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Welcome to divya's page.
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Comments ...

 +0  (nbme23#3)

okay but where in the question is it asking whether it's intention to treat or per protocol or as treated???

are we to assume its ITT if they don't mention anything or the part of the question that says "primary analysis" the giveway to ITT??

kpjk  I had the same doubt. I think if we were to consider "per protocol" then answer would have to be a mash of options A and B. There is no option that would be right for per protocol

 +1  (nbme23#45)

i don't think you need to think all that much. look at all the options and think of what happens when they increase. A, B, C, D and F all can cause interstitial edema. But increasing precapillary resistance definitely doesn't.

 +0  (nbme20#10)

FA 2019 Pg 415

Prosthetic heart valves and aortic stenosis may cause hemolytic anemia secondary to mechanical destruction of RBCs.

 +0  (nbme20#1)

For anyone interested, the current post exposure prophylaxis regimen contains - Tenofovir + Emtricitabine + Raltegavir

Link for PEP prophylaxis following occupational exposure

 +0  (nbme20#1)

uworld q id - 582 for reference gonadotropins increase aromatase activity.

Aromatase activity is increased by - 1) age 2) obesity 3) insulin 4) gonadotropins 5) alcohol

 +1  (nbme21#7)

Pregnant women are 20 times more likely to get infected with Listeria.

 +1  (nbme21#41)

The porphyrinogens following PBG conversion into Uroporphryinogen 3 cause photosensitivity because ONLY these react with oxygen on excitation by UV light.

Therefore deficiency of any of the following enzymes -

uroporphyrinogen decarboxylase coproporphyrinogen oxidase, proporphyrinogen oxidase and ferrrochelatase can cause photosensitivity.

But between answer choices B & C, C is right because of it's association with Hep C, raised AST ALT as @neonem said.

 +0  (nbme21#4)

C dip exotoxin inhibits protein synthesis(translation) via ADP ribosylation of EF 2.

 +3  (nbme21#48)

increase in cAMP (Gs) - beta2 - vasodilation

decrease in cAMP (Gi) - alpha2 - vasoconstriction

increase in IP3 DAG (Gq) - alpha1 - vasoconstriction

increase in cGMP - M3 - NO induced vasodilation

 +1  (nbme21#33)

look at the image

Immunosuppression causes reactivation of VZV.

 +1  (nbme21#18)

Currently Alzheimer's disease treatment includes -

1)Enhanced Ach transmission (Donepezil, Rivastigmine, Galantamine

2) Neuroprotection via antioxidants (Vitamin E)

3) NMDA receptor antagonism (Memantine)

 +2  (nbme21#37)

simply internal capsule has corticospinal and corticobulbar tracts pass thru it, hence the c/l hemiparesis of body and face.

If at all they want to know what specifically passes thru ic (which is practically NEVER), then anterior limb - thalamocortical tracts, genu - corticobulbar, posterior limb - corticospinal, all sensory

 +0  (nbme21#26)

Can anyone discuss what's responsible for inhibiting the processes given as other options?

 +0  (nbme21#12)

Why is there rhinorrhea in opioid withdrawal? And also, if stimulants like cocaine cause nasal vasoconstriction, shouldn't opioid withdrawal do the same?

 +1  (nbme21#18)

obvious answer choices between duodenal atresia and pyloric stenosis. duodenal atresia presents with bilious vomiting within 1st day of life. other features - double bubble on xray. whereas pt here has non bilious vomiting at 4th week of life.

 -4  (nbme21#41)

loperamide is basically diphenoxylate + atropine. atropine is added to reduce abuse potential by diphenoxylate.

divya  ugh sorry. this is wrong. idk why i always thought loperamide is diphhenoxylate

 +0  (nbme21#33)

agree with burak. they're trying to say that primary goal of treatment with supplemental o2 is to make sure there is no retinal damage.

Subcomments ...

The patient has ATN secondary to renal ischemia. Due to tubular necorsis, the patient will have an elevated FeNa. The patient's urine will also be dilute, but this will be reflected by the low urine osmolality, not the FeNa

mousie  Hypotension can also cause pre renal azotemia with a FENa <1%.... How do you know this is ischemic ATN and not hypotension induced Prerenal Azotemia? +1  
sympathetikey  I had the same thought as you @mousie, but I think "azotemia" and low urine output push it more towards ATN (looking back; I got it wrong too). Plus, the initially MVC / muscle damage probably caused some tubule injury by itself. +  
ajo  This might help clarify why the pt. has ATN rather than pre renal azotemia. The question did mention, though subtly, that the bleeding was controlled. That most likely indicates that his hypovolemia has been corrected. Developing azotemia 24 hrs after correction of hypovolemia is more suggestive of ATN (since he doesn't have hypovolemia anymore). I hope that helps and feel free to correct me, if I am wrong. +11  
ajo  In addition to my earlier comment, I just noticed the question also explicitly mentioned that he was fully volume restored. Which is consistent with my earlier assumption! +6  
gh889  Although initially, hypotension causes prerenal azotemia, the volume correction pushes you away from prerenal azotemia. but they want you to remember that in hypovolemia, the kidneys are also becoming ischemic, and so development of azotemia 24 hours later is more indicative of intrarenal azotemia due to ATN +  
sugaplum  for anyone who wants to see it: FA 2019 pg591 +1  
divya  i'm confused about one thing. if the tubules aren't working like they should, the bun:cr ratio falls right? doesn't that essentially mean azotemia reduces too? +  

submitted by krewfoo99(17),

Afterload and heart rate share an inverse relationship.

As the umbilical cord is compressed, there is an increase in systemic vascular resistance (Think of how the pressure would increase if you were to press down on a water hose). Thus, the afterload is increased and there is a compensatory decrease in heart rate.

divya  yeah, i too thought similarly. btw increase afterload --> increase in bp --> baroreceptor firing --> decrease in heart rate. is that it? +  

Patient has a ganglion cyst, which can spontaneously regress.

medschul  Mine would beg to differ >:O +5  
usmleuser007  Where would I have come across something like this (FA, Pathoma, or out of my S)? +1  
motherfucker2  I thought this bitch was a lipoma. Mother fucker +2  
divya  mf2 lipomas is fat. although fat may exist in liquid form, its still opaque, therefore negative transillumination. unlike ganglion cyst. +1  

submitted by jrod77(17),

The systolic pressure difference between the left ventricle and the aorta in this pt. is pretty significant, Whereas in a normal heart those systolic pressures should be just about equal. This hints at the fact that the left ventricle has to put in alot of work to push through the aortic valve. That extra pressure goes into opening the valve and does not appear in the aorta.

divya  why is left atrial pressure normal while pulm arterial and right ventricular pressures are high? +  

submitted by sajaqua1(262),

The single most important thing about this gross pathology is that the disease is multinodular. This indicates metastases from distant sites.

Liver abscesses are usualy singular, filled with creamy yellow pus, and may show a fibrous capsule. Cirrhosis often shows a yellow color due to fatty change as well as regenerative nodules, which are not present here. A focal nodular hyperplasia is a singular tumor of the liver, and this is multinodular. Hepatitis B is a little harder to distinguish because from what I can tell it can be multinodular in some cases, but this liver also shows none of the sclerosis from chronic inflammation that would likely accompany Hep B. Finally, we see no dark discoloration to indicate infarction.

monkd  It doesn't explain the sudden death, but I suppose they aren't asking for that! +1  
charcot_bouchard  I hate this type of ques. Here it is. Tell me what it is? +1  
divya  also, a liver infarct is unlikely due to rich dual blood supply. +  

submitted by luke.10(2),

picorna( coxsackie ) is more common than adenovirus but both can caause viral myocarditis

dulxy071  Yeah Adeno is what I went for unfortunately +  
divya  thank god for sketchy.. +2  

submitted by whossayin(7),

why can't "organification defect in T3 and T4" be the answer?

sugaplum  I think if it was organification defect you wouldn't have a normal T4 level in the serum. +3  
divya  because there would be an overall decrease in serum T3, T4 and increase in serum TSH levels. +  

submitted by aishu007(2),

can anyone explain why enterococcusfaecalis is the answer here?

priapism  Best I can guess is that both S. aureus and E. faecalis can cause UTI, but S. aureus is described as having clusters where as the other Gm+ cocci are in chains +3  
nala_ula  My doubt here in this question is the fact that Enterococcus faecalis is a normal gut microorganism that causes these different symptoms of sickness after genitoruinary or gastrointestinal procedures... but in this question there is no mention of any procedures. +  
fez_karim  its says chains, so not staph. only other is entero +  
temmy  according to first aid, staph aureus is not one of the high yield bugs for UTIs +  
temmy  uti bugs are E.Coli Staph saprophyticus Klebsiella pneumonia Serratia Marcescens Enterococcus Proteus mirabilis Pseudomonad aeruginosa +  
privatejoker  Where in FA 2019 does it list that C.coccus is specifically in chains? +  
privatejoker  E.Coccus* i mean +  
divya  @privatejoker FA 2018 Pg 134 table +  

submitted by sgarzon15(5),

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 neonem(302),

This is a case of acute gout. Monosodium urate crystals are taken up by neutrophils, leading to an acute inflammatory reaction. T-cells aren't really involved in gout (more rheumatoid arthritis).

hungrybox  Great explanation! So frustrating that I got this wrong, should have been easy. +1  
temmy  the way i thought about it was how did the neutrophils get there? the answer is via increased vascular permeability +3  
nor16  they, unfortunately, did not ask " how did neutrophils get there" but " whats the cause of the swelling " not to confuse with " what causes the swelling " +  
divya  absolutely right temmy. that's how i thought about it too. +  

submitted by tamey(0),

im a little confused isnt blocking ampulla of vater(hepatopancreatic ampula) would cause obstruction of both pancreatic duct and common bile duct and in this case the patient would have cholangits too, not only pancreatitis!!!

divya  true but none of the other options cause pancreatic duct dilation. options a, b and c would cause obstruction above the level of pancreas. +  
lilmonkey  It doesn't say ONLY pancreatitis, but just enough information to choose the correct answer. Maybe, in the test writers mind if they mention cholangitis and jaundice that would be too much hints :). +  

submitted by cantaloupe5(48),

This one was tricky but I think you could’ve done this one without knowledge of NMDA receptors. Stem told you that glutamate activates both non-NMDA and NMDA receptors but it activated only non-NMDA receptors in the early phase. That means NMDA receptors activate after non-NMDA receptors. That means something was delaying NMDA receptor activating and the only answer that made sense as the Mg inhibiting NMDA at resting potential. Once the cell is depolarized by non-NMDA receptors, NMDA receptors can be activated.

hungrybox  I forgot/didn't know this factoid and narrowed it to the correct answer and a wrong answer. Guess which one I chose? +5  
yotsubato  >That means something was delaying NMDA receptor activating and the only answer that made sense as the Mg inhibiting NMDA at resting potential. What makes the fasting gating kinetics choice incorrect then? +2  
imgdoc  NMDA receptors are both voltage gated and ligand gated channels. Glutamate and aspartate are endogenous ligands for this receptor. Binding of one of the ligands is required to open the channel thus it exhibits characteristics of a ligand channel. If Em (membrane potential) is more negative than -70 mV, binding of the ligand does NOT open the channel (Mg2+ block on the NMDA receptor). IF Em is less negative than -70 mV binding of the ligand opens the channel (even though no Mg2+ block at this Em, channel will not open without ligand binding. Out of the answer choices only NMDA receptors blocked by Mg2+ makes sense. Hope this helps. +2  
divya  sweet explanation imgdoc +  

submitted by divya(10),

loperamide is basically diphenoxylate + atropine. atropine is added to reduce abuse potential by diphenoxylate.

divya  ugh sorry. this is wrong. idk why i always thought loperamide is diphhenoxylate +  

submitted by priapism(3),

Per First Aid: antibodies against ABO blood types tend to be IgM or IgG, which is why the answer is IgG + complement and not IgA + complement

yotsubato  IgA also has no role in any hypersensitivity reaction +2  
divya  hi. where is this given in first aid? +