jgalt42

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What is the difference between osmotic and hydrostatic pressure?
 
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Hydrostatic Pressure is the pressure created from your blood pressure that pushes water and hydrophobic molecules into cells.

Osmotic Pressure is the gradient of water that is between the cells and capillaries. This gradient wants to push water into the capillaries.
 

sv3

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and i dont think they always oppose each other as well.................just something people tend to fall for i beleive
 

rocuronium

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Water will always move toward the higher solute concentration if it is able. Normally the osmotic pressure inside the vessel (resulting from the higher solute concentration when compared to the interstitium) counteracts the outward movement of water due to the hydrostatic pressure. This causes water movement in the direction of whichever force is stronger.

If, however, the solute concentration on the outside of the blood vessel is higher than inside, water will not only be pushed out by the hydrostatic pressure, it will be drawn out by osmosis as well. In this example the osmotic and hydrostatic pressure both cause water movement in the same direction.
 

Hemichordate

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Btw, is edema where the solute concentration in the cells is really high, so water flows into the tissues and you get swelling?
 

rocuronium

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Edema refers an abnormal accumulation of fluid. The mechanism you described is one way through which edema can occur.
 

Charles_Carmichael

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Btw, is edema where the solute concentration in the cells is really high, so water flows into the tissues and you get swelling?
No, I don't think that's right. Edema is when fluid accumulates in the interstitial space, not inside the cells (the cells will burst otherwise). Edema occurs when the hydrostatic pressure is too high (more fluid is being pushed out of the blood vessel) or if the oncotic pressure is too low (there's less of a force pulling fluid back into the blood vessel). Low serum albumin could be one reason for edema occurring, since albumin's main purpose is to provide an oncotic pressure and loss of albumin decreases the oncotic pressure that pulls fluid back into the blood vessels.
 

rocuronium

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Couldn't intracellular edema be a possibility if an inappropriate osmotic gradient existed between a cell and its extracellular fluid? For some reason water intoxication comes to mind.

I have always thought about edema in the way that you defined it, Kaushik, but your last post made me curious as to whether the above could still be classified as edema.

Regardless, other mechanisms for edema (in addition to those which Kaushik so perspicuously described) include problems with lymphatic drainage (think elephantiasis) or blood vessel permeability changes such as those seen with inflammation.
 
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RogueUnicorn

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Couldn't intracellular edema be a possibility if an inappropriate osmotic gradient existed between a cell and its extracellular fluid? For some reason water intoxication comes to mind.

I have always thought about edema in the way that you defined it, Kaushik, but your last post made me curious as to whether the above could still be classified as edema.

Regardless, other mechanisms for edema (in addition to those which Kaushik so perspicuously described) include problems with lymphatic drainage (think elephantiasis) or cell wall permeability changes such as those seen with inflammation.
edema is a general symptom, not a cellular phenomenon. the latter is just cell swelling and subsequent lysing.
 

Charles_Carmichael

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Couldn't intracellular edema be a possibility if an inappropriate osmotic gradient existed between a cell and its extracellular fluid? For some reason water intoxication comes to mind.

I have always thought about edema in the way that you defined it, Kaushik, but your last post made me curious as to whether the above could still be classified as edema.

Regardless, other mechanisms for edema (in addition to those which Kaushik so perspicuously described) include problems with lymphatic drainage (think elephantiasis) or cell wall permeability changes such as those seen with inflammation.
Water intoxication would result in cell swelling but, to be honest, I've never heard of cell swelling being called edema. I could be wrong, but the only factors influencing fluid accumulation that I have learnt about are hydrostatic pressure, oncotic pressure, blood vessel permeability, and lymphatic blockage (lymphedema). My understanding of edema is that it's accumulation of fluid in the interstitial compartment and not in the cells themselves. Hope this helps.

Also, I think you meant blood vessel permeability rather than "cell wall permeability" regarding inflammation. :p
 

Hemichordate

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My understanding of edema is that it's accumulation of fluid in the interstitial compartment and not in the cells themselves. Hope this helps.
Sorry that's what I meant to say in my original question- tissues have more proteins/solutes, thus water flows into the interstitial spaces.
 

sv3

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so for something common like inflammation, it's fluid accumilation in the interstitial tissue?
And this would due to increased vessel permeability right? (I dont think or know if oncotic or
hydrostatic play a role here?)

Any clue how the vessels themselves become more permeable?

thanks in advance
 

Charles_Carmichael

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Sorry that's what I meant to say in my original question- tissues have more proteins/solutes, thus water flows into the interstitial spaces.
Actually, the oncotic pressure of the interstitial space is very little compared to the oncotic pressure of the blood vessel. Tissues themselves will have more proteins, etc. but these are not floating around in the interstitum; they are inside the cells.

The force that drives fluid out of the capillary into the interstitial space is primarily the hydrostatic pressure. The oncotic pressure of the interstitum plays only a small part. Along the length of the capillary, the hydrostatic pressure decreases while the oncotic pressure remains relatively the same; the net pressure (calculated using the Starling equation) is dependent on the values of both hydrostatic pressure and oncotic pressure and determines whether fluid is pushed out of the capillary or is pulled into the capillary.

so for something common like inflammation, it's fluid accumilation in the interstitial tissue?
And this would due to increased vessel permeability right? (I dont think or know if oncotic or
hydrostatic play a role here?)

Any clue how the vessels themselves become more permeable?

thanks in advance
Yea, the fluid would accumulate in the interstitial space due to an increase in vascular permeability; there's also vasodilation. Tissue damage causes the release of various factors that are involved in vasodilation, increasing permeability, recruiting macrophages, etc. I would think that both hydrostatic pressure and tissue oncotic pressure would play a role in edema resulting from an inflammatory response; since the capillary is more permeable, there's a higher chance proteins will be pushed into the interstitium along with fluid and this would increase the tissue oncotic pressure which would help pull more fluid into the interstitium. I highly doubt that you would need to know the details regarding the inflammatory response for the MCAT though.

Hope this helps.
 

sv3

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Actually, the oncotic pressure of the interstitial space is very little compared to the oncotic pressure of the blood vessel. Tissues themselves will have more proteins, etc. but these are not floating around in the interstitum; they are inside the cells.

The force that drives fluid out of the capillary into the interstitial space is primarily the hydrostatic pressure. The oncotic pressure of the interstitum plays only a small part. Along the length of the capillary, the hydrostatic pressure decreases while the oncotic pressure remains relatively the same; the net pressure (calculated using the Starling equation) is dependent on the values of both hydrostatic pressure and oncotic pressure and determines whether fluid is pushed out of the capillary or is pulled into the capillary.


Yea, the fluid would accumulate in the interstitial space due to an increase in vascular permeability; there's also vasodilation. Tissue damage causes the release of various factors that are involved in vasodilation, increasing permeability, recruiting macrophages, etc. I would think that both hydrostatic pressure and tissue oncotic pressure would play a role in edema resulting from an inflammatory response; since the capillary is more permeable, there's a higher chance proteins will be pushed into the interstitium along with fluid and this would increase the tissue oncotic pressure which would help pull more fluid into the interstitium. I highly doubt that you would need to know the details regarding the inflammatory response for the MCAT though.

Hope this helps.

thanks very much. I bolded a comment above - doesnt oncotic pressure increase as fluid leaves the vessel, thus drawing fluid back in at the end of the vessel-tissue exchange?
 

Charles_Carmichael

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thanks very much. I bolded a comment above - doesnt oncotic pressure increase as fluid leaves the vessel, thus drawing fluid back in at the end of the vessel-tissue exchange?
Oops, yea good catch. :thumbup: I was typing fast and I meant to write that it increases. The oncotic pressure of the capillary would increase along the length of the capillary since the concentration of the solutes increases (as fluid is pushed out into the interstitium). The rest of my info looks right though (I just checked it over to make sure heh).
 

sv3

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Oops, yea good catch. :thumbup: I was typing fast and I meant to write that it increases. The oncotic pressure of the capillary would increase along the length of the capillary since the concentration of the solutes increases (as fluid is pushed out into the interstitium). The rest of my info looks right though (I just checked it over to make sure heh).
phew! had me worried! :highfive:
 

rocuronium

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Also, I think you meant blood vessel permeability rather than "cell wall permeability" regarding inflammation. :p
That is what I meant, yes. This thread seems to be attracting such mistakes.:D