Chapter 12: the hematopoietic and lymphoid system
Haematopoiesis: the differentiation of stem cells to mature blood cells under the influence of
growth factors and cytokines.
- Early precursor cells influenced by ILS
- Erythropoiesis influenced by erythropoietin
- Megakaryopoiesis influenced by thrombopoietin
- Myelopoiesis by GM-CSF and G-CSF
Needed to keep the number of cells stable.
Erythrocytes: filled with Hb. No nucleus. Are derived from myeloid stem cell. Life 150 days.
Neutrophils: segmented nuclei. Have granule. Short lifespan. Leave BM and circulate to tissue to
stick to endothelial cells. Clean up the mess of dead bacteria.
Lymphocytes: some have granules. B cells make antibodies. T cells for cellular response. Viral
infections a lot of activated lymphocytes.
Thrombocytes: small fragments of megakaryocytes. In the granule coagulation factors. Important in
the form of blood clot.
Decrease:
Erythrocytes = anaemia
Leuko/thrombo = can be due to production, maturation, survival, or distribution problem
Pancytopenia = all cells decreased. Can be due to constitutional, acquired, deficit B12, age or
malignancies.
Anaemia, causes are:
Increased destruction (haemolytic):
- Intrinsic by hereditary (membrane defect) or acquired.
- Extrinsic (transfusion)
Impaired production or blood loss
Leukopenia causes by decreased production (bone marrow hypoplasia, drugs, neoplastic &
myelodysplastic syndrome) or increased destruction (severe infections).
Increase:
- Acute leukaemia’s (AML, ALL); proliferation but no differentiation.
- Chronic myeloproliferative neoplasia; proliferation and differentiation
- Myelodysplastic diseases; bad quality of blood cells
- mast cytosis
- Localisation of tumors; NHL, Kahler and metastases.
Acute leukaemia’s: ALL vs AML
ALL: young age. Originate from B and T precursor. Prognosis depends on leukemic cells, organ
filtration and immunophenotype. Treatment is chemo and/or BM transplantation.
AML: incidence increase with age. Can arise in other BM diseases. Classified by genetic defect.
Changes the prognostic features. Inv3 (good prognose) inv16 (poor prognose).
Need to make distinction because different therapy and different prognosis.
Chronic leukaemia’s: CML and CLL
CML: stemcel disease. Translocation of 9,22. Can progress to AML. A lot of leukocytes with a huge
spleen.
CLL: (HNL): can happen outside the lymph nodes and inside. Other page more information about
HNL
Haematopoiesis: the differentiation of stem cells to mature blood cells under the influence of
growth factors and cytokines.
- Early precursor cells influenced by ILS
- Erythropoiesis influenced by erythropoietin
- Megakaryopoiesis influenced by thrombopoietin
- Myelopoiesis by GM-CSF and G-CSF
Needed to keep the number of cells stable.
Erythrocytes: filled with Hb. No nucleus. Are derived from myeloid stem cell. Life 150 days.
Neutrophils: segmented nuclei. Have granule. Short lifespan. Leave BM and circulate to tissue to
stick to endothelial cells. Clean up the mess of dead bacteria.
Lymphocytes: some have granules. B cells make antibodies. T cells for cellular response. Viral
infections a lot of activated lymphocytes.
Thrombocytes: small fragments of megakaryocytes. In the granule coagulation factors. Important in
the form of blood clot.
Decrease:
Erythrocytes = anaemia
Leuko/thrombo = can be due to production, maturation, survival, or distribution problem
Pancytopenia = all cells decreased. Can be due to constitutional, acquired, deficit B12, age or
malignancies.
Anaemia, causes are:
Increased destruction (haemolytic):
- Intrinsic by hereditary (membrane defect) or acquired.
- Extrinsic (transfusion)
Impaired production or blood loss
Leukopenia causes by decreased production (bone marrow hypoplasia, drugs, neoplastic &
myelodysplastic syndrome) or increased destruction (severe infections).
Increase:
- Acute leukaemia’s (AML, ALL); proliferation but no differentiation.
- Chronic myeloproliferative neoplasia; proliferation and differentiation
- Myelodysplastic diseases; bad quality of blood cells
- mast cytosis
- Localisation of tumors; NHL, Kahler and metastases.
Acute leukaemia’s: ALL vs AML
ALL: young age. Originate from B and T precursor. Prognosis depends on leukemic cells, organ
filtration and immunophenotype. Treatment is chemo and/or BM transplantation.
AML: incidence increase with age. Can arise in other BM diseases. Classified by genetic defect.
Changes the prognostic features. Inv3 (good prognose) inv16 (poor prognose).
Need to make distinction because different therapy and different prognosis.
Chronic leukaemia’s: CML and CLL
CML: stemcel disease. Translocation of 9,22. Can progress to AML. A lot of leukocytes with a huge
spleen.
CLL: (HNL): can happen outside the lymph nodes and inside. Other page more information about
HNL
