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

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if pth cant work on the the kidneys, then it cant activate vitamin D right? so loss of vitamin D would mean you lose calcium and po4 in your gut, and with PTH not working in the kidney, you cant excrete p04 so you would retain it, so maybe they balance each other out, making the p04 either normal, or id guess slightly decreased
 
That makes sense, thank you!!!

Another question, can we use aldosterone antagonists in say Liddle syndrome or licorice poisoning?
 
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That makes sense, thank you!!!

Another question, can we use aldosterone antagonists in say Liddle syndrome or licorice poisoning?

Aldo is low in both. Definitely can't use aldo antagonists in Liddle because the mechanism is completely unrelated to aldo receptors. Might work for licorice poisoning since the cortisol is acting on aldo receptors.
 
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H.Pylori --> decrease somatostatin levels --> increase gastrin levels indirectly.

Do you know how h.pylori decreases somatostatin levels? G cells are in antrum and duodenum? So wouldn't the inflammatory response damage G cells and reduce gastrin-secreting ability? Is it the duodenal G cells that are causing increased gastrin?

I've always had a problem with this concept. Once during GI I figured it out, but then promptly forgot it.
 
Do you know how h.pylori decreases somatostatin levels? G cells are in antrum and duodenum? So wouldn't the inflammatory response damage G cells and reduce gastrin-secreting ability? Is it the duodenal G cells that are causing increased gastrin?

I've always had a problem with this concept. Once during GI I figured it out, but then promptly forgot it.

Im sorry I dont. I remeber that some UW question explained this but not to much detail. I dont think you have to know much more about this concept than I just explained, at least for step 1 purpouses.
 
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here i have it typed from UW:
H. pyolori w/duodenal ulcers: H. pylori a/c antral gastritis is seen as early part of H. pylori (also damage to gastric mucosa is also due to immune reaction against h. pylori) H pylori associated antral gastritis decreases somatostatin producing cells(delta cells) so absence of somatostatin, leads to high gastrin levels, causing increased Hydrogen secretion by parietal cells. Which results in gastric fluid with a low ph, that isn’t neutralized by the duodenal bicarb production causing duodenal ulceration and duodenal gastric metaplasia. so its also the loss of somatostatin which increases acidity to cause duodenal ulceration.
 
in Burkitt's, the forms in the jaw and abdomen, are they arising within LN's within the jaw or abdomen? or are they thesmelves producing lymphoid type structures at these extranodal sites?
 
Confused about medical power of attorney (FA page 57).

"Can be revoked anytime patient wishes (regardless of competence)."

Should "competence" say "capacity"? Incompetent (e.g. minors) can't make legal decisions, can they? Also, regardless of if it's competence or capacity, can a patient with delirium revoke medical power of attorney even though delirium is a disqualifying factor for decision-making capacity?

Also what's the deal with STDs as reportable diseases? I distinctly remember doing a question that said the physician couldn't tell the patient's husband that the patient had HPV. So are STDs only reportable to public officials (who then can do the notifications)? Or is the confidentiality situation different depending on the STD (e.g. HIV vs HPV)?
 
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A/c to fischers ethics book, theres only certain reportable STD diseases, off the top of my head syph, hiv, were on the top of that list, cant remember the others, i think gonnorhea will check later. He said you have to encourage the patient to inform other partners, and if they dont wish to report to their partners, the physician has to report it to their partners but with concealing the identity of the patient
 
A/c to fischers ethics book, theres only certain reportable STD diseases, off the top of my head syph, hiv, were on the top of that list, cant remember the others, i think gonnorhea will check later. He said you have to encourage the patient to inform other partners, and if they dont wish to report to their partners, the physician has to report it to their partners but with concealing the identity of the patient

So...

Physician: It has come to my attention that one of your sexual partners has HIV. I can't tell you who though.

Patient's husband: Ok. Did you tell my wife?

Physician: I have to.. for the same reason I have to tell you.

Patient's husband: wtf
 
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not notifying the partners/public would mean the public is more at risk, and the public being at risk will always trump the patients own wishes, BUT at the same time you cant reveal information about the patient.
Side note: if theres an answer choice saying "encourage the patient to notifty partners" pick it.
 
not notifying the partners/public would mean the public is more at risk, and the public being at risk will always trump the patients own wishes, BUT at the same time you cant reveal information about the patient.
Side note: if theres an answer choice saying "encourage the patient to notifty partners" pick it.

I hope I get that lucky.
 
can someone explain, or provide some kind of resource on the findings of the myeloproliferative D/O chart on pg 404 in FA, Sattar mentioned all the cell lines would be increased, but its not what it says in the chart. In myelofibrosis it makes sense the rbcs are decreased bc your BM is fibrosed, so shouldnt your WBCS be down too? and why are your rbcs going down in CML etc. Things like that, please and thanks
 
Also what's the deal with STDs as reportable diseases? I distinctly remember doing a question that said the physician couldn't tell the patient's husband that the patient had HPV. So are STDs only reportable to public officials (who then can do the notifications)? Or is the confidentiality situation different depending on the STD (e.g. HIV vs HPV)?
Physician informs the local public health official and tells the patient that it's in everyone's best interest that patient informs the partner(s) about it since the public health department is going to inform the sexual partners in any case (without mentioning the personally identifiable details).
 
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Confused about medical power of attorney (FA page 57).

"Can be revoked anytime patient wishes (regardless of competence)."

Should "competence" say "capacity"? Incompetent (e.g. minors) can't make legal decisions, can they? Also, regardless of if it's competence or capacity, can a patient with delirium revoke medical power of attorney even though delirium is a disqualifying factor for decision-making capacity?
Yes it should say "capacity" since "competence" can only be decided by a court. Think it's being worked up as an errata in FA.
AFAIK delirious patient cannot revoke MPoA since the patient has clearly lost decision-making capacity.
 
Why is gastrin increased in H.pylori gastritis? (FA Page 353).

1. H. Pylori produces ammonia --> Alkaline pH near G cells --> directly stimulates G cells to produce Gastrin.
2. Chronic inflammation --> Cytokines --> Impaired somatostatin production & decreased D cells --> Decreased feedback inhibition of Gastrin release.

Remember, Gastrin stimulates acid secretion indirectly by inducing the release of histamine by ECL cells in Gastric fundus, although direct effect on parietal cells also plays a role. There are other ways by which ECL cells can stimulate parietal cells to stimulate acid release.
However, ultimately (Chronic atrophic gastritis) G cells also get destroyed leading to hypochlorhydria (late).
 
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I have a question about milestones. This is based on a question I got on the free 138 at Prometric today, but the info here is not exactly what's in the question, nor will it "ruin" the question for you.

FA says the child will do x motor activity by 8 months. One of the questions I did involved a 10-11month old child that has "started" to do x motor activity.

I know it's "normal" because I didn't get the question wrong. But shouldn't that be "delayed" since they should have started that motor activity 2-3 months ago?
 
can someone explain, or provide some kind of resource on the findings of the myeloproliferative D/O chart on pg 404 in FA, Sattar mentioned all the cell lines would be increased, but its not what it says in the chart. In myelofibrosis it makes sense the rbcs are decreased bc your BM is fibrosed, so shouldnt your WBCS be down too? and why are your rbcs going down in CML etc. Things like that, please and thanks
any takers?
 
I have a question about milestones. This is based on a question I got on the free 138 at Prometric today, but the info here is not exactly what's in the question, nor will it "ruin" the question for you.

FA says the child will do x motor activity by 8 months. One of the questions I did involved a 10-11month old child that has "started" to do x motor activity.

I know it's "normal" because I didn't get the question wrong. But shouldn't that be "delayed" since they should have started that motor activity 2-3 months ago?


I hate them damn milestones..
Any help in this regard will be highly appreciated by me too..
 
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I have a question about milestones. This is based on a question I got on the free 138 at Prometric today, but the info here is not exactly what's in the question, nor will it "ruin" the question for you.

FA says the child will do x motor activity by 8 months. One of the questions I did involved a 10-11month old child that has "started" to do x motor activity.

I know it's "normal" because I didn't get the question wrong. But shouldn't that be "delayed" since they should have started that motor activity 2-3 months ago?
As you pointed out that much delay could be normal.
If they wanted you to go down the developmental delay path then they will either give you very clear cut delay (e.g. 6 months) and /or give you something in the history or other findings of delayed development.
It also depends on the specific milestone e.g. some kids don't crawl and go straight to walking.
Maybe they was testing that particular fact.
 
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As you pointed out that much delay could be normal.
If they wanted you to go down the developmental delay path then they will either give you very clear cut delay (e.g. 6 months) and /or give you something in the history or other findings of delayed development.
It also depends on the specific milestone e.g. some kids don't crawl and go straight to walking.
Maybe they was testing that particular fact.

Good point. It doesn't help that "delayed" and "normal" are both available as answers for a situation when the milestone is 2 months delayed (by FA timeline). Chances are I'll get all of the milestone questions wrong anyway.. I suck at them.
 
Good point. It doesn't help that "delayed" and "normal" are both available as answers for a situation when the milestone is 2 months delayed (by FA timeline). Chances are I'll get all of the milestone questions wrong anyway.. I suck at them.
That's the one thing I refused to memorize in FA haha.
 
Good point. It doesn't help that "delayed" and "normal" are both available as answers for a situation when the milestone is 2 months delayed (by FA timeline). Chances are I'll get all of the milestone questions wrong anyway.. I suck at them.
I have yet to come across a person who doesn't suck at them except some with kids of their own.
Then there is nothing to memorize............
 
whats the cause of DIC in nephrotic syndrome? is it AT3? even though you'd urinate it out, you would have to still activate the fibrinolytic system etc wouldnt you?
 
A mnemonic to help remember the conversion of cholesterol to estradiol by the Theca and Granulosa cells in the ovaries:

LH stimulates the Theca cell: cholesterol is converted by desmolase to androstenedione

FSH stimulates the Granulosa cell: androstenedione is converted by aromatase to estradiol

I'l(L H)ave (The) (Ch)eescake (Des)sert (And) (SH)e'll (G)et (A)n (A)ppetizing (E)clair

LH - Luteinizing Hormone
The - Theca cell
Ch - Cholesterol
Des - Desmolase
And - Androstenedione
SH - (Follicle) Stimulating Hormone
G - Granulosa cell
A - Androstenedione
A - Aromatase
E - Estradiol
 
So even though dapsone is a sulfa drug it can be used for PCP prophylaxis in patients allergic to TMP/SMX (source = pharmcards)?
 
Viral complementation vs phenotypic mixing.

How are these different? In both cases there is no genetic exchange. In both cases one virus helps the other become infectious.
 
FA (p239) says lung cancer incidence has not changed significantly in women. I remembered this while doing a UW question a while back and it actually made me get the question wrong (because lung cancer was depicted as having a steep upslope over the past few decades). I believe UW also said in the explanation that lung cancer incidence has been steadily increasing in women. Anyone come across a question like this on the real deal?
 
FA (p239) says lung cancer incidence has not changed significantly in women. I remembered this while doing a UW question a while back and it actually made me get the question wrong (because lung cancer was depicted as having a steep upslope over the past few decades). I believe UW also said in the explanation that lung cancer incidence has been steadily increasing in women. Anyone come across a question like this on the real deal?

Magic8Ball.jpg
 
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FA (p239) says lung cancer incidence has not changed significantly in women. I remembered this while doing a UW question a while back and it actually made me get the question wrong (because lung cancer was depicted as having a steep upslope over the past few decades). I believe UW also said in the explanation that lung cancer incidence has been steadily increasing in women. Anyone come across a question like this on the real deal?

LC-Incidence-by-Sex.png


This what American Lung Association says:
The rate of new lung cancer cases (incidence) over the past 37 years has dropped for men (28% decrease), while it has risen for women (98% increase). In 1975, rates were low for women, but rising for both men and women. In 1984, the rate of new cases for men peaked (102.1 per 100,000) and then began declining. The rate of new cases for women increased further, did not peak until 1998 (52.9 per 100,000), and has now started to decline. (2011 data)
CDC:
http://www.cdc.gov/cancer/lung/statistics/race.htm
 
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So even though dapsone is a sulfa drug it can be used for PCP prophylaxis in patients allergic to TMP/SMX (source = pharmcards)?
Should not be the case unless it is TMP/SMX intolerance.
Which pharmcards are these, authors?
 
Should not be the case unless it is TMP/SMX intolerance.
Which pharmcards are these, authors?

Lange. Or maybe it was in Becker. One of those.

Edit: Nevermind, found it. It's Kaplan pharmcards and you're right it is bactrim "intolerance".
 
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Seminoma? Looks like testicular parenchyma on the left and tumor on the right (I think these are also known as "fried egg" cells with a lymphocytic infiltrate).

What are other "fried egg" associations?

Oligodendroglioma, ganglion cells (e.g. when identifying a normal segment of colon in Hirschsprungs), and dysgerminoma.
 
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