Official Step 1 High Yield Concepts Thread

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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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with the ca oxalate, isnt it that normally oxalate just simply doesnt get reabsorbed normally in the gut, but with crohns ileal trasmural damage, allows oxalate to be reabsorbed, which normally isnt suppose to, and gets into the bloodstream in abnormal amounts, and in the kidney it precipitates out? (this is what sattar said i think)
Yeah its because the calcium normally binding the oxalate in the gut is bound by fats so now you have all this free oxalate hanging around to get absorbed.
 
Yeah its because the calcium normally binding the oxalate in the gut is bound by fats so now you have all this free oxalate hanging around to get absorbed.

Can confirm. Just learned about this today. Crohn's was specifically mentioned in the lecture I watched, but I don't see a reason why any chronic fat malabsorption syndrome would be any different.
 
Your patient has asthma, HTN, and low HR. Your attending wants to prescribe a beta blocker and asks you which beta blocker would be suitable for your patient. Considering your patient's situation, which one(s) may be useful?
 
Your patient has asthma, HTN, and low HR. Your attending wants to prescribe a beta blocker and asks you which beta blocker would be suitable for your patient. Considering your patient's situation, which one(s) may be useful?

Either a non-selective or one of the partial agonists? I would be more concerned with severe bradycardia than exacerbating the asthma...
 
Non selective: Propranolol, but relatively contraindicated in asthma.
Partial agonists: Pindolol, acebutolol. Both of these are contraindicated in severe bradycardia.

Hmm, well the partial agonists (the ones with some ISA) were the ones I was thinking of because I have in my notes that they're used in pts with HTN and low-ish HR because they have less bradycardia, with pindolol having some vasodilation and bronchodilation as well because it's more non-selective than acebutolol.

Did I fudge my notes?
 
what should i know about treatment of enterococci for USMLE purpose (ampiciline + aminoglycosie , vancomycine , daptomycine or linezolide) ??
what is the treatment of recurrences of c.difficile?
 
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Reason for cyclic fever in Malaria?
Erythrocytic stage of the life cycle of parasite.
608px-Life_Cycle_of_the_Malaria_Parasite.jpg
 
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Why is the spleen critical in clearing encapsulated bacteria? Why is the spleen less critical (or unnecessary) in clearing other bacteria? Thanks.
 
Why is the spleen critical in clearing encapsulated bacteria? Why is the spleen less critical (or unnecessary) in clearing other bacteria? Thanks.
Splenic macrophages phagocytose opsonized encapsulated bacteria from the blood as they pass through splenic cords.
 
also the spleen has loads of players in the immune system(APC's etc), so they increase effectiveness of class switching(igB is an opsonizer) so yeah
 
Good/easy way to differentiate the murmur of tricuspid regurgitation from that of ventricular septal defect in a vignette?
 
Murmur intensity with TR increases on deep inhalation and VSD would decrease?

Sorry, I meant to say in terms of there being a holosystolic murmur in the tricuspid area. I was thinking more along the lines of TR being more likely seen in a IV drug abuser and VSD being more likely seen in a newborn.
 
Sorry, I meant to say in terms of there being a holosystolic murmur in the tricuspid area. I was thinking more along the lines of TR being more likely seen in a IV drug abuser and VSD being more likely seen in a newborn.
Or with carcinoid heart disease
 
What are the ACTH and cortisol levels (up, down, normal) in all of the following situations:

1) Intractable chronic asthma
2) Patient with rheumatoid arthritis diagnosed 5 years ago in whom NSAIDs are not effective
3) High blood pressure in man of 6-months' duration, cataract in left eye, impotence
4) Non-smoker, woman, 3-cm central coin lesion on CXR, 4-month history of ataxia
4) Patient with fasting glucose of 110, potassium of 3.7, sodium of 142, MRI of pituitary reveals no abnormality, no Hx of chronic disease, purple striae on upper-medial thighs bilaterally

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(Quote my comment if you want me to respond cuz I almost never check this thread)
 
Why do drugs have to be unionized to be able to permeate membranes?
Short answer: because ionized drugs will be repelled by the polarized cell membrane. Neutral molecules tend to work there way through cell membranes easier.

Now to answer this from my pharmacology-background part of my brain...
Study this pic
The-separation-of-charge-across-the-cell-membrane-forms-a-membrane-potential-5111221.png

Imagine a positively charge drug in the ex-fluid...It make get through the positive section of the membrane but will get stopped at the negative section. Same principle for negatively charge drug. Now, imagine a neutral drug...that sneaky bastard can glide through without being noticed (provided it's small enough)
However, this is not as simple as med school text make is seem. Technically some ionized drugs permeate but usually not enough to cause a physiological response.
 
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