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Welcome to xxabi’s page.
Contributor score: 224


Comments ...

 +33  (nbme24#43)
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Stnet obssrhitmo sv n-etesois.sr tSnte omoihtssrb is an uatec ncsulocio fo a coyonrar eyrrat ,ettns hwhic fnote tlreuss ni uteca ycoarron rneydsmo. Cna eb entevperd yb audl aenltteliatp apryeht ro ltueug-irdgn s.ttsen nso-itsRsee si eth aluadrg anrnwigro fo hte ntste neulm ued to omtenniail prfaoerlntoi,i gnrtusiel ni galinan o.mstpysm

sunshinesweetheart  so just to clarify - it's the "symptom-free for 3 months" that rules out thrombosis? +2
hpsbwz  It's moreso that at rest there's no changes, but during exercise there is. Like the pathophys of stable angina. +1
suckitnbme  I think it's more because of the 2-month history of PROGRESSIVE angina sx with exertion. This points to a chronic process rather than an acute event. +
alienfever  Drug-eluting stents prevent re-stenosis (rather than thrombosis) by releasing sirolimus which by blocking cell proliferation. +

 +2  (nbme24#47)
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sRBA elstru in hte wlgliofno cgaesnh: ineardesc niern, dacsrniee Agn I, sierednca ngA II, edrdceesa ndlsertaeoo dna adnchgnue yndiainrkb

famylife  ...and just to clarify, they directly inhibit the Ang II receptor (AT1) https://www.drugs.com/mmx/losartan-potassium.html +2
kpjk  I had a doubt- that wouldnt increased RAA lead to increased serum aldosterone as well. Now I understand that since the receptors are blocked- even the receptors to increase aldosterone secretion by Ang II would also get blocked... +2

 +11  (nbme24#45)
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nirCnieeta cacnelrea lslgityh tmessaereiotv GRF seueacb eceinirant si yaeomlretd rtseceed yb TPC


 +7  (nbme24#18)
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isetrAre of the tcarimesp dcro - uctrstlaei ,.a cuduts dfeernse ,.a ercacemsitr a.

roygbiv  https://i2.wp.com/obgynkey.com/wp-content/uploads/2017/06/A302767_1_En_1_Fig2_HTML.jpg?w=960 +1
roygbiv  Omg I keep adding comments instead of a post LOL +2

 +6  (nbme24#33)
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sotM oomcmn saecu fo eucta rtststoipia ni odrle nme is .E oi,Cl dna etnh mPseaodun.so

charcot_bouchard  Grandpa is monogamous. Sexual history was just to throw u off +9

 +5  (nbme24#2)
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ritgaSnt baet cskerlbo oefreb aaphl kadelbco in hotcmcrmoeoaopyh si naiictrdtdoenac. etBa osckrebl ccealn uto hte oaydtsrovlai eefctf fo hriaplpree tbea2- rrtncs,aeopdeo yelaipnltot igleand to ensdpopou harolepneartco-dpa ultioisnamt → vntiisnoorctcaso → ireenehtyvsp c.ssiri


 +7  (nbme24#23)
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NE si codrevtne ot EPI vai PMNT, wihch is dnudcie by .soitrloc

wowo  FA2019 p83 +2

 +1  (nbme20#13)
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eemrnpoN-natlo ttess rae tsniees,iv btu tno iccpsfei - P,RR RDLV


 +5  (nbme20#28)
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flewe  inghtolS .i ,(ccpoygrldee.lh  enn cghaetse→  doe)uis:ramisieti e  PcedapArdunToertsodci dAa+aT  nN +asrdsP /acdeeeeK→ aCu+2ppm otu→dafcin fyi vftio is aN+a nd rawet ihe nott e llc→ l wlcluiergsneall

endochondral1  can someone explain how to cross out the other choices> +1
endochondral1  what is hydropic degneration and where do i learn about it? why is it not the loss of plasma membrane integrity? +1
shaeking  Endochondral1, I had the same question. I tried figuring it out and this is what I came up with. The CHF and congestion of the lungs is reducing the amount of oxygen getting to the renal cells. With hypoxia there is decreased aerobic resp in mitochondria with decreased ATP. Without ATPase Na builds up and water follows. As far as the loss of membrane integrity. I think it would cause cellular destruction not just hydropic changes. This is my best guess. +2
charcot_bouchard  Membrane damage is irreversible stage of cellular injury. if membrane is damaged cell is dying & it will shrink. or totally destroyed by inflammation. they are specifically asking hydropic changes ie cellular swelling. which is the 1st sign of reversible cell injury due to failure of Na/K pump +1
winelover777  @endochondral1 Chapter 1 of Pathoma. Also FA 2019 p207 describes hydropic degeneration without saying those exact words in the first bullet under reversible cell injury. +1

 +7  (nbme20#45)
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Tieanlmr mpneCetlmo C9-5(C) sncDcefieiei encrseai yuesitsbtilipc ot nretuercr iNsraseei taarbmicee. ttesnaPi stom tfeon eprsten tiwh renterrcu mnsiintg.ei

lilyo  FA 2019 P. 107 Early and Terminal complement deficiencies. +1

 +0  (nbme20#5)
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aBcosr’ sipaaha: ixesevspre (tromo aahp)ias thiw tmamsaaimgr (pst ewara that yhte odt’n akem ee)sns - aera WrAenes c’ki aisapah: petricvee snr(yso)e ahaapsi hiwt adpmreii nopneomhrseci pt(s clka n)ihgtis

breis  Why would B be incorrect? I realize Broca is "technically lower" but A seems too low to be causing weakness of the lower 2/3 of the face? Am I missing something? +
shaeking  @breis B is incorrect because of the lower 2/3 of the face weakness. B isn't located on the motor cortex but in the premotor cortex, plus it isn't low enough for the lower two thirds of the face. https://thebrain.mcgill.ca/flash/a/a_06/a_06_cr/a_06_cr_mou/a_06_cr_mou.html https://www.sciencenews.org/blog/science-ticker/homunculus-reimagined +1
cienfuegos  @breis, per UW: "a/w r. hemiparesis (face & UE) bc close to primary motor cortex" +
almondbreeze  B is close to premotor cortex which is involved in learned or patterned skills & in planning movements. (i.e. two-hand coordination) slide 25/37 :https://www.slideserve.com/hal/the-motor-system-and-its-disorders +
almondbreeze  B is also close to frontal eye field; eyes look toward the lesion FA pg. 499 +
frijoles  I incorrectly picked C. When answering this, Broca's "broken speech" was my first thought, but I figured a lesion causing a facial droop would have to involve the motor strip so I prioritized that and chalked up the speech issue to dysarthria (I understand this is more of a "slurred speech" than broken, abrupt speech, but again, I simply misprioritized concepts.). So for the record, Broca area is part of the motor cortex? +1

 +2  (nbme20#24)
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icBcley arlehadnb jniury anlatiildtory esdamag rlaun reenv @ the okoh fo teh hamtae ebon


 +7  (nbme20#3)
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snStati aeseercd otslherocel yisnss,teh hwchi ienilrctyd tSstnia yctirnidel aceus ncresdiae LDL rceopter neepsioxrs no ptoecsayteh eearics(ns LLD crealncae ormf ocn.cial)trui

fatboyslim  SketchyPharm's "Statins" video explains this concept nicely and other lipid-lowering drugs +

 +11  (nbme20#8)
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I was enrdu the sospinmier ttha iths wsa an atrcio nti,icessod ued to s"ervee csteh pnia" as ewll sa het efsal elunm in eht t.aaro And HNT si eht 1# rkis aortfc orf trcaio iisdcne.sot eSoomen corcrte me fi i'm ow,nrg tbu I itkhn tshi si tairco ctdsinosei heartr htan tciaor s.nymeuar

chefcurry  I believe so, FA 2018 pg 299 +3
ergogenic22  It is dissection "extra lumen in the media of the proximal aorta" = "a longitudinal intimal (tunica intima) tear with dissection of blood through the media of the aortic wall" ... answer is still hypertension +1
breis  FA 2019: 301 +
pg32  First Aid says that aortic dissection causes widening of the mediastinum and is due to an intimal tear, so I thought it wasn't an aortic dissection. Can anyone help me understand why First Aid was wrong in this case? Thanks! +3
nephroguy  @pg32 The question stems states that there is no widening of the Aorta, not the mediastinum. Widening of the mediastinum is seen in dissection while widening of the aorta is seen in aneurysm. Also the intimal tear creates a false lumen between the intima and media. Hope that helps! +9

 +10  (nbme20#47)
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Teh irnutoda of natioc of lnSiyluicohncec si deeeindtmr by sti tlaibsmome by alasmp entesel.coshrai oS if trhee si armlboan mpaals raohsteecnisle ocl)id(snpr=aue,ehetsseo ti wlil adle to eyledad bsimleatom of incylhnuciloces as lelw as c,rviuiamm n,rieho and .coicena


 +6  (nbme20#13)
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cogncoerhBni oracaimcn = ugnl nacrec

ahtT egnib id,as ugln aaoadcocnnrmei ailsiyfceclp si sasodticae wiht itpphrhroecy ,yrtoraahsptoteoh chwhi is a iancosealrpatp nemoydsr zacdeetarcihr yb adligti nblgubc,i ahrtalirg,a njoti nsefofusi, nda osspseoitri of lurbatu ebnso

luke.10  why not systemic scleroderma since i did this question wrong and i chose systemic sclerosis scleroderma , can someone explain that ? +1
kernicterusthefrog  My best guess answer to that @luke.10 is that: a) there's no mention of any skin involvement (which there would be in order to be scleroderma) b) Scleroderma shows pitting in the nails, not clubbing c) There would be collagen deposition with fibrosis, not hypertrophy of the bone at joints Saying that, I also got this wrong! (but put RA...) so I'm not claiming to "get this" Hope my thought process helps, though! +5
yotsubato  This is in FA 2019 page 229 +8
larascon  I agree with @kernicterusthefrog on this one, Bronchogenic carcinoma = lung cancer. Squamous cell carcinoma gives you hypercalcemia (new bone formation; maybe?), commonly found in SMOKERS ... +3
waterloo  the clubbing is the symptom that takes out alot of the answer choices. It's super tricky. +
jawnmeechell  Plus the patient has an 84 pack-year smoking history, super high risk for lung cancer +
veryhungrycaterpillar  FA 2019 pg 229 is all paraneoplastic syndromes. There is no mention of bronchogenic carcinoma in any of them. There is adenocarcinoma, but that is most likely in non smokers, not in someone with 84 pack year of smoking history. Why does he have 5 upvotes for referencing first aid here, what am I missing? +2
jakeisawake  @veryhungrycaterpillar sounds like bronchogenic carcinoma is a general term for lung cancer. You are right that if a non-smoker gets lung cancer it is most likely adenocarcinoma as non-smokers rarely get small cell. However, smokers can get adenocarcinomas as well. The oncologist that I shadow sees this frequently. Adenocarcinoma of the lung causes hypertrophic osteoarthropathy per 229 in FA2019 +1
mangotango  @verhungrycaterpillar @jakeisawake Adenocarcinoma is the most common tumor in nonsmokers and in female smokers (like this patient), so adenocarcinoma would still be the most likely cancer for this pt over the others. Pathoma Pg. 96. +2
fatboyslim  Apparently bronchogenic carcinoma is basically an umbrella term for lung cancer. Source: https://radiopaedia.org/articles/lung-cancer-3 +

 +21  (nbme20#46)
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sloA fro eotsh fo uoy hwo ear yolaltt sllcusee kiel m,e uyrianr tctra oituorntbcs = ubcovrtiste ra.tpoyuh


 +2  (nbme20#33)
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Blie altss phle vseidosl lltgsaneos htat ehav dermof in the elradl,bglda used ni stinaept tyrcaoerfr to syreurg ro rpefre to ivoda i.t

xxabi  To add, bile salts are amphipathic which allows for the emulsification and solubilization of lipids in an aqueous environmen +3
md_caffeiner  To add more for people like me who dont even know what amphipathic means:, am·phi·path·ic /ˌamfəˈpaTHik/ (of a molecule, especially a protein) having both hydrophilic and hydrophobic parts +4

 +0  (nbme20#31)
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cnaiV dan ntpla aalldskio bnid bu,uiln-Bt whcih hntsiibi het oiafrtmon ro aiybmslssed ro ,bctluersomiu lvree.eipctsy

md_caffeiner  Vinca is a plant alkaloid and it has vinblastin, vincristine, which bind β-tubulin and inhibit its polymerization into microtubules Paclitaxel hyperstabilizes and prevents breakdown, its not a Vinca alkaloid. (FA+Wikipedia) +
md_caffeiner  What I mean is they are both derived from plants. +

 +7  (nbme20#7)
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iThs is a soslgolhyart dtuc syct. eTh slatyogrsol cudt yma erssitp nad elrstu ni a ystslohorgla cutd scty rc(cguoirn in delmiin nrea ihydo obne or ta eth esab of hte t)gno,ue suht lilw clsayilscla oevm up thiw islnwolawg or togeun rntusirpo.o

eTh feroman muecc of( teh tenu)og is teh nlaomr mrtnane of teh lrthoyossgal utdc

lilyo  I got it wrong though because the question clearly asks what does this structure (thyroglossal duct) DEVELOP from, not this structure eventually develops to form which structure. If it asked that then I would have picked option A but because it didnt that was the first option I crossed out. +14
misterdoctor69  It was a poorly worded question no doubt. But when they say "endoderm of foramen cecum" they're referring to the endoderm which is a primitive structure. The "foramen cecum" part is just a modifier that is added to describe what that endoderm would eventually become. +

 +2  (nbme20#47)
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5E-PD itibnrihso e..(g de,lslaiinf fadatlail) era aeddintci rof ED by yaw of giirsnacne dbloo wofl in het crsoup voracumsne (abeelld )D fo the pseni

dulxy071  I believe technically the answer would not be (B) as the corpus cavernosum isn't ACTED ON by PDE inhibitors ( per the words used in the question ) but rather simply fills as a result of PDE inhibitors acting on the internal pudis artery among many others to allow more blood flow into the corpus cavernosum for an erection +4

 -7  (nbme20#43)
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I ntkih tsi ttha eht CI ncaieotnd het bnemru "0" hichw aemsk it alyiltasistct fniaictnsgiin

kernicterusthefrog  You're thinking about CI for a **mean difference** b/w 2 variables. This question talks about **relative risk**, for which 'strugglebus' correctly asserts that *a CI including 1 fails to reject the null hypothesis*. #funwithformatting +
xxabi  Ahhhh you're right, I definitely had them mixed up! Thanks! +1
xxabi  #biostatsisthebaneofmyexistence +3
conradfussurefake  So am I the only one giving no shit about CI and going straight to what they're asking about. My understanding of the question is that they're asking about the difference in cosmetic results of both the procedure which are described in the stem as the same. The study isn't about wound infection rate!! +
fatboyslim  @conradfussurefake In the beginning of the Q stem it states "A randomized clinical trial is conducted to compare WOUND HEALING and cosmetic differences...", hence wound infection will affect wound healing. But the because the CI contained the value of 1, it is insignificant. +

 +4  (nbme20#33)
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eLda teim asib is sdeuac by lyare ittdcneoe iegbn fdescnuo iwth cinadeesr i.vlusvra lyare tntiedoec asmek it seme as ogthuh ravslviu ahs ieard,ecsn btu hte lrtnaua ristoyh of hte ssideae sha tno ebne .acidmept





Subcomments ...

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Cna neesomo eslaep ilayfrc teh raenws. Is deraseecd ncaeehred aems as eradecesd go?itganegar oduWnt;l tiinohnbii fo eht bI/IIIaI tecoprre neterpv ?agtegrgnaoi

xxabi  I'm not completely sure...but I think its because its aspirin, and aspirin doesn't work on IIb/IIIa receptors. That's why i picked decreased adherence of platelets, figured that was the closest thing to decreased aggregation that still made sense with aspirin's mechanism of action. Hope that helps! +1  
ihavenolife  Aspirin irreversibly inhibits COX which leads to decreased TXA2. TXA2 normally is a vasoconstrictor and induces platelet aggregation, so aspirin inhibits platelet aggregation by downplaying TXA2 not by interacting with IIb/IIIa receptor. (Source FA and UWorld) +17  
fallenistand  In this case, inhibition of COX-1 by aspirin will also reduce the amount of precursors for vascular prostacyclin synthesis, provided, for example, from adhering platelets https://www.ncbi.nlm.nih.gov/pubmed/9263351 +1  
niboonsh  inhibition of IIb/IIIa receptor is the moa of a completely separate class of drugs - Glycoprotein IIb/IIIa (abciximab, eptifabide, tirofiban) +  
t123  Bad question - TXA2 upregulates GpIIb/IIIa on platelets. So aspirin inhibits their expression. +1  


submitted by radshopeful(16),
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isTh tneaitp has ondmepetsadce flet aerht eilaf.ru seeptanmoDcino csorcu bcuseae fo hte rehtsa iiinlbtya ot peke pu whit anemdd any .gnoelr Thsi asled ot a deaceers in VS lnmiya ubseaec of a rtalciteonc isseu ihhwc dlsae to a readscee ni OC C(O = VS x .R)H ty,Lsla eth VVLED lwil be eddercaes uscabee het SV si reddascee vgeinal orme dbloo in het ltfe ticleenrv tefar telysso nseci ti atnnoc eb pdpmeu rdwf.aro oHep tshi eh!!lps

xxabi  Great explanation - I think you have a minor typo, LVEDV will be increased* bc SV is decreased +15  
smoothie  More blood left in the ventricle after systole is LVESV. I thought LVEDV increases because more blood remains after systole and on top of that blood from left atria from diastole is now also added. +5  


submitted by xxabi(224),
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I ikhtn tis atth teh CI eidtnonca eht rbnemu 0"" hihcw kesma it lastatcislity anntniigsfiic

kernicterusthefrog  You're thinking about CI for a **mean difference** b/w 2 variables. This question talks about **relative risk**, for which 'strugglebus' correctly asserts that *a CI including 1 fails to reject the null hypothesis*. #funwithformatting +  
xxabi  Ahhhh you're right, I definitely had them mixed up! Thanks! +1  
xxabi  #biostatsisthebaneofmyexistence +3  
conradfussurefake  So am I the only one giving no shit about CI and going straight to what they're asking about. My understanding of the question is that they're asking about the difference in cosmetic results of both the procedure which are described in the stem as the same. The study isn't about wound infection rate!! +  
fatboyslim  @conradfussurefake In the beginning of the Q stem it states "A randomized clinical trial is conducted to compare WOUND HEALING and cosmetic differences...", hence wound infection will affect wound healing. But the because the CI contained the value of 1, it is insignificant. +  


submitted by xxabi(224),
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I htink tis hatt eht CI dctinaeno eht burnem 0"" hwich eksma it lttcatiiylssa igifnainnscit

kernicterusthefrog  You're thinking about CI for a **mean difference** b/w 2 variables. This question talks about **relative risk**, for which 'strugglebus' correctly asserts that *a CI including 1 fails to reject the null hypothesis*. #funwithformatting +  
xxabi  Ahhhh you're right, I definitely had them mixed up! Thanks! +1  
xxabi  #biostatsisthebaneofmyexistence +3  
conradfussurefake  So am I the only one giving no shit about CI and going straight to what they're asking about. My understanding of the question is that they're asking about the difference in cosmetic results of both the procedure which are described in the stem as the same. The study isn't about wound infection rate!! +  
fatboyslim  @conradfussurefake In the beginning of the Q stem it states "A randomized clinical trial is conducted to compare WOUND HEALING and cosmetic differences...", hence wound infection will affect wound healing. But the because the CI contained the value of 1, it is insignificant. +  


submitted by ameanolacid(20),
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roAhoslicssteer si teh OTSM monomc uasce of relna trarey owiss..tetn.hsi buoscamurfirl aiylpdass ngeib teh DNCESO toms oomncm saeuc v(nee thhuog ti is enmpgitt ot hscoeo hist iotpno dosngericni eth taenip'st ir).cpedhoagm

xxabi  Is there a situation where you would pick fibromuscular dysplasia over atherosclerosis if given both options? Thanks for your help! +5  
baconpies  Atherosclerosis affects PROXIMAL 1/3 of renal artery Fibromuscular dysplasia affects DISTAL 2/3 of renal artery +36  
gonyyong  Why is there ↓ size in both kidneys? This threw me off +2  
kateinwonderland  @gonyyong : Maybe because narrowed renal a. d/t atherosclerosis led to renal hypoperfusion and decrease in size? +1  
drdre  Fibromuscular dysplasia occurs in young females according to Sattar Pg 67, 2018. +6  
davidw  Normally you will see Fibromuscular dysplasia in a young female 18-35 with high or resistant hypertension. She is older has a history type II DM predispose you to vascular disease and normal to moderate elevation in BP +5  
suckitnbme  @gonyyong there's bilateral renal artery stenosis. The decrease in size of both kidneys should be from atrophy due to lack of renal blood flow. +2  
tyrionwill  1 year ago, she did not present any physical or Lab abnormalities. This means she must not suffer fibromuscular dysplasia, otherwise she must have presented renal abnormalities for a long long time, or even before DM-2. +1  


submitted by lsmarshall(348),
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"eTh ecxta hmsnaimce fro mertor utnocdini yb nrei)ce(-dgβra2 sanotgis si litls u,nnkwon ubt tehre is msoe videcnee that ci(regeβ-d)a2rn atgoissn act elcytrid on .s.muel.c eoMr ent,yrelc ermtro ash eenb lteocaerrd lsyleco htiw m"alhkapoi.aye - HIN atbuilnipoc

tFrsi Aid oestmnni midspieyrohhryt ncgaius rmtore frmo diegrβaecn-r ntamituis.ol It lsao enmniots βsg2so-iatn niacsug mretro sa a deis eetcf.f sFitr dAi salo motnsien ia2ns-osβtg rviignd sipmotaus iotn cl,sle hihwc mya eonrutctib to mror.te atTh ,sdai moer icsaslc mmpotsys of pamkaiehloy are iedw QSR nad akeepd T wvsea no GE,C h,rhysamriat and uesmcl eska.esnw

okLniog uaordn no the irnnteet kosol keli fi prtaehy is eoutnicdn the rromet romf a aβg-osit2sn sselorve evoeitrm.

xxabi  Sketchy mentions tremor and arrhythmia as side effects! +1  
drpatinoire  Hypokalemia is more associated with U waves, flattened T, muscle cramps/spasm, those symptoms you mentioned is more typical in hyperkalemia. (I guess you made a typo..?) +  


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oHw do ouy know he ahs na itdacanrceer inlnagiu ihrane adn otn lafec apt?oimnic

sattanki  So as far as I understand, you don’t really get a bulging, defined abdominal mass with fecal impaction. Much more likely to see this with a hernia. +6  
xxabi  Fecal impaction can be palpated in the abdomen, since it'd be accumulating in the rectum and colon, not the groin. Hope that helps! +11  
pseudorosette  a little late but they also mention that the mass had bowel sounds hence it was an incarcerated bowel! :) +5  
waterloo  question said right groin, so idk, didn't think fecal impaction would be that low. + the bowel sounds made me think there is something at the groin that can make bowel sounds? --> Hernia. +  
thisshouldbefree  think in 3D. mass in right groin. in my head thats very low down below the belt line. i thought if its fecal impaction it would be on the left groin. next they hear bowel sounds over this mass in the right; if it was impaction right there i dont think youll be hearing anything, therefore the bowel loop is over there and is not impacted and thats what they hear. +  


submitted by strugglebus(154),
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eTh CI vluae edinoacnt ,1 hihcw neams tath sti isnftacnginii

sympathetikey  Correct. Per first aid: "If the 95% CI for odds ratio or relative risk includes 1, H0 is not rejected." +1  
xxabi  Ah that makes more sense, thanks! +  
drdanielr  Since the OR or RR is a ratio, if the two interventions are equal the ratio would be 1. So, if the CI includes 1, they are "the same" or not stat sig diff +  


submitted by usmleuser007(326),
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8htw/3e.nnpb1s/.uwmlvdiibph.c/m.w50t/g:on6

eeRlfi fo elrcanbaitt niap was uoddercp in xsi mhuna natiptse yb ltatiumnosi fo deecsoelrt aeenrtnymlp neialmtpd in teh racrrvnpiuleeit dan utleupadcreiaq rgya am.tert Teh lelve fo atnotsiuilm tunficefis to ndciue pain reeilf smees tno to elart hte tauec apni h.ltrsheod cartnIsedinimi ieettreivp olinittmsau uproddce nleearcot ot boht iodip-ncoealrdtmuuts anpi fereil nda hte giaclnase inocat of ortancic tcadoien;mi sthi secrpos ulcod be rvsreeed yb bseaecitnn mofr iatntmli.uso rmutliodutpanecoSdi- ferlie fo pain asw ervedsre by naxolnoe in fvei tuo of six pttaine.s sTeeh utsrsle ugsgste htat asyfcatirost aellitnaoiv fo etrspetnis npai in hnmuas mya be ioenbtda by lccreenoti nmu.otltiisa

usmleuser007  These questions seem unfair to test because they are based on experimental data. Guess they are there to limit a perfect score. +2  
xxabi  I just read it as patients take opioids to blunt or control pain. So if the electrode does the same thing (decrease pain), then an antagonist of opioids (naloxone) would bring the pain back? Idk if that reasoning is sound but that's the logic I used, I didn't even think of it as experimental. +21  
xxabi  Also its the only one that's an opioid antagonist from the list! +2  
redvelvet  they are writing these questions in an evidence-based manner because the questions in medicine cannot be produced by a self imagination or logic. But that doesn't mean that we have to know their exact evidence like this question. we can use our own basic knowledge and adjust it with logic. so opioids have an analgesic effect in the body and naloxone can revert it. +4  
champagnesupernova3  Anything that reduces pain by brain stimulation is increasing endogenous opiods like endorphins and encephalitis. +2  
champagnesupernova3  Enkephalins* not encephalitis +  


submitted by usmleuser007(326),
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s.d6ngow/bm:.tc5nm/e./hwp8.uiwibtlvhn10/3p

Rielef fo tctibaelnra aipn swa curopded ni xis numah psinttae yb ualimtisnot fo eoetecsdrl npelymaenrt mlpeatind ni teh eeuvirptlcnrrai and dpuaeqtlecuira argy me.atrt hTe level fo usanmtoliit tiuefcnsif to eciund npia eirlef semes ton ot taelr het eatcu pnia s.hlrhotde nIsmictnediair eiveirtetp ttnusmioial docurepd acteeornl to bhot -odcsenoatudulmrptii niap lirfee adn eth iaslgeanc tnicao of ictnroca mcatei;iodn hits escpros ucdlo be eerrvdes by ecsebnaint morf mitilosanut. ituaSrpioduetodmcn-l eelfri fo npia saw vsdeerer by eolxonna ni iefv tou fo xis ate.pstni Tehse stslrue gsgsuet ttah sftcsyitaaro aovnitliael of tpetsisenr apin in nhamus yam eb tebondia by irceetcnol tuio.lnisamt

usmleuser007  These questions seem unfair to test because they are based on experimental data. Guess they are there to limit a perfect score. +2  
xxabi  I just read it as patients take opioids to blunt or control pain. So if the electrode does the same thing (decrease pain), then an antagonist of opioids (naloxone) would bring the pain back? Idk if that reasoning is sound but that's the logic I used, I didn't even think of it as experimental. +21  
xxabi  Also its the only one that's an opioid antagonist from the list! +2  
redvelvet  they are writing these questions in an evidence-based manner because the questions in medicine cannot be produced by a self imagination or logic. But that doesn't mean that we have to know their exact evidence like this question. we can use our own basic knowledge and adjust it with logic. so opioids have an analgesic effect in the body and naloxone can revert it. +4  
champagnesupernova3  Anything that reduces pain by brain stimulation is increasing endogenous opiods like endorphins and encephalitis. +2  
champagnesupernova3  Enkephalins* not encephalitis +  


submitted by strugglebus(154),
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Atou dmo esdeias aer yaluslu gtsooeuyzrhe ro( so tyeh ntaw su ot susmae)

xxabi  How do you know is autosomal dominant? +3  
scpomp  Hereditary spherocytosis +  
fshowon  Isnt the mean corpuscular hemoglobin concentration increased in spherocytosis? Thats what through me off. +5  
charcot_bouchard  yes, would be inc in prev NBME. But this is batshit nbme 20. U have to identify spherocytes without central pallor in PBF +4  
charcot_bouchard  yes, would be inc in prev NBME. But this is batshit nbme 20. U have to identify spherocytes without central pallor in PBF +  


submitted by celeste(68),
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o,meAironad a slacs III iatniacmhtyrrh ru,gd has mpuieltl ffetces no aoicramydl aitilreapnozdo and penaatlzriorio ttha eakm it an retymleex ecietfefv irntrtcihhyaam gud.r w,ovreHe aaredoniom si istcoedsaa itwh a rebnmu fo eisd tefsfce, gniclndui dhytrio icydtnusfon ht(bo -yohp dna por,yhiidtseh)yrm ihcwh is edu ot 'oaiedorsnma ihgh dnioei onttcne and sti itcrde ioctx cftefe on teh o.hrityd (tmuetca.dopo)

celeste  The "**iod**" part of am**iod**arone reminds me of it's high **iod**ine content. +7  
xxabi  I think of it as the trifecta - gotta monitor LFTs, PFTs, and Ts (thyroid) when on amiodarone! +3  
sinforslide  Also, the patient presented with Afib; this might've been caused by transient hyperthyroidism as a prelude to Hashimoto's. In this case, if you give Amio, you'd cause serious hypothyroidism! +  
fatboyslim  Always monitor LFTs (liver), TFTs (thyroid), and PFTs (pulmonary) with amiodarone +  


submitted by xxabi(224),
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eliB lssta lhep doevsisl seoglalstn that eahv mfrdeo in teh ,eladglldabr udes in ttsiaepn etarrcyofr ot egrsyur or rpefer ot iaovd it.

xxabi  To add, bile salts are amphipathic which allows for the emulsification and solubilization of lipids in an aqueous environmen +3  
md_caffeiner  To add more for people like me who dont even know what amphipathic means:, am·phi·path·ic /ˌamfəˈpaTHik/ (of a molecule, especially a protein) having both hydrophilic and hydrophobic parts +4  


submitted by hayayah(990),
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etiPtna ahs ruaylemdl rna.aciocm Mitnlnaag oarpriliftneo of ralcpofluailra "C" lscel taht crdopue cnatilcoin adn heva ehesst of lcsel in na mlyoadi rasmo.t

xxabi  Just to add - patient likely has MEN 2A or 2B with the presence of medullary thyroid cancer and pheochromocytoma +6  
sympathetikey  @xxabi Was going to say the same thing. +  
dermgirl  The patient have MEN 2B (Medullary thyroid carcinoma + Pheochromocytoma) Page 351 FA. +