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Comments ...

 +2  (nbme22#24)

Essentially, we're trying to get to the renal artery from the femoral.

We cross through internal iliac (B) already to reach the aorta.

Remember the branches of the abdominal aorta: Celia -> SMA -> Renal -> IMA (FA 2020 pg. 363)

Celiac (A) and SMA (C) is superior to the renal so cross them out.

We're left with testicular artery.

Subcomments ...

submitted by sweetmed(144),
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heT Ham ttes si a tste duse in hte ssdongiai fo lxrpyasaom ruoltnanc lonemirbaguhoi .PNH() The sett lviovnes pngiacl der bodlo sllec ni limd dac;i a sotevpii tseulr earsein(dc RBC rgafyii)tl nacitdesi NHP

suckitnbme  It's so obscure of a test that wikipedia only has 4 sentences on it. +2  
pathogen7  FA2020 added the Ham test to PNH I believe! +  
pathogen7  Whoops no sorry I am wrong. They did add something called the EMA test to spherocytosis though. +  
snripper  Ham test has been replaced by flow cytometry now. So fck off, NBME. +1  
pseudomonalisa  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. +4  

submitted by lsmarshall(417),
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Syeoanvtinpbr si het eagttr of otanmtpieasns atnus(et ti;xon) umecls apsssm aer thrc.ccrisaeita nOly herto ewnsra oyu tmgih sicndroe si sltnyrieclcesoaeAhet nsice eh si a freram dan zzuobwdsr efotn ryarc su to teh rsmdpeoi ..d.nal ubt smmtyosp of a inhgiolercc torms rae santb.e

vshummy  Synaptobrevin is a SNARE protein. Why they couldn’t just give us SNARE I’ll never know. +45  
yotsubato  Cause they're dicks, and they watched sketchy to make sure our buzzwords were removed from the exam +46  
yotsubato  Oh and they read FA and did UW to make sure its not in there either +37  
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! +6  
qfever  So out of curiosity I checked out B) N-Acetylneuraminic acid It's sialic acid typical NBME +2  
alexxxx30  shocked they haven't started calling a "farmworker" a "drudge" <-- word I pulled from thesaurus. +3  
snripper  "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. +5  
mw126  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. +2  
wrongcareer69  Here's one fact I won't forget: Step 1 testwriters are incels +2  
baja_blast  FML +  
j44n  its not an ACH-E inhib because he doesnt have dumbell signs +  
flvent2120  I'm not even mad I got this wrong +  

G1 checkpoint: Cyclin D/CDK4 complex with p53 and rb G2 checkpoint: Cyclin B and CDK 1

Way to remember: G1 is associated with higher numbers D and 4 G2 is associated with B and 1


and also F@CK me and F@CK NBME!!!

snripper  But the question doesn't mention anything about which cyclin. How does this help? +1  
thyenman  @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). - +2  

submitted by diabetes(28),
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ihst iuonqset htye gvea uyo hte eswarn )to(.ioselitmsey

snripper  fck, am i retarded? +13  

submitted by neonem(572),
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sThi ainptet 'itsn ,gvteotipnanlhiy th'erye aElnHnRviPYi,gett hneec teh PC2O &;lt 40 mm Hg.

t'Lse wakl it rsbdk:wcaa yehT are tiahreelnyvinpgt ot tnespcaome orf hte lmbtcaioe odcsisai sauedc by rwaeddepsi y.apohix nlrpeayivtnigetH lslwao ouy ot bolw off roem O2.C

yWh aer yeth ix?ycoph Teh nsroep si yopxich ued to falmitnoianm nda tucea rrrsyepotai resstdis ymrodens morf teh emau.pnoni lAl teh icsteynok rofm the alrmnymifota clles aceus rdisceane nulpaormy cayilrpal eag,keal cihhw lboksc up eth avoarell mberamne os ttha 2O t'nac egt gruthho to eht .odbol

Why do htye vahe mebocialt ciadssio ni the irsft ael?pc oN ynoxge tg-&;- no nectoler oanstrrpt ncaih adn on CTA -&tg-; litcac ia.isdsoc

diabetes  no pneumonia it is UTI +3  
makinallkindzofgainz  The infection from the UTI spread to her lungs +  
makinallkindzofgainz  this is essentially urosepsis, one of the leading causes of sepsis +1  
cmun777  UTI -> Sepsis -> ARDS (exudative pathophysiology d/t increased pulmonary vasc permeability) +17  
peqmd  urosepsis +  
snripper  lmao I read it as upper respiratory tract infections, too. +3  
thisshouldbefree  she has an increased A-a gradient. +  

submitted by m-ice(340),
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The ooieh"ikdll of ssnmgii an osscn"itaiao efsrer to yeTp II The rkis of ypTe II errro is redetrespne by iThs olcdu eb nfesocud with o,rpew whcih si 1 - te.ab

usmleuser007  Just rereading this question without the stress, i got it quickly! Could't believe i missed something as simple as this. +2  
snripper  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... +1  

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dDi nyoena esle og wodn h:te 'shes veiposheynt so bymea ls'lhe tge sweaerohtu scieedfhnrri enrsoymd eaebcus oinghtn slee si knagmi esnse to em at tihs ??tonip? urtoe -

nsrTu to,u eseevr araamil anc asuec sralcuocadaivr lolepcas nad nynihspteoo.

redvelvet  me too :( +1  
abigail  me three :( +1  
yex  Me four :-/ +1  
link981  Slowly raising my hand as well +1  
tinydoc  Sammmme +1  
bullshitusmle  same here!!!:@ +1  
usmlecharserssss  patient has malaria with obvious picture and clinic, i answered because only thing associated with liver was hypoglycemia +12  
aisel1787  me five( +  
myoclonictonicbionic  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. +1  
alexxxx30  sammmeeeee +  
snripper  Dumbasses unite lmao +  
usmleaspirant2020  lol saaaaame! +  
usmleaspirant2020  lol saaaaame! +  
anechakfspb  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. +1  

submitted by sajaqua1(535),
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oenscayi,amtG sperid t,aomniaga nda agsiynmdphoo sa( wlel sa lamapr hymer)tae era lal nsgsi fo ssxcee The rvlie ni senatpit htiw acetiph isasdee is madeprii dan os ocnnat rleac gtsrenoe iflci.tnyufes ixS 21 oz eebsr aydil 72( ,oz or lhaf a )gaolln si oto cmu,h dna is tsdrneoygi ish .vreil

uslme123  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?! +6  
catch-22  The principle is you can get liver dysfunction without having HSM, ascites, etc. Liver disease is on a progressive spectrum. +12  
notadoctor  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. +  
charcot_bouchard  For Ascities u need to have portal HTN. Thats a must. (unless exudative cause like Malignancy) +2  
paulkarr  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". +4  
snripper  @paulkarr the problem was that the FA image was burned into my mind so without no ascites or edema threw me off of cirrhosis. +  
tyrionwill  cirrhosis doesn't present hepatomegaly, instead, the liver could be shrunken. +1  
avocadotoast  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. +1  

submitted by yogi(12),
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TIP - Pealttle + Ab sgoe ot nseepl - sydeL - owL plt t.orntcuAef lcepnmtysoe - laulsyu ptl ountc vrimope and elephrrPai olobd eamrs wsoh - JH sidoeb sa a sgni fo nlpaaise ( naurlce mtsearnn in CBR yaululs mreedov yb pe)es.ln I f tehre saw an rcsscyoea epslne h(hcwi was ton icnlotafun nwhe hte amni eelsnp was wgk)inor iwll aket rove the ftncuoin ydalglrau - HJ debiso liwl apirpsdea nda tPl ttsrsa to elsy - wchih sah dpehapen ni stih eacs n.csraeoi

spow  But why are there no bite cells? Question stem states that there is normal morphology? That's why I didn't pick accessory spleen +2  
makinallkindzofgainz  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) +3  
snripper  @spow Bite cells are associated with G6PD deficiency, not ITP. +1  
srdgreen123  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 +2  

submitted by hello(317),
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hWy are oorart"t cuff rte"a nda tro"taro fcuf stindie"nt ?rowng is ti cb hbot fo ehset odulw hows ngtpemniiem sgn?i si rthee a awy ot xDD oen from the tohre?

snripper  It can't be rotator cuff problems because abduction is normal up to 90 degrees. +2  

submitted by sne(48),
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I gthhtou of it ikel ehnw hes egts pu rfmo a poern os,optini esh si nagdscreie teh olbod ogngi to ehr eaht,r os os eht het xomyma aucsse oemr utronscbit.o sloA omsxmay secau yitn ,liobem hhicw can go ot teh tcseiysm niiuotclrca ugiscna iimn mbihrto in het rbina dna ibmls.

bigjimbo  Left atrial myxoma can mimic mitral stenosis (thus diastolic murmur) +1  
btl_nyc  RVOT obstruction would cause a systolic murmur that gets louder when standing, not diastolic. +2  
snripper  RVOT obstruction = Hypertrophic Obstructive Cardiomyopathy which causes diastolic dysfunction (S3) not a systolic murmur. +  

submitted by lfsuarez(143),
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hWne eitptsan rae nvige ccoitinNi i(acdiNnc)ia hyet ear dotl ot ecptex mmcono sdei seffcte to roucc shcu as thrwma dan dsener.s enO nac aivdo tsehe deis fetscfe by igatnk irpsnai

mcl  To expand on this, the flushing/warmth/redness is due to release of PGD2 and PGE2 which is why taking an NSAID helps. +17  
snripper  Doesn't acetaminophen inhibits COX 1-2, too? Why can't you use that instead of aspirin? Just wondering. +4  
raspberryslushy  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. +  
eagleeeee  I think the reason is that acetaminophen is inhibited peripherally and is mainly used to inhibit COX in the CNS +6  
whatup  The worst side effect of Niacin is hepatotoxicity. Acetaminophen is famously known for hepatoxicity so aspirin is a better answer +1  
doctordave  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) +2  

submitted by meningitis(546),
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Tennra agtses tarts at TEN ryeas dlo

atSeg I :

  • I is tl,fa sa in flta chets;
  • I is ,laeon as in on xaleus

aetSg II :()2 setag II rsstat at 11 o/y II( olok keil 11 )

  • 2 lslba lat(ecsurti nlamnet)rgee
  • 2 airhs (pibuc rihsa own igapnpe)ar
  • 2 rtebas sbdu romf

etgSa III 3:)( tartss ta 13 o/y

  • fI uoy ttaero 3, it slkoo leki lmsal etassrb aseBt(r dunoms mor;f)
  • fI uyo qgsigule het III yhte ookl ikle arsrycoc+leu ubipc hari
  • eendcsraI insep tlgneh nad esiz nca eb tnederespre by: II -;g&-t III
    yo(ur pines saw ntih II tbu own its ehkcrti I)II

etgSa VI (4:) rsttas at 14 y/o

  • istFr eii:mnga heT I in VI serrpetesn the ,hhigt dan eht V in VI sloko leki teh nsom ibpus betenew uory :legs
    N GENI:MA uoy evha rhia in nmso ibspu )V( tbu oyu vaeh a erobrd dtniegnia hte irha rofm wnirggo toni itg.shh
  • hTe V is n,yitop sa in onw hte ssabtre aer otipyn sai(red laorae ro oundm no nm)uod

taeSg V 5:)( 15 /oy

  • V has no dserrbo ganienidt ihar form nggrwio toin shithg ciupb( hair + hithg a)hri
  • 5 arsseinf(g in sandh) tglntfaine het aerlaos wneh braggbin hemt l(raeao etftanl at hist tsega dan no emro num"od on dumno")

meningitis  Sorry about the format, it came out wrong but I hope his helps. +1  
drdoom  looks good to me! +20  
gh889  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? +  
meningitis  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. +  
endochondral1  stage 3 breast mound is for females not males btw +2  
endochondral1  see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females +  
angelaq11  this is just too funny, I LOVE it! xD +3  
snripper  While this is impressive, this doesn't help with answering the question. +1  
yng  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. +  

submitted by drmohandes(103),
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Our tnetiap ahs a comitbela osisakall whti ira)tlp(a omsepycotarn ypiatrsoerr c.idssoai


ablictoeM aloislkas → +H sslo ro CH-O3 ng:ai

  • :mtinvgoi selo H+ (and eosl C-l/+)K
  • pool rscuidtei: osel +H da(n K)+


ileocbaMt doscai,si solebsip essauc ni siht ecotxn:t

  • texsvariadaari/lhe → sole C-O3H ad(n )+K ; Cl- topmyocarsen iercaens o(nmlra anoni )agp
  • aadmcteelizoa → loes -3OHC a(nd )K+ ; +H lsoa esdrsacee utb otn oheugn ot moroecev the loskisaal dascue by 3OCH- loss
  • rncolastipooen
snripper  This makes sense, thanks! +  
dysdiadochokinesia  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. +  
avocadotoast  @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 +  

submitted by yotsubato(1041),
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Wyh cnat tihs be texaisv?la oBht odulw sueca tcibmolea losakilsa whti ?

sup  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. +1  
miriamp3  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. +  
snripper  Why would laxatives cause anion gap MA? Isn't it similar to diarrhea? +  
castlblack  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. +4  

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The hometr is Rh - p;a&m sutef is hR +

gp 973 AF 2910 dniitnsaiAmtor fo tin-Da GgI to hR - tpnarneg heomrt uigndr rd3 tmsterire amp&; ayerl rpsupatmto ipreod (fi sfteu +)Rh

nrseePvt renlaamt i-taDn IGg rdtopuocni

ia-tnD IGg = ,O hR -

snripper  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. +1  
j000  the question is not asking what to give to the mother. it's asking what to give to the fetus. +1  

submitted by bobson150(14),
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ehT wgrodin of tihs tqiunoes ounefdsc .me hisT is ignaks hwcih" fo etehs leesssv si eth hhgi preressu syse"mt ghit?r So hte hghi pessreru isopreur laecrt is agniscu ideacners suerrpes itno het nfirrieo ?realct

welpdedelp  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 +13  
nc1992  Superior rectal not superior mesenteric. Took me a minute +  
hyperfukus  ugh am i ever gonna get these right EVER +5  
titanesxvi  why not the inferior mesenteric, since the superior rectal drains there +2  
thomasburton  @titanesxvi think it is because question says direct which is why superior rectal +2  
lilyo  thomasburton, so are they asking what vessels do internal hemorrhoids directly drain into? The order is Superior rectal vein--> Inferior mesenteric vein--> portal vein. +  
thomasburton  Yes exactly, so they do eventually reach IMV but not 'directly' +  
pg32  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. +3  
snripper  You just gotta know indirect vs. direct hemorrhoids. In this case, it's an indirect hemorrhoid (superior rectal vein) because of the rectal bleeding. +  
jesusisking  @titanesxvi DrDoom explained it pretty well below: "Defining tributary: Nice images make the term easier to recall. Smaller streams "pay tribute" to larger rivers (by flowing into them)" +  

submitted by usmlehulk(4),
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cna esoomen epesal xilnepa isth nuosei.qt i ouhgtth the tnpatie is cayaltul nigahv fletc ilp and la,taep btu yhw is het cterocr ransew gadsedsirn lony eth cltef

dentist  The question asks "the most likely cause of the facial finding involving the lip in this patient..." +5  
snripper  lmao. gottem +3  
ace9yak  cleft lip = 'processes' clef palate = 'shelves' +1  
mutteringly  Don't let a dentist tell you whats up :( +  

submitted by aesalmon(84),
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AF p.g 760 - ueflira of ifsuon fo the lmiyalaxr and dgemre lademi salna esrsepsoc aior(tnofm of iymarpr apt)ael

meningitis  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. +4  
redvelvet  a helpful photo +3  
snripper  @meningitis this is cleft lip, not cleft palate +2  

submitted by seagull(1583),
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If uyo 'ntod wnko thaw mucariloD eosd keil nya nolamr aunh.m heT fusco no whta nparsii tdoens' do, elnmay its' eonsdt' teffca PT miet nda otsm spill 'ntod rencasei tglniotc (alpeielsyc hiwt ipns.)ari iTsh si ohw I gciol ot hte ihgtr sa.nrwe

usmleuser007  If that's then thinking, then how would you differentiate between PT & PTT? +25  
ls3076  Why isn't "Decreased platelet count" correct? Aspirin does not decrease the platelet count, only inactivates platelets. +4  
drmohandes  Because dicumarol does not decrease platelet count either. +  
krewfoo99  @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) +3  
pg32  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. +4  
snripper  yeah, it wouldn't work. We'll need to know with Dicumarol is. +4  
jackie_chan  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 +3  
teepot123  di'coumarin'ol +  

submitted by seagull(1583),
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Im asol dvncinoec boklngci 2-LI is slao a nmaett?etr yWH is ahFTl-apN het ertbet wsarne eeh?r

amorah  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. +19  
sbryant6  Spot on. This image explains how Sirolimus blocks the effects of IL-2: +1  
krewfoo99  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. +  
snripper  Prednisone is a glucocorticoid (which inhibits IL-2 synthesis) is already being used with no effect. So TNF-alpha is the next option. +  
avocadotoast  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. +  

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AF 2910 o5ps1eD6 nyoane nwko owh ot ifeadrtteiefn teh cretpui beeladl aaopTrmsyon ebcrui and ?cuizr

footballa  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 +2  
snripper  Does Chagas have recurrent fever? Because that's what pointed me to African Sleeping Sickness. +  
baja_blast  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. +1  

submitted by cocoxaurus(55),
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lomtsA tgo kedcrit yb hsti noe ueebacs oatoaocrsmes saol esacsu ocbliatsotse srsotmOoaace toms ymloonmc ssmstazteaei ot unsgl g.uhoht

impostersyndromel1000  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 +2  
snripper  Also, osteosarcoma is less common in the elderly, more common in males <20 y/o (per F.A 2020) +2  
homersimpson  Osteosarcoma causes lytic bone lesions @cocoxarus +  

submitted by tissue creep(114),
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tLgfnii deha ielhw enro:p 1 Slcoaotmh ni lseim: 2 g oonsh:Cnimot 2 hmnsto

pg32  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 +1  
drschmoctor  @pg32 From being a parent! Otherwise little chance I'd remember all these milestones. +4  
drzed  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. +6  
snripper  Yeah, I don't see cooing anywhere. +  
teepot123  thankfully a lot of my friends on insta keep posting pics/vids of their babies reaching milestones so im well updated lol +1  
pjpeleven  Mnemonic: "Coo at Two" +1  

submitted by bubbles(70),
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Ccrhnoi arlen sfc:iucniynife

)1 orpo sphoahtep recaeancl &--gt; hhgi uemsr niacnorgi orshosohupp

2) ghhi mrues hhpotaesp ;t&-g- pcoexlmes ithw edlainvt oactin Ca --g;&t aC llafs

3) Ca alfls -;&-gt tgsrrgie HPT sixa

4) kyendi eulifra ;-g&-t creedsade ytacvtii fo r1aexldysoh-y ta eth nyiked -&g-t; ssel atiriclcol

makinallkindzofgainz  this guy renals +6  
paperbackwriter  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: +  
miriamp3  @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. +2  
paperbackwriter  @miriamp3 thank you! I will try out your strategy next time!! :) +1  
snripper  I thought renal insufficiency -> inability to reabsorb phosphate at PCT -> decreased phosphate? +2  

submitted by lnsetick(94),
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  • ncAPioer = yuro prsimta emlsl keil an AEP
  • ReeMUnc = hrste’e on ROMO in uoyr srae senci ’eehtry llfu fo wxa
  • -CEeCRYn = hwen uoy crsC,eeEi uroy rsoep ear giRCnY
  • cEusaoeBS = mSEBu is EPngEiS uot of yruo poser
hungrybox  as an ape i'm offended +31  
dr.xx  stop being an ape. evolutionize! +7  
dbg  as a creationist i'm offended +11  
maxillarythirdmolar  Also, Tarsal/Meibomian glands are found along the rims of the eyelid and produce meibum +  
snripper  So why is it apocrine? The dude is EXERCISING when playing football. +2  
qball  The question asks about "the characteristic odor" i.e. body odor coming from the APEocrine glands. The Eccrine glands secrete water and electrolytes. +1