270

[270]

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My goal is to get 270 on Step 1. I think I can do it, I'm not joking or trolling. I know it's a "meaningless" number and my life won't be any different if I get 250, 260, or 270. But, why do people climb everest?

Anyone wanting to trade "aha" insights feel free to do it in this thread. I welcome as many people as are interested to join me here in trading cool bits of insight.

Here's one: Why do thiazides and loop diuretics cause hyperglycemia?

Because they lower serum [K+], thereby depolarizing the beta-cell and inhibiting insulin secretion. In effect, low serum [K+] has the opposite effect on the ATP-sensitive K-channel that SUR's have. Maybe that's in First Aid, I don't know... It just dawned on me and I thought I would share.

And thanks to bigfrank, idiopathic, long dong, and everyone here that rocked the test and was kind enough to share their tips and tricks.

 

[woowoo]

depolarization of the B cells, opens Calcium channel, which then leads to an increase in intracellular calcium and a secretion of insulin.

i honestly don't know the mechanism of hyperglycemia in loops and thiazides, but i do know that depolarization of the B cell leads to insulin release.

 

[BlackNDecker]

Why do thiazides and loop diuretics cause hyperglycemia?

Because they lower serum [K+], thereby depolarizing the beta-cell and inhibiting insulin secretion. In effect, low serum [K+] has the opposite effect on the ATP-sensitive K-channel that SUR's have. Maybe that's in First Aid, I don't know... It just dawned on me and I thought I would share.

Wouldn't lowering extracellular K+ INCREASE the gradient for diffusion of K+ out of the cell? This would effectively HYPERPOLARIZE the cell. You are close...I think you meant to say "because they hyperpolarize the beta-cell and inhibit insulin secretion."

Where did you read that hyperglycemia is a feature of Loop diuretics? Your post is the only source I've read this...


SUR's and Glucose work via closure of K+ channels, which causes a net positive charge to build up inside the cell--> causing DEPOLARIZATION via the mechanism described above by Woowoo.

 

[Idiopathic]

Wouldn't lowering extracellular K+ INCREASE the gradient for diffusion of K+ out of the cell? This would effectively HYPERPOLARIZE the cell. You are close...I think you meant to say "because they hyperpolarize the beta-cell and inhibit insulin secretion." .

This is what he meant to say. And hyperglycemia is something that occasionally happens with these drugs, due to the hypokalemic potential, although there are other factors. The incidence is like 10-20% for HCTZ.

 

[nrosigh]

I think anything that lowers potassium can cause hyperglycemia - in fact, the therapy to prevent hyperglycemia with diuretics is to administer exogenous potassium.

Thiazides are definitely more "known" to potentiate hyperglycemia. I just looked up Loops in the big Katzung and it didn't mention hyperglycemia. But doing a pubmed search for "hyperglycemia and loop diuretics" yielded many results (here's one: http://www.ncbi.nlm.nih.gov/entrez/...t_uids=8288156&query_hl=2&itool=pubmed_docsum)

 

[270]

Thanks for the correction, BlackNDecker and Idiopathic. Low [K+] *hyperpolarizes* the cell. Kind of an silly way to get started...

Anyway, now we don't have to memorize "this or that diuretic causes hyperglycemia" because we know the mechanism.

Here's another one:

How do you distinguish a PTH adenoma from PTH hyperplasia?

Measure serum [Ca++]. Both can have high levels of PTH so that may not distinuish them. A PTH adenoma will cause very high calcium. PTH hyperplasia is by definition secondary hyperparathyroidism, most commonly in response to renal failure. The PTH is hyperplastic in response to LOW serum calcium, so the resulting serum calcium should be close to normal. This is probably obvious to many of you out there, but I was happy to figure it out.

 

[BlackNDecker]

One thing I've never been able to conceptualize is how HYERKALEMIA causes tall peaked T waves. 😕


If you have excess K+ in the ECF, that should decrease the chemical gradient of K+ and effectively decrease the outflow of K+...resulting in a lowered amplitude on EKG. But it doesn't...

Likewise, in hypokalemia, the lowered extracellular K+ would increase the outflow gradient which should result in a peaked amplitude on EKG. But it doesn't...

Why?

 

[270]

Great question! I never thought of that before.

Here's my attempt to explain as I understand it (no warranty here): The T wave is the repolarization of the ventricles. Hyperkalemia means the cell is already partially depolarized at rest, so maybe it's easier for the cell to repolarize? The peaked T wave is one of the first signs of hyperkalemia, the next change is an increased in QRS width, which makes more logical sense because there is less of an efflux gradient for [K+] so it takes longer for potassium to leave the cell....

You also see peaked T waves as one of the first signs of MI, this is probably due to an efflux of [K+] out of damaged cells producing localized hyperkalemia in the area of infarct (as opposed to systemic hyperkalemia, injury-hyperkalemia is only seen in the leads looking at the injured tissue).

One thing I've never been able to conceptualize is how HYERKALEMIA causes tall peaked T waves. 😕


If you have excess K+ in the ECF, that should decrease the chemical gradient of K+ and effectively decrease the outflow of K+...resulting in a lowered amplitude on EKG. But it doesn't...

Likewise, in hypokalemia, the lowered extracellular K+ would increase the outflow gradient which should result in a peaked amplitude on EKG. But it doesn't...

Why?

 

[Idiopathic]

Remember, repolarization on the EKG is the opposite of what you would expect to see, I think, because its happening in the reverse direction of depolarization.

As for the PTH stuff, Goljan has by far the best description of these cases in his chart that compares Ca with PTH. It takes into account all the scenarios that could be related. But what you say is true, and self evident. Just like any secondary process when compared to a primary process (reactive hyper-TSH versus Graves' disease for instance)

 

[dara678]

good thread ... i think it's a great idea to aim high 🙂 just don't be disappointed if you get a 269 😛

 

[YouDontKnowJack]

why stop at 270?

shoot for 281.

 

[BlackNDecker]

A gem from Goljan that even most microbiologists don't know:

The syphylitic chancre is painless because T. pallidum has a tropism for endothelial cells resulting in necrosis of small blood vessels --> which results in necrosis of the surrounding nerves. The blister has no innervation, thus you can't feel it.

 

[270]

Wow, that's great - we get two for one with that, since we can now remember that the syphilis ulcer is painless, AND we can remember the endartaritis it causes leading to aortic rupture.... cool!

Here's another Goljan gem: Why do you get hypercalcemia with sarcoid?
Because the activated macrophages (noncaseating granulomas) in the lung make 1-25 vitamin D!

The syphylitic chancre is painless because T. pallidum has a tropism for endothelial cells resulting in necrosis of small blood vessels --> which results in necrosis of the surrounding nerves. The blister has no innervation, thus you can't feel it.

 

[SaltySqueegee]

I want to rule the world too...

 

[surgwannabe]

Wow, that's great - we get two for one with that, since we can now remember that the syphilis ulcer is painless, AND we can remember the endartaritis it causes leading to aortic rupture.... cool!

Here's another Goljan gem: Why do you get hypercalcemia with sarcoid?
Because the activated macrophages (noncaseating granulomas) in the lung make 1-25 vitamin D!

And that's casued by the presence of 1-alpha-hydroxylase in macrophages.

lots of macrophages -> lots of 1-alpha-hydroxylase activity -> more 1,25 (OH) Vit D3

 

[zeloc]

Wow, that's great - we get two for one with that, since we can now remember that the syphilis ulcer is painless, AND we can remember the endartaritis it causes leading to aortic rupture.... cool!

Here's another Goljan gem: Why do you get hypercalcemia with sarcoid?
Because the activated macrophages (noncaseating granulomas) in the lung make 1-25 vitamin D!

They convert 25-hydroxyvitamin D3 into 1,25-hydroxy vitamin D3.

What are SUR's?

 

[Idiopathic]

What are SUR's?

Is that a pimp question or do you not know? Im not familiar with it as an acronym.

 

[270]

Sulfonylureas.

Is that a pimp question or do you not know? Im not familiar with it as an acronym.

 

[Idiopathic]

Sulfonylureas.

I see, it was mentioned earlier in the thread. never mind.

 

[lucky01]

My goal is to get 270 on Step 1. I think I can do it, I'm not joking or trolling. I know it's a "meaningless" number and my life won't be any different if I get 250, 260, or 270. But, why do people climb everest?

Anyone wanting to trade "aha" insights feel free to do it in this thread. I welcome as many people as are interested to join me here in trading cool bits of insight.

Here's one: Why do thiazides and loop diuretics cause hyperglycemia?

Because they lower serum [K+], thereby depolarizing the beta-cell and inhibiting insulin secretion. In effect, low serum [K+] has the opposite effect on the ATP-sensitive K-channel that SUR's have. Maybe that's in First Aid, I don't know... It just dawned on me and I thought I would share.

And thanks to bigfrank, idiopathic, long dong, and everyone here that rocked the test and was kind enough to share their tips and tricks.

Did you end up getting the 270 you were aiming for? Would love some tips and advice for a 250+

 

[pediadocto]

Did you end up getting the 270 you were aiming for? Would love some tips and advice for a 250+

Digging out an 11 yr old post for advice? lol..

 

[TheOther]

Digging out an 11 yr old post for advice? lol..

Gunners gon gun.