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Welcome to yex’s page.
Contributor score: 102


Comments ...

 +10  (nbme24#1)
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nicdrogAc ot nGol:ja 1"2B oaac(ilbmn) has cltoab in i.t urClacngtii ofrm fo afteol si ttyfoaemldlrtearhyt.ohe srpuoeP fo mliboaacn 2)B1( si to atek hte yehltm gorpu fof fo lhoydttmyt.aerlrotefeha ehnT s’it ecladl .tyretaadfltrhoeo fI ouy dotn’ get hte lmyteh pguor ffo fo taolef, yuo lliw not emak D.NA So, fi oyu rae 12B dfe, ouy tnc’a gte teh mtelhy prugo fof nad caonnt kmea .DAN If uyo aer edf in efoal,t uoy ta’nc amke DAN".

misterdoctor69  lmao +

 +2  (nbme24#13)
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hreTe rae nesiuqots tabou plgtinsin on tPtsesa nad .UW UW q id 18581 ohsws honrtea nsai.ocre Good giamse no the aotnixplane hogut.h suo,irplluaN bnesoone 39 /oy vilecp usrrseep &mpa; cponitsntiao dan osed tglninpsi ot fdaetece, abl alb ab.l E:mxa rerrgyulali relgedna uut.rse xD swa rtosipore ssslerauob eiurent oeiomlyam and ecrleecot wsa on hte opoints... nlnitSgip si ONT sjtu orf rleoctc.ee


 +6  (nbme24#43)
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shTi osal eerfrs to chnocir taalfimmoinn &pma; rnaglmoua aomntoifr.


 +1  (nbme24#34)
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I ktihn they era eferrirng to ktiyscluKh lecls = lmpnayruo uenorerioncnde csell .(PE)NC rdocgAnic to :Waieipkdi izeeSipadlc rwyaia pallhetiie llcse ttah ccoru as lytorisa cslel ro sa sclturse lelcda noeeielphuriatl odsibe E(N)B in teh gu.ln eThy aer elcodta in eht alasn pyersrtairo ietmul,eihp lygarnlae ausmco adn gohhouuttr hte ienrte taopesyrirr atcrt mfor het chrteaa ot eth nrtlaeim awi.yras hTey cna eb eht usecor fo saevlre ytesp fo glun -ecrcan tsmo toayl,bn aslml cell rmicaocna fo het lu,ng dna aroblhcni ncociirda trou.m


 +2  (nbme24#3)
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This asw no a rveposui M.BNE woH I tgo ?ti snaocItrtle rres)t(ipoo si who uoy egt to teh ebervatrl oiedsb; eht rhote seslevs aer it.rornae

medguru2295  this was nearly word for word on NBME 22. Slightly different wording maybe? +

 +5  (nbme23#7)
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mmH.m elWl ym dmin sah wblon off because awht ith ym dnim aws aernthdiyod icesn he swa in eht etsr.de sA nsoo sa ym indm edtrtsa ot awdren tboua lal fo eht tehor tnpsoio atth ucdlo aekm .n.esse. I tjsu ckildec adn domv!e

charcot_bouchard  Smart boi +5
usmlecharserssss  hiking in sahara desert SMH +3
cbreland  Simple = smart +




Subcomments ...

submitted by neonem(568),
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Tish atntpie has rmanulypo ,bsisofri iwhch esuacs a crserievtti nt(o tyr)putesvt-icbeo dsaei.es Senic hrtee was no lntuocaicaop oeexru,sp 'Im asmgunsi shti si idoaiictph mnlpyoaur sob.irsfi hTsi ecasus kihedntce arlaovle bsaenm,emr iilmitgn gsa iuidso.ffn eToferher, elvtunlyae O2 tn'ow eb able to fsudfei ucikyql oeunhg toni eht boold arssco the e-rrolavatllireaa ebmearmn, tgluisren in a rlgaer -aA .riefecenfd (I thikn e'etsrh rmlaolny a samll A-a rtna,dgei mrof 41-2 mm Hg, ubt nhew siht tegs too b,gi yuo gte x)ychoip

yex  UW q id 7648 +2  
melanoma  uw id 1526 +1  
feeeeeever  FA 2019 Pg. 661 +1  


submitted by dbg(149),
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TWF si wes"kneas of ntpalra ore"nislxofid ????? its' liek gsinya eeo"nitnsx o"nixhseilf T si ton hte olyn uoiobsv cahleticn kmiesta in eht wne sEBNM ...

karthvee  loool +2  
yex  Funny Board!! Yeahhhhh +  


yex  There is a Q on UWorld about rotator cuff tendinitis #380186 w/ a similar presentation... I kind of remembered about that, but honestly I do not know how I got it right. +  
yex  Correction: Q id is # 1732 +  


submitted by lsmarshall(415),
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Uear Clcye soDderirs t;g& aseltdoI everes moimpeeymranha &;g(t 01;00 i..,e no erhot eresve meaboilct rstbdusciane

hinOietrn snyaraamsrlcabet fnydcieice &tg; smto( ocnmmo raue elccy is)d. torioc eraaidda/aiciucmi, ehamoynraimepm

anOgicr eimciaAsd g;t& mm,ayrmnpaeioHe pa-gnnaio disio,acs ksosiet of(mr hmplgecoa)iyy

chuaneMmid-i y-AolcCa hyorgdeedaens cdifneeyci ;tg& naioareymepHm,m poctohketiy yaehcpyolmgi ee(ns ni onxtoi-dβia rissdod,er PTCEEX tnopsoladoyeyrderuhk)

eivLr osnuifdncyt &;gt yaeHmae,irnopmm FsTL msdese u,p delor p.t

lsmarshall  Summary of metabolic issues relating to hyperammonemia +7  
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +3  
notadoctor  Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria? +2  
charcot_bouchard  if it was mitochondrial disorder no one would escape +3  
wowo  figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB) + also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia +2  
artist90  i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong +4  
artist90  it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things 1-how does acidosis cause Hypoglycemia and Ketosis. 2-why is Ammonia elevated in these pts bc urea cycle will be fine? +  
yb_26  1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency 2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld) +1  
yex  According to UW, there is another question # 1341. This one refers to methylmalonic acidemia (ORGANIC ACIDEMIA). HYPOGLYCEMIA results from overall increased metabolic rate leading to increased glucose utilization and direct toxic (-) of gluconeogenesis by organic acids. The presence of hypoglycemia leads to increased free fatty acid metabolism that produces KETONES, resulting in a further anion gap met acidocis. Finally, organic acids also directly (-) the urea cycle, leading to HYPERAMMONEMIA. +11  


submitted by doodimoodi(62),
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Did no oen toncei atth eht dsdO taori on eth opt telf si wgr?on mA I isigmsn o?tgsnehmi fI ouy tlcualeac ti, tis' 6 utsj kile eht tpo rgthi o...ne.

mjmejora  thats actually really funny +  
yex  Because I said so, applies here... :-/ +1  
doodimoodi  Cant believe we pay $60 for this crap +41  
aisel1787  best comment doodimoodi) +1  
b1ackcoffee  that fucking threw me off on exam. I was like is there an effect modification by "Not drinking milk". the fuck! +1  


submitted by catch-22(76),
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I oduw do a eoveptsrtreic hotcro eeh.r I do'tn nthik shti souqient si orccetr adn vidsepro oto litelt itmnornafio ot get het rcocetr s.aenwr mei"T icfn"tifee si teh narpteo rdow ereh btu ehty pysmil ind'dt iesondrc that scitrevtpreeo chotor doluw be a bretet endsgi eher sa ognl sa hte lbaervsia rae oddc.e

sherry  I agree. I was hesitating between the two choices. I still think cohort study is better regarding the "risk". I hope this kind of questions wont pop out on the real thing. +2  
soph  I think key here was they were measuring risk though +  
yex  I also chose cohort, since it is comparing a given exposure. +  
raspberryslushy  I was also thinking retrospective cohort study - just as time efficient, can look at risk, and the Q stem said the cancer was common, and I think of case-control for rare conditions. It's like they forgot a cohort study could be retrospective. +1  
boostcap23  The classic example they always give for why not to do retrospective cohort is because patients who have whatever disease your testing for are more likely to remember all their risk factor exposures than a normal person that doesn't have any disease. Of course in this case I'm sure the people running the study would be the ones who figure out how much arsenic was in the water but this also would be very time consuming to figure out for each individual person in the study. Thus a case-control study where you look at a group of people with >50 arsenic exposure and a group <5 arsenic exposure and simply see who has cancer and who doesn't would be easier and take less time. +1  


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Snik ovpesird iunsialnot dan etpvnres etha lss.o iThs ase'ptint byod llwi ceptaenmos rof seidrenac etar of thea lsos yb anncgiiser baecmltio t.rae

davidw  This is directly from Goljan I) Hypovolemic shock may occur due to loss of plasma from the burn surface (refer to Chapter 5). • Loss of protein from the plasma loss may result in generalized pitting edema. II) Infection of the wound site and sepsis may occur. (a) Sepsis due to Pseudomonas aeruginosa is the most common cause of infection in burn patients. (b) Other pathogens include methicillin-resistant S. aureus and Candida species. (3) Curling ulcers may occur in the proximal duodenum (refer to Chapter 18). (4) Hypermetabolic syndrome may occur if >40% of the body surface is burned. +12  
yex  Can someone explain why is it not increased ECF? +24  
charcot_bouchard  i picked same. Increased ECF but cant remember why. Can you explain WHY it is increased ECF? what was ur reasoning +2  
isotopes  Burns would lead to a decrease in ECF because the protection from fluid loss is absent; it can lead to shock. :) +2  
tinydoc  My reasoning behind picking ↑ ECV was that your losing fluid but not electrolytes with the burn ⇒ the ecv would have increased osmolarity, so the fluid from the ICV would be pushed the the ECV. It made sense to me at the time. I guess technically its wrong because the loss of fluids and the gain of fluids would amount to pretty much the same thing. But the insulation and heat loss thing makes sense I guess. +  
yex  Increased ECF, bc I was thinking about the edema formation.... :-/ +3  
atbangura  I picked increased ECF because burns increase the capillary permeability coefficient, but now that I am going over it I realized that increasing the permeability would only transfer plasma volume to the interstitial volume, which are both a part of the ECF so therefore ECF would not change. SMH +5  
aisel1787  thanks +  
69_nbme_420  Burns (and Diarrhea) cause ISOsmotic volume contraction; Costanzo BRS Physio +  
tiagob  in severe burned patient, also has increased fluid in third spacing or interstitial (leading EDEMA). Different extracellular space is interstitial and vascular +  
peridot  I also wanted to add, another huge job of the skin is to prevent loss of fluid. Burn patients are easily dehydrated because they've lost that barrier. This helped me lean away from increased ECV - despite the edema (from one compartment to another) as others have mentioned above, there is a loss in overall ECV due to evaporation from body. +  


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diD nayoen else og odnw :hte sehs' ihysoevetpn so ameyb leh'sl gte eewhroasut ihcesdirfren dmoeynrs aubscee gntnoih seel si gamnik nssee to me ta tshi tpi?n??o eutor -

rTnus tuo, sveeer riaaalm cna uaecs vaaulasrodcirc eapclosl adn eyt.nhinsoop

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 +11  
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. +1  
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. +1  


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ikSn disvrepo aunilotsin nda sevrpten tahe ss.ol This t'iapsten dbyo lilw eepncmaost ofr ncairesed taer fo thea ssol yb siengcinra timeoblca t.rae

davidw  This is directly from Goljan I) Hypovolemic shock may occur due to loss of plasma from the burn surface (refer to Chapter 5). • Loss of protein from the plasma loss may result in generalized pitting edema. II) Infection of the wound site and sepsis may occur. (a) Sepsis due to Pseudomonas aeruginosa is the most common cause of infection in burn patients. (b) Other pathogens include methicillin-resistant S. aureus and Candida species. (3) Curling ulcers may occur in the proximal duodenum (refer to Chapter 18). (4) Hypermetabolic syndrome may occur if >40% of the body surface is burned. +12  
yex  Can someone explain why is it not increased ECF? +24  
charcot_bouchard  i picked same. Increased ECF but cant remember why. Can you explain WHY it is increased ECF? what was ur reasoning +2  
isotopes  Burns would lead to a decrease in ECF because the protection from fluid loss is absent; it can lead to shock. :) +2  
tinydoc  My reasoning behind picking ↑ ECV was that your losing fluid but not electrolytes with the burn ⇒ the ecv would have increased osmolarity, so the fluid from the ICV would be pushed the the ECV. It made sense to me at the time. I guess technically its wrong because the loss of fluids and the gain of fluids would amount to pretty much the same thing. But the insulation and heat loss thing makes sense I guess. +  
yex  Increased ECF, bc I was thinking about the edema formation.... :-/ +3  
atbangura  I picked increased ECF because burns increase the capillary permeability coefficient, but now that I am going over it I realized that increasing the permeability would only transfer plasma volume to the interstitial volume, which are both a part of the ECF so therefore ECF would not change. SMH +5  
aisel1787  thanks +  
69_nbme_420  Burns (and Diarrhea) cause ISOsmotic volume contraction; Costanzo BRS Physio +  
tiagob  in severe burned patient, also has increased fluid in third spacing or interstitial (leading EDEMA). Different extracellular space is interstitial and vascular +  
peridot  I also wanted to add, another huge job of the skin is to prevent loss of fluid. Burn patients are easily dehydrated because they've lost that barrier. This helped me lean away from increased ECV - despite the edema (from one compartment to another) as others have mentioned above, there is a loss in overall ECV due to evaporation from body. +  


yex  There is a Q on UWorld about rotator cuff tendinitis #380186 w/ a similar presentation... I kind of remembered about that, but honestly I do not know how I got it right. +  
yex  Correction: Q id is # 1732 +  


submitted by yotsubato(1019),
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saW ti jstu ,me or idd ge"a ta senot in re"ays aerapp GRIHT veoab eth rnbeum of nt,tspaei rareht htna teh man.e hhWic osdcuenf em for a dgoo 3 .imenstu

fulminant_life  Definitely was the same for me. I was so confused for like 5 mins +13  
d_holles  dude i almost didn't get the question bc of this ... i thought the age of onset was the actual age of onset (36) +7  
mellowpenguins  Are you serious. NBME strikes again with shitty formatting. +7  
yex  OMG!! Now I just realized that. Super confused and also thought onset of age was 36. :-/ +5  
monkey  what is 36 supposed to be? +1  
thomasburton  Think the number of people in that group +5  
paulkarr  Yup...was looking at it for a good 3 min before just doing the "fuck it..it's gotta be 99" +4  
arcanumm  Age of Onset is the Title of the table, which I didn't figure out until after exam was over. What terrible formatting. +3  


submitted by usmleuser007(395),
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.1 Acriot cDsailito rrePsues 1. ihHg RPT = ghih PD .2 Hihg HR = ighh DP 3. iHhg VS = hgih PD 2. tiAocr Stcloyis esusrrPe 1. ihHg iaCttrinytloc = gihh PS 2. ihHg VS = hhgi PS 3. Low eCoicpamln = ighh PS
yex  https://cvphysiology.com/Microcirculation/M012 This helps somehow, the first part about capillary pressure. +  
usmlelol  that's the exp part:: The average capillary hydrostatic pressure is determined by arterial and venous pressures (PA and PV), and by the ratio of post-to-precapillary resistances (RV/RA). An increase in either arterial or venous pressure will increase capillary pressure; however, a given change in PA is only about one-fifth as effective in changing PC as the same absolute change in PV. Because venous resistance is relatively low, changes in PV are readily transmitted back to the capillary, and conversely, because arterial resistance is relatively high, changes in PA are poorly transmitted downstream to the capillary. +  


submitted by mousie(216),
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naC meosone epalse lpnixae iths ot ?me I o'dnt dtndsurena hyw stgtrnia the erhto urdg udlwo ont ctonu as oeilxscun cr?aeitri

seagull  This has to do with Intention-to-treat analysis. Essentially, when participants are non-adherent but the data shouldn't be lost. They just undergo another statistical model to account for their changes. Here is a nice video https://www.youtube.com/watch?v=Kps3VzbykFQ&t=7s +22  
dr.xx  Where does the question mention "intention-to-treat"? +  
notadoctor  They seem to be pretty obsessed with "intention-to-treat" it's been asked in one way or another in all the new NBMEs that I've done. (Haven't done 24 as yet) +8  
wutuwantbruv  They don't, intention-to-treat is just the best way to go about it @dr.xx +  
smc213  Great for ITT: https://www.youtube.com/watch?v=Kps3VzbykFQ +4  
yex  I agree with @notadoctor !! +  
ergogenic22  i think if it were per protocol, both groups would be excluded, the ones that were inconsistent, the ones that dropped out, and the ones that switched. But answer choices only allow ITT or exclusion of one group. +  


submitted by whossayin(24),
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het ietousqn was vyre ooprly eordwd ni ym n,niiopo ayboynd sele eg?ear

niboonsh  yea it was a dumbass question, whoever is writing these questions is undoubtedly a crazy genius but homeboy (or homegirl...homeperson?) needs a few grammar lessons. +4  
yex  I agree. We know that it is a teratogen, but how does that question directs you to think about teratogenic effects instead of something physiologic? +5  
dr_jan_itor  The questions in the NBMEs by default are reject questions. So highly selective to be awful questsions. I am recieving regular heads up that the stems on the real thing lately are like 10-12 lines long. So these questions are not anywhere near like the test. NBME has f'd us good for this particular round of practice forms. +  


submitted by jotajota94(14),
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seU het iyrgaHnerde-bW atounqei

  1. Teka the qeuasr troo of 1106/,0 dna htta will gvei uoy the uqceenfyr fo eht sveeercsi eaelll = 01/4.
  2. aaltecuCl hte nyeqfuerc fo eht itandnmo llalee with +,1pq= hiwhc is =p .790.5
  3. hyTe rea iglnlet uoy to tccealual the feqyrunec fo hte iseaesd a,srriecr chhwi si with eht qutoenai pq2.
  4. Tyhe nwta loyn teh iassdee esrricra ni iwhhc dtoineel is psrent.e oT eltccalau ,shti seu hte q aulev (041)/ dna pmilutyl yb 8%0 in tshi olushd eigv uyo .2.00
  5. niFl,lay cutlaecal ofr q2P2 =.95).(200(0)7 .040 = 15/2.
yex  Nice! ...and we are supposed to read the stem and do all this in a minute or so? :-/ +23  
charcot_bouchard  Allele frequency 1/40. so carrier freq 1/20. 80% of 1/20 is 1/25 (80/100 x 1/20) +14  
dickass  Ah feck, 2pq got me +  
hello_planet  A handy shortcut for Hardy-Weinberg is that you generally can assume p ~= 1 if q if fairly low. It also tends to be easier to work in fractions if the answer choices are in fractions so you don't have to bounce back and forth between fractions and decimals. So with that, you send up with 2pq = 2 * 1 * 1/50 = 2/50 = 1/25. +6  
topgunber  hate this whole scramble thing: In one line: 2 * q * 80%. This is for diseased individuals (two q alleles).I = 1/1600 = q^2 The frequency of q = 1/40 Now carriers is 2 p q. P is close to one assuming HW eqm (p+q=1). There's an additional step in this question due to the two different mutations. so 2(q) = 1/20. 80% of these carriers are deletions so multiply 1/20 * 0.8 = 1/25 +  


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Cna ymbosode plaese eiapnxl hwy eht Kap hsa ot be 6 tsiande fo 0?1

masonkingcobra  Since an ionized form is charged (by definition), it will not easily cross a nonpolar lipid membrane. Thus, it is important to recognize the potential of the drug to ionize in order to predict its solubility and the degree to which it can be reabsorbed. The degree of ionization is determined by the drug’s pKa and the pH of its environment. Weak acids and bases are 50% ionized and 50% unionized when the surrounding pH equals the drug’s pKa. At 2 pH units above or below the pKa of the drug, nearly 100% of the drug is ionized or unionized. +3  
masonkingcobra  Basically weak acids are best excreted in alkaline urine, but weak bases are excreted more readily in acid urine. +  
masonkingcobra  In summary, because this is a weak acid at pKa 6, making the urine alkaline will result it its ionization and excretion. Ionized cant move through lipid membranes so can't get reabsorbed and is pissed out. +15  
yex  Following on masonkingcobra explanation: A pKa 4-9 can be either weak acid or base. Weak acid pKa 4-7; strong acid pKa 1-3 Weak base pKa 7-9; strong base pKa above 9 Differents pHs: stomach: 1-2 duodenum: 3-5 early jejunum: 5-7 late jejunum: 7-9 ileum: >9 urine: 4.5-8 Weak acids (pKa) gets absorbed in acidic (pH) environments and cleared in basic. Weak bases gets absorbed in basic environments and cleared in acidic. THIS DOES NOT APPLY TO STRONG BASES OR ACIDS!!!! The best explanation for this is a Biochem lecture from Pass Program and it is available on YouTube, its long but it is for sure worth it!! Look for 19 Biochemistry 1 from Pass Program on YouTube. +1