Official Step 1 High Yield Concepts Thread

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Transposony

Do or do not, There is no try
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Let's discuss our doubts/offer clarifications about mechanisms/concepts for Step 1

ASK ANY QUESTIONS here.

To kick start the thread here is something I didn't know:

1. Penicillin-binding proteins (PBPs) are actually enzymes (transpeptidases & carboxypeptidases) which cross-link peptidoglycan. Penicillins binds to these enzymes and inactivating them thereby preventing cross-linkiing of peptidoglycan.

2. Periplasmic space (Gram -ve) contain proteins which functions in cellular processes (transport, degradation, and motility). One of the enzyme is β-lactamase which degrades penicillins before they get into the cell cytoplasm.
It is also the place where toxins harmful to bacteria e.g. antibiotics are processed, before being pumped out of cells by efflux transporters (mechanism of resistance).

There are three excellent threads which you may find useful:

List of Stereotypes

Complicated Concepts Thread

USMLE images
 
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How many days post-MI?
original.jpg
 
Ipilimumab. It targets CTLA4 on the T cell allowing for increased proliferation of CTLs. Used for melanoma.

Nice. I was (wrongly) thinking abatacept or belatacept, which are both CTLA4s.. but they are Tcell inhibitors and aren't mabs like you asked for.
 
I was thinking of a certain pharmacological agent. Not in FA and don't know if HY but thought it was interesting as having a unique mechanism that activates the immune system.

Phloston has said that the mabs aren't super HY (except the obvious ones in FA), but my school really hammers them.. I guess they're becoming more popular clinically, but since USMLE questions are a few years behind that might be why they aren't tested often?


Antibiotic which is also a 5-lipoxygenase inhibitor ?

Minocycline. Btw, can anyone confirm or deny that zileuton is no longer available in the US? Our pharm teacher told us there are "currently no 5-lox inhibitors available in the US", but I didn't find anything online saying that zileuton had been completely discontinued.. I know one formulation of zileuton is gone, but according to wiki the other formulation is still available.
 
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Fat malabsorption leads to increased free oxalate which is taken up by the gut and leads to oxalate stones.
Normally Calcium binds oxalate in the gut. In Crohn's fat binds this Calcium leaving oxalate free to be absorbed.
Malabsorption causing fat to bind to calcium leaving oxalate to be absorbed and deposit in kidney
It's actually fat malabsorbtion, decreased calcium in the gut with increased oxalate absorption and resulting kidney stone formation. I'm disappointed in all of you.
 
Maybe nef?
Just read about it on wiki and it seems likely. We didn't learn about nef in micro though... maybe I need to look into HIV more.

I would say heterozygous CCR5 mutation, because homozygous CCR5 mutation leads to immunity.
Yeah that's true, but he was asking about a viral gene mutation. CCR5 is a host gene.
 
Just read about it on wiki and it seems likely. We didn't learn about nef in micro though... maybe I need to look into HIV more.


Yeah that's true, but he was asking about a viral gene mutation. CCR5 is a host gene.
Wouldn't a CCR5 mutation be in the human genome instead of the viral?

Derp. My bad guys. My vote would be for nef since that confers virulence.

I guess I'll add to the discussion with the following question: what's the effect of the nef protein on host immunity? (I'm thinking of two).
 
Derp. My bad guys. My vote would be for nef since that confers virulence.

I guess I'll add to the discussion with the following question: what's the effect of the nef protein on host immunity? (I'm thinking of two).
Downregulation of CD4 and IL2?
 
Just read about it on wiki and it seems likely. We didn't learn about nef in micro though... maybe I need to look into HIV more.
Yeah that's true, but he was asking about a viral gene mutation. CCR5 is a host gene.
Yes, that was the reason for posting this Qs.
 
with the ca oxalate, isnt it that normally oxalate just simply doesnt get reabsorbed normally in the gut, but with crohns ileal trasmural damage, allows oxalate to be reabsorbed, which normally isnt suppose to, and gets into the bloodstream in abnormal amounts, and in the kidney it precipitates out? (this is what sattar said i think)
 
What is a gardos channel and what condition may an inhibitor be used for?
Had no idea so looked it up.

The Gardos channel aka KCNN4 is a protein "pump" that expels intracellular potassium when activated by calcium. The red cells loose water along with calcium. The result is a higher intracellular Hb concentration. This promotes polymerization of deoxygenated HbS.

gardos.gif


Senicapoc for SCD.
 
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