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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loss of negative feedback. Conrad fischer: loss of negative feedback is one of the fundamentals of pathology. My bad for the error
 
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Tactile fremitus in pleural effusion? In lobar pneumonia? In pulmonary edema?

All three are fluid, so why aren't they all the same?
 
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dfib slim said:
Causes of differential and reverse differential cyanosis?
Click to expand...
Since no one is biting,

Differential cyanosis is caused by a patent ductus, you get lower extremity cyanosis when the shunt reverses. Not seen with coarctation of the aorta.

Reverse differential cyanosis is caused by transposition of the great vessels and you get the cyanosis in the upper body.
 
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seminoma said:
Tactile fremitus in pleural effusion? In lobar pneumonia? In pulmonary edema?

All three are fluid, so why aren't they all the same?
Click to expand...
up in lobar pneumonia and pulm edema
down in pleural effusion

depends on the location of the exudate/transudate; in lobar pneumonia and edema, it's w/in alveoli, in effusion it's between the pleural spaces
 
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in a genetically susceptible patient, what is a particular side effect after surgery that is treated with dantrolene?
 
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dfib slim said:
Yeast. Use use yeast to bake at higher temps.

Disregard, that's for systemic mycoses
Click to expand...

Yeah Candida is yeast at 20*, germ tubes at 37*.

syoung said:
up in lobar pneumonia and pulm edema
down in pleural effusion

depends on the location of the exudate/transudate; in lobar pneumonia and edema, it's w/in alveoli, in effusion it's between the pleural spaces
Click to expand...

Yup, in effusion the fluid "blocks" you from getting at the air in the lungs, thus dampening the sound.

syoung said:
in a genetically susceptible patient, what is a particular side effect after surgery that is treated with dantrolene?
Click to expand...

Malignant hyperthermia
 
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Can someone please explain FSH levels in PCOS? In first aid, it says FSH increased but on an NBME question the answer was that it's decreased.

It's my understanding you get a large increase in LH -> Theca cell makes tons of Androgens (more than granulosa cells can use) -> Androgens leak out into system and cause hirsuitism plus androgens converted to estrone by fat -> negative feedback on FSH so FSH decreases. Low FSH means granulosa cells cant convert androgens into Estradiol. So even though estradiol is low, overall "estrogen" is increased because of high estrone levels. Does that make sense?

So why does FA claim FSH is increased? Also why are Testosterone levels increased? Does it have anything to do with extra Androgens for the renal cortex (reticularis) to convert to T?

Thanks
 
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NoLollipops4U said:
Can someone please explain FSH levels in PCOS? In first aid, it says FSH increased but on an NBME question the answer was that it's decreased.

It's my understanding you get a large increase in LH -> Theca cell makes tons of Androgens (more than granulosa cells can use) -> Androgens leak out into system and cause hirsuitism plus androgens converted to estrone by fat -> negative feedback on FSH so FSH decreases. Low FSH means granulosa cells cant convert androgens into Estradiol. So even though estradiol is low, overall "estrogen" is increased because of high estrone levels. Does that make sense?

So why does FA claim FSH is increased? Also why are Testosterone levels increased? Does it have anything to do with extra Androgens for the renal cortex (reticularis) to convert to T?

Thanks
Click to expand...

Where does FA say FSH is increased in PCOS?

LH high --> theca cells make androgens --> fat converts to estrone --> FSH suppressed

The high T is from decreased SHBG 2/2 the obesity --> hyperinsulinism.
 
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seminoma said:
Where does FA say FSH is increased in PCOS?

LH high --> theca cells make androgens --> fat converts to estrone --> FSH suppressed

The high T is from decreased SHBG 2/2 the obesity --> hyperinsulinism.
Click to expand...

In FA 2014, it says that in the top right of the PCOS area in the "summary" of lab values for PCOS.

Interesting, I didn't know that obesity --> decreased SHBG.

Thank you. Im getting a little nervous, my exams in 2 weeks. I am doing fine on exams, but sometimes I just have something memorized rather than understanding the why.

I also just remembered that Theca cells convert some Androstenedione to testosterone anyways as well.
 
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NoLollipops4U said:
In FA 2014, it says that in the top right of the PCOS area in the "summary" of lab values for PCOS.

Interesting, I didn't know that obesity --> decreased SHBG.

Thank you. Im getting a little nervous, my exams in 2 weeks. I am doing fine on exams, but sometimes I just have something memorized rather than understanding the why.

I also just remembered that Theca cells convert some Androstenedione to testosterone anyways as well.
Click to expand...

Sure it's not in the errata? I'm pretty sure FSH is not increased.
 
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seminoma said:
Sure it's not in the errata? I'm pretty sure FSH is not increased.
Click to expand...
LH:FSH ratio should be > 2:1 or 3:1
FA15 says that both LH and FSH are up, but the ratio is much higher for LH which is probably more important to remember

Edit: FA14
 
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syoung said:
LH:FSH ratio should be > 2:1 or 3:1
FA15 says that both LH and FSH are up, but the ratio is much higher for LH which is probably more important to remember
Click to expand...

I just read the FA15 PCOS section this morning and I don't remember it saying FSH is up. It says LH/FSH is up (as in the ratio is up) for sure.
 
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A question about amyoptrophic lateral sclerosis. FA says "combined UMN and LMN deficits..."

edit: clarifying what I typed earlier.

Kaplan says

-spastic paralysis in lower limbs (UMN)
-flaccid paralysis in the upper limbs (LMN)

Any explanation of why that is?

Why no spastic paralysis in the upper limbs as well, or flaccid paralysis in the lower limbs?
 
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messengers said:
A question about amyoptrophic lateral sclerosis. FA says "combined UMN and LMN deficits..."

edit: clarifying what I typed earlier.

Kaplan says

-spastic paralysis in lower limbs (UMN)
-flaccid paralysis in the upper limbs (LMN)

Any explanation of why that is?

Why no spastic paralysis in the upper limbs as well, or flaccid paralysis in the lower limbs?
Click to expand...

You will not see spastic paralysis in the upper limbs, since the effect of flaccid paralysis will "override" the effect of spastic paralysis (since there are no functional LMN which can manifest the symptoms of the spastic paralysis). In terms of the flaccid paralysis in the LE, according to the KAPLAN, ALS commonly occurs in cervical enlargement, therefore the LMN for LE which are located in the ventral horn at the lumbar levels will not be affected by the condition, while there will be lateral sclerosis of the corticospinal tract (UMN) at the cervical level which project to LE, hence spastic paralysis for LE.
 
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Gynecologic cancers in order of incidence? Mortality? (in the US for both)

dfib slim said:
Berger vs Buerger disease and Langhans vs Langerhans cells?
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Berger = iga nephropathy. related to HSP, often within days of mucosal infection. "negative" IF that shows mesangial deposits.
Buerger = thromboangiitis obliterans. vasculitis a/w smoking. presents in younger men (before 30 in most cases I believe)

Langhans = fused macrophages/histiocytes --> giant cells as in granuloma
Langerhans = CD1a, S100 positive dendritic cells.
 
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What is/are the immunological receptor(s) bound by toxin in:

1) Septic shock caused by aspiration pneumonia in a 74-year-old stroke patient

2) Septic shock in a 16-year-old following a car accident in which he had epistaxis requiring nasal packing

(Quote me if you want my reply cuz I rarely check this thread)
 
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Phloston said:
What is/are the immunological receptor(s) bound by toxin in:

1) Septic shock caused by aspiration pneumonia in a 74-year-old stroke patient

2) Septic shock in a 16-year-old following a car accident in which he had epistaxis requiring nasal packing

(Quote me if you want my reply cuz I rarely check this thread)
Click to expand...

#1) hmmm this one has stumped me- aspiration pneumonia immediately made me think of klebsiella but that I know doesn't have any correlation to toxins. Also I know anaerobes can cause aspiration pneumonia. I don't know I'm stumped- god I feel stupid

#2) this is Staphylcoccus Aureus Toxic Shock Syndrome I believe, so the TSST binds to the v-beta region of the TCR and to the MHC of the antigen presenting cell as well to lead to polyclonal T-cell activation. well at least that's what I think it is
 
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Phloston said:
What is the mechanism of action of:

1) Irinotecan

2) Moxifloxacin

3) Etoposide

4) Pyrimethamine

5) Tegaserod

(Quote me if you want my reply cuz I rarely check this thread)
Click to expand...

so #1 is a topoisomerase I inhibitor
#2 is a fluoroquinolone so it's a bacterial topoisomerase II (dna gyrase) and IV inhibitor
#3 is also a anti-cancer drug and it acts via topoisomerase II inhibition
#4 Pyrimethamine inhibits bacterial dihydrofolate reductase so then Dihydrofolic acid cannot be converted into tetrahydrofolic acid
#5 Tegaserod is I think an IBD drug......haven't really reviewed GI since I had it in class so not so sure on it

also I'm kind of new on here so I wasn't sure if anyone is allowed to answer or only if we're 100%.... so forgive me if I was only supposed to answer if I was 100% sure with my answers
 
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FlashTime_91 said:
also I'm kind of new on here so I wasn't sure if anyone is allowed to answer or only if we're 100%.... so forgive me if I was only supposed to answer if I was 100% sure with my answers
Click to expand...
It's a free country ...........answer away.
This forum belongs to you as much as to any one of us, so, welcome!
 
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Can someone explain how estrogen (as in OCPs) prevents the physiologic estrogen peak --> LH surge from occurring? I get that the normal physiology requires estrogen to reach a critical level to switch from negative to positive feedback on LH.. and I also get that exogenous estrogen is at too low of a dose to initiate the LH surge, but how does the exogenous estrogen prevent the endogenous estrogen from going through its normal trough --> peak process?
 
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seminoma said:
Can someone explain how estrogen (as in OCPs) prevents the physiologic estrogen peak --> LH surge from occurring? I get that the normal physiology requires estrogen to reach a critical level to switch from negative to positive feedback on LH.. and I also get that exogenous estrogen is at too low of a dose to initiate the LH surge, but how does the exogenous estrogen prevent the endogenous estrogen from going through its normal trough --> peak process?
Click to expand...

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
 
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FlashTime_91 said:
#1) hmmm this one has stumped me- aspiration pneumonia immediately made me think of klebsiella but that I know doesn't have any correlation to toxins. Also I know anaerobes can cause aspiration pneumonia. I don't know I'm stumped- god I feel stupid

#2) this is Staphylcoccus Aureus Toxic Shock Syndrome I believe, so the TSST binds to the v-beta region of the TCR and to the MHC of the antigen presenting cell as well to lead to polyclonal T-cell activation. well at least that's what I think it is
Click to expand...
Don't feel stupid. It's definitely easier to pick the right answer out of a line up then to come up with it off the top.
I think you're on the right track with #1. Aspiration pna caused by gram neg anaerobes, the bacteria doesn't produce toxins but has LPS and binds to TLR4/CD14 leading to shock.
Your #2 explanation seems spot on, strong work.
 
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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. ?
 
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