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Welcome to snripper’s page.
Contributor score: 30

Comments ...

 +2  (nbme22#24)

Essentially, we're trying to get to the renal artery from the femoral.

We cross through internal iliac (B) already to reach the aorta.

Remember the branches of the abdominal aorta: Celia -> SMA -> Renal -> IMA (FA 2020 pg. 363)

Celiac (A) and SMA (C) is superior to the renal so cross them out.

We're left with testicular artery.

Subcomments ...

submitted by sweetmed(123),
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heT maH stte si a sett euds ni hte ssigodnai of aoxsaymrpl tonulacrn rubooalmgeiinh NP(H.) Teh tste slovenvi pgacnli erd loobd cslel ni dmli ai;dc a tisivope uelstr nesdceia(r RCB yrti)alifg icseantid PNH

suckitnbme  It's so obscure of a test that wikipedia only has 4 sentences on it. +1  
pathogen7  FA2020 added the Ham test to PNH I believe! +  
pathogen7  Whoops no sorry I am wrong. They did add something called the EMA test to spherocytosis though. +  
snripper  Ham test has been replaced by flow cytometry now. So fck off, NBME. +  
pseudomonalisa  I remember it like this: PNH occurs at night due to mild respiratory acidosis (slower respiratory rate), which activates complement which destroys RBCs. The test is essentially doing the same thing, putting cells into an acidic environment -> dead RBCs. +1  

submitted by lsmarshall(348),
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Sanvirypbeont si the trteag fo atamnpsotsine statnu(e tixo;)n emcusl saspms rae crachseairtitc. Oynl rheot esnwra ouy gthmi dcornsie si eetssecAaliyrotnhlec inces he is a frrmae nad wzrsobduz tfneo ryrca su ot teh isompdre .anl..d tub smotymsp fo a iegcirhlnco mstor ear tba.sne

vshummy  Synaptobrevin is a SNARE protein. Why they couldn’t just give us SNARE I’ll never know. +34  
yotsubato  Cause they're dicks, and they watched sketchy to make sure our buzzwords were removed from the exam +32  
yotsubato  Oh and they read FA and did UW to make sure its not in there either +28  
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! +4  
qfever  So out of curiosity I checked out B) N-Acetylneuraminic acid It's sialic acid typical NBME +1  
alexxxx30  shocked they haven't started calling a "farmworker" a "drudge" <-- word I pulled from thesaurus. +  
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. +2  
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. +  
wrongcareer69  Here's one fact I won't forget: Step 1 testwriters are incels +1  

G1 checkpoint: Cyclin D/CDK4 complex with p53 and rb G2 checkpoint: Cyclin B and CDK 1

Way to remember: G1 is associated with higher numbers D and 4 G2 is associated with B and 1


and also F@CK me and F@CK NBME!!!

snripper  But the question doesn't mention anything about which cyclin. How does this help? +1  
thyenman  @snripper I think the word choice of "mitotic cyclins" is suppose to show they wanted cyclin B which is produced in G2. This resource specifically refers to cyclin B with mitosis. CDKs and different cyclins are expressed at different stages of the cell cycle: cyclin D (G1), cyclin E (G1/S), cyclin A (S), cyclin B (mitosis). - +1  

submitted by diabetes(15),

this question they gave you the answer (osteomyelitis).

snripper  fck, am i retarded? +6  

submitted by neonem(503),
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sTih tnepati nti's thvpentanilo,gyi y'eterh PYnEnvilegt,RtaiH ecenh hte P2OC l;t& 04 mm Hg.

stLe' alwk it :bdcwksaar eTyh era gettpnhreyavlnii ot stoecnempa orf teh baltociem iicassod ucadse yb swdiardepe op.aihxy yrpettniHvlanegi olsawl oyu to bowl fof oemr 2.CO

Wyh era hyte cipy?ohx Teh nepors is pyiohcx deu to mlnminfataio adn uecat prietyasorr trdsisse drnsmyoe fomr the ean.onumpi llA eht tcksinyeo fmor eht tmrlfynoamai clsle aseuc sneecdiar umrplonya yllripaca ,eaegakl wichh clbsko pu hte lolaeavr eemranmb os hatt 2O cnt'a egt hhrugot ot het odob.l

Wyh do ehyt heva blocatiem iscasdoi ni eht rstfi pecl?a No xygeon g&t-;- on nlteerco ntsrrtopa incha adn no TCA &;--tg ccatli aicsdiso.

diabetes  no pneumonia it is UTI +2  
makinallkindzofgainz  The infection from the UTI spread to her lungs +  
makinallkindzofgainz  this is essentially urosepsis, one of the leading causes of sepsis +1  
cmun777  UTI -> Sepsis -> ARDS (exudative pathophysiology d/t increased pulmonary vasc permeability) +7  
peqmd  urosepsis +  
snripper  lmao I read it as upper respiratory tract infections, too. +  
thisshouldbefree  she has an increased A-a gradient. +  

submitted by m-ice(272),
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The iehkoilold" fo niismgs na tanocos"isai fseerr to ypTe II .reror eTh rkis of ypTe II rreor si srdeernpeet yb etba. sThi dcolu eb cudnfsoe wiht ,wroep cihhw is 1 - .btea

usmleuser007  Just rereading this question without the stress, i got it quickly! Could't believe i missed something as simple as this. +2  
snripper  Can't believe I spent 5 minutes on this and still got it wrong lmao. I was like, "it can't be 90% chance of missing an association, that's way too high." But I picked it nontheless... +  

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iDd aynnoe seel go dwon te:h essh' oysetphevni os aybme lhl'se egt tsrwahoeue iefhednrrcsi dymernso secaube ghotnin eesl is kinmga sesen ot me at tshi nt?p??io uteor -

nsruT ,otu rvesee lariama anc ceaus rcuadsorilaacv cepsolla and ystihnoo.enp

redvelvet  me too :( +1  
abigail  me three :( +1  
yex  Me four :-/ +1  
link981  Slowly raising my hand as well +1  
tinydoc  Sammmme +1  
bullshitusmle  same here!!!:@ +1  
usmlecharserssss  patient has malaria with obvious picture and clinic, i answered because only thing associated with liver was hypoglycemia +5  
aisel1787  me five( +  
myoclonictonicbionic  I was thinking that she is hypotensive which can cause an infarct of the pituitary (since pituitary is growing during pregnancy) and therefore she'd have secondary adrenal insufficiency. +  
alexxxx30  sammmeeeee +  
snripper  Dumbasses unite lmao +  
usmleaspirant2020  lol saaaaame! +  
usmleaspirant2020  lol saaaaame! +  
anechakfspb  me also :/ sitting there trying to figure it out during the test I thought I was so smart too - like "wow nbme, way to tie in micro and endocrine, not getting me though!" ... i was wrong. +  

submitted by sajaqua1(462),
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oaasie,mcGnyt epirds inoa,amtga dan pnomgyidahos as( lelw sa malrap earh)tmey rae all snigs fo exescs og.tsrene Teh vilre ni antstepi hitw tcahpei deisesa si eimiaprd dna so acnont cerla neetosrg st.icnylffeui Sxi 21 oz eresb dlaiy (72 z,o ro lfha a ol)glan is too cmh,u and is rsiedgtnyo hsi l.ierv

uslme123  No hepatosplenomegaly, ascites, or edema through me off. We that being said, I shied away from cirrhosis. I thought that he showed signed of depression, so I went with the thyroid. But who's to say he isn't injection anabolic steroids?! +4  
catch-22  The principle is you can get liver dysfunction without having HSM, ascites, etc. Liver disease is on a progressive spectrum. +11  
notadoctor  He likely has hepatitis B/C given his history of intravenous drug use. I believe both can have liver dysfunction but may or may not have ascites, whereas the type of damage we would expect from alcohol that would match this presentation would also show ascites. +  
charcot_bouchard  For Ascities u need to have portal HTN. Thats a must. (unless exudative cause like Malignancy) +2  
paulkarr  For anyone who needs it; the FA photo is kinda burned into my mind for these questions. NBME has some weird infatuation with this clinical presentation.. FA (2019) Pg: 383 "Cirrhosis and Portal HTN". +3  
snripper  @paulkarr the problem was that the FA image was burned into my mind so without no ascites or edema threw me off of cirrhosis. +  
tyrionwill  cirrhosis doesn't present hepatomegaly, instead, the liver could be shrunken. +1  
avocadotoast  Cirrhosis (most likely due to alcoholism in this patient) leads to an increase in sex hormone binding globulin, causing a relative increase in estrogen compared to androgens. Cirrhosis doesn't always have to present with ascites and adema. I agree with @catch-22 that liver disease is a spectrum. This patient does not have ascites because his liver is still able to produce enough albumin to maintain oncotic pressure in the blood. +1  

submitted by yogi(10),
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TPI - tetlaelP + bA eogs ot lsnpee - edLys - Low plt tforcuen.tA eytpcenolsm - yusulal lpt ucont opvmier and raepihlreP boodl mresa wsoh - JH sbeodi sa a nisg fo lnpasaie ( eurnlac etarsmnn in BRC auslyul dreveom by .nsl)eep If heert swa an ysaccoers eplnes h(cwih saw otn ilnuonactf wehn eth nmia lesnpe swa nko)irgw lilw aket eovr het uiftnnoc gaardlluy - HJ dseobi illw ppeadrias dna tlP rsttsa ot eyls - hhwic hsa epndehpa in tihs eacs osi.nreca

spow  But why are there no bite cells? Question stem states that there is normal morphology? That's why I didn't pick accessory spleen +2  
makinallkindzofgainz  Bite cells are seen when splenic macrophages take "bites" out of hemoglobin precipitates in G6PD deficiency, which doesn't have to do with our question. This patient had a splenectomy 3 months ago, 6 weeks later showed Howell-Jolly bodies (asplenia), and then today now has normal erythrocytes (spleen is working again somehow = accessory spleen) +3  
snripper  @spow Bite cells are associated with G6PD deficiency, not ITP. +1  
srdgreen123  Main takeaway is the HJ bodies. They're seen pretty much whenever you have no spleen. So if they dissapear, that means another spleen-like structure has showed up +1  

submitted by hello(251),
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Wyh era oottrar" ucff aetr" adn t"oortar fucf nteid"nits wn?org is ti cb hbot fo ehets lwduo whos pmeintgnime ?igsn si eethr a yaw ot DxD eno morf teh ?hreto

snripper  It can't be rotator cuff problems because abduction is normal up to 90 degrees. +1  

submitted by sne(36),
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I hottguh of it klei nhwe ehs egst pu mrfo a opren tpinosio, seh si nsadecirge eht dolob oggin to rhe ,ehatr so os het the moyxam seaucs meor .trsnctuoiob sloA ysxammo usace ytni bmoil,e hcihw nac go ot teh teymcsis racniiltuco ciagusn mini itohmbr in the inabr nad smbli.

bigjimbo  Left atrial myxoma can mimic mitral stenosis (thus diastolic murmur) +  
btl_nyc  RVOT obstruction would cause a systolic murmur that gets louder when standing, not diastolic. +2  
snripper  RVOT obstruction = Hypertrophic Obstructive Cardiomyopathy which causes diastolic dysfunction (S3) not a systolic murmur. +  

submitted by lfsuarez(132),
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nWhe ipentast are nvgie Nniciitco a)c(diiiNanc hety rea told ot etpcex mnmooc sedi cfesfet ot ourcc scuh sa twamrh nad Oen nca avodi sehte dise ffecets by tiknga npirasi

mcl  To expand on this, the flushing/warmth/redness is due to release of PGD2 and PGE2 which is why taking an NSAID helps. +11  
snripper  Doesn't acetaminophen inhibits COX 1-2, too? Why can't you use that instead of aspirin? Just wondering. +4  
raspberryslushy  I had this same question too, and had it narrowed down to those two choices. Ended up going w/aspirin but it was sort of a coin toss. Still not sure why it's not acetaminophen. +  
eagleeeee  I think the reason is that acetaminophen is inhibited peripherally and is mainly used to inhibit COX in the CNS +4  
whatup  The worst side effect of Niacin is hepatotoxicity. Acetaminophen is famously known for hepatoxicity so aspirin is a better answer +  

submitted by meningitis(413),
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Trnean tgasse trsat at TEN esayr dlo

tSeag :I

  • I is ,tfal as ni ltaf hsect;
  • I si aelon, as ni no sxulea ah.ris

Stgea II :2)( tsgae II ssartt at 11 oy/ II( kolo ilek 11 )

  • 2 asllb tituaec(slr lnrtameeegn)
  • 2 iarhs upc(ib rihsa onw narg)pipae
  • 2 trebsa bsud morf

ategS III :3() atsrts at 13 /o y

  • If ouy etaort 3, it ooslk kiel llmas tsbersa (Brstae oumsnd rom;f)
  • fI yuo sggqluie eth III yeht oklo leki csyaeolruc+r bucip hrai
  • recnasdeI nseip telgnh nad zesi can eb nredsreeetp b:y II --;> III
    (your ipens aws hitn II tub onw tsi rtcheik )III

Sgtea VI (:4) attssr ta 14 /y o

  • sFtri eig:mani Teh I in VI erntsepsre hte ih,thg dna het V in IV koslo leki teh noms pusbi etbnewe oury :gesl
    MGAINN :E you aveh riha in mson iubps V)( btu uoy evah a drrboe giednnita eht irah omrf wiorggn nito .htigsh
  • The V is tpnoyi, sa in own het sebatsr era ioynpt aried(s aeoalr ro udomn no nu)mod

agetS V ()5: 15 yo/

  • V ahs on erbdosr innaedgit hrai frmo nrwgiog itno hgisht cbp(ui irah + tghih )airh
  • 5 i(sgfsnera ni ha)nsd anigenlttf eht orlasae nehw gaigrbbn hetm eoarla( ftanelt at hsti esgat dan on mroe ou"ndm no dnm"u)o

meningitis  Sorry about the format, it came out wrong but I hope his helps. +1  
drdoom  looks good to me! +10  
gh889  According to FA2019, stage 2 ends at 11, stage 3 starts 11.5-13, and stage 4 starts at 13-15, where did you get your info from? +  
meningitis  You can change it to ENDS at 11, ENDS at 13, ENDS at 14... I simply have it as a range just like you stated in a couple of them. The importance is in how the kid presents because he/she will have some things mature but others not, the age will vary in questions. +  
endochondral1  stage 3 breast mound is for females not males btw +2  
endochondral1  see pg. 635 in FA it just pubertal. Idk if that correlates to the same stage as females +  
angelaq11  this is just too funny, I LOVE it! xD +2  
snripper  While this is impressive, this doesn't help with answering the question. +1  

submitted by drmohandes(73),

Our patient has a metabolic alkalosis with (partial) compensatory respiratory acidosis.


Metabolic alkalosis → H+ loss or HCO3- gain:

  • vomiting: lose H+ (and lose K+/Cl-)
  • loop diuretics: lose H+ (and K+)


Metabolic acidosis, possible causes in this context:

  • diarrhea/laxatives → lose HCO3- (and K+) ; Cl- compensatory increase (normal anion gap)
  • acetazolamide → lose HCO3- (and K+) ; H+ also decreases but not enough to overcome the alkalosis caused by HCO3- loss
  • spironolactone
snripper  This makes sense, thanks! +  
dysdiadochokinesia  I was able to break it down to diuretic or alcohol use and chose alcohol use under the assumption that the patient's serum Cl- levels were low (90; N = 95-105) since Cl- is also lost with vomiting. Im assuming that it was wrong for me to make the association between alcohol use and vomiting. +  
avocadotoast  @dysdiadochokinesia I think we can rule out alcohol use by looking at our patient's history and demographic. A 16yo girl who is dieting and constantly studying probably isnt getting turnt because 1) alcohol has empty calories (defeats the point of dieting), 2) why would you try to study when you're drunk, 3) where will this 16yo in social isolation get alcohol +  

submitted by yotsubato(806),
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Wyh ncat tihs be aes?taxliv thBo wduol esuca bcetolmia iaslolask wiht o.lh.iy.ekpama ?

sup  Laxatives would cause an anion gap metabolic acidosis due to loss of bicarbonate in the stool. You would see hypokalemia though as seen in this question. +1  
miriamp3  it took me a lot of time choosing between laxatives and diuretics and at the end I choose diuretics. but I didn't realize that the only thing I had to do was check if were a anion gap or not. +  
snripper  Why would laxatives cause anion gap MA? Isn't it similar to diarrhea? +  
castlblack  The above comments are incorrect. Diarrhea is a cause of normal-anion-gap metabolic acidosis (D in HARDASS from FA). Laxatives are wrong because they would lower HCO3- but in this scenario it is high. The low K+ and Cl- fits either case though. +3  

The mother is Rh - & fetus is Rh +

pg 397 FA 2019 Administration of anti-D IgG to Rh - pregnant mother during 3rd trimester & early postpartum period (if fetus Rh+)

Prevents maternal anti-D IgG production

anti-D IgG = O, Rh -

snripper  Not sure why you're getting downvoted, but this makes sense to me. Maybe because you're claiming that the fetus is Rh+ when it's not clearly stated? But take that away and your explanation still makes sense. +1  
j000  the question is not asking what to give to the mother. it's asking what to give to the fetus. +  

submitted by bobson150(6),
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eTh nogwdri of stih eosiqtun efcuodsn me. Thsi si inkgsa iwc"hh of sehte velesss si eth ighh sepusrre "ytmses tg?hir oS het hghi uessrrpe erirsupo eacltr is uncagis eidcasern peeurrss niot eth nifeirro rlcate?

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: Nice images make the term easier to recall. Smaller streams "pay tribute" to larger rivers (by flowing into them)" +  

submitted by usmlehulk(3),

can someone please explain this question. i thought the patient is actually having cleft lip and palate, but why is the correct answer addressing only the cleft lip.

dentist  The question asks "the most likely cause of the facial finding involving the lip in this patient..." +5  
snripper  lmao. gottem +2  
ace9yak  cleft lip = 'processes' clef palate = 'shelves' +  
mutteringly  Don't let a dentist tell you whats up :( +  

submitted by aesalmon(79),
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FA gp. 067 - iulaefr of usnfoi of hte yllamaixr nda dmeegr aeidml snlaa ersecposs onfroam(it of paymrir tale)pa

meningitis  I think Cleft palate could also be due to failure of fusion of lateral and medial nasal prominences.. but since the baby had lip involvement and the lateral nasals can be seen, I went with failure of Maxillary and medial nasal fusion. Someone correct me if im wrong. +3  
redvelvet  a helpful photo +2  
snripper  @meningitis this is cleft lip, not cleft palate +2  

submitted by seagull(1112),
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If uoy od'nt wkno what olrmauicD deso klie any naomlr h.uman ehT ofcus no htwa inrapsi oet'nsd o,d ynamle ti's 'sodnet fetcaf TP mtei nda msto lipsl dt'no aierescn iglcttno licypeeas(l wtih rn.i)aspi Tsih is owh I olicg ot hte irtgh r.naesw

usmleuser007  If that's then thinking, then how would you differentiate between PT & PTT? +11  
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. +2  
snripper  yeah, it wouldn't work. We'll need to know with Dicumarol is. +3  
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 +1  
teepot123  di'coumarin'ol +  

submitted by seagull(1112),
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Im soal nevonccid ibkgolnc 2LI- is laos a nttertea?m HyW is FpahT-Nal eht tertbe swenar hree?

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. +12  
sbryant6  Spot on. This image explains how Sirolimus blocks the effects of IL-2: +  
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. +  

FA 2019 p156 Does anyone know how to differentiate the picture labeled Trypanosoma brucei and cruzi?

footballa  This question is likely not important for two reason: They're both Trypansomastigotes, so of course they look almost the same. You can differentiate these two species clinically as they have very little clinical similarity in patient presentation. For these reasons there's little to no reason you would be expected to differentiate these two species by histology alone +2  
snripper  Does Chagas have recurrent fever? Because that's what pointed me to African Sleeping Sickness. +  
baja_blast  The history of travel to the Amazon is what pointed me to Cruzi over Brucei but agree it's a tough distinction to make here. In the absence of that detail I would have probably picked Tsetse fly. +1  

submitted by cocoxaurus(52),
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Asmtlo tog krdicet yb iths eon escabeu trcaoemssaoo osla scsaue aitbsleotcso erssaotmOaoc omts nmoymclo stasszmeitea to gnslu g.hhout

impostersyndromel1000  This was in pathoma, he said prostate cancer causes osteoblastic lesions and "the board examiners really want you to know that". also following the potential site of mets helps choose the answer +1  
snripper  Also, osteosarcoma is less common in the elderly, more common in males <20 y/o (per F.A 2020) +1  

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Liintfg ahde elhwi p:noer 1 Salon cmoith elsi:m 2 Com: sthngonoi 2 snothm

pg32  Where do you guys learn that cooing starts at 2 months? It isn't in first aid or boards and beyond so this was an annoying question for me +1  
drschmoctor  @pg32 From being a parent! Otherwise little chance I'd remember all these milestones. +3  
drzed  I'll get right on that @drshmoctor :). If only I could have a kid to memorize all these damn developmental milestones. That would make life easier haha. +5  
snripper  Yeah, I don't see cooing anywhere. +  
teepot123  thankfully a lot of my friends on insta keep posting pics/vids of their babies reaching milestones so im well updated lol +1  
pjpeleven  Mnemonic: "Coo at Two" +  

submitted by bubbles(63),
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nCciroh renla fnsucfici:iney

)1 orop opehthspa aeelcancr tg&--; hgih emrus ciingaonr hrpoupshoso

)2 high umser opahstehp -&;-tg xcpesemlo hiwt anevtdli ncioat aC -;-> aC lfals

3) Ca lfals --gt&; streigrg HTP iaxs

4) kindey eirlufa -t-g&; cderdeesa vtcyaiit of x-seohl1drayy ta eht eidynk g&t;-- less lcalirotci

makinallkindzofgainz  this guy renals +4  
paperbackwriter  Someone please help me with this (always trips me up): PTH causes increased vit D production in kidney... are we assuming the increased PTH can't catch up with the kidney failure? Is it the level prior to PTH compensation that they want? D: +  
miriamp3  @paperbackwriter what it works for me ;;;; is find the first abnormality so CKD low calcitriol (no D vit) ---> is gonna increase PTH ---> the kidney are not working (chronic, they don't tell u recently- you can;t revert a CKD so the kidney never going to catch up) --> increase inorganic phosphorus.--> always start with the problem. I also use this for celiac and types of shocks. start with the problem, and trust yourself. +2  
paperbackwriter  @miriamp3 thank you! I will try out your strategy next time!! :) +1  
snripper  I thought renal insufficiency -> inability to reabsorb phosphate at PCT -> decreased phosphate? +2  

submitted by lnsetick(84),
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  • oPenrciA = ouyr ispmrta llmse kile na APE
  • UenRecM = ’heetsr on MROO ni oryu easr iscen yhe’ret ufll of wxa
  • ReYC-CnE = nwhe uoy sECre,iec yuor eopsr aer iYgCRn
  • oaeusEScB = BmEuS si SEEPnig otu fo ryuo orspe
hungrybox  as an ape i'm offended +18  
dr.xx  stop being an ape. evolutionize! +6  
dbg  as a creationist i'm offended +9  
maxillarythirdmolar  Also, Tarsal/Meibomian glands are found along the rims of the eyelid and produce meibum +  
snripper  So why is it apocrine? The dude is EXERCISING when playing football. +1  
qball  The question asks about "the characteristic odor" i.e. body odor coming from the APEocrine glands. The Eccrine glands secrete water and electrolytes. +