Official Step 1 High Yield Concepts Thread

[Transposony]

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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[zhopv10]

Can someone explain like im 5 why high precision means more statistical power?

So remember that power is largely determined by sample size. So if you have like 5 people you are measuring there is probably going to be a fair amount of variation in their measurements and the data will not be as "precise" and he mean of that group will not be as apparent (thinking in histogram style type of image). Now if you increase your power (lots more people or whatever) your data will be more precise, I.e you will start being able to see a better representation of the mean of your data set. The representation gets better and better the more people you have. Hopefully that helps somewhat.


(As a side note I like to think of precision as imagining a target with the bullseye being the "truth" so precision would be tight grouping of shots but it doesn't necessarily have to be on the bullseye and then accuracy is on the bullseye but the grouping doesn't necessarily have to be tight. Ideally you would want right grouping on the bullseye.").


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[chillaxbro]

So remember that power is largely determined by sample size. So if you have like 5 people you are measuring there is probably going to be a fair amount of variation in their measurements and the data will not be as "precise" and he mean of that group will not be as apparent (thinking in histogram style type of image). Now if you increase your power (lots more people or whatever) your data will be more precise, I.e you will start being able to see a better representation of the mean of your data set. The representation gets better and better the more people you have. Hopefully that helps somewhat.


(As a side note I like to think of precision as imagining a target with the bullseye being the "truth" so precision would be tight grouping of shots but it doesn't necessarily have to be on the bullseye and then accuracy is on the bullseye but the grouping doesn't necessarily have to be tight. Ideally you would want right grouping on the bullseye.").


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Yes but you can also have 5 samples that are very precise vs 5 samples that arent precise. Why will the 5 sample with more precision mean more power?

 

[zhopv10]

Fair point, so power is 1-beta right? So beta is the chance of making a type II error (failure to reject a false null hypothesis, I.e. a false negative.) So there are a few things that go into that but in your example if you have imprecise data your chances of saying the null is true even though it is false goes up, thus beta is larger so you are subtracting a larger number from 1=power is decreased. If you have precise data that better estimated the true conclusion you are less likely to make a type II error, beta is smaller and thus you are subtracting a smaller number from 1 and thus power increases. Does that help?


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[zhopv10]

This shows how to calculate beta (well beyond the scope of step I) but it can help conceptualize what goes into beta which makes power make more sense if you want.


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[chillaxbro]

Thanks z . basically more precise = less likely to miss a true difference which makes sense

 

[chillaxbro]

So CNIII lesion = you have a down and out eye (at rest)

What happens to your eye in CN IV lesion at rest?

 

[TOKOY90]

So CNIII lesion = you have a down and out eye (at rest)

What happens to your eye in CN IV lesion at rest?

Just go opposite, little bit up and out

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[chillaxbro]

Just go opposite, little bit up and out

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nvm

 

[TOKOY90]

Isnt normal SO function down and out? so it should be up and in?

It's normal function is down and in. There is a lot of conflicting info around that since kaplan and dit and thieme atlas have down out but my neuro prof and first aid say it's down and in. That's what i would use

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[chillaxbro]

It's normal function is down and in. There is a lot of conflicting info around that since kaplan and dit and thieme atlas have down out but my neuro prof and first aid say it's down and in. That's what i would use

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Yeah u right. BTW somehow I learned it wrong for Head and Neck unit and then learned it wrong again for my neuro unit and I never noticed until now. oh well

 

[premed2000]

.

 

[aspiringmd1015]

why does a deficiency in hageman factor(12) cause thromboembolic complications instead of bleeding diathesis?

 

[aspiringmd1015]

@Transposony from uptodate : ''The phosphorus concentration in malignant cells is up to four times higher than in normal cells. Thus, rapid tumor breakdown often leads to hyperphosphatemia, which can cause secondary hypocalcemia. When the calcium concentration times phosphate concentration (the calcium phosphate product) exceeds 60 mg2/dL2, there is an increased risk of calcium phosphate precipitation in the renal tubules, which can lead to acute kidney injury. In addition, precipitation in the heart may lead to cardiac arrhythmias. Renal replacement therapy may be needed ''

UW says that the uric acid actually causes the nephropathy from cells being broken down, not the calcium and phosphate. i guess it could be both, but from a questoin standpoint in regards to tumor lysis id guess theyd try to go after the uric acid nephropathy concept rather than ca/p04

 

[aspiringmd1015]

confused about sulfatides and cord factor, can someone clear this for me. UW also states in the explanation that cordfactor inhibits phagolysosomal fusion.

Also how does low dietary calcium promote kidney stone formation? is it due to a compesnatory hyperparathyroidism? or oxalate which will then be absorbed due to the hypocalcemia

 

[aspiringmd1015]

how does distal RTA cause hypocitraturia? associated with an acidic ph, but how does that cause hypocitraturia?

 

[tasar1898]

@aspiringmd1015 That's true but keep in mind that due to widespread anti-uric acid drug ( uricases , febuxostat etc etc.. ) usage , the nephropathy due to hyperphospathemia/hypocalcemia is becoming more common and may actually surpass urate nephropathy soon..

 

[aspiringmd1015]

once you undergo full resolution with Hep B, are you still a carrier?

 

[Transposony]

once you undergo full resolution with Hep B, are you still a carrier?

No. Complete resolution mean that you are cured.
But you'll have Anti-HBe in addition of Anti-HBs whereas people with Vaccination will only have Anti-HBs.

 

[aspiringmd1015]

No. Complete resolution mean that you are cured.
But you'll have Anti-HBe in addition of Anti-HBs whereas people with Vaccination will only have Anti-HBs.

so to be a carrier of hepB you'd have to have Hbsag, as in be chronic hep, bc it says most cases of hepB undergo full resolution, while only a minor progress to chronicity. Transposony, help me with my other questions i posted above please! ^

 

[aspiringmd1015]

would HUS be classified as pre-renal or intrarenal kidney failure?

 

[Reperfused]

HIV is associated with Hodgkin or Non-Hodgkin Lymphoma?

 

[aspiringmd1015]

^actually both, in hodgkins its associated with lymphocyte depletion as well.

von gierke's is associated with underexcretion of overproduction of uric acid? i thought bc of the lactic acidosis, it would be associated with underexcretion as it competes with the acidic acid transported in the PCT.

 

[Reperfused]

Can we please come up with a list of drugs metabolized by Cytochrome P-450? The list given in FA is pretty short (Anti-epileptics, Theophylline, Warfarin, OCPs).
This will help us tackle drug interactions questions. I'll add the first one, Cyclosporine (RX question). Also would be nice if you can mention the source. Thanks

 

[aspiringmd1015]

why do you get acanthocytes with RPGN?

 

[worldbeater]

Can we please come up with a list of drugs metabolized by Cytochrome P-450? The list given in FA is pretty short (Anti-epileptics, Theophylline, Warfarin, OCPs).
This will help us tackle drug interactions questions. I'll add the first one, Cyclosporine (RX question). Also would be nice if you can mention the source. Thanks

Gotcha. An old post of mine:

http://forums.studentdoctor.net/threads/p450-interactions.1172788/#post-17188588

Relax. You just need a couple of mnemonics for what works with p450, and you can get all the questions right.

So p450 is the mechanism of how the liver metabolizes medications. They can be either 1) inducers 2) inhibitors or 3) dependent.

Inducers of p450 make the liver process medication faster, so it won't have it's intended effect over a long period of time. Warfarin being used up by another drug, and then causing clots, is a great example.

Inhibitors of p450 block the metabolism, so the medication won't be processed at all. Dependent means a handful of drugs work with other.

These are the drugs that we were taught:

1) p450 Inducers - BAG for CPR QTS
Barbiturates, alcohol, griseofulvin, carbamezapine, rifampin, quinidine, tetracyclines, spironolactone

2) p450 inhibitors - ID SMACK QUIN
INH, dapsone, sulfa drugs, macrolides, amiodarone, cimetidine, ketoconazole, quinolones

3) p450 dependent - WEPTD
Warfarin, estrogen, phenytoin, theophylline, digoxin

Match these lists to the questions your working on, you will see the pattern of what's going on.

 

[dempty]

Yes but you can also have 5 samples that are very precise vs 5 samples that arent precise. Why will the 5 sample with more precision mean more power?

Finer point-- a sample is the subset of the population. So a sample is made up of experimental units (patients, for example). A sample of 5 experimental units (I think you meant this one) is different than 5 samples (aka 5 groups selected from the population, could be of size 1, 15, etc.). This is probably worth clarifying for when you read or conduct research.

Fair point, so power is 1-beta right? So beta is the chance of making a type II error (failure to reject a false null hypothesis, I.e. a false negative.) So there are a few things that go into that but in your example if you have imprecise data your chances of saying the null is true even though it is false goes up, thus beta is larger so you are subtracting a larger number from 1=power is decreased. If you have precise data that better estimated the true conclusion you are less likely to make a type II error, beta is smaller and thus you are subtracting a smaller number from 1 and thus power increases. Does that help?

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In addition to larger sample sizes increasing precision, statistical power increases with precision because increased precision will allow you to more easily detect smaller effect sizes, because the estimate is more accurate. In other words, a lot of imprecision makes it hard to detect relatively smaller differences or effects that actually exist (which diminishes power). This imprecision could come from a small sample size or from poor measurement/lack of noise reduction techniques in the experimental design. Increasing the precision (decreasing uncertainty) will make it easier to detect (even smaller) true effects or differences (reject a false null) in comparison to a less precise measurement. Hope this helps clarify why the precision increases power for a given sample size.

It's normal function is down and in. There is a lot of conflicting info around that since kaplan and dit and thieme atlas have down out but my neuro prof and first aid say it's down and in. That's what i would use

So, the odd thing is that no one clarifies the context of what it appears the eye is doing when superior oblique functions or is tested. In isolation (by way of the trochlea and the muscle fibers), the superior oblique will intort, abduct, and depress the eye-- down and out. However, what many sources don't make clear is that the superior oblique is clinically tested by adducting and depressing the pupil (down and in). The superior oblique isn't the muscle that's adducting the eye, though, but adduction is needed to isolate the function of superior oblique to make sure it can depress the pupil (LR and IR could cause the same down and out movement if we didn't look medially).

 

[Reperfused]

Gotcha. An old post of mine:

http://forums.studentdoctor.net/threads/p450-interactions.1172788/#post-17188588

Thank you very much. This post is definitely helpful.

 

[tvelocity514]

What's the big differences b/t Pancoast tumor, SVC syndrome, and Thoracic outlet syndrome?
So far I have:
Pancoast: apex of lung, can cause thoracic outlet syndrome, hoarseness, horners, and SVC syndrome
SVC syndrome causes JVD, edema, face swelling. usually due to small cell ca of lung
Thoracic outlet syndrome: more neuro/vasc problems and positive adson test.

Pretty sure mediastinal mass (not pancoast) is MC cause of SVC syndrome (even though a pancoast could cause it)
Isn't one unilateral vs bilateral? I remember having a UWORLD Q on it and that was a big differentiating factor but forgot which is bilat.
@Phloston
@Transposony
@seminoma

Thanks!

 

[Transposony]

What's the big differences b/t Pancoast tumor, SVC syndrome, and Thoracic outlet syndrome?
So far I have:
Pancoast: apex of lung, can cause thoracic outlet syndrome, hoarseness, horners, and SVC syndrome
SVC syndrome causes JVD, edema, face swelling. usually due to small cell ca of lung
Thoracic outlet syndrome: more neuro/vasc problems and positive adson test.

Pretty sure mediastinal mass (not pancoast) is MC cause of SVC syndrome (even though a pancoast could cause it)
Isn't one unilateral vs bilateral? I remember having a UWORLD Q on it and that was a big differentiating factor but forgot which is bilat.

You pretty much got it.
Basically any mass in the mediastinum can cause Horner's/SVC syndrome/TOS depending on which structure it is compressing.
Pancoast tumor can lead to compression of SVC and/or can cause TOS.
TOS is usually described as having a benign cause & can be B/L since the classic cause is cervical rib/subclavius muscle.
SVC syndrome is usually described as having a malignant cause.

 

[faisal 2000]

why does immunosuppression therapy used to prevent graft rejection ?

 

[masterofnone101]

I believe its because if you supress your immune system your immune system is less likely to react to a graft rejection and attack your own cells.

 

[masterofnone101]

How does Hypophosphatemia lead to bone loss, osteomalacia, rickets again? I know the interaction of PTH but just forgetting how low phosphate in general is associated with those 3.

 

[zhopv10]

^high PTH drives calcium reabsorption from bone and kidney and phosphate excretion (phosphate trashing hormone) so that is one thing.

Hypophophatemia itself can lead to bone issues because it is one of the minerals that makes up the mineral extracellular matrix. Indeed that is where most of the body's phosphorus resides. There it is complex with calcium to make hydroxyapatite


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[faisal 2000]

what is the mechanism of gynecomastia due to spironolactone?

 

[Reperfused]

Why do we get negative PPD in Sarcoidosis?

 

[DerpStore]

Why do we get negative PPD in Sarcoidosis?

Sarcoidosis is characterized by intense foci of granulomatous inflammation in organs and lymphoid tissues but by paradoxical anergy in the periphery. This anergy leads to decreased delayed type hypersensitivity (type IV) in response to tuberculin proteins causing a negative PPD in patients with TB. The mechanism isn't completely clear but one theory is that an unknown antigen (possibly an infection) causes granuloma formation. These foci of chronic inflammation (granulomas) stimulate regulatory t-cells to proliferate to tone down the inflammation. The expansion of the T-regs is not enough to dampen down on the granulomas, but do suppress peripheral circulating CD4+ th cells leading to a state of anergy.

PPD/IGRA will exhibit very high specificity in sarcoidosis, but very low sensitivity.

http://jem.rupress.org/content/203/2/359.full

 

[Reperfused]

Sarcoidosis is characterized by intense foci of granulomatous inflammation in organs and lymphoid tissues but by paradoxical anergy in the periphery. This anergy leads to decreased delayed type hypersensitivity (type IV) in response to tuberculin proteins causing a negative PPD in patients with TB. The mechanism isn't completely clear but one theory is that an unknown antigen (possibly an infection) causes granuloma formation. These foci of chronic inflammation (granulomas) stimulate regulatory t-cells to proliferate to tone down the inflammation. The expansion of the T-regs is not enough to dampen down on the granulomas, but do suppress peripheral circulating CD4+ th cells leading to a state of anergy.

PPD/IGRA will exhibit very high specificity in sarcoidosis, but very low sensitivity.

http://jem.rupress.org/content/203/2/359.full

Thanks!!

 

[DerpStore]

Why does pentazocine cause opioid withdrawal symptoms if a patient is taking full opioid antagonist?

 

[Xavyer]

Why does the intact hCG remain normal but the beta-hCG increase in gestational trophoblastic disease?

 

[Xavyer]

what is the mechanism of gynecomastia due to spironolactone?

Spironolactone causes increased clearance of testosterone and increases estrogen levels. It isn't as specific to the aldosterone receptor as eplenerone and blocks the androgen receptors as well.

 

[faisal 2000]

what is the mechanism of Dupuytren contracture in cirrhosis ?



@Phloston
@Transposony

 

[Transposony]

what is the mechanism of Dupuytren contracture in cirrhosis ?

Nobody knows.

 

[faisal 2000]

how does Lambert-Eaton improve with exercise while myasthenia gravis do not ?
what is the mechanism of Tetrodotoxin and curare toxin?
can we differentiate b\w curare toxin and myasthenia gravis based on symptoms?

 

[Pushtothestars]

Start by being able to draw the steroid pathway. Whenever I have a CAH question I always go back to the mental image I have of the pathway and it never fails.

Umm pls share how u memorized this pathway

 

[seminoma]

Umm pls share how u memorized this pathway

Writing it out a bunch of times during my MS2 endocrine course. Start with the barebones one Sattar draws, then sequentially add things in from the FA chart. It's mainly important that you know the enzymes and where precursors go when each enzyme is deficient.

 

[seminoma]

What's the big differences b/t Pancoast tumor, SVC syndrome, and Thoracic outlet syndrome?
So far I have:
Pancoast: apex of lung, can cause thoracic outlet syndrome, hoarseness, horners, and SVC syndrome
SVC syndrome causes JVD, edema, face swelling. usually due to small cell ca of lung
Thoracic outlet syndrome: more neuro/vasc problems and positive adson test.

Pretty sure mediastinal mass (not pancoast) is MC cause of SVC syndrome (even though a pancoast could cause it)
Isn't one unilateral vs bilateral? I remember having a UWORLD Q on it and that was a big differentiating factor but forgot which is bilat.
@Phloston
@Transposony
@seminoma

Thanks!

In testing situations you shouldn't have an issue if you remember a few almost-common-sense things.

1. Pancoast: Vignette will almost always describe the CXR or just show you the CXR. There will not be signs of vascular congestion (no facial plethora).
2. SVC syndrome: Always gonna have facial swelling/redness and JVD. Might have some other stuff that overlaps with Pancoast (as you listed), but on the test there is always going to be the signs of venous obstruction.
3. Thoracic outlet syndrome: Always going to mention changes that relate to movement of the c-spine or the shoulder. Might be an old smoker, but more likely going to be someone without lung cancer risk factors.

I realize these are all simple things, but I don't mean to sound condescending. USMLE exams are all about pattern recognition and remembering the fact that the majority of the questions are meant to be answerable by the majority of the test-takers.

 

[Transposony]

This is an errata in FA.
Pigment stones due to increased amounts of bile salts reaching the cecum and solubilizing unconjugated bilirubin, allowing their reabsorbtion with subsequent hyperbilirubinobilia.

Normally, CB is secreted into the intestine as bile. In the intestine, CB cannot be absorbed due to large size and polarity unless intestinal enzymes cause deconjugation of CB to UB. This UB is rapidly converted to urobilinogen by bacterial reduction followed by urobilin, stercobilin etc. Some of this urobilinogen is absorbed and excreted into urine.
Normally, bile salts are primarily absorbed in the terminal ileum (95%) by active transport.
However, in terminal ileal disease these bile salts are not absorbed and therefore solubilize UB in the colon thereby preventing the bacterial reduction to urobilinogen.

I'm sorry, but maybe I'm having a 'foggy brain day' or something. If the bile salts aren't absorbed, that means you're going to be losing the bile into the feces. How would that result in pigment stones? Where is this excess billirubin coming from? I just checked Wiki, and it also says cholesterol stones, not pigment stones.

Here is the detailed discussion on this topic.

 

[MrWonderful]

.

 

[faisal 2000]

why there is low ceruloplasmin in wilson and menkes ?

 

[thisguy1225]

why there is low ceruloplasmin in wilson and menkes ?

Normally copper is excreted into bile but in these conditions you have a elevated copper due to difficult excretion. More ceruloplasmin is required to to bind to the copper, thus decreased ceruloplasmin.