Etiology, pathogenesis:
Histology:
The marrow is normo- or hypercellular with increased normoblastic erythropoiesis, which is organised in clusters. Erytropoietic precursors mature, often there is a left shift. Other hematopoietic lineages are normal.
Etiology, pathogenesis:
Histology:
The marrow is normo- or hypercellular with increased myelopoiesis, where neutrophils predominate. Myelopoietic precursors mature, often there is a left shift, however the number of myeloblasts is normal. Myeloid hyperplasia may sometimes be so extensive that it resembles hemoblastosis (leukemic reaction). Other lineages are either normal or also display reactive changes (for example an increased number of megakaryocytes caused by an inflammation).
Pictures
Myeloid hyperplasia:
Hyperplasia of granulopoesis, bone marrow, HE 100x (73026)
Hyperplasia of granulopoesis, bone marrow, PAS 100x (73027)
Etiology, pathogenesis:
Is most often caused by allergic disorders or parasitic infections, but other causes are also possible, for example. autoimmune diseases, dermathology deseases, Hodgkin's disease. When the cause is not identified, we talk of the hypereosinophilic syndrome which is near to myeloproliferative disorders.
Histology:
The marrow is normo- or hypercellular with an elevated eosinophil count. Other lineages remain normal.
Etiology, pathogenesis:
Histology:
The marrow is normocellular with an elevated megakaryocyte count. The megakaryocytes are separate and do not form larger clusters, there is a majority of immature hypolobulated forms. Other lineages are either normal or with reactive changes (myeloid hyperplasia caused by inflammation)
Pictures
Reactive thrombocytosis:
Reactive thrombocytosis, bone marrow, PAS 100x (73005)
Introduction:
Bone marrow failure either affects all hematopoietic lienages (aplastic anemia) or selectively only one of them (pure red cell aplasia, agranulocytosis, amegakaryocytic thrombocytopenia).
Etiology, pathogenesis:
Overall bone marrow failure may be congenital (such as Fanconi's syndrome) or aquired after exposition to myelotoxic agents (chemotherapeutics and other drugs, toxins, some (especially viral) infections etc.
Histology:
The marrow is hypocellular (0 – 30%) with reduced trilinear hematopoiesis. The depression of myelopiesis and megakaryocytes is usually more distinct than erytropoietic depression, therefore erytropoiesis relatively predominates. Lymphocytes, plasma cells, mast cells and macrophages with abundant iron deposits are reactively increased in number.
Classification:
Pure red cell aplasia may be acute or chronic. Chronic aplasia is either congenital (for example Blackfan-Diamond syndrome) or acquired (thymoma, systemic lupus erythematosus, autoimmune thyreoiditis).
Histology:
Bone marrow is normocellular or only slightly hypocellular with normal megakaryocytes and normal myelopoiesis. Erythropoietic islands are missing, separate normoblasts are sparsly dispersed. Lymphocytosis and plasmocytosis are usually reactive, the number of mast cells and macrophages with abundant iron deposits is increased.
Introduction:
Agranulocytosis rarely occures on its own, more often it exists as part of aplastic anemia.
Etiology, pathogenesis:
Autoimmune myelopoiesis inhibition, autoimmune diseases (rheumatoid arthritis, systemic lupus erythematosus), tumorous diseases (systemic mastocytosis), drugs, toxins.
Histology:
Bone marrow is hypocellular, with normal megakaryocytes and normal erythropoiesis. Myelopoiesis is significantly decreased or missing completely. Reactive lymphocytosis and plasmocytosis is usually present.
Introduction:
Amegakaryocytic thrombocytopenia is either congenital or acquired (amegakaryocytic thrombocytopenic purpura).
Introduction:
Autoimmune diseases, drugs, toxins, hepatic cirrhosis, lymphoproliferative disorders and other malignacies.
Histology:
Bone marrow is normocellular, erythropoiesis and myelopoiesis are normal. Megakaryocytes are substantially decreased in number or sometimes even completely missing.
Introduction:
Anemia is an abnormally low number of circulating erythrocytes leading to low hemoglobin levels in peripheral blood (less than 130 g/l in men or 120 g/l in women).
The classification of anemias is complex and since it is a part of hematology, this text will focus on basic types of anemias and the morphological changes they cause in the bone marrow.
Clinical signs:
Classification:
Introduction:
Posthemorrhagic anemia is caused by a sudden massive blood loss for example in severe injury (acute posthemorrhagic anemia) or repeated or prolonged blood losses (chronic posthemorrhagic anemia).
Histology:
Histology:
Introduction:
Anemia which arises from abnormal DNA synthesis caused by vitamin B12 or folate deficiencis. This leads to abnormal nuclear maturation of the hematopoietic cells and ineffective erythropoiesis. The anemia caused by B12 deficiency is also called pernicious anemia (apart from anemia, other symptoms such as atrophic glossitis, atrophic gastritis and neurologic disorders are often present).
Clinical signs:
Histology:
Pictures
Megaloblastic anemia, bone marrow:
Megaloblastic anemia, bone marrow, HE 100x (72608)
Introduction:
Anemia caused by inadeqaute iron deposits resulting from insufficient iron intake or increased loss (repeated or prolonged bleeding).
Clinical signs:
Microcytic hypochromic anemia.
Histology:
Introduction:
Anemia caused by decreased erythropoietin production in chronic kidney disorders.
Introduction:
Anemias caused by chronic diseases (chronic infection, chronic non-infectius inflammation, malignancies, chronic kidney and hepatic diseases).
Clinical signs:
Normocytic normochromic anemia.
Histology:
Introduction:
Anemias caused by excesive hemolysis. Hemolytic anemias are either congenital or acquired.
Clinical signs:
Normocytic normochromoc anemias.
Histology: