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 +0  (nbme24#27)

I just want to mention that kids squatting is very much suggesting a TOF in USMLE..lol. And her pulmonary murmur suggests pulmonary stenosis, which further supports TOF.


 +1  (nbme22#38)

Guys I have another thought.

Giving other choices are about his other abnormal values (increased creatine, glucose, uric acid), I guess the question is testing us which of these values will improve if his OSA is improved by CPAP.

Since OSA is one of the most important causes of idiopathic hypertension, it should come to us that once his OSA is treated, his hypertension will improve soon.

So "decreased BP" instead of other abnormal values.

(Thanks to my friends for hinting me about this!)





Subcomments ...

submitted by lsmarshall(262),

"The exact mechanism for tremor induction by β(2)-adrenergic agonists is still unknown, but there is some evidence that β(2)-adrenergic agonists act directly on muscle... More recently, tremor has been correlated closely with hypokalaemia." - NIH publication

First Aid mentions hyperthyroidism causing tremor from β-adrenergic stimulation. It also mentions β2-agonists causing tremor as a side effect. First Aid also mentions β2-agonists driving potassium into cells, which may contribute to tremor. That said, more classic symptoms of hypokalemia are wide QRS and peaked T waves on ECG, arrhythmias, and muscle weakness.

Looking around on the internet looks like if therapy is continued the tremor from a β2-agonists resolves overtime.

xxabi  Sketchy mentions tremor and arrhythmia as side effects! +1  
drpatinoire  Hypokalemia is more associated with U waves, flattened T, muscle cramps/spasm, those symptoms you mentioned is more typical in hyperkalemia. (I guess you made a typo..?) +  


submitted by vshummy(81),

So the best i could find was in First Aid 2019 pg 346 under Diabetic Ketoacidosis. The hyperglycemia and hyperkalemia cause an osmotic diuresis so the entire body gets depleted of fluids. Hence why part of the treatment for DKA is IV fluids. You might even rely on that piece of information alone to answer this question, that DKA is treated with IV fluids.

fulminant_life  I just dont understand how that is the cause of his altered state of consciousness. Why wouldnt altered affinity of oxygen from HbA1c be correct? A1C has a higher affinity for oxygen so wouldnt that be a better reason for him being unconscious? +4  
toupvote  HbA1c is more of a chronic process. It is a snapshot of three months. Also, people can have elevated A1c without much impact on their mental status. Other organs are affected sooner and to a greater degree than the brain. DKA is an acute issue. +1  
snafull  Can somebody please explain why 'Inability of neurons to perform glycolysis' is wrong? +3  
johnson  Probably because they're sustained on ketones. +1  
doodimoodi  @snafull glucose is very high in the blood, why would neurons not be able to use it? +1  
soph  @snafull maybe u are confusing bc DK tissues are unable to use the high glucose as it is unable to enter cells but I dont think thats the case in the neurons? +1  
drmomo  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909073/ states its primarily due to acidosis along wth hyperosmolarity. so most relevant answer here would be dehydration +  
drmohandes  I thought the high amount of glucose in the blood (osmotic pressure), sucks out the water from the cells. But you also pee out all that glucose and water goes with it. That's why you have to drink and pee a lot.. +3  
titanesxvi  Neurons are not dependent on insulin, so they are not affected by utilization of glucose (only GLUT4 receptors in the muscle and adipose tissue are insulin dependent) +5  
drpatinoire  @titanesxvi You really enlightened me! +  


submitted by neonem(364),

this patient has symptomatic aortic stenosis. This can be identified by the ventricular hypertrophy (to compensate for increased functional afterload from non-compliant aortic valve), midsystolic murmur and the location at the normal aortic area.

Per UpToDate on Clinical manifestations of Aortic Stenosis:

"Dizziness and syncope — Syncope occurs as a presenting symptom in approximately 10 percent of patients with symptomatic severe AS (or approximately 3 percent of all patients with severe AS) [3]. There are several proposed explanations for exertional dizziness (presyncope) or syncope in patients with AS, both of which reflect decreased cerebral perfusion. Exercise-induced vasodilation in the presence of an obstruction with fixed cardiac output can result in hypotension."

guillo12  What does "fixed cardiac output" signify? +  
usmleuser007  "fixed cardiac output" might mean that with the stenosis (ie. narrowed aortic valve) there is a limited or rather reduced cardiac output. Exercise would not increase cardiac output because the stenosis is caused by a mechanical (physical) rather than a biochemical process. Therefore, At any given moment the heart can not increase its output no matter how forcefully it contracts. +1  
fallot4logy  why not option A?arterial compression ? +  
sunshinesweetheart  @fallot4logy LVH does not lead to coronary artery compression. only reallyyyy rarely will pulmonary artery dilation cause coronary artery compression. plus that would cause angina but probably wouldnt decrease cerebral bloodflow to syncope. her murmur + LVH point us toward aortic stenosis which does cause those --> fixed CO +  
drpatinoire  @fallot4logy LVH can cause coronary artery compression, but typically leading to coronary ischemia after exercise (i.e. stable angina in this patient). The question is asking what leads to her syncope. Syncope actually means her brain is lacking blood supply abruptly. +  
rainlad  how do we rule out mitral valve prolapse in this case? +  
spow  @rainlad murmurs at the right upper sternal border are aortic in nature. Mitral murmurs are heard at left 5th intercostal at the midaxillary line. +  


submitted by yobo13(0),

Can someone explain why it can't be Crohn's since that would also cause a non AGMA?

drpatinoire  If she has Crohn, she has already lost a lot of K, HCO3-, then the compensatory system wouldn't let her keep losing electrolytes in her urine. +  


submitted by zbird(3),

This patient has Distal-Type I RTA which is explained by Normal Serum Anion gap (8) Metabolic acidosis with her positive urinary anion gap(+5).

krewfoo99  Why would the urine Potassium be so high if it is type 1 ? Shouldnt it be type 2? +  
drpatinoire  @krewfoo99 I think it's RTA2 (Fanconi syndrome), he is losing all kinds of Na, K, Cl which should be reabsorbed in PCT. +  


submitted by medstruggle(10),

Why is it not ovarian follicle cells? I thought the female analog of Sertoli and Leydig is theca/granulosa cells.

colonelred_  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +3  
brethren_md  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +2  
sympathetikey  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +3  
s1q3t3  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +2  
masonkingcobra  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
mcl  Wait, but did anyone mention that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen??? +20  
mcl  But seriously though, pathology outlines says sertoli-leydig tumor "may be suspected clinically in a young patient presenting with a combination of virilization, elevated testosterone levels and ovarian / pelvic mass on imaging studies." As for follicle cell tumors, granulosa cell tumors usually occur in adults and would cause elevated levels of estrogens. Theca cell tumor would also primarily produce estrogens. Putting the links at the end since idk if they're gonna turn out right lol Link pathology outlines for sertoli leydig granulosa cell tumor theca cell tumor +7  
bigjimbo  LOL +  
fallenistand  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +3  
medpsychosis  So after doing some intense research, UPtoDate, PubMed, an intense literature review on the topic I have come to the final conclusion that...... ...... ...... ...... Wait for it.... ..... ..... Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +5  
charcot_bouchard  Hello, i just want to add that Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
giggidy  Hold up, so I'm confused - I read all the posts above but I still am unsure - are sertoli-leydig cells notorious for producing androgen? +2  
subclaviansteele  Hold the phone.....Females can get sertoli leydig cell tumors which are notorious for producing androgen? TIL TL;DR - Females can get sertoli leydig cell tumors = high androgens +  
cinnapie  I just found a recent study on PubMed saying "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen" +1  
youssefa  Hahahahaha ya'll just bored +2  
water  Bored? you wouldn't think so if you knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +3  
nbmehelp  I dont get it +  
redvelvet  how don't you get it that females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen? +1  
drmomo  what if this means..... females can get Sertoli Leydig cell tumors, which are notorious for producing lots of androgen +  
sunshinesweetheart  hahahaha this made my day #futurephysicians #lowkeyidiots +  
sunshinesweetheart  @medstruggle look up placental aromatase deficiency (p. 625 FA 2019), it would have a different presentation +  
deathbystep1  i am sure i would ace STEP 1 if i only knew that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +1  
noplanb  Wait... I might actually never forget this now lol +1  
drmohandes  Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen. +1  
lilmonkey  Don't forget that females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens! You're welcome! +  
drpatinoire  Now I get it that females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens. Thank you very much.. So why choose Sertoli-Leydig cell tumor again? +  
dr_ligma  The reason is because females can get Sertoli-Leydig cell tumors, which are notorious for producing lots of androgens! This is easy to remember, as you can remember it through the simple mnemonic "FCGSLCTWANFPLOA" which stands for "Females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen!" +8  
minion7  after receiving a f*king score..... this post made me smile and thanks to the statement-- females can get sertoli-leydig cell tumours, which are notorious for producing lots of androgen! +  
djtallahassee  My worthless self put adrenal zona fasciculate but now I will never forget that females can get sertoli-leydig cell tumors, which are notorious for producing lots of androgen +  
medguru2295  Wait..... so can females get Sertoli Leydig cells that produce androgens then?????? +  


submitted by pg32(37),

The fact that the odds ratio in the top left is incorrect makes this question very difficult. It makes it appear as if the cookies are causative but the milk had some protective factor. So obnoxious.

drpatinoire  God I thought totally the same way as you did. I stared at this question for at least 5min and asked myself what's wrong with my statistics. +  


submitted by seagull(706),

A- primary motor cortex = wrong side of body (deficit of UMN on left side body)

B - Thalamus = sensory information conduit - motor deficits unlikely to originate from here

C - Pons - CNs 8,7,6,5, likely result in "locked in syndrome" or complete loss of motor function on right side + facial features.

D. Vermis - central body coordination. Damage results in ataxia

Not complete but maybe helpful..

yotsubato  C - Pons - CNs 8,7,6,5, likely result in "locked in syndrome" or complete loss of motor function on LEFT side + RIGHT sided facial features. Decussation occurs in medulla +1  
kard  Sorry if im mistaken, Isnt A) Somatosensory? +1  
krewfoo99  Yes i think A should be somatosensory. Primary motor cortex would be present in the precentral gyrus +  
drpatinoire  A is primary motor. A and the gyrus at right side of A compose the paracentral lobule. +  


submitted by madojo(48),

Ugh when you do it in uworld, write it down but still miss it.

Anyway going over other answers (pathoma): Fibrocystic changes of the breast --> benign, usually no discharge with this and you will usually have a lumpy breast or something palpable and it is hormone mediated. Pagets disease of the breast --> extension of ductal carcinoma in situ to lactiferous ducts and skin of nipple producing rash, so you see skin changes. No skin changes mentionedh ere. Prolactinoma --> gallactorhea not blood tinged

So per UW intraductal papilloma is a proliferation of papillary cels in a cyst wall or duct that may cause focal atypia - IT IS THE MOST COMMON CAUSE OF BLOODY NIPPLE DISCHARGE AND BREASTS WITHOUT BREAST MASS OR SKIN CHANGES

compare this to papillary carcinoma where you also have nipple discharge but you would see it in a post menopausal women.

drpatinoire  Upvote it wishing I could memorize it lol +