Official Step 1 High Yield Concepts Thread

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Transposony

Transposony

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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

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seminoma said:
The K+ backleak makes the lumen more positively charged. The Mg2+ and Ca2+ do whatever they can to get away from all the K+ floating around in the lumen. Eventually Mg and Ca find their way to the membrane and escape.

Btw, is that pic you attached from your classnotes? If so, I'm super jealous...
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haha no, that was borrowed from my friend googizzle. Cannot give my notes credit for that haha
 
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Transposony said:
Protease inhibitors e.g Indinavir

P.S. Please put a "spoiler alert" on the top if you are posting Qs from NBMEs or three main Q Banks for the people who has not yet done those Q Banks.
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I thought it would be nice to contribute for others here. I don't even read this thread really.
In one way or another literally everything people ask here will show up in a question bank. I will though.

Edit: I take that back after reading a few pages. Some of the stuff on here hasn't been in UW or Rx, both of which I'm done. So readers take things with a grain of salt, not need to be memorizing extra low yield details
 
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guys do you memorize all drug reaction in the general pharma pancreatits caused. didanosine steroid alcohol valproate azathioprine diuritics?
 
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This might be a bit tricky for some because it requires familiarity with cranial nerve neuroanatomy:

If you sever the sensory root of CN V, will all sensory to the face be affected? If yes, which nuclei/tracts will be affected? If no: what will remain intact, what nucleus/nuclei are spared, and why?
 
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seminoma said:
Lots of these are starting to tread into minutiae territory. Definitely more fun, but probably not super HY.
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I concur. My last question probably isn't too HY but it was something interesting I came across while doing some Neuro and I was reading some notes from class when I saw it.

I guess I'll answer my own question since nobody took the bait. Severing the sensory root of CN V will not take away all sensation from the face. Proprioception will remain intact for the TMJ so the jaw reflex will remain intact. Proprioception from the TMJ follows the motor tract of CN V and so severing the sensory root will not affect the reflex. The nucleus responsible for receiving proprioceptive input from the TMJ is the mesenecephalic nucleus.
 
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What about meds given with INH, cyclophosphamide, and methotrexate to reduce their respective side effects?
 
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faisal 2000 said:
when someone smoke just 2 or 3 cigarettes , how does lung get rid of Carcinogenesis of these cigarettes ?
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I feel like this is a trick question.. but larger particles = mucociliary elevator, smaller particles = alveolar macrophages (i.e. same mechanism as the other crap we inhale everyday)
 
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Mr. Mojo Risin said:
Loss of central sensitivity to CO2?
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Yup! In COPD there is chronic hypercapnia resulting in desensitization of central chemoreceptors. Normally respiratory drive is mediated primarily by the central chemoreceptors responding to CO2/H+. However, when the central chemoreceptors become desensitized, respiratory drive becomes controlled by peripheral chemoreceptors responding to hypoxemia. Thus, when you give supplemental O2 the peripheral chemoreceptors "turn off" and respiratory drive decreases.

This is also the reason you shouldn't give O2 to a patient with respiratory depression secondary to opioid overdose!
 
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