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Only the the black fly is associated with nematodes
Kidney is smaller than normal, suggesting less blood flow to it. Won't see shrunken kidney in the case of HTN.
I ruled out selection A since it is involving the interlobar artery. Renal artery stenosis involves the "renal artery" and the stem gives you fibromuscular dysplasia with renal artery stenosis.
the girl has tension headache. Triptans is not a drug of choice. NSAID, Acetaminophen, (or TCA for prophylaxis)
but question asks which drug she should take to /treat/ her headache? -> I fell into sumatriptan cause I know it didn't have prophylactic indications but more of a treatment. idk, was between the acetaminophen and sumatriptan, and would appreciate if someone can tell me why acetaminophen is the move for this patient.
for HA treatment you want to start off conservative anyway w/ Tylenol / NSAIDs before you move on to triptans. That and triptans are not used for tension HA
Triptans are used for migraine headaches by causing trigeminal vasoconstriction. They are not analgesics.
Yep. They tried to throw you off with the picture, but the wording in the stem says its a "photomicrograph" -- not exposed to plane polarized light, where you would see the negative birefringence.
Why is NBME so mean to us. Do those mean a lot in clinic？
@linwanrun1357 I highly doubt you would be looking at your own joint fluid aspirates instead of sending it to the lab.
what those yellow white nodules signify?
In clinic gout is typically a clinical diagnosis. If you can treat w/ NSAIDs instead of aspirate you would do that. You would aspirate if you are considering septic arthritis so you can get culture. I don't think anyone aspirate for heck of it.
@nnp, the yellow white nodules are tophus which is a sign of chronic gout, characterized histologically by aggregates of uric acid crystals, can show up as skin nodules most commonly on external ear, olecranon bursa or achilles tendon (pg 467 FA 2020)
If we assume that they are not carriers (in the recessive case)
Then how came it can be AR？！！
^exactly what's said above here. I think x-linked recessive is the least likely, but not impossible.
Only the the black fly is associated with nematodes
nodules can be hypo or hyperpigmented supposedly!
Could the pneumothorax also cause less ventilation due to decreased lung surface, retaining more CO2 causing respiratory acidosis? That's how I got to the answer at least.
I think pneumothorax would increase RR because you're probably hypoxic. Also I'm sure when you have a lung collapse on you you'd be scared and that would trigger your sympathetic so your RR will go up either way.
there is no bilateral lung opacities as you would see in ARDS
Was thinking some sort of infection b/c of the atelectasis so picked empyema but this makes sense!
does it need to be ARDS to cause "diffuse alveolar damage"?
Who can explain, the 12-y boy with stanner stage 2？？
I thought it should be stage 3....
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.
If there is a choice about asking what the patient is worried about. Is this right?
It does not sound like a dick :)
If this were about a treatment asking why hes worried would be right but hes kind of doing the hospital a favor so I dont think you're supposed to try to convince or pressure him
also, any patient participating in any research study can withdraw whenever they want. Answer E is wrong because he shouldn't have to go through hoops to quit, he can just drop out at any time.
Additional UW fun facts regarding Potassium and DKA:
use caution giving insulin and IV fluids to dehydrated hyperglycemic because i forces K in cells causing fast decrease of extracellular Potassium, thus give K supplementation even when serum K elevated
Seems like fatty change would require more than 1 weekend. I choose swelling since it's reversible and seems like something with a quick onset.
I think it's just a bad question. It should be "on weekends"
So his hepatocytes aren't dying ( ballon degeneration ) vs just damaged/increased FA synthesis due to increased NADH/citrate
It's not in pathoma, but I have it written in (so he or Dr. Ryan may have mentioned it) - Alcoholic hepatitis is generally seen in binge drinkers WITH A LONG HISTORY OF CONSUMPTION.
Do NOT think the answer of this question is right.
Cell swelling make more sense!
some asshole in suspenders and a bowtie definitely wrote this q, as I've seen both acute swelling and fatty change be used to describe one episode of drinking.
short term ingestion of as much as 80gm of alcohol (six beers) over one to several days generally produces mild , reversible hepatic steatosis . from big robin 8th edition page 858. Basically to develop alcoholic hepatitis with cellular swelling etc you have to have sustained long term ingestion of alcohol while steatosis can develop with a single six cap . hope that helps . ps i got it wrong too .
After even moderate intake of alcohol, lipid droplets accumulate in hepatocytes increasing with amount and chronicity of alcohol intake. (...) Fatty change is completely reversible if there is abstention from further intake of alcohol.
The swelling is caused by accumulation of fat, water and proteins. Therefore this will occur later. From big Robins 9th pg842.
Do not understand the breathing （choice C and D）
breath in and out are different?
I don't know if it's correct or not but how I approached C & D was that they both cause vasoconstriction in the arterioles (because this is the lung where hypoxia causes vasoconstriction), which decreases hydrostatic pressure through the capillaries and eventually decreases lymph flow. Maybe I completely got this question right for wrong reason, but I felt that it works with all of the answers.
For F) I was thinking that it would cause increased capillary oncotic pressure which causes more fluid to go into the capillary than into the lymph vessels...
Here's a picture: http://www.lymphedemablog.com/wp-content/uploads/2011/09/Lymphatics.gif