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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1. Flexor contracture of MCP. To correct the deformity which muscle tendon should you manipulate?

2. on a CT scan: blood is seen b/w liver and abdominal wall. Which artery is damaged? is this retroperitoneal hemorrhage as its outside liver. b/w liver and abd wall. ?

2 no should be intraperitoneal
 
Would it not just be via negative feedback which results in inhibition of FSH secretion by the exogenous estrogen? Decreased FSH -> decreased stimulation of aromatase -> no endogenous estrogen peak

OCPs w/ progesterone primarily suppress LH -> no LH surge -> no ovulation; estrogen primarily suppress FSH -> preventing development of a dominant follicle
 
Would it not just be via negative feedback which results in inhibition of FSH secretion by the exogenous estrogen? Decreased FSH -> decreased stimulation of aromatase -> no endogenous estrogen peak

That makes sense, but why doesn't that happen with endogenous estrogen (normal physiology w/o OCPs)? It has negative feedback until it reaches the point at which it switches to positive feedback... but that whole time it continued to rise even though there was negative feedback on LH/FSH, right?
 
That makes sense, but why doesn't that happen with endogenous estrogen (normal physiology w/o OCPs)? It has negative feedback until it reaches the point at which it switches to positive feedback... but that whole time it continued to rise even though there was negative feedback on LH/FSH, right?
see what I wrote above about estrogen from OCPs; does that help?
 
Pelvic anatomy has become a common topic lately on the step 1. So here's a few basic lymphatics questions for you all.

1) Cervical cancer is more likely to spread to what lymph node first?
2) How about uterine cancer?
3) a cancer in the upper anus?
 
Pelvic anatomy has become a common topic lately on the step 1. So here's a few basic lymphatics questions for you all.

1) Cervical cancer is more likely to spread to what lymph node first?
2) How about uterine cancer?
3) a cancer in the upper anus?

1 superficial inguinal?? if not superficial then internal inguinal
2 lumbar/para-aortic
3 internal iliac
 
Quick question, how does Hydrochlorothiazide causes hypokalmeia? it just blocks Na/Cl channel right?
 
Quick question, how does Hydrochlorothiazide causes hypokalmeia? it just blocks Na/Cl channel right?
HClT blocks Na/Cl in the distal tubule, which results in increased delivery of sodium to the collecting ducts and causes increased cellular uptake of Na from the lumen by apical Epithelial Na Channels (ENaCs). This then causes the basolateral Na/K exchanger to more actively exchange Na for K, which is then passively secreted into the lumen through apical channels, resulting in K loss.
 
These are antibodies against coagulation factors like prothrombin & protein C as well as activating complement.

My understanding from what I just read is that the antibodies you listed are two examples of antibodies that may be involved in antiphospholipid syndrome. Lupus anticoagulant is an example of an APS-inducing IgG antibody that alters the function of prothrombin and its interaction with membrane phospholipids such that it may serve to increase conversion to thrombin as well as promote the adhesion and aggregation of platelets.
 
Question for you guys. Where are main sites of Lipid, Protein, and Carbohydrates absorption in the GI tract?
 
Pelvic anatomy has become a common topic lately on the step 1. So here's a few basic lymphatics questions for you all.

1) Cervical cancer is more likely to spread to what lymph node first?
2) How about uterine cancer?
3) a cancer in the upper anus?

Could one of you see if my thinking regarding lymphatics in that region is correct:
so paraortic drains kidneys, testes, ovaries, and the uterus....superficial inguinal drains anal canal below the pectinate line, scrotum, skin below umbilicus, and then distal vagina and vuvla......internal illiac drains lower portion of rectum, anal canal above the pectinate line, bladder, prostate, and middle 1/3 of vagina?...external illiac: this is the one i'm confused about?- only thing I know is proximal vagina?

so using that knowledge I would have answered this as: #1) superficial inguinal 2) uterine 3) internal illiac
 
Besides choriocarcinoma what is an example of a reproductive system carcinoma that spreads hematogenously?
 
A patient is taking cimetidine. Now the doctor wants to put them on a statin as well for an unrelated health problem. What statin should they administer? (and why?)
 
A patient is taking cimetidine. Now the doctor wants to put them on a statin as well for an unrelated health problem. What statin should they administer? (and why?)

CIMETIDINE is a P450 inhibitor, and P450s metabolize most of the statins, except PRAVASTATIN which is transformed enzymatically in the liver cytosol
 
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

----------

(Quote my comment if you want me to respond cuz I almost never check this thread)

@Phloston

1) normal?
2) High ACTH High cortisol ... ( chronic pain-->inc CRH)
3) ACTH low. Cortisol High ( exogenous steroid)
4) ACTH high Cortisol High (Small cell lung ca paraneoplastic? but its nonsmoker not sure? ataxia points towards mets to brain?
5) ACTH low Cortisol High ( Cushing syndrome. striae + inc Na)
 
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CIMETIDINE is a P450 inhibitor, and P450s metabolize most of the statins, except PRAVASTATIN which is transformed enzymatically in the liver cytosol
Good job!

now a follow up question and one that I don't know the answer to myself- do these drugs all effect the same cytochrome P450 enzyme or different ones? I remember one time a person on one of these forums saying that on their real test they had been asked specifically which cytochrome P450 enzyme St. John's Wart enhanced......like what would the answer be? because in first aid it does not specify
 
Good job!

now a follow up question and one that I don't know the answer to myself- do these drugs all effect the same cytochrome P450 enzyme or different ones? I remember one time a person on one of these forums saying that on their real test they had been asked specifically which cytochrome P450 enzyme St. John's Wart enhanced......like what would the answer be? because in first aid it does not specify
when in doubt 3A4, if not that then 2D6... other than that i got nothing
 
Could one of you see if my thinking regarding lymphatics in that region is correct:
so paraortic drains kidneys, testes, ovaries, and the uterus....superficial inguinal drains anal canal below the pectinate line, scrotum, skin below umbilicus, and then distal vagina and vuvla......internal illiac drains lower portion of rectum, anal canal above the pectinate line, bladder, prostate, and middle 1/3 of vagina?...external illiac: this is the one i'm confused about?- only thing I know is proximal vagina?

so using that knowledge I would have answered this as: #1) superficial inguinal 2) uterine 3) internal illiac

@syoung - do you mind checking my reasoning ^ for one of the earlier questions?
 
Per my original post: 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
5) 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

@Phloston

1) normal?
2) High ACTH High cortisol ... ( chronic pain-->inc CRH)
3) ACTH low. Cortisol High ( exogenous steroid)
4) ACTH high Cortisol High (Small cell lung ca paraneoplastic? but its nonsmoker not sure? ataxia points towards mets to brain?
5) ACTH low Cortisol High ( Cushing syndrome. striae + inc Na)

1) ACTH and cortisol both low because these patients are on long-term prednisone. Exogenous steroids = most common cause of Cushing syndrome.

2) Same as #1. NSAIDs and steroids are used strictly for pain relief. This patient would also be on one or more DMARDs.

3) Most common endogenous cause of Cushing syndrome is Cushing disease. So ACTH high and cortisol high. The diagnosis would need to be confirmed, but these values should be the initial suspicion. Impotence is likely secondary to uncontrolled diabetes, as is the cataract.

4) ACTH high, cortisol high. This is a small cell bronchogenic carcinoma. USMLE textbooks stress paraneoplastic secretion of ACTH and/or ADH, but anti-Hu and anti-Yo antibodies associated with cerebellar dysfunction are actually really really HY. That is on the Step 1. And of course don't forget small cell causing Lambert-Eaton as well.

5) ACTH low, corisol high. Likely cortisol-secreting tumor of zona fasciculata. Corisol has subtle mineralocorticoid effects if present at high levels. Baseline sugars are up and electrolytes may or may not be perturbed. Lack of chronic disease suggests against exogenous steroids.
 
Could one of you see if my thinking regarding lymphatics in that region is correct:
so paraortic drains kidneys, testes, ovaries, and the uterus....superficial inguinal drains anal canal below the pectinate line, scrotum, skin below umbilicus, and then distal vagina and vuvla......internal illiac drains lower portion of rectum, anal canal above the pectinate line, bladder, prostate, and middle 1/3 of vagina?...external illiac: this is the one i'm confused about?- only thing I know is proximal vagina?

so using that knowledge I would have answered this as: #1) superficial inguinal 2) uterine 3) internal illiac
@syoung - do you mind checking my reasoning ^ for one of the earlier questions?
proximal vagina is probably internal iliac and distal vagina to superficial inguinal

okay i am a bit confused about anal canal vs anal skin lymphatic drainage.

what i have gathered so far is this:
till upper rectum-----------> Inferior mesenteric L.N ( is there a point of demarcation? if they say adenocarcinoma of rectum what are we to assume?)
lower Rectum-----------> Internal Iliac L N
anal canal above pectinate line---> internal iliac LN
below pectinate Line------> Superficial Inguinal LN

what about anal skin drainage ?

http://www.oganatomy.org/projanat/gross/41/four.htm
 
@Phloston
Per my original post: 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
5) 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



1) ACTH and cortisol both low because these patients are on long-term prednisone. Exogenous steroids = most common cause of Cushing syndrome.

2) Same as #1. NSAIDs and steroids are used strictly for pain relief. This patient would also be on one or more DMARDs.

3) Most common endogenous cause of Cushing syndrome is Cushing disease. So ACTH high and cortisol high. The diagnosis would need to be confirmed, but these values should be the initial suspicion. Impotence is likely secondary to uncontrolled diabetes, as is the cataract.

4) ACTH high, cortisol high. This is a small cell bronchogenic carcinoma. USMLE textbooks stress paraneoplastic secretion of ACTH and/or ADH, but anti-Hu and anti-Yo antibodies associated with cerebellar dysfunction are actually really really HY. That is on the Step 1. And of course don't forget small cell causing Lambert-Eaton as well.

5) ACTH low, corisol high. Likely cortisol-secreting tumor of zona fasciculata. Corisol has subtle mineralocorticoid effects if present at high levels. Baseline sugars are up and electrolytes may or may not be perturbed. Lack of chronic disease suggests against exogenous steroids.



thanks a lot.
looks like i missed a step there of linking chronic diseases with use of exogenous steroid.

couple of Queries.

1. doesn't long term prednisone will give us High cortisol level? i know endogenous cortisol is hydrocortisone formulation vs prednisone having Prednisolone as the active metabolite.
in other words exogenous steroid medication will not give us high plasma level of cortisol level or does it?

thanks !
 
Question
pudendal nerve block was administered. which of the following area will not be anesthetized?
a) labia minor
b)vestibule of the vagina
c) anterior Labia major
d) bulbs of the vestibule
 
@Phloston




thanks a lot.
looks like i missed a step there of linking chronic diseases with use of exogenous steroid.

couple of Queries.

1. doesn't long term prednisone will give us High cortisol level? i know endogenous cortisol is hydrocortisone formulation vs prednisone having Prednisolone as the active metabolite.
in other words exogenous steroid medication will not give us high plasma level of cortisol level or does it?

thanks !

Exogenous steroids (e.g., prednisone) exert negative feedback on hypothalamus and anterior pituitary --> decreases CRH and ACTH, respectively --> decreases cortisol. Exogenous steroids obviate the need for the zona fasciculata to secrete cortisol. We never give a patient cortisol. We give things like hydrocortisone, prednisone, fludrocortisone. Prednisone is big for chronic disease management. Hydrocortisone is generally good for secondary adrenal insufficiency. Fludrocortisone has the greatest mineralocorticoid effect and is good for Addison, where aldosterone is also low.
 
one of the WTF questions i have heard in a long time

a person goes for the hiking, used bottled water and cooked food. 3 days later present with myalgia, aches, abdominal pain. Dx is worm infection. what is the source of infection?
bites
ticks
fresh water infection

so can we quickly review parasites transmission?

hiking makes me think of tick bite--> which would be either lyme or Ricketsiaa infx. i don't recall worms.
 
okay i am a bit confused about anal canal vs anal skin lymphatic drainage.

what i have gathered so far is this:
till upper rectum-----------> Inferior mesenteric L.N ( is there a point of demarcation? if they say adenocarcinoma of rectum what are we to assume?)
lower Rectum-----------> Internal Iliac L N
anal canal above pectinate line---> internal iliac LN
below pectinate Line------> Superficial Inguinal LN

what about anal skin drainage ?

http://www.oganatomy.org/projanat/gross/41/four.htm

The USMLE will never give you something so ambiguous the same way a QBank will. You'll find that the NBMEs/USMLE will have a few odd ball questions, but they'll have clear cut answers.
 
one of the WTF questions i have heard in a long time

a person goes for the hiking, used bottled water and cooked food. 3 days later present with myalgia, aches, abdominal pain. Dx is worm infection. what is the source of infection?
bites
ticks
fresh water infection

so can we quickly review parasites transmission?

hiking makes me think of tick bite--> which would be either lyme or Ricketsiaa infx. i don't recall worms.

Myalgia, fever plus edema = Trichinella spiralis. But that's pork or bear meat.
Myalgia can also be cysticercosis (Taenia solium), but that's pork.
 
one of the WTF questions i have heard in a long time

a person goes for the hiking, used bottled water and cooked food. 3 days later present with myalgia, aches, abdominal pain. Dx is worm infection. what is the source of infection?
bites
ticks
fresh water infection

so can we quickly review parasites transmission?

hiking makes me think of tick bite--> which would be either lyme or Ricketsiaa infx. i don't recall worms.
Schistosomiasis from swimming in fresh water.
 
Long CAG repeats associated with what? What about short CAG repeats?
Long CAG repeats associated with Huntington's disease. Never heard of short CAG repeats leading to anything but I'll guess Huntington's as well. Maybe the farther you get from the normal amount of CAG repeats, in either direction, will lead to Huntington's?
 
Long CAG repeats associated with Huntington's disease. Never heard of short CAG repeats leading to anything but I'll guess Huntington's as well. Maybe the farther you get from the normal amount of CAG repeats, in either direction, will lead to Huntington's?

Shorter CAG = more sensitive androgen receptors = associated with prostate cancer. Also in Klinefelters the X chromosome with shorter CAG is preferentially inactivated, which is part of the reason why they have hypogonadism.
 
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