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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I think FA covers the important diseases, but the underlying physiology is not explained well. If you understand the lytes stuff in FA I think you're solid (e.g. why is NH3 synthesis decreased in Type 4 RTA or why does type 2 RTA initially have urine pH >5.5). If you just have it memorized I might be worried.

Edit: Although I guess that's true for most things in FA>
i was talking about page 537 in particular, but sounds good.
 
Just came across a UW question, where the explanation was talking about analgesic nephropathy, but the question made a distinction saying that patients on nsaids can develop papillary necrosis and interstitial nephritis. Are these two manifestations collectively called analgesic nephropathy? or what am i not following here
 
Just came across a UW question, where the explanation was talking about analgesic nephropathy, but the question made a distinction saying that patients on nsaids can develop papillary necrosis and interstitial nephritis. Are these two manifestations collectively called analgesic nephropathy? or what am i not following here

Correct. Analgesic nephropathy is a blanket term.
 
is it easy for you guys to disinguish FSGS and KW nodules(diabetic gn) just based on histology? Sorry guys, i know i have a **** load of ?'s but its bc im eager to clear my concepts, i only ask after doing my own fair share of googling. So on that note, is there a particular reason why we need to know the GLUT transporters are specific for D glucose, and not L-glucose
 
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with 11 hydroxlase deficiency, the increased in andorgens effect in boys arent listed, shouldnt they be the same as 21 hydroxylase deficiency? salt wasting/precocious puberty?
 
with 11 hydroxlase deficiency, the increased in andorgens effect in boys arent listed, shouldnt they be the same as 21 hydroxylase deficiency? salt wasting/precocious puberty?

The androgens made by the adrenals are weak. They are strong enough to mess with sexual development of girls, but for boys, they are by and large asymptomatic. DHT spikes in male puberty which is what's really needed for full male sexual development - a powerful androgen.
 
i see, but it states in FA that with 21 oh deficiency, you get precocious puberty in childhood, shouldnt that be seen in 11 too? unless in 21 the defect is higher up in the synthesis pathway so more androgens are being made with 21 oh deficiency?
 
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.
yeah, so is it pigment or cholesterol stones?
 
i see, but it states in FA that with 21 oh deficiency, you get precocious puberty in childhood, shouldnt that be seen in 11 too? unless in 21 the defect is higher up in the synthesis pathway so more androgens are being made with 21 oh deficiency?
I think it's because of what you said the defect in the pathway is higher upstream leading to more shunting towards sex hormones.
 
OK so on my COMSAE and NBME 15 I had some questions pop up about shoulder pain associated with pneumonia, and the different layers involved in this pain. Can anyone explain which layer (e.g. visceral pleura, diaphragmatic pleura, etc) is involved in referred shoulder pain from pneumonia? Does anyone have a good differential list for the different types of pain involved with lungs and surrounding pleura?
 
OK so on my COMSAE and NBME 15 I had some questions pop up about shoulder pain associated with pneumonia, and the different layers involved in this pain. Can anyone explain which layer (e.g. visceral pleura, diaphragmatic pleura, etc) is involved in referred shoulder pain from pneumonia? Does anyone have a good differential list for the different types of pain involved with lungs and surrounding pleura?

Visceral pleura is innervated only by autonomics and there's no pain afferents. All referred pleuritic pain is parietal pleura in origin.

Not sure what you mean about types of pain though. As far as I know, all pleuritic pain is worse on inspiration and is sharp/stabbing.
 
Visceral pleura is innervated only by autonomics and there's no pain afferents. All referred pleuritic pain is parietal pleura in origin.

Not sure what you mean about types of pain though. As far as I know, all pleuritic pain is worse on inspiration and is sharp/stabbing.

OK so referred shoulder pain with pneumonia is due to inflammation of the parietal pleura. Sorry about the unclear wording, but you jogged my memory about the visceral pleura having no pain afferents, thank you. The other options included (from memory, I think these are right): mediastinal pleura, visceral pleura, costal pleura, and I think maybe inflammation in the pleural space. So would the answer have been costal pleura?
 
OK so referred shoulder pain with pneumonia is due to inflammation of the parietal pleura. Sorry about the unclear wording, but you jogged my memory about the visceral pleura having no pain afferents, thank you. The other options included (from memory, I think these are right): mediastinal pleura, visceral pleura, costal pleura, and I think maybe inflammation in the pleural space. So would the answer have been costal pleura?

Haven't done NBME 15, and I probably will do it so I didn't read the last part of your post!
 
hmm did it have diagphragmatic pleura in there? isnt that why with cholecystitis you get referred pain to your shoulder? the diaphragm gets irritated(phrenic nerve)?
 
i read something on medscape a while ago about PPV is more common on the right, that would be for indirect, idk why for femoral. Liver maybe? more intraabdominal pressure on the right than the left bc of the liver(wild wild guess)
 
which hormones have a nuclear receptor? A/c UW, t3, Fatty acids, PPAR's and Retinoids are some hormones that have their actual receptors located in the nucleus and acting in the nucleus, and the other steroid hormone receptors located in the cytoplasm which after subsequent binding transolcate to the nucleus. Are there any other specific receptors that are however located within the nucleus?
 
i read something on medscape a while ago about PPV is more common on the right, that would be for indirect, idk why for femoral. Liver maybe? more intraabdominal pressure on the right than the left bc of the liver(wild wild guess)
Indirect inguinal hernia ---> Slower descent of testes on right and hence processus vaginalis closes later than left side.

Femoral hernia---> Sigmoid colon "splints" the femoral ring on left side.
 
missed an easy question about botulinum with a baby bc i was looking for classic galactosemia, anyways..whats the big deal with honey with clostridium? why honey? are there any other specific foods that are associated with it?
 
are there any other HY food assocations we should know? besides the Honey-botulinum, sucrose for aldolase B def, wheat products for celiac? Aspartame for PKU's another one
 
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are there any other HY food assocations we should know? besides the Honey-botulinum, sucrose for aldolase B def, wheat products for celiac? Aspartame for PKU's another one

You mean like the giant list for food poisoning, implicated foods, and associated microbes? As far as food avoidance for molecular defects those usually just make sense. Like avoiding lactose for lactase deficiency, protein for urea cycle defects (and CKD), gout-related foods etc. Also p450 foods (i.e. grapefruit juice) and other common food-drug interactions like milk and quinolones/tetracyclines. There are also things like goitrogens, soy-based products, etc that are probably lower yield.

Edit: Also my favorite one (because it's counterintuitive to me) is citrus fruit --> alkalinize urine.
 
Because it will most likely present before there is enough time for enough transudate to develop (>500mL) into clinically evident ascites.

UW says it's because there's no sinusoidal congestion, which didn't make sense to me. It also implies Budd Chiari would cause ascites. I thought BC could be very rapid in presentation as well?
 
UW says it's because there's no sinusoidal congestion, which didn't make sense to me. It also implies Budd Chiari would cause ascites. I thought BC could be very rapid in presentation as well?

There isn't sinusoidal congestion with portal vein thrombosis, but ascites can be caused by other things besides portal hypertension/sinusoidal congestion. If you obstruct all the venous drainage from the gut you're going to have a problem. If there's partial portal vein thrombosis and the patient develops chronic disease from it they can develop ascites.

Budd Chiari will present acutely as well, but the obstruction is after the liver so there will be sinusoidal congestion --> ascites.

Portal vein = prehepatic obstruction. Budd Chiari = hepatic vein = posthepatic obstruction. Portal vein thrombosis can't cause sinusoidal congestion just like RV failure can't cause pulmonary htn. Budd Chiari causes portal htn just like LV failure causes pulmonary htn.

At least that's my understanding.
 
Radiation treatment makes opthalmopathy worse bc of the loss of feedback inbition on TSH? and those retroorbital fibroblats express TSh receptors correct? UW says this is especially common in smokers, whats the association?
 
Can someone clarify the relationship between carcinoma in-situ and benign vs malignant? Just did a UW question about bronchioloalveolar carcinoma (i.e. adenocarcinoma in-situ) and wasn't sure if it is benign because it hasn't inavded, or malignant because it has the potential to invade (and is called a "carcinoma").
 
"
  • Bronchioloalveolar carcinoma (BAC) of the lung is the only form of CIS that can kill directly because, in rare cases (the "pneumonic form"), it expands greatly and fills the lungs, preventing breathing and causing other dire effects on the host. Thus, the pneumonic form of BAC is a true malignant entity, but is not "invasive" in the classical sense. For this reason, it is considered a form of CIS by pathologists, but not by oncologists or surgeons and inclusion of this form of cancer among the types of CIS is controversial.
"
 
"
  • Bronchioloalveolar carcinoma (BAC) of the lung is the only form of CIS that can kill directly because, in rare cases (the "pneumonic form"), it expands greatly and fills the lungs, preventing breathing and causing other dire effects on the host. Thus, the pneumonic form of BAC is a true malignant entity, but is not "invasive" in the classical sense. For this reason, it is considered a form of CIS by pathologists, but not by oncologists or surgeons and inclusion of this form of cancer among the types of CIS is controversial.
"

Thanks, so would CIS elsewhere be considered benign or malignant? For example, cervical CIS or Bowen's disease or breast DCIS/LCIS?
 
Thanks, so would CIS elsewhere be considered benign or malignant? For example, cervical CIS or Bowen's disease or breast DCIS/LCIS?

I think the point of that article is that it is not cancer and hence malignant vs benign is non-applicable. A high grade dysplasia is a carcinoma in situ meaning carcinoma that hasn't become a carcinoma yet. The Wiki quote calls it malignant in that it will kill a person, but is not truly a carcinoma.
 
I think the point of that article is that it is not cancer and hence malignant vs benign is non-applicable. A high grade dysplasia is a carcinoma in situ meaning carcinoma that hasn't become a carcinoma yet. The Wiki quote calls it malignant in that it will kill a person, but is not truly a carcinoma.

But it is a cancer if it's a monoclonal proliferation. My understanding of malignant vs benign is malignant = risk of mets, benign = never going to metastasize. Since CIS need to progress to full blown carcinoma (i.e. invade through the basement membrane) before going to nodes or distant sites, technically CIS can never metastasize because once it goes through a basement membrane it is renamed to carcinoma and any mets from that point are from the carcinoma, not the CIS.
 
it specifically said that it resembles ACD in the explanation, so i thought maybe because of the associated necyrolysis erthyema there could be some associated hemolysis or something?
 
Can someone explain how capitation pay helps promote preventative care? I get that capitation = fixed pay per patient, but how is a physician's cost ever going to exceed his/her pay? It's not like the physician pays out of pocket for the patient's surgery, hospital fees, lab tests, etc.. So even though capitation won't pay you more if you do more tests, I don't see how doing more tests would hurt a capitation-paid physician.

UW QID 8456

@Winged Scapula @cabinbuilder
 
Can someone explain how capitation pay helps promote preventative care? I get that capitation = fixed pay per patient, but how is a physician's cost ever going to exceed his/her pay? It's not like the physician pays out of pocket for the patient's surgery, hospital fees, lab tests, etc.. So even though capitation won't pay you more if you do more tests, I don't see how doing more tests would hurt a capitation-paid physician.

UW QID 8456

@Winged Scapula @cabinbuilder

Here:
Capitation was meant to be a step up in terms of creating better incentives for efficiency, cost control, and preventive care in health care. Under capitation, a doctor, medical group, hospital or integrated health system receives a certain flat fee every month for taking care of an individual enrolled in a managed health care plan, regardless of the cost of that individual's care (usually with a few exceptions built into the contract for unusual types of care). Given that the majority of individuals enrolled in a health plan will never use health care services within any given month, capitation arrangements should naturally 'balance out' the 'high utilizers' of health care in health plans with those enrolled members who use little or no health care every month. What's more, because the physician, hospital or health system is responsible for the enrolled member's health regardless of cost, in theory, capitation motivates the health care provider to provide health screenings (mammograms, pap smears, PSA tests), immunizations, prenatal care, and other preventive care to enrolled members, and to focus on keeping the member healthy through good primary care (and less reliance on costly medical specialists).

To read more check this link: http://www.pbs.org/wgbh/pages/frontline/shows/doctor/care/capitation.html
 
Here:
Capitation was meant to be a step up in terms of creating better incentives for efficiency, cost control, and preventive care in health care. Under capitation, a doctor, medical group, hospital or integrated health system receives a certain flat fee every month for taking care of an individual enrolled in a managed health care plan, regardless of the cost of that individual's care (usually with a few exceptions built into the contract for unusual types of care). Given that the majority of individuals enrolled in a health plan will never use health care services within any given month, capitation arrangements should naturally 'balance out' the 'high utilizers' of health care in health plans with those enrolled members who use little or no health care every month. What's more, because the physician, hospital or health system is responsible for the enrolled member's health regardless of cost, in theory, capitation motivates the health care provider to provide health screenings (mammograms, pap smears, PSA tests), immunizations, prenatal care, and other preventive care to enrolled members, and to focus on keeping the member healthy through good primary care (and less reliance on costly medical specialists).

To read more check this link: http://www.pbs.org/wgbh/pages/frontline/shows/doctor/care/capitation.html

Thanks I think I understand all that, but it doesn't explain why a physician would care about the patient's health care costs since the physician doesn't cover those costs.

For example if you have a diabetic patient you could teach them about the need to check their feet everyday for ulcers or you could just wait until they need an amputation. According to the UW question the capitation pay system motivates the physician to prevent ulcers --> amputation because it's cheaper for them. What I don't understand is how the physician is "harmed" if they don't prevent the patient from needing an amputation. All that's going to happen is the physician refers the patient to a surgeon. The physician doesn't have to pay for the surgery.
 
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Thanks I think I understand all that, but it doesn't explain why a physician would care about the patient's health care costs since the physician doesn't cover those costs.

For example if you have a diabetic patient you could teach them about the need to check their feet everyday for ulcers or you could just wait until they need an amputation. According to the UW question the capitation pay system motivates the physician to prevent ulcers --> amputation because it's cheaper for them. What I don't understand is how the physician is "harmed" if they don't prevent the patient from needing an amputation. All that's going to happen is the physician refers the patient to a surgeon. The physician doesn't have to pay for the surgery.

It is not unusual for large groups or physicians involved in primary care network models to also receive an additional capitation payment for diagnostic test referrals and subspecialty care. The primary care physician will use this additional money to pay for these referrals. Obviously, this puts the primary care provider at greater financial risk if the overall cost of referrals exceeds the capitation payment, but the potential financial rewards are also greater if diagnostic referrals and subspecialty services are controlled. Alternatively, some plans pay for test and subspecialty referrals via fee-for-service arrangements but are more typically paid via contractually agreed-upon fee schedules that are discounted 10% to 30%, compared to the local usual and customary fees.

So basically I think it is all dependent on the capitation contract signed, as the paying parties are mostly in charge of the terms, I think they have a set amount of money they cut from the money given to the Physician monthly per referral.

If that didn't answer it then I'll reply back during Residency.
 
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thats because in accordance with the USMLE, physicans ALWAYS care.
The hypophosphatemia in aluminum hydroxide, and osteodystrophy, is this somehow associated with increased PTH? or it is due to the binding of p04 in the gut decreasing its absorption? Before anyone asks me to google this, i did, and found a bunch of bs about it.
 
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