welcome redditors!to snoo-finity ... and beyond!
Welcome to linwanrun1357's page.
Contributor score: 4

Comments ...

 +0  (nbme24#25)

I just think plams are not protected by the melanin and got this right.

 -2  (nbme24#23)

F**K this question!

Know exactly what the disease is without knowing what the f**king "generalized malabsorption" means!!

 +0  (nbme24#18)


This looks better for the 3 arteries

 +0  (nbme24#9)

NOTE: Microfilaria:

Microfilariais an early stage in the life cycle of certain parasitic nematodes in the family Onchocercidae.--wiki

linwanrun1357  Only the the black fly is associated with nematodes

Subcomments ...

submitted by keycompany(142),

Why would deposition of fibrinoid deposits (i.e. fibrinoid necrosis/malignant HTN) be wrong?

amorah  Kidney is smaller than normal, suggesting less blood flow to it. Won't see shrunken kidney in the case of HTN. +1  
linwanrun1357  I have done so research showing that it should deposit collagen (see below). Anyway, fuck this question! http://www.pathologyoutlines.com/topic/heartfibromusculardysplasia.html +  

This is aspirin-intolerant asthma. Acetaminophen only inhibits COX within the CNS, so doesn’t cause the leukotriene shunting that characterizes that disease.

linwanrun1357  why not triptans? +1  
joyceeepan  the girl has tension headache. Triptans is not a drug of choice. NSAID, Acetaminophen, (or TCA for prophylaxis) +  

submitted by neonem(305),

These are gout crystals. I suppose the best way to differentiate this case from pseudogout is that the crystals are sharp & needle-shaped and not rhomboid-shaped.

sympathetikey  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. +7  
linwanrun1357  Why is NBME so mean to us. Do those mean a lot in clinic? +  

submitted by trazabone(7),

My understanding is that if parents are unrelated by blood to those affected, we assume that they are not carriers (in the recessive case). Therefore, if we have a male father affected with x-linked recessive married to a non-carrier, there's no way any of his offspring would be affected.

"If one parent is not a carrier, then a child can only inherit a disease allele from the other parent. In these problems, we can assume that any individual marrying into the family is not a carrier." https://www.cs.cmu.edu/~genetics/units/instructions/instructions-CP.pdf

linwanrun1357  If we assume that they are not carriers (in the recessive case) Then how came it can be AR?!! +  
catscan1979  ^exactly what's said above here. I think x-linked recessive is the least likely, but not impossible. +1  

NOTE: Microfilaria:

Microfilariais an early stage in the life cycle of certain parasitic nematodes in the family Onchocercidae.--wiki

linwanrun1357  Only the the black fly is associated with nematodes +  

submitted by brethren_md(54),

Onchocerca Volvulus via female blackfly. Black flies, black skin nodules, "black sight" (aka Blindness). Question stem here describes the black nodules seen in Onchocerca.

linwanrun1357  There is no black in the stem~~!! +1  

submitted by keycompany(142),

This patient has a pneumothorax. Hyperventillation is not enough to compensate for the overall decrease in lung surface area.

_yeetmasterflex  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. +1  
duat98  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. +1  
kateinwonderland  Arterial blood gas studies may show respiratory alkalosis caused by a decrease in CO2 as a result of tachypnea but later hypoxemia, hypercapnia, and acidosis. The patient's SaO2 levels may decrease at first, but typically return to normal within 24 hours. (https://journals.lww.com/nursing/Fulltext/2002/11000/Understanding_pneumothorax.52.aspx) +1  
linwanrun1357  How about choice C, --ARDS? +  
bullshitusmle  there is no bilateral lung opacities as you would see in ARDS +1  

submitted by lsmarshall(228),

"In the years preceding physical puberty, Robert M. Boyar discovered that the gonadotropin pulses occur only during sleep, but as puberty progresses they can be detected during the day. By the end of puberty, there is little day-night difference in the amplitude and frequency of gonadotropin pulses.

Some investigators have attributed the onset of puberty to a resonance of oscillators in the brain.[89][90][91] By this mechanism, the gonadotropin pulses that occur primarily at night just before puberty represent beats." - Wiki

linwanrun1357  Who can explain, the 12-y boy with stanner stage 2?? I thought it should be stage 3.... +  

The disease here is fructose bisphosphatase deficiency. In it, IV glycerol or fructose doesn’t help because both enter the gluconeogenesis pathway below fructose bisphophatase. Galactose on the other hand enters above it. I don’t think you really need to know this to choose the correct answer since the clinical picture of fasting hypoglycemia that is corrected w/ some sort of sugar that can enter the gluconeogenesis pathway should clue you into the right answer.

neonem  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. +9  
vshummy  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! +11  
drmomo  glycerol and fructose both enter the pathway thru DHAP and glyceraldehyde-3-ph. Galactose enters thru Gal-1-ph to glu-1-ph conversion +1  
linwanrun1357  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.... +  
krewfoo99  According to uworld, fructose infusion will not increase blood glucose levels in Von Gierkes Disease as well +  
atbangura  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. +  
lilyo  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. +  

submitted by hungrybox(317),

The 2 commandments of ethics questions:

  1. Don't ever pick an answer where you sound like a dick
  2. Don't ever consult the ethics committee

Served me well on this question.

linwanrun1357  If there is a choice about asking what the patient is worried about. Is this right? It does not sound like a dick :) +1  
champagnesupernova3  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 +  

submitted by nala_ula(49),

In diabetic ketoacidosis, there is increased acid in the extracellular space. According to FA there is a transcellular shift due to decreased insulin that leads to more H+ entering the cell in exchange for K+. This leads to hyperkalemia with depleted intracellular stores of K+. There is also osmotic diuresis that leads to increased K+ loss in the urine and total body K+ depletion. The question asks that is most likely to decrease with insulin therapy: serum potassium concentration will decrease as K+ is now exchanged for H+ inside the cell.

cienfuegos  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 +1  
linwanrun1357  Why urine K+ does not decrease? +  

It’s acute alcohol consumption so fatty change more likely. Cellular swelling indicates alcoholic hepatitis which requires chronic alcohol consumption (See FA 2019 pg 385). At least that’s the logic I used to pick fatty change.

seagull  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. +17  
nc1992  I think it's just a bad question. It should be "on weekends" +8  
uslme123  https://webpath.med.utah.edu/LIVEHTML/LIVER145.html +3  
uslme123  So his hepatocytes aren't dying ( ballon degeneration ) vs just damaged/increased FA synthesis due to increased NADH/citrate +  
sympathetikey  @seagull I agree! +  
et-tu-bromocriptine  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. +  
linwanrun1357  Do NOT think the answer of this question is right. Cell swelling make more sense! +1  
fkstpashls  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. +3  

submitted by hayayah(516),

Lymph flow rate is usually low. It is influenced primarily by the rate of lymph formation. For example, if blood capillary pressure is increased by arterial vasodilation or venous constriction, the flow rate of lymph increases. Also, the flow rate is affected by compression of lymphatics by contraction of neighboring musculature and by negative intrathoracic pressure (breathing).

Interstitial pressure (so pressure in the ECF, which would increase if given IV saline) and lymph flow are positively related. A small increase in interstitial volume greatly increases its pressure, promoting lymph flow that acts to restore the interstitial volume to normal.

more on this topic: https://www.ncbi.nlm.nih.gov/books/NBK53448/

linwanrun1357  Do not understand the breathing (choice C and D) breath in and out are different? +