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Welcome to krewfoo99’s page.
Contributor score: 87


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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cmaCuil rontCeaab si an aandtic hicwh nca leahcte nad rcasdeee nevtfiecsesfe of hteor dsrgu ushc sa tatscliceyenr nda olluqosinoneufr


 +4  (nbme24#33)
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HPV hsa hghi fitanyfi rfo ousmqsau mheipetu.li euTr lacov rodsc hvae qssuumoa mhlpieeitu, tsuh VPH estdn ot wgor htere

suckitnbme  Specifically stratified squamous epithelium I believe. +1

 +0  (nbme24#33)
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say,Bcalil cueta tapstrosi is dsucae yb agorsnims hwchi uesca TUI as.lo


 -2  (nbme24#50)
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ihTs cluod iyelsa eb sfnedouc with musuaqoS ellC maCanrico sa they rae rdisbgcnei a .sasm uBt i inkht teh eyk cffreedine si htat ehty netomni A.MTIPSLAAE fI it saw laipda,yss tnhe it uowdl vahe ebne acrc.en

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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oilcf cdia nwhe ti esnter teh yodb is in eht ofmr of mftrltohedoaertyhaltey (TFH ea.t)dtlhmye tI notsead tsi emlthy guorp ot iivnmta 2B1 ot eoebmc FHT h(te acteiv omfr wichh as a DNA sucr.e)pror eh T iamnivt 12B hiwt tsi yhtlem ogpru oges no to cibenom tihw eycnehmoiot to mrfo itn.mhinoee


 +1  (nbme24#2)
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ugLn mouevl wlil dscreeea in obiyste oahnytelitopnvi osmedrny. nEev otuhhg shit eianttp is eeb,so eh has lla het lnacciil rtefseau fo seepl napea

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 uyo eevr teg fseudnoc itwh hte maadgri me:remerb

CN 4,231,, - ibCainMNdr ,,756,8 - nosC NP 1092,,111, - uMdalle

iScne ylno neo utrretucs ni hte iadgamr si igomnc otu of eht lladume hent ti sah eb het augsv enevr

faus305  haha hey I do that +

 +2  (nbme24#17)
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yWh dulow dsdaeerce moevment tuhohrg hte brraceele qcudatau be rn?ogw htWi all teh dbilu fo lobdo ni hte SCF attcr iwtohtu aprosto,nbi nlotduw nemtmvoe salo be cddeserea ghortuh the uuatdc?qe

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 hnkti oeoqriuhcln arsisnteec town eb fpceices to avxvi nad sutel,vhao ngkmia ti the ncoirrect wen.ars iornqhCuleo ecreaitsns nca ppayl ot .P ipuFcaarlm dan P. Maalarei

yOln xvvai dna volae sauec oethnyipoz shtu kigamn ahtt eht emor ralce aesrwn


 +1  (nbme24#22)
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BEV risvu nsifontcei B cell.s sA a penrssoe teher is vacietre hotcsyliysomp fropai(oritlen of C+8D otxtcoyic T Leoysyht.p)cm In VIH, uoy liwl ehva a edseecar in HT cesll ginadel to aedercse in C8D T .elslc uhTs BEV will lareiopfrte roem eyfrel as hte ieummn pnrsseoe wdrtoas it DC8( )escll rae ub.dnlet Tish si ohw i ogt to eth .snwaer


 +3  (nbme24#3)
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RNIT - oBne wrrmao ornpesissu, aLtcci dcsiosA,i RIamnaiANTeN - itHxtyo,capiteo hreIneraatgss thioriibn )sgert(a - tMyyphoa gnsiuca( reIdansce ieerCatnin it)oearKens saPe irItbisnoh i)narv( - otdoLprpsy,yih yplraymHceei, IG corniltenae (thnki of arlonhom eef)fcs

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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Imeag owssh hnaSort uaCcluls

)1 gSrahotn Cuslcula in sdulat - seiunamM iAmmmoun hhaso)p t2eP gorhtSan lcsCualu ni inCdrleh - ieCsnty

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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hWy luowd rernfopsi eb teh owrng aners?w otdnuWl icaulcountma of xtioc oprisnte esuac teh llec ot eougrdn soitpspoa ?

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 alaclbisy wtha tish is nsiyag tath NDA liwl be mtiasdtrent to hte nyepogr not S.NRA o AND liwl cpletirea in teh G2 asehp nda tasrfren of DNA aratlemi ot ynproge ilwl ccour ni the M s.ahpe ehT RAN amy be utmdaet adn niamkg fdceeteiv tpr,cudso utb tihs lwli otn arsittnm onit eht yeg,npor thsu ont feinaftgc esespic lvursiva aedbs on NAR umntito.as

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: https://pure.mpg.de/rest/items/item_1940413/component/file_1940417/content) 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 hawt sittsuinoa iwll bHH eb fodrme 3( hpala aihcn t)eldeios?n

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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nCa oomesne ilanpex twha teh iucrpet is pesudspo ot so?hw Is it sosdpupe ot eb entdsemge urshnito?epl

titanesxvi  yes do to B12 deficiency +

 +7  (nbme23#50)
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Aotadrlfe nad htare atre aehrs na veienrs i.nsaploirthe

sA eth bulilcima dorc si m,pcrdseeos eerht si na insacree ni ciesymst acuslarv atiensescr Tkhni( of how teh reesupsr wuold iceansre if uoy wree ot pessr dnwo on a erawt h)es.o ,hsTu the leftaoadr is iaeecnsrd and treeh si a acemtonysorp deeercas ni teahr rta.e

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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ltWdoun the OHMC urmrmu be sbet earhd in eth taciro area?

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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ernEiheippn satc tloyms on Btea soerrctpe. taBe rpeecrsto ear G uepoc.dl

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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yM isnngeor:a

As you og lewbo eas ,evlel teher is an aeersnic in rtcmahosipe rpesu.rse rsIeacne ni hte respuser yam ucesa uupertr of spualrlueb sbelb daigenl to oaremxnho.tpu

Not seru fi htsi is inrelyet rcocrte .hotguh


 -1  (nbme23#23)
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Anonye know yhw ehart onsusd lwodu eb saittdn ni POCD bierta?cxoean

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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Anyoen nwok hyw rtaeh dosnus odulw be ttnisda ni ODCP etcn?obxaraie

marat  Cause lungs are overextended +5
marat  overexpanded +3

 +2  (nbme23#41)
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nI sroadb and end,oyb It is isda hatt hitdr drgeee erhat klcob si ued to clokb ni the HIS euenkrijP et.ymss oS hwy uodwl loantiab fo VA neod saeuc isht sd?eseia

lotnWud crosdniettu of patr of fetl nervcltie eb a rebtet earwsn ?

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(1389),

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(15),
  • 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.)

https://step-prep.org/tutoring/

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(1389),
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If you odt'n kown waht uDoarmilc sedo leki any omanrl nu.ham eTh uscof no htaw pirsnia eot'dns d,o almeny 'its od'ntes affcet TP item nda omst lilsp don't eeianrcs gttolcni elyplcs(eai ithw )ri.psani This is how I goilc ot hte gitrh nwae.sr

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(1389),
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mI soal ednciocvn nikolbgc IL-2 is alos a enaettrtm? WyH is hpaalFT-N eht etbtre sawner e?rhe

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: https://image.slidesharecdn.com/11-150813013011-lva1-app6892/95/11immunosuppressants-30-638.jpg?cb=1439429471 +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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hwy si hits so /i/ nokw sit iacbs btu ?.?it.lls.

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(316),
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toMoprsisol is a rtlgnoianadsp agoanl EP2G)( thta sact no hte osmhtac ot rmotpoe mcuus trteopncoi of hte otcamhs ,ilgnni ubt losa satc ni het seturu to aocreugen iocrnn,attoc hwich kesma it eluusf orf natio.rbo

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 eth rhtoe ndha , uneri imtopusas is gihh ugehno , so fi eeisurzs sr=ybyit;o&gdmholas &g=t; uyibramgnlioo t&;=g ATN g=&t; hghi aomstusip reicnxteo , hwy no?t

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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This tniapet ash silatTepyD- I TAR whchi is ilxpenead by mNarlo rmSeu nAino agp ()8 Mceoalitb scidaios wiht rhe piiovtes yiranur ninao )ga(+.p5

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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Why dluoc shit tno be lxstarucavera islom?syeh In AF ti ayss caute ytmohlice ssniartfuno enatrcoi anc be edu ot AOB itlcpomabitniiy or xsarlevaartcu mlssyh.ioe

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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hwo ddi uyo wnko ti swa a rsrbrytawe hammaoinge nad not a orpt newi tsn?Iia uotthgh I had iths neo 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) https://www.aafp.org/afp/1998/0215/p765.html +  
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(72),
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aWht angtaeure od we ahev ttha eht eooatrmm is nggoi to stop mkniosg ni eht ptteranma by n"sia"kg hmi ot od ?.o.s

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(1389),
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A- yrrmaip omtro cxteor = rwngo iesd of doyb diti(efc fo MUN no flet idse obdy)

B - maTulahs = oessnry ioamoftrinn iotnudc - ormot tfeciisd klluiyne to ginrteaoi mfro ereh

C - Pnso - CNs 86,,5,,7 yikell rlutes ni dkleo"c in nomesd"yr or tmceleop olss fo motro ncufotin on tghri eids + ilacaf sa.ureetf

D. isemVr - ntrcael boyd taooidonic.nr agamDe rslteus ni aixaat

toN elptmoec btu abmey ehlu..lpf

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(316),
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ttieCmoivep bshniriiot sceinrea hte mK of eht tutersas.b ehT Km eentsrrpse woh yseali a sbtratues nac bdni hte icetav i,tes twih a weolr mK rieerengntps ysea bg,idinn nda a hgeirh Km enaginm more ftfdiucl.i fI you add a eottivpmcei onrbtiii,h iekl laohnet in ihst s,eac ti mksae ti remo ctlififud rof teh tamehlno ot bidn het aeitvc ie,ts bcueeas ti stum optmcee hwti eht nt.ehaol

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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out fo tiicuyrso, yhw are TAS nda LTA hi?gh si hatt sgnayi teh TINR sued was ennsiaoiedd hihwc del ot aicsinetarpt a?ols

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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heT asiesde heer si costfuer paitsbshaeshop niifee.ccdy In ,it IV rclolegy or trofusec dnoet’s hple ubaesec tobh neert eht igslgnesoocunee pwayhat blewo otescufr pbiasoah.hpset seatoGacl no the hreot hand etenrs bovae .ti I ’tnod ntkih you aeyllr deen ot wkon siht to sheoco teh retrcoc ewsnra cnesi the caiilnlc purctei fo nfagtis ioyemagyhclp atht is derccoetr /w smeo srot of ruags hatt nca enert eth golessecunngieo aytahpw hluods lcue oyu nito het rtgih .aenswr

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(316),
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hTsi anwom has rmalyxsoPa caltornNu lbmoHeoan.gruii Tihs tosm tfeno erpnests ni a onugy tdalu who hsa spieosed of dakr urnei ni the eddilm fo hte gnhti or wenh kingwa pu in the rnmnog.i It's cdaues by lmnpotecem cyitavit ertlicyd isagatn eth p'tanseti wno BRsC. terinCa idllogcsyip era eeendd on eth BCR ucasfre to teerpnv ataktc ofmr tenm,empcol hte omts lebnato fo ihcwh rae C55D and CD9.5 ansiePtt hwti PHN evah a iomatsc otuintma ni ihchw hyet olst cuofintn fo a APIG eeynmz edeend orf rorepp aeensrttonip dna nemtathatc fo D5C/D559C on teh RBC ceuasfr. eereTfrho the wnesra si a ctefde in a lelc mabmerne ahrnco r.teipon Wuothti ,hsit pmmelnecot ttcaska sRC.B

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_(98),
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etiutlrtaAbb skir = cinnedeic in exspoed – ceinincde ni nsdopexue

= 3/0,0001 kesrmso)( - 00,033/0 noso)rnmk(se
= 00.3 - 001.
= 002. (so hte aaubtretblti srki si oubta 2)%

piylnpgA ti ot a plpntoaiuo fo :001,00

= 02.0 * 10000,
= 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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aCbmlooo si an eey lnrtioaamby thta osrcuc bfeeor .hbitr e'rhTey gsmiisn ipcsee fo uietss ni stcsuuretr atth mfor hte .eye

  • Cmlbosooa fgciftane teh rsii, iwhch letrsu in a eholk"ye" arpeaenapc of hte ppiu,l lgeenalyr do nto eald ot iosvni sos.l

  • loomosCab lvonvnigi teh ateirn lesrtu ni sviion loss ni siiepfcc tpasr of het aluisv df.lei

  • eraLg eilartn obmslocao or oseht geffticna teh optci neevr acn aceus lwo snii,ov cwhih nasem vsoiin sols hatt nnotac be tpelmcloye cdrtercoe hiwt slasegs or otccatn .elessn

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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Btu deonts' tcsaueub oimndcbe eenatiogdner dela to ieipmmarnt ni DMLC, nsrcierlpaoleeb adn irnopotcsaicl tcar?t I get eth xtaiac gati - bMoCr./enLrslDclieeap uBt eht snitaenos to n,picpikr otlnuw'd taht be the smichntlaaoip ta?ctr thaT is ont llusauy fdaeceft in tacusbeu ibmcndoe neeigrnae.tdo

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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But o'dsnet btcusaue dmbnicoe edeairtnoneg dael to nirapmmeti in C,LDM rorenalpsbelice nda srconplcotiia rat?ct I tge het aixtca agti - irleensLco/elra.pCbMD But eth sensnitoa ot ikipcrpn, w'lnutdo that be eth paicamtnishlo ct?rta taTh si nto uslylau eefafctd in atebsucu nodiembc eirt.dnngaeoe

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(151),
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icdArcgon ot anolGj, chymyaoepilt vrae is oen fo hte tsom omomcn esucsa fo hrCaudiBd-i sedrnoy.m ocAgdcnri to FA, rhCBi-adiud is adsasitceo oerm gyalenler hwti labuhpeegyoclra tes,ast myyceoaitlhp aevr, paopstrmut te,tass nad C.HC

epctHia ssiicrohr nac be erdlu tou daebs no the item rsoeuc of the 'ntpsaiet toeiennastpr - eh swa ifen 2 swkee gao dna eth modbnlaia napi etardts na uroh oga.

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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The ayw I lddecexu ltdavansiioo was :itsh hte mtsaphiycte cetrpero ttah lisedta si β,2 hihcw si not mtsudelait by epinrhrnopeeni. oS ot tstuealim teh ro,tecpre the elltsate ogliagnn uwdlo evah had ot rftis utsmietla eht rendaal eudamll ot eserael ernpeipnihe ateel(tls oot ghhi ot sauttlemi eht d.lla)eum

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


submitted by welpdedelp(215),
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mcaotosohmH,eris aak brn"eoz sdtia.eb"e ntaonC eb nsddoiA edu ot eht hiempacerygyl nad rmlano PB

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(87),
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dWltonu teh OMCH rrmuum be tebs hraed ni the orcita a?are

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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it is aomnrl iaidonarirt ot hte IHGTR ken?c hatw odes ti mae?n

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


submitted by sajaqua1(516),
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aeesBuc eth sab'by tmheor has peyT 1 sabiDeet uetlmsil, it si aubeslipl atth eyht dah teldvaee blood gsocleu esvlel rgunid ro osylhrt rfoeeb b.hrit nIluins oesd tno sorcs teh aae,lcnpt utb uscelgo eods, os idrgnu irthb eht onteaen uwold ehav enbe yyhgr.meplccei sTih loduw dale ot the lotnaena panarecs slgereain inslni,u gvindri oclesug noti sllce dna irtgunn nwdo inosnco;slgeueeg iths is yhw het bayb is ymihgpleycoc rhgit wn.o

B) aeeDecdsr ynlcgoeg teiocta-nnorcn I dont' wkon teh gyeolcgn nitnrccaooetn dromecpa ot an dtalu i,tatepn but a rcseeaed ni nclgoegy netaoncrocint wdolu acneitdi coegosl/lgcynuge ese,real hcwhi dwolu otn eb a ccehigmylypo teta.s )C cseareeDd ylnggceo yashsnet taiivc-yt csreeedad enoclgyg yaetnssh yivtitac sdticeain nyreeg mloaatc,bis nad udlow elad ot hihgre rsuem uscelog elvsl.e D) cesadereD mresu sniulni rie-onntcctona esrecedad meurs lnnusii wodlu dael to hhreig vlseel fo scuoegl in .urems E) dcneasreI seumr nkilueil-ins rthogw -rfotac GIF sdoe ton bndi ylnera sa lewl to iinlnsu tpecsrore as usnnili ods,e adn os udlow veah ot be in emyltexer hghi rcnestioanntco to veha stih cfefe.t FIG is scaistdaeo itwh sticmao tgwhor nda scemul depveeo.mnlt

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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heT uiteqnso says eyht tndo' sspednor ot tnsiadca EHTN asks wichh you ot tiydeifn ihchw grud si het toms cefivetfe at nsgspisuepr cdia or,icdoutpn TON hwta eth mtso tevefcefi anitcda .is The esnrwa is IP.'Ps

I iwll s,ya ,herwevo I wsa oligkon rof hmgseonit klei .eoedoitcrt

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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m’I ton teh btes at het itanacsluocl fo C/IEFC,F ubt syaicallb you are iinfguns a otprcniyeh sonluiot ntoi het ma.lain yIll,iniat hits si lal gigon ot go ntoi eht eraralxcltleu cp,aes sa nya VI niusinfo lwli d.o Snice it si egrhih ahtn intoosci nlit,souo aretw si goign ot go orfm hte lriencllatrua spaec ot hte tlaerlurcxale aepcs to yrt to bnacael ti uot, os het rlaltcaenriul pacse lilw heva cesredead vmuloe and dainceers tiylolmsoa n(csei ylno rewat si glvne,ia gnmiak ti emor ncta).dcenerot

So yuo wnko fro seur FCI mulevo is raddcesee dna otoamsylil eac,dsrien dan het uclletrxaeral elmuvo lilw eb a.inrecdse I ikhnt teh omalitoyls of the raxlrealtlcue sacep si hte tyickr tpra adn eht ptar hwree abyme seeomon lese nca pehl with hte clsactiaonlu tbu lbasciayl si’t htyincopre onguhe that the matslioyol liwl tlisl eb aindesce.r

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 kinth yeht mhtig be nisrbdiecg a..ntn.ngioa sru.e AT2X is sresipbolen orf pleaettl aeorsgotagig,n ti aym be gibonuncrtti ot shomb,srito shut ecmhisai to the caarcdi ute.iss

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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nI daiiontd ot het rsieouvp pnnteaoil:ax

eSh is rino eifdeictn dan leicac tefscfa the milxraop ddueou.nm I" euckFd Bttarin"y = rnoI, tFloa,e 12B rof ,dmnuuoDe ejuumJn dna uIlme

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