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

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Oh duh... PCC-induced Vit. C deficiency. I was totally thinking the other way on that one with what vitamin deficiency causes PCC. D'oh!

Great question.
 
What vitamin(s) would be deficient in a vegan (doesn't eat milk & eggs) v/s a vegetarian (does eat milk & eggs) ?
 
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Exception to the rule of Step 1 "never going to court for consent to treatment" ?
 
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PTT is usually affected in von Willebrand disease.
Also, ristocetin assay can differentiate.
Yup, that's what I was getting at. The addition of normal plasma will cause agglutination in a patient with vWD but not BSS.
 
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During exercises such as heavy weight lifting, does blood flow increase or decrease to the muscle? Why?
 
why there is no development of collateral circulation in pre ductal coaractation ?

The body is a lazy POS and won't do anymore work than it needs to. The fetus normally circulates deoxygenated O2 to the lower body and therefore it doesn't see a preductal coarctation as a problem. No problem = not gonna do anything to fix it (lazy POS).

In postductal coarctations, development of collateral flow causes an increase in retrograde flow through which artery(ies)?
 
What vitamin(s) would be deficient in a vegan (doesn't eat milk & eggs) v/s a vegetarian (does eat milk & eggs) ?

Wouldn't pigeonhole this one. Tons of non-vegan vegetarians have low B12, including those I've seen in clinic who have needed B12 injections. I also have a relative who is pescetarian who had to have a B12 injection. Veganism is just on the extreme side of things, which is why a greater % of them will have low B12.
 
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I can't get my head around this concept.
Since translation is responsible for synthesis of proteins and most enzymes and initiation factors are required for translation are proteins, how were these made to start with?
Is it a chicken or the egg dilemma ?
 
Does anyone knows how HY is CCA tail of t-RNA ?
It is mentioned is FA but not many details are given.
 
I can't get my head around this concept.
Since translation is responsible for synthesis of proteins and most enzymes and initiation factors are required for translation are proteins, how were these made to start with?
Is it a chicken or the egg dilemma ?

We are medical students, not philosophers!

I'll bite... G0?
 
I can't get my head around this concept.
Since translation is responsible for synthesis of proteins and most enzymes and initiation factors are required for translation are proteins, how were these made to start with?
Is it a chicken or the egg dilemma ?
Ribozymes?
 
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The body is a lazy POS and won't do anymore work than it needs to. The fetus normally circulates deoxygenated O2 to the lower body and therefore it doesn't see a preductal coarctation as a problem. No problem = not gonna do anything to fix it (lazy POS).

In postductal coarctations, development of collateral flow causes an increase in retrograde flow through which artery(ies)?
Intercostal arteries
 
During exercises such as heavy weight lifting, does blood flow increase or decrease to the muscle? Why?
During exercise, blood flow increases due to locally produced mediators causing vasodilation but with the prolonged contraction of heavy lifting I'd think the vessels would be compressed and flow would decrease.
 
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During exercise, blood flow increases due to locally produced mediators causing vasodilation but with the prolonged contraction of heavy lifting I'd think the vessels would be compressed and flow would decrease.

With a reactive hyperemia once contraction ends.
 
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Genetic mutation will most commonly affect which of the following:
1. Spacer DNA
2. Introns
3. Exons
4. 28 subunit of 60S ribosome
5. Elongation factors
 
During exercise, blood flow increases due to locally produced mediators causing vasodilation but with the prolonged contraction of heavy lifting I'd think the vessels would be compressed and flow would decrease.
I think it's other way around.
Local mediators can't accumulate unless the flow is decreased?
 
Genetic mutation will most commonly affect which of the following:
1. Spacer DNA
2. Introns
3. Exons
4. 28 subunit of 60S ribosome
5. Elongation factors
Statistically wouldn't it be spacer DNA because that's what makes up most of the genome?
 
I think it's other way around.
Local mediators can't accumulate unless the flow is decreased?
Exercising muscle produces vasodilator metabolites like lactate and adenosine which causes dilation of the arterioles in those areas.
 
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Exercising muscle produces vasodilator metabolites like lactate and adenosine which causes dilation of the arterioles in those areas.
Muscles contraction compresses blood vessels in the muscles which causes vasodilator metabolites accumulation leading to autoregulation of local arterioles.
Unless the blood flow decreases there will not an accumulation of these metabolites and hence no dilation of the local arterioles.
 
Muscles contraction compresses blood vessels in the muscles which causes vasodilator metabolites accumulation leading to autoregulation of local arterioles.
Unless the blood flow decreases there will not an accumulation of these metabolites and hence no dilation of the local arterioles.

As he said, blood flow does decrease because the muscle is contracted blocking flow. During this period of stasis, blood vessels begin to dilate without an increase in flow. Once contraction ends, the area sees hyperemia due to the pent up vasodilation until it can all be washed away.
 
Doesn't the swelling cause them to just pop off? The swelling due to the Na+/K+ ATPase shutting down and influx of water.
Protein synthesis requires energy (4 HE-P per AA) and when the source of energy dries up these ribosomes find no incentive to sit on the toilet.
 
During exercise, blood flow increases due to locally produced mediators causing vasodilation but with the prolonged contraction of heavy lifting I'd think the vessels would be compressed and flow would decrease.

Yup. During weight lifting blood flow is decreased. During cardio type stuff it is increased.
 
Which ones?
A HY point about coaractation of aorta-The blood flow in the intercostal arteries is reversed below the defect.
Also, for a coarctation that is proximal to the left subclavian, the right subclavian will have it's normal blood supply, so the pulse will be strong, but the left subclavian will not receive it's blood supply, hence the weak pulses.

Some great discussion about coaractation of aorta here
703899-fig1.jpg
 
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