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Welcome to davidw’s page.
Contributor score: 48


Comments ...

 +0  (nbme24#33)
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sI sith nfuod in horte soerrucse orhte neht buP edm res?atcil

mission260  Costanzo says " One of the earliest events of puberty is the appearance of large nocturnal pulses of LH during REM sleep. " also, I am aware of how late this answwer is :P +6




Subcomments ...

submitted by ameanolacid(24),
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ioorlsehAsetrsc si het SOMT mmonoc suaec of alern aryrte w.t.ssti.nisohe busacloumrirf sldaiaysp bgnei eth CDESON stmo oncmom caues vene( hghtou it is imtepntg ot hseoco itsh tinopo idnrcogsien hte npeat'sti dprec)ahmg.io

xxabi  Is there a situation where you would pick fibromuscular dysplasia over atherosclerosis if given both options? Thanks for your help! +5  
baconpies  Atherosclerosis affects PROXIMAL 1/3 of renal artery Fibromuscular dysplasia affects DISTAL 2/3 of renal artery +45  
gonyyong  Why is there ↓ size in both kidneys? This threw me off +3  
kateinwonderland  @gonyyong : Maybe because narrowed renal a. d/t atherosclerosis led to renal hypoperfusion and decrease in size? +1  
drdre  Fibromuscular dysplasia occurs in young females according to Sattar Pg 67, 2018. +10  
davidw  Normally you will see Fibromuscular dysplasia in a young female 18-35 with high or resistant hypertension. She is older has a history type II DM predispose you to vascular disease and normal to moderate elevation in BP +9  
suckitnbme  @gonyyong there's bilateral renal artery stenosis. The decrease in size of both kidneys should be from atrophy due to lack of renal blood flow. +3  
tyrionwill  1 year ago, she did not present any physical or Lab abnormalities. This means she must not suffer fibromuscular dysplasia, otherwise she must have presented renal abnormalities for a long long time, or even before DM-2. +2  
rockodude  a little surprised that atherosclerosis leading to bilateral renal artery stenosis and shrunken kidneys could happen that quickly after everything was A okay the year prior +  


davidw  If the Infarct was on the right side they you would have a decrease in PCWP +  
usmile1  yes exactly. Cardiogenic shock always has decreased CO and increased SVR. PCWP is the tricky part. If its right sided, there isn't enough blood making it to the LA (which is what PCWP measures) thus PCWP would decrease. If it is left sided, as indicated in this question by the crackles in the lungs, the blood is backing up in the left side of the heart so the PCWP would go up. +6  


submitted by welpdedelp(219),
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No ietd if,ndciceey teh tepitan dha esescx teconrea eud to hsi tied

sympathetikey  Would never have thought of that. Thanks +8  
medschul  that's messed up dog +18  
hpkrazydesi  Excess carotene in what way? sorry if thats a stupid question +  
davidw  this is directly from Goljan "Dietary β-carotenes and retinol esters are sources of retinol. β-carotenes are converted into retinol. (a) Increased β-carotenes in the diet cause the skin to turn yellow (hypercarotenemia). Sclera remains white, whereas in jaundice the sclera is yellow, which can be used to distinguish the two conditions. (c) Vitamin toxicity does not occur with an increase in serum carotene" +7  
davidw  β-Carotenes are present in dark-green and yellow vegetables. +  
hyperfukus  ohhhh hellllll no +7  
dashou19  When I was a little kid, I like to eat oranges, like I could eat 10 oranges at once, and after a few days, I could tell that I turned yellow... +6  
cbreland  I'm okay with missing this one +4  


submitted by welpdedelp(219),
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oN eitd ifcie,cyend het tieatpn hda eescsx neartceo ued ot sih tdie

sympathetikey  Would never have thought of that. Thanks +8  
medschul  that's messed up dog +18  
hpkrazydesi  Excess carotene in what way? sorry if thats a stupid question +  
davidw  this is directly from Goljan "Dietary β-carotenes and retinol esters are sources of retinol. β-carotenes are converted into retinol. (a) Increased β-carotenes in the diet cause the skin to turn yellow (hypercarotenemia). Sclera remains white, whereas in jaundice the sclera is yellow, which can be used to distinguish the two conditions. (c) Vitamin toxicity does not occur with an increase in serum carotene" +7  
davidw  β-Carotenes are present in dark-green and yellow vegetables. +  
hyperfukus  ohhhh hellllll no +7  
dashou19  When I was a little kid, I like to eat oranges, like I could eat 10 oranges at once, and after a few days, I could tell that I turned yellow... +6  
cbreland  I'm okay with missing this one +4  


submitted by dr.xx(144),
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SSsRI udcrope a netsasudi esiernca in ullaaetxrrcle TH5- in eht dsloar arhep DR,() nad tihs lasde to iaohiiiuobtntn of rnrstioceeog sorunne.

nt1g7pp:es5srt//jgou.p2t4.hcerr/5/n4o/t/

davidw  Pg 483 in firstaid has a good table of where the neurotransmitters work +6  


submitted by mousie(211),
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pelh ihwt iths one ..a.see.pl is itsh ecuebsa eh ahs yherpTG ADN toClsohrele NAD ciory.smcln.oh loyn LL ecinicyedf uapwdliolxen lla of teseh isfngid?n I osech DLL R ediyicnfec ebausce I segus I hghuto it owlud cueas lal fo tehm to esnricae tub si tish tepy fo eidycifenc loyn iecasdasot hiwt hhig ?DLL

sympathetikey  First off, do yourself a favor and check this out - https://www.youtube.com/watch?v=NJYNf-Jcclo The LDL receptor is found on peripheral tissues. It recognizes B100 on LDL, IDL, and VLDL (secreted from the liver). Therefore, an issue with that would cause an increase in those, but mainly LDL. Since in this question we see that Triglycerides and Chylomicrons are elevated, that points towards a different problem. That problem is in the Lipoprotein Lipase receptor. This is the receptor that allows tissues to degrade TGs in Chylomicrons. So, if it's not working, you get increased TGs and Chylomicrons. Additionally, you get eruptive xanthomas, which are the yellow white papules the question refers to. +8  
davidw  There is much easier way go to page 94 in first aid. This kid has Type 1 Hyper-Chylomicronemia which is I) Increased Chylomicrons, Increase TG and Increased Cholesterol. It can be either Lipoprotein Lipase or Apolipoprotein CII Deficiency +12  
bulgaine  The video sympathetikey referred to only mentions pancreatitis in type IV but according to page 94 of FA 2019 it is also present in type I Hyper-chylomicronemia which is what the question stem is referring to with the abdominal pain, vomiting and increased amylase activity +  
dentist  thats not the only difference in that video.... +  
paulkarr  Pixorize has a set of videos on all the lipid disorders that made it a breeze to answer. Pixorize is basically sketchy but for biochem and other basic science subjects. +2  
futurelatinadr  Pancreatitis was a huge clue for me to think of hyperchylomicronemia +  


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inkS dvpseori ulaintiosn dna nrevsept heat so.ls Tsih neptia'st bydo will nopcametes rfo caeisrned reta of haet slso by ngnarciise bimlaetoc reta.

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? +19  
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. :) +1  
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. +  


submitted by mcl(586),
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brise  Wouldn't that be more long term? +3  
sugaplum  I think Epo would indicate Rcc or renal failure, she seems like she has "just" refractory HTN, and no other sx to indicate anemia. +  
davidw  She has Fibromuscular dysplasia which should be in your differential for a young female with hypertension ( along with Conns syndrome and pheochromocytoma). it typically causes stenosis and aneurism formation of the renal arteries leading to elevated renin. +2