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Hematopoiesis and Anemia Insights

1. Regulation of erythropoiesis is described for 7 conditions: decreased RBC survival increases EPO and reticulocytes but decreases RBC mass; iron, B12, and folate deficiencies increase EPO and decrease reticulocytes and RBC mass, causing anemia. Kidney disease decreases all three. Lung disease increases EPO, reticulocytes, and RBC mass, causing secondary polycythemia. A Jak-2 mutation leads to constitutively increased EPO and primary polycythemia. 2. Megaloblastic anemia results from folate or B12 deficiencies, which impair DNA synthesis and cause ineffective hematopoiesis

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98 views3 pages

Hematopoiesis and Anemia Insights

1. Regulation of erythropoiesis is described for 7 conditions: decreased RBC survival increases EPO and reticulocytes but decreases RBC mass; iron, B12, and folate deficiencies increase EPO and decrease reticulocytes and RBC mass, causing anemia. Kidney disease decreases all three. Lung disease increases EPO, reticulocytes, and RBC mass, causing secondary polycythemia. A Jak-2 mutation leads to constitutively increased EPO and primary polycythemia. 2. Megaloblastic anemia results from folate or B12 deficiencies, which impair DNA synthesis and cause ineffective hematopoiesis

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Flower
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Regulation of Erythropoiesis

[EPO] Retic% RBC mass


This is reticulocytotic
1 ↓RBC survival ↑ ↑ ↓
2 Iron Deficiency ↑ ↓ ↓ In 2-5 we have anemia
(↓BC mass); it’s due to
3 B12 Deficiency ↑ ↓ ↓
ineffective hematopoiesis
4 Folate Deficiency ↑ ↓ ↓ (because we lack the
5 Kidney disease ↓ ↓ ↓ ingredients to make retics.

we have 2o polycythemia
6 Lung disease (↓PaO2) ↑ ↑ ↑ (i.e. polycythemia
secondary to lung disease)
EPO uses jak-stat pathway.
When the’re a utation,the
7 Jak-2 mutation (on) ↓ ↑ ↑ receptor will be
onstitutively on; this is
primary polycythemia
Megaloblastic anemia:
1. Mechanism:↓ DNA syntheisis → ↓nuclear division but normal cytoplasm →
nuclear: cytoplasmic desynchrony → ineffective hematopoiesis→ Intramedullary
HEMOLYSIS, i.e. when fragile red blood cell (RBC) precursors are destroyed in the
BM prior to release into the circulation.
2. Anemia: RPI <2
3. Macrocytosis (↑MCV)
4. Pancytopenia
5. Hypersegemented Neutrophiles (classic for megaloblastic anemia)
6. ↑Homocysteine.
7. ↑ LDH and unconjucated Billirubin.
8.

9. This impaired DNA synthesis delays nuclear maturation.


a. Causes a block in cell division in all rapidly dividing cells, leading to large, nucleated
hematopoietic cells with an open chromatin pattern
a. Cells that are affected include RBCs, leukocytes, megakaryocytes, and intestinal
epithelium.
b. Cellular RNA synthesis and protein synthesis are not affected.
• Cytoplasmic volume continues to expand→ ↓nuclear division but normal cytoplasm →
nuclear: cytoplasmic desynchrony → ineffective hematopoiesis→ Intramedullary
HEMOLYSIS, i.e. when fragile red blood cell (RBC) precursors are destroyed in the BM
prior to release into the circulation. .
10. Ineffective hematopoiesis is present in either folate or B12 defciencies.
a. Megaloblastic precursors outside the BM sinusoids are phagocytosed and destroyed by
BM MPs.
b. Megaloblastic precursors undergo apoptosis, causing pancytopenia (anemia,
neutropenia, and thrombocytopenia).
11. Folate and B12 play two important roles in
a. conversion of homocysteine to methionine and
b. DNA synthesis

Two most common causes are folate or B12 deficiency.

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