Lecture 5b: Destruction of Red Blood Cells

A. Fate of the RBC’s:


The erythrocytes have no nucleus, no endoplasmic reticulum and no mitochondria. But there is some glucose oxidation which can produce ATP


This ATP is necessary for: 1. flexibility of the membrane 2. membrane ion transport 3. keep Fe in ferrous format otherwise; ferri-format = (methemoglobine) which is not suitable for oxygen binding.

3. The RBC test:

All RBC’s (7 micron wide) will at one moment or another flow through the spleen. But the spleen consists of the narrowest capillaries (3 micron) in the body! If the membrane of an old RBC is no longer flexible enough, it will break (=hemolysis) and the life of this RBC is terminated!


There is enough glucose and ATP to keep the RBC membrane flexible for about 120 days!


In the old Olympics (Greeks) they already practiced doping by removing the spleen in young athletes. This will leave more (older) RBC’s in the circulation, thereby increasing the oxygen transportation.


But eventually the RBC’s will die but now they don’t break down in the spleen but elsewhere in the body; in the capillaries of the brain, the heart or in the muscles. This will, in time, lead to decrease in the quality of these organs. These young athletes typically died young!



B. Destruction process of the RBC’s:


In the spleen, the components of the old destroyed RBC’s are recycled!


Fe => Transferrin => Ferritin. In other words, the iron is stored and saved.


The globine is converted back into its amino acids which can be used for building other proteins.


The heme is processed in a very special manner:


The heme is converted, still in the spleen, first into biliverdin which is then converted into bilirubin.


This bilirubin then appears in the blood and is bound to the blood transport protein: albumin.


This bilirubin is called “free” or “indirect” bilirubin (depending on the book or the teacher or the country that you are being taught this).


This free or indirect bilirubin is then transported by the blood to the liver


This bilirubin is now called “conjugated” (!) or “direct” bilirubin. Whatever its name, this type of bilirubin is secreted into the bile.


The bile flows into the intestine, where the bilirubin is converted, by the intestinal bacteria, into urobilinogen.


This urobilinogen is absorbed by the blood and either goes back to the liver (to go back to the bile, to make a loop), or excreted by the kidney (as urobilin) or excreted via the stool (as stercobilin).


Important; the stercobilin gives the stool its characteristic brown colour. If you don’t have stercobilin, then the stool becomes pale like clay. This is an important diagnostic tool to discover diseases of the gall bladder or the bile duct!




C. Jaundice:


Why is this story about bilirubin so important? In one word: jaundice (yellow colour of the skin and the whites of the eye). Medical name: icterus.


When someone turns “yellow”, that means that something is wrong with the bilirubin processing. This is very useful because it reveals that there is a pathology somewhere in the body. It works like a marker.

3. Hemolytic jaundice:

In this case, too much RBC’s are being destroyed which increases the “free” bilirubin. This can be due to poisoning, a defect in the RBC, mismatched transfusion etc.

4. Hepatocellular jaundice:

When the liver cells are diseased (such as in hepatitis), then they will be less able to conjugate the bilirubin. This will also increase the “indirect” bilirubin

5. Obstructive jaundice:

This occurs when the bile in the liver does not reach the intestine due to obstruction of the bile ducts (gallstones!) or to cholestasis (no bile flow). This will lead to an increase in the conjugated bilirubin.


Because it is possible, in the lab, to differentiate between the conjugated and the free bilirubin, it is possible to have an idea of the location or the type of the disease. That is why the jaundice story is so useful to make a diagnosis.





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