Sickle Cell Anemia
Early twentieth-century descriptions of sickle cell anemia in Western literature noted that sickling was related to low levels of oxygen, and before mid-century Linus Pauling and Harvey Itano demonstrated through protein electrophoresis that the hemoglobin of patients with the disease is different than that of normal individuals. In the subsequent decades, a more complete understanding of the disease was culled. According to modern medicine, sickle cell anemia is caused by a point mutation in one nucleotide within the sequence of 438 bases coding for the hemoglobin beta chain. A shift in the seventeenth nucleotide from a thymine base to an adenine base in the DNA of genes encoding hemoglobin causes a switch in the sixth amino acid, from glutamic acid to valine, in people with sickle cell anemia. The change of this one amino acid results in hemoglobin (generally referred to as hemoglobin S) that responds to oxygen deficiency by stacking into filaments and clustering in red blood cells containing the mutated protein in such a way that their shape is distorted. Initially, cells experiencing the distortion, or sickling, can resume their normal shape when they are reintroduced to oxygen. However, over time, they lose this ability and the sickle shape becomes permanent.
Blood flow from the body (aka the systemic circuit) returns to the heart via two large vessels known as the superior and inferior venae cavae. In some cases, a patient is born with an absent inferior vena cava; which is a problem if you want all the deoxygenated blood from your lower half to return to the heart. When this happens, the azygous vein, one of the veins that drains into the superior vena cava, can be used instead. This vein will be much larger than normal due to the need for increased blood flow. Instead of draining into the inferior vena cava, blood vessels in the lower half of the body drain into the enlarged azygous vein.
Hematopoietic stem cells (HSC) are multipotent stem cells that give rise to all the blood cell types from the myeloid (monocytes and macrophages, neutrophils, basophils, eosinophils, erythrocytes, megakaryocytes/ platelets, dendritic cells), and lymphoid lineages (T-cells, B-cells, NK-cells).
HSC = hematopoietic stem cell
Progenitor = progenitor cell
L-blast = lymphoblast,lymphocyte
Mo-blast = monoblast, monocyte, myeloblast
Pro-M = promyelocyte, myelocyte
Meta-M = metamyelocyte, neutrophil, eosinophil, basophil
Pro-E = proerythroblast
Baso-E = basophilic erythroblast
poly-E = polychromatic erythroblast
Ortho-E = Orthochromatic, erythroblast, erythrocyte, promegakaryocyte, megakaryocyte, platelet
Acute lymphoblastic leukemia is a malignant cancer of the bone marrow in which early lymphoid precursors proliferate replaced the normal hematopoietic cells of the marrow. Acute lymphoblastic leukemia do from the other malignant lymphoid disorders by the help of immunopheno cells, which is like B- or T-precursor cells.Cytochemistry, Cytogenetic and Immunochemistry indicator aid in categorizing the malignant lymphoid clone.
Coloured scanning electron micrograph (SEM) of a blood clot (thrombus) in an arteriole (small blood vessel) of a salivary gland. Red blood cells (erythrocytes, red) are trapped within a fibrin protein mesh (thread-like), which is formed in response to chemicals secreted by platelets, fragments of white blood cells (large, round). Clots are formed in response to cardiovascular disease or injuries to blood vessels. Magnification: x1650 when printed 10 centimetres wide.
DIC With Microangiopathic Hemolytic Anemia
34 y/o female, Hb 8.6 g/dL, MCV 104.5 fL, MCHC 32.8 g/dL, platelets 11,000/uL, WBC 59,000/uL. Patient had a history of disseminated non-small cell carcinoma of the lung. She presented to the ER in extremis and expired within a few hours of admission.
Morphology: Thrombocytopenia, 4+ schizocytes, 3+ spherocytes, 4+ polychromatophilic rbc.
Diagnosis: Disseminated carcinomatosis with DIC