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

USMLE images
 
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bestcoast027 said:
Is "sensitivity of a positive test" the same thing as PPV?
Click to expand...
No. Sensitivity is the number of people that have the dz and test + for the dz (TP) out of the total number of people that actually have the dz regardless of test result (TP + FN).

PPV is the chance that given a positive test result, the individual actually has the dz (TP/(TP+FP)).
 
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FalconSlice said:
No. Sensitivity is the number of people that have the dz and test + for the dz (TP) out of the total number of people that actually have the dz regardless of test result (TP + FN).
Click to expand...
What you are describing is the sensitivity of a test.
What he is asking is sensitivity of a positive test?
 
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Can someone explain the physio behind these two situations:
1) Long term COPD pt given supplement O2 -> respiratory drive goes down
vs
2) Pt. overdose on opiates, given supplemental O2 -> respiratory drive goes down (A firecracker card says this is is contraindicated but I just want to know exactly why)
 
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Can someone explain do we include "lost to follow up patient number" in the calculation of incidence rate in the denominator? do we consider them as been at risk or not.
 
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Krasmyc said:
Can someone explain do we include "lost to follow up patient number" in the calculation of incidence rate in the denominator? do we consider them as been at risk or not.
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They are no longer at risk and can no longer be part of the denominator just like when they die or develop the disease.
 
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images


Diagnosis, cause and mechanism?
 
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In serum sickness(type 3 HS), are the antigens the immunoglobins you injected the patient with, and the antibody from your own immune system, or is the antibody the actual immunoglobin you injected(i.e. horse immunoglobin) and binding up the antigen its suppose to be working against(antivenin or something) and then those immune complexes settle out into different tissues?
 
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during an experiment Rat leg was cut. Which of the following won't regrow?
neural crest cell
NMJ
Myelin.

@Transposony any idea? i guess they are testing us on permanent cell concept. in that case its muscle and neuron. I am not sure if there are any neural crest cell in an adult only the mature derivatives. which will make me think of NMJ.

also embryogenesis of limb development. How and when?

thanks
 
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Krasmyc said:
during an experiment Rat leg was cut. Which of the following won't regrow?
neural crest cell
NMJ
Myelin.

@Transposony any idea? i guess they are testing us on permanent cell concept. in that case its muscle and neuron. I am not sure if there are any neural crest cell in an adult only the mature derivatives. which will make me think of NMJ.

also embryogenesis of limb development. How and when?

thanks
Click to expand...

Neural crest cell. NMJ's can be damaged and regenerate. The neuron it's part of must be intact, which I think is the implication when it specifically says "NMJ". Same thing is true of myelin. Neural crest tissues tend to be permanent tissues.
 
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Kapooya said:
What genetic abnormality makes a patient susceptible to warfarin skin necrosis and why?
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Protein C or S deficiency. C and S have shorter half-lives than factors II, VII, IX, and X (all of which are dependent on Vitamin K) and thus Warfarin depletes levels of C and S faster than II, VII, IX, and X. In patients with C or S deficiency these levels drop precipitously when on warfarin, putting the patients in a hypercoaguable state before the other factors catch up -> warfarin skin necrosis.
 
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stepone2015 said:
Neural crest cell. NMJ's can be damaged and regenerate. The neuron it's part of must be intact, which I think is the implication when it specifically says "NMJ". Same thing is true of myelin. Neural crest tissues tend to be permanent tissues.
Click to expand...
thanks
 
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what will happen to testosterone level in a patient who is taking finasteride?

i think negative feedback loop is dependent on testosterone not DHT. so there shouldn't be any change? or does DHT also has a negative feedback effect?
 
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Krasmyc said:
what will happen to testosterone level in a patient who is taking finasteride?

i think negative feedback loop is dependent on testosterone not DHT. so there shouldn't be any change? or does DHT also has a negative feedback effect?
Click to expand...

Finasteride blocks T-->DHT. Testosterone will increase some.
 
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Krasmyc said:
what will happen to testosterone level in a patient who is taking finasteride?

i think negative feedback loop is dependent on testosterone not DHT. so there shouldn't be any change? or does DHT also has a negative feedback effect?
Click to expand...
seminoma said:
Finasteride blocks T-->DHT. Testosterone will increase some.
Click to expand...

I'd actually reckon it stays pretty much the same. We don't need DHT to exert hypothalamic/anterior pituitary negative feedback I wouldn't think, so less DHT shouldn't prompt a significant increase in LH. And then I'd also guess that transient increases in testosterone secondary to mere decreased conversion to DHT would simply be buffered by SHBG. Yet again, I haven't looked at any article on this stuff to confirm (which would have taken me the same amount of time as writing this post), but that's just my two cents.
 
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In terms of keeping things HY though:

1) MOA of clopidogrel
2) Name three drugs with MOA same as clopidogrel
3) Of those three drugs in #2, which one causes neutropenia?
4) What drug used to treat an enveloped, linear DNA virus causes neutropenia?
5) The organism treated by the drug in #5 causes what classic infection in immunocompromised patients?
6) Name three risk factors for SCC of esophagus
7) What kind of metaplasia is seen in Barrett esophagus? Frame your answer as ___ is converted to ___. And be as specific as possible.
8) Of the following, which one(s) is/are reversible: hyperplasia, hypertrophy, metaplasia, dysplasia, neoplasia, desmoplasia
9) MOA of dipyridamole
10) What are the male/female manifestations of the urethral folds, genital tubercle, urethral sinus, labioscrotal swelling?
11) Which aortic arch derivative gives rise to a structure closest to that which is most often ruptured in epidural hematoma?
 
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@Phloston 273 (1 point different than my "goal" score)
2) Name three drugs with MOA same as clopidogrel - prasugrel, ticagrelor, ticlopidine
7) What kind of metaplasia is seen in Barrett esophagus? Frame your answer as NKSS is converted to non-ciliated columnar with goblets. And be as specific as possible.
3) Of those three drugs in #2, which one causes neutropenia? ticlopidine

faisal 2000 said:
which drugs can cause Parkinson like syndrome ??
Click to expand...

Any D2 antagonist.
 
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@Phloston
1) MOA of clopidogrel - ADP receptor blocker on platelets
6) Name three risk factors for SCC of esophagus - Smoking, achalasia, Plummer-Vinson syndrome
11) Which aortic arch derivative gives rise to a structure closest to that which is most often ruptured in epidural hematoma? - 1st arch, Maxillary artery-->middle meningeal
seminoma said:
Any D2 antagonist.
Click to expand...
OTC antidote?
 
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@Phloston
4) What drug used to treat an enveloped, linear DNA virus causes neutropenia? Ganciclovir
5) The organism treated by the drug in #4 causes what classic infection in immunocompromised patients? CMV retinitis
9) MOA of dipyridamole --> increases cAMP in platelets by inhibiting it's degradation by PDE3--> Less ADP--> Less platelet aggregation.
It is also an adenosine uptake inhibitor--> increased extracellular concentration of adenosine --> Vasodilation.
 
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aspiringmd1015 said:
In serum sickness(type 3 HS), are the antigens the immunoglobins you injected the patient with, and the antibody from your own immune system, or is the antibody the actual immunoglobin you injected(i.e. horse immunoglobin) and binding up the antigen its suppose to be working against(antivenin or something) and then those immune complexes settle out into different tissues?
Click to expand...
The antigens are foreign proteins you are injected with. You form antibodies against those proteins. The complexes get deposited in different tissues leading to complement-mediated damage.
 
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dfib slim said:
Nice score, was this from an online NBME? Makes my 258 seem inadequate. Got some work to do, haha.
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No lol, it's just my made up goal because I think it looks good when you write it down on a piece of paper.

For all I know I'll fail the NBME I'm taking right now (first day of dedicated woo!)
 
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so its a
dfib slim said:
The antigens are foreign proteins you are injected with. You form antibodies against those proteins. The complexes get deposited in different tissues leading to complement-mediated damage.
Click to expand...
so youre actually prouding antibodies against foreign injected antibodies(in the case of passive immunization)
 
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@Phloston

8) Of the following, which one(s) is/are reversible: hyperplasia, hypertrophy, metaplasia, dysplasia, neoplasia, desmoplasia

10) What are the male/female manifestations of the urethral folds, genital tubercle, urethral sinus, labioscrotal swelling?
genital tubercle: Penis/Clitoris+erectile tissue under majora
urethral sinus: All the glands
urethral folds: Spongy Urethra/Minora
labioscrotal swelling: Scrotum/Majora
 
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dfib slim said:
Seems like you've been putting in work, you'll probably kill it.
Click to expand...

Satisfied I guess. Not sure exactly what the correlation is since the two charts I have give 2 different scores.. Do you guys have a correlation for the offline NBMEs?

Anyway, on topic, Triple therapy for h.pylori?
 
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why do muscarinic antagonists cause flushing of skin? This is probably a really dumb question but I just can't wrap my head around it
 
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