted by ameanolacid(26),
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'olduCnt eb SLA /cb he hda enrossy AnvvmL..eineltoS. is tdcnsytiil olny trom.o oNt oamyrenlSgyii (wichh si eprpu ieemtrxsite rsesyon hnte rootm talre no) bc I esusamd by eth rgonwdi tath lal 4 ixmerttesei eerw v.lonvedi vOb ton s,sPnkaionr and otn lpoio bc gaa,ni eh ash romto + .snysoer

sympathetikey  Probably in part due to early age presentation, but I hear you +5  
wowo  FA2019 p518 - process of elim for other spinal cord lesions +2  
cbreland  Also syringomyelia wouldn't have a position sense issue +  


submitted by usmile1(109),
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frmo yaBsp;and-rdoBoem& o rActi istsosen asdel to cnpSyoe, nn,Aiga nda teLf ather el afy.ciupornSe si deu to eaiufrl to isaecenr acaridc uotupt eud to disceenar lro.fedtaa nA iang is due ot csniaedre PLVED wichh eadsl ot sdeederca acrroyon lbdoo wol.f dnA ftel earth iraulef is eud ot aneisedcr LDP.VE

cbreland  Great, same thought process, murmur made me think of aortic stenosis, supported by the LV hypertrophy in stem. Then you have syncope during exercise because the heart is not able to keep up with the demands of the body +  


submitted by newrose(9),

Can someone clarify why Prostacyclin was wrong? I knew the CHALK thing but for some reason had trouble ruling out prostacyclin since it's a vasodilator

cassdawg  My best answer for this is that the best answer is adenosine because it is asking for which is involved in the mechanism of reactive hyperemia (which involves similar mechanisms to autoregulation) of blood flow, which involves CHALK. While vasodilators like PGI2 (protacyclin) are vasodilators it is released at a base level by the lungs and endothelium, and releasedat higher levels in instances such as inflammation. Prostacyclin is not released in reactive hyperemia. If you want a refresher about active v reactive hyperemia: https://slideplayer.com/slide/2541224/9/images/3/Arteriole+Resistance%3A+Control+of+Local+Blood+Flow.jpg. They are both mediated by metabolic intermediates. as mentioned above. +2  
cbreland  I picked prostacyclin for the same reason. Adensine and the other CHALK metabolites makes sense though. I guess that's why your arteries/veins dilate when working out +1  


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otnipo B) e(th eccrrot otonpi sa pre menb) :het ttiapen has a nimi lntame atste fo 2,330/ os htta uohdsl nmea thta hse tsn'i aelpbac of kmgina rhe nwo nseic!isdo os htwas hte ipnto in akltngi to hre aelvypirt huoiwtt rhe eru?dhgat

ntpoio A) is wgnro ceseuba yuo tnac tusj dihe hte disoanigs mofr het iaptetn nad eahrs ti twhi eht flmayi

ipntoo C map;& uD)yo ancton risgdarde het etst or tperae eht ttse sa htbo het stet rea sivoipe,t RPR is a nirecsnge tets thiw esls ctieycpifis utb hutoiaiecrmnmitaognlg si a yghlih ispciecf ttes os seh ndlfyetie sah llphs!iiys

tnoipo )E ndotse ekma sseen uesebca why owdul uyo od alubrm rpteucun fro si?ylpslih!

i nkhti htye rtgfoo to igve an potnio )F utsj nkearfi ertat erh ofr sylh!l!i!ips

saturdaynightpalsy  "Patients with suspected neurosyphilis should undergo lumbar puncture and subsequent VDRL, FTA-ABS and/or PCR of cerebrospinal fluid" per my notes and the internet Lumbar puncture is used to diagnose neurosyphilis, so that's what I put. +2  
saturdaynightpalsy  To add to that, I didnt choose the other answers you listed for the same reasons you listed. +1  
ac3  which of the following is the NEXT BEST STEP meaning you wouldnt want to jump straight to a lumbar puncture especially when there are answer choices that suggest discussing the diagnosis with the patient first. If you went to the doctor and they diagnose you they will discuss this with you before ordering additional testing. +1  
yerpderp  23/30 is also just mild cognitive impairment so I just thought she still had decision making capability as 24/30 is still normal +2  
cbreland  Are we expected to interpret MCI scores +  


submitted by haliburton(213),
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iiIfxbmnla is a phN-FlaTa inhboiri.t from pebmud -FTNα sha eebn ddtsarnetoem ot evah a rntcela relo in het oths eospsern atnsiag eo,lirsubtucs cnnduligi galnruaom iftnmoaro adn the mtaoenintcn of adeessi .,)5114( yot,Nalb tdoienbisa sagtina αNT-F ndcieud otaitnaivecr of buclestouris

bigjimbo  TB can spread to psoas L1-2 often, which then goes to the actual L1-L2 vertebrae itself (Potts or osteomyelitis) +6  
cbreland  I get why the TNF inhibitor would cause Tb and it literally said osteomyelitis, but the question says "gram stain is negative". Does that mean it doesn't gram stain?? I read it as it having a negative gram stain and crossed out Tb osteomyelitis as a result +  
jsanmiguel415  Mycobacterium doesn't gram stain due to mycolic acid in it's membrane. It'll take the carbol-fuschin stain (acid fast) or grow on a lowenstein-jensen culture but not gram +1  
doctordave  What threw me off was that 'she has not had fever'. Figured there's no way it could be TB +  


submitted by colonelred_(105),
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s’eH nptgisnere hitw aiclcss ssgin fo vamitin 3B fcynieedci i;ina)nc( inncia si eiqdrure to mofr the aoorctcf N+DA dinneiaocm(ti naeenid u.ieciedld)not

bigjimbo  B3 Niacin deficiency = Pellegra = diarrhea, dermatitis, dementia death. = Niacin combines with adenine to become NAD+ https://www.aocd.org/page/Pellagra +11  
cbreland  Noted lack of niacin, not making NAD. Did not think about what NAD stands for, instead went down a rabbit hole +11  


submitted by yex(101),
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mHmm. lWle my inmd hsa lnwbo ffo ebesuac athw iht my ndim swa onhaitdyrde secin he aws in eth esdt.re As nsoo sa my ndim edtatrs ot nderwa butoa lal of eht herot ntsooip ahtt ucdol kaem n.eess.. I jsut ekdlicc and v!emod

charcot_bouchard  Smart boi +5  
usmlecharserssss  hiking in sahara desert SMH +3  
cbreland  Simple = smart +  


submitted by mousie(216),
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I csohe NPA for shit ,eon asw eth enral .a resnmysau and went gihtr rfo it ubt PAN wlduo veah eorm cymitsse indsingf e(r,evf twigeh ,sosl adeh hcae) nda ysullau tefesfc dimedl aeg MEN sv moeWn ni MD.F

cbreland  Fibromuscular dysplasia = middle aged female with HTN... Maybe it'll stick this time 🤯 +  


submitted by wired-in(67),
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ctnMnaeanei sode raomufl si Cs(s × lC × )aut ÷ F

heerw Css is tssyeatdta-e ttager amlpsa c.nco of rugd, lC si eac,nacler uta si oasged neiltvra mpa&; F si b.yiltabaiivlioa

eeNithr adseog atnielrv ron iavaoaiilibyltb si ivgen, os igirongn steho p&;am ggugnlip ni hte rsnembu ecr(falu ot ntcorve stuin to ykg)d/agm:/

=(21 /muLg × 1 m00g1/0 gu) × 0.0(9 /krh/Lg × 0100 /1mL L × 24 h1/r y)da
= 2592. /mag/kdyg

.hchw.i. st'in ayn of the anwser hcsoice ds.eitl eThy tusm eavh nuerdod .009 kr/h/gL ot .01 kh/gr,/L dan ndogi os eigsv axctyle 82.8 gk//agdym eic(ohc )C

lispectedwumbologist  That's so infuriating I stared at this question for 20 minutes thinking I did something wrong +75  
hyoid  ^^^^^ +11  
seagull  lol..my math never worked either. I also just chose the closest number. also, screw this question author for doing that. +9  
praderwilli  Big mad +9  
ht3  this is why you never waste 7 minutes on a question.... because of shit like this +8  
yotsubato  Why the FUCK did they not just give us a clearance of 0.1 if they're going to fuckin round it anyways... +18  
bigjimbo  JOKES +1  
cr  in ur maths, why did u put 24h/1day and not 1day/24h? if the given Cl was 0.09L/hr/kg. I know it just is a math question, but i´d appreciate if someone could explain it. +1  
d_holles  LMAO games NBME plays +2  
hyperfukus  magic math!!!!! how TF r we supposed to know when they round and when they don't like wtf im so pissed someone please tell me step isn't like this...with such precise decimal answers and a calculator fxn you would assume they wanted an actual answer! +1  
jean_young2019  OMG, I've got the 25.92 mg/kg/day, which isn't any of the answer choices listed. So I chose the D 51.8, because 51.8 is double of 25.9......I thought I must have make a mistake during the calculation ...... +6  
atbangura  They purposely did that so if you made a mistake with your conversion like I did, you might end up with 2.5 which was one of the answer choices. SMH +3  
titanesxvi  I did well, but I thought that my mistake was something to do with the conversion and end up choosing 2.5 because it is similar to 25.92 +2  
makinallkindzofgainz  The fact that we pay these people 60 dollars a pop for poorly formatted and written exams boggles my mind, and yet here I am, about to buy Form 24 +16  
qball  Me after plugging in the right numbers and not rounding down : https://i.kym-cdn.com/entries/icons/original/000/028/539/DyqSKoaX4AATc2G.jpg +1  
frustratedllama  Not only do you feel like you're doing sth wrong but then that feeling stays for other questions. sucks so baad +  
fexx  'here.. take 50mg of vyvanse.. I just rounded it up from 30.. dw you'll be fine' (totally doing this with my patients 8-)) +1  
cbreland  I was so close to picking 2.5 because I thought I did a conversion error. 5 minutes later and still didn't feel comfortable picking 28.8😡 +  


submitted by sympathetikey(1349),
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cyukL eu,cntodid tbu lgoknoi cbk,a I leeivbe tahw ehty weer ingog orf is atwh she uosldh eahv eben iceadvtcna rfo at 6 toshnm of ega encs(i hteer aer on rptanpae mossmpt.)y

Hpe B ceniavc is uyasull genvi at ir,thb 1 htn,om and 6 hnosmt fo ag,e so i'ts erpytt nparittmo ttha she eb avdntiaecc aianstg ,ti luenss she yledara sah t,i ni ihhcw seca seh duhlso eb ttaered ot vioda icosr.rsih

ls3076  how can we actually be expected to know vaccination schedules... there must be some other reason the answer is correct +4  
cbreland  I don't think we need to know that the vaccination schedules, but that the only other answer with a vaccine was adenovirus. I figured that there would have more symptoms if she had adenovirus (plus didn't fit the typical military recruit/swimmer demographic) +  
koko  Why does it have to be something with a vaccine? RSV Is extremely common in babies,shouldn’t screen for that? +  


submitted by lfsuarez(141),
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rAswen E

Inricgano ossporhhuP ; oatharirPyd erooHmn ; Coiirlcatl

reDdeeacs ; cesdnIaer ; Ddaseecre

sTih eipnatt is usfnrefig frmo alecci super, hhcwi ni hits seac has suacde imaVtin D oopimatabnlsr nad forteeehr sedceread urmse .cilmuca eTh doby wlli oendsrp ot the darecdese muiaclc aiv itenoescr fo PTH. shiT wlli hnte esuac ropousohhps swanigt ot rcuoc in the olaprmxi cluvndtoeo lb.ueut

kuhnboom  Why does Calcitriol not increase with the increased PTH? Wouldn't the increased PTH stimulate the kidneys to make more activated vitamin D. +1  
batmane  vitamin d malabsorption --> dec calcitriol +4  
peridot  @kuhnboom Yes, while PTH stimulates the kidneys to make more active vitamin D (calcitriol), you need vitamin D precursors to begin with in order to do that. If you have vitamin D malabsorption, then the activated form won't be high even with high levels of PTH. Therefore, calcitriol is decreased. +  
cbreland  Also, Vitamin D causes Ca and Phosphate absorption in the intestines. A lack of activated vitamin D would cause more Ca/Phosp wasting +  


submitted by monkd(18),
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Am I zrcya ro did ldUowr tno avhe a uotnsiqe ttha asetdt intStas rea eth osmt fieecetvf grud lrdaesegrs of leienabs diispl. This gciol rhtew ym .ffo

adisdiadochokinetic  You are not crazy. I got this question wrong for the same reason but here's why I think NBME was going with fibrates. You can use the Friedewald equation to calculate LDL cholesterol from the values they give. This equation is LDL= Total Cholesterol-HDL Cholesterol-(Triglycerides/5). The Triglycerides/5 term is an estimate for VLDL. If you calculate it in this case you get an LDL of 120 which is firmly normal and thus the patient would ostensibly not benefit from statin therapy. +14  
hello36654  omg when the hell am I going to remember this equation? Jesuusssssss, this kind of details makes me want to give up on STEP +4  
almondbreeze  Her goal LDL should still be <100, bc she has 3 CHD risk equivalents (https://www.aafp.org/afp/2002/0301/p871.html#afp20020301p871-t3) CHD risk equivalent=the major risk factors that modify LDL goals 1) age(M>45, F>55), 2) smoking status, 3) hypertension(>140/90), 4) ow HDL level (<40), and 5) family history. (https://www.aafp.org/afp/2002/0301/p871.html#sec-4) +  
almondbreeze  *low HDL level (refer to table 3 of the article) +  
makinallkindzofgainz  These guys are hitting up attending-level cardiovascular risk factor calculations, meanwhile I picked statins because I think I remember that they help the heart +12  
jimdooder  So I ended up going with fibrates because of her age (39). I vaguely remember being taught that statins are really only recommended for patients >40 because the big study that came out about them was in the 40-75 age group. I think this might contribute to the question but I'm not totally sure. https://en.wikipedia.org/wiki/Statin#Primary_prevention +  
ytho  This question inspired my screen name +2  
cbreland  "Statins are always the answer", "Fat Female 40 Fertile", "Fibrates can cause gallstones". I feel lied to +  
brise  I'm not sure if this question is correct. I chose statins according to what an attending told me and UWOLRD 2, I just went back to check and on uworld 2, you only consider giving fibrates if their TG levels are above 1,000. So idk what the nbme is smoking. Or if doctors actually write these questions. +  


submitted by welpdedelp(225),
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oN dite ndecycf,iie teh peattni had xesecs anoercet ued to sih ited

sympathetikey  Would never have thought of that. Thanks +9  
medschul  that's messed up dog +19  
hpkrazydesi  Excess carotene in what way? sorry if thats a stupid question +  
davidw  this is directly from Goljan "Dietary β-carotenes and retinol esters are sources of retinol. β-carotenes are converted into retinol. (a) Increased β-carotenes in the diet cause the skin to turn yellow (hypercarotenemia). Sclera remains white, whereas in jaundice the sclera is yellow, which can be used to distinguish the two conditions. (c) Vitamin toxicity does not occur with an increase in serum carotene" +7  
davidw  β-Carotenes are present in dark-green and yellow vegetables. +  
hyperfukus  ohhhh hellllll no +7  
dashou19  When I was a little kid, I like to eat oranges, like I could eat 10 oranges at once, and after a few days, I could tell that I turned yellow... +6  
cbreland  I'm okay with missing this one +4  


submitted by aneurysmclip(149),

what I'm thinking is, normally the perineal body is cut during a posterior episiotomy. so reading over the question again, the last line "which is at greatest risk for damage IF this incision is TORN FURTHER during delivery" Torn further being the key imo.

as for why it isn't bulbospongiosus or ischocavernosis -> https://en.wikipedia.org/wiki/Transverse_perineal_muscles#/media/File:1116_Muscle_of_the_Female_Perineum.png

cbreland  why do I feel like this was supposed to be an easy question +  


submitted by jrod77(28),
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The yilotscs pesreurs ceffrndeie enteebw eth tlef nerctievl dan hte toaar ni isht p.t is retpty itn,scinigfa Waseerh in a rnaolm ehrat hotse syoscitl seeussrrp hslodu be tjsu ubtao quale. Tish itnsh at teh ctaf htat hte eltf ierlcnvet ash to put in tlao of krow ot hspu hghoutr het tarcoi a.evvl ahTt axrte srupeesr esog inot negnpoi teh lvvae and esdo not aperap in het .raaot

divya  why is left atrial pressure normal while pulm arterial and right ventricular pressures are high? +6  
leaf_house  @divya It looks like the left atria can dilate in response to severe aortic stenosis, which I think would bring up the minimum diastolic pressure of LA (and I guess lower max systolic pressure?) like dilated cardiomyopathy. Link: https://www.ahajournals.org/doi/10.1161/CIRCIMAGING.116.005156 +  
cbreland  @divya I was on the same page, I saw that the left atrium was normal so I went to look at the right side of the heart and saw pressure elevations. Went with pulmonic stenosis.. Jumped the gun😔 +  


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etatPni sha a igaglnon cts,y ihwhc nca uossonnyatlpe sre.esrg

medschul  Mine would beg to differ >:O +28  
usmleuser007  Where would I have come across something like this (FA, Pathoma, or out of my S)? +5  
motherfucker2  I thought this bitch was a lipoma. Mother fucker +9  
divya  mf2 lipomas is fat. although fat may exist in liquid form, its still opaque, therefore negative transillumination. unlike ganglion cyst. +4  
beanie368  Only knew this because I have one that comes and goes... +4  
cbreland  I thought these were like a 1-way valve? Didn't think it would regress if that was a case? +  


submitted by sh_nu(3),
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hTsi Q codul be wdaseern tow aw,ys eon thohurg lmntoieiina ro gnownik who to tiyfdien teh el!cu wNo via aiinmtloien A.. .) naylmi seen in DSAI niespatt ( Q mest sdoe nto eicrtd Q ahtt a)wC)y loFu llisngem raarehdi t)"aftD y" Treeh seden to eb a tdria " esy emyTaElPgAHO + neel"yepmSaglo ip"gikns e"rvef yieap"ptoac"nn yam sola heva skin vlnteveomni E ) fuol gelsilnm negre algianv hdercsaig

)B *UCEL QRU PNIA + ecrlu

cbreland  I marked off Entamoeba because I thought it always caused bloody diarrhea... damn +1  
aakb  between Giardia and Entamoeba -- giardia doesn't invade intestinal wall but entamoeba does (per sketchy) +  
pfebo  Entamoeba: flask-shaped ulcers, Liver abscess +  


submitted by cbay0509(3),

the hallmark of meningioma is its relation to a meningeal surface hence relation to sulcus

https://usmlemate.blogspot.com/2019/02/nbme-19-block-2-answers-with-explanation.html

cbreland  I really wanted to pick GBM/astrocytoma here +  


submitted by aliyah(26),
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tefAr teh 4D+C slcle emoebc fecint,ed eth +DC8 sclle llik t.mhe

cbreland  Same for the macrophages and dendritic cells that would be infected. Intracellular pathogen that would need to have CD8 T cell mediated death +  


submitted by cassdawg(1101),

Penicillin can cause a direct Coombs + autoimmune hemolytic anemia

The Direct Coomb's test involves anti-Ig antibody (Coombs reagent) added to patient’s RBCs. RBCs agglutinate if the RBCs are already coated with antibodies (indicating that the body is making antibodies that bind the RBCs). RBCs tagged with antibodies are destroyed in the spleen. Penicillin is thought to act as a hapten binding with proteins on the RBCs and triggering an antibody response against the penicillin-RBC complex [FA2020 p423]

cbreland  To add, LDH would be increased with many types of hemolytic anemia. Not be the best answer, not as specific +  
kevin  Penicillins and cephalosporins act as haptens, alpha-methyldopa causes direct Abs against self Ag on RBC. - Dr. Sattar +2  


submitted by paloma(8),
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nrdccAigo ot ,UW lolchoa besau is a rkis rtocfa rof cuasravla .ecsrsoin Teh mots ocmmno ites si eht lmfroea ,dhea whcih npterses hiwt pnia hatt is edebtxaaerc by ithweg ainegbr ithotuw nmlfarmiyato gnsis on yahslcpi tixome.nnaai

cbreland  Similar thought process over here, didn't get a whole lot from the MRI other than lack of symmetry, but pt with alcohol problems was the key for me. Just played the odds +  


submitted by privwill(23),
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epSt by e:tps

  1. pH = wol = icsidosa
  2. HCO3 = lwo = disacsio
  3. OC2 = hgih = cossaiid

,So wtah Iev' narleed si tha,t in ,ecsenes eotbilacm asdocisi ysalaw satek piotryir ni tehes c.ieoanssr It's neditve atht eth nsproe is ont gic,toepmsnna utb you tnaw ot aeulcalct ayyawn by isgnu rtWein = .15 3()OHC + 8 .
fI you luataclce uyo lwli see taht het excdpeet si 3.5.0

  1. If OC2 is hherig atnh dteecxep = ntctocnoiam oreiatpyrsr isacoids
  2. If C2O si rweol hant exctedep = conotcamtni tioyesrprar aslaisolk

eHre it is gihreh tnah detpcxee 5)6( os octnctamnio iaerroptsry sco.aiids

I egssu fi you wnaetd ot rtsat hitw het rroipyresat iossdaic ouy vowudel' atenk onti ioetodcsnnrai htta tbcaioernba luhvo'sed eogn up ot opnemctase. It 'itndd os s'it o.tpaucmeesndn toN ersu fi st'eerh a raumlfo to elaualtcc het etrho fustf

makinallkindzofgainz  don't forget to add the +/- 2 to the end of Winter's formula. You have a tiny range in which CO2 can fall within +2  
cbreland  I started with respiratory acidosis and thought that any compensation would have an increased HCO3-. HCO3- is lower than normal levels, so that would mean met. acidosis as well. No math involved like you alluded to +  


submitted by chandlerbas(97),
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tno sure fi yuo all aevh nees teh uwlrdo acrht dDx for bkac pani tub i nfudo ti llarey puehlf.l lil saremuzmi it rhee: nictondoi yke( teurfnetdai:g e)ereav stttoohirreias i(taosoinlp rvedeile htiw ts)re, tyuolachdiapr - isdc rteihrnieaonsatai(d ot teh gle aak geulsea )igs,n lspani oitasisesnnp( wtih t),asndngi dvrpnoieotpdsyhea(erlyl wtih exse,icre and noiddnmta at rt,es) pilsan tmstn(saecsnotaiast npi,a soerw ta nhgt,i not eevdiler yb ntlopiisoa ,sea)cgnh rbetlrvae oifclyottoelsime(as nsen,edsret aeutc abck ,apni dan e,erv)f tarico cdosenstii sr(eeev selaroretrtsn a,nip iindgarat ot eht acbk)

cbreland  What page in FA is this? +