Page 40 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Erythrocytes can to a certain extent be bound to haptoglobin
(→ p. 38). This reduces the glomerular filtra-
Erythrocytes (red blood cells [RBCs]) are tion of Hb and thus its elimination (hemoglo-
formed in bone marrow from nucleus-contain- binuria).
ing erythroid precursor cells (→ B and p. 29 A)
and reach the bloodstream as nucleus-free and
mitochondria-free, disc-shaped cells (ca. 7.5 × Erythropoiesis, Anemia
2 µm). They can be severely deformed within
the blood capillaries, which greatly facilitates Anemia is the term given to the reduction in
both their passage and the exchange of sub- the number of erythrocytes, in the concentration
stances and gases with the surrounding tis- of hemoglobin and/or in the hematocrit as long
sues. RBCs that have recently entered the as the total blood volume is normal. Shortly
blood will retain net-like residues of organ- after acute major blood loss, in dehydration,
elles (reticulocytes) for another one or two or in hyperhydration the blood volume must
days. With a normal life-span of RBCs of about first be normalized before anemia can be diag-
110–120 days, the proportion of reticulocytes nosed. Using the erythrocyte parameters mean
is normally 1–2%. corpuscular volume (MCV) and mean corpus-
Erythrocytes contain a large amount of he- cular hemoglobin (MCH) (→ A), anemias can
moglobin (Hb), their mean corpuscular hemo- be classified according to cell volume (MCV:
globin concentration (MCH) normally being microcytic, normocytic, or macrocytic) and ac-
Blood 300–360 g per litre RBCs (→ A). Since a normal cording to the ratio of Hb concentration/eryth-
rocyte count (MCH: hypochromic, normochro-
RBC has a volume (MCV) of 80–100 fL, it con-
3 tains 26–35 pg Hb (MCH). mic, or hyperchromic). Pathogenetic division
The high hemoglobin content largely con- of the anemias reflects the individual steps of
tributes to intracellular osmolality so that, to erythropoiesis as well as the life-span of the
avoid osmosis-induced entry of water, the in- erythrocytes circulating in blood (hemolytic
tracellular ion concentration has to be held at anaemia; → B). Finally, acute or chronic blood
+
+
a lower level than that in plasma. Na -K -AT- loss can also lead to anemia.
Pase is essential for this, the required ATP Disorders of erythropoiesis (→ B) may occur
(adenosine 5′-triphosphate) in the RBCs (be- as a result of 1) lack or absence of differentia-
cause of the absence of mitochondria) coming tion of pluripotent, hemopoietic stem cells
from anaerobic glycolysis. Volume regulation it- (aplastic anemia in panmyelopathy or acute
self happens indirectly, especially via the vol- myeloid leukemia); 2) transient (viral infec-
ume-sensitive ion transporters that can lower tion) or chronic reduction of only the erythro-
–
+
the K and Cl content of RBCs (→ p.10f.). If cytic precursor cells (isolated aplastic anemia)
ATP production ceases or the membrane is due to autoantibodies against erythropoietin
damaged, the RBCs swell and thus have a or against membrane proteins of the precursor
shorter survival time (premature hemolysis). cells; 3) erythropoietin deficiency in renal fail-
The RBCs regularly leave the arterioles in ure (renal anemia); 4) chronic inflammation or
the pulp of the spleen and reach the small tumors that can activate, among others, eryth-
pores in the splenic sinuses. Old and abnor- ropoiesis-inhibiting interleukins (secondary
mally fragile erythrocytes are separated out anemia); 5) abnormal cell differentiation (inef-
and destroyed in the region of these pores. fective erythropoiesis), which in addition to
The fragments are phagocytized by the macro- gene defects may mainly be due to a deficiency
phages in the spleen, liver, bone marrow, etc. in folic acid or vitamin B 12 (megaloblastic ane-
and broken down (extravascular hemolysis in mia; → p. 34); 6) abnormal Hb synthesis (mi-
the reticuloendothelial system [RES], or more crocytic hypochromic anemia; → p. 36ff.).
precisely, the mononuclear phagocytotic sys-
tem [MPS]; → p. 44). The liberated heme is bro-
ken down into bilirubin (→ p.168), the liber-
30 ated iron is reused (→ p. 38). If there is intra-
vascular hemolysis, Hb that has been released
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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