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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seminoma said:
Can you guys help clarify the varus/valgus stress tests for me?

In the MCL test (abnormal passive abduction) you are exerting a medially directed (laterally originating) force, which (if MCL is injured) will result a valgus deformity (i.e. knee moves medially and distal tib/fib move laterally). So the force originates laterally, but pushes medially.. which is considered a valgus force.

In the LCL test (abnormal passive adduction) you are exerting a laterally directed (medially originating) force, which will result in a varus deformity (i.e. knee moves laterally, distal tib/fib moves medially). So the force originates medially, but pushes laterally.. which is a varus force.

So basically varus "deformity" and varus "force" are in opposite directions (same for valgus force/deformity)?
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It's opposite of you are referring the origin of the force.

If you think of it as the direction of the force then it would be the same.

A lateral force of the knee is a varus stress test resulting in a varus deformity.
 
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how do atypical antipsychotic drugs lead to tradive dyskinasia (what is the mechanism byonid that) ?
 
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faisal 2000 said:
how do atypical antipsychotic drugs lead to tradive dyskinasia (what is the mechanism byonid that) ?
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I hope you know that TD is not a major SE for atypicals, and it is much MORE significant for the first generation anti-psychotics. But the low incidence of TD with atypicals can be attributed to the same mechanism as for the FGA >> D2 antagonism in the Nigrostriatal pathway >> upregulation of postsynaptic D2 receptors (with prolonged duration --- TIME and technically increasing Vmax for the drug) >> over-excitation of the nigrostriatal pathway = TD. Even though, atypicals primarily work through antagonism of D2C receptor found in the mesolimbic system, than D2A receptor found in the nigrostriatal pathway, the drug is not that selective as we wish, especially with increased doses hence overflow of antagonism at a different pathway is likely. But, overall this is not a big deal in comparison to the FGAs.
 
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Ethics question for you guys.

Obviously no romantic relationships with current patients, but what's the deal with a former (but not current) patient?

FA says never say "there can be no relationship while you are a patient," because this implies that a relationship is possible if the individual is no longer a patient.

UW (QID 10464) says relationships with former patients are acceptable on a case-by-case basis.

Really not a big deal except for the fact that the UW question has both "explain to the patient that romantic relationships with current or former patients is always unethical" and "explain that romantic relationships with current patients is always unethical" as answers.

FA is implying that romantic relationships with former patients is always unethical. UW is saying romantic relationships with former patients is a gray area.

What say you (for testing... not what is your opinion about patient relationships irl)?
 
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seminoma said:
Ethics question for you guys.

Obviously no romantic relationships with current patients, but what's the deal with a former (but not current) patient?

FA says never say "there can be no relationship while you are a patient," because this implies that a relationship is possible if the individual is no longer a patient.

UW (QID 10464) says relationships with former patients are acceptable on a case-by-case basis.

Really not a big deal except for the fact that the UW question has both "explain to the patient that romantic relationships with current or former patients is always unethical" and "explain that romantic relationships with current patients is always unethical" as answers.

FA is implying that romantic relationships with former patients is always unethical. UW is saying romantic relationships with former patients is a gray area.

What say you (for testing... not what is your opinion about patient relationships irl)?
Click to expand...

I remember that question mostly because of the answer choices.
I believe that in "Khans 100 cases" it pretty much says that both current and former patients are a big no-no. Also, I think FA pretty much says that it´s not ok to date former ones as well. I hope step 1 is not going to have us choose between these two, but if it will I´ll pick "current and former". But then again, behavioral is my weakest subject on UW.
 
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seminoma said:
Ethics question for you guys.

Obviously no romantic relationships with current patients, but what's the deal with a former (but not current) patient?

FA says never say "there can be no relationship while you are a patient," because this implies that a relationship is possible if the individual is no longer a patient.

UW (QID 10464) says relationships with former patients are acceptable on a case-by-case basis.

Really not a big deal except for the fact that the UW question has both "explain to the patient that romantic relationships with current or former patients is always unethical" and "explain that romantic relationships with current patients is always unethical" as answers.

FA is implying that romantic relationships with former patients is always unethical. UW is saying romantic relationships with former patients is a gray area.

What say you (for testing... not what is your opinion about patient relationships irl)?
Click to expand...
If you're a psychiatrist, never appropriate.
If you're not a psychiatrist, you can if they are not a current patient.
Source: Dr. Fischer, USMLE Medical Ethics
 
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a decrease in TPR increase your venous return because of more forward flow into your veins right? so on the cardiac vascular function curve it says it only increases your venour return but not your EDV. How is that possible?
 
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seminoma said:
Ethics question for you guys.

Obviously no romantic relationships with current patients, but what's the deal with a former (but not current) patient?

FA says never say "there can be no relationship while you are a patient," because this implies that a relationship is possible if the individual is no longer a patient.

UW (QID 10464) says relationships with former patients are acceptable on a case-by-case basis.

Really not a big deal except for the fact that the UW question has both "explain to the patient that romantic relationships with current or former patients is always unethical" and "explain that romantic relationships with current patients is always unethical" as answers.

FA is implying that romantic relationships with former patients is always unethical. UW is saying romantic relationships with former patients is a gray area.

What say you (for testing... not what is your opinion about patient relationships irl)?
Click to expand...

I believe I had read somewhere that it's generally acceptable that one could see a prior patient after two years have passed. I would guess the basis for that is to prevent the subconscious urge (both ways) to end the patient-physician relationship (which could be deleterious to the patient) in order for there to immediately be something intimate.
 
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reduced glucose tolerance( that you see with sleep deprivation) does that mean reduced isnulin secretion, or some sort of insulin resistance that develops where insulin cant drive glucose into the cell? or what does it mean lol?
 
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aspiringmd1015 said:
reduced glucose tolerance( that you see with sleep deprivation) does that mean reduced isnulin secretion, or some sort of insulin resistance that develops where insulin cant drive glucose into the cell? or what does it mean lol?
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I think insulin tolerance generally refers to downregulation of insulin receptors. Therfore insulin secretion will rise to compensate --> which will lead to further downregulation --> eventually the pancreatic B-cells will not be able to keep up the production.
 
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Does anyone know whether any protease inhibitors other than Ritonavir inhibit CYP450? Furthermore, do any NNRTIs other than Nevirapine induce CYP450?

Also, I just noticed that UWorld changed from recommending specific anticonvulsants for various seizure disorders to instead making general statements about "narrow-spectrum" and "broad-spectrum" anticonvulsants (other than Ethosuximide for Absence). Does anyone have any more insight into this?

Danke!
 
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pathologyDO said:
3 types of vasculitis associated with RPGN and their key differentiating labs/signs?
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All cause RPGN (nephritic syndrome):
- Goodpasture syndrome: Hematuria, hematoptysis. Anti-GM ab --> linear depostion on IF.
- Granulomatosis with polyangitis (Wegeners): Granulomas in upper+lower resp tract (can cause hematoptysis) + kidneys (hematuria). c/PR3-ANCA + , - IF (pauci-immune)
- Microscopic polyangitis: Necrotizing vasculitis (w/o granulomas) in lower resp tract only (vs Wegeners) + kidney involvement. p/MPO-ANCA +, - IF

Once again: Primary biliary cirrhosis vs Primary sclerosing cholangitis (in terms of histopath/autoantibodies)?
 
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Radiolucent said:
All cause RPGN (nephritic syndrome):
- Goodpasture syndrome: Hematuria, hematoptysis. Anti-GM ab --> linear depostion on IF.
- Granulomatosis with polyangitis (Wegeners): Granulomas in upper+lower resp tract (can cause hematoptysis) + kidneys (hematuria). c/PR3-ANCA + , - IF (pauci-immune)
- Microscopic polyangitis: Necrotizing vasculitis (w/o granulomas) in lower resp tract only (vs Wegeners) + kidney involvement. p/MPO-ANCA +, - IF

Once again: Primary biliary cirrhosis vs Primary sclerosing cholangitis (in terms of histopath/autoantibodies)?
Click to expand...

I asked for vasculitis causes, which goodpasture is not. The 3 vasculitis causes are Wegners, Microscopic polyangiitis, and Churg-Strauss (this one is not in FA)

Wegners -> c-ANCA and will be associated with sinusitis
Microscopic Polyangiitis -> p-ANCA, non-granulomatous
Churg-Strauss -> p-ANCA, Eosinophilia, Asthma, granulomatous vasculitis
 
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pathologyDO said:
I asked for vasculitis causes, which goodpasture is not. The 3 vasculitis causes are Wegners, Microscopic polyangiitis, and Churg-Strauss (this one is not in FA)

Wegners -> c-ANCA and will be associated with sinusitis
Microscopic Polyangiitis -> p-ANCA, non-granulomatous
Churg-Strauss -> p-ANCA, Eosinophilia, Asthma, granulomatous vasculitis
Click to expand...
Henoch schonlein(mostly in the childeren) --> igA deposition in blood vessels wall , palpable purpura on buttocks and legs , hematuria
 
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what happen if you scratch your ear strongly and deeply ?
which nerves will irritate due to this process ?
 
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faisal 2000 said:
Henoch schonlein(mostly in the childeren) --> igA deposition in blood vessels wall , palpable purpura on buttocks and legs , hematuria
Click to expand...


Good info, but IgA nephropathy has little to do with RPGN other than IgA nephropathy can result in RPGN
 
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faisal 2000 said:
what happen if you scratch your ear strongly and deeply ?
which nerves will irritate due to this process ?
Click to expand...
Bradycardia/hypotension (vasovagal response) due to stimulation of the auricular branch of vagus nerve.

V3 supplies the anterior half of the external auditory canal.
Tympanic membrane (inner surface) is supplied by the glossopharyngeal nerve.


Q: Nerve supply of Stapedius muscle and the classic lesion/sequelae ?
 
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Transposony said:
Bradycardia/hypotension (vasovagal response) due to stimulation of the auricular branch of vagus nerve.

V3 supplies the anterior half of the external auditory canal.
Tympanic membrane (inner surface) is supplied by the glossopharyngeal nerve.
Click to expand...
i think also facial nerve can be damaged because it can cross tympanic membrane i am not sure about that but i had encountered q mention that this nerve will damage due to using pencil to clean your ear
 
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- where does vit B12 stored ? which conditions will cause vit B12 deficiency ?
- how does expressionless face developed due to Parkinson's disease ?
 
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