Official Step 1 High Yield Concepts Thread

[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

 

[stepone2015]

Did she forget to take her insulin and now is in DKA?

Yes, that was the idea. But the question is, why does she have DKA if she has T2DM?

 

[stepone2015]

Not sure, but is it destruction of pancreatic islet cells via pancreatic adenocarcinoma; poor prognosis.

A good thought, but a 20 year history of DM is incompatible with that theory of pancreatic cancer. She'd be long dead if that were the case.

 

[dfib slim]

Yes, that was the idea. But the question is, why does she have DKA if she has T2DM?

She had T2DM for over 20 years, maybe her pancreas burned out.

 

[stepone2015]

She had T2DM for over 20 years, maybe her pancreas burned out.

Yup, that's it.

 

[aspiringmd1015]

Whats the other name for the lactase enzyme?

 

[seminoma]

FA page 423 says t-tubules are part of sarcoplasmic reticulum. That's wrong... correct? T-tubules are part of plasma membrane.

 

[stepone2015]

FA page 423 says t-tubules are part of sarcoplasmic reticulum. That's wrong... correct? T-tubules are part of plasma membrane.

Definitely. Should say 'are associated with'.

 

[dfib slim]

FA page 423 says t-tubules are part of sarcoplasmic reticulum. That's wrong... correct? T-tubules are part of plasma membrane.

I saw that in the proposed errata but I don't think it made it into the final draft. I changed mine to "T-tubules (extensions of the plasma membrane) are juxtaposed with terminal cisternae (part of the sarcoplasmic reticulum)". Made more sense this way.

 

[Transposony]

I saw that in the proposed errata but I don't think it made it into the final draft. I changed mine to "T-tubules (extensions of the plasma membrane) are juxtaposed with terminal cisternae (part of the sarcoplasmic reticulum)". Made more sense this way.

What about "T-tubules (extensions of the plasma membrane) are juxtaposed with terminal cisternae of the sarcoplasmic reticulum".

 

[seminoma]

Brown Sequard syndrome.

Why is there ipsilateral loss of pain/temperature at the level of the lesion? Doesn't the LST ascend 1-2 levels before entering the cord as the Lissauer tract? If so, shouldn't pain/temperature at the level of the lesion be spared (because the axons enter, synapse, and decussate above the level of the lesion)?

 

[stepone2015]

Brown Sequard syndrome.

Why is there ipsilateral loss of pain/temperature at the level of the lesion? Doesn't the LST ascend 1-2 levels before entering the cord as the Lissauer tract? If so, shouldn't pain/temperature at the level of the lesion be spared (because the axons enter, synapse, and decussate above the level of the lesion)?

It is spared for a couple levels below the lesion. Where does it say that it isn't?

 

[Transposony]

Brown Sequard syndrome.

Why is there ipsilateral loss of pain/temperature at the level of the lesion? Doesn't the LST ascend 1-2 levels before entering the cord as the Lissauer tract? If so, shouldn't pain/temperature at the level of the lesion be spared (because the axons enter, synapse, and decussate above the level of the lesion)?

Are you sure?

Contralateral pain and temperature loss below level of lesion (due to spinothalamic tract damage)
Ipsilateral loss of all sensation at level of lesion

If you are asking why ipsilateral loss of pain/temperature at the level of the lesion as part of "ipsilateral loss of all sensations" then it is due to the fact that the pain and temperature fibres (1st order neurons) enter the spinal cord in the lateral division of the dorsal root and then ascend or descend one or two segments in the Lissauer tract and then synapse on second-order neurons in the outer laminae of the dorsal horn.

Hope I am making sense. Had to look it up.

 

[seminoma]

It is spared for a couple levels below the lesion. Where does it say that it isn't?

FApg 472

 

[stepone2015]

FApg 472

If it hits the cell bodies in the DRG, it can affect that level.

 

[aspiringmd1015]

^exactly, AT the level of the lesion, everything is lost, motor, sensory etc. Basically you cant feel Shi!t at the level of the hemisection.

 

[seminoma]

If it hits the cell bodies in the DRG, it can affect that level.

^exactly, AT the level of the lesion, everything is lost, motor, sensory etc. Basically you cant feel Shi!t at the level of the hemisection.

Brown sequard is cord hemisection. DRG isn't in the cord...

And if the lesion hit the DRG then you would have bilateral loss of sensation at the lesion, not just ipsilateral?

 

[psylocke]

Brown sequard is cord hemisection. DRG isn't in the cord...

And if the lesion hit the DRG then you would have bilateral loss of sensation at the lesion, not just ipsilateral?

Yeah... Sensation loss will be of dermatomal distribution depending on the location of the injured DRG.

 

[Transposony]

Brown sequard is cord hemisection. DRG isn't in the cord...

And if the lesion hit the DRG then you would have bilateral loss of sensation at the lesion, not just ipsilateral?

There are three types of P&T fibers at a given level of the spinal cord:
1. 1st order neurons entering the spinal cord ipsilaterally
2. 1st order neurons which has already entered the spinal cord 1-2 levels below and which are ascending in the Lissauer tract ipsilaterally
3. 2nd order neurons which have crossed from the other side and ascending as the LST.

So, in Brown-Sequard all of these will be injured but to answer your original question, it will be #1 fibers which will cause the ipsilateral loss of pain/temperature at the level of the lesion.

 

[aspiringmd1015]

the dorsal root gangion isnt in the cord, but after the neurons make its first snapse in the DRG, the second order neuron from there enters the dorsal column

 

[aspiringmd1015]

for maternal PKU, does the infant have to be deficiency in the enzyme? or is it the accumulation of the phenylketones that overhwlems the capacity of the infant to hydroxlate it as well even if the infant has normal levels

 

[seminoma]

There are three types of P&T fibers at a given level of the spinal cord:
1. 1st order neurons entering the spinal cord ipsilaterally
2. 1st order neurons which has already entered the spinal cord 1-2 levels below and which are ascending in the Lissauer tract ipsilaterally
3. 2nd order neurons which have crossed from the other side and ascending as the LST.

So, in Brown-Sequard all of these will be injured but to answer your original question, it will be #1 fibers which will cause the ipsilateral loss of pain/temperature at the level of the lesion.

Nice, thanks. I always forget that they ascend after they enter the cord.

the dorsal root gangion isnt in the cord, but after the neurons make its first snapse in the DRG, the second order neuron from there enters the dorsal column

I think we're talking about different things. Nothing synapses in the DRG, and the spinothalamic tract isn't in the dorsal column.

for maternal PKU, does the infant have to be deficiency in the enzyme? or is it the accumulation of the phenylketones that overhwlems the capacity of the infant to hydroxlate it as well even if the infant has normal levels

Fetus has normal phe hydroxylase. That's probably the only thing step 1 will test about maternal PKU.

 

[seminoma]

Page 479 FA15. "Ciliary body (middle), Cornea (outer), Iris (middle)" is referring to what?

 

[aspiringmd1015]

the sensory neurons that come in from the periphery synapse in the Dorsal root gangion dont they?

 

[aspiringmd1015]

Page 479 FA15. "Ciliary body (middle), Cornea (outer), Iris (middle)" is referring to what?

i was going to say uveal tract, but thats iris, ciliary body, and the choroid.

 

[seminoma]

the sensory neurons that come in from the periphery synapse in the Dorsal root gangion dont they?

No, the DRG houses the neuron cell bodies. Synapse is in the dorsal horn.

 

[aspiringmd1015]

No, the DRG houses the neuron cell bodies. Synapse is in the dorsal horn.

okay my bad, but there you go, if it synapses in the dorsal horn, a hemisection-lose all sensation

 

[seminoma]

What a bunch of jerks. Just noticed that FA put an "ipsilateral" leptomeningeal angioma on the contralateral side of the accompanying port-wine stain (page 491). Could've just photoshopped the pic before publishing.

 

[Transposony]

Page 479 FA15. "Ciliary body (middle), Cornea (outer), Iris (middle)" is referring to what?

They are referring to the layers of the globe of the eye.
Therefore,
Outer --> Sclera continues as cornea
Middle --> Iris and Ciliary body are continuations of Choroid
Most likely something to do with their developmental origin but I don't think they are going to ask the embryology of the eye except the corneal limbus (neural crest).

 

[Transposony]

What a bunch of jerks. Just noticed that FA put an "ipsilateral" leptomeningeal angioma on the contralateral side of the accompanying port-wine stain (page 491). Could've just photoshopped the pic before publishing.

Why are you assuming that they are from the same patient?

 

[seminoma]

Why are you assuming that they are from the same patient?

I'm not. I'm just saying that making the images show ipsilateral lesions would be better to drive the point home. Or, at the very least, if you happen to remember the images from FA and not the text then you would at least guess ipsilateral correctly.

 

[Radiolucent]

Yes, that was the idea. But the question is, why does she have DKA if she has T2DM?

Eventually patients with T2DM have complete destruction of pancreatic islets --> possibility of DKA.

Edit: Nvm, didnt see that that one already was answered.

 

[Radiolucent]

A 37 year old female comes to the office with 2 weeks high fever, night sweats and fatigue. She returned from a vacation in southern Europe 4 weeks ago where she went to a goat cheese festival. She also came back from a hiking trip 2 weeks ago and recalls having multiple bites on her legs. She denies drinking unbotteled water during these trips. Physical examination reveals a mildly enlarged liver and the doctor notices a strange moldy odor coming from the patient. No rash or skin change can be seen. CBC and chest X-ray is normal.
Which of the following is the most likely pathogen?

a. Ascaris lumbricoides
b. Rickettsia prowazekii
c. Francicella tularensis
d. Salmonella typhi
e. Hymenolepis nana
f. Brucella melitensis
g. Leptospia interrogans

 

[seminoma]

A 37 year old female comes to the office with 2 weeks high fever, night sweats and fatigue. She returned from a vacation in southern Europe 4 weeks ago where she went to a goat cheese festival. She also came back from a hiking trip 2 weeks ago and recalls having multiple bites on her legs. She denies drinking unbotteled water during these trips. Physical examination reveals a mildly enlarged liver and the doctor notices a strange moldy odor coming from the patient. No rash or skin change can be seen. CBC and chest X-ray is normal.
Which of the following is the most likely pathogen?

a. Ascaris lumbricoides
b. Rickettsia prowazekii
c. Francicella tularensis
d. Salmonella typhi
e. Hymenolepis nana
f. Brucella melitensis
g. Leptospia interrogans

F? Only thing I know to associate with Goats.

 

[seminoma]

FA (page 506) says 40% of deaths in children <1 year old are due to physical abuse. Yet the top 3 causes of death in children <1 (page 60) are congenital malformations, preterm birth, SIDS. Not sure how those numbers add up.

Any input?

 

[stepone2015]

A 37 year old female comes to the office with 2 weeks high fever, night sweats and fatigue. She returned from a vacation in southern Europe 4 weeks ago where she went to a goat cheese festival. She also came back from a hiking trip 2 weeks ago and recalls having multiple bites on her legs. She denies drinking unbotteled water during these trips. Physical examination reveals a mildly enlarged liver and the doctor notices a strange moldy odor coming from the patient. No rash or skin change can be seen. CBC and chest X-ray is normal.
Which of the following is the most likely pathogen?

a. Ascaris lumbricoides
b. Rickettsia prowazekii
c. Francicella tularensis
d. Salmonella typhi
e. Hymenolepis nana
f. Brucella melitensis
g. Leptospia interrogans

Ascaris. Caused biliary tree infection leading to symptoms seen.

 

[seminoma]

Ascaris. Caused biliary tree infection leading to symptoms seen.

Pretty sure ascaris tends to cause eosinophilia and pulmonary infiltrates on CXR..?

 

[Transposony]

Fever, night sweats and hepatitis fits quite well into Brucellosis.
South Europe & Goat cheese are good pointers.
Only thing missing from a typical presentation is myalgia.

 

[stepone2015]

Fever, night sweats and hepatitis fits quite well into Brucellosis.
South Europe & Goat cheese are good pointers.
Only thing missing from a typical presentation is myalgia.

I was looking for an undulant pattern. Think that threw me off.

 

[seminoma]

Fever, night sweats and hepatitis fits quite well into Brucellosis.
South Europe & Goat cheese are good pointers.
Only thing missing from a typical presentation is myalgia.

Just remembered that the smelly sweat is a pretty strong indicator too.

 

[Transposony]

I was looking for an undulant pattern. Think that threw me off.

Yes classically the undulant fever is associated with udders and unpasteurized milk and that's the reason they are not going to give it to you on the test.
It's a great question where you have to pick the "best answer" and exclude others based on the info provided.
Never knew about the characteristic "smell" but now I know.
One clue which always helps me to narrow down the choices is that "night sweats" are associated with overactive Lymphocyte/Macrophages, probably due to increased cytokine release.
So I always look for condition which might be causing inflammation usually of the granulomatous kind (Granulomatous hepatitis in this case).

 

[Transposony]

Has anyone come across Bronchiolitis obliterans (especially in relation to transplant and rejection) in any of the QBanks or NBMEs?
I am trying to figure out if it is HY for Step 1

 

[Radiolucent]

Fever, night sweats and hepatitis fits quite well into Brucellosis.
South Europe & Goat cheese are good pointers.
Only thing missing from a typical presentation is myalgia.

Just remembered that the smelly sweat is a pretty strong indicator too.

Nice. As you pointed out the characteristic smell of sweat, the likely unpasteurized milk ingestion, and location (mediterranean) and symptoms points to Brucellosis.

Ascaris. Caused biliary tree infection leading to symptoms seen.

Ascariasis is of course a possible Dx but less likely than brucellosis because of no mention of eosinophilia, pulmonary/gi symptoms. Also, Ascaris is most often spread by contaminated water which is not very likely in this patient.

Has anyone come across Bronchiolitis obliterans (especially in relation to transplant and rejection) in any of the QBanks or NBMEs?
I am trying to figure out if it is HY for Step 1

Only seen it once and in relation to transplantation (UW). No other mention in FA (IIRC), UW, Rx and the real thing.

 

[seminoma]

Has anyone come across Bronchiolitis obliterans (especially in relation to transplant and rejection) in any of the QBanks or NBMEs?
I am trying to figure out if it is HY for Step 1

UW has at least 2 questions about it.

 

[aspiringmd1015]

in FA, it has schistoma heamtoboium a/c with pulmonary HTN, is that correct? or should it be portal HTN

 

[seminoma]

FA 590 - "Malignant breast tumors usually arise from terminal duct lobular unit"
FA 591 "Invasive ductal most common of all breast cancers"
FA 589 "DCIS, Invasive Ductal Carcinoma arise from Major duct" (image)

???

 

[dartmed]

Question: how do you distinguish Albright hereditary osteodystrophy from ESRD in terms of lab values for calcium, phosphate, and PTH? They both would look the same, right?

I am thinking you might be able to use the cAMP levels assuming that you might have some preserved function for ESRD, so PTH can still act on it?

 

[Transposony]

FA 590 - "Malignant breast tumors usually arise from terminal duct lobular unit"
FA 591 "Invasive ductal most common of all breast cancers"
FA 589 "DCIS, Invasive Ductal Carcinoma arise from Major duct" (image)

???

Looks like they didn't update the figure on page 589.

 

[aspiringmd1015]

Question: how do you distinguish Albright hereditary osteodystrophy from ESRD in terms of lab values for calcium, phosphate, and PTH? They both would look the same, right?

I am thinking you might be able to use the cAMP levels assuming that you might have some preserved function for ESRD, so PTH can still act on it?

PTH cant act on it regardless though right? the receptor would have to be funcitonal for PTH to increase c-amp

 

[aspiringmd1015]

with PTH not working can you still hydroxylate vit d in the kidney? if not then your po4 will be low in heriditary osteodystrophy

 

[dartmed]

with PTH not working can you still hydroxylate vit d in the kidney? if not then your po4 will be low in heriditary osteodystrophy

I was under the impression that PTH directly acts on PCT to decrease the PO43-?

I thought PTH would activate the 1alpha-hydroxylase, which would form calcitriol. Calcitriol acts on the small intestine to reabsorb more calcium and acts on the bone to increase the phosphate levels. So, in Albright hereditary osteodystrophy, if PTH can't work on the kidneys, then you would see elevated phosphorus, low levels of calcium with high levels of PTH with decreased levels of cAMP

Similarly, in ESRD, you would see high levels of phosphorus, low levels of calcium, and low levels of Vitamin D.

For your question on whether you would see normal Vitamin D activity, I don't know? I guess if you did, you wouldn't be able to maintain the homeostasis for calcium and phosphorus. So, high calcium levels would be regulated by calcitonin and high phosphorus wouldn't be regulated by PTH. So, you would see normocalcemic and hyperphosphate levels if the homeostasis was disrupted.