Anasarca and glomerulonephritis

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shouldBstudying

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Been scratching my head over this one -

Had a question on a popular qbank that was discussing the causes of anasarca. The question stem basically described a man with anasarca, marked HTN, and UA with trace protein and a bunch of RBCs. The answer for the cause of his peripheral edema was acute glomerulonephritis.

The explanation given was somewhat circular in reasoning - third spacing--> decreased volume sensed by the kidney-->activation of RAS-->peripheral constriction & inc capillary hydrostatic pressure-->third spacing

But my question is - what causes the third spacing to begin with?? I understand this process completely if you apply this to nephrotic syndrome - but for this, I'm puzzled.

Any thoughts/clarification would be greatly appreciated.

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Been scratching my head over this one -

Had a question on a popular qbank that was discussing the causes of anasarca. The question stem basically described a man with anasarca, marked HTN, and UA with trace protein and a bunch of RBCs. The answer for the cause of his peripheral edema was acute glomerulonephritis.

The explanation given was somewhat circular in reasoning - third spacing--> decreased volume sensed by the kidney-->activation of RAS-->peripheral constriction & inc capillary hydrostatic pressure-->third spacing

But my question is - what causes the third spacing to begin with?? I understand this process completely if you apply this to nephrotic syndrome - but for this, I'm puzzled.

Any thoughts/clarification would be greatly appreciated.

From Physiology, first year med school: J = K (Hydro_cap - Hydro_int) - (Oncotic_Cap - Oncotic_Int)

You get edema either from

1. vasoDILATION (increased capillary permeability), K, the permeability coefficient. Think of sepsis, burns, local inflammation.

2. increased hydrostatic pressure, meaning you have to have obstruction to outflow. Think compression, clots, cancer, and CHF. This gives you dependent edema; back up of blood at the spot of increased hydrostatic pressure. So, by definition, NOT anasarca... if you had right heart failure, all the fluid would end up in your feet.

3. decreased oncotic pressure, meaning you have a low albumin. That is Cirrhosis, Nephrosis, and Gastrosis. Meaning, liver impairment (you can't make the protein in the first place), nephrotic syndrome (loss of albumin through urine), and protein losing enteropathies or malnutrition (you don't bring in enough protein). Because there is low albumin everywhere, there is redistribution of fluid into the third space. I.e. ANASARCA.

Bottom line: Anasarca yes in Oncotic pressure, Anasarca No in Hydrostatic pressure...dependent peripheral edema yes hydrostatic pressure, dependent peripheral edema no oncotic pressure

It is strange that your patient had only mild proteinuria. When I read the question, I thought he straight up had nephrotic syndrome (hypercholesteremia, edema, proteinuria, and hypercholesteremia). If he had nephrotic-range proteinuria, his albumin would be low, and he would get anasarca.

They might be getting at acute volume overload if his GFR dropped as a result of the glomuerlonephritis, but they didnt give you that information, and it should be more dependent edema.

It seems that they are getting at Nephritic syndrome (HTN, hematuria, and azotemia). But Nephritic syndrome isn't really associated with anasarca. I have a feeling they are meaning volume overload from azotemia and decreased GFR as a product of nephritic syndrome. This could cause peripheral edema, because excess fluid would third space as well, but would be more likely to be dependent with gravity, rather than anasarca.

Are you sure the details in the question stem are correct?
 
From Physiology, first year med school: J = K (Hydro_cap - Hydro_int) - (Oncotic_Cap - Oncotic_Int)

You get edema either from

1. vasoDILATION (increased capillary permeability), K, the permeability coefficient. Think of sepsis, burns, local inflammation.

2. increased hydrostatic pressure, meaning you have to have obstruction to outflow. Think compression, clots, cancer, and CHF. This gives you dependent edema; back up of blood at the spot of increased hydrostatic pressure. So, by definition, NOT anasarca... if you had right heart failure, all the fluid would end up in your feet.

3. decreased oncotic pressure, meaning you have a low albumin. That is Cirrhosis, Nephrosis, and Gastrosis. Meaning, liver impairment (you can't make the protein in the first place), nephrotic syndrome (loss of albumin through urine), and protein losing enteropathies or malnutrition (you don't bring in enough protein). Because there is low albumin everywhere, there is redistribution of fluid into the third space. I.e. ANASARCA.

Bottom line: Anasarca yes in Oncotic pressure, Anasarca No in Hydrostatic pressure...dependent peripheral edema yes hydrostatic pressure, dependent peripheral edema no oncotic pressure

It is strange that your patient had only mild proteinuria. When I read the question, I thought he straight up had nephrotic syndrome (hypercholesteremia, edema, proteinuria, and hypercholesteremia). If he had nephrotic-range proteinuria, his albumin would be low, and he would get anasarca.

They might be getting at acute volume overload if his GFR dropped as a result of the glomuerlonephritis, but they didnt give you that information, and it should be more dependent edema.

It seems that they are getting at Nephritic syndrome (HTN, hematuria, and azotemia). But Nephritic syndrome isn't really associated with anasarca. I have a feeling they are meaning volume overload from azotemia and decreased GFR as a product of nephritic syndrome. This could cause peripheral edema, because excess fluid would third space as well, but would be more likely to be dependent with gravity, rather than anasarca.

Are you sure the details in the question stem are correct?


Thanks for the detailed response.

You are right about your last comment - they are getting at nephritic syndrome, which as you mentioned (and the reason I was confused) is not associated, to my knowledge, with generalized edema, but more peripheral and gravity-dependent.

The stem definitely mentioned "facial edema making it difficult for the patient to open his eyes in the morning" and "generalized body edema" with trace proteins and >50 RBCs on a UA. I suppose with a more careful read the periorbital/facial edema in the morning could be more gravity-dependent/hydrostatic pressure driven, but I'm not sure what to make of the "generalized body edema"

Appreciate your confirmation that I dont have to go back and re-take first year phys :D and my reasoning behind my confusion wasnt way out of whack
 
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