A clearly basic question on ESR.

[Old Style Nanny]

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Could someone be kind enough to post a one line explanation why exactly the ESR changes in each of these conditions?

infections
inflammation
malignancy
pregnancy
polycythemia
sickle cell anemia
congestive heart failure
microcytosis
hypofibrinogenemia

Thanks!

 

[Coug42]

Erythrocyte Sedimentation Rate (ESR)

Mechanism Tested:
Products of Inflammation (ex. Fibrinogen) coat RBCs and cause Red Blood Cell Aggregation making them fall faster in test tube

Conditions with Effects on ESR:
Elevated ESR -
Infection
Inflammation (ex. Temporal Arteritis)
Cancer
Pregnancy (increased fibrinogen)
SLE
Polymyalgia Rheumatica

Low ESR -
Sickle Cell Disease (changed shape)
Polycythemia (too many)
CHF (unknown)

 

[Old Style Nanny]

I guess my question is, how does changed shape, number, etc. affect rouleaux formation.

 

[Ycut]

I guess my question is, how does changed shape, number, etc. affect rouleaux formation.

In inflammatory conditions increased fibrinogen causes rouleaux formation which increases mass and cause to settle more rapidly than single rbc
In other conditions such as sickle cell anemia and polycythemia there is problem with shape and number (for comparison-toilet bowl clogged with toys of various shapes which cant be flushed due to confined pipe space and for polycythemia - too many tissue papers clogging the pipe)

 

[tiedyeddog]

So, a simplistic way to think about this is:

high ESR = pro-inflammatory state

low ESR = RBC number/shape altered (plus CHF)?

 

[Old Style Nanny]

In other conditions such as sickle cell anemia and polycythemia there is problem with shape and number (for comparison-toilet bowl clogged with toys of various shapes which cant be flushed due to confined pipe space and for polycythemia - too many tissue papers clogging the pipe)

Agreed about the pro-inflammatory states, but this analogy above doesn't quite make sense to me. How can RBCs clog a test tube of uniform diameter? Could you clarify?

And with polycythemia, even if there are lots of tissue papers, why should the rate at which they fall down change?

I was reasoning out that in polycythemia, it must have something to do with the negative charge of the erythrocytes (zeta potential). I was thinking maybe increased number of RBCs = increased force with which each of the RBCs in the lower part of the test tube repels the ones on the upper part thereby slowing down the rate of sedimentation. Although it is just my hypothesis and I have no idea how to search for a corroboration.

Anyway, if this information is not common knowledge, then I guess it would not be tested on the step. So I may just memorize it and move on.

 

[tiedyeddog]

Agreed about the pro-inflammatory states, but this analogy above doesn't quite make sense to me. How can RBCs clog a test tube of uniform diameter? Could you clarify?

And with polycythemia, even if there are lots of tissue papers, why should the rate at which they fall down change?

I was reasoning out that in polycythemia, it must have something to do with the negative charge of the erythrocytes (zeta potential). I was thinking maybe increased number of RBCs = increased force with which each of the RBCs in the lower part of the test tube repels the ones on the upper part thereby slowing down the rate of sedimentation. Although it is just my hypothesis and I have no idea how to search for a corroboration.

Anyway, if this information is not common knowledge, then I guess it would not be tested on the step. So I may just memorize it and move on.

I think you need to think of it like this, SUPER simply ESR depends on two thing:

(Procoagulative inflammatory factors) / (Intrinsic RBC factors, like Shape and Number).

If you keep the inflammatory factors levels the same and increase the RBC #, you have less factors coating RBCs. Less coating of RBCs = less thromogenesis.

please, if my line of thinking is wrong someone please correct it, ESR is kind of confusing to me...

 

[Ycut]

Agreed about the pro-inflammatory states, but this analogy above doesn't quite make sense to me. How can RBCs clog a test tube of uniform diameter? Could you clarify?

And with polycythemia, even if there are lots of tissue papers, why should the rate at which they fall down change?

I was reasoning out that in polycythemia, it must have something to do with the negative charge of the erythrocytes (zeta potential). I was thinking maybe increased number of RBCs = increased force with which each of the RBCs in the lower part of the test tube repels the ones on the upper part thereby slowing down the rate of sedimentation. Although it is just my hypothesis and I have no idea how to search for a corroboration.

Anyway, if this information is not common knowledge, then I guess it would not be tested on the step. So I may just memorize it and move on.

Yes thats not going to be tested so heavily

Polycythemia-think of tube diameter that allows free flow of 20 rbc but insted of 20 now u got 200 which increases resistance (lets view through physio this increase rbcs increases viscosisty which in turn increases resistance which decreases flow-R=viscosity x length/radius to the 4th power)
sickle cells can wedge between normal cells and impede sedimentation)

Anyway thats my view on this process and someone can provide better explanation 😉

 

[Old Style Nanny]

Polycythemia-think of tube diameter that allows free flow of 20 rbc but insted of 20 now u got 200 which increases resistance (lets view through physio this increase rbcs increases viscosisty which in turn increases resistance which decreases flow-R=viscosity x length/radius to the 4th power)

By that logic, why does ESR decrease in microcytosis then? 🙂

 

[Ycut]

By that logic, why does ESR decrease in microcytosis then? 🙂

That question must be addressed to God i guess 😉

(So from previous discussions on rouleaux formation-which increased mass and ESR i deduce that decrease in size decreases mass compared to normal RBCs and decreases ESR)

 

[Old Style Nanny]

That question must be addressed to God i guess 😉

(So from previous discussions on rouleaux formation-which increased mass and ESR i deduce that decrease in size decreases mass compared to normal RBCs and decreases ESR)

Touché!

 

[Akarat]

By that logic, why does ESR decrease in microcytosis then? 🙂

I don't know much about ESR, but could it be that in case of microcytosis, there's an increase in the total surface area? I'm assuming that although the RBCs are smaller, the total number of RBCs is increased. More total surface area with a constant level of inflammatory factors means that there is less coating of each RBC, and therefore a decrease in ESR.

 

[Old Style Nanny]

I don't know much about ESR, but could it be that in case of microcytosis, there's an increase in the total surface area? I'm assuming that although the RBCs are smaller, the total number of RBCs is increased. More total surface area with a constant level of inflammatory factors means that there is less coating of each RBC, and therefore a decrease in ESR.

Not necessarily. Microcytosis only implies small cells with no implication on the number. On the other hand, microcytosis accompanied by anemia is when there is reduction in the number of cells.

As far as I have understood, the RBCs are generally made smaller because there is less Hb and the body tries to maintain a proper MCHC in each cell. So, I don't see why microcytosis should increase the number of cells produced. Do you have a reference where you had read that?

 

[Akarat]

Not necessarily. Microcytosis only implies small cells with no implication on the number. On the other hand, microcytosis accompanied by anemia is when there is reduction in the number of cells.

As far as I have understood, the RBCs are generally made smaller because there is less Hb and the body tries to maintain a proper MCHC in each cell. So, I don't see why microcytosis should increase the number of cells produced. Do you have a reference where you had read that?

I assumed that the body would compensate for a deficiency in oxygen content by increasing the number of RBCs. However, from what you've typed and the fact that I haven't taken the hematology portion of my courses yet leads me to believe that I'm incorrect in that assumption.

 

[pak90]

I think ESR is mostly based on the fact that RBCs are negatively charged, they push each other away. During inflammation for example, the inflammatory proteins circulating will neutralize the negative charges causing RBC clumping.
I'm still unsure why microcytic anemia decreases ESR, but I just use this analogy: small cells are less likely to come into contact with each other -> less likely to clump.