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

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[PowerDan]

why there is low ceruloplasmin in wilson and menkes ?

Due to defective copper efflux pumps/transporters. ATP7A in case of Menke's and ATP7B in Wilson's.

 

[PowerDan]

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.

Copper is deficient, not elevated in Menke's.

 

[faisal 2000]

why homocysteine levels will be high in PCOS ?

 

[Pholston]

why homocysteine levels will be high in PCOS ?

It is just an observed association.
No-one knows why.

 

[faisal 2000]

.

 

[tarsuc]

Goljan says Acute GlomeruloNephritis (pg 517) labs are similar to prerenal azotemia, while FA pg 553 says its similar to intrinsic.

Any inputs, guys?

 

[MrWonderful]

Might I add some HY Drug Facts and ADRs

 

[faisal 2000]

is there any changes in ECG in case of hypo/hypernatremia ?





@Phloston
@Transposony

 

[sloop]

is there any changes in ECG in case of hypo/hypernatremia ?





@Phloston
@Transposony

Hyponatremia would carry the theoretical risk of QRS prolongation and ventricular conduction delay, however my limited understanding is that the hypothesis that this has any practical significance is far from established.

My guess is that with any problems with sodium/water homeostasis severe enough to impact the ECG directly, you'll probably be more worried about associates RAAS-induced issues with potassium than the sodium. But I'm not a cardiologist.

I don't think Step 1 would test you on ECG manifestations of issues with sodium metabolism.

 

[seminoma]

Hyponatremia would carry the theoretical risk of QRS prolongation and ventricular conduction delay, however my limited understanding is that the hypothesis that this has any practical significance is far from established.

My guess is that with any problems with sodium/water homeostasis severe enough to impact the ECG directly, you'll probably be more worried about associates RAAS-induced issues with potassium than the sodium. But I'm not a cardiologist.

I don't think Step 1 would test you on ECG manifestations of issues with sodium metabolism.

Haven't been on sdn in close to a year or more.. Can't believe you're able to keep up with step 1 stuff as a ms4. My ms4 brain is worthless lol.

 

[sloop]

Haven't been on sdn in close to a year or more.. Can't believe you're able to keep up with step 1 stuff as a ms4. My ms4 brain is worthless lol.

Haha, mine is too. Counting down the days until march day. To be fair I don't think a sodium ECG question is actually a step 1 question. The thread showed up in my alerts so I took a stab.

You were a great support during the whole process of step 1 and beyond. I honestly think the board exam support forums are the best of SDN.

 

[Brorthopedic]

According to Uworld - "Increase in LV contractility increases total SV and could lead to an increase in afterload"

Can someone explain to me why it isn't a decrease in afterload? Stem didn't mention anything about an AR.

 

[chromuffin]

According to Uworld - "Increase in LV contractility increases total SV and could lead to an increase in afterload"

Can someone explain to me why it isn't a decrease in afterload? Stem didn't mention anything about an AR.

What QID? Was there any indication of increased TPR?

 

[Brorthopedic]

What QID? Was there any indication of increased TPR?

QID 943, choice D explanation

 

[chromuffin]

QID 943, choice D explanation

Hmm.. I haven't don't it. This goes completely against Frank Starling's Curve for Inotropy though. I would suspect some condition like CHF has the patient severely decompromised and the patient is then given dobutamine or milrinone to compensate. Are you paraphrasing the wording? I've never heard of increased inotropy causing increased afterload. I've heard of increased afterload causing increased inotropy..

 

[Brorthopedic]

Hmm.. I haven't don't it. This goes completely against Frank Starling's Curve for Inotropy though. I would suspect some condition like CHF has the patient severely decompromised and the patient is then given dobutamine or milrinone to compensate. Are you paraphrasing the wording? I've never heard of increased inotropy causing increased afterload. I've heard of increased afterload causing increased inotropy..

Nope, that's a straight quote. Patient has MR in the stem though.


@Pholston

 

[Transposony]

is there any changes in ECG in case of hypo/hypernatremia ?

I completely agree with my esteemed colleague sloop here as no significant changes on the ECG occurs with hypo/hypernatraemia.

However, they might put in an experimental question to test your understanding of movement of various ions across the membrane.
Therefore, hypernatremia can theoretically lead to prolongation of the QT interval because of an increase in the duration of the action potential. This happens due to high extracellular Na levels causing an increase in the gradient across the membrane. Increased extracellular Na causes more Ca to exit the cell via Na/Ca exchanger on the sarcolemma. This results in decreased levels of intracellular Ca levels for cardiac myocyte contraction causing a negative inotropic effect.
Similarly, it can cause other theoretical ECG changes like reduction in the P and QRS amplitude.
Hyponatremia, therefore, can have opposite effect.

But always remember, Na (hypo/hypernatremia) almost always affects brain.

 

[faisal 2000]

how can we differentiate b\w thoracic outlet syndrome and Injury to the medial cord of the brachial plexus beside presence of Adison sign in thoracic outlet ?

 

[AlteredScale]

how can we differentiate b\w thoracic outlet syndrome and Injury to the medial cord of the brachial plexus beside presence of Adison sign in thoracic outlet ?

Adsons/Halsteds/Wright's Hyperabduction test are all pretty sensitive tests for Thoracic O/S and they can help localize it as well (Wrights being impingement by the pec minor, halsteds being impingement by clavicle). The best way I've come across differentiating these two has been essentially that TOS is exacerbated with motion whereas median cord injury presents with constant s/s.

 

[faisal 2000]

Adsons/Halsteds/Wright's Hyperabduction test are all pretty sensitive tests for Thoracic O/S and they can help localize it as well (Wrights being impingement by the pec minor, halsteds being impingement by clavicle). The best way I've come across differentiating these two has been essentially that TOS is exacerbated with motion whereas median cord injury presents with constant s/s.

what about areas of numbness and atrophy? what happen if there is isolated medial cord lesion?

 

[faisal 2000]

how can kidney diseases cause hyperprolactinemia ?

 

[IM/EM/CCM]

Decreased renal excretion of prolactin!!

how can kidney diseases cause hyperprolactinemia ?

 

[faisal 2000]

i have encounter Q somewhere mention that hypothyroidism can associated with hypokalemia.
anyone knows the mechanism ?