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Welcome to vshummy’s page.
Contributor score: 163


Comments ...

 +9  (nbme24#50)
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oS eth tesb i uldoc dinf aws in rsFit Adi 2091 gp 364 ruend ieciatDb .tiasooscediK hTe lehypiagrcyme nad krmlaeeyhpia usaec an soctimo desriusi so teh eritne oydb sgte ldpdetee fo .sdiufl Heecn hwy ptra of hte tnteermta for KDA is IV udifs.l You ghmit even eyrl no htat ceipe of niroatnfmoi nelao ot anrswe hsti isunoet,q htat ADK si aetredt hwti VI .lidfus

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

 +6  (nbme24#46)
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I nkhit orem yra,gneell prienot dglinof nseaphp at the RER nda the setm yssa the oternip dt’eson dfol el.oypprr lfi,ccSiyaple the toms mmcono CF tiauonmt si a dsfieoldm trieopn and eht toierpn is iateerdn ni eht RRE nda otn dttapnsrroe to the ecll mrbmanee - AF 2109 gp 06.

uroosisyed5  Which makes sense if we think about the pathophys of elevated Cl- and Na intracellularly. Both of these ions go up inside the cells due to the retention of the misfolded proteins in the RER. +
lilyo  I actually disagree with this reasoning. The pathophysiology in CFTR is not due to accumulation of misfolded proteins. It is due to decreased/absent ATP gated transmembrane Chloride channel. According to Uworld, the miscoded protein is detected by the Endoplasmic Reticulum. The abnormal protein is targeted for destruction by the proteasome and never reaches the cell surface. There is NO retention of misfolded protein, there is degradation of misfolded protein and therefore absence of chloride channels on the membrane. This is what leads to impaired removal of salt from the sweat as well as decreased NaCl in mucus. I dont think the answer should be ER. Can anyone tell me if I am missing something here that makes the answer ER as opposed to cytoplasm? Because the way I see if is misfolded proteins go form the ER into the cytoplasm to reach the proteasome and then be destructed. Uworld questions ID are 805, 802, 1514, and 1939. +15
drdoom  @lilyo The CFTR is a transmembrane protein. Like all proteins, its translation begins in the cytosol; that said, CFTR contains an N-terminus “signal sequence”, which means as it is being translated, it (and the ribosome making it!) will be transported to the Endoplasmic Reticulum.^footnote! As it gets translated, its hydrophobic motifs will emerge, which embeds the CFTR protein within the phospholipid bilayer of the ER itself! That means the protein will never again be found “in the cytosol” because it gets threaded through the bilayer (which is, in fact, how all transmembrane proteins become transmembrane proteins at the cell surface -- they have to be made into transmembrane proteins in the ER first!). +8
drdoom  @lilyo (continued) So, yes, ultimately, these misfolded proteins will be directed toward a proteasome for degradation/recycling, but that will happen as a little vesicle (or “liposome”); the misfolded protein, in this case, is not water-soluble (since, by definition, it has hydrophobic motifs which get “threaded through” a bilayer to create the transmembrane pattern), which means you won’t find it in the cytosol. +5
drdoom  ^footnote! : The movement of active* ribosomes from the cytosol to the Endoplasmic Reticulum is why we call that area of ER “rough Endoplasmic Reticulum (rER)”; on electron microscopy, that section was bespeckled with little dots; later, we (humans) discovered that these dots were ribosomes! +1
drdoom  * By “active ribosomes”, I just mean ribosomes in the process of converting mRNA to protein! (What we call “translation” ;) +1
wrongcareer69  How many goddamn ways are they going to test us on CF. I'm so over this! +2
furqanka  also in FA, under alpha 1 antitrypsin, its says 'Misfolded gene product protein aggregates in hepatocellular ER". might be the same concept. +5
joanmanuel26  According to Kaplan; All proteins that are synthesized in the ER must fold correctly in order to be transported to the golgi aparatus and then to their final destinations. If the mutation cause a misfolded protein, the result will be the loss of the protein function and, in some cases, accumulation of the protein in the ER. +
drdoom  @lilyo Thinking about this more. You will not find the (misfolded) protein in the cytosol. The misfolded protein may be inside a proteasome—and a proteasome may live in the cytosol—but the misfolded protein itself will never appear in the cytosol. The products of its degradation might (constituent amino acids or small peptides) but if you had an antibody for the misfolded protein and asked it “Where is the misfolded protein?”, the antibody would answer: “Most of what I could find appears to be in the rER.” +
yesa  Check out the calnexin cycle, usually proteins that are made in the RER and misfolded get tagged and 'refolded' and then scanned again for proper folding...and if they really can't be refolded, they're degraded then and there! So the only place misfolded CFTR could accumulate if misfolded is....RER... (Link to calnexin cycle: https://www.google.com/search?q=uggt+in+rer&sxsrf=ALeKk02X8jH8eveQ2IVM9IsVOlO47Qjh5A:1597110732938&source=lnms&tbm=isch&sa=X&ved=2ahUKEwiI75yPhZLrAhUTZjUKHWxgCaIQ_AUoBHoECAwQBg&biw=886&bih=1045#imgrc=4UYRaaYQDDFbDM) +

 +5  (nbme23#26)
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eagP 295 no siFrt iAd 9102 drune uelaarsRvocn s.eesiDa Mani susaec of alner trryae :osnstsei obruuFlmracis sldyaisap ni teh asldit /2r3d fo alren yerart ro ntsegmlea crhseb,an saulylu yogun ro dgaidmd-ele em.fleas


 +6  (nbme23#24)
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Tihs esqniuot si odwr fro dwro ni Fsrit idA 9120 eapg 442 renud M.CL -- I tdi'd rzleeia ti wsa rhete ilnut I got it wrogn.

vshummy  "Very low leukocyte alkaline phosphatase (LAP) as a result of low activity in malignant neutrophils vs benign neutrophilia (leukemoid reaction) in which LAP is increased due to increased leukocyte count with neutrophilia in response to stressors (eg, infections, medications, severe hemorrhage)." +5




Subcomments ...

This patient has chronic (6 weeks) symptomatic hypotension while not coincidentally on three BP meds: a diuretic, a beta blocker, and an ACE inhibitor. The most likely explanation and easiest/fastest intervention is to reduce her polypharmacy.

vshummy  Sure.. while we ignore her coarctation.... I mean I get it, stop the hypotension first but. +  
derpymd  @vshummy She has subclavian steal syndrome, not coarctation. Otherwise, yes, stop the hypotension -- address the SSS when she's hemodynamically stable +  


submitted by colonelred_(107),
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Teh sdsiignao is rwsbrrtaye ahaeginmom, lynmmcoo epsnahp ni ,ksdi ntfoe rleosves no sit won as eyht teg l.dore

shaeking  A strawberry hemangioma is normally pink or red (which is why it is named strawberry). The description has a flat purplish lesion which makes me think of a port wine stain on the face. How do you know to think of strawberry hemangioma over port wine based on this question stem? +3  
seagull  the age is key here. Newborns have strawberry hemangiomas typically on their face. Sturge-Weber could also be the case but none of the answer choices matched to that description. +1  
vshummy  I would agree with Sturg Webber nevus flammeus but I also noticed First Aid says it's a non-neoplastic birth mark so I should have known not to pick malignant degeneration or local invasion. Also because capillary hemangiomas don't have to be flat but the nevus flammeus is consistently flat. But I'm also reading on Wiki that the nevus flammeus doesn't regress so they must be trying to describe strawberry hemangioma even though I don't agree with their color choice... +  
nala_ula  Maybe (and I can only hope I'm right and the test makers are not -that much of- sadists) they would have made sure to write "in a cranial nerve 5 (either ophthalmic or maxillary) distribution" if it were Sturge-Weber. +1  
j44n  this is literally on every NBME along with the 10,000 ways to not get a boner +1  


submitted by karljeon(118),
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I dt'on konw fi reteh is an quoeinat ofr ts,hi tbu I bslyailac dpmeup tuo yveer vidioins raoscs het alebt to egt %~5 on .vrgeaea

reHe they er:0 4a0 / 0,600 = 0250607. / ,0605 = 300500 4. / 5503, = 5006. 003 / 5,050 = 0205 05.9 / 04,08 = 05.20

The vraagee of heste %s rof lla the sarye = .o.%5S 85 'satht sceol noguhe ot %5.

seagull  good work. I found this question annoying and gave up doing those considering the amount of time we are given. +4  
vshummy  Well just don’t include the intake year... because that messed me up.. +15  
_yeetmasterflex  How would we have known not to include the intake year? From average **annual** incidence? +  
lamhtu  Do not include intake year because the question stem is asking average annual incidence. The 4000 positives at intake could have acquired HIV whenever, not just in the last year. +8  
neels11  literally didn't think there was an actual way to figure this out. but my thought process was: okay incidence means NEW cases. so the annual average at the end of 5 years would be: (# of NEW people that tested positive at the end of year 5) / (# of people at that were at risk at the beginning of year 5) <--- aka at the end of year 4 250/5050 = 4.95% also if you look at year 5: you'll see that the at risk population is 4800 when 300 new cases were found the year before. 5050 at the end of year 4 MINUS the 300 new cases at the end of year 4 should give you 4750 as the new population at risk. but notice that end of year 5 we have 4800. idk if that means 50 people were false positives before or 50 people were added but in incidence births/death/etc don't matter it's kind of like UWORLD ID 1270. assuming average annual incidence is the same as cumulative incidence this was just a bunch of word vomit. sorry if it was unbearable to follow +  


submitted by lsmarshall(417),
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rnveobypaSnti si hte treatg of mnpsaneisttoa ansteut( ioxn;t) eucmls pssasm era seahtacrici.ctr lynO rhtoe snrawe uyo gtmhi cnrdosei si eehsttraocnlAcleyeis nscie he si a aerrfm dan urwszdboz ntfeo racyr us to eht oidsempr ..na.ld but spysmotm of a clghiiroecn msrot ear bset.an

vshummy  Synaptobrevin is a SNARE protein. Why they couldn’t just give us SNARE I’ll never know. +45  
yotsubato  Cause they're dicks, and they watched sketchy to make sure our buzzwords were removed from the exam +46  
yotsubato  Oh and they read FA and did UW to make sure its not in there either +37  
soph  This toxin binds to the presynaptic membrane of the neuromuscular junction and is internalized and transported retroaxonally to the spinal cord. Enzymatically, tetanus toxin is a zinc metalloprotease that cleaves the protein synaptobrevin, an integral neurovesicle protein involved in membrane fusion. Without membrane fusion, the release of inhibitory neurotransmitters glycine and GABA is blocked. -rx questions! +6  
qfever  So out of curiosity I checked out B) N-Acetylneuraminic acid It's sialic acid typical NBME +2  
alexxxx30  shocked they haven't started calling a "farmworker" a "drudge" <-- word I pulled from thesaurus. +3  
snripper  "You shouldn't memorize buzzwords. You gotta learn how to think." Lemme pick another random ass word that doesn't have anything to do with critical thinking skills and use it instead. +5  
mw126  Just as an FYI, there are multiple "SNARE" Proteins. Syntaxin, SNAP 25, Synaptobrevin (VAMP). From google it looks like Tetanospasmin cleaves Synaptobrevin (VAMP). Botulism toxin has multiple serotypes that target any of the SNARE proteins. +2  
wrongcareer69  Here's one fact I won't forget: Step 1 testwriters are incels +2  
baja_blast  FML +  
j44n  its not an ACH-E inhib because he doesnt have dumbell signs +  
flvent2120  I'm not even mad I got this wrong +  


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The sisdeea heer si utsecfro ohbhpesaasptis ednefyii.cc In ti, VI logyelcr ro ruftseco od’setn ehpl sbeecua btho tener hte negceloosngeusi awptyah bweol ceroufts otapsieh.pbhsa Gleasctoa on eth ehtro dhan trsene oevab ti. I tdon’ htikn ouy aeryll ened to nwko this ot coeohs eth tcrecor asnerw isnce eth llinccai uierpct fo afigtns ilmgyecpoyah atth is crrdeceto w/ mose sotr fo ugras hatt nac enetr hte enooegliucsegns whaatyp odushl ceul uyo noti het ihrgt wre.ans

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. +25  
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. +4  
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. +  
shayokay  You had to know that fructose and glycerol enter glycolysis at DHAP/G3P, and galactose enters glycolysis at G6P (gal-> gal-1-p -> glu-1-p -> glu-6-p). This means that one of the 3 enzymes between G6P and DHAP/G3P is not functioning properly. Most likely this would be fructose-1,6-bisphosphatase because there does not appear to be anything wrong with glycolysis. "Fructose-1,6-bisphosphatase (FBP1) deficiency is characterized by episodic acute crises of lactic acidosis and ketotic hypoglycemia, manifesting as hyperventilation, apneic spells, seizures, and/or coma. Acute crises are most common in early childhood; nearly half of affected children have hypoglycemia in the neonatal period (especially the first 4 days) resulting from deficient glycogen stores. Factors known to trigger episodes include fever, fasting, decreased oral intake, vomiting, infections, and ingestion of large amounts of fructose." https://www.ncbi.nlm.nih.gov/books/NBK550349/ +1  
shayokay  Also, even though Von Gierke is categorized as a glycogen storage disease it is really a problem with gluconeogenesis not glycogen breakdown. So even if you thought this was VG, you still could have gotten the right answer. In VG, any monosaccharide other than glucose (fructose, galactose, glycerol, etc.) will not raise the plasma glucose level because they all require gluconeogenesis to be converted into glucose and this cannot happen because there is no glucose-6-phosphatase. This is why the treatment for VG is frequent oral glucose in the form of cornstarch and avoidance of fructose and galactose. +  


submitted by m-ice(340),
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etisirincnV si a hioemcarpehtteuc dgur ttha itlsezaibs ocretuilbums dan vtpeesnr meth romf iseigsbnd.slma The clel ni hte cpiutre is suckt ni ,pehanasa thiw mretubiclosu cethdata to its sohom,cosemr ublean to lupl ehmt prata auecsbe it onactn sliesdbmeas ist ous.erubtmlic

vshummy  So I get that by process of elimination cyclophosphamide, cyclosporine, doxorubicin, and 5-fluorouracil are not related to microtubules but vincristine in First Aid 2019 says it prevents microtubule formation, doesn’t stabilize it because the one that stabilizes microtubules is paclitaxel. +  
vshummy  Okay, I realize now- the picture is stuck in metaphase, not anaphase. Both paclitaxel and vincristine stop the cell in metaphase but by two different mechanisms. Vincristine prevents mitotic *spindle* formation while paclitaxel prevents mitotic spindle *breakdown*. Mitotic spindle is needed to pull the chromosomes apart before anaphase begins. +15  
azibird  No, I think you were right to begin with. Without spindle formation the cell should be stuck in prophase (vincristine). Without breakdown it should be stuck in metaphase (paclitaxel). Metaphase is shown here with spindle fully formed, so it should be paclitaxel. +  
sars  I agree with the logic stated above. It could also be that the researchers added Drug X later on in M-phase, so therefore maybe the microtubules aren't even fully formed to fully reach metaphase. I think they're harping on "pick the best answer" +  
sars  I agree with the logic stated above. It could also be that the researchers added Drug X later on in M-phase, so therefore maybe the microtubules aren't even fully formed to fully reach metaphase. I think they're harping on "pick the best answer" +  


submitted by m-ice(340),
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eitniVcrnis si a ceuiohrpthmatcee gurd taht iblaszsiet uteubsimrloc nad vesptnre meth rmfo gbsdnimise.sla Teh clel ni hte rtuicpe si kstuc in p,esahaan hwit bimurlsetcou dhaactet to ist cmh,oomseors bulane to pllu mthe parta useebca it cnntoa edasbmliess tsi trlbsceu.iuom

vshummy  So I get that by process of elimination cyclophosphamide, cyclosporine, doxorubicin, and 5-fluorouracil are not related to microtubules but vincristine in First Aid 2019 says it prevents microtubule formation, doesn’t stabilize it because the one that stabilizes microtubules is paclitaxel. +  
vshummy  Okay, I realize now- the picture is stuck in metaphase, not anaphase. Both paclitaxel and vincristine stop the cell in metaphase but by two different mechanisms. Vincristine prevents mitotic *spindle* formation while paclitaxel prevents mitotic spindle *breakdown*. Mitotic spindle is needed to pull the chromosomes apart before anaphase begins. +15  
azibird  No, I think you were right to begin with. Without spindle formation the cell should be stuck in prophase (vincristine). Without breakdown it should be stuck in metaphase (paclitaxel). Metaphase is shown here with spindle fully formed, so it should be paclitaxel. +  
sars  I agree with the logic stated above. It could also be that the researchers added Drug X later on in M-phase, so therefore maybe the microtubules aren't even fully formed to fully reach metaphase. I think they're harping on "pick the best answer" +  
sars  I agree with the logic stated above. It could also be that the researchers added Drug X later on in M-phase, so therefore maybe the microtubules aren't even fully formed to fully reach metaphase. I think they're harping on "pick the best answer" +  


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yWh duowl it ton be aemian fo coirhcn isdesea htwi desradeec smeru srnrinatfre rnoatcconen?it

lispectedwumbologist  Nevermind I'm stupid as fuck I see my mistake +2  
drdoom  be kind to yourself, doc! (it's a long road we're on!) +21  
step1forthewin  Hi, can someone explain the blood smear? isn't it supposed to show hypersegmented neutrophils if it was B12 deficiency? +1  
loftybirdman  I think the blood smear is showing a lone lymphocyte, which should be the same size as a normal RBC. You can see the RBCs in this smear are bigger than that ->macrocytic ->B12 deficiency +23  
seagull  maybe i'm new to the game. but isn't the answer folate deficiency and not B12? Also, i though it was anemia of chronic disease as well. +  
vshummy  Lispectedwumbologist, please explain your mistake? Lol because that seems like a respectible answer to me... +9  
gonyyong  It's a B12 deficiency Ileum is where B12 is reabsorbed, folate is jejunum The blood smear is showing enlarged RBCs Methionine synthase does this conversion, using cofactor B12 +1  
uslme123  Anemia of chronic disease is a microcytic anemia -- I believe this is why they put a lymphocyte on the side -- so we could see that it was a macrocytic anemia. +3  
yotsubato  Thanks NBME, that really helped me.... +1  
keshvi  the question was relatively easy, but the picture was so misguiding i felt! i thought it looked like microcytic RBCs. I guess the key is, that they clearly mentioned distal ileum. and that is THE site for B12 absorption. +6  
sahusema  I didn't even register that was a lymphocyte. I thought I was seeing target cells so I was confused AF +  
drschmoctor  Leave it to NBME to find the palest macrocytes on the planet. +5  
zevvyt  so i guess size is more important than color cause those are hypochromatic as fuck +  
yesa  The NUCLEUS of a lymphocyte should be the same size as a normal RBC, which is not the case here. Under normal circumstances RBCs are not as big as lymphocytes, so this is truly extraordinary = megaloblastic anemia. +  


submitted by vshummy(163),
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Tihs eoiusnqt si ordw ofr rwdo ni irsFt diA 0219 eapg 442 rednu ML.C -- I 'ditd ezrleia it swa heret luint I got ti w.nrgo

vshummy  "Very low leukocyte alkaline phosphatase (LAP) as a result of low activity in malignant neutrophils vs benign neutrophilia (leukemoid reaction) in which LAP is increased due to increased leukocyte count with neutrophilia in response to stressors (eg, infections, medications, severe hemorrhage)." +5  


submitted by docred123(7),
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naC eemoons aslpee erruhtf enxipla itsh n?suoetqi Wtha asoiatsiitcbtl aalinssy suolhd I eb khgtnnii b?auot

vshummy  I got this wrong but best I could come up with was this was about Bradford Hill Criteria for establishing causality. And of the 9 included, F has the most that are actually included in the information given to us. I chose D but I think since we don't know about other study results, we can't include it as directly answering the question about *this* study. https://en.m.wikipedia.org/wiki/Bradford_Hill_criteria Someone double check me here: A: biologic plausibility is a weak point in the criteria, according to the wiki. Also probably not true in regards to this study. B: Sensitivity is not part of the criteria C: " " D: We don't know about consistency E: " B " +26  
mousie  Found this ... still confused about why A and D are wrong though... https://stats.stackexchange.com/questions/534/under-what-conditions-does-correlation-imply-causation +1  
2zanzibar  The three criteria for causality are: 1) empirical association (i.e. strength of association; a change in independent variable correlates or is associated with a change in dependent variable), 2) time order (i.e. temporal relationship; the independent variable must come before change in the dependent variable, or plainly stated, cause must come before effect). and 3) nonspuriousness (i.e. dose-response gradient; the relationship between 2 variables is due to a direct relationship between the two, not because of the actions of changes in a third variable... this can be evinced by a dose-dependent response). +10