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Comments ...

 +1  (nbme16#11)

You should be thinking of something like Enterococcus. They had a GU procedure and subsequent cardiac issues.

When I hear soft S1, i think that the patient must have had a issue with the closing of either the mitral or tricuspid valves. Playing odds, this should be the mitral valve. You also here an early diastolic murmur, so you might be thinking volume overload (S3).

 -1  (nbme23#33)

Best comment i read was to treat this like it's a VIPoma. You would get all three electrolyte/metabolic disturbances.


 +1  (nbme23#36)

Likely an inhibition of 21-hydroxylase. This is the most common of the congenital adrenal hyperplasias. Presents in infancy or childhood.

Another symptom they may have that I've seen around is vomiting!! Took me a while to find it, but they are salt wasting by having no aldosterone, so the loss of electrolytes is causing increased ICP.

 +2  (nbme23#42)

The question says they don't responds to antacids THEN asks which you to identify which drug is the most effective at suppressing acid production, NOT what the most effective antacid is. The answer is PPI's.

I will say, however, I was looking for something like octeotride.

drdoom  lucid. nice catch.
maddy1994  WHY not blockage of h2 receptors
krewfoo99  @maddy1994. PPI are more effective than H2 blockers in suppression of gastric acid

 -3  (nbme23#12)

FA 19, pg. 305 - May see Mitral regurgitation due to impaired mitral valve closure.

I always find it important to remember that once you get pathology somewhere in the heart, you can expect pathology everywhere behind it, over time.

So in this case you start with HCM -> Mitral regurg -> LA dilation -> A.fib -> LA/LV failure -> Pulm edema -> RHF -> etc.

It's always a matter of time.

mario  wrong q bro @ maxillarythirdmolar

 +4  (nbme21#50)

Lol uhhh also the scaphoid is literally fractured in the X-ray

 +1  (nbme21#39)

I'm sure it's related to the activating effect of Cortisol on phenylethanolamine-N-methyltransferase, converting NE to Epi. Sounds like a synergistic thing to me. (FA.83)

alexv0815  this was my thought too

 +0  (nbme20#25)

Where does the role of B1 stimulation of RAAS come into this? Wouldn't the B1 action cause decrease RAAS? That being said, I can also understand if that's a long term thing and this is a question about the immediate effects...?

Subcomments ...

submitted by usmleuser007(278),

Treat this like a VIPoma (Watery diarrhea, achlorhydria = reduced HCl in the lumen, & hypokalemia)

this will lead to metabolic acidosis d/t loss of bicarb in stool

btl_nyc  Chloride is increased though. +  
maxillarythirdmolar  This comment is gold. @btl_nyc, this is actually accute. you would expect hyperchloremia https://www.ncbi.nlm.nih.gov/books/NBK507698/ +  

submitted by usmleuser007(278),

PPI side-effects: + increased risk for C. diff + Increased risk for resp infections + can cause hypomagnesia + decrease absorption of (Ca2+, Mg2+, & iron) + increased risk of osteoporotic hip fractures (d/t low serum calcium)

imnotarobotbut  That's not the right answer tho, the answer is the binding of PGE to it's receptor +  
tinydoc  Can someone explain to me why the PPi answer is wrong if it increases the risk of C Dif wouldnt that also cause severe diarrhea. PPIs make a lot more sense to be given to this patient in the first place. +1  
maxillarythirdmolar  Keep it simple, stupid. +1  
roaaaj  @tinydoc You are correct about PPI increasing the risk of C. diff, but there was no history of antibiotic use. +  

submitted by sympathetikey(752),

I see what they're saying (this was my second choice) but at the same time I feel like a backup of blood would activate the baroreceptors and cause decreased sympathetic activity to the SA & AV node.

sympathetikey  (choice E) +  
meningitis  Could you elaborate? Is this related to: less "preload" from mother circulation causes lowered HR? +  
meningitis  Or backflow of blood and causes a Reflex Bradycardia? still confused on this question. +  
kentuckyfan  So I think the subtle difference in choice E is that there would be a negative CHRONOTROPIC effect, no inotropic effect (contractility). +7  
maxillarythirdmolar  if anything, inotrophy could go UP not down as diastole prolongs and LVEDV increases --> Starling equation bullshit +  

submitted by gh889(66),

compression of the common peroneal nerve as it wraps around the neck of the fibula causes decreased sensation from the superficial peroneal nerve, responsible for the anterolateral aspect and dorsum of the leg and foot

Deep peroneal nerve is sensory to the webspace between the hallux and 2nd digit


maxillarythirdmolar  You might be able to damage the superficial peroneal nerve with damage to the lateral malleolus but the description in the stem has deficits in the end targets of both the deep and superficial peroneal nerves +1  

submitted by mousie(135),

Your pituitary lactotrop cells hypertrophy during pregnancy to produce increasing amounts of prolactin - part of the pathophysiology of Sheehan's syndrome... increased blood loss during delivery can cause ischemic necrosis of pituitary

tinydoc  I thought the elevated Estrogen and progesterone depress the function of Prolactin until delivery. I guess you needed to know that it decreases its function by downregulating receptors or something as opposed actually decreasing the prolactin production. I picked gonadotrophs. This was a fair question but I reasoned it out and arrived at the wrong conclusion. +3  
maxillarythirdmolar  Specifically, the estrogen is stimulating lactotrophs as progesterone is preventing the prolactin from actually working on the breasts. So it's the estrogen that is stimulating the lactotrophs to grow, and you would see the effects of this growth if it weren't for the progesterone preventing the action of prolactin (their secretory product) on the breasts. +7  
dul071  why not somatotrophs. she's understress. wouldn't that increase the production of GH +  

submitted by cbrodo(29),

The posterior columns (Fasciculus cuneatus/Fasciculus gracilis) carry information to the brain regarding proprioception, vibration, discriminative touch and pressure. Physical exam findings suggest a lesion here (the spinothalamic tract carries pinprick/pain and temperature, and these were normal). Since the patient has abnormal findings in the lower extremities, and normal findings in the upper extremities, the answer is Fasciculus gracilis. This is because information from body areas below the level of T6 is carried by gracilis and information from body areas above the level of T6 is carried by cuneatus.

kai  kick Goals (gracilis) with your feet Cook and eat (cuneatus) with your hands +3  
temmy  i remember gracilis is for legs by saying i have graciously long legs and they are inside while arms can spread out to remember their orientation on the spinal cord +2  
jess123  I remember it as gracilis = grass so feet haha +4  
link981  Just to add found on page 492 on FA 2018. +  
charcot_bouchard  Hey Temmy, I can spread my legs too :) +  
maxillarythirdmolar  I can't feel GRACIE's ~fine touch~ as she ~vibrates~ my balls. +3  
cat5280  Could someone please explain why you were able to eliminate the spinocerebellar tracts? +  
drzed  Lmao I remember gracilis because of the gracilis muscle in the legs! +1  
alexxxx30  cat5280...so spinocerebellar tract does 4 things to know 1. proprioception in the Romberg test 2. intention tremor if damaged 3. shin to knee test 4. dysdiadochokinesia (being able to rapidly pronate/supinate the upper extremity) yes the patient has proprioception issues, but the other symptom of vibration loss points us more to a fasciculus gracilis issue. If the patient had presented with proprioception and and intention tremor then we would think spinocerebellar +  
alexxxx30  adding to my comment^ I would commit these 4 things to memory as I have gotten several questions concerning this topic (there were 2 questions on this exam where spinocerebellar tracts are involved). Memorize them and it might get you 1-2 extra points! +  

submitted by beeip(104),

This has been a tough concept for me to get, but I think I'm finally there:

The stem is describing primary adrenal insufficiency, or Addison's.

  • ACTH is being over-produced to stimulate the adrenals to produce cortisol, but they can't respond, either due to atrophy or destruction (TB, autoimmune: DR4, etc.)
  • The first 13 amino acids of ACTH can be cleaved to form α-MSH, which stimulates melanocytes, causing hyperpigmentation
jotajota94  Good job! Also, cortisol is involved in maintaining blood pressure. which was decreased in the patient. +6  
tinydoc  Decreased Na and increase K+ --- Hypoaldosteronisim Hypoglycemia, and hypotension --- Hypocortisolism so the adrenals arent working ---- adrenal Insufficiency the Hyperpigmentation comes from the increase ACTH as ACTH is from Proopiomelanocorticotropin. SO - increased ACTH also increases a -MSH ---> Hyper pigmentation. +9  
hungrybox  thank u for this answer +  
bilzcop  Ugh! I misread the question and chose ACTH :( +2  
cienfuegos  @bilzcop: same +  
cienfuegos  @bilzcop: let's never do it again, k? +1  
maxillarythirdmolar  Why does this patient have elevated BUN and creatinine?? +  

submitted by whoissaad(47),

Where is this even from? My mind's going hay wire trying to understand this.

sahusema  Hardy Wineberg equilibrium square root 900 = 30 1/2 of all offspring will be carriers so 30*.5 = 15 simple as that +4  
maxillarythirdmolar  this deserves a million upvotes. +1  

This is what I thought but not sure if it’s correct. There is a UWorld q where it describes co-administration of cortisol and epinephrine. Cortisol significantly enhances the effect of epi because cortisol has a permissive effect on maintaining the adrenergic receptors.

194orbust  per UWorld, "cortisol exerts a permissive effect on many hormones to help improve the response to a variety of stressors. For example, cortisol increases vascular and bronchial smooth muscle reactivity to catecholamines". FA also uses the effect of cortisol on catecholamine responsiveness as the lone example for a permissive drug interaction (FA2018 pg 229). The difference here is that we're talking about exogenous glucocorticoid and adrenergic agonist. I guess it was expected for us to assume that the mechanism is analogous for the analogous drugs +1  
maxillarythirdmolar  I'm sure it's related to the activating effect of Cortisol on phenylethanolamine-N-methyltransferase, converting NE to Epi. Sounds like a synergistic thing to me. (FA.83) +3  

submitted by lnsetick(68),
  • APocrine = your armpits smell like an APE
  • ceRUMen = there’s no ROOM in your ears since they’re full of wax
  • EC-CRYne = when you ECercise, your pores are CRYing
  • SEBaceous = SEBum is SEEPing out of your pores
hungrybox  as an ape i'm offended +15  
dr.xx  stop being an ape. evolutionize! +6  
dbg  as a creationist i'm offended +3  
maxillarythirdmolar  Also, Tarsal/Meibomian glands are found along the rims of the eyelid and produce meibum +  
snripper  So why is it apocrine? The dude is EXERCISING when playing football. +  
qball  The question asks about "the characteristic odor" i.e. body odor coming from the APEocrine glands. The Eccrine glands secrete water and electrolytes. +  

submitted by haliburton(171),

Peri- or postpartum cardiomyopathy (PPCM) is a rare, life-threatening heart disease of unclear origin and is characterized by heart failure of sudden onset between the final weeks of pregnancy and 6 months after delivery. link to pubmed The clinical picture of PPCM corresponds to a dilated cardiomyopathy (DCM) with signs of severe heart failure.

maxillarythirdmolar  For anyone wanting to understand why^ the tl;dr is that prolactin gets cleaved into two toxic metabolites. Treatment is something like bromocriptine (and therefore no more breast feeding) to stop prolactin release. Lastly, you can treat with regular HF meds. +1  

submitted by cantaloupe5(60),

Hypo/hyperthyroidism is diagnosed with TSH w/ reflex to T4 (this just tells the lab if TSH is normal don’t check T4 but if TSH is abnormal, check T4 too). TSH wasn’t an option so T4 is the best answer.

hello  I don't get why this was downvoted... +  
maxillarythirdmolar  To take it a step further, Goljan mentions that there are a myriad of things circulating in the body, often in a 1:2 ratio of free:bound, so in states like this you could acutally see disruption of this ratio as the body maintains its level of free hormone but further increases its level of bound hormone. Goljan also mentions that you'd see the opposite effect in the presence of steroids and nephrotic syndromes. So you could see decreased total T4 but normal free T4 because the bound amounts go down. +  

submitted by assoplasty(75),

I think the concept they’re testing is the increased TBG levels in pregnancy, and not just hyperthyroidism in general.

When screening for hypo/hyperthyroidism, TSH levels are ALWAYS preferentially checked because they are more sensitive to minute differences in T3/T4. Often times TSH levels can demonstrate a change even when T3/T4 levels are in the subclinical range. The only exception to this would be in pregnancy (and I guess maybe liver failure? I doubt they would ask this though). High estrogen levels prevents the liver from breaking down TBG, leading to increased TBG levels in the serum. This binds to free T4, decreasing the amount of available free T4. As a compensatory mechanism, TSH levels are transiently increased and the RATE of T4 production is increased to replenish baseline free T4 levels. However the TOTAL amount of T4 is increased.

The question is asking how to confirm hyperthyroidism in a pregnant woman --> you need to check FREE T4 levels (because they should be normal due to compensatory response). You cannot check TSH (usually elevated in pregnancy to compensate for increased TBG), and you cannot check total T4 levels (will be increased). You got the answer right either way but I think this is a different reasoning worth considering, because they can ask this concept in other contexts of hyper-estrogenism, and if they listed “TSH” as an answer choice that would be incorrect.

hungrybox  Extremely thorough answer holy shit thank u so much I hope you ACE Step 1 +5  
arkmoses  great answer assoplasty, I remember goljan talking about this in his endo lecture (dudes a flippin legend holy shit) but it kinda flew over my head! thanks for the break down! +2  
whoissaad  you mean total amount of T4 is "not changed"? 2nd para last sentence. +  
ratadecalle  @whoissaad, in a normal pregnancy total T4 is increased, but the free T4 will be normal and rest of T4 bound to TBG. If patient is hyperthyroid, total T4 would still be increased but the free T4 would now be increased as well. +  
maxillarythirdmolar  To take it a step further, Goljan mentions that there are a myriad of things circulating in the body, often in a 1:2 ratio of free:bound, so in states like this you could acutally see disruption of this ratio as the body maintains its level of free hormone but further increases its level of bound hormone. Goljan also mentions that you'd see the opposite effect in the presence of steroids and nephrotic syndromes. So you could see decreased total T4 but normal free T4 because the bound amounts go down. +1  

submitted by temmy(92),

please help according to winters equation the patient has a normal anion gap

ergogenic22  winter's formula is to look at the compensation to see if it is appropriate. PCO2 = 1.5[HCO3-] + 8 +/- 2 In this case, 1.5* 10 (Pt's bicarb) +8 +/-2 = 21 to 25 Pt's PO2 is 23, so compensation is appropriate. If PCO2 was below 21, it would be concomitant respiratory alkalosis +4  
ergogenic22  in other words, winter's formula is not necessary for this question +2  
the_sacramento_kings  lol unless you want to make sure its not A. +1  
hello  @ergogenic22 Someone might use Winter's formula to rule out choice A. +  
maxillarythirdmolar  respiratory depression of alcohol should rule out "A" +  
baja_blast  Isn't the low pCO2 enough to rule out A? +  

submitted by hayayah(884),

Definition of adjustment disorder:

Emotional symptoms (eg, anxiety, depression) that occur within 3 months of an identifiable psychosocial stressor (eg, divorce, illness) lasting < 6 months once the stressor has ended.

If symptoms persist > 6 months after stressor ends, it is GAD.

hello  Yep, and I think what we are supposed to take from this Q is: The only info. we have for this patient is that he ended chemo 2 months ago and has been calling the doctor a lot -- this is supposed to mean he has been calling a lot since ending chemo 2 months ago. His frequent calls starting after ending chemo and within 3 months of the stressor fits with the above-stated definition of "adjustment disorder" with anxiety. I stressor in this case could possibly be either the actual illness or the ending of chemo/treatment. It probably does not matter much in this case. +1  
charcot_bouchard  I think doing uw done me wrong here. Adjustment disorder isnt diagnosed when symptom match another disorder --- it was like never a right answer. But ofc its right answer in nbme +3  
maxillarythirdmolar  Just to add to that, the tingling in his fingers may seem like a distraction/it probably is. Likely has some relation to his Chemo. +3  

submitted by neonem(450),

Obstructive uropathy causes a postrenal azotemia --> when prolonged, tubular damage ensues. This leads to an acute tubular necrosis, characterized by necrotic plugs in the tubular system as seen in the image

meningitis  Does anyone know the relevance of the stem saying: "during this time she also has been crying frequently"? +12  
usmleuser007  Think the postrenal azotemia is d/t her pregnancy. With the increasing in size fetus, the pelvic cavity is being compressed and thus there is pressure on the ureters. This leading to the presentation. As per above --- the crying maybe just d/t her pain and emotional stress caused by worrying about possible complications regarding her fetus. +2  
maxillarythirdmolar  My gut tells me it must be some sort of transient change in placental size with hormonal changes. It's reminiscent of what you might expect for breast changes during the menstrual cycle, imo +  

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