Benign hematology lecture includes:
Tips and tricks in cbc reading, approach to anemia, approach to plat count disorders, indications of lymph node biopsy
This document provides information about Idiopathic Thrombocytopenic Purpura (ITP), including:
- ITP is a blood disorder characterized by a decreased number of platelets, which can cause easy bruising and bleeding.
- There are two main forms - acute (seen in children and resolves in <6 months) and chronic (onset at any age and lasts >6 months).
- The cause is unknown in most cases but involves antibodies destroying platelets. Diagnosis involves ruling out other causes through testing.
- Treatment options depend on severity but may include steroids, IVIg, splenectomy, thrombopoietin receptor agonists, and experimental agents.
This document contains 15 multiple choice questions about idiopathic thrombocytopenic purpura (ITP). ITP is a diagnosis of exclusion defined by premature platelet destruction and immune-mediated mechanism. It is distinguished from other causes of thrombocytopenia through testing and examination. Treatment involves steroids as first line, with splenectomy as subsequent option if steroids are ineffective. Platelet transfusions are not generally recommended for treatment of ITP but may be used to prevent bleeding in severe cases.
Polycythemia vera is a chronic myeloproliferative disorder characterized by an absolute increase in red blood cells, total blood volume, leukocytosis, thrombocytosis, and splenomegaly. It is caused by a clonal proliferation of a hematopoietic stem cell. Symptoms include headaches, visual disturbances, thrombosis, pruritus, and splenomegaly. Diagnosis involves meeting certain criteria including elevated hematocrit. Treatment involves phlebotomy to reduce red blood cell mass and hydroxyurea or interferon-alpha to reduce platelet and white blood cell counts and reduce risk of thrombosis.
Myeloproliferative neoplasms (MPNs) are a group of disorders where the bone marrow produces too many red or white blood cells. The presentation outlines the history, classification, signs and symptoms, causes related to genetic mutations like JAK2, diagnosis through blood and bone marrow tests, and treatments including medications, radiation, surgery, and stem cell transplant. MPNs include chronic myeloid leukemia, polycythemia vera, essential thrombocythemia, myelofibrosis, and rare disorders like chronic neutrophilic leukemia and mast cell disease.
1. Polycythemia vera (PV) is a chronic myeloproliferative neoplasm characterized by an overproduction of red blood cells without an identifiable stimulus. It commonly presents with erythrocytosis, splenomegaly, thrombosis, and pruritus.
2. The main cause of PV is a mutation in the JAK2 gene, but some patients have mutations in exon 12. Diagnosis requires tests to distinguish absolute from relative erythrocytosis. Treatment focuses on phlebotomy and medications to control symptoms and prevent complications.
3. Primary myelofibrosis (PMF) is a chronic myeloproliferative neoplasm involving clonal proliferation and
This document provides information about how to interpret a complete blood count (CBC). It discusses the components of blood that are analyzed in a CBC, including red blood cells, hemoglobin, white blood cells, and platelets. It describes normal ranges for CBC parameters and potential abnormalities that may be detected, such as anemia, infections, and bone marrow disorders. The CBC is presented as a relatively inexpensive test that can help diagnose various blood diseases, bone marrow conditions, and other organ abnormalities.
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.
This document discusses tumors of infancy and childhood. It begins by describing tumor-like lesions such as hamartomas and choristomas. It then discusses common benign tumors including hemangiomas, lymphangiomas, and sacrococcygeal teratomas. Malignant tumors that are discussed include leukemias, lymphomas, brain tumors, liver tumors, kidney tumors, soft tissue sarcomas, and bone tumors. Specific malignant tumors that are common in different age groups are also outlined. The document concludes by discussing characteristics of common childhood cancers like leukemia, lymphomas, brain tumors, and others.
This document provides information about Idiopathic Thrombocytopenic Purpura (ITP), including:
- ITP is a blood disorder characterized by a decreased number of platelets, which can cause easy bruising and bleeding.
- There are two main forms - acute (seen in children and resolves in <6 months) and chronic (onset at any age and lasts >6 months).
- The cause is unknown in most cases but involves antibodies destroying platelets. Diagnosis involves ruling out other causes through testing.
- Treatment options depend on severity but may include steroids, IVIg, splenectomy, thrombopoietin receptor agonists, and experimental agents.
This document contains 15 multiple choice questions about idiopathic thrombocytopenic purpura (ITP). ITP is a diagnosis of exclusion defined by premature platelet destruction and immune-mediated mechanism. It is distinguished from other causes of thrombocytopenia through testing and examination. Treatment involves steroids as first line, with splenectomy as subsequent option if steroids are ineffective. Platelet transfusions are not generally recommended for treatment of ITP but may be used to prevent bleeding in severe cases.
Polycythemia vera is a chronic myeloproliferative disorder characterized by an absolute increase in red blood cells, total blood volume, leukocytosis, thrombocytosis, and splenomegaly. It is caused by a clonal proliferation of a hematopoietic stem cell. Symptoms include headaches, visual disturbances, thrombosis, pruritus, and splenomegaly. Diagnosis involves meeting certain criteria including elevated hematocrit. Treatment involves phlebotomy to reduce red blood cell mass and hydroxyurea or interferon-alpha to reduce platelet and white blood cell counts and reduce risk of thrombosis.
Myeloproliferative neoplasms (MPNs) are a group of disorders where the bone marrow produces too many red or white blood cells. The presentation outlines the history, classification, signs and symptoms, causes related to genetic mutations like JAK2, diagnosis through blood and bone marrow tests, and treatments including medications, radiation, surgery, and stem cell transplant. MPNs include chronic myeloid leukemia, polycythemia vera, essential thrombocythemia, myelofibrosis, and rare disorders like chronic neutrophilic leukemia and mast cell disease.
1. Polycythemia vera (PV) is a chronic myeloproliferative neoplasm characterized by an overproduction of red blood cells without an identifiable stimulus. It commonly presents with erythrocytosis, splenomegaly, thrombosis, and pruritus.
2. The main cause of PV is a mutation in the JAK2 gene, but some patients have mutations in exon 12. Diagnosis requires tests to distinguish absolute from relative erythrocytosis. Treatment focuses on phlebotomy and medications to control symptoms and prevent complications.
3. Primary myelofibrosis (PMF) is a chronic myeloproliferative neoplasm involving clonal proliferation and
This document provides information about how to interpret a complete blood count (CBC). It discusses the components of blood that are analyzed in a CBC, including red blood cells, hemoglobin, white blood cells, and platelets. It describes normal ranges for CBC parameters and potential abnormalities that may be detected, such as anemia, infections, and bone marrow disorders. The CBC is presented as a relatively inexpensive test that can help diagnose various blood diseases, bone marrow conditions, and other organ abnormalities.
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.
This document discusses tumors of infancy and childhood. It begins by describing tumor-like lesions such as hamartomas and choristomas. It then discusses common benign tumors including hemangiomas, lymphangiomas, and sacrococcygeal teratomas. Malignant tumors that are discussed include leukemias, lymphomas, brain tumors, liver tumors, kidney tumors, soft tissue sarcomas, and bone tumors. Specific malignant tumors that are common in different age groups are also outlined. The document concludes by discussing characteristics of common childhood cancers like leukemia, lymphomas, brain tumors, and others.
The document provides guidelines for the diagnosis, treatment indications, response assessment, and supportive management of chronic lymphocytic leukemia (CLL). It summarizes updates to the understanding of genomic alterations in CLL like TP53 mutations and their prognostic role. It also discusses clinical staging, assessment of organomegaly and lymphadenopathy, response criteria for novel drugs, and monitoring of minimal residual disease. Diagnosis of CLL requires verification through blood smear, immunophenotyping and genetics. Prognostic markers like immunoglobulin variable gene mutational status, cytogenetics, serum markers, and immunophenotype are also covered.
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
This document provides an overview of thrombocytopenia and its causes and classification. It discusses the normal physiology of platelet production and defines thrombocytopenia. The four main causes of thrombocytopenia are outlined as artifactual, deficient platelet production, accelerated platelet destruction, and abnormal platelet distribution. Specific causes under each category are then examined in more detail over several paragraphs.
This lecture includes definitions and roles of every lab test included in a complete blood count (CBC) panel along with how to interpret high or low values of each. Provided by www.DiscountedLabs.com , a site that provides affordable blood tests to consumers in the United States without the need of a doctor's visit. https://www.discountedlabs.com/popular-tests
This document summarizes various platelet disorders including their causes, characteristics, diagnosis and treatment. It discusses decreased platelet production from bone marrow issues as well as increased platelet destruction from immune or non-immune causes. Specific disorders covered include idiopathic thrombocytopenic purpura, hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, sequestration, Kasabach-Merritt syndrome, and others. Diagnostic tests and treatment approaches are provided for each condition.
This document discusses thrombotic thrombocytopenic purpura (TTP). It begins by presenting a case of a 32-year-old woman presenting with headaches, difficulty speaking and moving her tongue, and numbness. Her exam and labs show thrombocytopenia and schistocytes. The document then discusses the differential diagnosis, epidemiology, terminology, definitions, types, presentations, investigations, and treatment of TTP, with a focus on plasma exchange therapy to remove antibodies and replace deficient ADAMTS13 protease.
Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of mature-appearing B lymphocytes in the blood, bone marrow, lymph nodes, and spleen. It is considered a clonal B cell malignancy caused by a defect in apoptosis that allows long-lived, non-cycling lymphocytes to accumulate over time. CLL cells typically express CD5, CD19, and CD23 and have mutations that dysregulate pathways controlling cell survival and apoptosis. Prognosis depends on clinical features and genetic abnormalities - deletion of 13q or mutated IgVH correlate with better prognosis while deletion of 11q or 17p indicate poorer prognosis. CLL can transform into an aggressive lymphoma called Richter's syndrome over time.
There are two main types of chronic leukemia: chronic myeloid leukemia (CML) and chronic lymphocytic leukemia (CLL). CML accounts for around 15% of leukemia cases and results from a genetic abnormality known as the Philadelphia chromosome. It commonly presents in middle age with symptoms of excessive white blood cell production. CLL is the most common chronic lymphoid leukemia, typically affecting older adults, and is characterized by the accumulation of abnormal lymphocytes in the blood and bone marrow. Staging systems such as Rai or Binet are used to determine prognosis and treatment approaches for CLL patients.
Chronic myeloid leukemia is a type of cancer that affects white blood cells. It is caused by a genetic abnormality that results in excessive production of white blood cells. There are typically no symptoms in the early chronic phase, but later symptoms may include fatigue, fever, enlarged spleen, and weight loss. Diagnosis involves blood and bone marrow tests to detect the genetic abnormality. Treatment primarily uses targeted drug therapies such as imatinib to control the disease. Without treatment, it may progress to more advanced phases with worse symptoms.
Dr. Nahar K discusses disorders of platelets, including thrombocytopenia and platelet function disorders. Platelets play a key role in hemostasis by adhering to injury sites, aggregating with other platelets to form plugs, and releasing compounds to stimulate clot formation. Disorders can be qualitative defects in platelet function or quantitative defects in platelet number. Thrombocytopenia can be caused by increased platelet destruction, disorders of platelet distribution or pooling, or decreased platelet production. A thorough history, physical exam, blood smear, and functional platelet tests are used to evaluate the cause and guide treatment if needed to prevent bleeding risks.
This document discusses the approach and management of thrombocytopenia and immune thrombocytopenic purpura (ITP). It defines thrombocytopenia and its causes, provides diagnostic criteria for ITP, and outlines treatment approaches including corticosteroids, IVIG, anti-D, thrombopoietin receptor agonists, splenectomy, rituximab, and experimental therapies. It also addresses management of severe bleeding, pregnancy-associated thrombocytopenia, and thrombocytopenia in the settings of HIV and hepatitis C infection.
This document discusses microangiopathic hemolytic anemia (MAHA) and thrombotic thrombocytopenic purpura (TTP). It recommends ordering tests like LDH, haptoglobin, reticulocyte count, and ADAMTS13 level if MAHA is suspected. ADAMTS13 levels below 10% are specific for TTP, caused by acquired or hereditary deficiencies of the von Willebrand factor cleaving protease ADAMTS13. Initial treatment for suspected TTP includes plasma exchange while waiting for test results. Differential diagnoses are discussed including thrombotic microangiopathies, autoimmune hemolytic anemia, immune thrombocytopenic purpura, and aplastic
Hematology is the study of blood and blood-forming organs. Key topics covered include hematopoiesis, the production of blood cells; normal blood volume and components; red blood cell production and function; white blood cell types and roles; platelet function; and common blood disorders such as anemias, leukemias, and bleeding/clotting disorders. Diseases are discussed in relation to abnormal cell counts or functions that can cause symptoms like fatigue, bleeding, or infection.
This document provides information on chronic myelogenous leukemia (CML), including its definition, history, epidemiology, etiology, pathogenesis, clinical features, diagnosis, disease course, treatment, and more. Some key points:
- CML is a stem cell disease characterized by increased white blood cells, anemia, splenomegaly, and the Philadelphia chromosome.
- It has three phases: chronic, accelerated, and blast crisis. Treatment depends on the phase and may include tyrosine kinase inhibitors like imatinib, interferon, chemotherapy, and stem cell transplantation.
- The disease is caused by the BCR-ABL fusion gene which results in uncontrolled tyrosine kinase activity and increased proliferation of
Simple way to explain primary haemostatic anomalies
Easy to teach
Platelet function as well as disorders of granules and their release reaction. A reader will find a few better resources.
Outline is from introduction to explanation of every single anomaly. Happy reading
The document discusses chronic lymphocytic leukemia (CLL), including its definition, epidemiology, etiology, pathogenesis, clinical symptoms, diagnosis, staging, prognosis, and treatment. Some key points:
- CLL is characterized by the proliferation and accumulation of small, mature lymphocytes in the blood, bone marrow, and lymphoid tissues. It most commonly affects elderly adults.
- Diagnosis is based on blood cell counts and immunophenotyping of lymphocytes. Prognosis depends on factors like clinical stage, genomic abnormalities, and biomarker expression levels.
- Treatment involves chemotherapy, chemoimmunotherapy, targeted therapies, and supportive care. The appropriate treatment approach depends on a patient's risk
The document discusses thrombocytopenia, defined as a platelet count below 150,000/mm3. Various causes of thrombocytopenia are covered, including decreased production, immune-mediated causes, and sequestration. A history and physical exam can help diagnose the cause, while tests like CBC, smear, and bone marrow exam provide further information. Treatment depends on the underlying condition but may involve steroids, IVIG, splenectomy, or platelet transfusions.
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.
1) The document discusses Acute Myeloid Leukemia (AML), including its classification, epidemiology, etiology, clinical presentation, laboratory findings, and specific subtypes defined by genetic abnormalities such as AML with t(8;21), inv(16), and t(15;17).
2) It describes the key features of different AML subtypes including their morphology, immunophenotype, genetics, and prognosis. Specific attention is given to abnormal cells, staining patterns, and genetic translocations that characterize each subtype.
3) The FAB and WHO classification systems are introduced and compared, noting the WHO system incorporates immunophenotyping, cytogenetics, and molecular characteristics
Interactive talk on common hematological and oncological emergencies - which if not noticed early can lead to irreversible complications and death .
Intended to be used for educational purposes for the fertile minds in medicine .
The document provides guidelines for the diagnosis, treatment indications, response assessment, and supportive management of chronic lymphocytic leukemia (CLL). It summarizes updates to the understanding of genomic alterations in CLL like TP53 mutations and their prognostic role. It also discusses clinical staging, assessment of organomegaly and lymphadenopathy, response criteria for novel drugs, and monitoring of minimal residual disease. Diagnosis of CLL requires verification through blood smear, immunophenotyping and genetics. Prognostic markers like immunoglobulin variable gene mutational status, cytogenetics, serum markers, and immunophenotype are also covered.
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
This document provides an overview of thrombocytopenia and its causes and classification. It discusses the normal physiology of platelet production and defines thrombocytopenia. The four main causes of thrombocytopenia are outlined as artifactual, deficient platelet production, accelerated platelet destruction, and abnormal platelet distribution. Specific causes under each category are then examined in more detail over several paragraphs.
This lecture includes definitions and roles of every lab test included in a complete blood count (CBC) panel along with how to interpret high or low values of each. Provided by www.DiscountedLabs.com , a site that provides affordable blood tests to consumers in the United States without the need of a doctor's visit. https://www.discountedlabs.com/popular-tests
This document summarizes various platelet disorders including their causes, characteristics, diagnosis and treatment. It discusses decreased platelet production from bone marrow issues as well as increased platelet destruction from immune or non-immune causes. Specific disorders covered include idiopathic thrombocytopenic purpura, hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, sequestration, Kasabach-Merritt syndrome, and others. Diagnostic tests and treatment approaches are provided for each condition.
This document discusses thrombotic thrombocytopenic purpura (TTP). It begins by presenting a case of a 32-year-old woman presenting with headaches, difficulty speaking and moving her tongue, and numbness. Her exam and labs show thrombocytopenia and schistocytes. The document then discusses the differential diagnosis, epidemiology, terminology, definitions, types, presentations, investigations, and treatment of TTP, with a focus on plasma exchange therapy to remove antibodies and replace deficient ADAMTS13 protease.
Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of mature-appearing B lymphocytes in the blood, bone marrow, lymph nodes, and spleen. It is considered a clonal B cell malignancy caused by a defect in apoptosis that allows long-lived, non-cycling lymphocytes to accumulate over time. CLL cells typically express CD5, CD19, and CD23 and have mutations that dysregulate pathways controlling cell survival and apoptosis. Prognosis depends on clinical features and genetic abnormalities - deletion of 13q or mutated IgVH correlate with better prognosis while deletion of 11q or 17p indicate poorer prognosis. CLL can transform into an aggressive lymphoma called Richter's syndrome over time.
There are two main types of chronic leukemia: chronic myeloid leukemia (CML) and chronic lymphocytic leukemia (CLL). CML accounts for around 15% of leukemia cases and results from a genetic abnormality known as the Philadelphia chromosome. It commonly presents in middle age with symptoms of excessive white blood cell production. CLL is the most common chronic lymphoid leukemia, typically affecting older adults, and is characterized by the accumulation of abnormal lymphocytes in the blood and bone marrow. Staging systems such as Rai or Binet are used to determine prognosis and treatment approaches for CLL patients.
Chronic myeloid leukemia is a type of cancer that affects white blood cells. It is caused by a genetic abnormality that results in excessive production of white blood cells. There are typically no symptoms in the early chronic phase, but later symptoms may include fatigue, fever, enlarged spleen, and weight loss. Diagnosis involves blood and bone marrow tests to detect the genetic abnormality. Treatment primarily uses targeted drug therapies such as imatinib to control the disease. Without treatment, it may progress to more advanced phases with worse symptoms.
Dr. Nahar K discusses disorders of platelets, including thrombocytopenia and platelet function disorders. Platelets play a key role in hemostasis by adhering to injury sites, aggregating with other platelets to form plugs, and releasing compounds to stimulate clot formation. Disorders can be qualitative defects in platelet function or quantitative defects in platelet number. Thrombocytopenia can be caused by increased platelet destruction, disorders of platelet distribution or pooling, or decreased platelet production. A thorough history, physical exam, blood smear, and functional platelet tests are used to evaluate the cause and guide treatment if needed to prevent bleeding risks.
This document discusses the approach and management of thrombocytopenia and immune thrombocytopenic purpura (ITP). It defines thrombocytopenia and its causes, provides diagnostic criteria for ITP, and outlines treatment approaches including corticosteroids, IVIG, anti-D, thrombopoietin receptor agonists, splenectomy, rituximab, and experimental therapies. It also addresses management of severe bleeding, pregnancy-associated thrombocytopenia, and thrombocytopenia in the settings of HIV and hepatitis C infection.
This document discusses microangiopathic hemolytic anemia (MAHA) and thrombotic thrombocytopenic purpura (TTP). It recommends ordering tests like LDH, haptoglobin, reticulocyte count, and ADAMTS13 level if MAHA is suspected. ADAMTS13 levels below 10% are specific for TTP, caused by acquired or hereditary deficiencies of the von Willebrand factor cleaving protease ADAMTS13. Initial treatment for suspected TTP includes plasma exchange while waiting for test results. Differential diagnoses are discussed including thrombotic microangiopathies, autoimmune hemolytic anemia, immune thrombocytopenic purpura, and aplastic
Hematology is the study of blood and blood-forming organs. Key topics covered include hematopoiesis, the production of blood cells; normal blood volume and components; red blood cell production and function; white blood cell types and roles; platelet function; and common blood disorders such as anemias, leukemias, and bleeding/clotting disorders. Diseases are discussed in relation to abnormal cell counts or functions that can cause symptoms like fatigue, bleeding, or infection.
This document provides information on chronic myelogenous leukemia (CML), including its definition, history, epidemiology, etiology, pathogenesis, clinical features, diagnosis, disease course, treatment, and more. Some key points:
- CML is a stem cell disease characterized by increased white blood cells, anemia, splenomegaly, and the Philadelphia chromosome.
- It has three phases: chronic, accelerated, and blast crisis. Treatment depends on the phase and may include tyrosine kinase inhibitors like imatinib, interferon, chemotherapy, and stem cell transplantation.
- The disease is caused by the BCR-ABL fusion gene which results in uncontrolled tyrosine kinase activity and increased proliferation of
Simple way to explain primary haemostatic anomalies
Easy to teach
Platelet function as well as disorders of granules and their release reaction. A reader will find a few better resources.
Outline is from introduction to explanation of every single anomaly. Happy reading
The document discusses chronic lymphocytic leukemia (CLL), including its definition, epidemiology, etiology, pathogenesis, clinical symptoms, diagnosis, staging, prognosis, and treatment. Some key points:
- CLL is characterized by the proliferation and accumulation of small, mature lymphocytes in the blood, bone marrow, and lymphoid tissues. It most commonly affects elderly adults.
- Diagnosis is based on blood cell counts and immunophenotyping of lymphocytes. Prognosis depends on factors like clinical stage, genomic abnormalities, and biomarker expression levels.
- Treatment involves chemotherapy, chemoimmunotherapy, targeted therapies, and supportive care. The appropriate treatment approach depends on a patient's risk
The document discusses thrombocytopenia, defined as a platelet count below 150,000/mm3. Various causes of thrombocytopenia are covered, including decreased production, immune-mediated causes, and sequestration. A history and physical exam can help diagnose the cause, while tests like CBC, smear, and bone marrow exam provide further information. Treatment depends on the underlying condition but may involve steroids, IVIG, splenectomy, or platelet transfusions.
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.
1) The document discusses Acute Myeloid Leukemia (AML), including its classification, epidemiology, etiology, clinical presentation, laboratory findings, and specific subtypes defined by genetic abnormalities such as AML with t(8;21), inv(16), and t(15;17).
2) It describes the key features of different AML subtypes including their morphology, immunophenotype, genetics, and prognosis. Specific attention is given to abnormal cells, staining patterns, and genetic translocations that characterize each subtype.
3) The FAB and WHO classification systems are introduced and compared, noting the WHO system incorporates immunophenotyping, cytogenetics, and molecular characteristics
Interactive talk on common hematological and oncological emergencies - which if not noticed early can lead to irreversible complications and death .
Intended to be used for educational purposes for the fertile minds in medicine .
Idiopathic thrombocytopenic purpura (ITP) is an immune-mediated disorder characterized by low platelet counts. It most commonly presents as bruising or bleeding in otherwise healthy children. While severe bleeding is rare, treatment may be required to raise platelet counts to prevent bleeding. For children with no or minor symptoms, the guidelines recommend initial observation over corticosteroids or IVIG due to low risk and lack of evidence for benefit of active treatment. Hospitalization is typically not required if prompt hematology follow-up can be provided.
UGIB in children can have various causes. This case discusses a 1.5 year old male presented with bloody vomiting for 2 days. His history revealed splenomegaly since 2 weeks of age, anemia, and recurrent malaria attacks. Imaging showed splenomegaly, peri-portal fibrosis, portal vein thrombosis, and collateral formation; findings suggestive of non-cirrhotic portal hypertension likely due to chronic portal vein thrombosis. The child was managed conservatively with medications while further workup including endoscopy and biopsy were pending.
approach to a bleeding child with blood disorders.pptxtsholanangmaoka
This document describes the approach to three cases of bleeding in children. Case 1 involves a 5-month-old male with intracranial bleeding and seizures who was found to have a subdural hematoma requiring surgery. Despite resuscitation efforts, the child did not survive the surgery. Case 2 is a 2-year-old male with bruising and a very low platelet count, consistent with thrombocytopenia. Case 3 involves a 1-year-old male with knee swelling and fever, who was found to have a low platelet count, consistent with disseminated intravascular coagulation. The document provides definitions of types of bleeding, the stages of hemostasis, differential diagnoses, and management strategies for bleeding
This document provides information about neonatal sepsis, including its definition, classification, causes, risk factors, clinical features, diagnostic tests, management, and prevention. Some key points:
- Neonatal sepsis is a systemic bacterial infection occurring in newborns, defined as a positive blood culture within the first month of life. It is a major cause of neonatal mortality and morbidity.
- It can be classified as early-onset (before 72 hours of life) or late-onset (after 72 hours) sepsis. Early onset is usually caused by maternal genital tract bacteria, while late onset is caused by environmental and healthcare-associated bacteria.
- Risk factors include prematurity, prolonged rupture of membranes, chorio
A 60 year old male presented with severe vomiting, diarrhea and low urine output. On examination, he had a low volume pulse and hypotension. Laboratory findings showed blood urea of 150 mg/dl and serum creatinine of 4.2 mg/dl. A kidney biopsy revealed acute tubular injury. The diagnosis is acute renal failure.
The document discusses signs and symptoms that may indicate cancer in pediatric patients and how to evaluate those signs and symptoms. It provides guidance on when to suspect cancer based on conditions that mimic cancer, common symptoms of childhood cancers, and test that should be performed during initial workup. Specific guidance is given for symptoms like fever, vomiting, headaches, lymphadenopathy and when to perform procedures like bone marrow aspiration, biopsy and imaging tests.
This document provides information on pediatric sepsis for first responders. It begins with introducing the speaker and their experience with EMS and sepsis. It then discusses the challenges of recognizing sepsis in pediatric patients and the impact EMS can have by recognizing it early and transporting patients quickly. The rest of the document covers assessment of pediatric patients for sepsis, treatment guidelines including fluid resuscitation and pressors, and discusses some screening tools and criteria for identifying sepsis. It emphasizes the ABCs (airway, breathing, circulation) approach and following treatment algorithms.
Presentation at the SRMO weekly teaching for Shellharbour Hospital ED - by Dr Mahsa Fateminayyeri, MD - trainee, who covers an approach to sepsis in the ED setting, and highlights the value of a sepsis pathway to expedite antibiotic treatment and provide early resuscitation in order to promote good outcomes
This document discusses hemophilia, von Willebrand disease, disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), and other platelet disorders. It provides information on the clinical presentation, diagnosis, and treatment of these conditions. Key points include that hemophilia A and B are sex-linked recessive disorders caused by a deficiency in coagulation factors VIII and IX respectively, and DIC is a consumptive coagulopathy caused by excessive thrombin production that requires treatment of the underlying condition.
1) Liver abscesses can be either pyogenic (caused by bacteria) or amoebic (caused by the parasite Entamoeba histolytica).
2) Pyogenic liver abscesses are more common in western countries and are usually caused by E. coli or Klebsiella pneumoniae, while amoebic liver abscesses are more common in Asia and Africa.
3) The most common causes of pyogenic liver abscesses are infections that spread from the biliary tract, while amoebic liver abscesses usually originate from ingesting cysts of E. histolytica through contaminated food or water.
- Pancytopenia in neonates is defined as hemoglobin <13g/dl in males and <12g/dl in females, absolute neutrophil count <1500 cells/mm3, and platelet count <150×103 cells/mm3.
- The causes of pancytopenia can be inherited or acquired and include aplastic anemia, myelodysplastic syndrome, infections, medications, and nutritional deficiencies.
- Clinical manifestations include fatigue, infections, bruising, and bleeding. Diagnosis involves blood tests, bone marrow biopsy, and ruling out other causes through differential diagnosis.
- Treatment depends on the underlying cause but may include blood transfusions, medications, managing infections, and stem
The document provides information on evaluating and diagnosing thrombocytopenia, including:
1) Normal platelet counts range from 150,000-450,000/microL and are slightly higher in females and younger people. Thrombocytopenia is defined as a platelet count below 150,000/microL.
2) The basic mechanisms of thrombocytopenia include decreased platelet production, ineffective production, increased destruction, increased consumption, and sequestration.
3) Diagnosing thrombocytopenia involves ruling out pseudothrombocytopenia, examining the blood counts, bone marrow, and performing additional lab tests to determine the underlying cause and guide treatment.
This patient has longstanding SLE with quiescent disease activity currently. She has a history of fetal loss and blood clots while pregnant previously. She is seeking contraceptive options other than barrier methods. Given her history of APL antibodies and blood clots, progesterone-only contraceptives like the progesterone IUD or depot medroxyprogesterone would be safest options to avoid estrogen which could increase her risk for further clotting issues.
Dental Management of Patient with Leukemia toteata
This document discusses a case of a 52-year-old female patient presenting with severe bleeding gums and bruising. It provides background information on leukemia, including that it is cancer affecting white blood cells in the bone marrow and blood. It describes the types of leukemia, signs and symptoms, diagnostic tests, and management including chemotherapy, radiation therapy, and bone marrow transplants. It also discusses dental considerations for patients with leukemia, such as preventing infection and bleeding during treatment.
The document discusses opportunistic infections (OIs) that commonly affect HIV patients. It begins by defining OIs as infections caused by pathogens that take advantage of a weakened immune system. It then lists some examples of common bacterial, viral, fungal and parasitic OIs and describes how the risk of OIs increases as CD4 cell count declines. The document focuses on describing several specific OIs in more detail, including their causative pathogens, routes of transmission, clinical manifestations, diagnosis and treatment approaches. It concludes by emphasizing that adherence to antiretroviral therapy is the best way to prevent OIs by restoring immunity.
This document contains 12 questions related to hematology for pediatric practical exams. Each question provides clinical information about a pediatric patient and asks for the diagnosis, relevant investigations, treatment, or other information. The answers are then provided, detailing the bone marrow diagnosis, differential diagnoses, inheritance patterns, prognostic factors, or other requested information for each clinical scenario.
This document discusses thrombocytopenic purpura (TP), a condition characterized by low platelet count and bruising. It describes the main types of TP, including immune (idiopathic) TP, thrombotic thrombocytopenic purpura, and drug-induced TP. Epidemiology and pathogenesis are covered. A case study demonstrates the clinical presentation and diagnosis of a 12-year-old male with immune thrombocytopenic purpura. Treatment options are outlined, including steroids, immunoglobulins, thrombopoietin receptor agonists, and splenectomy. Differential diagnoses and references are also provided.
Similar to Tips and tricks in cbc reading.pptx (20)
This document provides an overview of evaluating pediatric patients with thrombocytopenia. It defines degrees of thrombocytopenia and associated bleeding risks. The evaluation involves obtaining a detailed history, clinical assessment, and initial laboratory tests including a complete blood count and peripheral blood smear. The history aims to identify potential etiologies such as infections, drugs, recent illness or procedures. The clinical exam evaluates for signs of bleeding and possible underlying conditions. The blood tests can help determine if thrombocytopenia is real or pseudo, and provide clues to possible causes through findings on the peripheral smear. Further testing may then be guided by these initial findings.
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Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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1. Course
Benign Hematology
Mustafa Selim, MD
Lecturer of Pediatric Oncology, NCI, Cairo University – Consultant of Pediatric Oncology, CCHE - 57357 Egypt
Clinical fellowship program trainer (CCHE-57357/Dana-Farber Cancer Institute pediatric Oncology Fellowship)
17. Thrombocytopenia in a child
Tips & Tricks in
CBC reading
Labs:
• Thrombocytopenia < 150,000
• Plat clumps = pseudothrombocytopenia (plat aggregate in the syringe before
reaching the anticoagulant)
• Associated anemia or pancytopenia?
Examination and history:
• Patient is ill appearing?? → do PT, PTT, TT (DIC?)
• Congenital anomalies? (cyanotic heart, Fanconi A, DKC, TAR)
• Organomegaly or lymphadenopathy
• Drugs (sulfa, quinidine, heparin, anticonvulsants, vaccines like measles and varicella)
18. Plat< 150,000 in a child
No plat clumps
No anemia or pancytopenia
Critical ill
Macrothrombocytes
Not critical ill
No congenital anomalies or drugs
See morphology
No
Macrothrombocytes
PT, PTT, INR
↑ spleen → Malaria, portal HTN, Gaucher disease
↑ liver & lymphadenopathy → lymphoma, leukemia, MDS
Prolonged Normal
Acute febrile illness – chronic ill
Spleen size & liver size & lymph nodes
Acute fever → sepsis, EBV, CMV, HIV, parvovirus
Chronic ill → HIV,
HUS/TTP, autoimmune or
connective tissue disease
20. Immune thrombocytopenia
Tips & Tricks in
CBC reading
Past (idiopathic thrombocytopenic purpura)
Diagnosis: if the platelet counts are repeatedly below 100 × 109/µL
The detection of isolated thrombocytopenia in the presence of otherwise normal leukocyte
and erythrocyte parameters is usually sufficient for an initial diagnosis
A blood smear must always be examined.
Gender:
o In pediatric boys are more often affected than girls
o In middle age, women are more likely to develop ITP
than men. After age 60 years, men predominate again.
Pathophysiology
21. Immune thrombocytopenia
Tips & Tricks in
CBC reading
Clinical Presentation
o The central clinical symptom of ITP is the increased bleeding tendency.
o Petechiae and mucosal hemorrhages are typical.
o Many ITP patients also complain of exhaustion and fatigue, including
depressive disorders
24. Immune thrombocytopenia
Tips & Tricks in
CBC reading
Prognosis and risk indicators
Phases of the disease and treatment goals
Indications for bone marrow biopsy
25. Tips & Tricks in
CBC reading
Immune thrombocytopenia
Pre-treatment considered factors
26. Tips & Tricks in
CBC reading
Immune thrombocytopenia
First line therapy
27. Tips & Tricks in
CBC reading
Immune thrombocytopenia
o Early response: plat count ≥ 30 x 109/L and at least doubling baseline at 1 week
o Initial response: plat count ≥ 30 x 109/L and at least doubling baseline at 1 month
o Durable response: plat count ≥ 30 x 109/L and at least doubling baseline at 6 months
o Remission: plat count > 100 x 109/L at 12 months
Definition of response
28. Tips & Tricks in
CBC reading
Immune thrombocytopenia
Pre-treatment considered factors
First line therapy
o Early response: plat count ≥ 30 x 109/L and at least doubling baseline at 1 week
o Initial response: plat count ≥ 30 x 109/L and at least doubling baseline at 1 month
o Durable response: plat count ≥ 30 x 109/L and at least doubling baseline at 6 months
o Remission: plat count > 100 x 109/L at 12 months
Definition of response
29. Tips & Tricks in
CBC reading
Immune thrombocytopenia
Diagnostic workup for patients with persistent or chronic ITP
30. Tips & Tricks in
CBC reading
Second-Line Treatment
with TRAs
32. Thrombocytosis
Tips & Tricks in
CBC reading
Thrombocytosis (> 450,000)
Mild > 500,000 Moderate > 700,000
Severe > 900,000 Extreme > 1000,000
Etiology:
Primary (caused by a process that is intrinsic to megakaryocyte)
Reactive (caused by a process that is extrinsic to megakaryocyte)
Thrombocytosis in children is almost always a reactive response, most often
infectious or inflammatory (interleukin-6 & c-reactive protein).
1/3 of the circulating platelets are normally sequestrated within the spleen.
Stress like exercise or surgery are commonly cause thrombocytosis.
Down syndrome, ↑ plat is very common by the 2nd month of life for 1st year.
33. Thrombocytosis
Tips & Tricks in
CBC reading
Primary thrombocytosis is very rare:
o Familial: mutation in thrombopoietin gene (TPO) or MPL
o Acquired: Essential thrombocythemia, polycythemia vera, primary
myelofibrosis, chronic myeloid leukemia, MDS
Essential thrombocytosis is also very rare (diagnosis of exclusion).
Hematological disorders for reactive thrombocytosis:
o Iron deficiency anemia (at diagnosis or during therapy)
o Megaloblastic anemia
o Hemolysis
o Sickle hemoglobinopathies (functional asplenia→ Howell-jolly bodies)
Initial labs: cbc, retic, peripheral smear, ESR, hepatic functions, urine analysis, cxr.
34. C
• Tips & Tricks in CBC
reading
B
D
• Practical approach to
anemia
Agenda
• Plat count
abnormalities
• Lymphadenopathy
A
41. Always put yourself in the
others shoes. If you feel
that it hurts you,
it probably hurts the
person too.
42. C
• Tips & Tricks in CBC
reading
B
D
• Practical approach to
anemia
Agenda
• Plat count
abnormalities
• Lymphadenopathy
A
43. Generalized Lymphadenopathy
• Enlarged lymph nodes:
The neonate: generally, not palpable
Childhood: cervical & axillary (>1 cm) - inguinal(>1.5cm) – epitrochlear (>5 mm)
Generalized lymphadenopathy = ≥ non-contiguous lymph node groups
• History: should include
Travel (TB, histoplasmosis)
Pets (scratch and toxoplasmosis)
Allergies
Sexual (HIV)
B symptoms (fever, drenching sweats, weight loss >10% in previous 6 months)
Flu like symptoms without weight loss suggest viral infection
44. Generalized Lymphadenopathy
• Examination:
Concomitant splenomegaly suggests a systemic disorder
Massive splenomegaly & adenopathy suggestive storage disease
Tenderness, warmth, and erythema are usually due to bacterial infection
Fluctuance suggests secondary abscess formation
• Labs:
Initial screening: cbc, blood smear, ESR, LDH, uric acid, hepatic and renal functions.
CMV screening if cp suggests infection + atypical lymphocytes are noted.
Mild ↑ AST & ALT suggest viral infection
↑ uric acid, BUN, ↓ ca→ tumor lysis syndrome
Mediastinal widening on cxr → suggest malignancy or (TB – sarcoidosis)
↑ WBC, shift to left, ↑ ESR → suggest bacterial infection
45. Generalized Lymphadenopathy
• Most common infection: EBV, CMV, varicella, rubella, mumps, measles, TB,
syphilis, HIV
• Red flags for malignant nodes:
Usually are fixed, large, firm or rubbery or matted.
Painless, progressive ↑ size
Supraclavicular adenopathy
Associated pancytopenia, ↑ LDH, ↑ uric acid
• Biopsy should be done if:
If adenopathy continues to increase over 2 weeks
If adenopathy fails to resolve over 6 weeks
If B symptoms present
If lymph nodes became firm or matted or supraclavicular adenopathy
55. Blood is made of two major components:
plasma + cells.
CBC = complete blood count→ is a group of
tests that evaluate the cells that circulate in
blood, including RBCs, WBCs, and PLTs.
Collected in purple tube (EDTA)
Unit volume: per cubic millimeter (mm3) =
one microliter = µL
WHAT cbc?
56. Automated
counting
Erythrocytes Leukocytes Thrombocytes
Count 4-5.5 x 106/µL 4-11 x 106/µL 150 - 450 x 109/µL
Size 7 microns 8 – 20 microns 3 – 4 microns
Life span 120 days 7 – 10 days
• Coulter principle: electrical impedance: resistance
or change in current when cell passes between
electrodes in NaCL solution
• Flow cytometry: uses lasers to measure both forward and side scatter
• Forward scatter measures size.
• Side scatter measures granularity
57. WHY cbc?
CBC is the 1st most common investigation performed in both in-
patient and out-patient setting.
CBC is inexpensive maneuver.
CBC is available everywhere.
CBC can help in diagnosis
Blood disorders,
BM abnormalities,
Organ dysfunction
59. HOW cbc?
RBCs (4-5.5 x 106/µL) HB (normal 12-16 g/dl) Hematocrit (normal 35-45%)
Rule of 3
RBCs x 3 = HB
HB X 3= hematocrit (% of blood that is made by packed RBCs)
↑ Hematocrit
Polycythemia, diarrhea, dehydration, burn, hear or lung or kidney problems
↓ Hematocrit
Anemia, hemolysis, bleeding, nutritional deficiences
60. HOW cbc?
Reticulocytes (normal; 0.5 -1.5%)
Immature red cells containing residual RNA
Indicate rate of new RBC production.
↓ if the anemia due to BM problem.
↑ if the anemia due to problem outside the BM (eg; hemolytic anemia)
Supervital stain
61. Normal
(0.5 -1.5%)
Newborn
(2 -6%)
• Aplastic anemia
• Anemia of chronic disease
• Nutritional anemias (↓ vit B12 - ↓ folate)
• Myelodysplastic syndrome
• Cirrhotic liver
• Hemolytic anemias
• Hemorrhage
• Response to treatment
• Pregnancy
• Leukemia
Reticulocytes
Indicator of rapid RBCs production
Decreased erythropoiesis
62. • The reticulocyte count is expressed as a % of the total number of RBCs.
• 1-2% in the setting of a normal hemoglobin.
• In patients with moderate or severe anemia, the reticulocyte count may appear elevated, but
in absolute terms, it may be insufficient for the degree of anemia. Therefore, the reticulocyte
count must be corrected using the following formula:
Corrected reticulocyte count = reticulocyte % × (patient Hct/normal Hct)
• If the corrected reticulocyte count is >2%, then the bone marrow is producing RBCs at an
accelerated pace
Corrected reticulocyte count
63. • The ratio of immature reticulocytes to the total number of reticulocytes
• IRF in many situations increase before the total reticulocyte count increase
Post transplant or chemotherapy.
Monitoring the efficacy of therapy in nutritional anemia.
Evaluate optimal timing for stem cell collection following mobilization.
Immature reticulocyte fraction (IRF)
64. • MCV, mean corpuscular volume
• MCH, mean corpuscular hemoglobin
• MCHC, mean corpuscular hemoglobin concentration
• RDW, red cell distribution width
Red Blood Cell Indices
65. • MCV, mean corpuscular volume
• MCH, mean corpuscular hemoglobin
• MCHC, mean corpuscular hemoglobin concentration
• RDW, red cell distribution width
Red Blood Cell Indices
• = Mean cell volume
• Definition → is a measure of the average volume of a red blood cell
• Calculation→ MCV = Hct/RBCs x 10
Normal: 80-100 Fl (femtoliters)
High (macrocytic, >100 FI) – low (microcytic, < 80 FI)
• Some conditions that present with high MCV without megaloblastic cells. ??
• MCV can be normal with low HB?? Hypovolemic or recent hemorrhage
PS, where a normal RBC is about the size of a normal lymphocyte nucleus.
66. • MCV, mean corpuscular volume
• MCH, mean corpuscular hemoglobin
• MCHC, mean corpuscular hemoglobin concentration
• RDW, red cell distribution width
Red Blood Cell Indices
• Definition → MCH is the average weight of hemoglobin per red cells (give the color of the cell)
• Calculation→ MCH = HB / RBCs x 10
Normal: 27 - 32 pg (picogram)
High (with macrocytic anemia) – low (with microcytic anemia)
67. • MCV, mean corpuscular volume
• MCH, mean corpuscular hemoglobin
• MCHC, mean corpuscular hemoglobin concentration
• RDW, red cell distribution width
Red Blood Cell Indices
• Definition → MCHC is the average concentration of hemoglobin per erythrocyte
• Calculation→ MCHC = = HB / Hct x 100
Normal: 32 – 36%
68. • MCV, mean corpuscular volume
• MCH, mean corpuscular hemoglobin
• MCHC, mean corpuscular hemoglobin concentration
• RDW, red cell distribution width
Red Blood Cell Indices
• It is a measure of the range of variation of RBC volume that is reported as part of a standard CBC.
• Normal: 11.5 – 14.5%
• Elevated RDW in 2/3 of deficiencies of Vitamin B12 or folate.
• Elevated RDW is a hallmark of iron deficiency anemia.
• Normal in anemia of chronic disease, hereditary spherocytosis, acute blood loss, aplastic anemia.
• Elevated RDW & normal MCV→ there is a mixture of large and small RBCs.
69. • MCV, mean corpuscular volume (Hct/RBCs x 10)
• MCH, mean corpuscular hemoglobin (weight> color, HB / RBCs x 10)
• MCHC, mean corpuscular hemoglobin concentration (HB / Hct x 100)
• RDW, red cell distribution width (range of variation of RBC volume)
Red Blood Cell Indices
72. If you don’t use it, you lose it
Tips & Tricks in
CBC reading
73. C
• Tips & Tricks in CBC
reading
B
D
• Practical approach to
anemia
Agenda
• Plat count
abnormalities
• Lymphadenopathy
A
74. C
• Tips & Tricks in CBC
reading
B
D
• Practical approach to
anemia
Agenda
• Plat count
abnormalities
• Lymphadenopathy
A
75. 2
3 Ask about drug or infection history
4 The RBC indices, particularly the MCV + RDW are extremely
helpful in DD.
Do not forget
1/3 of the children with newly diagnosed leukemia will have normal total WBC, but their ANC
mostly reduced
2 The 1st step in evaluating anemia
Is to determine whether other cell lines are also affected??
4
5
1
Peripheral smear should be reviewed to ensure that there are
no errors with the automated counts.
Drugs can cause anemia, neutropenia, and thrombocytopenia like chemotherapy, trimethopri,m/sulfamethoxazole.
Acute viral infections are the most common cause anemia with thrombocytopenia or leukopenia (mild and transient, in chronic
infection like HIV and EBV)
76. Tips & Tricks in
CBC reading
Persisting abnormalities in the full blood count that remain
unexplained should prompt an opinion from a hematologist.
77. Tips & Tricks in
CBC reading
Questions
• A male patient, 8 years old,
presented to ER with URTs &
fever.
• Cbc was done as a routine
work up before giving iv 3rd
generation antibiotic
78. Tips & Tricks in
CBC reading
Questions
1. Do Peripheral smear 2. Consult hematologist 3. Reassure the family 4. Repeat cbc after 48 h
• A male patient, 8 years old,
presented to ER with URTs &
fever.
• Cbc was done as a routine
work up before giving iv 3rd
generation antibiotic
79. Tips & Tricks in
CBC reading
Questions
1. Do Peripheral smear 2. Consult hematologist 3. Reassure the family 4. Repeat cbc after 48 h
• A male patient, 8 years old,
presented to ER with URTs &
fever.
• Cbc was done as a routine
work up before giving iv 3rd
generation antibiotic
Peripheral smear: no abnormal cells. Numerous Plat clump in the smear. Suggest repeat cbc in blue top tube
Acute viral illness is the most common cause of anemia with thrombocytopenia or leukopenia (mild & transient)
83. Microcytic hypochromic Anemia
Tips & Tricks in
CBC reading
1. IDA
2. Thalassemia
3. Chronic illness or infection
4. Pb poisoning
5. Rare disorders (sideroblastic anemia, Protein caloric malnutrition,
metabolic defects of Fe absorption)
84. Microcytic anemia (↓ MCV)
↓ Fe oral or blood loss
1. History
* No HSM, Hb > 9 g/dl
↓ RBC + ↑ RDW
FH of anemia or thalassemia
Mediterranean/ Asian/ African
Trial oral Fe
↓ serum Fe, ↑𝑻𝑰𝑩𝑪,"↓ TS," ↓ ferritin, ↔ retic, ↔ bilirubin
Rare Causes
IDA
Trait
Chronic infection or inflammation
Hb
Electrophoresis
↑ RBC + ↔↑ RDW
↓ serum Fe, ↓ 𝑻𝑰𝑩𝑪, ↑ ferritin
Pb poisoning
2. Lab
Intermedia/major
* HSM, Hb < 9 g/dl
↔ ↑ serum Fe, ↔ ↑ ferritin, ↑ retic, ↑ bilirubin
Sidroblastic anemia
Metabolic defect Fe absorption & metabolism
85. Tips & Tricks in
CBC reading
1. IDA:
Confirmed by trial of oral Fe supplementation.
Not necessary to do (↓ serum Fe, ↑𝑻𝑰𝑩𝑪,"↓ TS," ↓ ferritin), ↔ bilirubin.
TTT:
Fe therapy for at least 3-4 months
Correct the cause like; change in diet or management of blood loss)
A dimorphic population (microcytic hypochromic cells + normocytic
normochromic cells)→ early in the disease or with Fe treatment.
Mentzer index: (MCV/RBC)
Benefit: to differentiate IDA from thalassemia minor.
IDA: > 13 - Thalassemia minor: < 13
Microcytic hypochromic Anemia
86. Tips & Tricks in
CBC reading
Which is the first stage of iron deficiency?
a. Negative iron balance
b. Decreased iron stores
c. Decrease MCV
d. Decrease in Hemoglobin
87. Tips & Tricks in
CBC reading
Which is the first stage of iron deficiency?
a. Negative iron balance
b. Decreased iron stores
c. Decrease MCV
d. Decrease in Hemoglobin
88. Tips & Tricks in
CBC reading
1. IDA:
Stages of IDA:
1) Loss of storage Fe: ↓ ferritin, ↓ stainable marrow Fe
2) Loss of circulating Fe: ↓ serum Fe, ↓ transferrin saturation
3) Loss of functional Fe: ↓ Hb, ↓ MCV, ↑ RDW, ↑ TIBC
NB;
• Transferrin saturation: serum iron/TIBC
• Serum iron fluctuates with iron ingestion (if you just ate a steak, it will
be high even u are iron deficient)
Microcytic hypochromic Anemia
89. Tips & Tricks in
CBC reading
1. IDA:
IDA which fails to respond to oral Fe:
1) IDA due to blood loss
2) Poor compliance or incorrect Fe dose
3) Concurrent illness (anemia of infection or inflammation)
4) Malabsorptive syndrome (Fe absorption test)
5) Failure to utilizee Fe
6) Hemoglobanthy (β-thalassemia / α-thalassemia/ sickle cell anemia)
7) Pb poisoning
8) Sidroblastic anemia
Microcytic hypochromic Anemia
90. Tips & Tricks in
CBC reading
2. Thalassemia
Lab: ↓ HB (microcytic hypochromic), ↔ RDW
Morphology: target cells
Other labs; ↑ retic, ↑ bilirubin, ↔ ↑ serum Fe, ↔ ↑ ferritin.
History: age of manifestations and clinical presentation
Confirmed by HB electrophoresis
β-thalassemia (major/intermediate) β-thalassemia / (trait) α-thalassemia
HSM present absent
HB < 9 g/dl > 9 g/dl
Normoblastemia Present Absent
Normoblastemia, the presence of nucleated erythrocytes in peripheral blood (prominent in severe forms of β-
thalassemia)
Microcytic hypochromic Anemia
91. Tips & Tricks in
CBC reading
2. Thalassemia
α-thalassemia (trait) β-thalassemia (trait)
Mild microcytic anemia & not responsive to iron & normal iron panel
• Num of encoding genes 4 2
• Pick up during neonatal period yes No
• HB A2 ↔ ↑
Microcytic hypochromic Anemia
92. Tips & Tricks in
CBC reading
Major cause of death in thalassemia major is due to?
a. Endocrinopathies
b. Cardiomyopathies
c. Liver Failure
d. Infection
93. Tips & Tricks in
CBC reading
Major cause of death in thalassemia major is due to?
a. Endocrinopathies
b. Cardiomyopathies
c. Liver Failure
d. Infection
94. Tips & Tricks in
CBC reading
The co-inheritance of alpha thalassemia with beta thalassemia:
a. Increases the severity of symptoms
b. Decreases the severity of symptoms
c. Does not effect
d. Variable effects
95. Tips & Tricks in
CBC reading
The co-inheritance of alpha thalassemia with beta thalassemia:
a. Increases the severity of symptoms
b. Decreases the severity of symptoms
c. Does not effect
d. Variable effects
96. Tips & Tricks in
CBC reading
3. Many infections and inflammatory disorders cause
leukocytosis and/or thrombocytosis are frequently
accompanying anemia of acute infection
Toxic granulation, Dohle bodies and vacuolization
3. Anemia of chronic disease:
Most of cases normocytic normochromic anemia.
20 – 30% can be microcytic
(↓ serum Fe, ↓ 𝑻𝑰𝑩𝑪, ↑ ferritin)
4. Pb poisoning:
Anemia is a late sign of Pb poisoning.
Anemia usually due to concomitant IDA.
Basophilic stippling is not consistently present
Sky blue inclusions in
cytoplasm of neutrophils
Microcytic hypochromic Anemia
97. Tips & Tricks in
CBC reading
5. Rare disorders
• Sideroblastic anemia: anemia, reticulocytpenia, abnormal Fe
deposition in BM erythroblasts.
• Protein caloric malnutrition,
• Metabolic defects of Fe absorption
Microcytic hypochromic Anemia
98. Tips & Tricks in
CBC reading
Which of the following is earliest recognizable change in RBC
morphology in case of iron deficiency?
a. Hypochromia
b. Anisocytosis
c. Target cells
d. Poikilocytosis
99. Tips & Tricks in
CBC reading
Which of the following is earliest recognizable change in RBC
morphology in case of iron deficiency?
a. Hypochromia
b. Anisocytosis
c. Target cells
d. Poikilocytosis
100. Normocytic normochromic Anemia
Tips & Tricks in
CBC reading
1. Hemorrhage
2. Hemolysis (immune vs non-immune)
3. Anemia of chronic infection
4. Hypersplenism
5. BM disorders
101. Normocytic anemia (↔ MCV)
Blood loss
1. History
↔ ↑ retic, ↔ bilirubin
No blood loss
Hemorrhage
Hemolysis
Combs test, LDH,
haptoglopin
↑
2. Lab
Macro-ovalocytosis and/or
hypersegmentation
retic & bilirubin
Blood smear
↓
No Macro-ovalocytosis
and/or hypersegmentation
102. Tips & Tricks in
CBC reading
The least severe form of sickle cell disease is:
a. Hb SS
b. Hb Sβ0
c. Hb Sβ+
d. SCD with hereditary persistence of fetal hemoglobin (S/HPFH)
103. Tips & Tricks in
CBC reading
The least severe form of sickle cell disease is:
a. Hb SS
b. Hb Sβ0
c. Hb Sβ+
d. SCD with hereditary persistence of fetal hemoglobin (S/HPFH)
104. Tips & Tricks in
CBC reading
The most common cause of death in childhood with sickle cell
disease is:
a) Pulmonary hypertension
b) Sudden death of unknown etiology
c) Renal failure
d) Infection
e) Myocardial infarction
105. Tips & Tricks in
CBC reading
The most common cause of death in childhood with sickle cell
disease is:
a) Pulmonary hypertension
b) Sudden death of unknown etiology
c) Renal failure
d) Infection
e) Myocardial infarction
106. Tips & Tricks in
CBC reading
True regarding sickle cell trait are all, except:
a. Is associated with normal growth and life expectancy
b. The ratio of HbA to HbS is 50:50
c. Impaired urine–concentrating ability and haematuria can occur
d. Splenic infarction is possible at very high altitudes
107. Tips & Tricks in
CBC reading
True regarding sickle cell trait are all, except:
a. Is associated with normal growth and life expectancy
b. The ratio of HbA to HbS is 50:50
c. Impaired urine–concentrating ability and haematuria can occur
d. Splenic infarction is possible at very high altitudes
108. Macrocytic Anemia
Tips & Tricks in
CBC reading
1. ↓ B12 level
2. ↓ folate level
3. Drug induced
4. Reticulocytosis
5. BM failure disorders
6. Liver disease
7. Hypothyroidism
8. Rare, congenital deficiency of transcobalamin II or intrinsic factor
110. Tips & Tricks in
CBC reading
Macrocytic anemia may be seen with all the following
conditions, except:
a. Liver disease
b. Copper deficiency
c. Thiamine deficiency
d. Orotic aciduria
111. Tips & Tricks in
CBC reading
Macrocytic anemia may be seen with all the following
conditions, except:
a. Liver disease
b. Copper deficiency
c. Thiamine deficiency
d. Orotic aciduria
112. Tips & Tricks in
CBC reading
1. Vitamin B12 deficiency
Lab: ↓ HB (macrocytic),
Morphology: macro-ovalocytosis + neutrophil hyper segmentation.
In the absence of malnutrition megaloblastic anemia is uncommon.
****************************************
Serum B12 is usually diagnostic
↓ B12 commonly due to pernicious anemia
↓ B12 can be due to ileal disease, malabsorption, vegan diet.
Definition of neutrophil hypersegmentation
Equal or more than 5% of PMNs with 5 nuclear lobes
Equal or more than 1% of PMNs with 6 lobes
Macrocytic Anemia
113. Tips & Tricks in
CBC reading
2. Folate deficiency
Lab: ↓ HB (macrocytic),
Morphology: macro-ovalocytosis + neutrophil hyper segmentation.
In the absence of malnutrition megaloblastic anemia is uncommon.
****************************************
Serum folate reflects recent intake,
RBC folate reflects longer term intake (more reliable)
↓ folate can be due drugs (phenytoin, trimethoprim), malabsorption,
goat milk, ↑ turnover (pregnancy and hemolysis)
Vitamin B12 deficiency should be excluded before ttt to avoid
irreversible neurological damage.
Macrocytic Anemia
114. Tips & Tricks in
CBC reading
3. Drug induced
Lab: ↓ HB (macrocytic),
Morphology: macro-ovalocytosis + neutrophil hyper segmentation.
In the absence of malnutrition megaloblastic anemia is uncommon.
****************************************
Drugs induced macrocytic anemia are the most common cause of
macrocytic anemia in children in industrialized communities.
Chemotherapy (6-mp – hydroxyurea)
Anticonvulsant (carbamazepine, valproic acid, phenytoin, phenobarbital)
Sulfa drugs
Macrocytic Anemia
115. Tips & Tricks in
CBC reading
Lab: ↓ HB (macrocytic),
Morphology: no macro-ovalocytosis & no neutrophil hyper segmentation.
Macrocytic Anemia
4. Reticulocytosis (↑ retic)
Reticulocytes 20% large normal cbc→ ↑ the overall MCV
5. BM failure syndromes (↔/↓ retic)
Diamond Blackfan Anemia (congenital anomalies, presents in the first 3 months of life)
Fanconi anemia (↑ HbF, congenital anomalies, chromosomal breakage test)
Dyskeratosis congenita
Nb; normal MCV in full term neonate 98 – 118 fl
Down associated with with macrocytosis
116. Sum up
Macrocytic Anemia
Tips & Tricks in
CBC reading
1. ↓ B12 level (macro-ovalocytosis + neutrophil hyper segmentation)
2. ↓ folate level (macro-ovalocytosis + neutrophil hyper segmentation)
3. Drug induced (sulfa, anticonvulsant, chemotherapy)
4. Reticulocytosis (normocytic RBC, no macro-ovalocytosis & no neutrophil hyper segmentation,↑ retic)
5. BM failure disorders (no macro-ovalocytosis & no neutrophil hyper segmentation, ↔/↓retic)
6. Liver disease
7. Hypothyroidism (excessive membrane lipids)
8. Rare, congenital deficiency of transcobalamin II or intrinsic factor
118. Neonatal anemia
Retic count
< 2 % retic
Direct Combs test +ve
↑ Indirect bilirubin
> 5 – 8 % retic
Direct Coombs test & indirect bilirubin
Direct Combs test -ve
↑ Indirect bilirubin
Direct Combs test -ve
↔ Indirect bilirubin
MCV
↑ → Megaloblastic anemia
↓ → Blood loss - α-thalassemia
↔ →
• Blood loss
• Infection
• BM replacement: NB, ALL, LCH, osteopetrosis
• DBA
119. Neonatal anemia
• Neonatal pallor is a sign of asphyxia, shock, hypothermia, hypoglycemia, and anemia.
• Time:
o At birth: usually hemorrhage or severe alloimmunization.
o < 48 hours: internal or external hemorrhage.
o > 48 hours: usually hemolytic and associated with jaundice
• Capillary samples can average 3.5 g/dl higher than venous samples.
• Reticulocytes reached normal level 0-1% by 7 days of life.
• Anemia without jaundice is usually due to hemorrhage.
• Shock can trigger DIC; DIC can cause hemolytic anemia.
• G6PD screening results are common false negative in mild variants due to reticulocytosis.
120. Neonatal anemia
• α-thalassemia manifest in neonate because both Hb A and F contains α-chains.
• Critically ill neonates (eg; bronchopulmonary dysplasia) often develop anemia and
reticulopenia.
• Megaloblastic anemia is rare in newborn.
• B 12 deficiency can be seen in:
Breast fed infants of vegan B12 deficient mothers
Infants with GI abnormalities (NEC – short gut syndrome)
• Folate deficiency can be seen in:
Infants receiving goat milk or boiled milk
Malabsorption
122. Anemia in sickle cell disease
Hb concentration
Compared to the baseline
> 2 g/dl below baseline
Ill patient (low or normal BP)
Normal spleen
High retic (> 15%)
1-2 g/dl below baseline
Well patient
Spleen size & retic count
Normal spleen
Low retic (< 5%)
Enlarged spleen
↑ retic (> 5%)
Spleen size & liver size & retic count
↑ spleen → Acute splenic sequestration crisis
↑ liver → Acute hepatic sequestration crisis
↑ retic (> 5%) ↓↓ retic (<1%)
Transient aplastic crisis
(Parvo virus B19)
BM necrosis: Rare in pediatric, due to
repeated Vaso occlusive infarction
123. Anemia in sickle cell disease
• Acute splenic sequestration (ASSC):
It can be acute, subacute, chronic
ASSC is less common in HbSc disease.
Splenomegaly + anemia + thrombocytopenia (↑ retic )
Death may occur in few hours.
Immediate TTT→ correct hypovolemia and anemia
Goal of blood transfusion: to prevent shock (not to restore Hb to normal).
Mostly will need splenectomy (recurs in 50%)
• Transient aplastic crisis (TAC)
It is exacerbation of anemia due to infection mostly parvo virus B19
Severe anemia (↓ retic )
Goal of blood transfusion: to prevent congestive heart failure and shock
↑ risk of stroke is associated with severe anemia