Intravascular Versus Extravascular Hemolysis - USMLE Forums
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  #1  
Old 08-29-2009
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Blood Intravascular Versus Extravascular Hemolysis

Intravascular Hemolysis
The RBCs are lysed within the blood vessel such as by mechanical damage of a heart valve, or because of complement fixation as in paroxysmal nocturnal hemoglobinuria.
The hemoglobin is released into the blood and immediately bound by haptoglobin for clearance in the liver.
If the hemolysis is too much, haptoglobin get consumed and extra hemoglobin set free in the circulation (that's why hemoglobinemia).
This free hemoglobin reaches the kidney and get's filtered and then reabsorbed in the form of Iron.
Again if hemolysis is beyond the reabsorptive capacity of the renal tubules, hemoglobin will appear in the urine (hemoglobinuria, and urinary hemosiderin appears).
Because the fact that RBSs are lysed in the blood, its LDH is released into the circulation raising it's levels. (recall that LDH is mainly a cytoplasmic enzyme that's why it's available in the nucleus-free mitochondria-free RBC).
Schitiocytes are essentially broken up and fragmented RBCs.

Extravascular Hemolysis
RBCs are coated with antibodies or have abnormal shape of membrane or abnormal inclusion (such as Heinz bodies in G6PD) and so they are attacked prematurely by the liver and spleen phagocytes.
The engulfed hemoglobin is converted into iron for recycling and the globine portion becomes billirubin later.
So as no hemoglobin is released into the circulation, no haptoglobin is consumed and no hemoglobinemia or uria is observed.
As the RBC is not lysed in the circulation, no LDH is elevated.
Sometimes, the phagocytes spit up the RBCs back again after chewing up some membrane and therefore we may see spherocytes in the peripheral blood smear. Differentiate the two main cause of spherocytosis by doing osmotic fagility (positive in congenital spherocytosis) and DCT (positive in AutoImmune Hemolytic Anemia).

Have a look this quick table for comparison

Intravascular Versus Extravascular Hemolysis-intravascular-extravascular-hemolysis.jpg

Last edited by lee-usmle; 08-29-2009 at 01:29 PM.
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  #2  
Old 08-30-2009
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G6PD deficiency
does it cause intravascular or extravascular hemolysis?

Your post hinting to extravascular, but then how come see red urine in these patients?
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G6PD and Rh incompatibility cause extravascular hemolysis if they are mild
When they go severe, the RBCs can be destroyed within the circulation resulting in intravascular hemolysis
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Old 04-10-2011
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Sorry. Could you post a list about causes of intravascular and extravascular hemolysis. Thank you very, very much.

Last edited by bibyology; 04-10-2011 at 07:19 AM. Reason: false typing
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Old 10-02-2011
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Could you ever have any conditions that there is increased indirect bilirubin but no anemia, liver function tests normal, Comb test negative ?
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  #6  
Old 10-03-2011
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Gilbert syndrome,,criggler nijar(sorry don't know exact spelling)
raised bilirubin
normal LFTs
normal blood smear
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  #7  
Old 10-08-2014
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Quote:
Originally Posted by lee-usmle View Post
Intravascular Hemolysis
The RBCs are lysed within the blood vessel such as by mechanical damage of a heart valve, or because of complement fixation as in paroxysmal nocturnal hemoglobinuria.
The hemoglobin is released into the blood and immediately bound by haptoglobin for clearance in the liver.
If the hemolysis is too much, haptoglobin get consumed and extra hemoglobin set free in the circulation (that's why hemoglobinemia).
This free hemoglobin reaches the kidney and get's filtered and then reabsorbed in the form of Iron.
Again if hemolysis is beyond the reabsorptive capacity of the renal tubules, hemoglobin will appear in the urine (hemoglobinuria, and urinary hemosiderin appears).
Because the fact that RBSs are lysed in the blood, its LDH is released into the circulation raising it's levels. (recall that LDH is mainly a cytoplasmic enzyme that's why it's available in the nucleus-free mitochondria-free RBC).
Schitiocytes are essentially broken up and fragmented RBCs.

Extravascular Hemolysis
RBCs are coated with antibodies or have abnormal shape of membrane or abnormal inclusion (such as Heinz bodies in G6PD) and so they are attacked prematurely by the liver and spleen phagocytes.
The engulfed hemoglobin is converted into iron for recycling and the globine portion becomes billirubin later.
So as no hemoglobin is released into the circulation, no haptoglobin is consumed and no hemoglobinemia or uria is observed.
As the RBC is not lysed in the circulation, no LDH is elevated.
Sometimes, the phagocytes spit up the RBCs back again after chewing up some membrane and therefore we may see spherocytes in the peripheral blood smear. Differentiate the two main cause of spherocytosis by doing osmotic fagility (positive in congenital spherocytosis) and DCT (positive in AutoImmune Hemolytic Anemia).

Have a look this quick table for comparison

Attachment 32
Thanku this is very helpful
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