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Manual differential. Blood differential test |
Manual differential.What’s in a Differential?
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. The absolute numbers for total WBC count and each type of leukocyte are in thousands per cubic millimeter or alternatively, per microliter. In the above example, cell size as volume is compared with granularity and lobularity to categorize the WBCs. In the example below, WBC size and cell complexity are compared to categorize the cell population present to produce an automated WBC differential 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.
The following terms are used in describing the morphology of WBC's, as seen on a standard peripheral blood smear:. 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:. 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:.
An increase in the number of circulating lymphocytes may normally be observed in infants and young children. Pathologic processes with lymphocytosis may include:. Protein can be better characterized and quantified by immunoelectrophoresis. Serum proteins are first separated in an electric field and then react with antibodies introduced in the support medium. Each arch of precipitation can then be identified and measured. WBC are classified into granulocytes, lymphocytes, and monocytes.
Granulocytes owe their name to the presence of distinct cytoplasmic granulation. Three varieties are recognized: neutrophils or polymorphonuclear granulocytes , eosinophils, and basophils.
A more primitive stem cell gives rise to lymphoid cells as well as to the myeloid precursor. Under the influence of poietins and microenvironmental factors, the stem cells evolve through a series of intermediate steps into the mature blood elements. Stem cells resemble lymphocytes morphologically. They can be recognized by growth characteristics in vitro in semisolid media containing different growth factors.
In the evolution of the neutrophilic granulocyte, the first cell identifiable morphologically is the myeloblast. As maturation progresses, the myeloblast becomes first a promyelocyte and later a myelocyte.
These developmental stages constitute predominantly a proliferative compartment, in which the cell number increases geometrically. The next form, the metamyelocyte, is unable to undergo further mitosis but transforms into a band. About half of the intravascular polymorphonuclear cells are circulating, maintaining a dynamic equilibrium with the other half, which are marginated against the vascular endothelium.
Only the circulating neutrophils are accounted for in the WBC count. The half-life of mature neutrophils in circulation is about 7 hours. They irreversibly traverse the vascular endothelium into the tissues, where they die after 1 or 2 days. The main function of neutrophilic granulocytes is phagocytosis of bacteria. This is a complex multistage process that includes engulfment of the organism, incorporation into the cytoplasm, and fusion with a lysosome where enzymes are liberated that will destroy the bacterium while a burst of energy is generated.
Eosinophils and basophils have a similar development. They are not able to reenter the blood. Heavy concentrations of eosinophils are found in the GI tract, lung, and skin. The precise function of these complex cells is not well known. They possibly play a role in defense against multicellular parasites and in limiting inflammation.
Their physiologic role is also not known with precision. In their granules they carry heparin and histamine. IgE can be found bound to their surface. Macrophages and lymphocytes are known collectively as mononuclear leukocytes. Both play important roles in cellular and humoral immunity. These cells are able to exit and reenter circulation, retaining their function. They may spend time in the tissues or in lymph nodes. The cells of the monocyte—macrophage system have their origin in the bone marrow, deriving from the CFU-GM.
In tissues, they become macrophages. Monocyte—macrophages phagocytose bacteria and particulate material, play a role in the inflammatory reaction, and are important in the immune apparatus where they process antigenic material and "communicate" with T lymphocytes through a cell—cell interaction process.
Monocytes are able to secrete interleukin, a substance that potentiates B and T lymphocytes. They participate in fibrinolysis by secreting plasminogen activators. Lymphocytes are immune cells fundamental in cellular and humoral immunity. They belong to the B b ursa or b one marrow or T t hymus systems. Both cells are morphologically indistinguishable. The B system is responsible for synthesis of antibodies.
When a B cell is properly stimulated, it proliferates first and transforms later into a plasma cell, the effector limb of the immune arch. Each B lymphocyte is able to synthesize only one species of antibody. The T system constitutes the cellular immune system and regulates the whole immune apparatus.
Several subsets of T cells can be identified with monoclonal antibodies specific against different membrane antigens.
For instance, helper T cells favor the function of B cells, whereas suppressor T cells inhibit them. Some T cells are responsible for cell-mediated cytotoxicity; natural killer NK lymphocytes are responsible for nonspecific lysis of certain cells. WBC disorders can be classified as quantitative or qualitative. In quantitative alterations all cells appear normal but are present in abnormal quantities, either in excess or in defect of normal values.
In qualitative defects, abnormal appearing cells or extrinsic cells are found in circulation. Granulocytes can be increased in circulation by four different mechanisms: increased production, decreased egress from the circulation, demargination, and release from storage compartments.
Most instances of neutrophilia are secondary to a pathologic process outside the marrow. It can occur in infectious diseases, especially acute bacterial infections; neoplasia, either affecting the myeloid system chronic myelogenous leukemia and other myeloproliferative disorders or secondary to a solid tumor paraneoplastic syndrome ; inflammation secondary to tissue necrosis, metabolic and collagen diseases, hypersensitivity reactions; hemorrhage; hemolysis; and stress. Neutropenia is due in the great majority of cases to decreased production of granulocytes.
Antineoplastic agents and extensive radiation therapy produce neutropenia almost invariably. Drugs such as phenothiazines, phenylbutazone, and allopurinol can induce neutropenia through idiosyncratic reactions. Infections, most often viral but also bacterial or rickettsial, can lower the polymorphonuclear count. Other conditions causing a decrease in WBC production include cyclic neutropenia, congenital disorders, and idiopathic neutropenia.
If peripheral consumption exceeds production, neutropenia and concomitant marrow hypercellularity will result. It can be seen in hypersplenism, Felty's syndrome, and in the presence of antineutrophil antibodies. The risk of infection increases when the absolute granulocyte count falls below per microliter. Gram-negative sepsis is common in this setting.
Qualitative abnormalities of neutrophils include functional defects in chemotaxis, phagocytosis, and bacterial killing. They can be due to extrinsic or intrinsic abnormalities of the granulocyte. Extrinsic abnormalities include treatment with antineoplastic agents and corticosteroids, deficiencies of complement and opsonizing antibody, hypophosphatemia, and sickle cell disease. Several abnormalities of cytoplasmic granulation can be found.
Toxic granules appear in the cytoplasm of neutrophils during infectious processes and represent probably phagocytic vacuoles. The May-Hegglin anomaly is characterized by large inclusion bodies in the cytoplasm of polymorphonuclear cells associated with thrombocytopenia and giant platelets. The cell is functionally normal. Monocytosis can follow chronic infectious disorders tuberculosis, brucellosis , rheumatic diseases lupus, rheumatoid arthritis , chronic inflammatory bowel disease, and some malignant processes Hodgkin's and non-Hodgkin's lymphoma.
Monocytes play an important role in other chronic granulomatous diseases: sarcoidosis, histiocytosis X, and storage diseases Gaucher's disease, Niemann—Pick disease. Eosinophilia occurs in association with hypersensitivity reactions, parasitic infestations, cancers Hodgkin's disease, eosinophilic leukemia , connective tissue disorders rheumatoid arthritis, polyarteritis nodosa , and the syndrome of pulmonary infiltrates with eosinophilia.
Basophilia can be found in chronic myelogenous leukemia and other myeloproliferative disorders, Hodgkin's disease, and some chronic inflammatory and infectious disorders. Lymphocytopenia can be seen mainly in association with several congenital diseases of the immune system or following treatment with corticosteroids, antineoplastic agents, or radiation. Lymphocytosis can accompany some infections, both acute and chronic, usually viral, Addison's disease, and autoimmune diseases.
Acute leukemia results from the malignant proliferation of cells of the myeloid acute nonlymphoblastic leukemia or ANLL or lymphoid acute lymphoblastic leukemia or ALL progeny. Untreated it is rapidly fatal. The clinical picture stems predominantly from bone marrow failure but also from infiltration of normal tissues by the leukemic cells.
Anemia produces weakness, easy fatigability, dyspnea, palpitations, orthostasis, and pallor. Granulocytopenia results in infection, often with gram-negative organisms, but also with low-grade pathogens. Thrombocytopenia is manifested as purpura: epistaxis, petechiae, easy bruisability, and gum bleeding. Infiltration of tissues results in lymphadenopathy and hepatosplenomegaly more common and more marked in ALL than ANLL , chloromas, and, in monocytic leukemia, gum hypertrophy.
In childhood ALL the long bones of the inferior limbs are predominantly affected. In the peripheral blood a normochromic normocytic anemia is found. Platelets are decreased, often to very low values. The total white cell count may be very elevated, normal, or low. In most cases blasts will be found.
These are large, immature-looking cells with a high nucleus to cytoplasm ratio. Myeloblasts have a thin, lacy chromatin and well-defined nucleoli. Monocytoid or promyelocytic features may be found in AML blasts. Lymphoblasts have a coarser chromatin with less sharply delineated nucleoli and a slightly basophilic cytoplasm with few granules. The bone marrow examination will show hypercellularity, decrease or absence of normal hemopoietic precursors, and infiltrations with blasts.
Histochemistry and cell surface markers can be helpful in these circumstances. It appears that these cells are early B cell precursors. Large mediastinal lymphadenopathy is commonly found. B cell ALL is very rare. Chronic myelogenous leukemia CML affects middle-aged patients median age at diagnosis is 40 to 45 years.
A juvenile form of the disease has been recognized. Patients present most often with signs of anemia or after finding a left upper quadrant abdominal mass. On physical examination the dominant finding is splenomegaly, which can be enormous, penetrating into the pelvis and extending across the midline. Areas of infarction can result in tenderness on areas of the splenic surface. Palpable lymph nodes are seldom greater than 1 cm in diameter. Examination of the peripheral smear confirms the diagnosis.
The anemia is mild to moderate. Platelet count may be elevated, and counts above 10 6 per microliter are not uncommon; thrombocytopenia is rare.
These platelets may be functionally impaired. The most striking abnormality is found in the white cell series. WBC counts are elevated, sometimes so that leukostasis may occur. Cells of all stages of granulopoiesis including early progenitor cells are found in the peripheral blood to the extent that it can resemble a bone marrow aspirate. Basophil and eosinophil counts are increased. The bone marrow appears hypercellular with a very heavy predominance of myeloid elements.
Megakaryocytes are increased. It results from the translocation of the long arm of chromosome 22 to chromosome 9. The cell primarily affected by the neoplastic process is an early stem cell. As a consequence, the Ph 1 chromosome can be found in neutrophils, erythroid precursors, megakaryocytes, and monocytes. Treatment of CML improves symptoms but not survival. After a median of 3 to 4 years, the disease evolves into a blastic phase that resembles an aggressive acute leukemia on clinical and laboratory grounds.
CML is a myeloproliferative disorder together with essential thrombocythemia, polycythemia vera, and agnogenic myeloid metaplasia. It is not seen in children.
In the majority of patients it results from the malignant proliferation of B lymphocytes, although occasionally a T cell CLL is found. Malignant cells resemble mature lymphocytes but have different morphologic features than their normal counterparts. Patients can be diagnosed while asymptomatic when a high lymphocyte count is found incidentally. A count higher than 15, lymphocytes per microliter is necessary to make the diagnosis.
After a variable asymptomatic period, lymphadenopathy will develop. It sometimes can be massive. Splenomegaly is common. As the disease progresses, anemia and thrombocytopenia will appear. Hypogammaglobulinemia develops in almost all patients, increasing the risk of infections, predominantly with encapsulated gram-positive organisms. Autoimmune hemolytic anemia and hypersplenism are common. The natural history of the disease is measured in years.
T cell CLL is a more aggressive disease. The skin is commonly involved and splenomegaly is seen early in the course of the disease. Multiple myeloma results from the monoclonal proliferation of a plasma cell.
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