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Welcome to miriamp3’s page.
Contributor score: 7


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 +2  visit this page (nbme22#49)
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I wasn't sure, but then I realize he is going to die, he is in a hospice + the best you can do is made him feel without pain. BUT at the end what made me decide was The reason of the medication. At this point you really don't care about controlling everything else.

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madamestep  Also, bone pain is excruciating. You're not going to make someone in hospice just scream in writhing agony for months. +




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submitted by yotsubato(1208), visit this page
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Why cant this be laxatives? Both would cause metabolic alkalosis with hypokalemia... ?

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sup  Laxatives would cause an anion gap metabolic acidosis due to loss of bicarbonate in the stool. You would see hypokalemia though as seen in this question. +1
miriamp3  it took me a lot of time choosing between laxatives and diuretics and at the end I choose diuretics. but I didn't realize that the only thing I had to do was check if were a anion gap or not. +
snripper  Why would laxatives cause anion gap MA? Isn't it similar to diarrhea? +
castlblack  The above comments are incorrect. Diarrhea is a cause of normal-anion-gap metabolic acidosis (D in HARDASS from FA). Laxatives are wrong because they would lower HCO3- but in this scenario it is high. The low K+ and Cl- fits either case though. +4


submitted by mattnatomy(46), visit this page
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Answer = C. (Decreased hepatic VLDL synthesis)

Nicotinic acid = Niacin. Niacin works by:

  1. Inhibiting lipolysis (hormone sensitive lipase) in adipose tissue)

  2. Reducing hepatic VLDL synthesis

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johnthurtjr  Well color me surprised. I was completely thrown off here. +34
miriamp3  @almondbreeze go to the cardiovascular pharmacology you will see a draw of lipid lowering agents and you will find niacin en two places ++one on the adipose tissue and the second one in the liver by the vldl production. in the text in the same page is also mention it FA 2018 pg 313. +
djeffs1  I still don't quite see how C corresponds to those 2 processes... +


submitted by usmleuser007(464), visit this page
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Just note why other answers are not correct:

  1. Egophony is an increased resonance of voice sounds heard when auscultating the lungs, often caused by lung consolidation and fibrosis.

    • a. It is due to enhanced transmission of high-frequency sound across fluid, such as in abnormal lung tissue, with lower frequencies filtered out.
  2. Whispered pectoriloquy refers to an increased loudness of whispering noted during auscultation with a stethoscope on the lung fields on a patient’s torso.

    • a. Usually spoken sounds of a whispered volume by the patient would not be heard by the clinician auscultating a lung field with a stethoscope.

    • b. However, in areas of the lung where there is lung consolidation, these whispered spoken sounds by the patient (such as saying ‘ninety-nine’) will be clearly heard through the stethoscope.

    • c. This increase in sound exists because sound travels faster and thus with lower loss of intensity through liquid or solid (“fluid mass” or “solid mass,” respectively, in the lung) versus gaseous (air in the lung) media.

    • d. Whispered pectoriloquy is a clinical test typically performed during a medical physical examination to evaluate for the presence of lung consolidation, which could be caused by cancer (solid mass) or pneumonia (fluid mass).

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titanesxvi  why not wheezing? +
miriamp3  @titanesxvi because the dx is CHF +1
leaf_house  I get why crackles are more likely in CHF, but wouldn't it also cause whispered pectoriloquy, if fluid allows better transmission of sound? +
weirdmed51  @tita wheeze is asthma +
umpalumpa  Guys, why not whispered pectoriloquy, egophony? FA2020 pg680: pulmonary edema causes "bronchial breath sounds, late inspiratory crackles, whispered pectoriloquy" +1


submitted by bubbles(79), visit this page
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Chronic renal insufficiency:

1) poor phosphate clearance --> high serum inorganic phosphorous

2) high serum phosphate --> complexes with divalent cation Ca --> Ca falls

3) Ca falls --> triggers PTH axis

4) kidney failure --> decreased activity of 1-hydroxylase at the kidney --> less calcitriol

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makinallkindzofgainz  this guy renals +9
paperbackwriter  Someone please help me with this (always trips me up): PTH causes increased vit D production in kidney... are we assuming the increased PTH can't catch up with the kidney failure? Is it the level prior to PTH compensation that they want? D: +
miriamp3  @paperbackwriter what it works for me ;;;; is find the first abnormality so CKD low calcitriol (no D vit) ---> is gonna increase PTH ---> the kidney are not working (chronic, they don't tell u recently- you can;t revert a CKD so the kidney never going to catch up) --> increase inorganic phosphorus.--> always start with the problem. I also use this for celiac and types of shocks. start with the problem, and trust yourself. +4
paperbackwriter  @miriamp3 thank you! I will try out your strategy next time!! :) +1
snripper  I thought renal insufficiency -> inability to reabsorb phosphate at PCT -> decreased phosphate? +3
skonys  Can someone explain why calitriol is low? Is it just that his kidneys are fucked and he can't make it? So PTH is increasing to try to lower the phos and raise the vit d but the kidneys are like "lol, I can't" +
madamestep  @skonys pretty much yup! In early renal failure you'll see high PTH levels but NORMAL Ca and Phos. Becuase it's able to keep up but barely. At a certain point though, the kidney bows out and PTH is high, Phos is high, Ca2+ is low, EPO is low, calcitriol is low, Creatine is high, BUN is high. +


submitted by haozhier(23), visit this page
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I chose C because I thought it has been four weeks so it must have been acute tubular necrosis. Can anyone explain? Thanks!

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miriamp3  @haozhier if you are deciding to think that he had a ATN because of the 4 weeks.. then he should be by now in the recovery phase(polyuria, Bun/cr fall) But he is with HF and his urine output has progressively decrease. So AKI prerenal HF Bun/cr >20. the only one is D. Don't get confused with the rest of the information. +
jesusisking  I thought the same thing so chose C as well! +


submitted by seagull(1933), visit this page
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What a terrible picture. They they covered up part of it with lines. WTF

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sympathetikey  Agreed. +18
catch-22  Start at the pontomedullary junction and count from superior to inferiorly (or medially to laterally): VI, VII, VIII, IX. +3
yotsubato  I looked at the left side (cause the nerves arent frazzled up). Saw 7 and 8 come out together nicely. Then picked the right sided version of 8 +15
lolmedlol  why is it not H or I on the right side; the stem says he has hearing loss on the right side, so the lesion should be ipsilateral no? +4
catch-22  You're looking at the ventral aspect of the brainstem. +11
catch-22  ^Also, you know it's the ventral aspect because you can see the medullary pyramids. +1
amarousis  think of the belly of the pons as a pregnant lady. so you're looking at the front of her +6
hello  which letter is CN IX in this diagram? +
miriamp3  there is no VI nerve. That's the thing. The VI nerve should be in the angle between the pons and the medulla. Parallel to the pyramid. It goes V then VII and then VIII. I make the same mistake and I thought it was the picture but there is no VI par in the photo. They know We count from superior to inferior. +
jesusisking  Don't G and H lowkey look like VII and VIII? I chose H b/c of that +
ljennetten  G and H are CN VII and VIII on the left side, while this guy has right sided hearing loss. CN VI is not labeled in this photo, but is the smaller nerve that arises medial to CN VII and us cut most of the way up the pons. +1
prolific_pygophilic  Mother Fuckers took this with a disposal camera then deep fried it. What is this grainy ass picture +1
soccerfan23  There's over a million pics of the brainstem on the internet and of course, the NBME picked the worst quality, most blurry one for this Q. +


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