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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This is a good idea for a thread. I have a question:
If someone was diagnosed with Gonorrhea, would you treat only for Gonorrhea, treat for Gonorrhea and screen for Chlamydia, or treat both Gonorrhea and Chlamydia?

This question applies to someone who was diagnosed with Chlamydia as well - would you also co-treat Gonorrhea?

Kaplan Microbiology says to co-treat if you're diagnosed with one of them. SketchyMicro says treat for only the one your were diagnosed with, and if possible choose an answer that also screens for the other. Which is correct?
 
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Treat both Gonorrhea and Chlamydia since they frequently co-infect.
 
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What will happen in a patient with Acetaminophen ingestion with a P450 inducer?
 
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Macaroon_Berry said:
This is a good idea for a thread. I have a question:
If someone was diagnosed with Gonorrhea, would you treat only for Gonorrhea, treat for Gonorrhea and screen for Chlamydia, or treat both Gonorrhea and Chlamydia?

This question applies to someone who was diagnosed with Chlamydia as well - would you also co-treat Gonorrhea?

Kaplan Microbiology says to co-treat if you're diagnosed with one of them. SketchyMicro says treat for only the one your were diagnosed with, and if possible choose an answer that also screens for the other. Which is correct?
Click to expand...

You always treat for both.
 
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Transposony said:
Treat both Gonorrhea and Chlamydia since they frequently co-infect.
Click to expand...
seminoma said:
You always treat for both.
Click to expand...

Treat for both only if gram(-) diplococci are seen on gram stain. If you see nothing, you only Tx for chlamydia cuz you know gonorrhea isn't there. I think one of my slides years ago had an error in it where I said you Tx for both regardless, but it's only if you see the diplococci.
 
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Phloston said:
Conditions in which you see schistocytes (5) vs spherocytes (2)?
Click to expand...
Intravascular (schistocytes) v/s extravascular hemolysis (spherocytes).
Intravascular (schistocytes) : Microangiopathic hemolytic anemias ( DIC, HUS, TTP ), PNH, mechanical valve
Extravascular hemolysis (spherocytes): Hereditary spherocytosis and autoimmune hemolytic anemia.
Haptoglobin levels decreased in intravascular and normal in extravascular hemolysis.
 
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Phloston said:
Treat for both only if gram(-) diplococci are seen on gram stain. If you see nothing, you only Tx for chlamydia cuz you know gonorrhea isn't there. I think one of my slides years ago had an error in it where I said you Tx for both regardless, but it's only if you see the diplococci.
Click to expand...

Didn't know this. We've been taught that you treat every chlamydia infection for both :(.
 
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Just wanting to make sure on this one.. Goljan RR lists "Factor V deficiency" as a cause for hypercoagulability. It should say "Factor V Leiden" instead, right?

V deficiency = bleeding
V Leiden = clotting
 
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seminoma said:
Just wanting to make sure on this one.. Goljan RR lists "Factor V deficiency" as a cause for hypercoagulability. It should say "Factor V Leiden" instead, right?

V deficiency = bleeding
V Leiden = clotting
Click to expand...
Yes
 
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Phloston said:
Hmm tacrolimus, niacin, gatifloxacin, thiazides...
Click to expand...
Thiazides, Diazoxide, atypical antipsychotics, etc
Any drug (e.g. as above) or condition (i.e. hypokalemia) which keep the beta cells hyperpolarized i.e. keep the K+ channels open will lead to hyperglycemia over a period of time.
Unless the K+ channels are closed (or IOW the beta cell depolarizes) there will be no calcium entry to stimulate insulin release.
Tacrolimus has a slightly different MOA as well as other mechanisms for insulin resistance. It binds to an intracellular protein, FKBP-12, and forms a complex with calcium, calmodulin, and calcineurin since calcineurin is expressed in the beta cell. So, less calcium to stimulate insulin release from beta cells.
 
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Phloston said:
Treat for both only if gram(-) diplococci are seen on gram stain. If you see nothing, you only Tx for chlamydia cuz you know gonorrhea isn't there. I think one of my slides years ago had an error in it where I said you Tx for both regardless, but it's only if you see the diplococci.
Click to expand...
Makes sense.
Although some books still mention treating for both IIRC.
 
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In a patient on Proton Pump Inhibitors the Gastrin levels will go up which will induced release of histamine from ECL-like cells.
So is is correct to say that a patient on Proton Pump Inhibitors will have raised histamine levels?
My question is, do these patients have other (systemic) symptoms related to raised histamine since the PP is already blocked or histamine metabolized quickly?
 
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Transposony said:
Intravascular (schistocytes) v/s extravascular hemolysis (spherocytes).
Intravascular (schistocytes) : Microangiopathic hemolytic anemias ( DIC, HUS, TTP ), PNH, mechanical valve
Extravascular hemolysis (spherocytes): Hereditary spherocytosis and autoimmune hemolytic anemia.
Haptoglobin levels decreased in intravascular and normal in extravascular hemolysis.
Click to expand...

Nice.

Was thinking DIC, HUS, TTP, mechanical hemolysis and HELLP syndrome for schistocytes (obviously the list wouldn't be limited to that).

For spherocytes was thinking hereditary spherocytosis and drug-/infection-induced hemolytic anemia (which is basically autoimmune as you've said).
 
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seminoma said:
Only ones I can think of are vanc (rapid infusion) and caspa/micafungin. I think there's one more though? Niacin is via PG release, so not niacin.
Click to expand...
Polyenes (Amphoterrible) and Meperidine.
Good point regarding Niacin.
 
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Maybe we can make this a HY concepts in pharm thread? Then make new threads for path, micro, etc?
 
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seminoma said:
Maybe we can make this a HY concepts in pharm thread? Then make new threads for path, micro, etc?
Click to expand...

I like this idea. @Transposony do you have privileges to change the thread name to Official Step 1 HY Pharm Concepts Thread?

What do people think about me making individual "HY ___ Concept" threads? Yea or nay?
 
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What non-peptidoglycan inhibiting drugs have anti-pseudomonal activity? I have 6-7 drugs in mind.

And what (one) carbapenem does not have anti-pseudomonal activity?
 
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seminoma said:
Maybe we can make this a HY concepts in pharm thread? Then make new threads for path, micro, etc?
Click to expand...
Seems like a good idea but I am not sure since then you will have to look for a specific thread to post a question.
Here, you can post whatever you like and also on the real deal it's all random concepts!
 
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seminoma said:
What non-peptidoglycan inhibiting drugs have anti-pseudomonal activity? I have 6-7 drugs in mind.

And what (one) carbapenem does not have anti-pseudomonal activity?
Click to expand...
Fluoroquinolones.
Ertapenem

Which Fluoroquinolone has anaerobic activity?
 
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What is the most differentiating feature between Atropine poisoning, TCA overdose and Amphetamine toxicity since they all have s/s of sympathetic over-activity?
 
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Reason for the difference in blood lactate levels between Von Gierke and Cori disease?
 
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it's like all these drugs are second nature to you guys. did you all continually review them after learning them the first time in class?
 
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dfib slim said:
Flushing, dryness, urinary retention, agitation, constipation, mydriasis.
Click to expand...
Great.
To summarize the differentiating feature are:
Atropine poisoning --> dry skin (Muscarinic block as sweating is sympathetic muscarinic mediated)
TCA overdose --> dry skin with arrhythmia and hypotension (Muscarinic and alpha 1 block)
Amphetamine toxicity --> warm and sweaty skin (as sweating is sympathetic muscarinic mediated)
They all have s/s of sympathetic over-activity.
 
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dextor2003 said:
did you all continually review them after learning them the first time in class?
Click to expand...
It's a continuous process and fun since it one of those rare Step 1 subjects which you are actually going to use in clinical practice.
 
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