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I don't think you could have *totally* ruled out the other answers - I picked glycogen breakdown because it sounded kind of like Von Gierke disease (glucose-6-phosphatase) to me: characterized by fasting hypoglycemia, lactic acidosis, and hepatomegaly since you're not able to get that final step of exporting glucose into the blood. However, I guess in this case you wouldn't see that problem of glycerol/fructose infusion not increasing blood glucose. Nice catch.
I think you were super smart to catch Von Gierke! Just to refine your answer b/c I had to look this up after reading your explanation, von gierke has a problem with gluconeogenesis as well as glycogenolysis. So they’d have a problem with glycerol and fructose but also galactose since they all feed into gluconeogenesis before glucose-6-phosphatase. Great thought process!
glycerol and fructose both enter the pathway thru DHAP and glyceraldehyde-3-ph. Galactose enters thru Gal-1-ph to glu-1-ph conversion
In this cause (fructose bisphosphatase deficiency.,),fructose should help to increase serum glucose, bcz it can become into glucose-6-P by hexokinase.
Therefore, this question makes me confused....
According to uworld, fructose infusion will not increase blood glucose levels in Von Gierkes Disease as well
I believe Von Gierke is not a plausible answer choice because a galactose infusion would still not see an elevation in glucose levels. Remember, galactose could be converted to galactose 6 phosphate, but in order to complete gluconeogenesis and allow glucose to leave the Liver for an increase of its concentration in the blood, the patient would still need glucose 6 phosphatase which is eliminated in Von Gierke.
So what disease is this??? I mean couldnt we have just answered the question based on the fact that the patient responds to galactose being infused and we know that galactose feeds into gluconeogenesis?? I am so confused.
Its Hereditary Fructose intolerance right? gets sick after fructose and I guess glycerol can jump in via aldolase B on this pathway via page 74 of FA2019. It looked like a fructose thing to me so I just marked out the other ones and moved on.
@djtallahassee I was wondering same, but hereditary fructose intolerance also results in inhibition of glycogenolysis :/ confusing question.
A much simpler way to think about this, without trying to figure out a diagnosis, I looked at the time frame for when the child was presenting. He has eaten poorly for 3 days, by now, his glycogen breakdown is gone. His body would be trying to make glucose, therefore, gluconeogenesis is impaired, not glycogen breakdown.
if fructose kinase is not available (fructose intolerence), then some fructose may go to F-6-P by hexokinase, then goes to G6P if gluconeogenesis is needed. however this patient's fructose kinase was intact, so no fructose would have go to F6P, so there would be no blood glucose increment after injection of fructose.
That's so infuriating I stared at this question for 20 minutes thinking I did something wrong
lol..my math never worked either. I also just chose the closest number. also, screw this question author for doing that.
this is why you never waste 7 minutes on a question.... because of shit like this
Why the FUCK did they not just give us a clearance of 0.1 if they're going to fuckin round it anyways...
in ur maths, why did u put 24h/1day and not 1day/24h? if the given Cl was 0.09L/hr/kg. I know it just is a math question, but i´d appreciate if someone could explain it.
LMAO games NBME plays
magic math!!!!! how TF r we supposed to know when they round and when they don't like wtf im so pissed someone please tell me step isn't like this...with such precise decimal answers and a calculator fxn you would assume they wanted an actual answer!
OMG, I've got the 25.92 mg/kg/day, which isn't any of the answer choices listed. So I chose the D 51.8, because 51.8 is double of 25.9......I thought I must have make a mistake during the calculation ......
They purposely did that so if you made a mistake with your conversion like I did, you might end up with 2.5 which was one of the answer choices. SMH
I did well, but I thought that my mistake was something to do with the conversion and end up choosing 2.5 because it is similar to 25.92
The fact that we pay these people 60 dollars a pop for poorly formatted and written exams boggles my mind, and yet here I am, about to buy Form 24
Not only do you feel like you're doing sth wrong but then that feeling stays for other questions. sucks so baad
'here.. take 50mg of vyvanse.. I just rounded it up from 30.. dw you'll be fine' (totally doing this with my patients 8-))
I was so close to picking 2.5 because I thought I did a conversion error. 5 minutes later and still didn't feel comfortable picking 28.8😡
This is directly from Goljan
I) Hypovolemic shock may occur due to loss of plasma from the burn surface (refer to
• Loss of protein from the plasma loss may result in generalized pitting edema.
II) Infection of the wound site and sepsis may occur.
(a) Sepsis due to Pseudomonas aeruginosa is the most common cause of infection in burn patients.
(b) Other pathogens include methicillin-resistant S. aureus and Candida species.
(3) Curling ulcers may occur in the proximal duodenum (refer to Chapter 18).
(4) Hypermetabolic syndrome may occur if >40% of the body surface is burned.
Can someone explain why is it not increased ECF?
i picked same. Increased ECF but cant remember why. Can you explain WHY it is increased ECF? what was ur reasoning
Burns would lead to a decrease in ECF because the protection from fluid loss is absent; it can lead to shock. :)
My reasoning behind picking ↑ ECV was that your losing fluid but not electrolytes with the burn ⇒ the ecv would have increased osmolarity, so the fluid from the ICV would be pushed the the ECV. It made sense to me at the time. I guess technically its wrong because the loss of fluids and the gain of fluids would amount to pretty much the same thing. But the insulation and heat loss thing makes sense I guess.
Increased ECF, bc I was thinking about the edema formation.... :-/
I picked increased ECF because burns increase the capillary permeability coefficient, but now that I am going over it I realized that increasing the permeability would only transfer plasma volume to the interstitial volume, which are both a part of the ECF so therefore ECF would not change. SMH
Burns (and Diarrhea) cause ISOsmotic volume contraction; Costanzo BRS Physio
in severe burned patient, also has increased fluid in third spacing or interstitial (leading EDEMA). Different extracellular space is interstitial and vascular
I also wanted to add, another huge job of the skin is to prevent loss of fluid. Burn patients are easily dehydrated because they've lost that barrier. This helped me lean away from increased ECV - despite the edema (from one compartment to another) as others have mentioned above, there is a loss in overall ECV due to evaporation from body.