Welcome to notyasupremeโs page.
Contributor score: 48
Comments ...
notyasupreme
lol jk, just looked it up and apparently I know shit about the female anatomy!
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abelaia
probably classic overthink. likely to do with the type of blood culture grown. Staph vs. E. coli.
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notyasupreme
Lol, never mind I realize, it's a scar and that's type III collagen!
+6
i_hate_it_here
It is also the disulfide bonds that add to tensile strength of collagen, while the inter-chain fibril cross-linking that leads to elastins elasticity FA2020 pg: 51&52
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xw1984
I think the Q emphasized postoperatiive. Maybe the production of elastin does not increase much comparing to collagen.
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topgunber
i think they would refer to elastin in cases of arteriolar compliance
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nbmeanswersownersucks
I think it's more because a spontaneous microdeletion would not really explain the previous lost pregnancies whereas an unbalanced translocation in the mom could. And I think it could be any of the big trisomies (13, 18, 21) but 21 is most common.
+5
m0niagui
so, it is the mother that has Down's Sd?
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jj375
No, the mother doesnt have down syndrome. As far as I know, the mother has a BALANCED translocation - for example (totally made the chromosome # up) she may have a piece of chrom 11 and chrom 4 swap places. However they are balanced since they are both there, no genetic material is missing os she looks healthy and is fine. BUT when her eggs are made, some eggs may get the chrom 11 (+ piece of chrom 4) and then her regular copy of chrom 4...Now that baby also gets a chromosome 4 from the dad. The baby will end up with 3 copies of part of chrom 4 but 1 part of chrom 11! So the kid is unbalanced and may die in utero (spontaneous abortions). I hope that was clear Here is a photo that may help: https://accessmedicine.mhmedical.com/data/books/hoff2/hoff2_c006f005.png
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chaosawaits
I think the point is that no matter which disease you think it is, whether trisomy 13, 18, 21 or even Turner syndrome, in all those genetic disorders, the most common cause is an unbalanced chromosome rearrangement. I don't think you're actually supposed to know the disease.
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an1
@chaosawaits The MCC is not actually unbalanced chromosomes (robertsonian ~ 4%). the most common is nondisjunction (~95%). also a point from UW was that robertsonian defects will often have a family hx of recurrent miscarriages. we don't have a fam hx of this woman but she herself has a hx which could also help us diagnose. and secondly, gonadal mosaicism could have been ruled out easily because gonadal is fatal, only somatic can result in survival!
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Subcomments ...
tinylilron
so PE was on my differential... why do we immediately jump to pleurisy???
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etherbunny
...and if aspirin doesn't work, what are the chances of ibuprofen doing much better?
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len49
Stone cold normal vital signs and recent viral infxn symptoms points significantly towards viral pleurisy. Aspirin did relieve the symptoms a bit as well. She gets zero points on the Well's criteria, not sure why PE would be super high on someone's differential.
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dnazmzm
What is "splinting"....?
+1
lilmonkey
Respiratory splinting is defined as reduced inspiratory effort as a result of sharp pain upon inspiration (severe pleuritic chest pain).
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charcot_bouchard
Post viral pericardial effusion should be on someone differential!!
I pick EKG.
+1
charcot_bouchard
even in amboss says do a EKG to rule out other cause like peri effusion
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charcot_bouchard
Replace all pericardial effusion with Pericarditis. Thats what was in my head
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charcot_bouchard
Ok. i got my answer.
sx is unilateral. if it was pericardial shit would be in middle
on cardiac exam no abnormalities. pericarditis would have scracthing sounds
chest xray showed no abnormalities than means no pleural effusion either if it was in someones mind.
+1
notyasupreme
^^ i guess that makes sense but this q makes me mad
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notyasupreme
lol jk, just looked it up and apparently I know shit about the female anatomy!
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szsnikaa
Brain abscesses are secondary to septic emboli via hematogenous spread. Edema often forms around these abscesses leading to a mass effect (+ Babinski & Mild Hemiparesis on the left).
+10
kingfriday
Guy has a valve replacement -> he then has a new murmur, fever, and FND - he probably has endocarditis due to staph epidermidis.
Carotid artery occlusion wouldn't cause more issues (i think vision in particular would be included) in addition to more severe deficits. There would also be no fever.
Venous sinus thrombosis would also not present with fever and also probably include vision problems
Encephalitis would probably present with AMS and seizures - may or may not be nuchal rigidity
Hydrocephalus: wet wacky wobbly- not seen here
+5
tinylilron
So the brain abscess would be due to staph epidermis rather than strep pyogenes, right?
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notyasupreme
^^ yeah, pretty sure I read on Anki that it's usually S aureus initially that commonly causes it, then becomes epidermitis
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notyasupreme
Tbh, I don't think he has dysthymia lol. I think he has some form of somatic symptom disorder or some Munchausen ass shit. First of all, why does he have a massive binder full of records about vague medical complaints? Sorry I curse so much, I'm from NY
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lubdub
Yea, this one made me think more than I'd hope lactose intolerance would have.
If the lactose can't be broken down (by the lactase in the brush boarder) then it stays in the lumen (malabsorption) letting all the gut bugs digest it (make gas) and allowing for osmotic diarrhea. Osmotic =/= secretory
+5
jlbae
Ah ok, ty. That makes sense. It's kinda coming back to me from M2 GI lectures now lol. So then an example of secretory would be a viral gastroenteritis where electrolytes are being actively secreted into the GI lumen.
+1
notyasupreme
I think of secretory diarrhea like secreting alllll the time, so they have to shit in the night time too.. as opposed to lactose which is osmotic diarrhea, with some acidic ass bullshit going on in the bowels. Anyways, if you're too pedantic on this question, you may get it wrong
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jlbae
They might refer to MGP as "relative afferent pupil defect" on the NMBE
+1
lindasmith462
is there anything differentiating this from acute angle closure glaucoma? She's a little young for ACG but a little old for MS. both would present w/ sudden painful vision loss and a pupil poorly responsive to light. (answer is still optic nerve though)
+1
notyasupreme
^^ Probably would have had vomiting, nausea, and other factors that suggest that it's angle closure glaucoma.. +mid-dilated pupil
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notyasupreme
I wish they would just give the BMIs, nobody got time to be deciding if she's obese
+1
saffronshawty
OHHH wait, is there secondary hyperaldosteronism due to the renal artery stenosis? that explains things..
+2
adong
yea elevated renin
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notyasupreme
I think it's because of the location.. I was between those two choices, but figured one said the adrenal veins, when this is 2/2 renovascular stenosis
+1
madojo
He's not really symptomatic "mild nonproductive cough but is otherwise feeling." Why wouldnt you give demeclocycline to treat the SIADH.
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notyasupreme
@madojo, I agree.. I put the same answer as you, but I guess fluid restriction is the FIRST line treatment of all.. Lol, these Anki that give you all three (+conivaptan) never tell you which is the right one in these cases.
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beans123
demeclocycline is neurotoxic, UW says only to use it if salt tablets and fluid restriction fail
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osler_weber_rendu
What about the insufficient sample size? 40 patients per group seems low
+1
notyasupreme
Lol, for some reason I read it as the same physician evaluating, but then I re-read it after reviewing and I realized I have no comprehension skills hahahaha
+2
notyasupreme
Agreed! This is worded so badly, and is so classic NBME! I guess it couldn't have been the others because increase in peripheral vascular resistance isn't technically counted as the aorta.
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welpdedelp
Same lol. A question I had was I thought lymphangitis was supposed to precede some sort of injury, obv not lol but was the lymph node the main giveaway?
+1
keyseph
I think the key distinguishing features are the red streaks leading to an area of local lymphadenopathy. Otherwise, cellulitis would be a viable option if given.
+6
notyasupreme
I thought lymphangitis is seen more with erysipelas
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lm4
or prior treatment with radiation caused fibrosis of pericardium --> constrictive pericarditis --> cardiac tamponade
+5
notyasupreme
Doesn't tamponade not cause pulmonary edema / crackles since it's usually right sided heart failure? I picked it anyways, but remember a UWorld question about that vs. AR
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alimd
did you pay fucking $30?
+2
cheesetouch
some institutions give students UpToDate access
+6
cbreland
I knew that misoprostol (PGE1) can be used for abortions by forcing uterine contractions, so I figured the answer had something to do with prostaglandins
+11
rthavranek
I knew prostaglandins increased uterine contraction, but I also thought PGE2 caused cervical ripening and since there was a closed cervix, I eliminated that choice. I had no idea what was going on so I just picked oxytocin since that would increase uterine tone without dilation, though my reasoning seems to be incorrect
+2
utap2001
Great, the above message deserve $30.
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notyasupreme
I think also it said that the fetus releases oxytocin and steroids, which I guess is stupid wording that makes it not right. Anyways, fuck the curve on NBME 18 :)
+4
okokok1
if anyone didn't know what "PPROM" stood for it is: Preterm Premature Rupture Of Membranes"
+4
aakb
I was between the prostaglandin answer and stressed fetal production and release of oxytocin and the reason I didn't pick oxytocin was if the cervical os is closed (membranes ruptured 32 hrs ago and contractions been going on for 12) and there's no effacement, it didn't seem like that baby actually wanted to come out so I thought that's not what's happening here. Plus mom has a fever so inflamed maternal decidua seemed to fit.
+2
helppls
If there was an increase in Pgs why did she not have a ripened cervix?
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leemax
read it again guys-option E-stressed fetal production and release of OXYTOCIN.
good nbme,got me there!
+1
gabriellerenai
I think a key thing is that oxytocin is never the primary initiator of labor even in full term labor (it mainly controls Phase 3 and 4): via up to date - "It is unlikely that oxytocin provides the trigger for the initiation of labor, but the release of oxytocin during labor results in more forceful uterine contractions and undoubtedly facilitates delivery of the fetus and placenta."
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epiglotitties
@leemax doesn't the fetus produce oxytocin? and its clearly stressed, a fetal heart rate of 210 is high isnt it? Still don't get why that couldnt be the answer..
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fatboyslim
I got this wrong and chose oxytocin. But now I recall a UW question saying oxytocin receptors on the uterus don't play much of a role in uterine contractions until about the late 3rd trimester. This fetus is 27 weeks gestation.
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underd0g
Why can't the answer be plasma cell infiltration?
+2
notyasupreme
@underd0g I put that too, but I think if you look at the histo picture, it literally shows all the eosinophilic looking bullshit from amyloidosis, and it was specifically asking the cardiac symptoms. The cause of MM is plasma cell, but the cause of the cardiac is the primary amyloid deposition = restricitive cardiomyopathy
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trishasingh
In multiple myeloma there is overproduction of immunoglobulin light chain that causes majority of the symptoms, like bence jones proteins in the urine and infiltration of organs like the kidneys and the heart. It causes diastolic dysfunction of the heart. Other infiltrative diseases, like haemochromatosis and sarcoidosis also cause diastolic dysfunction of the heart.
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ih8payingfordis
This is a case of primary amyloidosis from deposition of Ig Light chains (AL). FA 2019 pg 212
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cienfuegos
I think this is it
-pulmonary fibrosis increases elastic recoiland widens airway 2/2 increased outward force (radial traction) by fibrotic tissue thus decreasing airflow resistance thus supernormal expiratory flow rates (higher than nl following correction for lung volume)
+4
notyasupreme
^ Why do I feel like this is literally not english, I have no clue what's being said here. Can someone else explain it?
+2
skonys
Radial Traction is basically the force that the surrounding scaffold of the lung parenchyma exerts on a brochial tube to keep it patent when youre breathing.
In restrictive lung disease (interstitial pulmonary fibrosis) youre adding more fibrous scaffolding around the tube which keeps BIG open. These patients have a greater than FEV1 than you would think. They are taking in less air into their restricted lungs but that lung tissue has a much hhigher elastic recoil so what air they bring in is forced out through patent brochioles that are held open.
In some obstructive lung diseases like emphasema, you have elastases tearing up the scaffolding holding the tubes open and these tubes naturally want to collapse so they do. They have less "traction" force radially around the tube holding it open so air is trapped.
+2
yotsubato
I think that this question is phrased atrociously,
Just like the rest of the NBME
+26
b1ackcoffee
exactly how does maternal hashimoto can cause cretinism?
+1
notyasupreme
@b1ackcoffee, it's not maternal hashimoto, basically you just have to disregard the ENTIRE question stem and the last part of the sentence (if the mom's TSH goes up) means that there's hypothyroidism going on, which causes cretinism.
+5
medschul
Would pheo have a normal resting BP though?
+16
meningitis
I was trying to justify these tricky questions but very true medschul.. It shouldn't have normal resting BP. Sometimes it seems these NBME always have a trick up their sleeve. Im getting paranoid lol
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nala_ula
The reason why the patient probably has normal HTN is because Pheochromocytoma has symptoms that occurs in "spells" - they come and go. Apparently in that moment, when the physician is examining her, she doesn't have the HTN, but like @meningitis explained, so many adrenergic hormones around leads to double the vasoconstriction when the patient stands up.
+10
meningitis
Thank you @nala_ula for your contribution! Really filled in the gap Iwas missing.
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nala_ula
No problem! Thank you for all your contributions throughout this page!
+2
mjmejora
I thought the pheochromocytoma was getting squeezed during sitting and releasing the epinephrine then. kinda like how it can happen during manipulation during surgery. Got it right for sorta wrong reasons then oh well.
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llamastep1
When she sits in the examination table there would be a normal activation of the sympathetic system from the stress of getting examined which is amplified by the pheo. Cheers.
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sammyj98
UpToDate: Approximately one-half have paroxysmal hypertension; most of the rest have either primary hypertension (formerly called "essential" hypertension) or normal blood pressure.
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notyasupreme
Damn llama, that is WAYYY too much of an inference. Maybe if they said she was nervous in general or something, but not everyone gets stressed out by a doctor hahaha
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jakelong377
Itโs not about being stressed infront of doctor. When u stand sympathetics activate to prevent orthostatic hypotension, to counter it adrenal medulla released catecholamines so much so that pheochromocytoma patients would appears with flushed skin n such
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notyasupreme
I thought from the 5 Ps of pheochromocytoma, Pallor was one of them? That's what threw me off from keeping it the same.. Or atleast the anking deck says pallor.
+1
saqeer
the way i understand it the pallor is because of the sever vasoconstriction during an episode of catcholamine release but in general anything leading to polycythemia can lead to flushing
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lee280
For some reason, I had two answers that I felt like both made absolute sense to me. As explained above, that totally came to my mind and I knew this was the case. When I thought about Metoprolol blocking B1 receptors in a patient with an ejection fraction of only 30%, I was thinking this could as well be a contraindication, not sure if it's an absolute one or relative. Now, am I right if I said that Beta-blockers are only contraindicated in acute decompensated HF? and can be used unless otherwise? Someone, please help me clarify this, so then this distinction can come clean in my thoughts. Thanks
+2
notyasupreme
I thought the same thing as you, I think we're just overthinking the most important thing - never give antihypertensive with Viagra lmfao. I totally thought too deep into it.
+4
topgunber
sildenafil does make sense, especially since hes on 2 vasodilators. I picked diltiazem because the pt has systolic heart failure. thought it was contra indicated to give CCB to systolic heart failure because you could further decrease contractility. Either way never give NTG and viagra
+1
sexymexican888
Yeah @topgunber I also picked diltiazem.... I guess they were looking for "COMBINATION" rather than a specific contraindication
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pakimd
@lee280 you are right in saying that beta blockers are only contraindicated in acute decompensated heart failure. this is because beta blockers, which would normally prevent the deleterious effects of neurohormones like norepinephrine on cardiac remodeling that occurs in HFrEF, will further impair cardiac output in decompensation. hope this helps :)
+1
leap1608
The answer to all your queries lies in the fact that a combination of Metoprolol and vasodilators would actually be beneficial in dampening the REFLEX TACHYCARDIC effect of nitrates, hydralazines etc. Hence, decreasing the work load on the heart.
+1
notyasupreme
I guess I wasn't sure because it said FSH and LH levels were normal, so I assumed the problem was with progesterone. But I thought too deep into it and should've just went with my gut.
+2
feochromocytoma
Clopmiphene is usually the answer for infertility with NORMAL anatomy and NORMAL appearing labs
+4
sexymexican888
Yeah I made the same mistake by choosing progesterone BUT they are used for contraception (pill, IUD etc) and for the PROGESTIN challenge EXCLUDES (if +withdrawl bleed its hormonal PCOS etc) uterine bleeding due to anatomic defects (which will have no withdrawal bleeding i.e asherman)
so as far I know its not used as fertility treatment
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notyasupreme
Lol, never mind I realize, it's a scar and that's type III collagen!
+6
i_hate_it_here
It is also the disulfide bonds that add to tensile strength of collagen, while the inter-chain fibril cross-linking that leads to elastins elasticity FA2020 pg: 51&52
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xw1984
I think the Q emphasized postoperatiive. Maybe the production of elastin does not increase much comparing to collagen.
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topgunber
i think they would refer to elastin in cases of arteriolar compliance
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lee280
I agree, at the start, I got a bit confused because I felt like the question was probably less specific than it would have been, but NBME being NBME this is really expected. When you think about it more closely, once you consume the meal then ghrelin will peak and start dropping.
+21
notyasupreme
I agree, I had B at first but then thought too deep into it. I thought if she ATE a meal, she'd be full and low ghrelin. Annoying to get a question wrong on something so simple.
+2
radzio1
Also got this question wrong. A really bad explanation what they want from the curve...
+1
shieldmaiden
Basically she is eating at peak ghrelin (B) its drops, then she likely eats a snack on E
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bboucher
They ask what point ''represent the consumption of a meal'' by mean there is no reason you're ghrelin would start dropping before you even started eating (point C which is I guess the other you might have guess) in contrast to B where it follows a natural physiologic cycle where it increase because you get hungry --> You eat because you're hungry --> Abdominal distention due to the food start decreasing ghrelin.
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ali_hassan
I get it now, but when I was doing the test it made absolutely no sense, I was stuck between B - C - D. Word your questions better NBME!
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chaosawaits
I'm reading the question now and I still think "the consumption of a meal" means that the meal has been consumed. I feel like this is really a black & blue dress and once again, I'm not in on the joke.
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chaosawaits
I think the question is actually worded properly because of the lag before ghrelin is released. As you consume the meal, ghrelin release slows down, such that the peak arises by the end of the meal. Therefore B is the right choice because at the end of consumption of the meal is the peak of amount of ghrelin. It's not like as soon as you take a bite of cream of wheat, the ghrelin levels immediately shoot down. Maybe?
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motherhen
Why does albumin solution not have this effect?
+3
notyasupreme
I think it's because albumin in saline is hypertonic, which would cause the opposite effect of what the experiment was going for. Fluid would go across the capillaries into the vasculature, rather than vice versa.
+4
notyasupreme
Ask me why I thought this was Friedreich Ataxia and not CMT fml lol
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fatboyslim
@notyasupreme because Friedreich's has hammer toes?
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notyasupreme
It's actually funny because the question stem makes it seem like it's an MCAD deficiency (presence of dicarboxylic acid) and all the symptoms, but then treat it with MCAD. Whatever, I got it right but it just felt like a weird question to me.
+4
nbmeanswersownersucks
yeah I was confused too but I also think the negative serum carnitine is supposed to help r/o MCAD deficiency since that usually has elevated serum carnitine.
+1
baja_blast
If Carnitine was an option here, how could we differentiate this from primary carnitine deficiency? Would it have been possible?
+11
melanoma
the presence of dicarboxylic aciduria is more related to mcad/lcad deficiency. the patient receives medium chain tryglicerides because he has the enzyme to metabolize it.
+10
topgunber
just a few things, sure it sounds like mcad but lcad would present similarly, except in MCAD, giving medium chain triglycerides would worsen symptoms as compared with LCAD. + Similarly when fatty acids cant undergo Beta oxidation they undergo omega oxidation- which is why there is increased dicarboxlic acids (i.e. dont just jump for MCAD when you see dicarboxilic acids). Last of all it would be difficult to differentiate but if the patient were deficient in carnitine the treatment with MCADs would not show improvement because carnitine is required to shuttle the fatty acid into the MTs.
+2
topgunber
'a 'weird question' because my school never asked it'
+1
sexymexican888
According to UWORLD: Primary carnitine deficiency elevated muscle triglycerides. MCAD, will not
+2
This is hilarious, did anyone else think it could be viral pericarditis, which in another question required prompt evaluation with an echo. I initially thought EKG, then echo, then NSAIDs as the order. Apparently, we just skip the diagnosis and go straight to NSAIDs in these patients now. Unbelievable.