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Comments ...

 +0  (nbme18#8)

did anybody else second guess the heck out this answer just because he's got a pH of 7.2 and he's hanging out in an outpatient clinic? I haven't done my clinicals yet but it seems like this guy would be struggling..

myoclonictonicbionic  EXACTLY... 7.2 for 6 months without any drastic symptoms.. that doesn't sound right

 +1  (nbme20#35)

maybe I overthought this one, but doesn't she have free air in the bottom left? Or is that the bottom of the pleural space...

ibestalkinyo  That's probably the most inferior portion of the right lung

Subcomments ...

submitted by meningitis(273),

When standing up, the body normally activates sympathetic system to avoid orthostatic hypotension.

But since there is now an additive effect of the pheochromocytoma adrenergics, it will lead to a hypertension

(i.e: Double vasoconstriction = Pheo adrenergics + Sympathetic system)

sympathetikey  Brilliant. +2  
medschul  Would pheo have a normal resting BP though? +1  
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 +  
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. +5  
meningitis  Thank you @nala_ula for your contribution! Really filled in the gap Iwas missing. +1  
nala_ula  No problem! Thank you for all your contributions throughout this page! +1  
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. +  
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. +  
sammyj98  UpToDate: Approximately one-half have paroxysmal hypertension; most of the rest have either primary hypertension (formerly called "essential" hypertension) or normal blood pressure. +  

submitted by mrglass(7),

Why would this not be acute transplant rejection leading to ARDS? The creatinine is elevated, and I see any reason why it would be elevated beyond rejection

sammyj98  I selected the same. I think part of the question wanted us to recognize that the pt was not receiving CMV prophylaxis (hinted that they are getting TMP-SMX but no Gancyclovir) so they're at really high risk for CMV specifically. UpToDate: •Universal prophylaxis with valganciclovir or ganciclovir is typically given to patients at risk for cytomegalovirus (CMV) reactivation (eg, seropositive recipients and those with seropositive donors). The duration of therapy often depends on the type of organ transplanted, the risk status of the patient, and individual institutional practice. Some transplant centers prefer to use a pre-emptive approach (eg, routine CMV viral load monitoring within initiation of treatment when reactivation becomes evident) for specific patient populations. (See 'Cytomegalovirus' above.) +  

submitted by hayayah(620),

Also, you shouldn't be seeing end-organ damage or increased renin / kidney response with a previously healthy patient that just developed essential HTN. The body doesn't want to increase renin when it has HTN. However, if you have stenosis, the kidneys freak out because they're not getting enough flow and think the whole body isn't either, so they activate the RAAS system. When you give them an ACE-I, the renin is still being produced by the kidney, it just isn't being converted to angiotensin-II.

To eliminate other choices:

  • He has increased renin activity so you can eliminate primary aldosteronism. That has inc. aldosterone, dec. renin.
  • No signs or sxs of Cushing's so that's eliminated.
  • 11-B-hydroxylase deficiency would sxs with the genitalia. You'd have dec. renin activity (aldosterone-like effects still present).
  • Essential HTN: explained above
sammyj98  I like you sticking up for the kidneys, thinking they're increasing Renin for the benefit of the whole body, but lets face it, the kidneys are a couple selfish dicks who want the high blood pressure all for themselves. LeftVentricularSolidarity +  

submitted by drdoom(375),

This is an interesting one. I like to remember it this way: in people with narcolepsy, all the “right kinds” of sleep are happening at all the “wrong times” of day. During the day, when a power nap would typically throw you immediately into REM, this kid is only entering Stage 1 or 2 (lightest sleep = slightest noises jar him back to reality). At night, when he should peacefully drift into Stage 1, 2, and so on, he instead completely zonks out. Classic narcolepsy.

From UpToDate: “Narcolepsy can be conceptualized as a disorder of sleep-wake control in which elements of sleep intrude into wakefulness and elements of wakefulness intrude into sleep.”

chextra  Isn't REM a rather light sleep stage? Brain waves during REM are very similar to awake states. I think you even wake up briefly in the middle of REM sleep. I don't think FA gave me a great understanding of narcolepsy, but I see it as going from awake to REM (light) for any kind of sleep, daytime or night time. +  
sammyj98  I'm definitely not ace on this subject, but I think the brain waves present in REM are similar to wakefulness because of the dreaming component. I think of it as though the brain has to go through a process of hypnotizing the body into a state of relaxation, and then properly paralyzing it, and then it can simulate wakefulness (dreaming) to go through with it's defragging of the hard drive. So REM is actually the deepest sleep because the body is fully paralyzed. Please someone correct me, this is probably an inacurrate perspective. +1  
pg32  FA says that narcolepsy has nocturnal AND NARCOLEPTIC sleep episodes that start with REM sleep... So is @drdoom correct? FA seems to disagree regarding the daytime sleep pattern. +  

submitted by sugaplum(128),

phenylpropanolamine is an alpha agonist that stimulates urethral smooth muscle contraction. - from uptodate, however, it also says it is not recommended treatment anymore

ugalaxy  α1 stimulation (via α1 agonist) constricts the bladder sphincter thereby, preventing sudden bouts of micturition during coughing/sneezing (abdominal stress). +5  
sammyj98  I thought that B3 stimulation stopped urination +5  
adong  @sammyj98 B3 would facilitate bladder relaxation +  
hvancampen  @sammyj98- were you thinking of oxybutynin? (thats what I thought of!) According to FA, its used for urge incontinence not stress. +  
drzed  Nah he/she's talking about Beta-3 receptors which are Gs coupled. Gs increases cAMP thus it would cause smooth muscle relaxation -> bladder relaxation! +  
donttrustmyanswers  From Mayo: "There are no approved medications to specifically treat stress incontinence in the United States. The antidepressant duloxetine (Cymbalta) is used for the treatment of stress incontinence in Europe, however." +1  

submitted by momof21234(3),

the patient has asbestos which is restrictive (clue was pleural plaques) DLCO is decreased in intra-thoracic conditions (interstitial lung dz etc) and normal on extra-thoracic conditions (muscular issues)

usmlecharserssss  how FEV1/FVC is normal i cannot get that +1  
sammyj98  I think this is standard for restrictive lung diseases. In obstructive the airways collapse during expiration so it's hard to expire, but there's a long drawn out end to epiration as little by little it escapes, leading to a decreased FEV1/FVC. In restrictive pt's just aren't able to move and expand their lungs enough, so when they expire it's of a small volume, but there isn't any collapse involved. It's like a normal expiration just with a restricted volume, making the FEV1/FVC normal. +  
spow  @usmlecharserssss In restrictive lung diseases, the ratio is either normal or increased. +  
drzed  And the reason why FEV1/FVC is either normal or increased in restrictive lung disease is very simple: the FEV1 and FVC both decrease because you are restricting airflow, but the FVC will decrease MORE than the FEV1, and thus because the denominator is larger, the fraction either stays normal, or increases slightly Contrast this to obstructive lung disease where you have an obstruction to air FLOW, e.g. the FEV1 will decrease more than the FVC, leading to a low ratio by defition +1  
llamastep1  To add to what @drzed said, fibrosis causes radial traction on the airways therefore increasing FEV1/FVC. Theres a Uworld q on it +