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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Transposony said:
A HY point about coaractation of aorta-The blood flow in the intercostal arteries is reversed below the defect.
Also, for a coarctation that is proximal to the left subclavian, the right subclavian will have it's normal blood supply, so the pulse will be strong, but the left subclavian will not receive it's blood supply, hence the weak pulses.

Some great discussion about coaractation of aorta here
Click to expand...

You're oversimplifying a little but yea, retrograde blood flow in the intercostals supplied by the descending aorta is increased. However, not ALL the intercostals have increased retrograde flow. The internal thoracic gives rise to the anterior intercostals, in which anterograde flow is increased (because the coarctation is distal to the subclavians). The posterior intercostals originate from the descending aorta. Retrograde flow is increased in the posterior intercostals due to the increased anterograde flow seen in the anterior intercostals (the anterior and posterior intercostals anastomose). This increased retrograde flow through the posterior intercostals helps perfuse the descending aorta territories.
 
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seminoma said:
You're oversimplifying a little but yea, retrograde blood flow in the intercostals supplied by the descending aorta is increased. However, not ALL the intercostals have increased retrograde flow. The internal thoracic gives rise to the anterior intercostals, in which anterograde flow is increased (because the coarctation is distal to the subclavians). The posterior intercostals originate from the descending aorta. Retrograde flow is increased in the posterior intercostals due to the increased anterograde flow seen in the anterior intercostals (the anterior and posterior intercostals anastomose). This increased retrograde flow through the posterior intercostals helps perfuse the descending aorta territories.
Click to expand...
Yeah, I was trying to say the same thing but not in so many words. AFAICS it is obvious that the blood is flowing from internal mammary via intercostals towards aorta.
http://circ.ahajournals.org/content/90/2/937.full.pdf
 
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Phloston said:
Didn't know this caused HTN. Perhaps you've taught me something new / do you have an article stating this? I do recall long-term licorice consumption (eg., licorice tea) causing hypokalaemia though.
Click to expand...

It's a classic question we get in the US at least: http://en.wikipedia.org/wiki/Glycyrrhizin

Only happens with real licorice, not just like Twizzlers.
 
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Phloston said:
Didn't know this caused HTN. Perhaps you've taught me something new / do you have an article stating this? I do recall long-term licorice consumption (eg., licorice tea) causing hypokalaemia though.
Click to expand...
They taught us that in class. There is a molecule in licorice, glycyrrhizic acid that apparently blocks 11-beta hydroxysteroid dehydrogenase 2. So the kidney is unable to convert cortisol to cortisone and you get a mineralocorticoid effect. Hypokalemia, hypernatremia and hypertension to follow.
 
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stepone2015 said:
It's a classic question we get in the US at least: http://en.wikipedia.org/wiki/Glycyrrhizin

Only happens with real licorice, not just like Twizzlers.
Click to expand...
dfib slim said:
They taught us that in class. There is a molecule in licorice, glycyrrhizic acid that apparently blocks 11-beta hydroxysteroid dehydrogenase 2. So the kidney is unable to convert cortisol to cortisone and you get a mineralocorticoid effect. Hypokalemia, hypernatremia and hypertension to follow.
Click to expand...

Cheers, guys. Didn't realize it was due to a mineralicorticoid-like effect. I guess that makes sense though.
 
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68-year-old,jaundice,stomach pain,
“dark urine”,itching of the
skin,rapid weight loss of 21lb
CBC within narmal limits
Total bilirubin:238μmol/l
GGT:300U/l
ALP:360U/l
AST:80u/l
ALT:75u/l
Urinalysis positive bilirubin,normal urobilinogen
Serum amylase:elevated

What is the most probable diagnosis for this patient?
Which labtory tests provided the most information
 
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History:38-year-old white
female,jaundice,right upper
quadrant abdominal
pain,nausea,vomiting,itching

skin.She has a history of

intravenous drug use and alcohol

abuse.
what is your diagnosis ?
 
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1. Test of choice for a newborn to an HIV+ mother and WHY ?

2. Test of choice for detecting viral load and WHY ?
 
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Phloston said:
Cheers, guys. Didn't realize it was due to a mineralicorticoid-like effect. I guess that makes sense though.
Click to expand...
seminoma said:
Agreed, thanks for sharing guys. US MD student here.. Never heard of the licorice/HTN relationship.
Click to expand...

The vignette was usually something like a kid presents to PCP with new onset hypertension. History will hint at British/European relatives and maybe a mention of candy would be made.

The UK/Europe has more authentic licorice lying around. The backstory is that the relative came to visit with a bag of the stuff, and the kid just stuffed his face with a ton of it.
 
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faisal 2000 said:
is hypersensitivity pneumonitis type III or IV ? why ?
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Both.

Second exposure = Type 3 because preformed (from the first exposure) IgG + antigens form immune complexes.
Subsequent exposures = Type 4 because T cells pop in and you get granulomas.
 
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In a patient with laterally displaced PMI how can heart sounds be used to distinguish between dilated cardiomyopathy and chronic systemic HTN?
 
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seminoma said:
In a patient with laterally displaced PMI how can heart sounds be used to distinguish between dilated cardiomyopathy and chronic systemic HTN?
Click to expand...
S4 with chronic HTN.
Could have panvalvular regurg with dilated carduomyopathy?
 
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Diagnosis?
upload_2015-2-1_18-18-10.jpeg
 
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CodeRedDew said:
http://library.med.utah.edu/WebPath/HEMEHTML/HEME001.html

That's the same picture from the WebPath page, saying it's a normal smear. Am I missing something because it looks normal to me lol
Click to expand...
Sometime they put completely normal findings (heart sounds, gross pathology, histology etc) on the real test just to make sure that we can recognize them.
I posted this to stress the point of not falling into the trap of looking for a pathology where none exists.
 
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Transposony said:
Sometime they put completely normal findings (heart sounds, gross pathology, histology etc) on the real test just to make sure that we can recognize them.
I posted this to stress the point of not falling into the trap of looking for a pathology where none exists.
Click to expand...
yeah, had an Rx question with normal vaginal discharge as the answer
 
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In Acetaminophen overdose cytochrome P450 will cause the formation of........................................
 
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stepone2015 said:
I was taught that carbon tetrachloride creates tons of free radicals in the liver via metabolization and caused chemical hepatitis. That's wrong?
Click to expand...

Yeah, forgot to mention free radicals. They cause the ribosomes to detach, leading to impaired apolipoprotein synthesis, resulting in fatty change. Liver necrosis is seen too.
 
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CCL4>>>>SER>>>>Free radicals (CCl3-) >>>> Lipid peroxidation.
Lipid peroxidation causes:
1. Membrane damage to RER>>>>Ribosomes detach>>>>impaired apolipoprotein synthesis >>>> fatty change.
2. Plasma membrane damage>>>>>>Ca2+ influx>>>>>All that jazz.
 
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CodeRedDew said:
Pathogenesis is definitely multifactorial; however, since the CYPP450 metabolism to NAPQI is so critical, I would assume that it would be due to the predominance of CYP enzymes in Zone 3 of the liver. I don't think the details really matter though.

http://toxsci.oxfordjournals.org/content/65/2/166.full
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2836803/
Click to expand...
I could not find anywhere in these articles where it says "there is predominance of CYP enzymes in Zone 3 of the liver".
Did I miss it or you are just assuming it?
 
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Transposony said:
I could not find anywhere in these articles where it says "there is predominance of CYP enzymes in Zone 3 of the liver".
Did I miss it or you are just assuming it?
Click to expand...

Those articles were just showing that acetaminophen toxicity was multifactorial. Here's another article below that provides the info you're looking for.

-----
"There is a zonal distribution of P450 in the liver acinus as the centrilobular region of the liver generally contains a higher amount of P450 than the periportal zone."

It also goes on to state that toxicity is multifactorial → "Interestingly, this may, along with other factors (lower oxygen tension, lower levels of GSH), contribute to the initiation and increased toxicity of agents oxidized by CYP2E1 to reactive products including CCl4, acetaminophen, benzene and ethanol itself in the centrilobular zone."

Source: http://www.sciencedirect.com/science/article/pii/S2213231714001207 -- it's also in First Aid
 
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