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 +0  (nbme21#7)

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


 +0  (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.


 +0  (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


 +0  (nbme21#33)

look at the image

Immunosuppression causes reactivation of VZV.


 +0  (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)


 +1  (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.


 -1  (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 ...

submitted by sgarzon15(4),

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(257),

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 +2  
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(2),

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(35),

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? +4  
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. +1  
divya  sweet explanation imgdoc +  


submitted by divya(1),

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 +1  
divya  hi. where is this given in first aid? +