Thank you so much for the awesome vide!! I have a question at 7:56, why is the pressure at the end of the efferent managed to be kept the same? i.e. if the afferent resistance is kept normal while the efferent dilates and decrease resistance, wouldn't the pressure at the glomerulus still be 60 mmHg but the pressure at the end of the efferent be higher than 10 mmHg?
Thank you for the kind words! Thats a great question. In actuality, changes in afferent/efferent arteriole resistance would affect the total peripheral resistance (TPR) resulting in corresponding changes to *both* arterial and venous pressures. Reflecting this in the model would obscure the local pressure changes (e.g., glomerular hydrostatic pressure) caused by changes in afferent/efferent arteriole resistance. To simplify, the model assumes no changes in TPR (i.e., changes in afferent/efferent resistance offset by opposing changes in resistance elsewhere). With this assumption, pressures on arterial and venous compartments stay constant, thereby highlighting the local pressure changes. I hope that helps!
@@PeteMeighan. Firstly, I must thank you for this video. It is perhaps the most insightful explanation of the topic, creating a clear and easy-to-understand theoretic framework, yet not losing necessary details in the process. Secondly, I would be grateful if you could help with a concept of physiology regarding haemodynamics that has bothered me for quite a bit. In medicine, there is a heuristic that when there is a partial obstruction in a blood vessel or a downstream increase in resistance, the proximal pressure increases. Sometimes I have heard this being reduced to "blockage causes more blood to accumulate before it and push on the blood vessel walls", but I doubt that that is scientific. My personal qualms are with liver cirrhosis and portal hypertension (PH), but this can apply elsewhere too. What exactly causes this proximal pressure increase? Is it intrinsically associated with a physics expression-a property of the system? Or is it secondary to a body's response, an extrinsic change in the system, for instance, increased cardiac output or something of the sort? Usually articles try to explain PH with The Hagen-Poiseuille equation, namely, that increased resistance increases the pressure drop, hence increases the proximal pressure. I find that unfounded, because-why would the pressure increase, rather than the flow get reduced? A pressure increase would demand an additional body's input of energy into the system. For this reason, I think the answer lies in the body's tendency of maintaining constant flow, meaning that there is a response mechanism of the body with the increased pressure's being the result rather than the primary driver. But the exact response of the body escapes me (especially since this is the venous system and is not as straightforward as the arterial system). If it is possible, I would greatly appreciate your opinion on this, or perhaps a source where this concept is explained in more detail. Thank you for your time.
@@ArchPandara I sincerely appreciate the kind words. Thank you very much. This is an excellent question. Although intrinsic and extrinsic regulatory processes might be at play, I suspect the increased proximal pressure caused by an obstruction can be approached with conservation principles. The explanation you mention (i.e., "blockage causes more blood to accumulate before it and push on the blood vessel walls") is close to the truth but is missing an important feature: the fluid energy of blood. Fluid energy is determined by BOTH the hydrostatic pressure AND the kinetic energy (also gravitational potential energy, which we can probably ignore here). Blood flowing through the vasculature has a finite amount of fluid energy in the form of kinetic energy (due to its motion) and pressure (determined by blood volume and vascular compliance). In accordance with Bernoulli’s Principle, pressure and kinetic energy are interconvertible. In the context of a vascular obstruction, the loss of kinetic energy imposed by the obstruction is converted to an increased pressure (i.e., exertion of force against the vasculature walls). This increased pressure is sustained by a constant flow of blood “colliding” with the stagnant blood impeded by the obstruction. I think that accounts for the phenomenon you describe. Hope that helps. Let me know if you have any follow up questions!
So to put this entire conversation in simpler terms: For example, if there is a blockage in a pipe, the hydrostatic pressure before the blockage will in crease since the liquid has nowhere to flow to and will hence accumulate?
![[Re:all TREASURE] EP.6 in 방콕ㅣ🚩 쩡캠의 방콕 투어 빵 마이 와이 👍](http://i.ytimg.com/vi/uyFw-nItA_s/mqdefault.jpg)
This is perfect! I'm currently studying renal physiology in med school and this is exactly what I was looking for. Thank you so much!
Glad it was helpful! Good luck to you!
Yes!!
I am studying for the MCAT, and all your videos on renal physiology were much better than the Kaplan book!
This video is exactly what I’ve been looking for!
Thanks so much 😃
Your welcome--glad it was helpful!
thank you for the excellent explanation
thank you so much for your video, I was struggling to understand this, but you just explained it so easily :)
Thank you so much for explaining! This was very clear
Glad it was helpful!
It was verry helpful to me,
Thank u
You are genius thanku Sir
Best video
Thankyou!
Thankyou so much Sir ❤️
Please make more videos on renal physiology
Thank you so much for the awesome vide!! I have a question at 7:56, why is the pressure at the end of the efferent managed to be kept the same? i.e. if the afferent resistance is kept normal while the efferent dilates and decrease resistance, wouldn't the pressure at the glomerulus still be 60 mmHg but the pressure at the end of the efferent be higher than 10 mmHg?
Thank you for the kind words! Thats a great question. In actuality, changes in afferent/efferent arteriole resistance would affect the total peripheral resistance (TPR) resulting in corresponding changes to *both* arterial and venous pressures. Reflecting this in the model would obscure the local pressure changes (e.g., glomerular hydrostatic pressure) caused by changes in afferent/efferent arteriole resistance. To simplify, the model assumes no changes in TPR (i.e., changes in afferent/efferent resistance offset by opposing changes in resistance elsewhere). With this assumption, pressures on arterial and venous compartments stay constant, thereby highlighting the local pressure changes. I hope that helps!
@@PeteMeighan. Firstly, I must thank you for this video. It is perhaps the most insightful explanation of the topic, creating a clear and easy-to-understand theoretic framework, yet not losing necessary details in the process.
Secondly, I would be grateful if you could help with a concept of physiology regarding haemodynamics that has bothered me for quite a bit. In medicine, there is a heuristic that when there is a partial obstruction in a blood vessel or a downstream increase in resistance, the proximal pressure increases. Sometimes I have heard this being reduced to "blockage causes more blood to accumulate before it and push on the blood vessel walls", but I doubt that that is scientific. My personal qualms are with liver cirrhosis and portal hypertension (PH), but this can apply elsewhere too.
What exactly causes this proximal pressure increase? Is it intrinsically associated with a physics expression-a property of the system? Or is it secondary to a body's response, an extrinsic change in the system, for instance, increased cardiac output or something of the sort?
Usually articles try to explain PH with The Hagen-Poiseuille equation, namely, that increased resistance increases the pressure drop, hence increases the proximal pressure. I find that unfounded, because-why would the pressure increase, rather than the flow get reduced? A pressure increase would demand an additional body's input of energy into the system. For this reason, I think the answer lies in the body's tendency of maintaining constant flow, meaning that there is a response mechanism of the body with the increased pressure's being the result rather than the primary driver. But the exact response of the body escapes me (especially since this is the venous system and is not as straightforward as the arterial system).
If it is possible, I would greatly appreciate your opinion on this, or perhaps a source where this concept is explained in more detail. Thank you for your time.
@@ArchPandara I sincerely appreciate the kind words. Thank you very much.
This is an excellent question. Although intrinsic and extrinsic regulatory processes might be at play, I suspect the increased proximal pressure caused by an obstruction can be approached with conservation principles. The explanation you mention (i.e., "blockage causes more blood to accumulate before it and push on the blood vessel walls") is close to the truth but is missing an important feature: the fluid energy of blood. Fluid energy is determined by BOTH the hydrostatic pressure AND the kinetic energy (also gravitational potential energy, which we can probably ignore here). Blood flowing through the vasculature has a finite amount of fluid energy in the form of kinetic energy (due to its motion) and pressure (determined by blood volume and vascular compliance). In accordance with Bernoulli’s Principle, pressure and kinetic energy are interconvertible. In the context of a vascular obstruction, the loss of kinetic energy imposed by the obstruction is converted to an increased pressure (i.e., exertion of force against the vasculature walls). This increased pressure is sustained by a constant flow of blood “colliding” with the stagnant blood impeded by the obstruction. I think that accounts for the phenomenon you describe. Hope that helps. Let me know if you have any follow up questions!
So to put this entire conversation in simpler terms: For example, if there is a blockage in a pipe, the hydrostatic pressure before the blockage will in crease since the liquid has nowhere to flow to and will hence accumulate?