Step 1 Complicated Concepts Thread

[TheSeanieB]

ASK AND ANSWER TOUGH QUESTIONS RELATED TO STEP 1.

Starting with me:
physiologic chloride shift - When CO2 diffuses into a RBC, it quickly converts with H2O to H+ and HCO3- so that CO2 will continue to passively diffuse into the RBC. The HCO3- is then excreted into the plasma by a Cl-/HCO3- exchanger. When the RBC enters the pulmonary capillaries, the process reverses. HCO3- is taken up by exchange for a Cl-. It combines with H+ to creates CO2 +H2O. The CO2 then diffuses out of the RBC and ultimately into the alveoli. This process allows for maximal CO2 excretion by a RBC.

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[Choo]

Hypoglycemia is an adverse effect of diabetic medications. Diabetics usually are alerted to this by the symptoms they experience.

Alpha cells can get destroyed or jacked up in type 1.

 

[Transformers]

Question on Emphysema:

I get the reason why you get air trapping (hence increased compliance or loss of elastic recoil of the lung) due to destruction of elastin....

However, can someone explain why you get an increased tendency for the lungs to collapse as you expire (hence the basis for "pink puffers"

 

[Choo]

Question on Emphysema:

I get the reason why you get air trapping (hence increased compliance or loss of elastic recoil of the lung) due to destruction of elastin....

However, can someone explain why you get an increased tendency for the lungs to collapse as you expire (hence the basis for "pink puffers"

Airways collapse to due damage to the small airways and the increased velocity pulls that junk shut. It's bernoulli's principle or some other nerd stuff. You can purse the lips to create back pressure to keep the airways open. I think that is the pink puffer. The lungs can collapse when bulla explode.

 

[Transformers]

Question on "malignant risk for polyps"...just to relate genetic mutations with the physical/histological features of the polyp according to UW...\

=> So the APC mutation itself relates to the development of the polyp and its features (epithelial dysplasia and villous histology) correct while the K-ras specifically just increases the size right?

 

[Transformers]

In the context of renal failure, d you first get renal osteodystrophy and then progress to osteitis fibrosa cystica a more downstream complication? I ask this because both UWorld and FA equate the term "subperiosteal thinning" with both osteitis fibrosa cystica and renal osteodystrophy

 

[loveoforganic2]

Sounds right

 

[Transformers]

another quick question on diabetes path on the arterioles of the kidney....pathoma hits at two important concepts....

1.) the one thats tested is of course the context of nephrotic syndrome aka the preferental NEG of the EFFERENT arteriole leading to mesengial sclerosis and KW nodules

2.) the other one that is touched on in in the cardiac section of blood vessels, specifically the path of arteriolosclerorosis...Both benign HTN and diabetes lead to hyaline arteriosclerosis and one of the downstream complications is the arteriolosclerosis of the AFFERENT arteriole....leading to something called "arteriolonephrosclerosis" is this really characteristic of diabetes? In this case, although not mentioned, but what I am inferring, I presume you would thus expect a pre-renal azotemia correct?

 

[wanderer]

another quick question on diabetes path on the arterioles of the kidney....pathoma hits at two important concepts....

1.) the one thats tested is of course the context of nephrotic syndrome aka the preferental NEG of the EFFERENT arteriole leading to mesengial sclerosis and KW nodules

2.) the other one that is touched on in in the cardiac section of blood vessels, specifically the path of arteriolosclerorosis...Both benign HTN and diabetes lead to hyaline arteriosclerosis and one of the downstream complications is the arteriolosclerosis of the AFFERENT arteriole....leading to something called "arteriolonephrosclerosis" is this really characteristic of diabetes? In this case, although not mentioned, but what I am inferring, I presume you would thus expect a pre-renal azotemia correct?

What exactly is your question? DM affects both afferent and efferent but efferent is the more important and early effect which causes hyperfiltration, this is followed by damage to the afferent.
I should note that this isn't my strongest subject so there's a chance I'm not 100% correct.

 

[Transformers]

Are all the movement disorders in FA (p.417) contralateral with the exception of intention tremor (cerebellum)

 

[CaptainSSO]

Question on Emphysema:

I get the reason why you get air trapping (hence increased compliance or loss of elastic recoil of the lung) due to destruction of elastin....

However, can someone explain why you get an increased tendency for the lungs to collapse as you expire (hence the basis for "pink puffers"

My understanding is that adjacent alveoli essentially help hold each other open due the elastin, looking basically something like this: )(

The collapsing pressure of each alveoli helps hold the other one open.

When the elastin is hydrolyzed, at low volumes the alveolus collapses due to loss of support by the contiguous alveolus, resulting in dynamic compression of the airways.

Like someone mentioned, when emphysema patients purse their lips they decrease the diameter of their airway, increasing its resistance, which increases the pressure. The increased pressure in the alveoli helps hold them open.

 

[CaliAtenza]

just had a quick question about alosteric regulation of Glucokinase/Hexokinase. Why is that Glucokinase is less suspectible to regulation by its product, Glucose-6-phosphate? Also, when exactly does the product regulate this enzyme? Is it just a simple situation where the level gets high and it turns down the enzyme or is it something else? That wasnt very clear to me, Kaplan wasnt clear on it either...

 

[Smashingdude]

just had a quick question about alosteric regulation of Glucokinase/Hexokinase. Why is that Glucokinase is less suspectible to regulation by its product, Glucose-6-phosphate? Also, when exactly does the product regulate this enzyme? Is it just a simple situation where the level gets high and it turns down the enzyme or is it something else? That wasnt very clear to me, Kaplan wasnt clear on it either...

Well, that is explained by the Km for both these enzymes. To put it simply, all tissues get glucose inside and trap them by putting a phosphate. This is done by Hexokinase. However, the liver has a variant of this enzyme called Glucokinase. Both have negative inhibition by their product, which is G6P.

The key is that both these enzymes have different Km and affinity for glucose. That is, Hexokinase has a very low Km, meaning a high affinity for glucose, implying that a small amount of glucose saturates it, and will cause the build up of product and inhibit it. (Remember Km is inverse to affinity). However, you can't have this enzyme in the liver. The liver acts like a sponge after a meal. It sucks in all the glucose and traps it so that it can release it later on. If the liver had the same Hexokinase enzyme, it would only take in a bit of glucose, and then get saturated, and all the glucose will stay outside.

To counter this, the body uses a different enzyme in the liver. Its Glucokinase. It has a high Km, meaning a low affinity for glucose. You need to give a LOT of glucose to satisfy it. Therefore, the liver can suck in a lot of glucose, till this enzyme gets saturated and satisfied.
Also, Glucokinase has a high Vmax compared to Hexokinase (meaning more active sites, more glucose taken up in the liver).

There is actually a pathology when there is a mutation of Glucokinase. Its a variation of Diabetes called MODY (Maturity Onset Diabetes of the Young). In this case, this mutation prevents the liver from sequestering all that glucose, and glucose levels stay high in the blood after a meal, giving insulin resistance ultimately, and diabetes.

Hope that helps!

 

[tvelocity514]

Bump for the current students who want to read through this thread for their boards

 

[walakin25]

your welcome @tvelocity514 haha

 

[tarsuc]

awesome thread. Lets continue this. shallwe?

 

[tarsuc]

What are the dopamine receptors involved in the Mesolimbic , mesocortical, tuberoinfundibular and nigrostriatal pathway pathologies? d2 or d1?

Is it wrong to classify them like this. D2 - ML and MC (since anti psych act on d2); d1 and d2 - NS (parkinsonism both pathways); TI pathway?

 

[Daitong]

Well, that is explained by the Km for both these enzymes. To put it simply, all tissues get glucose inside and trap them by putting a phosphate. This is done by Hexokinase. However, the liver has a variant of this enzyme called Glucokinase. Both have negative inhibition by their product, which is G6P.

The key is that both these enzymes have different Km and affinity for glucose. That is, Hexokinase has a very low Km, meaning a high affinity for glucose, implying that a small amount of glucose saturates it, and will cause the build up of product and inhibit it. (Remember Km is inverse to affinity). However, you can't have this enzyme in the liver. The liver acts like a sponge after a meal. It sucks in all the glucose and traps it so that it can release it later on. If the liver had the same Hexokinase enzyme, it would only take in a bit of glucose, and then get saturated, and all the glucose will stay outside.

To counter this, the body uses a different enzyme in the liver. Its Glucokinase. It has a high Km, meaning a low affinity for glucose. You need to give a LOT of glucose to satisfy it. Therefore, the liver can suck in a lot of glucose, till this enzyme gets saturated and satisfied.
Also, Glucokinase has a high Vmax compared to Hexokinase (meaning more active sites, more glucose taken up in the liver).

There is actually a pathology when there is a mutation of Glucokinase. Its a variation of Diabetes called MODY (Maturity Onset Diabetes of the Young). In this case, this mutation prevents the liver from sequestering all that glucose, and glucose levels stay high in the blood after a meal, giving insulin resistance ultimately, and diabetes.

Hope that helps!

mind = blown

 

[navigator]

So I get why you'd avoid giving live attenuated vaccines to patients with T cell deficiencies (i.e. SCID and DiGeorge), but why do we also want to avoid giving live vaccines to patients with XLA?

In XLA, aren't T cells (and the cell-mediated response needed to overcome mild infections caused by live vaccines) working just fine?

EDIT: Nvm on this one, the whole point is to generate antibodies and memory B cells to mount immune response against future infection -> so immunizing XLA pts with attenuated vaccines in attempt to produce endogenous antibodies is just silly

 

[navigator]

Why can't we treat XLA/Bruton's with BMT? Wouldn't the transplanted bone marrow exhibit new hematopoietic stem cells without the BTK mutation, thus fixing the problem?