Official Step 1 High Yield Concepts Thread

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

Transposony

Do or do not, There is no try
10+ Year Member
Joined
Nov 10, 2011
Messages
1,811
Reaction score
999
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

Members don't see this ad.
 
Last edited:
  • Like
Reactions: 5 users
can we say Guillain Barre is type II since there are autoantibodies against gangliosides ? and also it is type IV since Subsequent exposures to c.jejenum will make th1 which already sensitize to the bacteria bind to it and deposition in the axon and causes GBS isn't it ?
 
Members don't see this ad :)
Name a few P-glycoprotein inhibitors.

Hint: for one of the drugs I'm thinking of, there have been reports of people recreationally taking loperamide with this common OTC medication.
 
Name a few P-glycoprotein inhibitors.

Hint: for one of the drugs I'm thinking of, there have been reports of people recreationally taking loperamide with this common OTC medication.

Verapamil is the only one I know of. It's used with some anticancer drugs.
 
  • Like
Reactions: 1 user
What do Marfan's and Polycystic Kidney disease have in common besides berry aneurysms?

For what it's worth, I'm not sure if Marfan is actually associated with berry aneurysms. FA 2014 had it, but DIT mentioned that Up-To-Date states that it may not be associated, and FA 2015 took it out.
 
  • Like
Reactions: 1 user
For what it's worth, I'm not sure if Marfan is actually associated with berry aneurysms. FA 2014 had it, but DIT mentioned that Up-To-Date states that it may not be associated, and FA 2015 took it out.

Yeah, I believe the association is with increased risk of rupture of berry aneurysms (for Marfan), not increased incidence of berry aneurysms.
 
Members don't see this ad :)
Yeah, I believe the association is with increased risk of rupture of berry aneurysms (for Marfan), not increased incidence of berry aneurysms.
Interesting article.
http://stroke.ahajournals.org/content/30/8/1632.full
We conclude that there exists no evidence that Marfan syndrome is associated with an increased prevalence of intracranial aneurysms. This conclusion implies that the already extensive and costly evaluations pursued in these patients do not need to include serial intracranial radiographic studies intended to rule out these lesions.
 
Last edited:
What biochemical compound is associated with adverse cardiovascular complications?

In what two vitamin deficiencies would this compound be elevated?
 
For what it's worth, I'm not sure if Marfan is actually associated with berry aneurysms. FA 2014 had it, but DIT mentioned that Up-To-Date states that it may not be associated, and FA 2015 took it out.

Well regardless, I was going for MVP.
 
  • Like
Reactions: 1 user
Thiazides open potassium channels --> inhibits insulin release. Same mechanism by which it induces vasodilation.

Yeah, that's the big picture. K+ loss causes K+ to exit all cells. Open K+ channels with K+ efflux prevents the Ca+ influx and thus results in decreased insulin secretion.
 
  • Like
Reactions: 2 users
Bacteria using reorganization of actin polymerization to facilitate motility from cell to cell ?
 
CBC differences between Fanconi's anemia and Diamond-Blackfan anemia?
 
  • Like
Reactions: 1 user
In FA, it states that a DECREASED interval between S2 and Opening Snap relates to INCREASED severity

Can someone please explain to me why that's the case? I was trying to reason that the longer it takes to snap open, the greater the pressure building up in the LA and the increase in severity........This doesn't make sense to me as I think an increased interval between S2 and OS would mean the valves are really really stenosed, thus more serious
 
can we say Guillain Barre is type II since there are autoantibodies against gangliosides ? and also it is type IV since Subsequent exposures to c.jejenum will make th1 which already sensitize to the bacteria bind to it and deposition in the axon and causes GBS isn't it ?

It's mixed type-II/-IV. The literature confirms that. This was causing issues in the FA errata. And people will likely continue to submit errata claiming it's either II or IV, but the point being that the USMLE doesn't assess every detail about everything. And they likely would never assess something so debated/borderline either. The USMLE would literally just care that you know it's a syndrome of peripheral nerves / Schwann cells.
 
  • Like
Reactions: 1 users
CBC differences between Fanconi's anemia and Diamond-Blackfan anemia?

I know this seems really LY, but there's a UWorld question for 2CK that comes down to you knowing the difference about the thumbs in Fanconi vs Diamond-Blackfan anemias. Fanconi can present with absent thumbs/radius; Diamond-Blackfan can present with a triphalangeal thumb. Stupid, I know. But UW 2cK assesses it! And the chance of that showing up on the real deal is probably zero percent.
 
  • Like
Reactions: 3 users
1- how does Desmopressin work in treatment of von willebrand disease ?
2- how does liver detoxified substances like carcinogens?
 
Last edited:
It's mixed type-II/-IV. The literature confirms that. This was causing issues in the FA errata. And people will likely continue to submit errata claiming it's either II or IV, but the point being that the USMLE doesn't assess every detail about everything. And they likely would never assess something so debated/borderline either. The USMLE would literally just care that you know it's a syndrome of peripheral nerves / Schwann cells.
Not sure what are we talking about here?:unsure:
 
In FA, it states that a DECREASED interval between S2 and Opening Snap relates to INCREASED severity

Can someone please explain to me why that's the case? I was trying to reason that the longer it takes to snap open, the greater the pressure building up in the LA and the increase in severity........This doesn't make sense to me as I think an increased interval between S2 and OS would mean the valves are really really stenosed, thus more serious

As MV Stenosis becomes more severe LA pressure gets higher. This is why you can use PWCP to monitor progression; higher LAP means worsening disease. As LAP gets higher and higher, it is able to force the MV open more quickly. Thus, the shorter gap between S2 and OS.

Look at how high LAP is when the AV closes. Yeah MV is stenosed, but as LV pressure drops during isovolumetric relaxation, the LA/LV pressure gradient is going to get high really fast if LAP is high from the start.
HD004%20mitral%20stenosis.gif
 
Last edited:
  • Like
Reactions: 3 users
Top