Plasma cell neoplasms represent a spectrum of diseases characterized by abnormal plasma cell proliferation and monoclonal immunoglobulin production. Multiple myeloma is the most common and clinically significant plasma cell neoplasm, presenting as multiple tumor masses of neoplastic plasma cells scattered throughout the skeletal system. Other related conditions include monoclonal gammopathy of undetermined significance (MGUS), Waldenstrom macroglobulinemia, solitary plasmacytoma, and heavy chain disease.
This document discusses leukemias and provides information about leukemoid reactions. It defines a leukemoid reaction as a high white blood cell count with neutrophilia usually in response to infection, which can mimic chronic myelogenous leukemia or acute myeloid leukemia. The document notes that serum leukocyte alkaline phosphatase is normally elevated in leukemoid reactions, distinguishing it from CML where it is depressed. Features suggesting a leukemoid reaction rather than leukemia include toxic granulation, a high LAP score, and an obvious cause of the neutrophilia such as infection. The document provides several potential causes of leukemoid reactions and discusses methods for distinguishing leukemoid reactions from leukemia.
This document provides an overview of hemolytic anemia, including definitions, pathogenesis, classification, clinical features, laboratory findings, and approaches. Hemolytic anemia is characterized by increased red blood cell destruction. It can be hereditary or acquired. Specific hereditary forms discussed include hereditary spherocytosis, elliptocytosis, and pyropoikilocytosis, which are caused by red blood cell membrane defects. Clinical features may include pallor, jaundice, splenomegaly, and gallstones. Laboratory findings aid in diagnosis and include peripheral smear showing abnormal red blood cells, reticulocytosis, and elevated bilirubin. The document also discusses hemolytic anemia evaluation and differential diagnoses.
Waldenstrom macroglobulinemia (WM) is a rare type of non-Hodgkin lymphoma where abnormal lymphocytes in the bone marrow produce too much IgM protein, thickening the blood. This causes weakness, fever, enlarged lymph nodes, and other symptoms. Doctors diagnose WM through blood tests, bone marrow biopsies, and imaging to detect IgM protein and bone marrow changes. Treatment options include chemotherapy, plasma exchange, biotherapy, and sometimes radiation therapy, as current treatments do not usually cure WM but rather control it by periods of treatment and breaks as the disease returns.
The document discusses various myeloproliferative neoplasms (MPNs) including classic MPNs such as polycythemia vera, essential thrombocythemia, and primary myelofibrosis as well as atypical MPNs. It provides details on the diagnostic criteria, signs and symptoms, genetic mutations involved, and treatment approaches for these different MPNs. Chronic myelogenous leukemia is also examined as it represents a distinct MPN characterized by the Philadelphia chromosome genetic abnormality.
technique of preparing imprint smear# comparision with frozen sections# application and its role in thyroid ,paathyroid,breast,skin,head and neck and mucinous tumors# advantages and limitations
The document discusses myeloproliferative disorders (MPDs), which are clonal stem cell disorders characterized by increased blood cell counts and enlarged spleen and bone marrow. It focuses on chronic myeloid leukemia (CML), describing it as a MPD caused by a genetic mutation that results in uncontrolled white blood cell growth. CML progresses through chronic, accelerated, and blast phases, with symptoms ranging from fatigue to organ enlargement. Diagnosis involves blood and bone marrow tests detecting elevated white and platelet counts and the Philadelphia chromosome genetic abnormality associated with CML.
This document provides an overview of myelodysplastic syndrome (MDS). It discusses the history and changing definitions of MDS, current WHO classification, clinical features, pathogenesis involving genetic and epigenetic abnormalities, dysplastic changes seen in the bone marrow, and identification of blast cells. MDS is a heterogenous stem cell disorder characterized by cytopenias, dysplasia, and increased risk of acute myeloid leukemia. The disease results from acquired mutations in hematopoietic stem/progenitor cells and involves dysregulated apoptosis, ineffective hematopoiesis, and genetic and epigenetic changes.
This document discusses leukemias and provides information about leukemoid reactions. It defines a leukemoid reaction as a high white blood cell count with neutrophilia usually in response to infection, which can mimic chronic myelogenous leukemia or acute myeloid leukemia. The document notes that serum leukocyte alkaline phosphatase is normally elevated in leukemoid reactions, distinguishing it from CML where it is depressed. Features suggesting a leukemoid reaction rather than leukemia include toxic granulation, a high LAP score, and an obvious cause of the neutrophilia such as infection. The document provides several potential causes of leukemoid reactions and discusses methods for distinguishing leukemoid reactions from leukemia.
This document provides an overview of hemolytic anemia, including definitions, pathogenesis, classification, clinical features, laboratory findings, and approaches. Hemolytic anemia is characterized by increased red blood cell destruction. It can be hereditary or acquired. Specific hereditary forms discussed include hereditary spherocytosis, elliptocytosis, and pyropoikilocytosis, which are caused by red blood cell membrane defects. Clinical features may include pallor, jaundice, splenomegaly, and gallstones. Laboratory findings aid in diagnosis and include peripheral smear showing abnormal red blood cells, reticulocytosis, and elevated bilirubin. The document also discusses hemolytic anemia evaluation and differential diagnoses.
Waldenstrom macroglobulinemia (WM) is a rare type of non-Hodgkin lymphoma where abnormal lymphocytes in the bone marrow produce too much IgM protein, thickening the blood. This causes weakness, fever, enlarged lymph nodes, and other symptoms. Doctors diagnose WM through blood tests, bone marrow biopsies, and imaging to detect IgM protein and bone marrow changes. Treatment options include chemotherapy, plasma exchange, biotherapy, and sometimes radiation therapy, as current treatments do not usually cure WM but rather control it by periods of treatment and breaks as the disease returns.
The document discusses various myeloproliferative neoplasms (MPNs) including classic MPNs such as polycythemia vera, essential thrombocythemia, and primary myelofibrosis as well as atypical MPNs. It provides details on the diagnostic criteria, signs and symptoms, genetic mutations involved, and treatment approaches for these different MPNs. Chronic myelogenous leukemia is also examined as it represents a distinct MPN characterized by the Philadelphia chromosome genetic abnormality.
technique of preparing imprint smear# comparision with frozen sections# application and its role in thyroid ,paathyroid,breast,skin,head and neck and mucinous tumors# advantages and limitations
The document discusses myeloproliferative disorders (MPDs), which are clonal stem cell disorders characterized by increased blood cell counts and enlarged spleen and bone marrow. It focuses on chronic myeloid leukemia (CML), describing it as a MPD caused by a genetic mutation that results in uncontrolled white blood cell growth. CML progresses through chronic, accelerated, and blast phases, with symptoms ranging from fatigue to organ enlargement. Diagnosis involves blood and bone marrow tests detecting elevated white and platelet counts and the Philadelphia chromosome genetic abnormality associated with CML.
This document provides an overview of myelodysplastic syndrome (MDS). It discusses the history and changing definitions of MDS, current WHO classification, clinical features, pathogenesis involving genetic and epigenetic abnormalities, dysplastic changes seen in the bone marrow, and identification of blast cells. MDS is a heterogenous stem cell disorder characterized by cytopenias, dysplasia, and increased risk of acute myeloid leukemia. The disease results from acquired mutations in hematopoietic stem/progenitor cells and involves dysregulated apoptosis, ineffective hematopoiesis, and genetic and epigenetic changes.
This document discusses the classification and diagnosis of non-Hodgkin lymphoma (NHL) using cytology. It begins by outlining the WHO classification system for lymphomas which incorporates cytology, immunophenotype, genetics, and clinical findings. Flow cytometry is the main diagnostic tool for NHL classification. The document then describes the normal histology and cytology of lymph nodes before focusing on the cytological features and immunophenotypes of common B-cell and T-cell NHL subtypes such as follicular lymphoma, mantle cell lymphoma, and marginal zone lymphoma. Accurate classification requires integrating cytological findings with immunophenotyping and genetics.
Hereditary spherocytosis is an inherited condition related to RBC destruction. its diagnosis is require to differentiate immune hemolytic anemia and G-6-P-D deficiency anemia
Special stains are used in hematology and cytology to identify specific molecules that are not visible with routine staining. They can determine if certain molecules are present or absent, where they are located, and how much is present. Examples of special stains discussed in the document include fetal hemoglobin stain, Prussian blue for sideroblasts, methyl violet for Heinz bodies, Papanicolaou stain in cytology, and Masson Fontana silver stain to identify melanin and argentaffin granules. These stains help characterize and diagnose blood and cellular abnormalities.
D dimer test and sample collection procedure anjalatchi
Normally D-dimer levels are undetectable or detectable at very low levels, but they rise sharply when the body breaks down clots. D-dimer tests help in ruling out pulmonary embolisms in hospitalised Covid-19 patients
Sansar Babu Tiwari presented a slide presentation on hematology focusing on eosinophilia. The presentation included:
1. Analysis of a peripheral blood smear showing 53% eosinophils, with normal RBC and platelet morphology.
2. A discussion of eosinophil morphology, differentiation, and granule composition. Eosinophils arise from bone marrow and traffic to tissues, where they play roles in immunity and tissue damage.
3. An overview of the causes of eosinophilia, which can be secondary/reactive to conditions like parasites, allergies, and drugs, or primary/clonal due to disorders like cancers, idiopathic hypereosin
This document defines urine casts and describes their types. Urine casts are cylindrical structures formed by condensation of proteins in the renal tubules. There are cellular casts containing cells and acellular casts without cells. The most common acellular cast is the hyaline cast, seen in conditions like fever and dehydration. Granular casts indicate conditions like kidney disease. Waxy casts signify advanced kidney disease. Cellular casts contain red blood cells, white blood cells, or epithelial cells, indicating various pathological conditions.
This document discusses the evaluation of lymphadenopathy. It outlines the key steps in evaluation which include determining the size and characteristics of palpable lymph nodes, identifying accompanying symptoms, examining the distribution of enlarged lymph nodes, and considering epidemiological factors. A variety of diagnostic tests are described based on the location and suspected causes of lymphadenopathy including blood tests, imaging studies, biopsies and cultures. The goal of evaluation is to arrive at an accurate diagnosis and guide further treatment.
Sickle cell anemia is a hereditary blood disorder caused by a genetic mutation that results in abnormal hemoglobin and sickle-shaped red blood cells. It affects approximately 90,000-100,000 people in the United States, primarily those of African descent. Symptoms include episodes of severe pain, organ damage, infections, and stroke due to sickled cells blocking blood flow. While there is no cure, treatment focuses on pain management, blood transfusions, medications, and in some cases stem cell transplants or gene therapy.
This document discusses various hemoglobin derivatives that are formed due to ligands binding to the heme part of hemoglobin or changes in the iron oxidation state. It specifically describes carboxyhemoglobin which is formed when hemoglobin binds to carbon monoxide, preventing oxygen transport. Other derivatives discussed include methemoglobin and sulfhemoglobin. The document also examines hemoglobinopathies such as sickle cell anemia, caused by a single amino acid substitution, and thalassemias which involve impaired globin chain synthesis. Clinical manifestations and treatments for various hemoglobin derivatives and disorders are summarized.
This document discusses Perls stain, which is used to identify iron deposits in tissue samples. It provides background on pigments in living tissue, including endogenous pigments like hemosiderin and hematogenous pigments. The history of Prussian blue and its use as Perls stain is described. The principle of the stain is that hydrochloric acid releases ferric ions from hemosiderin, which then react with potassium ferrocyanide to form insoluble Prussian blue pigment. Staining protocols, quality control, and clinical applications for identifying iron deposits in organs are covered.
This document discusses sideroblastic anemia, which is caused by an abnormal accumulation of iron in the mitochondria of red blood cell precursors called ring sideroblasts. There are several types of sideroblastic anemia, including hereditary forms caused by genetic mutations and acquired forms caused by drugs, toxins, or diseases. The condition is characterized by ring sideroblasts seen on bone marrow biopsy along with ineffective red blood cell production and iron overload. Treatment depends on the underlying cause but may include blood transfusions, vitamin supplements, iron chelation therapy, or bone marrow transplant in severe cases.
This document discusses the classification and characteristics of various types of non-Hodgkin lymphoma (NHL). It describes the historical classifications of NHL from the 1940s to the current 2008 WHO classification. It then provides details on specific NHL subtypes, including small lymphocytic lymphoma/chronic lymphocytic leukemia, follicular lymphoma, mantle cell lymphoma, and marginal zone B-cell lymphoma. For each subtype, it discusses immunophenotype, genetic abnormalities, clinical features, histopathology, immunostaining patterns, and differential diagnosis.
This document provides an overview of bronchoalveolar cytology. It discusses the history of exfoliative cytology and various sampling methods used including sputum, bronchial brushings, bronchial washings, and bronchoalveolar lavage. The cytology of normal respiratory tract cells and benign cellular changes are described. Infections that can be identified include pneumonia, tuberculosis, herpes simplex, cytomegalovirus, adenovirus, and various fungal infections. The characteristic cytological findings of these conditions are summarized.
Hemolytic anemia is characterized by accelerated red blood cell destruction and vigorous blood regeneration. It can be classified as intrinsic or extrinsic, congenital or acquired. The site of red blood cell destruction can be intravascular or extravascular. Common causes of hemolytic anemia include hereditary spherocytosis, thalassemias, sickle cell anemia, glucose-6-phosphate dehydrogenase deficiency, paroxysmal nocturnal hemoglobinuria, and immune-mediated hemolytic anemia. Evaluation of hemolytic anemia involves determining whether the anemia is hemolytic, the site of red blood cell destruction, the etiology, and severity through blood smears, reticulocyte counts, LDH and
Experiment No - 3 aims to perform an Alcian blue stain to identify acid mucopolysaccharides in a fungal sample such as Cryptococcus neoformans. The Alcian blue stain uses a blue dye that binds to acid mucopolysaccharides, allowing identification of fungi containing these substances under a microscope. The process involves staining tissue sections with Alcian blue solution followed by rinsing in distilled water and dehydration using concentrated alcohol solutions to preserve the stained sample.
This document discusses sideroblastic anemia, a type of anemia where the bone marrow produces abnormal red blood cells called ringed sideroblasts that cannot incorporate iron efficiently. Ringed sideroblasts have iron granules accumulated in mitochondria around the nucleus. Sideroblastic anemia can be hereditary or acquired through toxins, drugs, nutritional deficiencies, or other conditions. Symptoms include paleness, dizziness, fatigue, and organ enlargement. Diagnosis involves blood tests showing low hemoglobin and iron studies. Bone marrow biopsies reveal excess ringed sideroblasts. Treatment depends on the severity and cause but may include blood transfusions, iron chelation therapy, vitamins, or
Hemolytic anemia occurs when the bone marrow is unable to increase production to make up for the premature destruction of red blood cells and the abnormal breakdown of red blood cells either in the blood vessels (intravascular hemolysis) or elsewhere in the body (extravascular). It has numerous possible causes, ranging from relatively harmless to life-threatening. The general classification of hemolytic anemia is either inherited or acquired. Treatment depends on the cause and nature of the breakdown.Symptoms of hemolytic anemia are similar to other forms of anemia (fatigue and shortness of breath), but in addition the breakdown of red cells leads to jaundice and increases the risk of particular long-term complications such as gallstones and pulmonary hypertension.
1. Cytology of body fluids involves examining fluids from various body cavities including cerebrospinal fluid, pleural fluid, peritoneal fluid, pericardial fluid, and synovial fluid. Specimen collection and laboratory analysis includes gross examination, cell counts, biochemical analysis, and microscopic examination.
2. Transudates and exudates are distinguished based on characteristics like protein content and cell differentials. Infection, inflammation, and malignancy can be identified by analyzing changes in fluid characteristics.
3. Cytology of body fluids provides diagnostic information for conditions affecting various organ systems. Proper collection and analysis of physical and chemical properties aids in differential diagnosis.
This document discusses endometrial hyperplasia and carcinoma. It defines endometrial hyperplasia as an abnormal increase in the endometrium that can progress to carcinoma. Causes include prolonged estrogen stimulation without progesterone. Hyperplasia is classified as simple or complex depending on morphological features and risk of progression. Endometrial carcinoma is more common in postmenopausal women and often presents with abnormal bleeding. Risk factors include obesity, diabetes, and infertility. The document also discusses leiomyoma and leiomyosarcoma of the uterus, defining them, describing their morphology and microscopic features, and distinguishing between them.
Haemolytic anaemias are a group of anemias caused by the premature breakdown of red blood cells in the bloodstream or spleen. There are two main types - intrinsic defects that cause red blood cell damage from within, such as hereditary spherocytosis, and extrinsic defects that cause damage from outside factors like immune mediated hemolysis. Symptoms include anemia, jaundice, splenomegaly and gallstones. Laboratory tests show signs of increased red blood cell breakdown like elevated bilirubin and LDH, as well as signs of the bone marrow attempting to compensate with reticulocytosis and nucleated red blood cells. Intravascular hemolysis specifically causes hemoglobinemia,
Multiple myeloma is a cancer of plasma cells that produce abnormal proteins called monoclonal proteins (M proteins). The most common M protein is IgG, followed by IgA. In some cases, only free light chains are produced. Free light chains can cause kidney damage and are detected in urine as Bence Jones proteins. Myeloma cells secrete cytokines like IL-6 that support their growth and cause bone damage. Patients experience symptoms like bone pain, fractures, anemia, and kidney problems. Diagnosis involves tests to detect M proteins in blood and urine and check for organ damage and immune suppression.
This document discusses the classification and diagnosis of non-Hodgkin lymphoma (NHL) using cytology. It begins by outlining the WHO classification system for lymphomas which incorporates cytology, immunophenotype, genetics, and clinical findings. Flow cytometry is the main diagnostic tool for NHL classification. The document then describes the normal histology and cytology of lymph nodes before focusing on the cytological features and immunophenotypes of common B-cell and T-cell NHL subtypes such as follicular lymphoma, mantle cell lymphoma, and marginal zone lymphoma. Accurate classification requires integrating cytological findings with immunophenotyping and genetics.
Hereditary spherocytosis is an inherited condition related to RBC destruction. its diagnosis is require to differentiate immune hemolytic anemia and G-6-P-D deficiency anemia
Special stains are used in hematology and cytology to identify specific molecules that are not visible with routine staining. They can determine if certain molecules are present or absent, where they are located, and how much is present. Examples of special stains discussed in the document include fetal hemoglobin stain, Prussian blue for sideroblasts, methyl violet for Heinz bodies, Papanicolaou stain in cytology, and Masson Fontana silver stain to identify melanin and argentaffin granules. These stains help characterize and diagnose blood and cellular abnormalities.
D dimer test and sample collection procedure anjalatchi
Normally D-dimer levels are undetectable or detectable at very low levels, but they rise sharply when the body breaks down clots. D-dimer tests help in ruling out pulmonary embolisms in hospitalised Covid-19 patients
Sansar Babu Tiwari presented a slide presentation on hematology focusing on eosinophilia. The presentation included:
1. Analysis of a peripheral blood smear showing 53% eosinophils, with normal RBC and platelet morphology.
2. A discussion of eosinophil morphology, differentiation, and granule composition. Eosinophils arise from bone marrow and traffic to tissues, where they play roles in immunity and tissue damage.
3. An overview of the causes of eosinophilia, which can be secondary/reactive to conditions like parasites, allergies, and drugs, or primary/clonal due to disorders like cancers, idiopathic hypereosin
This document defines urine casts and describes their types. Urine casts are cylindrical structures formed by condensation of proteins in the renal tubules. There are cellular casts containing cells and acellular casts without cells. The most common acellular cast is the hyaline cast, seen in conditions like fever and dehydration. Granular casts indicate conditions like kidney disease. Waxy casts signify advanced kidney disease. Cellular casts contain red blood cells, white blood cells, or epithelial cells, indicating various pathological conditions.
This document discusses the evaluation of lymphadenopathy. It outlines the key steps in evaluation which include determining the size and characteristics of palpable lymph nodes, identifying accompanying symptoms, examining the distribution of enlarged lymph nodes, and considering epidemiological factors. A variety of diagnostic tests are described based on the location and suspected causes of lymphadenopathy including blood tests, imaging studies, biopsies and cultures. The goal of evaluation is to arrive at an accurate diagnosis and guide further treatment.
Sickle cell anemia is a hereditary blood disorder caused by a genetic mutation that results in abnormal hemoglobin and sickle-shaped red blood cells. It affects approximately 90,000-100,000 people in the United States, primarily those of African descent. Symptoms include episodes of severe pain, organ damage, infections, and stroke due to sickled cells blocking blood flow. While there is no cure, treatment focuses on pain management, blood transfusions, medications, and in some cases stem cell transplants or gene therapy.
This document discusses various hemoglobin derivatives that are formed due to ligands binding to the heme part of hemoglobin or changes in the iron oxidation state. It specifically describes carboxyhemoglobin which is formed when hemoglobin binds to carbon monoxide, preventing oxygen transport. Other derivatives discussed include methemoglobin and sulfhemoglobin. The document also examines hemoglobinopathies such as sickle cell anemia, caused by a single amino acid substitution, and thalassemias which involve impaired globin chain synthesis. Clinical manifestations and treatments for various hemoglobin derivatives and disorders are summarized.
This document discusses Perls stain, which is used to identify iron deposits in tissue samples. It provides background on pigments in living tissue, including endogenous pigments like hemosiderin and hematogenous pigments. The history of Prussian blue and its use as Perls stain is described. The principle of the stain is that hydrochloric acid releases ferric ions from hemosiderin, which then react with potassium ferrocyanide to form insoluble Prussian blue pigment. Staining protocols, quality control, and clinical applications for identifying iron deposits in organs are covered.
This document discusses sideroblastic anemia, which is caused by an abnormal accumulation of iron in the mitochondria of red blood cell precursors called ring sideroblasts. There are several types of sideroblastic anemia, including hereditary forms caused by genetic mutations and acquired forms caused by drugs, toxins, or diseases. The condition is characterized by ring sideroblasts seen on bone marrow biopsy along with ineffective red blood cell production and iron overload. Treatment depends on the underlying cause but may include blood transfusions, vitamin supplements, iron chelation therapy, or bone marrow transplant in severe cases.
This document discusses the classification and characteristics of various types of non-Hodgkin lymphoma (NHL). It describes the historical classifications of NHL from the 1940s to the current 2008 WHO classification. It then provides details on specific NHL subtypes, including small lymphocytic lymphoma/chronic lymphocytic leukemia, follicular lymphoma, mantle cell lymphoma, and marginal zone B-cell lymphoma. For each subtype, it discusses immunophenotype, genetic abnormalities, clinical features, histopathology, immunostaining patterns, and differential diagnosis.
This document provides an overview of bronchoalveolar cytology. It discusses the history of exfoliative cytology and various sampling methods used including sputum, bronchial brushings, bronchial washings, and bronchoalveolar lavage. The cytology of normal respiratory tract cells and benign cellular changes are described. Infections that can be identified include pneumonia, tuberculosis, herpes simplex, cytomegalovirus, adenovirus, and various fungal infections. The characteristic cytological findings of these conditions are summarized.
Hemolytic anemia is characterized by accelerated red blood cell destruction and vigorous blood regeneration. It can be classified as intrinsic or extrinsic, congenital or acquired. The site of red blood cell destruction can be intravascular or extravascular. Common causes of hemolytic anemia include hereditary spherocytosis, thalassemias, sickle cell anemia, glucose-6-phosphate dehydrogenase deficiency, paroxysmal nocturnal hemoglobinuria, and immune-mediated hemolytic anemia. Evaluation of hemolytic anemia involves determining whether the anemia is hemolytic, the site of red blood cell destruction, the etiology, and severity through blood smears, reticulocyte counts, LDH and
Experiment No - 3 aims to perform an Alcian blue stain to identify acid mucopolysaccharides in a fungal sample such as Cryptococcus neoformans. The Alcian blue stain uses a blue dye that binds to acid mucopolysaccharides, allowing identification of fungi containing these substances under a microscope. The process involves staining tissue sections with Alcian blue solution followed by rinsing in distilled water and dehydration using concentrated alcohol solutions to preserve the stained sample.
This document discusses sideroblastic anemia, a type of anemia where the bone marrow produces abnormal red blood cells called ringed sideroblasts that cannot incorporate iron efficiently. Ringed sideroblasts have iron granules accumulated in mitochondria around the nucleus. Sideroblastic anemia can be hereditary or acquired through toxins, drugs, nutritional deficiencies, or other conditions. Symptoms include paleness, dizziness, fatigue, and organ enlargement. Diagnosis involves blood tests showing low hemoglobin and iron studies. Bone marrow biopsies reveal excess ringed sideroblasts. Treatment depends on the severity and cause but may include blood transfusions, iron chelation therapy, vitamins, or
Hemolytic anemia occurs when the bone marrow is unable to increase production to make up for the premature destruction of red blood cells and the abnormal breakdown of red blood cells either in the blood vessels (intravascular hemolysis) or elsewhere in the body (extravascular). It has numerous possible causes, ranging from relatively harmless to life-threatening. The general classification of hemolytic anemia is either inherited or acquired. Treatment depends on the cause and nature of the breakdown.Symptoms of hemolytic anemia are similar to other forms of anemia (fatigue and shortness of breath), but in addition the breakdown of red cells leads to jaundice and increases the risk of particular long-term complications such as gallstones and pulmonary hypertension.
1. Cytology of body fluids involves examining fluids from various body cavities including cerebrospinal fluid, pleural fluid, peritoneal fluid, pericardial fluid, and synovial fluid. Specimen collection and laboratory analysis includes gross examination, cell counts, biochemical analysis, and microscopic examination.
2. Transudates and exudates are distinguished based on characteristics like protein content and cell differentials. Infection, inflammation, and malignancy can be identified by analyzing changes in fluid characteristics.
3. Cytology of body fluids provides diagnostic information for conditions affecting various organ systems. Proper collection and analysis of physical and chemical properties aids in differential diagnosis.
This document discusses endometrial hyperplasia and carcinoma. It defines endometrial hyperplasia as an abnormal increase in the endometrium that can progress to carcinoma. Causes include prolonged estrogen stimulation without progesterone. Hyperplasia is classified as simple or complex depending on morphological features and risk of progression. Endometrial carcinoma is more common in postmenopausal women and often presents with abnormal bleeding. Risk factors include obesity, diabetes, and infertility. The document also discusses leiomyoma and leiomyosarcoma of the uterus, defining them, describing their morphology and microscopic features, and distinguishing between them.
Haemolytic anaemias are a group of anemias caused by the premature breakdown of red blood cells in the bloodstream or spleen. There are two main types - intrinsic defects that cause red blood cell damage from within, such as hereditary spherocytosis, and extrinsic defects that cause damage from outside factors like immune mediated hemolysis. Symptoms include anemia, jaundice, splenomegaly and gallstones. Laboratory tests show signs of increased red blood cell breakdown like elevated bilirubin and LDH, as well as signs of the bone marrow attempting to compensate with reticulocytosis and nucleated red blood cells. Intravascular hemolysis specifically causes hemoglobinemia,
Multiple myeloma is a cancer of plasma cells that produce abnormal proteins called monoclonal proteins (M proteins). The most common M protein is IgG, followed by IgA. In some cases, only free light chains are produced. Free light chains can cause kidney damage and are detected in urine as Bence Jones proteins. Myeloma cells secrete cytokines like IL-6 that support their growth and cause bone damage. Patients experience symptoms like bone pain, fractures, anemia, and kidney problems. Diagnosis involves tests to detect M proteins in blood and urine and check for organ damage and immune suppression.
Plasma cell dyscrasias are a group of disorders characterized by the abnormal proliferation of plasma cells that produce a monoclonal immunoglobulin or paraprotein. The most common types are multiple myeloma, monoclonal gammopathy of undetermined significance, Waldenström macroglobulinemia, and primary amyloidosis. Multiple myeloma is defined as the neoplastic proliferation of plasma cells in the bone marrow that secrete a monoclonal protein, commonly resulting in osteolytic bone lesions, hypercalcemia, renal insufficiency, and anemia. Diagnosis requires the presence of clonal bone marrow plasmacytosis along with other clinical or laboratory features. Treatment options continue to advance but currently include chemotherapy, st
Monoclonal gammopathies of undetermined significanceDrChirag Parmar
Monoclonal gammopathies of undetermined significance (MGUS) is an asymptomatic pre-malignant disorder characterized by a monoclonal protein level <3 g/dL, bone marrow plasma cells <10%, and no organ damage from the plasma cell disorder. MGUS has a risk of progression to multiple myeloma, amyloidosis, or other related disorders. Larger M-protein level, IgM or IgA type, and abnormal bone marrow plasma cells or serum free light chain ratio indicate a higher risk of progression. MGUS is typically detected incidentally during workup for suspected multiple myeloma. Management involves monitoring for progression through regular bloodwork and testing.
ACUTE MYELOID LEUKEMIA is a neoplastic disease characterized by
infiltration of the blood,
bone marrow, and
proliferative, clonal undifferentiated cells of the hematopoietic system.
Plasma cell disorders are a group of lymphoid neoplasms involving the expansion of a single plasma cell clone secreting monoclonal immunoglobulins. Multiple myeloma is a malignant plasma cell disorder characterized by proliferation of plasma cells in the bone marrow, resulting in anemia, bone lesions, hypercalcemia and renal failure. Treatment involves alkylating agents, glucocorticoids, immunomodulatory drugs and proteasome inhibitors. New targeted therapies and personalized treatment approaches based on disease risk factors are improving outcomes.
Multiple myeloma is a cancer of plasma cells that produces abnormal proteins. It most commonly affects people over age 65 and is more common in African populations. Symptoms include bone pain, infections, anemia, kidney problems, and neurological issues. Diagnosis requires the presence of clonal plasma cells in bone marrow, monoclonal proteins in blood or urine, or biomarkers of malignancy. Initial tests evaluate for paraproteins, organ damage, tumor burden, and prognosis.
Plasma cell disorders are characterized by the disproportionate proliferation of a single clone of plasma cells resulting in monoclonal immunoglobulins. The most common types are monoclonal gammopathy of undetermined significance (MGUS), multiple myeloma, and solitary plasmacytoma. Diagnosis involves detecting the monoclonal protein by serum and urine protein electrophoresis and bone marrow biopsy. Risk stratification uses tools like ISS staging and FISH. Treatment depends on disease stage and eligibility for stem cell transplant, and may include chemotherapy, corticosteroids, immunomodulatory drugs, proteasome inhibitors, and autologous stem cell transplant.
This document provides information on multiple myeloma. Key points include:
- Multiple myeloma is a neoplastic proliferation of plasma cells producing monoclonal immunoglobulins that can cause symptoms.
- It occurs more commonly in older adults, blacks, and those with radiation/chemical exposure. Common signs are anemia, bone pain, elevated creatinine, and hypercalcemia.
- Diagnosis requires clonal plasma cells ≥10% on bone marrow biopsy or related end organ damage like kidney impairment. Staging involves tests like SPEP, UPEP, and imaging to identify bone lesions.
This document provides an overview of acute myeloid leukemia (AML). It discusses the etiology, classification, clinical features, laboratory findings, treatment including induction chemotherapy, post-remission therapy such as stem cell transplantation, and prognostic factors of AML. The key points are that AML is a cancer of the myeloid line of blood cells, its incidence increases with age, and treatment involves induction chemotherapy to achieve remission followed by post-remission therapy to prevent relapse.
The document discusses acute myeloid leukemia (AML), including its pathophysiology, signs and symptoms, laboratory diagnosis, classification, and genetic abnormalities. AML results from the uncontrolled growth of immature myeloid cells in the bone marrow, preventing normal blood cell production and leading to symptoms like infections, anemia, and bleeding. Diagnosis involves blood and bone marrow tests to identify the percentage and type of immature blast cells present and any genetic mutations driving the cancer.
Multiple myeloma is a malignant plasma cell disorder characterized by a monoclonal paraprotein, bone lesions, and excess plasma cells in the bone marrow. It has an incidence of approximately 50 cases per million population and occurs more commonly in black individuals and males. The cause is unknown but involves abnormal plasma cells secreting an immunoglobulin. Symptoms include bone pain, bone marrow failure, infections, and renal failure in some cases. Laboratory tests show anemia, elevated sedimentation rate, paraprotein, increased or abnormal free light chains, and lytic bone lesions on imaging. Related disorders include monoclonal gammopathy of undetermined significance, solitary plasmacytoma, plasma cell leukemia, and amyloidosis.
Multiple myeloma is a cancer of plasma cells that results in overproduction of monoclonal proteins. It most commonly affects people over age 60 and accounts for 10-15% of hematologic cancers. The malignant plasma cells accumulate in the bone marrow and cause bone lesions through secretion of cytokines that increase osteoclast activity. Diagnosis requires the presence of clonal plasma cells or monoclonal proteins in addition to other criteria. Staging systems evaluate disease severity based on blood counts, calcium levels, bone lesions, and monoclonal protein levels. Treatment may include chemotherapy, steroids, autologous stem cell transplant, immunomodulatory drugs, and management of complications like renal failure, bone lesions, and infections.
This document discusses multiple myeloma, a plasma cell disorder. It begins with an overview of plasma cell disorders and defines multiple myeloma. It then covers the epidemiology, etiology, pathophysiology, clinical features, diagnostic tests including serum protein electrophoresis and immunofixation, bone marrow examination, skeletal survey, staging, prognostic factors. It also discusses related conditions like monoclonal gammopathy of undetermined significance, smoldering myeloma, non-secretory myeloma, solitary plasmacytoma, extramedullary plasmacytoma. It concludes with discussing criteria for diagnosing multiple myeloma and initial treatment approaches.
Plasma cell dyscrasias are a group of disorders characterized by the proliferation of plasma cells that secrete monoclonal immunoglobulins (M proteins). This includes conditions ranging from benign monoclonal gammopathy of unknown significance (MGUS) to malignant multiple myeloma. Multiple myeloma is diagnosed based on the presence of a monoclonal protein, clonal plasma cells in bone marrow, and end organ damage like hypercalcemia, renal insufficiency, anemia, or lytic bone lesions. It involves the pathological proliferation of plasma cells in the bone marrow that can cause osteolytic bone lesions, hypercalcemia, renal failure, and immunosuppression. Prognosis is worse in cases with deletions of chromosomes 13 or 17
Plasma cell neoplasms are clonal proliferations of plasma cells that produce monoclonal proteins. The key types are plasma cell myeloma, monoclonal gammopathy of undetermined significance, and plasmacytoma. Plasma cell myeloma is characterized by clonal plasma cell proliferation in the bone marrow causing osteolytic lesions and organ dysfunction. Diagnosis involves identifying monoclonal proteins by serum and urine protein electrophoresis and bone marrow biopsy showing clonal plasma cell infiltration. Genetic testing can further classify myeloma into hyperdiploid and non-hyperdiploid subtypes associated with different prognoses.
Multiple myeloma - Etiopathogenesis, Clinical features, Advances in ManagementChetan Ganteppanavar
Multiple myeloma is a cancer of plasma cells that accumulate in the bone marrow. It causes anemia, bone lesions, high calcium levels, and kidney damage. The disease arises from post-germinal center plasma cells and is characterized by genetic abnormalities. Myeloma cells interact with the bone marrow microenvironment to gain growth and drug resistance advantages. Treatment involves systemic therapy to control disease progression and supportive care for complications. High-dose chemotherapy with autologous stem cell transplantation is the standard initial treatment for eligible patients.
This document provides information about multiple myeloma, including its definition, epidemiology, pathogenesis, clinical presentation, diagnostic criteria, staging system, imaging, laboratory findings, and treatment options. Key points include:
- Multiple myeloma is a neoplastic plasma cell disorder characterized by clonal proliferation of malignant plasma cells in the bone marrow.
- It accounts for 1% of cancers and 13% of hematological malignancies in Western countries. Median age at diagnosis is 70 years.
- Pathogenesis involves genetic alterations in plasma cells following activation in lymph nodes, resulting in monoclonal protein production and bone marrow homing.
- Clinical features include bone lesions, hypercalcemia, renal impairment, anemia, and infections.
Hysterectomy is the surgical removal of the uterus. There are different types depending on what organs are removed, including total hysterectomy where the uterus and cervix are removed, and subtotal where only the uterus is removed. It can be performed through open abdominal surgery, laparoscopic abdominal surgery, or vaginally. Hysterectomy is commonly performed to treat conditions like fibroids, endometriosis, uterine prolapse, or cancers of the cervix or uterus. The procedure involves preparing the surgical site, making incisions, clamping and cutting ligaments, and removing the uterus through the vagina. Post-operative complications can include pelvic hemorrhage, injury to surrounding organs, or prolapse.
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Dic and vitamin k deficiency pathologyAshish965416
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Plasma cell myeloma pathology (1)
1. h . d.~
Heavy-c a1n 1sease
• Rare disorder
• Bone marrow shows variable increase in plasma cells
• In Heavy chain disease, there is synthesis and secretion of free H chain
fragments.
• It is seen in a diverse group of disorders including
• CLUSLL,
• Lymphoplasmacytic lymphoma,
• An unusual small bowel lymphoma that occurs in malnourished populations.
2. Waldenstrom macroglobulinemia
(Lymphoplasmacytic lymphoma)
• It is rare B cell lymphoproliferative disorder, characterised by
lymphoplasmacytic proliferation in marrow with secretion of lgM
Monoclonal protein
• Classic features are anemia, lymphadenopathy, hepatosplenomegaly &
features of hyperviscosity syndrome t,
• WHO classification has grouped it under lymphoplasmacytic lymphoma
• So, WM is lymphoplasmacytic lymphoma with bone marrow involvement &
lgM monoclonal gammopathy.
3. • It inevitably progresses to multiple myeloma, although
progression can take IO- 20 years o►longer.
• Progression to classic MM is commoner in patients with
solitary osseous plasmacytoma then in extraosseous
plasmacytomas.
4. Solitary Myeloma (Plasmacytoma)
•About 3-5% of plasma cell neoplasms present as a solitary lesion of
either bone or soft tissue.
• The bony lesions, with single localised collection of plasma cells in
bone, tend to occur in the same lo~tions as in multiple myeloma.
• Extraosseous lesions- in the lungs, oronasopharynx or nasal
sinuses.
• Modest elevations of M proteins in the blood or urine may be found
in some patients.
6. MGUS Vs Smoldering MM Vs Multiple Myeloma
Investigations MGUS
Bone marrow <10%
plasma cells
M component <30g/L
Lytic lesions in No bony lesions
bones
Myeloma related Not present
organ damage/
CRAB
Myeloma defining Not present
event
Smoldering
MM
>10-60%
>30g/L
No bl.'y
lesions
Not present
Not present
Multiple myeloma
>60°/4 clonal or >10%
clonal plasma cells
with CRAB/ MOE
>35g/L
Present
Present
Present
7. Indolent myeloma
• Have upto 3 lytic bone lesions without bone pain
• Marrow plasmacytosis I0-30 % ~
• Mcomponent at intermediate levels
• No anemia, Normal calcium & creatinine levels
8. Asymptomatic/ Smoldering MM
• It is an intermediate stage between MGUS and MM, (formerly known as
smoldering multiple myeloma). ~
• Clonal bone marrow plasmacytosis: I0-30%
• Serum Mcomponent >3gm%
• Patients are asymptomatic, without any anemia or lytic bone lesions,
• No myeloma related end organ damage (CRAB)
• 75% of patients progress to MM ov,
er a period of 15 years
9. • Approx I% of patients with MGUS progress to an overt muftipfe
myefoma per year. Therefore, it is considered pre-neopfastic
condition.
• Life long foHow up with serum M component levefs and Bence Jones
protein in urine is warranted.
10. Monoclonal Gammopathy of
Undetermined Significance (MGUS)
• MGUS is a relatively benign proliferation of plasma cells resulting in secretion of
Monoclonal proteins
• It is the m/c plasma cell dyscrasia, occurring in about 3-5% of patients > 70 yrs of
age.
• Patients with MGUS have
• <3 gm/dl of monoclonal protein in the serum
• No Bence Jones proteinuria,
• Clonal BM plasma cells < I0%,
• Patients r asymptomatic, with no features of myeloma associated end organ damage,
• No bone lesions on skeletal survey.
11. CLINICAL VARIANTS
• Non-secretory myeloma: rare (I%), myeloma cells synthesize lgs but do not
secrete lgs in plasma, so, lg levels are not increased, therefore M component is absent
• lg is demonstrated in cytoplasm of myeloma cells by IF or lmmunoperoxidase
studies
• Have low incidence of renal insufficiency
• Lytic bone IEt!ons are present, bone marrow reveals increase in plasma cells.
• Plasma cell leukemia:when plasma cells in PBF have a count >2xI0
9
/L or >20% of
differential count.
-Represent terminal stage of MM.
12. Treatment
• Despite advancement in therapy of myeloma, it is still incurable disease
• Asymptomatic myeloma patients do not require therapy
• The main aim is to have prolonged progression free survival &
symptomatic improvement.
• Treatment is started if there is evidence of end organ damage (CRAB)
• Melphalan, ~ednisolone
• Bisphosphonates (inhibitors of osteoclast mediated bone resorption)
• Bone marrow stem cell transplantation.
13. Prognosis
• Prognosis is variable; median survival is 4-7 years.
• Patients with multiple bony lesions, if untreated, rarely survive for more than 6-12
months,
• Translocations involving cyclin DI are associated with a good outcome,
• Poor prognostic factors are
• Deletions of~3q, I7p, and the t(4; 14)
• High tumour load, Higher stage of MM
• Diffuse pattern of marrow involvement
• Raised ~2 microglobulin levels, High S. creatinine
14. Durie-Salmon staging system
• International staging system, developed over 40 years ago to provide
a practical way to measure MM tumor burden
• Patients are categorized as stage I, II or Ill depending on the degree
of anemia. hypercalcemia. levels of M protein in the serum and urine.
and bone lesions.
~
• In addition, stages are further divided into category A or B if serum
creatinine is <2 mg% or ~2mg%.
15. Diagnosis
• The diagnosis depends on the
• Identification of abnormal monoclonal plasma cells in the
bone marrow,
• M protein in the serum or urine on electrophoresis,
• Evidence of end-organ damage .
• Clinical picture consistent with MM
16. Serum protein electrophoresis
Albumin ~ a2 P y
A.NORMAL SERUM PATTERN
Polydooal immuooglobolins
('Middle panel')
Albumin ~ ~ p
B.BENIGN POLYCLONAL
GAMMOPATHY
y
Myeloma(M)-band
('Bottom panel')
Albumin ~ <iz
C,MONOCLONAL GAMMOPATHY
(PLASMA CELL MYELOMA)
y
17. -
AL a Cllt
T.,. • - 6.AO_._.
A.a. - 3_s,
_, - 0..23
_, - o.-
• - '.30
,... - o ....
•
~or••Ial Electrophoretic Pattern
•Pe1·formed on serum or urlne
•In this procedure, proteins separated by electrophoresis within gel, are reacted with speclflc antisera.
After extensive washing ofthe gel, only proteins that are cross-linked b;v antlsera are retained.
-
18. • Urine examination for presence of Bence Jones proteins.
• Electrophoretic studies on Serum or urine: to screen patient for
presence of monoclonal immunoglobin or M band
• In 99% of patients, there is increased levels of M lgs in the blood and/or
light chains, i.e. Bence Jones proteins, in the urine
• lmmunofixation: done to confirm the suspected monoclonal lg and classify
it. The most common serum monoclonal lg is lgG (in 55% of pts), lgA-25%.
• Serum free light chain assay,
• Imaging studies incluiJng X-rays, MRI, CT Scan to identify bone lesions.
19. Investigations
• PBF:
• Anemia; normocytic normochromic with rouleaux formation
• TLC, DLC is normal, Raised ESR
• Platelet count normal with increased bleeding time
• Bone marrow shows increased number of plasma cells (30-90%),
• Raised S. calcium due to extensive osteolytic lesions
• Renal function tests are abnormal,
~
• Raised ~2 microglobunn levels indicating high tumour load.
20. Clinical features
• In early stages, patient complains of weakness, fatigue & weight loss,
• Later, various clinical manifestations are
• Pallor
• Bone pains, pathological fractures, leading to Hypercalcemia due
to bone resorption,
• Neurological manifestations like confusion, lethargy
~• Recurrent infections (due to decreased production of normal lg)
• Bence Jones proteinuria, Renal failure
• Hypergammaglobinemia, Hyperviscosity in lgM myeloma
21. Clinical features
• Insidious onset
•The clinical features are due to the effects of
• Infiltration of organs, particularly bo~es, by the neoplastic
plasma cells;
• Production of excessive immunoglobulins,
•The suppression of normal humoral immunity.
22. •With progressive disease, plasma cell infiltrate is seen in spleen,
liver, kidneys, lungs, lymph nodes or other soft tissues.
23. • Cytologic variants are d/t abnormal synthesis and
secretion of lg, which leads to intracellular accumulatio
of intact or partially degraded lg. Such variants include
• Flame cells with fiery red cytoplasm;
• Mott cells having multiple, blue, grapelike cytoplasmi
droplets;
~
• Russell bodies (have cytopfasmic inclusions) or
• Dutcher bodies (nuclear inclusions)
, I
•
24. • Neoplastic plasma cells like t'eir benign counterpart usually
have a perinuclear clearing and an eccentrically placed nucleus.
• C. .
• ••
•
25. • Bone marrow examination reveals increased number of
monoclonal plasma cells, plasmablasts (with vesicular nuclear
chromatin & a prominent single nucleolus), or bizarre,
multinucleated cells (I0-90%).
• Plasma cells infiltrate the marrow diffusely or in sheets that
com lace normal hemato oietic elements.
,, .
• ·-(.
I
!Vo
26. ----------=----------------
• High level of serum M proteins causes red cells in smears of
peripheral blood to appear as a stack of coins, referred to as
rouleaux formation. Although characteristic, it is not specific.
• Rarely, tumor cells flood the peripheral blood, giving rise to
Plasma cell leukemia. . ~
3
• - ·
; . . .........
✓~ .
~ -. o<i)
(._r' 0 •
-
~ ~
27.
28. Morphology
• MM presents most often as multifocal, destructive bone lesions
composed of plasma cells throughout the skeletal system.
• Most commonly affects axial skeleton bones & other bones including
•Vertebral Column, Ribs, Skull, Pelvis, Femur, Clavicle & Scapula.
•The bone lesions appear radiographically as punched-out defects,
usually 1-4 cm in diameter. ~
~
• Lesions begin in the medullary cavity, erode cancellous bone and
progressively destroy the bony cortex, often leading to pathologic
fractures.
29. Revised IMWG criteria for diagnosis of Multiple
Myeloma (20 14)
• Out of proposed 3 myeloma defining events (MDEs) one
must be present regardless of presence or absence of CRAB
features. These are:
• ~60% clonal plasma cells in BM
• Involved/ uninvolved free light chain ratio > I00
· >I focal lesion on MRI (~Smm in size)
30. Diagnostic criteria for multiple myeloma
(IMVfG 2011)
• Clonal plasma cells ~ I 0% on bone marrow biopsy,
• Monoclonal protein in serum or urine,
• Evidence of myeloma related end organ damage (CRAB)
• HyperCalcemia (S. Ca> I I .5mg%)
• Renal insufficiency (S. Creatinine> I.9mg%)
~
• Anemia (Hb< I Ogm%)
• Lytic Bone lesions
• In absence of end organ damage, clonal plasma cells>60%
31. • The proliferation & survival of myeloma cells is dependent on
various cytokines, like IL-6, which is produced by neoplastic plasma
cells and normal stromal cells in the marrow.
• IL-6 and MIP-1 a, activate osteoclasts, resulting in bone destruction
(the major pathological feature of MM).
• Other factors released from tumor cells, like modulators of Wnt
pathways, a~ potent inhibitors of osteoblast function.
• The net effect is a marked increase in bone resorption, which leads
to hypercalcemia and pathologic fractures.
32. Etiology and Pathogenesis
• MM is associated with rearrangements involving lg Heavy chain gene
locus and various proto-oncogenes.
• Translocations involving chr 14 with oncogene cyclin DI on chr I Iq 13
and cyclin D3 on chr 6p2 I.
• Deletions of chromosome 17p (poor outcome).
• Plasma cell w.ukemia (a highly aggressive form of the ds) is associated
with rearrangements involving MYC gene.
• Mutations involving components of the NF-KB pathway (which supports
B-cell survival).
33. Multiple Myeloma
• Multiple myeloma is a malignant neoplasm of plasma cells; B cell
neoplasm.
• Usually presents as multiple tumor masses of neoplastic plasma
cells scattered throughout the skeletal system.
•Accounts for I% of all malignancies & I0-20% of all hematologic
malignancits.
• It is chiefly a disease of the elderly, with a peak age of incidence
around 65-70 years with slight male preponderence.
35. ✓ Benign proliferations are important as there is increased risk
of their transformation to MM
✓ Of all the plasma cell dyscrasias, Multiple Myeloma is the
commonest & clinically most important.
36. Plasma cell Neoplasms/ dyscrasias
• Plasma cell dyscrasias are subclassified into 2 groups:
I. Malignant proliferations:
✓ Multiple myeloma
✓ Waldenstrom macroglobulinemia
✓ Solitary Plasmacytoma
✓ Heavy chain disease
2. Relative~ benign proliferations:
✓ Monoclonal Gammopathy of Uncertain Significance (MGUS)
✓ Primary amyloidosis
✓ POEMS syndrome- osteosclerotic myeloma
37. Plasma cell Neoplasms
• Monoclonal lg, or M component refers to structurally homogenous
proteins synthesized by neoplastic plasma cells.
• These have high MW (~ 1,60,000), so they are restricted to plasma and
extracellular fluid and are not excreted in urine in absence of glomerular
damage.
• Neoplastic plasma cells synthesize complete immunoglobulins of same class,
with excess of light chains or rarely, heavy chains.
• In contrast, Polyclonal proteins are lgs of different types and are produced
in response to antigenic stimulation by various plasma cell clones during
infections, inflammatory conditions etc.
38. Plasma cell Neoplasms
• In immunoglobulins produced by normal plasma cells, the
production and coupling of heavy (H) and light (L) chains
are tightly balanced, but neoplastic plasma cells usually
synthesize excess of light chains or rarely, ~ chains.
• Light chains produced are either Kappa or Lambda
(never both) & Heavy chains are either alpha, gamma or
mu depending on particular class of immunoglobulins.
• Free light chains are small in size, so are excreted in
urine. These light chains are known as Bence Jones
Light
Chain
Heavy
Chain
39. Plasma cell Neoplasms
• Normal plasma cells transform into malignant plasma cells
(known as myeloma cells) and produce large quantities of
an abnormal immunoglobulins called Monoclonal proteins
(M component).
•Collectively, the plasma cell neoplasms account for about 15%
of the deaths caused by lymphoid neoplasms.
40. Plasma cell Neoplasms
• Plasma cell neoplasmsare abnormal
pro1
1iferation of plasma cells and represent a
spectrum of diseases called plasma cell
dyscrasias.
• It is associated with production of
monoclonal immunoglobulins (lgs), which
serve as tumour markers.
• Also known as monoclonal gammopathy
paraproteinemias, dysproteinemia.
llultiplll,eloN
!lont-
41. Plasma cells
• Plasma cells, also called plasma B cells, are
white blood cells that originate in the bone
marrow and secrete large quantities of proteins
called antib?ies in response to specific
substances called antigens.
• These cells are large lymphocytes with abundant
basophilic cytoplasm, an eccentric nucleus,
perinuclear halo with characteristic cartwheel
or clock face arrangement.
I
42. Blood stem cell
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Red blood
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