Questions Renal and Respiratory?

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socrates89

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I have a few questions please answer if you can

Which segment of the Nephron has the lowest osmolarity and highest osmolarity with and without the presence of ADH? I'm getting different answers from various sources

What is the reason for Prolonged QT interval on ECG in hypocalcemia and shortened QT on ECG with hypercalcemia

Terminal broncial epithelium? is it Pseudostratifed ciliated or Ciliated Cuboidal Epithelium? FA says peudo while most sources say Ciliated cuboidal

What is the change in compliance in Asthma? Is it similar to obstructive disease in general or different?

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I have a few questions please answer if you can

Which segment of the Nephron has the lowest osmolarity and highest osmolarity with and without the presence of ADH? I'm getting different answers from various sources

With ADH: highest osmolarity = medullary collecting duct; lowest osmolarity = DCT, NOT the distal ascending loop.

Without ADH: highest osmolarity = trough of loop of Henle; lowest osmolarity = medullary collecting duct.

What is the reason for Prolonged QT interval on ECG in hypocalcemia and shortened QT on ECG with hypercalcemia

The plateau phase of the cardiomyocyte action potential is created by calcium influx. If you increase extracellular calcium (i.e. increasing the gradient), the rate of ion flow increases, thereby shortening the plateau phase, so the QT-interval decreases. The opposite is the case with hypocalcaemia. The QT-interval reflects the rate of repolarization. The influx of calcium counteracts the efflux of potassium during the plateau, effectively prolonging repolarization. The quicker calcium moves across, the quicker potassium becomes unopposed and the cell repolarizes.

Terminal broncial epithelium? is it Pseudostratifed ciliated or Ciliated Cuboidal Epithelium? FA says peudo while most sources say Ciliated cuboidal

I've seen this change depending on the source. Off the top of my head, GT QBank had said cilia is lost at the terminal bronchioles, but UWorld said cilia is present till the respiratory bronchioles. In general, I would just be aware that the typical pseudostratified columnar ciliated epithelium becomes more cuboidal toward the respiratory bronchioles, but that cilia is still present at that level, even if density is attenuated at certain areas. Then beyond that, it's simple squamous without cilia. On the real USMLE, I'd put respiratory bronchioles are cuboidal and ciliated only because UWorld had that.

What is the change in compliance in Asthma? Is it similar to obstructive disease in general or different?

Compliance is expansion whereas elasticity is ability to retract. Asthma affects expiration but not inspiration because it's small-airway obstructive disease. Compliance should be normal because that's an attribute of inspiration, not expiration.

In contrast, be aware that ARDS and pulmonary oedema have decreased compliance. I have seen this in practice questions before.


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Now that I answered your questions, maybe you can do dirty work for me on my hepatitis thread?? Thanks!
 
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The plateau phase of the cardiomyocyte action potential is created by calcium influx. If you increase extracellular calcium (i.e. increasing the gradient), the rate of ion flow increases, thereby shortening the plateau phase, so the QT-interval decreases. The opposite is the case with hypocalcaemia. The QT-interval reflects the rate of repolarization. The influx of calcium counteracts the efflux of potassium during the plateau, effectively prolonging repolarization. The quicker calcium moves across, the quicker potassium becomes unopposed and the cell repolarizes.

I'm new to this forum, but thought I should start contributing. Calcium has a profound affect on Voltage gated sodium channels. In hypercalcaemia, they increase the voltage threshold needed to activate sodium channels - hence, this leads to decreased membrane excitability. Thus, this is reflected by a prolonged QT interval. Calcium influx into the cell has no bearings on membrane excitability. This is dictated primarily by funny channels and subsequent activation of voltage gated sodium channels
 
I'm new to this forum, but thought I should start contributing. Calcium has a profound affect on Voltage gated sodium channels. In hypercalcaemia, they increase the voltage threshold needed to activate sodium channels - hence, this leads to decreased membrane excitability. Thus, this is reflected by a prolonged QT interval. Calcium influx into the cell has no bearings on membrane excitability. This is dictated primarily by funny channels and subsequent activation of voltage gated sodium channels

I think you're confusing potassium with calcium. Potassium levels have >>> more of an effect than calcium on the threshold of sodium channel excitability. You've said yourself that calcium influx into the cell has no bearings on membrane excitability. You're right. That's because that's potassium, not calcium.

The mechanism of calcium channel blockers should not be confused with hyper-/hypocalcaemia in general. Blockers work at the nodal cells, thereby increasing the PR-interval. But serum levels alter the plateau phase (cardiomyocyte QT-interval) by simply changing the rate of Ca2+ influx, as dependent on the magnitude of the gradient in place.
 
haha no you're right - I don't know what I was thinking. I must've got confused with something else *face palm*
 
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