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 +0  (nbme24#37)

Which type of cell we r going to find in blisters?, neutrophils?


 +1  (nbme21#47)

why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain +

usmle11a  i believe increase 25OHcholecalciferol indicates the storage capacity of vit D, which wont be affected in case of CKD. it goes like this, kidneys wont respond to regular PTH, loses Ca and cant execrete PO4, PTH gets made and tries to burn bone to produce Ca, resulting in elevated levels of Ca and PO4, Ca will bind the calcium and go to kidneys, yet same story all over. add to that the fact that 1 oh hydroxylase wont be able to function in a dead kidney.

 +0  (nbme21#21)

why not C?. It´s not supose that it improve the efectivity of insulin?

yb_26  thiazolidinediones (pioglitazone) increase insulin sensitivity (in muscles and liver) through activation of peroxisome proliferator-activated receptor-gamma (PPAR) I think they are asking about primarily mechanism of action, that's why it is E
cienfuegos  UW explanation regarding the genes upregulated 1. GLUT4: insulin responsive on adipocytes/skeletal increases G uptake 2. adiponectin: cytokine secreted by adipocytes increases # of insulin responsive adipocytes and stims FA oxidation 3. PPAR family also plays significant role in pathogenesis of metabolic syndrome




Subcomments ...

submitted by i-de-liver(0),

Does anyone know why this is Uric Acid not N. gonorrhea? All I see in the micrograph are neutrophils. Is that white line in the middle of the picture that overlays the lymphocyte supposed to be the needle-shaped uric acid? Or is it because she's an old lady and usually septic Arthritis is from S. Aureus, so it would more like by uric acid and not gonorrhea since she's older?

maverick95  I struggled between those two answer choices as well. I thought that the large needle shape right in the middle was a uric acid crystal which helped push me towards Uric Acid as my answer. I also took into account that she was older (even though STIs are rampant among the elderly) she didn't really seem to have any other symptoms or history of STI/gonorrhea. I figured with her age that she just wasn't able to excrete Uric Acid enough, and got a gout. Something a pathologist told me one time was that they put the focus of the picture in the middle of the shot. So considering the uric acid-looking shape was right in the middle, I figured that's what they wanted us to focus on with the picture. Hope this helps. +1  
i-de-liver  Ah gotcha! I guess I shouldn't have thought that the thing in the middle was an artifact lol... thank you!! +  
a1913  I believe it's because: 1) there is nothing given that would be risk factors for this woman to have N. gonorrhea 2) The thing in the middle is indeed an MSU crystal, just not under polarized light 3) apparently we get acute inflammation and increase in WBCs with crystal-induced arthropathies, per Table 11-2 on page 8 here (10 page document, top of page of interest will say p. 260) --> http://downloads.lww.com/wolterskluwer_vitalstream_com/sample-content/9781582558752_Mundt/samples/Chapter_11.pdf Also take a look at the pics on the previous page, left column for an example. I got this wrong as well, but I definitely won't again! lol +  
cr  i had the same problem, Whats about the fever?, could be present in gout? +  


submitted by ferrero(16),

A very similar question I have seen in Qbanks will ask why a patient with right heart failure does not develop edema and the answer is increased lymphatic drainage. I got this question wrong originally because I answered along this line of reasoning but I think in this case it all has to do with WHERE the extra pressure is coming from. In this question the pt has diastolic hypertension so you can think about the pressure as coming "forward" so constricting precapillary sphincters can prevent an increase in pressure in the capillary bed. However for right heart failure this extra fluid is coming from the OPPOSITE direction (backwards from the right heart) and constricting precapillary sphincters can do nothing (on opposite side of capillary bed) - the only way to prevent edema is to increase lymphatic drainage.

seagull  The question clearly lead us to think about Osmotic pressure by talking about protein and urine. I wonder how many people used that line of reasoning (like myself)? +11  
mousie  Great explanation, I chose lymphatic drainage for the same reasoning (similar Q on different bank) +1  
sympathetikey  My reasoning was much more simplistic (maybe too simple) but in my mind, systolic BP is determined by Cardiac Output and diastolic BP is determined by arterioles. Therefore, what comes before the capillary and regulates resistance? Arterioles. That's why I said that pre-capillary resistance. +13  
cr  the main difference between the 2 cases is that in this case the patient has high BP +  
link981  So in kindergarten language the question is essentially asking how high pressure in the arterial system is NOT transmitted to the venous system (which is where EDEMA develops). But you know they have to add all this info to try confuse a basic principle and make you second guess yourself. (Got it wrong by the way) because of what @ferrero said of Qbank questions. +  
hello  @ferrero what are you talking about? lymphatic drainage is the wrong answer... +  
hello  ok never mind. i got it. hard to understand b/c it was a big block of text. +  


submitted by wired-in(27),

Maintenance dose formula is (CssCltau)/F where Css is steady-state target plasma conc. of drug, Cl is clearance, tau is dosage interval & F is bioavailability.

Neither dosage interval nor bioavailability is given, so ignoring those & plugging in the numbers (careful to convert units to mg/kg/day): (12 ug/mL * 1 mg/1000 ug) * (0.09 L/hr/kg * 1000 mL/1 L * 24 hr/1 day) = 25.92 mg/kg/day

...which isn't any of the answer choices listed. They must have rounded 0.09 L/hr/kg to 0.1 L/hr/kg, and doing so gives exactly 28.8 mg/kg/day (choice C)

lispectedwumbologist  That's so infuriating I stared at this question for 20 minutes thinking I did something wrong +18  
hyoid  ^^^^^ +2  
seagull  lol..my math never worked either. I also just chose the closest number. also, screw this question author for doing that. +2  
praderwilli  Big mad +4  
ht3  this is why you never waste 7 minutes on a question.... because of shit like this +5  
yotsubato  Why the FUCK did they not just give us a clearance of 0.1 if they're going to fuckin round it anyways... +6  
bigjimbo  JOKES +  
cr  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. +  
d_holles  LMAO games NBME plays +  
hyperfukus  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! +  
jean_young2019  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 ...... +  
atbangura  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 +  


submitted by sgarzon15(3),

Thank you glitter zone of sketchy pharm. I shall never forget you

cr  why not C?. It´s not supose that it improve the efectivity of insulin? +  
cr  why not C?. It´s not supose that it improve the efectivity of insulin? +  
divya  because insulin uptake by adipose and muscle tissue is not limited to thiazolidinediones but also and mainly by metformin. and glitazones' primary MOA is PPAR gamma stimulation which then increases insulin sensitivity to other tissues. +  


submitted by haliburton(83),

this is a cervical spinal cord section. the cuneate fasciculus is intact (UE) vibration and proprioception, but the white section is the gracile fasciculus (LE) and is damaged. I think the lateral portion that is uneven is just natural/artifact.

arezpr  thorax section +3  
guillo12  How do you know the gracile fasciculus is damage?!?! +1  
cr  which parte of the image its damage?, the pink? or black? +  
usmile1  the pink park yes +1  
d_holles  If you look at https://en.wikipedia.org/wiki/Gracile_fasciculus#/media/File:Spinal_cord_tracts_-_English.svg you can see that the closer to the center = legs, while further away = arms. +1  
hyperfukus  i still don't see where the damage is lol! FML +  
hyperfukus  i finally figured it out lol that was a slow moment i hope im not this slow on step yikes! +  
angelaq11  @hyperfukus I had the same problem at first, marked it and then came back. If you remember, in the spinal cord the white matter and gray matter are "reversed" compared to the brain. That said, if the butterfly shaped region (ie, the gray matter) is colored (in this case) lilac and the rest (ie, white matter) is blackish, the only thing that is actually abnormal, is the region where the dorsal columns are, because it stains just like the normal gray matter. After that, you have to think about which fasciculus is damaged, the gracilis or the cuneatus. The gracilis is medial while the cuneatus is lateral (picture someone with glued legs and open arms). Hope this helped +1  


submitted by sgarzon15(3),

Thank you glitter zone of sketchy pharm. I shall never forget you

cr  why not C?. It´s not supose that it improve the efectivity of insulin? +  
cr  why not C?. It´s not supose that it improve the efectivity of insulin? +  
divya  because insulin uptake by adipose and muscle tissue is not limited to thiazolidinediones but also and mainly by metformin. and glitazones' primary MOA is PPAR gamma stimulation which then increases insulin sensitivity to other tissues. +  


submitted by hayayah(399),

Secondary hyperparathyroidism (usually d/t chronic renal failure).

Lab findings include ↑ PTH (response to low calcium), ↓ serum calcium (renal failure), ↑ serum phosphate (renal failure), and ↑ alkaline phosphatase (PTH activating osteoBlasts).

haliburton  also remember that in renal failure, 1-alpha-hydroxylase activity is down, so there will be less activation of 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol, which is a key mechanism causing hypocalcemia. +1  
cr  why not increased 25-hydroxycholecalciferol?, with the same logic haliburton explain +  
nala_ula  Increased phosphate, since the kidneys aren't working well, leads to the release of fibroblast growth factor 23 from bone, which decreases calcitriol production and decreased calcium absorption. The increase in phosphate and the decrease in calcium lead to secondary hyperparathyroidism. +1  
privatejoker  Probably a dumb question but how do we definitively know that the ALP is elevated if they give us no reference range in the lab values or Q stem? Everything stated above definitely makes sense from a physiological standpoint, I was just curious. +