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Welcome to schep’s page.
Contributor score: 20

Comments ...

 +1  (nbme18#40)

Why is this Chlamydia? I thought we give erythromycin ointment at birth to prevent conjunctivitis-->blindness from Neisseria gonorrhoeae

schep  In looking through FA, conjunctivitis from gonorrhea occurs 2-5 days after birth while chlamydia occurs 1-2 weeks after birth +2
tekkenman101  Also gon. conjunctivitis is more often purulent while chlamydia is watery discharge. +

 +1  (nbme21#27)

A refresher on the branches of external carotid artery-SALFOPMaxS

Superior thyroid, Ascending pharyngeal, Lingual, Facial, Occipital, Posterior auricular, Maxillary and Superficial temporal

 +0  (nbme13#6)

FYI since I didn't know the difference

Nitric oxide=NO

Nitrous oxide=N2O

 +1  (nbme13#1)

I thought lytic bone lesion-->multiple myeloma-->hypercalcemia

but I suppose that calcium isn't involved in the process of creating the lytic lesion, that would be IL-1 and TNF

 +0  (nbme13#26)

carbon monoxide inhibits the final step of ETC, cytochrome oxidase

Subcomments ...

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PCP si a vpht-oiteydaceins nad iiiedacvstos ehcettasin ahtt elgyrlnae csat sa a nwrode btu anc oasl csaue inedicrbel snogersgia uldeopc thiw napi iynnitsetsvii (eth pesmanur .ug)rd leacriVt stuygmsna is a myoclonm etdmnineo lhcpsayi amxe di.nfing

azibird  FA specifically mentions hypertension and tachycardia, so I ruled it out immediately. But you're right, it's a hallucinogen, I thought it was a stimulant. +1  
azibird  "PCP (10mg/kg, s.c.) causes hypertension that is associated with decrease or tendency to decrease the levels of epinephrine and norpinephrine in the hypothalamus and the brainstem regions." "Over 50% of adult patients present with the classic toxidrome of PCP intoxication: violent behavior, nystagmus, tachycardia, hypertension, anesthesia, and analgesia." +  
schep  I spent so much time on this question. I also ruled out cocaine, methamphetamine and PCP because (I thought) his vitals didn't match. Then I was forced to convince myself that someone on oxy or a benzo would suddenly get violent... +1  

submitted by aneurysmclip(151),

She's vomiting - Metabolic Alkalosis > loss of HCL > ie; acid, there would be increased HCO3 Anion gaps are usually with metabolic acidosis because in alkalosis there is high HCO3 which keeps gap normal. For the K+ > vomiting > loose water along with the vomit > decreased blood volume > RAAS activation > aldosterone secretes H+ and K+ > hypokalemia

schep  Dirtyusmle has a good video on this topic if you're like me and struggle with renal +1  

submitted by schep(20),

Why is this Chlamydia? I thought we give erythromycin ointment at birth to prevent conjunctivitis-->blindness from Neisseria gonorrhoeae

schep  In looking through FA, conjunctivitis from gonorrhea occurs 2-5 days after birth while chlamydia occurs 1-2 weeks after birth +2  
tekkenman101  Also gon. conjunctivitis is more often purulent while chlamydia is watery discharge. +  

submitted by sugaplum(376),
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FA 1902 gP 012
oilcrn ysoepc essacu tenesynrhpio dna icprxonyoethti

schep  it can also cause gingival hyperplasia +1  

submitted by pppro(23),
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IV rdgu besau + R etahr ealuifr msomytps ent(cdeosg rvi:)el thkin idcpsirut fnunfyeiciics

fukprometric  why couldn't it be something cirrhosis related given his IVDU? I was thinking that the increased systolic pressure was a sign of portal HTN from cirrhosis so he'd also have a portosystemic shunt, but that was wrong +1  
schep  I picked portosystemic shunt, too. Looking at the question now, I should have focused on the fact that he is IV drug user, has a fever and has signs of right heart failure (back up of blood into the liver) which makes me think endocarditis +  
jaramaiha  Portal HTN wouldn't give him a fever, but those septic emboli would. TBH to go 10+ years as IVDU w/ no heart conditions, he seems to have played his luck, but luck has run out :( +  

submitted by johnthurtjr(144),
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hrse'e a oeggol

johnthurtjr  FTR I had no idea this was a thing, and was pretty disappointed in myself when the google search had it in big bold letters right in my face. +3  
drdoom  via @johnthurtjr link: "Testosterone and other androgens have an erythropoietic stimulating effect that can cause polycythemia, which manifests as an increase in hemoglobin, hematocrit, or red blood cell count." +3  
meningitis  I guess that's another reason for steroids and doping up. +8  
drschmoctor  For once I feel like I've been led astray by Pathoma. My instinct was to go with hemoglobin, but I talked myself out of it after remembering Dr. Sattar saying that the reason why women have lower hemoglobin is due to menstruation. +2  
fexx  F U testosterone! and F U NBME 22 question +1  
schep  I only knew this because there are three (at least three, maybe more that I don't know) contraindications to giving testosterone replacement therapy: +OSA +prostate cancer +hematocrit >50% +2  
drdoom  ^ linkify @drdoom +  

submitted by haliburton(214),
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:oehptgan tccocyprocus

mteTtnrae tpoo:nis pmAho :B dnsbi eersrgotol &t;-g sroep ni afnlug abmermne tg&;- aeslk e .nsctotn cna dad n:stcyuilFoe crvedonte to -UF5 to niibtih ilneccu dica tsnishsye

1tt6icce.pnosbeo0ygyumtmsfteli/1lo//icho:1./d/uol4rsslp1mtbe /oib/e01rohyntedclsimis4et.lo.8tueablc1t/i:mpg/bm/ospmro5p1-cht

passplease  How did you know it was cryptoccocus and not something else like candidiasis? +1  
jsanmiguel415  Was stuck between cryptococcus and candida as well. I think the tip might be that Candida is in mold form at higher (body) temp. But amphotericin b can be used for both and given that it's a serious infection you would probably just go straight for that instead of fluconazole. +  
schep  Patients with T cell dysfunction (HIV) are more susceptible to cutaneous candida infections (esophagitis, etc). Patients with neutropenia (chemotherapy, post-transplant) are more susceptible to invasive candida infections (bloodstream infection, meningitis) +  

submitted by seagull(1567),
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tuo fo ,syrtuioci hwo yam opeepl kewn ht?is ontd( eb shy to say yuo idd ro d?)idnt

My ovytper tncuoaied dt'nid airignn sthi ni em.

johnthurtjr  I did not +3  
nlkrueger  i did not lol +  
ht3  you're definitely not alone lol +  
yotsubato  no idea +  
yotsubato  And its not in FA, so fuck it IMO +1  
niboonsh  i didnt +  
imnotarobotbut  Nope +  
epr94  did not +  
link981  I guessed it because the names sounded similar :D +14  
d_holles  i did not +  
yb_26  I also guessed because both words start with "glu"))) +27  
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle. +1  
jaxx  Not a clue. This was so random. +  
ls3076  no way +  
hyperfukus  no clue +  
mkreamy  this made me feel a lot better. also, no fucking clue +1  
amirmullick3  My immediate thought after reading this was "why would i know this and how does this make me a better doctor?" +7  
mrglass  Generally speaking Glutamine is often used to aminate things. Think brain nitrogen metabolism. You know that F-6-P isn't an amine, and that Glucosamine is, so Glutamine isn't an unrealistic guess. +4  
djtallahassee  yea, I mature 30k anki cards to see this bs +4  
taediggity  I literally shouted wtf in quiet library at this question. +1  
bend_nbme_over  Lol def didn't know it. Looks like I'm not going to be a competent doctor because I don't know the hexosamine pathway lol +21  
drschmoctor  Is it biochemistry? Then I do not know it. +5  
snoochi95  hell no brother +1  
roro17  I didn’t +  
bodanese  I did not +  
hatethisshit  nope +  
jesusisking  I Ctrl+F'd glucosamine in FA and it's not even there lol +  
batmane  i definitely guessed, for some reason got it down to arginine and glutamine +2  
waterloo  Nope. +  
monique  I did not +  
issamd1221  didnt +  
baja_blast  Narrowed it down to Arginine and Glutamine figuring the Nitrogen would have to come from one of these two but of course I picked the wrong one. Classic. +1  
amy  +1 no idea! +  
mumenrider4ever  Had no idea what glucosamine was +  
feeeeeever  Ahhh yes the classic Glucosamine from fructose 6-phosphate question....Missed this question harder than the Misoprostol missed swing +1  
surfacegomd  no clue +  
schep  no idea. i could only safely eliminate carbamoyl phosphate because that's urea cycle +  
kernicteruscandycorn  NOPE! +  
chediakhigashi  nurp +  
kidokick  just adding in to say, nope. +  
flvent2120  Lol I didn't either. I think this is just critical thinking though. The amine has to come from somewhere. Glutamine/glutamate is known to transfer amines at the least +1  

submitted by cassdawg(1148),

The big hint here is EXTREME respiratory depression which is characteristic of opioid overdose, so he should be given naloxone. [FA2020 p570 has drug intoxication and withdrawal syndromes]

bingcentipede  And he was also taking codeine, a mu opiod agonist. So naloxone would be able to reverse the codeine specifically. +1  
schep  Flumazenil-GABA antagonist, used to treat benzodiazepine OD Fomepizole-competitive inhibitor of alcohol dehydrogenase, used to treat ethylene glycol and methanol OD hemodialysis-can be used for severe lithium ODs, not sure what else propranolol-nonselective beta blocker; not sure if it treats any ODs in particular +2  
deadbeet  The HR made me waste way too much time on this question. Don't think tachycardia is the norm for opoid OD. +2  
prostar  the reason for increase HR is hypotension(and the reason for hypotension is opioid induced mast cell release- histamine-vasodilation) +2  

submitted by cassdawg(1148),

Ibutilide is a Class III antiarrhythmic drug. Most Class III antiarrhythmics are associated with Torsdaes de Pointes as a complication [FA2020 323]

Other drugs associated with Torsades de Pointes are drugs that induce prolonged QT including: Class IA antiarrhythmics, some antibiotics like macrolides, antipsychotics like haloperidol, TCAs, and some antiemetics like ondansetron [FA2020 p294].

schep  I vaguely recall that methadone also prolongs QT +  

submitted by andro(189),

Patient with Primary Hypothyroidism (problem with the gland itself ) treated with T3

  • In normal physiology T4 is converted to T3 and less commonly ( rT3) . As such most of the T3 in the body is derived from the peripheral deiodination of T4 to T3
  • Also note that TSH secretion by anterior pituitary is under negative feedback control by both Free T3 and T4

So what happens when we give our Patient T3.
- firstly , we inhibit secretion of TSH from the pituitary gland . ( TSH decreases ).

This means less stimulation of the Thyroid and less hormone production . The Throid hormone it primarily makes and releases is T4 , ( and so T4 decreases ) . Naturally you would also expect a decrease in T3 but patient is taking exogenous T3( and so T3 increases )

schep  I messed this up because I know treatment of primary hypothyroidism is usually with levothyroxine (T4). I totally skimmed the part where we are told she is being treated with T3 +1  
jdc_md  ^nbme is asshoe! +1  
topgunber  side note thyroglobulin would also be low and is asked on uworld +2  
cheesetouch  Thyroxine = T4 +1  

submitted by cassdawg(1148),

Hormone sensitive lipase (HSL) is the enzyme which degrades triglycerides stored within adipocytes (FA2020 p93). Thus, it makes sense that it is activated in times of fasting and suppressed in the fed state.

Insulin would inhibit HSL, as insulin is a fed state enzyme secreted by the pancreas and would want to trigger storage of triglycerides.

In contrast glucagon is secreted in response to hypoglycemia by the pancreas and will trigger fasted state activation. In terms of the fed/fast state I always think of glucagon and epinephrine kind of like a superhero and their side kick, because they usually work together in the fasting state on similar targets to ensure the body has enough energy (this helps me remember that epinephrine and glucagon are fasting state hormones). Here though is epinephrine's big action away from glucagon, where glucagon has minimal effect and epinephrine has the big action of activating HSL! Glucagon has a minor role and other catecholamines and ACTH can also serve to activate HSL as well.

Another example of the synergistic work of glucagon and epinephrine is in glycogen breakdown (FA2020 p85). Both will trigger cAMP increase and protein kinase A activation which will phosphorylate glycogen phosphporylase and activate it (FAST PHOSPHORYLATE! Hormone sensitive lipase is actually phsophorylated to activate it as well).

FUN FACT: Hormone sensitive lipase actually got its name because it was sensitive to epinephrine!

flapjacks  In Type 1 DM, the glucagon response to hypoglycemia is not functional and these individuals are reliant on the epinephrine-stimulated hepatic glycogenolysis. I recall this by remembering you can administer glucagon to these patients if they're having a hypoglycemic episode. They can respond to it, but they aren't releasing it. +1  
passplease  How did you eliminate thyroxine? As it also plays a role in lipolysis. I was thrown off my the low blood pressure and therefore did not select epinephrine. Why would they still have a low blood pressure? +  
jackie_chan  ^ they have low blood pressure because DKA causes a lot of dehydration (vomiting, diuresis due to osmotically active glucose in urine) so low BP Thyroxine I eliminated because remember that thyroxine is unique in that it functions similar to a steroid hormone and acts in the nucleus to upregulate expression of many genes. I figured hormone-sensitive lipase needs to be activated, not stimulated to upregulate expression, so I thought about EPI and beta-3 stimulation. fuckPeter +  
schep  I figured since he has low BP/dehydrated, his body would try to maintain cardiac output by increasing sympathetic tone (releasing epinephrine). In hypovolemic shock, systemic vascular resistance is up because of this compensation. +  
j44n  also thyroxine works like a steroid hormone meaning it takes a while to cause its effect +  
flvent2120  That'd be cool if it were called "epinephrine sensitive lipase" +  

submitted by enbeemee(13),
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i tge hwy s'ti lfgneal,il btu is het cpscfeii ronase htta LSP si rnowg si aceebsu 'ist ustj tno who teh vacneci is ?dema SPL olwdu alos ilcite an mmuien ,einrtaoc ?hgtir

nor16  Lipid A of LPS can be sensed by CD14 of macrophages causing shock, its not a protein, so no immune reaction as in vaccination (humoral, IgG class switch via Th2 and B Cells). +3  
eclipse  actually they do use LPS as adjuvant in vaccines +1  
eclipse  actually they do use LPS as adjuvant in vaccines +2  
hyperfukus  TLRs recognize common motifs called pathogen-associated molecular pattern (PAMP) in bacteria, fungi, viruses, and other pathogens. TLR signaling in the modulation of innate immunity + adaptive immunity against pathogens, TLR agonists: CpG-DNA, flagellin, and lipid became essential candidates of effective+safe vaccine adjuvants. TLR agonists improve the efficacy of vaccine, reducing TCR-based selection thresholds and enhancing the magnitude and quality of memory T-cell response. +2  
hyperfukus  some extra info in case they ask another annoying q +3  
aturner713  Not sure if this matters for this or not, but Neisseria spp. have lipoOLIGOsaccharide (LOS) and not lipoPOLYsaccharide (LPS) +3  
schep  I don't understand why LPS couldn't be the answer also. UWorld question ID 45 specifically says that they are using LPS as a conjugate +  
jp1003  I think it's because Neisseria does have LPS. They have LOS instead. +1  
jp1003  *does not have LPS +1  

submitted by peridot(68),

I am for some reason learning about this for the first time so I'll write a bit about euthyroid sick syndrome in case it helps someone.

It's a disease of exclusion - the thyroid hormones are whack but the thyroid gland itself seems to be totally fine. Specifically, T3 levels are low, rT3 is high (the activity of different deiodinases are off, so rT3 is made more and degraded less, though it doesn't seem like the rT3 level has any other clinical implications). As the other comments have mentioned, TSH and T4 are typically normal, although they can be decreased as well in severe cases.

Euthyroid sick syndrome is typically due to an underlying critical illness or starvation - the body stops making the hormones as an extreme measure to save energy and resources. The treatment is to treat the underlying illness; thyroid hormone therapy is not recommended as its effectiveness is inconclusive.

In this question stem, the patient has an underlying illness. Her thyroid gland works fine (responds appropriately to TSH). Classic case of euthyroid sick syndrome.

Given that her T4 levels are normal, we can rule out B, D, and E. I'm a dumdum and put C because I had no idea what euthyroid sick syndrome was. But given that her TSH level is also normal, it's not an issue with the hypothalamus or pituitary gland.

(Sources: wiki page and this article)

schep  Thanks! I, too, am hearing about this for the first time +  

submitted by usmleuser007(397),
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alIlf eels al:isf tnoe atth ohter awenrs cehcsio are CODP pesyt

dragon3  (except sarcoidosis) +2  
leaf_house  I got hung up on why this couldn't be sarcoid, and I think no lymphadenopathy is one of the reasons you wouldn't pick it here. (Though it seems like it can cause alveolar septal thickening: +  
lovebug  Restrictive VS Obstructive ! very good point! THX! +  
schep  if it were sarcoid, wouldn't the biopsy show noncaseating granulomas? +1  

So I must have misunderstood - the arcuate arteries are in the cortex which is why I picked cortex - but we're saying the renin will always be highest in the cortex? - p. 564 FA

schep  This was my thinking, too. I didn't think about JG cells or where renal corpuscles are. I picked which part of the kidney is perfused by arcuate artery. I get jittery when I get these questions right for the wrong reason... +1  

Why is this VSD? Is it just because she is 3 years old? I was stuck between MVP, VSD.

schep  I picked VSD because of the description of the murmur-loud, harsh, holosystolic, radiates over precordium and palpable thrill at left sternal border (I think because high pressure blood is moving from LV-->RV so you can feel a thrill) MVP is late systolic, crescendo murmur with midsystolic click +1  
castlblack  rule out all diastolic murmurs including -aortic regurg, -mitral stenosis, -PDA (no sound in diastole so cant be continuous). Rule out all murmurs that are heard on A and M sites, -aortic stenosis, -mitral regurg. Coarctation of the aorta is heard between the scapula I read so rule that out too. Rule out crescendo decrescendo murmurs, because holosystolic murmurs are like they sound: the same throughout systole. -pulmonic stenosis, -atrial septal defect. (AS has already been ruled out) You are now left with tricuspid regurg and VSD. Use harsh, high pitched descriptors to pick VSD. Tricuspid is described as blowing just like mitral regurg. Tricuspid regurg is a close candidate because it is heard in the same place as VSD, can be due to congenital malformation e.g. ebstein anomaly. It is also seen in rheumatic fever and endocarditis, but no other symptoms are mentioned so this question is leaning toward congenital malformation. +