Leucocytes csbrp
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Leucocytes csbrp
- 1. Disorders of LeucocytesDisorders of Leucocytes Dr.CSBR.Prasad, M.D.
- 2. In the center of the field are a band neutrophil on the left and a segmented neutrophil on the right. 2CSBRP-Sep-2011
- 3. A normal mature lymphocyte is seen on the left compared to a segmented PMN on the right. An RBC is seen to be about 2/3 the size of a normal lymphocyte. 3CSBRP-Sep-2011
- 4. Here is a monocyte. It is slightly larger than a lymphocyte and has a folded nucleus. Monocytes can migrate out of the bloodstream and become tissue macrophages under the influence of cytokines. Note the many small smudgy blue platelets between the RBC's 4 CSBRP-Sep-2011
- 5. In the center of the field is an eosinophil with a bilobed nucleus and numerous reddish granules in the cytoplasm. Just underneath it is a small lymphocyte. Eosinophils can increase with allergic reactions and with parasitic infestations. 5 CSBRP-Sep-2011
- 6. There is a basophil in the center of the field which has a lobed nucleus (like PMN's) and numerous coarse, dark blue granules in the cytoplasm. They are infrequent in a normal peripheral blood smear, and their significance is uncertain. A band neutrophil is seen on the left, and a large, activated lymphocyte on the right. 6 CSBRP-Sep-2011
- 7. • Name different types of T-cells 7CSBRP-Sep-2011
- 8. • Name some cells without nucleus 8CSBRP-Sep-2011
- 9. • What are stab cells? 9CSBRP-Sep-2011
- 10. • What is a plasma cell? 10CSBRP-Sep-2011
- 11. This hypersegmented neutrophil is present along with macro-ovalocytes in a case of pernicious anemia. Compare the size of the RBC's to the lymphocyte at the lower left center. 11CSBRP-Sep-2011
- 12. Lymphocyte (blue circle), spherocytes and polychromatic cells (Red circle). 12CSBRP-Sep-2011
- 13. 13CSBRP-Sep-2011
- 14. The RBC's in the background appear normal. The important finding here is the presence of many PMN's. An elevated WBC count with mainly neutrophils suggests inflammation or infection. A very high WBC count (>50,000) that is not a leukemia is known as a "leukemoid reaction". This reaction can be distinguished from malignant WBC's by the presence of large amounts of leukocyte alkaline phosphatase (LAP) in the normal neutrophils. 14CSBRP-Sep-2011
- 15. The RBC's here are smaller than normal and have an increased zone of central pallor. This is indicative of a hypochromic (less hemoglobin in each RBC) microcytic (smaller size of each RBC) anemia. There is also increased anisocytosis (variation in size) and poikilocytosis (variation in shape). 15CSBRP-Sep-2011
- 16. Here is a hypersegmented neutrophil that is present with megaloblastic anemias. There are 8 lobes instead of the usual 3 or 4. Such anemias can be due to folate or to B12 deficiency. The size of the RBC's is also increased (macrocytosis, which is hard to appreciate in a blood smear). 16CSBRP-Sep-2011
- 17. The nucleated RBC in the center contains basophilic stippling of the cytoplasm. This suggests a toxic injury to the bone marrow. Such stippling may also appear with severe megaloblastic anemia. 17CSBRP-Sep-2011
- 18. The WBC's seen here are "atypical" lymphocytes. They are atypical because they are larger (more cytoplasm) and have nucleoli in their nuclei. The cytoplasm tends to be indented by surrounding RBC's. Such atypical lymphocytes are often associated with infectious 18CSBRP-Sep-2011
- 19. If most of the neutrophils appear bilobed, this is indicative of an uncommon condition known as Pelger-Huet anomaly, an inherited condition. This is the heterozygous form. The homozygous form is fatal. Just be aware of this condition when you get back a manual differential count with mostly bands, but the WBC count is normal or the patient shows no signs of infection or inflammation. 19CSBRP-Sep-2011
- 20. Here is another view of a peripheral blood smear in a patient with CML. Often, the numbers of basophils and eosinophils, as well as bands and more immature myeloid cells (metamyelocytes and myelocytes) are increased. Unlike AML, there are not many blasts with CML. 20CSBRP-Sep-2011
- 21. Here is a smear of bone marrow aspirate from a patient with multiple myeloma. Note that there are numerous well-differentiated plasma cells with eccentric nuclei and a perinuclear halo of clearer cytoplasm. There is also an abnormal plasma cell with a double nucleus. 21CSBRP-Sep-2011
- 22. This is a normal plasma cell as seen in a bone marrow smear at high magnification. Note the eccentric nucleus as well as the perinuclear halo containing the Golgi apparatus. The remaining cytoplasm containing abundant rough endoplasmic reticulum is dark blue. 22CSBRP-Sep-2011
- 23. A history of recurrent bacterial infections and giant granules seen in peripheral blood leukocytes is characteristic for Chediak-Higashi syndrome. This disorder results from a mutation in the LYST gene on chromosome 1q42 that encodes a protein involved in intracecellular trafficking of proteins. Microtubules fail to form properly, and the neutrophils do not respond to chemotactic stimuli. Giant lysosomal granules fail to function. Soft tissue abscesses with Staphylococcus aureus are common. Other cells affected by this disorder include platelets (bleeding), melanocytes (albinism), Schwann cells (neuropathy), NK and cytotoxic T cells (aggressive lymphoproliferative disorder). 23CSBRP-Sep-2011
- 24. White Cell Differential Count • Manual methods • Automated methods 24CSBRP-Sep-2011
- 25. An example of a CBC with automated WBC differential count is shown above. The absolute numbers for total WBC count and each type of leukocyte are in thousands per cubic millimeter (or alternatively, per microliter). 25CSBRP-Sep-2011
- 26. Absolute counts The absolute white blood cell counts are most useful, and are calculated by multiplying the % of each cell type counted by the total WBC count. Simple percentages may be misleading, since an apparent percentage increase in one constituent may actually be due to a significant and absolute decrease of another type of WBC. For example, 99% lymphs with an absolute WBC count of 1300/microliter means neutropenia, not lymphocytosis. Always consider the WBC percentages in the context of the total WBC count. 26CSBRP-Sep-2011
- 28. HematopoiesisHematopoiesis • Upto 2months --- Yolk sac • Upto 7th month --- Liver • After 7th month --- BM major site (starts producing from 3rd month) • At birth --- BM is the only site 28CSBRP-Sep-2011
- 29. • Distribution of hemopoietic BM in children and adults. HematopoiesisHematopoiesis 29CSBRP-Sep-2011
- 30. HematopoiesisHematopoiesis • Two critical properties of STEM CELLs: 1-Self Renewal (regenerate their own population) & 2-Differentiate towards matured cells 30CSBRP-Sep-2011
- 31. • Hemopoietic stem cells (HSCs) - have great capacity for self renewal - Pleuripotent - most of them are not in cycle • Committed progenitors (lineage restricted) - self renewal is very limited - there after a fraction divide actively - they acively generate matured cells • Early recognizable precursors (ex: Mye.blast, Proerythroblast) - cannot self renew - proliferate, differentiate and die HematopoiesisHematopoiesis 31CSBRP-Sep-2011
- 33. HematopoiesisHematopoiesis • Stem cell proliferation and differentiation -- is mediated by many soluble factors -- stem cell and stromal cell interaction in BM 33CSBRP-Sep-2011
- 34. Examples for soluble factors: c-kit and FLT-3 ligand at stem cell level GM-CSF at CFU-GM level Clinical application: some of the factors are available by recombinant technology for therapeutic use include: 1. EPO 2. GM-CSF 3. G-CSF 4. TPO HematopoiesisHematopoiesis 34CSBRP-Sep-2011
- 36. Stem cell and stromal cell interaction: BONE MARROW MICROENVIRONMENT HematopoiesisHematopoiesis 36CSBRP-Sep-2011
- 37. HematopoiesisHematopoiesis BONE MARROW MICROENVIRONMENT BM is a vast network of thin walled BVs (sinusoids) lined by --single layer of endothelium and --discontinuous basement membrane --and adventitial cells. --extracellular matrix (cell adhesion proteins- fibronectin, laminin, Type-IV collagen, hemonectin & glycosaminoglycans) 37CSBRP-Sep-2011
- 38. BONE MARROW MICROENVIRONMENT Erythroblasts and also progenitors exhibit the property of adherence to stromal cells. This is mainly mediated by Fibronectin When the cells differentiate they become non-adherent HematopoiesisHematopoiesis 38CSBRP-Sep-2011
- 39. HematopoiesisHematopoiesis BONE MARROW MICROENVIRONMENT For blasts & progenitor cells of granulocytic leneage hemonectin acts as anchoring molecule 39CSBRP-Sep-2011
- 40. HematopoiesisHematopoiesis Sources of CSF: 1. Activated MØ – M-CSF, G-CSF 2. Activated T-cells – Lymphokines, GM-CSF, IL-3, γ-IF 3. Endotoxins (stimulate T-cells) – G-CSF secretion 4. Fibroblasts & Endothelial cell (when they are exposed to IL-1 & TNF)- M-CSF, G-CSF, GM-CSF 40CSBRP-Sep-2011
- 41. 41CSBRP-Sep-2011
- 42. 42CSBRP-Sep-2011
- 43. Neutrophilia An increase in the absolute neutrophil count, it can be increased transiently with stress and exercise by a shift of neutrophils from the marginating pool to the circulating pool. Pathologic processes that result in neutrophilia include: • Infection • Toxins: metabolic (uremia), drugs, chemicals • Tissue destruction or necrosis: infarction, burns, neoplasia, etc • Hemorrhage, especially into a body cavity • Rapid hemolysis • Hematologic disorders: leukemias, myeloproliferative disorders 43CSBRP-Sep-2011
- 44. Neutropenia – A decrease in the absolute neutrophil count. Pathologic processes that result in neutropenia include processes that decrease production or increase destruction. Diseases that decrease neutrophil production include: • Aplastic anemia • Toxins that damage marrow • Collagen vascular diseases (such as SLE) • Myelphthisic marrow processes such as marrow infiltration by infections or metastatic carcinomas • Hematologic malignancies such as leukemias • Myeloproliferative disorders • Radiation therapy • Chemotherapy • Congenital disorders – Diseases that increase neutrophil destruction include: • Splenomegaly with hypersplenism • Infection • Immune destruction 44CSBRP-Sep-2011
- 45. Lymphocytosis – An increase in the number of circulating lymphocytes may normally be observed in infants and young children. Pathologic processes with lymphocytosis may include: • Acute infections, including pertussis, typhoid, and paratyphoid • Infectious mononucleosis, with "atypical" lymphocytosis • Viral infections, including measles, mumps, adenovirus, enterovirus, and Coxsackie virus • Toxoplasmosis • HTLV I 45CSBRP-Sep-2011
- 46. Lymphopenia – A decrease in the number of circulating lymphocytes may be seen with: • Immunodeficiency syndromes, including congenital (DiGeorge syndrome, etc) and acquired (AIDS) conditions • Corticosteroid therapy • Neoplasia, including Hodgkin's disease, non- Hodgkin's lymphomas, and advanced carcinomas • Radiation therapy • Chemotherapy 46CSBRP-Sep-2011
- 47. Monocytosis • An increase in the number of circulating monocytes may be seen with: – Infections: such as brucellosis, tuberculosis and rickettsia, Bacterial endocarditis – Myeloproliferative disorders – Hodgkin's disease – Gastrointestinal disorders, including inflammatory bowel diseases and sprue 47CSBRP-Sep-2011
- 48. Monocytopenia • A decrease in the number of circulating monocytes may be seen with: – Early corticosteroid therapy – Hairy cell leukemia 48CSBRP-Sep-2011
- 49. Eosinophilia • An absolute increase in the number of circulating eosinophils may occur with: – Allergic drug reactions – Parasitic infestations, especially those with tissue invasion – Extrinsic asthma – Hay fever – Extrinsic allergic alveolitis ("farmer's lung") – Chronic infections – Hematologic malignancies: CML, Hodgkin's disease 49CSBRP-Sep-2011
- 50. Eosinopenia • An absolute decrease in the number of circulating eosinophils may occur with: – Acute stress reactions with increased glucocorticoid and epinephrine secretion – Acute inflammation – Cushing's syndrome with corticosteroid therapy 50CSBRP-Sep-2011
- 51. Basophilia and Basopenia – An absolute increase in the number of circulating basophils may occur with myeloproliferative disorders and with some allergic reactions. – An absolute decrease in the number of circulating basophils may occur with the same conditions that lead to eosinopenia 51CSBRP-Sep-2011
- 52. Left shift An absolute increase in neutrophils with an increase in bands, and sometimes an increase in immature forms such as metamyelocytes or myelocytes Hypersegmentation Polymorphonuclear leukocytes normally have 3 or 4 lobes, but 5 or 6 or more lobes indicate hypersegmentation; seen most often with megaloblastic anemias, sometimes with myeloproliferative disorders, or following chemotherapy (methotrexate) Toxic granules Increased number and prominence of the azurophilic (primary) granules; seen most often with bacterial infections and in association with cytoplasmic vacuolization Döhle body Irregularly shaped blue staining area in the cytoplasm due to free ribosomes or RER; seen with infections Smudge cell / Basket cell A ruptured cell remnant, classically associated with fragile lymphocytes in CLL Pelger-Huet anomaly An autosomal dominant condition with neutrophils that are mostly bilobed in the heterozygote (normal function) and unilobate in the homozygote (fatal ) May-Hegglin anomaly Rare disorder with large, prominent Döhle-like bodies Chediak-Higashi syndrome Rare disorder with large neutrophilic granules representing abnormal lysosomes 52CSBRP-Sep-2011
- 53. Agranulocytosis • Deficiency of granulocytes • Recognised as a distinct entity in 1922 • Drugs are the common culprits • Early recognition is associated with good prognosis 53CSBRP-Sep-2011
- 54. Symptomatology: • Chills & fever • Extreme prostration • Ulceration of gums, tonsils, soft palate, tongue, pharynx (in severe cases ulcerations may be gangrenous) • Sepsis • Death Agranulocytosis 54CSBRP-Sep-2011
- 55. Drugs that are associated with AGC: 1. Analgesics: phenylbutazone, phenacetin, indimethacin, acetyl salicylic acid, ibuprofen 2. Antiepileptics: barbiturates, hydantoin 3. Antibacterials: chloramphenicol, vancomycin, INH, PAS 4. Miscellaneous: penicillamine, cimetidine, quinine, gold salts 5. Chemicals: benzene Agranulocytosis 55CSBRP-Sep-2011
- 56. Mechanism: Immunologically mediated Evidences: 1-Reintroduction of the drug is associated with reduction in polys 2-Serum from the patient, reduces the granulocyte count in normal persons 3-Patient’s serum lysed granulocytes in vitro Agranulocytosis 56CSBRP-Sep-2011
- 57. Hematological findings: 1. Deficiency of granulocytes 2. No anemia 3. No thrombocytopenia 4. BM may show mild hypoplasia Agranulocytosis 57CSBRP-Sep-2011
- 58. Monitoring blood counts is mandatory when the following drugs are used: 1. Gold salts 2. Thiouracil 3. Anticancer drugs Agranulocytosis 58CSBRP-Sep-2011
Notes de l'éditeur
- In the center of the field are a band neutrophil on the left and a segmented neutrophil on the right.
- A normal mature lymphocyte is seen on the left compared to a segmented PMN on the right. An RBC is seen to be about 2/3 the size of a normal lymphocyte.
- Here is a monocyte. It is slightly larger than a lymphocyte and has a folded nucleus. Monocytes can migrate out of the bloodstream and become tissue macrophages under the influence of cytokines. Note the many small smudgy blue platelets between the RBC's.
- In the center of the field is an eosinophil with a bilobed nucleus and numerous reddish granules in the cytoplasm. Just underneath it is a small lymphocyte. Eosinophils can increase with allergic reactions and with parasitic infestations.
- There is a basophil in the center of the field which has a lobed nucleus (like PMN's) and numerous coarse, dark blue granules in the cytoplasm. They are infrequent in a normal peripheral blood smear, and their significance is uncertain. A band neutrophil is seen on the left, and a large, activated lymphocyte on the right.
- This hypersegmented neutrophil is present along with macro-ovalocytes in a case of pernicious anemia. Compare the size of the RBC's to the lymphocyte at the lower left center.
- The size of many of these RBC's is quite small, with lack of the central zone of pallor. These RBC's are spherocytes. In hereditary spherocytosis, there is a lack of spectrin, a key RBC cytoskeletal membrane protein. This produces membrane instability that forces the cell to the smallest volume--a sphere. In the laboratory, this is shown by increased osmotic fragility. The spherocytes do not survive as long as normal RBC's. With hemolysis, there is increased RBC production, evidenced by the reticulocyte at the upper left center.
- A manual WBC differential count is performed by having a person trained in peripheral blood morphology review the stained blood smear and manually count 100 white cells (or 50 cells in the case of severe leukopenia). The major advantage is that the observer can determine subtle differences in morphology and observe additional changes in RBC morphology and platelets. The major disadvantage is the need for a trained person to spend increased time (with increased cost) needed to scan the smears. Also, there can be some inter-observer variation. A standard complete blood count is performed on an automated laboratory instrument that quantitates the number of WBC's present. Some instruments are also able to perform an "automated" WBC count. The advantages of the automated WBC differential are speed, low cost per test, and the precision from the large number of cells counted. The disadvantages include the initial cost of buying the instrument, inability to distinguish subtle differences in morphology, more marked abnormalities, and lack of information about RBC's or platelets.
- An example of a CBC with automated WBC differential count is shown above. The absolute numbers for total WBC count and each type of leukocyte are in thousands per cubic millimeter (or alternatively, per microliter).
- In children almost all bones are involved in hemopoiesis and in adults it is confined to calvaria, upper ends of humori, femora, pelvic bones, vertebraand rib cage. In adults distribution mimics “a person wearing T-shirt, a cap and shorts”.
- HSCs have two essential properties that are required for the maintenance of hematopoiesis: pluripotency and the capacity for self-renewal. Pluripotency refers to the ability of a single HSC to generate all mature hematopoietic cells. When an HSC divides at least one daughter cell must self-renew to avoid stem cell depletion. Self-renewing divisions are believed to occur within a specialized marrow niche, in which stromal cells and secreted factors nurture and somehow maintain the HSCs.[2] As you may have already surmised from their ability to migrate during embryonic development, HSCs are not sessile. Particularly under conditions of marked stress, such as severe anemia, HSCs are mobilized from the bone marrow and appear in the peripheral blood. In such circumstances, additional HSC niches are sometimes induced or “unveiled” in other tissues, such as the spleen and liver, which can then become sites of extramedullary hematopoiesis. The marrow response to short-term physiologic needs is regulated by hematopoietic growth factors through effects on the committed progenitors. Since mature blood elements are terminally differentiated cells with finite life spans, their numbers must be constantly replenished. In at least some divisions of HSCs, a single daughter cell begins to differentiate. Once past this threshold, these newly committed cells lose the capacity for self-renewal and commence an inexorable journey down a road that leads to terminal differentiation and death. However, as these progenitors differentiate they also begin to express receptors for lineage-specific growth factors, which stimulate their short-term growth and survival. Some growth factors, such as stem cell factor (also called c-KIT ligand) and FLT3-ligand, act on very early committed progenitors. Others, such as erythropoietin, granulocyte-macrophage colonystimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF), and thrombopoietin, act on committed progenitors with more restricted potentials. Feedback loops that are mediated through growth factors tune the marrow output, allowing the numbers of formed blood elements (red cells, white cells, and platelets) to be maintained within appropriate ranges.
- FIGURE 13-1 Differentiation of blood cells. CFU, colony forming unit; SCF, stem cell factor; Flt3L, Flt3 ligand; G-CSF, granulocyte colony-stimulating factor; GM-CSF, granulocyte-macrophage colony-stimulating factor; LIN–, negative for lineage-specific markers; M-CSF, macrophage colony-stimulating factor. Robbin’spath 8th Ed. ======================================= HSCs have two essential properties that are required for the maintenance of hematopoiesis: pluripotency and the capacity for self-renewal. Pluripotency refers to the ability of a single HSC to generate all mature hematopoietic cells. When an HSC divides at least one daughter cell must self-renew to avoid stem cell depletion. Self-renewing divisions are believed to occur within a specialized marrow niche, in which stromal cells and secreted factors nurture and somehow maintain the HSCs.[2] As you may have already surmised from their ability to migrate during embryonic development, HSCs are not sessile. Particularly under conditions of marked stress, such as severe anemia, HSCs are mobilized from the bone marrow and appear in the peripheral blood. In such circumstances, additional HSC niches are sometimes induced or “unveiled” in other tissues, such as the spleen and liver, which can then become sites of extramedullary hematopoiesis. The marrow response to short-term physiologic needs is regulated by hematopoietic growth factors through effects on the committed progenitors. Since mature blood elements are terminally differentiated cells with finite life spans, their numbers must be constantly replenished. In at least some divisions of HSCs, a single daughter cell begins to differentiate. Once past this threshold, these newly committed cells lose the capacity for self-renewal and commence an inexorable journey down a road that leads to terminal differentiation and death. However, as these progenitors differentiate they also begin to express receptors for lineage-specific growth factors, which stimulate their short-term growth and survival. Some growth factors, such as stem cell factor (also called c-KIT ligand) and FLT3-ligand, act on very early committed progenitors. Others, such as erythropoietin, granulocyte-macrophage colonystimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF), and thrombopoietin, act on committed progenitors with more restricted potentials. Feedback loops that are mediated through growth factors tune the marrow output, allowing the numbers of formed blood elements (red cells, white cells, and platelets) to be maintained within appropriate ranges.
- FIGURE 13-1 Differentiation of blood cells. CFU, colony forming unit; SCF, stem cell factor; Flt3L, Flt3 ligand; G-CSF, granulocyte colony-stimulating factor; GM-CSF, granulocyte-macrophage colony-stimulating factor; LIN–, negative for lineage-specific markers; M-CSF, macrophage colony-stimulating factor. Robbin’spath 8th Ed. ======================================= HSCs have two essential properties that are required for the maintenance of hematopoiesis: pluripotency and the capacity for self-renewal. Pluripotency refers to the ability of a single HSC to generate all mature hematopoietic cells. When an HSC divides at least one daughter cell must self-renew to avoid stem cell depletion. Self-renewing divisions are believed to occur within a specialized marrow niche, in which stromal cells and secreted factors nurture and somehow maintain the HSCs.[2] As you may have already surmised from their ability to migrate during embryonic development, HSCs are not sessile. Particularly under conditions of marked stress, such as severe anemia, HSCs are mobilized from the bone marrow and appear in the peripheral blood. In such circumstances, additional HSC niches are sometimes induced or “unveiled” in other tissues, such as the spleen and liver, which can then become sites of extramedullary hematopoiesis. The marrow response to short-term physiologic needs is regulated by hematopoietic growth factors through effects on the committed progenitors. Since mature blood elements are terminally differentiated cells with finite life spans, their numbers must be constantly replenished. In at least some divisions of HSCs, a single daughter cell begins to differentiate. Once past this threshold, these newly committed cells lose the capacity for self-renewal and commence an inexorable journey down a road that leads to terminal differentiation and death. However, as these progenitors differentiate they also begin to express receptors for lineage-specific growth factors, which stimulate their short-term growth and survival. Some growth factors, such as stem cell factor (also called c-KIT ligand) and FLT3-ligand, act on very early committed progenitors. Others, such as erythropoietin, granulocyte-macrophage colonystimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF), and thrombopoietin, act on committed progenitors with more restricted potentials. Feedback loops that are mediated through growth factors tune the marrow output, allowing the numbers of formed blood elements (red cells, white cells, and platelets) to be maintained within appropriate ranges.
- The bone marrow is a unique microenvironment that supports the orderly proliferation, differentiation, and release of blood cells. It is filled with a network of thin-walled sinusoids lined by a single layer of endothelial cells, which are underlaid by a discontinuous basement membrane and adventitial cells. Within the interstitium lie clusters of hematopoietic cells and fat cells. Differentiated blood cells enter the circulation by transcellular migration through the endothelial cells. The normal marrow is organized in subtle, but important, ways. For example, normal megakaryocytes lie next to sinusoids and extend cytoplasmic processes that bud off into the bloodstream to produce platelets, while red cell precursors often surround macrophages (so-called nurse cells) that provide some of the iron needed for the synthesis of hemoglobin. Diseases that distort the marrow architecture, such as deposits of metastatic cancer or granulomatous disease, can cause the abnormal release of immature precursors into the peripheral blood, a finding that is referred to as leukoerythroblastosis
- The bone marrow is a unique microenvironment that supports the orderly proliferation, differentiation, and release of blood cells. It is filled with a network of thin-walled sinusoids lined by a single layer of endothelial cells, which are underlaid by a discontinuous basement membrane and adventitial cells. Within the interstitium lie clusters of hematopoietic cells and fat cells. Differentiated blood cells enter the circulation by transcellular migration through the endothelial cells. The normal marrow is organized in subtle, but important, ways. For example, normal megakaryocytes lie next to sinusoids and extend cytoplasmic processes that bud off into the bloodstream to produce platelets, while red cell precursors often surround macrophages (so-called nurse cells) that provide some of the iron needed for the synthesis of hemoglobin. Diseases that distort the marrow architecture, such as deposits of metastatic cancer or granulomatous disease, can cause the abnormal release of immature precursors into the peripheral blood, a finding that is referred to as leukoerythroblastosis
- The bone marrow is a unique microenvironment that supports the orderly proliferation, differentiation, and release of blood cells. It is filled with a network of thin-walled sinusoids lined by a single layer of endothelial cells, which are underlaid by a discontinuous basement membrane and adventitial cells. Within the interstitium lie clusters of hematopoietic cells and fat cells. Differentiated blood cells enter the circulation by transcellular migration through the endothelial cells. The normal marrow is organized in subtle, but important, ways. For example, normal megakaryocytes lie next to sinusoids and extend cytoplasmic processes that bud off into the bloodstream to produce platelets, while red cell precursors often surround macrophages (so-called nurse cells) that provide some of the iron needed for the synthesis of hemoglobin. Diseases that distort the marrow architecture, such as deposits of metastatic cancer or granulomatous disease, can cause the abnormal release of immature precursors into the peripheral blood, a finding that is referred to as leukoerythroblastosis
- The bone marrow is a unique microenvironment that supports the orderly proliferation, differentiation, and release of blood cells. It is filled with a network of thin-walled sinusoids lined by a single layer of endothelial cells, which are underlaid by a discontinuous basement membrane and adventitial cells. Within the interstitium lie clusters of hematopoietic cells and fat cells. Differentiated blood cells enter the circulation by transcellular migration through the endothelial cells. The normal marrow is organized in subtle, but important, ways. For example, normal megakaryocytes lie next to sinusoids and extend cytoplasmic processes that bud off into the bloodstream to produce platelets, while red cell precursors often surround macrophages (so-called nurse cells) that provide some of the iron needed for the synthesis of hemoglobin. Diseases that distort the marrow architecture, such as deposits of metastatic cancer or granulomatous disease, can cause the abnormal release of immature precursors into the peripheral blood, a finding that is referred to as leukoerythroblastosis.
- Extreme reduction / complete disappearance of granulocytes in the blood.
- Antibodies form against drug or its metabolite by its combination with a protein on the surface of neutrophils. (Hapten + Granulocyte Protein)=Neoantigen Resulting in stimulation of immune system with antibody production.