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Welcome to krewfoo99’s page.
Contributor score: 88

Comments ...

 +1  (step2ck_form7#17)

QID: 15710

If the patient is asymptomatic no treatment needed.

If the pt had reflux symptoms then give medical therapy ( He dosent have symptoms now even though he had an ulcer in the past)

If GERD refractory to medical therapy then surgery is indicated .

 +1  (step2ck_form7#39)

According to wiki:

Most common infections in multiple myeloma are Pneumonia and Pyelonephritis. Pneumonia is caused by strep, staph, and klebsiella. Pyelonephritis is caused by E. Coli and other gram negatives

 +0  (step2ck_form7#15)

Im assuming OC pills over IUD since its less invasive. However, the risk of adverse effects would be higher.

 +0  (step2ck_form7#18)

u world: QID 4806.

Begin antiviral supression at 36 weeks. If there are lesions/prodromal symptoms during the time of delivery then do C section. If no lesions of prodormal symptoms during time of delivery, then Vaginal delivery.

 +4  (nbme18#21)
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mCluiac Ceobntraa is na naadcit hhwci can lcthaee nad sceeeadr tvefsesfeenic of hoter sdgru ucsh sa reycttceniasl and floneuisqulonro

 +4  (nbme24#33)
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VPH has ighh fntifiay for uoquasms teiu.hmleip rueT laocv ocdsr aevh mqssaouu pluie,etihm utsh HPV ntsde to grow htere

suckitnbme  Specifically stratified squamous epithelium I believe. +1

 +0  (nbme24#33)
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,aaylBscli utcae pttirsoas si scedau by omgsnsiar whhci aecus ITU as.lo

 -2  (nbme24#50)
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isTh udloc aiylse eb denuscfo twih uomuasqS Clle cnaoraCmi sa etyh aer bdcenrgisi a Btu i htink the yke eefnciredf si atth yhet tnimneo SPA.ETIAALM fI ti was daipla,ssy nteh ti wudol heva bnee neaccr.

usmlecrasherss  metaplasia also can lead to cancer FA p206 2019 +
suckitnbme  Dysplasia is not cancer since it is, in theory, still reversible. Only when it becomes irreversible is it a carcinoma. +1

 +1  (nbme24#1)
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oflci daic enwh it neetrs eht yobd si in eht ofmr fo rytloeheytmladoreahtft HTF( al.dyt)etmeh It dnsatoe its ehtlym ogrpu to avminit 21B to ceebmo HTF the( acitve mfor chiwh as a NDA rcorur)es.p Te h mtinaiv 2B1 wiht sti thylem orupg geos no ot encbomi twih oeoitmcnehy to rmfo iei.hnmtnoe

 +1  (nbme24#2)
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Lugn oeluvm iwll adrsecee ni oiyetbs tnpoyantolevihi .odmsnery evEn ohghut tshi apttnei si b,seoe eh has lal teh ialcclni seatreuf of lesep peana

j44n  also the lung volume would't have an "episodic" decrease. It would be constant due to the weight on their chest. +

 +12  (nbme24#4)
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fI oyu ever gte secnufod htiw hte amriadg m:ebemerr

CN 31,2,,4 - rnNibaC Mdi 68,,5,7 - n NPsCo 91112,,10, - eudlalM

eicSn ylon neo uuetscrtr ni the gdramia si nigmco tou of hte ulealmd tehn ti hsa be het vsagu veern

faus305  haha hey I do that +

 +2  (nbme24#17)
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Wyh dlowu eerdcaeds vomteemn truhohg het beecelrar adcqtuua eb rngow? ihtW all hte idulb fo bdool ni the CFS acttr wiottuh riatnp,obos tlwuond mmvneeto oals eb dadeersce huhrgto hte ad?uucqte

ergogenic22  this would cause a non-communicating hydrocephalus with enlarging of the lateral and 3rd ventricles but normal 4th ventricle and subarachnoid space +1

 +0  (nbme24#41)
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I inhkt noolrcqiueh sinctesrae wnot eb icecpfse ot vxiva and vhsl,otuea gknima it eth itecrrnco nrae.sw qiolronCehu rnteeasisc anc pplya to .P rcaalpmiuF nda .P alMaeira

nlyO ivvax adn voael cseua inzeyotohp htus mainkg htat hte remo cealr weasnr

 +1  (nbme24#22)
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EVB ursvi ofisenctni B esc.ll As a eosrsnep hrete si taeericv oytsclshpyiom oiof(terinrlap fo CD+8 ctoyitocx T sLpmytye)hc.o In ,HVI oyu lilw hvea a deesearc in TH clels igdnlea ot aesedcer ni C8D T husT BEV iwll oefrreialtp remo erlfey sa eht mmnieu sesnoper woatdrs it D(8C sllec) era etb.dunl shiT is ohw i got ot eth .aernws

 +4  (nbme24#3)
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RNTI - neoB mrwaro sseuop,nisr accitL Ai,isdosc IT NamRANnaie - ,acoixHytpoetti grstah rsaIene rihiobitn ta(er)gs - toaypMyh sg(acinu enaersIcd eteanrnCii sr)eKisanae Ptoe iInsbrhito v)ina(r - horpdtpsoyLy,i mprHeia,ylecy IG aorenneltic (tinhk of omaonlhr ecsf)ef

madojo  building off on this... answer choice A would be something like Maraviroc, and B is basically the same thing as A because a fusion inhibitor would be something like Maraviroc where you don't have any interaction with CCR5 and gp120. +1
overa  ^ With B, they are referring to Enfuvirtide, which blocks FUSION via gp41 blockade. Maraviroc blocks ATTACHMENT by preventing gp120 binding the chemokine receptor CCR5 on macrophages mainly. -lolnotacop +2

 +3  (nbme23#35)
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Igmea oswsh Shartno sllcuaCu

1) otganhrS lCuuaslc ni utsdal - msuMiena umminmoA Phpao 2s)hte rgaoSnht alsucCul in eiChlrdn - nytCesi

cuteaf  The history of recurrent pyelonephritis + fever is also a giveaway that this was due to a bacterial infection. +

 +3  (nbme23#22)
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Why uowld pesrfoirn be the rnwog wnras?e tuldWno ctcniuuaomla fo xcoit tnesopir ueasc het cell ot oundgre ssapoptoi ?

ergogenic22  Bortezomib does not directly activate perforin. It directly inhibits the proteasome which → enables CD8+ T cells to initiate apoptosis → via perforin release (in essence a downstream effect). +4
drzed  Exactly, it triggers the cells to undergo apoptosis which means that it can either be cell mediated (perforin and granzyme via FAS/FASL) OR it could also be through the intrinsic pathway (e.g. mitochondrial; cytochrome c) +
powerhouseofthecell  Question: But how do CD8 cells have a role in this process exactly in the vignette? Is it saying that when the proteins build up, only then do CD8 cells come and instead of MHC I presenting to proteasomes, they present it to CD8 to initiate apoptosis? +

 +8  (nbme23#19)
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oS iaylbsacl wath ihst is nyaigs ttah AND illw be iramnestttd to hte nrypoge nto SNR.A o DAN iwll crpaitele ni hte G2 aehps adn rnrtfesa of AND taramlei to pgroeyn lliw rccuo ni teh M epa.hs Teh ANR mya eb mdtueat dna kimnag tvefidece r,upsotdc utb sthi lliw ont armtstni otin hte ygron,pe tuhs nto aentfgifc pessiec luvvrais esdab on NAR mti.nastou

bk2458  makes sense!! +
almondbreeze  good work +1
tyrionwill  the question asks the reason of no impact on its survival. if a protein translated from a wrong mRNA loses its function, how can we say the bacteria will still survive well? if there is always fatal error happened during mRNA transcription, and always leading to fatal dysfunctional protein, how can the bacteria and its progeny still survive? so the point will be whether the fatal errors will always happen during transcription? I dont know... +
tyrionwill  actually FA and NBME seem to have made a wrong statement that RNA polymerase has no proofreading function. RNA polymerase has more fidelity to DNA than DNA polymerase by 2 ways: 1) highly selection of correct nucleotide, and 2) proofreading. (Jasmin F Sydow and Patrick Cramer, RNA polymerase fidelity and transcriptional proofreading: however, if survival of the species refers only to the reproduction of progeny, mRNA mutation has nothing with the progeny. +1

 +1  (nbme23#33)
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In twha sutositani iwll HbH eb fremod (3 hlpaa inahc )snol?eietd

ergogenic22  one parent has 2 deletions on the same gene, the other parent has 1 deletion, and the offspring receives all three. In this question, both parents have alpha 1 deletion +
ergogenic22  actually its possible that they both have 2 gene deletions, but regardless, a-thalassemia trait is more likely +
ergogenic22  and someone above said Asian people are cis-2 deletion so the offspring will not receive two deletion from one parent +
ergogenic22  ↑↑ I made a mistake by confusing trans and cis cis has deletions on the same chromosome and can pass two deletions to off spring, therefore a chance of allowing HbH +

 +0  (nbme23#28)
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naC eeonsom lpiaxne thwa teh recpiut is sepopuds to ?sowh Is ti pudessop ot be dgseetmne hltiuroepn?s

titanesxvi  yes do to B12 deficiency +

 +7  (nbme23#50)
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flteaodAr and ertha trea hesra na rieesvn

As eht mbailulic ocrd is reepcd,sosm terhe is an ernscaei in tmciesys uavclsar atiersesnc kT(nih fo who eht uerpsser ulodw seearcin if you erew ot rpsse wodn no a raetw s.ohe) ,Tshu the daolftera is rcaieends dna hetre is a mtroeanopcys eseaerdc in aehrt t.ear

divya  yeah, i too thought similarly. btw increase afterload --> increase in bp --> baroreceptor firing --> decrease in heart rate. is that it? +2

 +0  (nbme23#12)
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lWtdoun eth CMHO urmurm be etsb herad in eht tiocra ?eaar

krewfoo99  Correction: Shouldnt it be heard best in the left upper sternal border? +
usmlehulk  In FA 2018 page 303. patients with HOCM presents with MItral regurgitation due to impared mitral valve closure. Hence this explains the murmur. +1

 +3  (nbme23#49)
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epiiehEnrnp satc tyomsl no Btea sc.orteper Beat spteorrce rae G .ocdulep

baja_blast  Alpha receptors are also G-coupled and are another potential site of action for Epinephrine (at high doses according to SketchyPharm Sympathomimetics) +

 -3  (nbme23#21)
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My :agnsneori

sA uyo og blweo aes elvl,e eerht si na eanisrce ni tcpreihasom e.psrsure Icenersa ni hte srseuepr amy sucea reurptu fo barpuselul slbbe dgelnia to exaruoptm.hon

Nto seur fi sith is telyrnie eorrcct thhgu.o

 -1  (nbme23#23)
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yeonnA onwk hwy hreta onsdus uwold be indttsa ni DOPC rc?naxeaiobet

yng  Patient is usually obese (blue bloater) --> diaphragm movement is limited --> can't take deep breaths, and in extreme cases, the chest size increased and causing distant heart sound. +1

 +0  (nbme23#23)
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neoyAn kwno ywh ehtra nsodus oluwd eb atntisd ni ODPC rn?teciexaabo

marat  Cause lungs are overextended +5
marat  overexpanded +3

 +2  (nbme23#41)
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In odrabs dna deby,no It si dsia atth thdir edegre htrea bcokl is ued ot kcolb ni eth HSI enurikPje m.ystse oS wyh ouwdl nltaioab fo AV neod useac shit sesaide?

nlWudot osnertctudi of rpat of fetl vrinetelc be a rteetb waensr ?

brbwhat  Had the same doubt, Read the part again and found this. Type 2 Is caused when purkinje is hanging by a thread and therefore some impulses conducted, some not. Chb is caused by purkinje not conducting impulses from san, some lower pacemaker ie purkinje or his is depolarising by itself hence venrticles beat independently. There is BLOCK in purkinje for conduction from san. Among options the only thing that establishes this block is avn ablation. +

Subcomments ...

Can anyone help explain to me why he has lower extremity hyperreflexia and upper extremity resting tremor? I can't find anything that associates those symptoms to Schizophrenia.

krewfoo99  I think its because his hypothyroidism is being overtreated with levothyroxine. +  

submitted by seagull(1405),

My understanding is that occult blood is commonly due to an upper GI bleed. Wouldn't the colon produce gross blood? I'm hopelessly lost in these matters.

krewfoo99  Yeah I am lost in this one too. Maybe colonoscopy is the right answer to rule out other serious causes of GI Bleeding (Ex: Cancer). +  

submitted by step_prep5(25),
  • Woman with complicated/prolonged delivery with excessive postpartum bleeding who does not have retained placenta, genital tract trauma or history of coagulopathy, and therefore most likely has uterine atony (most common cause of postpartum bleeding and commonly seen after prolonged/difficult delivery)
  • Causes of post-delivery bleeding is 4 T’s: (1) aTony (most common) (2) Trauma (3) Thrombin (coagulopathy) (4) Tissue (retained placenta, etc.)

krewfoo99  Yes but how do you know that the placenta is not retained? +  

submitted by russnels(13),

Anybody have any good insights as to what is going on here? Does surgery somehow cause hypokalemia? Or does this have to do with digoxin toxicity? I'm not sure how surgery fits in. Thanks in advance!

misscorona  Looking at UpToDate, hypokalemia is listed as one of few postoperative electrolyte abnormalities. Surgical stress releases aldosterone which leads to hypokalemia. Hypokalemia is a known cause of premature ventricular contractions. Digoxin toxicity can cause premature ventricular contractions but it seems like this patient was on these medications prior to surgery and this may be less likely contributor. Side note, digoxin can lead to hyperkalemia. +2  
yotsubato  Ah so it is a BS question.... Ugh. +2  
krewfoo99  I think surgery/stress will lead to increase in cortisol which acts like aldosterone to cause hypokalemia leading to premature ventricular contractions +  

submitted by seagull(1405),
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If oyu 'dnot owkn hatw iurlamDco soed ielk nya oanlmr .mauhn Teh ocfsu on hawt ipisarn netosd' ,od meylan 'tis tnsde'o efcfat TP mtei dan mots lpils nd'ot eriacnse ctltgnoi lpalicseye( ihwt sinia.rp) ihTs is owh I oilcg ot het ghrit swaern.

usmleuser007  If that's then thinking, then how would you differentiate between PT & PTT? +18  
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(1405),
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mI losa doccnniev gcobkiln -I2L si osal a nr?tmtteae HWy is Fph-TNlaa eht eetbtr rwneas rhee?

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. +16  
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. +  

submitted by sunny(4),
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hyw si hsit so //i oknw tis basci tub ..l?il?s.t

krewfoo99  I think its neutrophils because they mention myelosupression and rapidly dividing cells. +2  
wishmewell  Ya, Neutrophils, basophils, macrophages, eosinophils are considered Myeloid cells. While the rest of the T cells are from the Lymphoid lineage, The Immunoglobulins come from B cells ( lymphoid lineage). +6  
cuthbertallg0od  Myelosuppression refers to bone marrow suppression as a whole, including lymphocytes. I got it wrong too and no clue why its neutrophils, but I don't think that's why +  
cuthbertallg0od  Maybe they're looking for us to pick "losing innate immunity" (maybe worse than losing adaptive?), which wouldn't refer to complement here since the problem isn't in the liver +  
scrambledeggs  FA2020 p.424 Neutropenia: Absolute neutrophil count < 1500 cells/mm3. Severe infections typical when < 500 cells/mm3. Causes: Sepsis/postinfection, drugs (including chemotherapy), aplastic anemia, SLE, radiation +1  
kmichaels  Pretty sure the idea is that it's just the fact that you classical follow neutrophils. All cytotoxic T-cell activity is talking about ACTIVITY not counts. NK cells we just don't really measure those I think haha +1  

submitted by m-ice(321),
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loMtrissopo is a rdalnntispaog lagnoa )EG2P( ttha asct on eht tsomcha ot peotmro cumsu ocrpottien fo het cthsmoa ln,ngii tbu lsoa stca ni teh ertusu to oeunaegcr irtc,nnoaotc hhciw kasem it uflseu for boroani.t

usmile1  perfect except it is a PGE1 analog, not 2 +2  
krewfoo99  PGE2 will increase uterine tone (Pg. 270 FA 2018) +  
drmohandes  Misoprostol prevents NSAID-induced peptic ulcers. Side-effect: also gets rid of baby. +  

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in eht throe dhan , rneui itsaspumo si hhgi guhone , so if rezseusi haysgto=;lryob&dsim gt&;= olygmiibraonu &;t=g TAN =t&;g high saupimsot erncxotie , wyh ?ont

krewfoo99  True but hypokalemia would occur in the recovery phase. So weeks after the inciting phase. +1  
therealslimshady  Acute rhabdomyolysis would lead to hyperkalemia, not hypokalemia, because cells are packed with K+ +  

submitted by zbird(2),
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iThs tnitpae ash -sypTilaDte I RAT hhicw is leepdianx yb Nlorma mSuer onAin gap 8)( bocilateM siiodsca iwht her isvptieo ayrurni onani g)+p(5a.

krewfoo99  Why would the urine Potassium be so high if it is type 1 ? Shouldnt it be type 2? +  
drpatinoire  @krewfoo99 I think it's RTA2 (Fanconi syndrome), he is losing all kinds of Na, K, Cl which should be reabsorbed in PCT. +  
misterdoctor69  @Drpatinoire: it can't be RTA2 because the urine anion gap (UAG) is positive (+), which implies that the patient is unable to secrete H+ (via NH4+, which couples w/ Cl-). RTA2 on the other hand has a negative (-) UAG because RTA2 affects only the proximal tubule's ability to reabsorb bicarbonate (i.e. H+ secretion via NH4+ in the distal convoluted tubule is unaffected). +  

submitted by roygbiv(20),
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hyW udclo tshi not eb resxcavturala s?shmieylo nI FA ti says uctae loiyhctem irunntoafss nrteioca cna be deu ot ABO oiaynctbtipmiil or rraavausetlcx ssiolmy.he

niboonsh  because extravascular hemolysis is associated w jaundice. Intravascular hemolysis would have hemoglobinuria but that's not an answer +1  
niboonsh  i mean that is the answer lol +  
krewfoo99  According to pathoma: Intrvascular haemolysis will lead to haemoglobin binding to haptoglobin. This complex will travel to the kidneys and be excreted. This will lead to red colored urine and haemosiduria (Note: This can also lead to acute tubular necrosis) Extravascular haemolysis is when macrophages break down the RBC. Then the Haeme is converted to biliverdin then bilirubin and conjugated in liver, and then excreted. +4  
paperbackwriter  If you look under the "clinical presentation" column of the blood transfusion reactions chart (pg114), it says that hemoglobinuria is with intravascular hemolysis and jaundice is with extravascular. Makes sense because with extravascular hemolysis your splenic macrophages are are chewing up the RBCs and sequestering it in the spleen so you don't get "spillover" -- i.e. clean urine. +1  

submitted by medskool123(26),
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owh did ouy wnok it aws a ayserrrwbt onhegmiama adn tno a trpo weni tsiI?na otuhhtg I adh tsih noe ni eth bnak

kateinwonderland  Me too! TABLE 1 Classification of Vascular Lesions Vascular malformations (flat lesions) -Salmon patch (also known as nevus simplex or nevus telangiectaticus) -Port-wine stain (also known as nevus flammeus) Hemangiomas (raised lesions) -Superficial hemangioma (also known as capillary nevus hemangioma) -Deep hemangioma (also known as cavernous hemangioma) +  
krewfoo99  Because they describe the lesion as cavernous vascular channels +  
covid2019  After looking into it, port wine stain comes as part of Sturge Weber SYNDROME. Given that this child was coming in for a well-child examination, they're implying there's no other symptoms (SWS would have signs of other vascular malformations like in the CNS--> epilepsy). +  

submitted by whoissaad(73),
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What eueragnat do we heva ttha teh toraemmo is gingo ot tops minsokg in het ternpmaat by ig""nsak imh ot od .?.so

krewfoo99  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. +1  

submitted by seagull(1405),
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A- mpiryar morto cterox = orgnw esid fo byod ict(dief fo NUM on eftl sdei ob)dy

B - sThlauma = noessyr annriotifmo cduoint - ormto ifcisedt uiklleny ot gaieinort mfro eehr

C - sPno - sNC ,87,,6,5 klliye erutls ni "eclokd in no"mysedr or tmepceol olss fo otomr iofcnnut no rtghi sied + fiacal aersut.ef

D. emrVis - rlatenc yodb io.rocnatondi ameaDg elssurt ni ataiax

tNo elcpmote btu amyeb p..llhufe

yotsubato  C - Pons - CNs 8,7,6,5, likely result in "locked in syndrome" or complete loss of motor function on LEFT side + RIGHT sided facial features. Decussation occurs in medulla +2  
kard  Sorry if im mistaken, Isnt A) Somatosensory? +2  
krewfoo99  Yes i think A should be somatosensory. Primary motor cortex would be present in the precentral gyrus +  
drpatinoire  A is primary motor. A and the gyrus at right side of A compose the paracentral lobule. +  

submitted by m-ice(321),
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vpCetitoeim bntrishiio nesraiec eth Km fo eht sattsur.eb heT Km ssreeterpn owh slyaie a bsertatus nac nidb het vteaci is,et twhi a erlwo Km gennrteserpi eysa nb,gdiin and a reihgh Km anmigne orem .ifitudfcl fI uoy dad a ievcpmeotit iiihronb,t ilek nhoelat ni this eacs, ti kseam it eorm iucliftdf ofr het oletmnha to dnib eht ticvae sei,t eceuabs it umst ctmpoee ithw eth e.talhno

deathbystep1  but how is ethanol a "inhibitor" of alcohol dehydrogenase? isnt the concept that both ethanol and methanol compete for the same binding site of alcohol dehydrogenase and hence ethanol displaces methanol preventing its metabolism? if ethanol were to be a inhibitor it would have to shut off the enzyme, which is does not. +  
krewfoo99  @deathbystep1 Competitive inhibitor simply means increasing concentration of a particular substrate will allow more binding of the substrate to the enzyme. Thus the substrate with the higher concentration will competitive inhibit the other substrate by binding to the enzyme. It dosent necessarily shut off the enzyme +3  

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tou fo yrtciu,soi hyw ear AST dna TAL h?ghi si htat iyangs eth RTIN edsu swa enidoiadesn cihwh lde ot eatpsnctiria s?aol

krewfoo99  AST and ALT will not be elevated in pancreatitis, they will only be increased during liver damage. NRTI causes hepatoxicity (although FA 2018 states NNRTI causes hepatotoxicity, NRTI could also be an option considering the two classes are similar. The hepatoxicity will cause an increase in ALT and AST +  

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hTe ieassed eher is stceofru pabshsiaphtose .icefdcieny In ,ti VI croeygll or usctofer ts’dnoe leph ecsubae bhto rnete eth snoilgneeoucseg pawthya ewblo eusfoctr hbopp.stahseia saaoctlGe no teh othre ahdn tenres eoavb .it I n’dto tkinh oyu llarye dnee to wkno sith ot ooeshc eth cctrroe wraesn csien eht lniiccla cutirpe fo gasfint aeylygcpohmi taht is ertccedor /w smeo stro fo ugras atht can renet teh elusceeginognso ayawpht dsohlu clue you oint het ihgrt s.wnrea

neonem  I don't think you could have *totally* ruled out the other answers - I picked glycogen breakdown because it sounded kind of like Von Gierke disease (glucose-6-phosphatase) to me: characterized by fasting hypoglycemia, lactic acidosis, and hepatomegaly since you're not able to get that final step of exporting glucose into the blood. However, I guess in this case you wouldn't see that problem of glycerol/fructose infusion not increasing blood glucose. Nice catch. +24  
vshummy  I think you were super smart to catch Von Gierke! Just to refine your answer b/c I had to look this up after reading your explanation, von gierke has a problem with gluconeogenesis as well as glycogenolysis. So they’d have a problem with glycerol and fructose but also galactose since they all feed into gluconeogenesis before glucose-6-phosphatase. Great thought process! +22  
drmomo  glycerol and fructose both enter the pathway thru DHAP and glyceraldehyde-3-ph. Galactose enters thru Gal-1-ph to glu-1-ph conversion +2  
linwanrun1357  In this cause (fructose bisphosphatase deficiency.,),fructose should help to increase serum glucose, bcz it can become into glucose-6-P by hexokinase. Therefore, this question makes me confused.... +  
krewfoo99  According to uworld, fructose infusion will not increase blood glucose levels in Von Gierkes Disease as well +  
atbangura  I believe Von Gierke is not a plausible answer choice because a galactose infusion would still not see an elevation in glucose levels. Remember, galactose could be converted to galactose 6 phosphate, but in order to complete gluconeogenesis and allow glucose to leave the Liver for an increase of its concentration in the blood, the patient would still need glucose 6 phosphatase which is eliminated in Von Gierke. +1  
lilyo  So what disease is this??? I mean couldnt we have just answered the question based on the fact that the patient responds to galactose being infused and we know that galactose feeds into gluconeogenesis?? I am so confused. +1  
djtallahassee  Its Hereditary Fructose intolerance right? gets sick after fructose and I guess glycerol can jump in via aldolase B on this pathway via page 74 of FA2019. It looked like a fructose thing to me so I just marked out the other ones and moved on. +1  
paperbackwriter  @djtallahassee I was wondering same, but hereditary fructose intolerance also results in inhibition of glycogenolysis :/ confusing question. +  
amt12d  A much simpler way to think about this, without trying to figure out a diagnosis, I looked at the time frame for when the child was presenting. He has eaten poorly for 3 days, by now, his glycogen breakdown is gone. His body would be trying to make glucose, therefore, gluconeogenesis is impaired, not glycogen breakdown. +2  
tyrionwill  if fructose kinase is not available (fructose intolerence), then some fructose may go to F-6-P by hexokinase, then goes to G6P if gluconeogenesis is needed. however this patient's fructose kinase was intact, so no fructose would have go to F6P, so there would be no blood glucose increment after injection of fructose. +  

submitted by m-ice(321),
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ihTs mowan hsa amalrxoPys luartnocN oraul.mboneiHgi hiTs otsm fenot esspnetr ni a uyogn talud owh ahs deseosip fo kadr einru in eht leddmi of het ithng or hnwe gwnika pu ni eth i.nrmgon tIs' escuad by elmnmoptec vyattici ritcldey gaastni eht ptneitas' nwo .CRsB nreatCi piilyocdlgs are eededn on the RBC asfeurc to eevptrn attkca ofmr n,ltecpmeom het msot nabotel of iwchh aer C55D nda .9C5D Pttnasei tihw PHN ehva a tmscoia imnttuoa ni wihch ehty sotl oitunnfc fo a GAIP ezenym dedeen rfo erporp ernntapsieto adn aaenthctmt of DD5/C55C9 on het BCR s.ucrfea rrfeoheeT eht eawsnr si a etcefd in a ecll embemarn hnaroc io.epntr htuWtio si,ht oetcnpmlem atskatc BRsC.

usmleuser007  I knew the disorder and its pathophysiology. But sometimes the answer choices are so wordy or colorful that you still get it wrong.... +19  
sunshinesweetheart  I got this one right but now upon review I'm having trouble ruling out hereditary spherocytosis ("abnormal cell morphology") answer choice. It helps that the dark urine is in the mornings, but is it officially ruled out because of her age? like this is obvi an acquired mutation if someone's 33? +  
krewfoo99  @sunshinesweetheart Hereditary Spherocytosis is a autosomnal dominant condition. The patient in the question stem has had dark urine since the past 2 months (acute presentation). Since spherocytosis is hereditary, it wont be present as a acute condition +5  

submitted by colonelred_(100),
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aubttebrlAti iksr = cinecdien ni xeesdpo – cecnienid ni epudxseno

= /3010,00 oke)rmss( - ,0033/00 kn)omesrsn(o
= 0.03 - 001.
= 020. s(o teh tbbuattlreai skri is otabu 2%)

gplpynAi it ot a puootlpani of 0001,:0

= 020. * 001,00
= 200

charcot_bouchard  What if i tell you this is a ques of Attributable risk % in exposed? AR= 0.02 / IR in exposed (30/1000) = 0.6667 30 case in 1000. So 300 case in 10,000 0.6667 x 300 = 200 or in another word 66% cases of 100 lung cancer cases in smokers is actually due to smoking. so in 300 cases of smokers 200 is actually due to smoking +4  
charcot_bouchard  This is a mind fuck. Lemme tell u guys if any consolation while doing the ques during test i did it with AR = 0.02; NNH = 1/0.02 = 50. 50 persons smoke to cause 1 cancer. 10K smoke to cause 200 cancer. +1  
ls3076  Sorry if this is a stupid question. Why is it incorrect to simply apply the same proportion (30 cancer per 1000 smokers) to 10,000 smokers? +2  
krewfoo99  @is3076 Thats exactly what is did. I still dont understand how that is wrong. But i guess they want us to think about it in terms of AR +  
hhsuperhigh  @Is3076 and @Krewfoo99, If a person doesn't smoke, the natural risk of getting lung cancer is 30/3000=1%. The smoker's risk is 30/1000=3%. This 3% is not purely contributed by smoking, but mixed with the natural risk. So for calculating the pure contribution made by smoking, you should use 3%-1% which is 2%. And this 2% is the pure contribution of smoking. Not all smokers get lung cancer, the same thing, not all lung cancer among smokers are attributed by smoking. They may get lung cancer anyway despite smoking or not. +10  

submitted by hayayah(1056),
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ooombCla is na eey mroyatalnib ahtt surcco eeobfr birh.t hy'eerT sgminis isecep fo tsusie in urescrstut atth mrfo hte ee.y

  • maCoobsol taefinfgc teh iris, hhiwc srutel in a ke"oeh"ly aaanrcppee of eht lu,ppi rneelaygl do nto lead to insvio sol.s

  • moslbCooa ilgvonnvi het iteran lesutr ni oivins sosl in ispicfce tsarp of eht laiuvs dlie.f

  • gareL tnralei ocsoomabl ro tohse gncifeaft het ctpoi ernve cna acesu wlo siino,v hhicw snaem svnioi lsos ahtt nncaot eb letpmeclyo ecedrotcr tiwh elsasgs ro cnacott lne.sse

mousie  thanks for this explanation! +  
macrohphage95  can any one explain to me why not lens ? +  
krewfoo99  @macrophage95 Lens are an interal part of the refractive power of the eye. Without the lens the image would not be formed on the retina, thus leading to visual loss +4  
qfever  Do anyone know why not choroid? +1  
adong  @qfever, no choroid would also be more detrimental to vision since it supplies blood to the retina +2  
irgunner  That random zanki card with colobomas associated with a failure of the choroid fissure to close messed me up +11  
mnemonicsfordayz  Seems like the key to this question is in what is omitted from the question stem: there is no mention of vision loss. If we assume there is no vision loss, then we can eliminate things associated with visual acuity (weird to think of in 2 week old but whatever): C, D, E, F. Also, by @hayayah 's reasoning, we eliminate E & F. If you reconsider the "asymmetric left pupil" then the only likely answer between A & B is B, Iris because the iris' central opening forms the pupil. I mistakenly put A because I was thinking of the choroid fissure and I read the question incorrectly - but it's a poorly worded question IMO. +  
mamed  Key here is that it doesn't affect vision- the only thing would be the iris. All others are used in vision. Don't have to know what a coloboma actually is. +2  
azibird  The extra section of that Zanki card specifically says that a coloboma "can be seen in the iris, retina, choroid, or optic disc." Don't you dare talk trash about Zanki! +1  

submitted by amarousis(22),
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tBu ts'oned cuubtsae inbdcome genotdrneiae alde ot pteaimnrim ni CDL,M serlcobnleparei dan strincoocipla tctra? I gte the taixac itag - elLrbCcrMo.seinlp/aeD But the estsnnaoi ot kiinc,ppr 'udwlont atht be eth ataislcmhniop c?attr taTh si not llysauu tfaefdce in buaesuct denobimc raoigentneed.

krewfoo99  It would affect the dorsal column tract and the spinothalamic tract. It wont affect the spinocerebellar tract (Thus Rombergs sign in B12 deficiency will be positive) All three of the tracts are affected in Friedrichs Ataxia +  
krewfoo99  Sorry. Just checked on FA. It will also affect the spinocerebellar tract +  
spow  Sensation to pinprick is DCML +  
meli  UWORLD ID:65 "many patients develop neurologic manifestations due to: axonal degeneration of the peripheral nerves, leading to numbness, paresthesia, and depressed motor reflexes." So, I think the sensation to pinprick was describing the paresthesia! +  

submitted by amarousis(22),
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uBt so'tdne utcasbeu ibdenocm tdnieaorngee aled to tnmmiireap in CDML, lesrpcnlaoreibe nda locipacitrson trc?at I etg eht ctxaia agti - CnrrlcMsea.poeDeilLb/ tuB het nisansote ot ci,ipnrkp ludn'tow tath be eth socthaimnplia rtct?a Taht si ton uasuyll cadeffte ni ebuacuts cdbmneio nteedr.nioaeg

krewfoo99  It would affect the dorsal column tract and the spinothalamic tract. It wont affect the spinocerebellar tract (Thus Rombergs sign in B12 deficiency will be positive) All three of the tracts are affected in Friedrichs Ataxia +  
krewfoo99  Sorry. Just checked on FA. It will also affect the spinocerebellar tract +  
spow  Sensation to pinprick is DCML +  
meli  UWORLD ID:65 "many patients develop neurologic manifestations due to: axonal degeneration of the peripheral nerves, leading to numbness, paresthesia, and depressed motor reflexes." So, I think the sensation to pinprick was describing the paresthesia! +  

submitted by notadoctor(152),
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cocndrAgi to Glnj,oa iehtampcyloy arev is noe of the sotm oncmom csseau fo B-uddihraiC myode.nsr goccnrAdi to F,A -CdBduiraih si soaestdaci emro ygeralenl with yghepearcolulba s,etats yteoilyamphc are,v smputpraot sstae,t adn C.CH

taipcHe riiocsrhs cna be delur tuo sdaeb no teh emit uroces fo eth e'ianptst isnoetaneprt - he was ifen 2 wekes oag adn eht ladinbamo anip atsrtde na urho og.a

krewfoo99  Also in cirrhosis, the liver wont be enlarged or tender on palpation +1  
almondbreeze  @krewfoo99 Good job. accoring to FA2019 pg.368, congestive liver disease (hepatomegaly, ascites, varices, abdominal pain, liver failiure) seems to be the key in Budd-Chiari SD +2  

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ehT ywa I ldeduxce adontaiovils saw t:hsi eth imhectyatps oepcrrte htta dstaeli is 2β, chwih is ton ttsiuamedl yb erepepoih.rninn oS ot mitaetlsu eht ,eorrectp teh taelelst aoiglnng odluw ehav had to tirsf satuelitm hte alerand dlmulae to seralee epeenhpinir tselaetl( oto ighh ot tieatumls eht ae.u)llmd

krewfoo99  But isint beta 1 (heart rate) also stimulated by Epinephrine? +  

submitted by welpdedelp(216),
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shsHiemmtocoroa, kaa breon"z tede".ibas otannC be nsdodiA edu to teh irgyeapmhyelc dan mraonl BP

alexb  I missed this bc didn't notice it was a middle-aged guy w/ just 3 year hx of Type 1 DM. +2  
tinydoc  I got it mixed up with primary adrenal insufficiency and the acth ⇒ hyperpigmentation. +11  
maddy1994  testicular atrophy &hepatomegaly helped me out to eliminate the options..when i was left with ferritin and saw pigmentation it clicked that it is hemochromatosis +3  
krewfoo99  Symptoms of Darkening of skin, liver dysfunction, diabetes, with testicular atrophy will always be hemochromatosis +3  

submitted by krewfoo99(88),
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lnoWtud het COMH murumr be tbse drahe in hte tocair rae?a

krewfoo99  Correction: Shouldnt it be heard best in the left upper sternal border? +  
usmlehulk  In FA 2018 page 303. patients with HOCM presents with MItral regurgitation due to impared mitral valve closure. Hence this explains the murmur. +1  

submitted by kimcharito(14),
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ti is lnrmao naoitrirdia ot teh HIGRT k?nec wtah osde it ?aemn

krewfoo99  @kimcharito Aortic stenosis radiates to the carotids FA pg. 285 (2018) +1  

submitted by sajaqua1(519),
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ueesaBc teh a'sybb mertho hsa eTyp 1 iDteabse liseml,ut it si ebspliual atht yhte hda tvleedea obldo ouglces lseelv udgnri or tyhsrlo efreob Iulnnsi oesd ont cssor the npaael,tc tub ousgcle oesd, so igndur briht eht ennoaet wodul aevh bene iecyep.lrmycgh siTh olwud elad ot hte nnoatlae ncaepsra elinrasge nnu,ilsi nigdirv ucseolg tnoi llces dna iutrnng owdn goneslugiee;ncso this si hyw het abby si limhgyycceop rihgt ow.n

)B ecarDesed oneycggl enan-ctcntroio I 'ontd knwo eht nolcyegg rocntoencaint rceapdmo to an adutl ,tpienta but a esdcreae ni gnogcyle acorncntoeint udolw itneiacd oselcyggonulec/g laseeer, hhwci ouwdl tno be a cglcyhpiemyo ttes.a C) sraDeeecd egyonglc tasseynh vaytt-ici edadrcsee cynoeglg easyhtns tvyciiat tdcaienis erygen aml,cbaitos dan wuold dela to iehghr ermsu eoslucg )D aedesceDr serum nisliun riacnt-ectonno eeredacsd ermsu snuinli lodwu dale ot eghirh eeslvl fo lgseouc ni re.usm E) Indscerea sremu nusillien-ki gothrw f-ctrao FGI seod nto nbid nealry sa ellw to nuniils rsetercop as silunin ,odes nad so uwldo vhea to be in lyextemre ghih ictntsrnencaoo ot aevh thsi fcet.ef GIF is soadseaitc hitw moictas htgrwo dan suemcl

yotsubato  His glycogen concentration is high, since he's been hyperglycemic with lots of insulin until birth. +3  
alexb  Also explains why he's 12 pounds. +3  
krewfoo99  Also, think of it like this: Insulin causes hypoglycemia, thus this baby must have increased insulin. It is also an anaobolic hormone which is clear by the babys weight. Insulin increases glycogen synthase activity, and causes an increase in concentrations of glycogen. Decrease in insulin would do exactly the opposite +1  
tyrionwill  fetus of a mom with DM will develop pancreatic beta cell hyperplasia, which leads to insulinemia trying to reduce the blood glucose. after birth, the excessive blood glucose will be automatically withdrawn while the insulin at that moment is still high, which leads to hypoglycemia. +2  

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The ustoiqne says eyth 'ntod rpoedssn ot asdictan HTEN kssa hwcih uoy ot iftieydn hhciw gdur si eth stmo ftfeeevic at uepssrngisp adic dnp,ocurtoi NOT waht the otms eevftiecf indatca .is ehT enwasr si PsP'.I

I iwll ,sya erhew,ov I swa iklogon orf eomntgihs ekil eortdiot.ce

drdoom  lucid. nice catch. +1  
maddy1994  WHY not blockage of h2 receptors +3  
krewfoo99  @maddy1994. PPI are more effective than H2 blockers in suppression of gastric acid +1  

submitted by aladar50(40),
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I’m ont het bets at hte naalluotcics of EFC/F,IC tub bcyillasa uyo aer nigsnuif a tnyoehpcri toliusno ntio teh aln.ami Ilya,nilit htsi is lla gingo ot go itno eth xeacutrleallr ,capes as ayn VI sfoiunin illw o.d nSeci it si ihregh nhat sionitoc tsion,olu teawr si ggnoi to go ormf teh eircltullanra paecs ot hte lcuatalerlxer espac ot try ot leabnac ti to,u os eht ientacrlrlalu pesac wlil ehva dedeercas melvou dna eneiscdra olmtoayils (cnsie nlyo trwae si e,alving mkgnia it emor ne)dc.taceotrn

oS oyu wonk orf esru CFI ulmvoe si ardeecdse adn yisallomot inceresda, adn teh leearltacurxl lomveu iwll eb er.snceadi I tikhn the tyaoolisml of eth lexarlretucal ecaps si the rikytc atpr and teh artp herwe beaym osnemeo esle anc plhe hwit eth ccslnolauiat but laalcbiys tsi’ ityrpehonc egnohu atth teh olomisyalt will illst eb icnes.dare

btl_nyc  Since hypertonic solution was added, osmolality has to go up. The degree of the hypertonicity doesn't really matter. The fluid flowing out of the ICF will increase ICF osmolality. Since water follows salt, the water's gonna flow only until the ECF and ICF have the same tonicity. So if the ICF osmolality went up, the ECF osmolality also had to go up, because they both need to be equal after the water is done equilibrating. +18  
krewfoo99  ECF fluid is hypertonic because we infused an hypertonic solution. ECF volume is going to go up because A) we added more volume via injection B) Sodium attracts water, and since hypertonic solution was given water goes from ICF to ECF ICF volume decreases because the water is going to ECF. This causes an increase in Intracellular osmolarity, since you have more solutes compared to water (Less water to dilute it) +1  

submitted by jrod77(27),
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I ikthn yhet tmigh eb dgiibecnsr ngaani.tno.. sr.ue XT2A is osnpelsbrei rof eeptaltl aggegoanr,otis ti yam be nrtgbutnioci ot ibrt,ssmoho tuhs asheimci ot het ridccaa eui.sts

sympathetikey  Agreed. I'm pissed though because PGE2 mediates pain, which is why I picked it. +33  
he.sanchez14  If im not mistaken, the question describes unstable angina. Unstable angina is due to thrombosis with incomplete occlusion. So, yes TXA2 is responsible for the thrombus that is causing the symptoms in this patient. I'm also pissed because I also went straight for the PGE2 +5  
vik  hahah, seems like all in same boat like me +  
yb_26  thromboxane A2 is also vasoconstrictor, so my thoughts were about vasospastic angina +4  
youssefa  Went for PGE2 ... shit +  
need_answers  I went for leukotriene B4, what the hell was I doing....SHIT +12  
hopsalong  I picked Leukotrine B4 thinking that the neutrophil infiltration was the source of the pain, seems wrong lol. +  
bballhandler11  Sometimes it helps me to think of it in a general, non med school textbook kind of way. When answering, I narrowed it down to PGE2 and TXA2 as well. Then I asked myself, if someone is experiencing chest pain, would I recommend Aspirin or Advil? That's helped on a few over the counter pharm questions. +7  
ususmle  same here I M PISSED PGE2 +3  
krewfoo99  Maybe PGE2 isint the answer because it mediates pain and fever during episodes of acute inflammation? Thus making TXA2 more likely. +2  
djtallahassee  ditto on the looked at it for 2 seconds and went PGE2 +1  

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In iddainto to eth rvuposie xp:enalniota

She si roni dnefiitec and licace catseff het oxailprm e.umdnodu I" eudkcF rB"ytiant = ronI, a,ltoeF 2B1 ofr o,emDdnuu Jnujmeu dna luIem

krewfoo99  Great analogy lol. But just a correction, First Aid states that Celiac Disease affects distal duodenum and proximal jejunum. But you are right, it would still cause iron deficiency anemia as it affects the duodenum. +3  
fexx  OR you could just remember 'Iron Fist Bro' (F includes folate and fat, B includes B12 and bile salts) +4