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Welcome to titanesxvi’s page.
Contributor score: 81


Comments ...

 +10  (nbme24#22)
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  • drotcudA slemscu dna cgisrlia aer aernintevd yb teh tartrooub envre
  • xrlEeant buolieq is devntarien by eth ooyigcaispithrl enver
  • boottrrua sntrneiu is renvndtiae by het ototrruab niutnsre erven S2–5)(L
  • rmiifsiroP si nrvtadeeni yb eht aiiscct rvene -L)S(35

 +3  (nbme24#20)
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hTees otoscermel lscel ideettafirfne ntoi hcdlanorotbss atth romf hte isacrltagoiun sprocusrre fo the aailx neotkels nda snoeb of het caanril baes fmo(r teentr ermboi)


 +0  (nbme23#28)
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Heer si a ogdo crroeuse

sIkegpl_sn:s/sod_ewom.do/nnbwp_wnsoiwamlccoepo/detsc/rurh/mttsye.lam


 +0  (nbme23#28)
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ywh tno radecsee AC yitcivat ni the mriolaxp ubu?lte sith saol oclud aedl ot botaimlec oiasid.sc

ergogenic22  carbonic anhydrase inhibitors can cause Type 2 RTA but it is not the cause here (cystinosis) +
doublethinker  Yeah, I said CA too. Problem is that CA deficiency wouldn't lead to lack of reabsorption of all the ions listed. +

 +2  (nbme22#4)
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heT rheto nsewasr ear owngr a:cebsue fi( I am wrgno eelpsa ocrectr me)

)A hisT uodwl eb treu ni a npiaett hwti ilerv or rcheoitnp rmneysdo

)C Tsih doulw be trcoecr fi hte ew cesreain lalrycpia aryibplteeim meaxpe(l spi)sse

D) iThs si eltf ather eraufil

E) iTsh dculo eb RDSA ton( rues )otghhu

)F alncynMagi


 +4  (nbme22#6)
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ohep itsh gamie phel to aennsurtdd i,t eht pspmu odt'n work beuesca ckla of TAP





Subcomments ...

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Juts ecbsuea ’hes anihvg nrtuctpo(d)ee esx deno’ts name he sdon’et vhea ipmesl ecuiofnsti omcnnuile.soso ehT xes eipimsl ’she loas sgiskin omeoe!sn nitrgahPsiy + lhpmy soned + augitfe = .moon

titanesxvi  The triad of classic symptoms for infectious mononucleosis is lymphadenopathy (swollen glands), splenomegaly (large spleen), and exudative pharyngitis accompanied by high fever, malaise, and often hepatosplenomegaly (large liver and spleen) +2  


submitted by fahmed14(29),
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neamisHti lapys a rmoja oler in eth ilncdraa gnsis fo t.onimfmalani It pehls mtideae lniivsotadoa dna lucvrasa mlaibterieyp via( oeihdnltale llec nt.no)cracoit sheTe two fuontiscn rae eldaayr rtnyocar ot A, ,B ,C adn D. By rinsnegcia lufdi in eht artliiseintt epcs,a ouy nca oeanrs htta teher lliw eb arineceds yhlpm .folw

youssefa  If more transudates are leaking into the interstitium wont this dilute the interstitial proteins and cause a decrease in oncotic pressure and increase in interstitial hydrostatic pressure? +12  
titanesxvi  @youssefa I think because it is an exudate from increased permeability of venules, the oncotic pressure in the interstitium is not going to decrease +6  
thotcandy  @youssefa transudate is like pulmonary edema due to CHF, no proteins, just fluid congestion and leaking out. That would decrease interstitial oncotic pressure because it has very little protein. Exudate due to inflammation/histamine has a high amount of protein (due to inc permeability) so the IOP doesn't change. +6  


submitted by vshummy(161),
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oS eth bste i ulcdo fidn wsa ni tsiFr dAi 9201 pg 634 undre tiDibace dias.oetcoKis hTe yarhgecilepym nda lkmayairheep ausce an cioomts usdirsie os eht nriete oybd gets ltpedeed of si.fdlu Hnece wyh prta fo het etermatnt for KAD is IV isd.flu ouY igthm enev reyl no atth ecipe fo ninriaotomf laone to nwsera shit ,inoesutq ttah DAK is tereadt ihtw VI d.lifsu

fulminant_life  I just dont understand how that is the cause of his altered state of consciousness. Why wouldnt altered affinity of oxygen from HbA1c be correct? A1C has a higher affinity for oxygen so wouldnt that be a better reason for him being unconscious? +6  
toupvote  HbA1c is more of a chronic process. It is a snapshot of three months. Also, people can have elevated A1c without much impact on their mental status. Other organs are affected sooner and to a greater degree than the brain. DKA is an acute issue. +6  
snafull  Can somebody please explain why 'Inability of neurons to perform glycolysis' is wrong? +3  
johnson  Probably because they're sustained on ketones. +3  
doodimoodi  @snafull glucose is very high in the blood, why would neurons not be able to use it? +2  
soph  @snafull maybe u are confusing bc DK tissues are unable to use the high glucose as it is unable to enter cells but I dont think thats the case in the neurons? +1  
drmomo  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909073/ states its primarily due to acidosis along wth hyperosmolarity. so most relevant answer here would be dehydration +1  
drmohandes  I thought the high amount of glucose in the blood (osmotic pressure), sucks out the water from the cells. But you also pee out all that glucose and water goes with it. That's why you have to drink and pee a lot.. +7  
titanesxvi  Neurons are not dependent on insulin, so they are not affected by utilization of glucose (only GLUT4 receptors in the muscle and adipose tissue are insulin dependent) +25  
drpatinoire  @titanesxvi You really enlightened me! +  
mutteringly  I don't make the connection of what titanesxvi said to the question - can someone explain? +  
motherhen  @mutteringly it explains why the answer choice "inability of neurons to perform glycolysis" is wrong +1  


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Wyh si ti htat eht oupayrmnl aylcipalr gedwe srsspeueere si dsernec?ia no p.g 730 of AF 1209 it sysa ti nca eb iradceesn or readeescd /:

giggidy  Depends on where the infarct is I guess? Crackles in lung base means increased left sided pressure and therefore PCWP. At least that's how I thought of it. +9  
titanesxvi  Because think the circulation as a closed circuit, in this case the heart isn't pumping well and the pressure is going to backup. that is why the PCWP is increased +4  
mw126  It depends if the patient goes into heart failure because of the infarct or whatever the insult is. The crackles in the lungs gave it away. If crackles are present then there is blood backing up. the increased pressure in the pulmonary vasculature causes leaking into the alveoli which we hear as crackles when the lung expands. +  


submitted by krewfoo99(93),
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aCn emnsoeo ieanpxl hatw teh peucirt is osesudpp ot wsh?o sI ti sspdeuop ot be mstnedeeg n?pulerohtsi

titanesxvi  yes do to B12 deficiency +  


submitted by wired-in(67),
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acnnMtaniee deso uralmof is ssC( × lC × ut)a ÷ F

erweh ssC is aeatsdeyt-ts agtetr aalsmp cnc.o fo ug,dr lC is nr,elcacea tua si sgodea teinalrv ;pm&a F si bai.olablivyiita

tNieerh easogd vinrlate onr yobtlaiaaiilibv si vne,ig os ggrnoini seoht p;ma& gipgnlgu in eth rmuenbs refcla(u to tecvonr iutsn to gkd/y:/ma)g

1 =2( mgL/u × 1 00m01/g u)g × 9.0(0 hLrg//k × 0001 m1/L L × 24 r1h/ y)ad
= 259.2 gk//mgady

.ichw.h. itn's ayn fo het ewnras occihse dits.le Tyeh tmus heva nuoddre 0.09 Lkrg/h/ to 1.0 ,/L/grhk dna idogn os gevis ecalxyt 8.82 /mygdagk/ icoe(hc )C

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


submitted by hello(311),
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ciwhh elttre si CN IX in hits ?dgrmaia

titanesxvi  A think is D, but it is not very clear +1  
usmlecharserssss  A WHAT anatomical structure is this ???????? +  


submitted by lfsuarez(141),
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Fsirt rhtae usnod )S(1 is gnrteaeed by owt thera sv:laev eht amitrl levva dna dsciitrup ev.lav leyNra msuoaeulitsn icnlsgo fo htsee lvesva aorlmyln ereganets a lsegin S1 ud.son iSpgltnti of eht 1S dosun si haedr henw lmtiar nda ciusditrp selvva cleos ta llhgtiys ertifnefd it,sem tiwh alluyus het mlrtai clsongi oebref tcipsruid

yotsubato  Then why the fuck is it describing a mitral valve sound in the tricuspid area +25  
dr.xx  it's describing a splitting S1 — consisting of mitral and tricuspid valve closure — that is best heard at the tricuspid (left lower sternal border) and mitral (cardiac apex) listening posts. +35  
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +4  
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +1  
drzed  It shouldn't matter where you hear a split sound. For example, no matter where you auscultate on the heart, the second heart sound in a healthy individual will always be A2 then P2 (whether you are at the mitral listening post or the aortic listening post) The key is recognizing that the right sided valves in healthy individuals will always close later (e.g. the heart sounds are S1 S2, but more specifically M1 T1 A2 P2). The reason for this is simple: if you take a breath in, you will increase preload on the right side of the heart, and thus the greater volume will cause a delayed closure of the valve. This is physiologic splitting, and is better appreciated in the pulmonary and aortic valves because they are under greater pressure, and thus louder, but it can also be heard in the first heart sound. +10  
alexxxx30  yes agreed!! This question is mostly asking if you understand a few basic things regarding cardio physio. The left side of the heart is the higher pressure side so left sided valves will close first. The right side of the heart is the lower pressure side, which means right sided valves will open first. [Left closes first, Right opens first]...Secondly, it requires you to know what S1 and S2 sounds come from. S1 is the mitral/tricuspid valve closing and S2 is the Aortic/pulmonary valves closing. So really the question asks what is the first component of S1 (mitral or tricuspid closes first). And since we know that the left side will always close first, it must be mitral valve closure. Sorry if that was a long explanation. +10  
jesusisking  Thanks @alexxxx30, you the man! RIP Kobe +  


submitted by lfsuarez(141),
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tisFr aehtr nsuod (1)S is aneeerdtg yb otw rateh v:levsa teh matril aelvv dan uistdpirc a.levv rlNaye iulsutmnoase sgiocnl fo steeh aelvvs rllnmoya eesrganet a ensgil S1 osdun. Slgptniti of eth 1S dsonu si eradh nwhe tamlir and ctruiisdp aselvv locse ta igsltylh dnfefrite tme,si ihtw asluylu teh iatlrm osigcnl ebrofe psdtuiicr

yotsubato  Then why the fuck is it describing a mitral valve sound in the tricuspid area +25  
dr.xx  it's describing a splitting S1 — consisting of mitral and tricuspid valve closure — that is best heard at the tricuspid (left lower sternal border) and mitral (cardiac apex) listening posts. +35  
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +4  
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +1  
drzed  It shouldn't matter where you hear a split sound. For example, no matter where you auscultate on the heart, the second heart sound in a healthy individual will always be A2 then P2 (whether you are at the mitral listening post or the aortic listening post) The key is recognizing that the right sided valves in healthy individuals will always close later (e.g. the heart sounds are S1 S2, but more specifically M1 T1 A2 P2). The reason for this is simple: if you take a breath in, you will increase preload on the right side of the heart, and thus the greater volume will cause a delayed closure of the valve. This is physiologic splitting, and is better appreciated in the pulmonary and aortic valves because they are under greater pressure, and thus louder, but it can also be heard in the first heart sound. +10  
alexxxx30  yes agreed!! This question is mostly asking if you understand a few basic things regarding cardio physio. The left side of the heart is the higher pressure side so left sided valves will close first. The right side of the heart is the lower pressure side, which means right sided valves will open first. [Left closes first, Right opens first]...Secondly, it requires you to know what S1 and S2 sounds come from. S1 is the mitral/tricuspid valve closing and S2 is the Aortic/pulmonary valves closing. So really the question asks what is the first component of S1 (mitral or tricuspid closes first). And since we know that the left side will always close first, it must be mitral valve closure. Sorry if that was a long explanation. +10  
jesusisking  Thanks @alexxxx30, you the man! RIP Kobe +  


submitted by keycompany(308),
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yTep I asDbteei is irhecezaadrtc sa the ttsdouceirn fo eicnpatrca essitl (pcilcaiseylf tbae )ecsll by Tl-.elsc Teh most elyikl sceua rof pyogalmcehiy oinglwfol suniiln tstainrda,mniio tfeeeor,rh si hte tnuiserdotc fo hapla llecs ahtt odurnsru eth eabt l.lces hisT wodlu sauec deceerads sellve of nicgtclarui agcou.ngl

titanesxvi  I think rather that high insulin is going to block the release of glucagon +6  
melanoma  the answer is not correct +1  
melanoma  his answer +1  
prolific_pygophilic  I actually think this has some merit. I believe there is a U world question that talks about how very long history of T1DM (20 years in this patient) can progress to destruction of alpha cells and hence impaired release of glucagon and episodes of hypoglycemia. Thats how I reasoned it. The first answer is also possible. +  


submitted by yotsubato(1019),
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3p5 si utaetmd dan anct idnb eht TTAA ob,x so hwta pnheaps ot pinasoctnitrr of nbyhrtiiio npestori?

Is ylalbcsia hwat isth qtesnoiu is tnrigy to k.a.s.

oS on ATTA oxb mtpreoro =&t;g reeedDsac gnbiidn of ARN elrpmaoeys

link981  You said it, they are "trying" to ask. Should use better grammar. +3  
titanesxvi  This is on first aid, and says that the promoter region is where RNApolymerase binds +  
nootnootpenguinn  Hakuna NO-TATA box... thank you for this explanation! +  


submitted by enbeemee(13),
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secyhtk syas taht osas'pik ahs tgnifritlian cspoeyylmht, os hyw wdoul rglea geetaggsar of aytalipc lheypmoytcs eb cotnric?re

titanesxvi  Bcz I think vascular is the key thing here, whereas atypical lynphocytes would be more of EBV +2  
d10s  the lymphocytes seen in kaposi sarcoma are not atypical. +3  


submitted by g8427(0),
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If meos one can hlep em sedunadnrt bc im a bit .eodncfsu I uddnnsrate the ttghouh osesprc adn I airelezd tath tihs swa an AR esasdie dan I olas tgo eht /14 caeffet,d 2/1 eracirr adn 1/4 ntfduf.eace tBu I shceo %0 bc I eugridf fi it aws na AR aeidsse teh 1 cihdl lryadea eseadsdi asw hozomyosgu fteecdaf 1(/4 detefc)af. ihchW dela me ot ikthn htta eht ethor tsirse aws hirtee a ciarerr ro otn etadeffc ta .lal mA I tusj rveo tgikinhn shit ro am I otn lulyf rtsgndndiaune asthw ogngi on?

rush  you have to think about each child individually, doesn't matter what the siblings have. The question states what are the odds of the child getting the disease. So regardless of the other siblings it still is Mom (1/2) dad (1/2) which makes it 1/4 AR +  
titanesxvi  But how do we know that the parents are heterozygous for the mutation +  
need_answers  we know that the parents have to be heterozygous Aa X Aa because on a 2x2 table, the only way the daughter could be homozygous for an AR is by having both parents be carriers (Aa) so the question was asking what are the chances the sister has the same alleles (aa) and there is only a 25% of having the same alleles. +  


submitted by usmleuser007(395),
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utJs ntoe hyw reoht aesrnws rea tno eorccr:t

  1. nbpEnshogy&;soip an sirdnecea saoerncne fo vecio ssuodn rahde nweh ultugnatcsia teh gulsn, nfote acdues by lgnu nnoitloaoiscd and o.iifsrsb

    • .a tI is ude ot deannche tniinosrmass of hyqu-fnrigchee onsdu oascsr ,iudlf uhsc as ni rmbnalao lgnu ,situes tiwh weolr neueeicrfsq reifdlet .tuo
  2. dhWeerspi eeopby;p&rcnrotssfilueqr to an nesicdaer lsdsnoeu ngpn&dnbrbfhioptpn;&s;wessioe udginr cutliatnaosu iwht a hopcstseeto no the nugl sdlefi no a taist’pen osr.ot

    • a. Ulyausl pseokn snsudo of eesbs;;nbppuspwvraenhimod&&l yb teh tanipte oldwu ton be arehd yb het inlcncaii sniauugltcta a ulgn fdeil wiht a t.phetsceoos

    • b. Hreeovw, ni rasea of teh lgun reewh eehtr usnpi&blgn;s dootl,niiocans sethe hwserpeid eknspo unosds by eht pnatite cshu( sa asiyng eetnniy-n’n‘)i will be alclyre daerh hgutrho teh oc.psttheeos

    • .c siTh ricneaes in nusod iexsst ceeausb snudo atvrsel aertsf nad uths iwth leowr slos fo stnienity rughhot iqilud or dsilo l“ufdi( sa”sm or i“lsdo ”am,ss vesriept,ylec ni het gn)lu svrsue egsoasu ria( in the l)ngu d.amie

    • d. eprWesidh oqpoyelctiru is a ciinlcal tste ypcyltlia ereomdfpr idnrug a aicdmle cpsalhyi anemoniixta to lueaveat orf hte ceeenrsp lg&n;unbsopf nioidlntaco,os ichwh ocldu eb edsauc yb crcnae (soidl a)sms ro upmenonai diuf(l sam.s)

titanesxvi  why not wheezing? +  
miriamp3  @titanesxvi because the dx is CHF +  
leaf_house  I get why crackles are more likely in CHF, but wouldn't it also cause whispered pectoriloquy, if fluid allows better transmission of sound? +  


submitted by marbledoc(0),
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hWy uwlod oyu ksa het tipneat to inedftyi teh osrp dan con?s I do’nt etg het ahcpraop !eerh

someduck3  There was a question about this in Uworld. for *stubborn* patients who are "not ready to quit" just yet you use the motivational approach. The technique acronym is OARS: Open ended questions, Affirmation, Reflect, Summarize. +6  
yotsubato  Additionally the guy himself says "I know smoking is bad for me" Like he knows its bad, he doesnt care, but give him nicotine replacement and maybe he'll quit... +5  
usmleuser007  I didn't think nicotine replacement was a good answer choice b/c if he isn't ready to quit then why would he agree to use alternatives. +  
usmleuser007  People who smoke and are addicted like the feel of the cigs and environmental ques. Using replacements would be more challenging. The second best answer choice would have been Rx. +  
titanesxvi  why not detail the long-therm health effects of smoking? +  
seracen  @ titanesxvi: I assume because they always like the most "open ended" response. If you start detailing the long term effects, the patient might interpret that as attempting to convince, and might resist or feel pressured. By having the patient elucidate what they consider pros and cons, you allow it to be an open discussion. +  
suckitnbme  Also because the patient states he already knows smoking hurts him in the long run so it may come off as lecturing on something he already knows. I view this as what is the least-judgmental way to facilitate the patient moving on to the next step of the stages of change model largely of their own volition. +2  
usmlehulk  i choose the option c which is initiate a pulmunary function test. why is that a wrong choice? +2  
makinallkindzofgainz  @usmlehulk - he's asymptomatic, knows it is not good for him in the long run, but is not quite ready to make a change. It is best to talk with him about the pros/cons of cessation so that maybe he will make the decision to quit smoking soon. Ordering a pulmonary function test is not going to be useful. Let's say it's decreased. Ok, so what? It doesn't change management in this patient right now. +1  
rainlad  Think of it as motivational interviewing +1  
tulsigabbard  Still don't like the answer given that the patient already stated that he knows that it can do him harm in the long run. It seems like overkill. +3  


submitted by bobson150(12),
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Teh nirdogw fo ihst tesiuoqn cusfnode e.m iTsh si ansgki cwihh" fo eseht eevlsss is the ighh seprures smsty"e gtrh?i oS eth ihgh espsreru siruoepr altecr is cnugsai nedrseaic eepurrss tnio eht riifreon c?teral

welpdedelp  Superior rectal comes from the inferior mesenteric vein which comes from the splenic vein --> portal veins Thus, this dude had cirrhosis so it would "back-up" into the superior rectal vein. FA 2018: p360 +13  
nc1992  Superior rectal not superior mesenteric. Took me a minute +  
hyperfukus  ugh am i ever gonna get these right EVER +5  
titanesxvi  why not the inferior mesenteric, since the superior rectal drains there +2  
thomasburton  @titanesxvi think it is because question says direct which is why superior rectal +2  
lilyo  thomasburton, so are they asking what vessels do internal hemorrhoids directly drain into? The order is Superior rectal vein--> Inferior mesenteric vein--> portal vein. +  
thomasburton  Yes exactly, so they do eventually reach IMV but not 'directly' +  
pg32  Also worded poorly because the varicosities are connections between the superior rectal and the middle/inferior rectal veins of the systemic circulation. So the blood could be in both the superior rectal vein and the middle/inferior rectal vein as that is what a varicosity is. +2  
snripper  You just gotta know indirect vs. direct hemorrhoids. In this case, it's an indirect hemorrhoid (superior rectal vein) because of the rectal bleeding. +  
jesusisking  @titanesxvi DrDoom explained it pretty well below: "Defining tributary: https://i.imgur.com/2zDxPbW.png Nice images make the term easier to recall. Smaller streams "pay tribute" to larger rivers (by flowing into them)" +  


submitted by sklawpirt(30),
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hayayah  pg. 47 on FA got the good visuals! +5  
notadoctor  COPII* proteins are needed to coat vesicles from the RER to Golgi. "Two(COPII) steps forward; one(COPI) step back." Anterograde goes RER -> Golgi -> Lysosomes/Secretory Vesicles -> Plasma membrane +23  
titanesxvi  why not small lysosomes? +3  
varunmehru  and I thought large lysosomes due to lack of enzymes to degrade +  
samsam3711  The size of the lysosome is not affected by the presence or absence of protein, but its function is compromised (eg. protein is getting stuck in the RER) +  
fattyacid  I hope this helps to whomever was lost like me Null mutation: A mutation (a change) in a gene that leads to its not being transcribed into RNA and/or translated into a functional protein product. For example, a null mutation in a gene that usually encodes a specific enzyme leads to the production of a nonfunctional enzyme or no enzyme at all. +2  
pingra  I think you made a typo: COPII (RER -> cis-Golgi); COPI (trans-golgi -> cis-golgi and cis-golgi -> RER), clathrin (endocytosis and trans-golgi -> lysosome) +  
kevin  So my thought process was if there is no COP signal then instead of going to Golgi it would be sent astray into cytoplasm, akin to how in I-cell Dx the enzymes get sent out of the cell since there is no trafficking signal (therefore I presumed large lysosome due to eating the aggregated protein). Are we saying without COP or Clathrin that the vesicle will simply stay put where it is? If I can get a reply before my exam (2 weeks) that'd be much appreciated +