Anemias PowerPoint Presentation PDF

ANEMIAS MISS RIMSHA NOOR DEFINITION Anemia is a medical condition characterized by a decrease in the number of red blood cells (RBCs) or a decrease in the amount of hemoglobin in the blood. Hemoglobin is a protein in red blood cells that binds to oxygen and carries it to tissues and or...

ANEMIAS MISS RIMSHA NOOR DEFINITION Anemia is a medical condition characterized by a decrease in the number of red blood cells (RBCs) or a decrease in the amount of hemoglobin in the blood. Hemoglobin is a protein in red blood cells that binds to oxygen and carries it to tissues and organs throughout the body. Anemia results in a reduced oxygen- carrying capacity of the blood, leading to various symptoms. CLASSIFICATION Anemia can be classified based on various criteria, including the size of red blood cells (RBCs), the amount of hemoglobin, and the underlying cause. Here are some common classifications: Based on Red Blood Cell Size (MCV - Mean Corpuscular Volume): Microcytic Anemia: RBCs are smaller than normal. Normocytic Anemia: RBCs are of normal size. Macrocytic Anemia: RBCs are larger than normal. Based on Hemoglobin Content (MCH - Mean Corpuscular Hemoglobin): Hypochromic Anemia: RBCs have reduced hemoglobin content. Normochromic Anemia: RBCs have normal hemoglobin content. Based on Underlying Cause: Iron-deficiency anemia: Caused by insufficient iron for proper hemoglobin synthesis. Vitamin B12 deficiency anemia: Caused by a lack of vitamin B12, which is crucial for RBC production. Folate deficiency anemia: Caused by a lack of folate (vitamin B9), essential for RBC formation. Hemolytic anemia: Caused by the destruction of red blood cells at a rate faster than their production. Aplastic anemia: Characterized by a decrease in the number of red blood cells due to bone marrow failure. Chronic diseases anemia: Associated with chronic inflammatory diseases. ETIOLOGY A. Iron-deficiency Anemia: Causes: Inadequate dietary intake of iron. Chronic blood loss (e.g., gastrointestinal bleeding, menstruation). B. Vitamin B12 Deficiency Anemia: Causes: Inadequate dietary intake (common in vegetarians). Malabsorption issues, such as pernicious anemia (autoimmune destruction of intrinsic factor, needed for B12 absorption). C. Folate Deficiency Anemia: Causes: Inadequate dietary intake. Malabsorption issues. D. Hemolytic Anemia: Causes: Inherited Conditions: Sickle cell anemia, thalassemia. Acquired Conditions: Autoimmune hemolytic anemia, certain infections. E. Aplastic Anemia: Causes: Idiopathic (unknown cause). Exposure to certain drugs or toxins (e.g., chemotherapy, radiation). F. Chronic Diseases Anemia: Causes: Chronic inflammatory condition (e.g. chronic kidney disease). Systemic illnesses affecting erythropoietin production MORPHOLOGY Microcytic Anemia: Small, pale RBCs under the microscope. Example: Iron-deficiency anemia. Normocytic Anemia: Normal-sized RBCs. Example: Anemia of chronic disease. Macrocytic Anemia: Larger RBCs, often with immature forms (megaloblasts). Example: Vitamin B12 deficiency anemia. Hypochromic Anemia: RBCs with reduced color (pale) due to decreased hemoglobin content. Example: Iron-deficiency anemia. Normochromic Anemia: RBCs with normal color. Example: Anemia associated with chronic diseases. Sickle Cell Anemia: Crescent-shaped RBCs under certain conditions. Example: Sickle cell disease. SYMPTOMS Fatigue and Weakness: Reduced oxygen delivery to tissues leads to fatigue and weakness. Pale Skin: Decreased red blood cell count can result in paleness. Shortness of Breath: The body compensates by increasing heart rate and respiratory rate to deliver more oxygen. Dizziness and Lightheadedness: Insufficient oxygen supply to the brain can cause dizziness. Cold Hands and Feet: Reduced blood flow to extremities can cause them to feel cold. Headache: Insufficient oxygen supply to the brain may lead to headaches. Irregular Heartbeat: The heart may pump faster to compensate for decreased oxygen-carrying capacity. Chest Pain: Severe anemia may strain the heart, leading to chest pain. IRON DEFICIENCY ANEMIA Iron deficiency anemia (IDA) is a common type of anemia that occurs when there is insufficient iron to support the production of hemoglobin, the oxygen-carrying protein in red blood cells (RBCs). PATHOPHYSIOLOGY 1. Iron Metabolism: Absorption: Iron is primarily absorbed in the duodenum and upper jejunum. Transport: Transferrin, a plasma protein, transports iron in the blood. Storage: Iron is stored in the form of ferritin and hemosiderin, primarily in the liver, spleen, and bone marrow. 2. Development of Iron Deficiency: Inadequate Dietary Intake: Consuming insufficient iron-rich foods. Increased Iron Requirements: During periods of growth, pregnancy. Impaired Absorption: Conditions like celiac disease or inflammatory bowel diseases can hinder iron absorption. Chronic Blood Loss: The most common cause of iron deficiency anemia. Occurs through gastrointestinal bleeding (ulcers, tumors, inflammation), menstruation, 3. Depletion of Iron Stores: Exhaustion of Ferritin Reserves: Initially, iron deficiency may not manifest as anemia, but ferritin stores start depleting. Decline in Serum Iron: Serum iron levels decrease as stored iron is mobilized for use. 4. Hypochromic, Microcytic RBCs: Insufficient Hemoglobin Synthesis: Without enough iron, the synthesis of hemoglobin is impaired. Reduced Size of RBCs (Microcytosis): New RBCs produced are smaller than normal. Decreased Hemoglobin Content (Hypochromasia): RBCs appear paler due to lower hemoglobin content 5. Increased Erythrocyte Protoporphyrin (EP): EP Accumulation: In the absence of sufficient iron, protoporphyrin accumulates in the RBCs. Increased EP Levels: Measured as free erythrocyte protoporphyrin (FEP) in laboratory tests. 6. Erythropoiesis and Anemia: Erythropoietin Release: The kidneys release erythropoietin in response to low oxygen levels, stimulating the bone marrow to produce more RBCs. Ineffective Erythropoiesis: Iron deficiency leads to the production of small, pale RBCs that are less efficient in carrying oxygen. Anisocytosis and Poikilocytosis: Variability in RBC size (anisocytosis) and shape (poikilocytosis) may be observed. CLINICAL MANIFESTATIONS Fatigue and Weakness: Due to reduced oxygen delivery to tissues. Pallor: Paleness of the skin, conjunctiva, and mucous membranes. Shortness of Breath: Resulting from the body's attempt to compensate for reduced oxygen-carrying capacity. Headache and Dizziness: Insufficient oxygen supply to the brain. Cold Hands and Feet: Reduced blood flow to extremities. LABORATORY FINDINGS Low Serum Iron: Reflects decreased iron availability. Low Ferritin Levels: Indicates depleted iron stores. High Total Iron-Binding Capacity (TIBC): Reflects the body's attempt to mobilize iron. Low Hemoglobin and Hematocrit: Confirm anemia. Microcytosis and Hypochromasia: Observed in a peripheral blood smear. TREATMENT Iron Supplementation: Oral or intravenous iron to replenish iron stores. Addressing Underlying Causes: Treating conditions contributing to chronic blood loss or impaired absorption. VITAMIN B12 DEFICIENCY ANEMIA Vitamin B12 deficiency anemia is a condition characterized by a lack of sufficient vitamin B12, leading to impaired DNA synthesis in red blood cell (RBC) production. This deficiency can result from inadequate dietary intake, malabsorption issues, or other factors affecting the absorption of vitamin B12. PATHOPHYSIOLOGY 1. Vitamin B12 Metabolism: Dietary Intake: Vitamin B12 is primarily obtained from animal products (meat, fish, dairy). Intrinsic Factor: In the stomach, vitamin B12 binds to intrinsic factor, a glycoprotein secreted by gastric parietal cells. Absorption: The vitamin B12–intrinsic factor complex is absorbed in the ileum of the small intestine. 2. Causes of Vitamin B12 Deficiency: Inadequate Dietary Intake: Common in strict vegetarians and vegans. Malabsorption: Conditions affecting the stomach, such as pernicious anemia or atrophic gastritis, can reduce intrinsic factor production or function. Ileal Disorders: Surgical removal of the terminal ileum or diseases affecting the ileum can impair absorption. Competition for B12 Absorption: Conditions like bacterial overgrowth in the small intestine can consume available vitamin B12. 3. Inadequate DNA Synthesis in Erythropoiesis: Role of Vitamin B12: Essential for the synthesis of DNA and RNA, including the maturation of RBCs in the bone marrow. Effect on Cell Division: Vitamin B12 deficiency leads to impaired cell division and larger, immature RBCs (macrocytes). 5. Morphological Changes in RBCs: Macrocytic Anemia: Larger-than-normal RBCs (macrocytes) are produced due to impaired DNA synthesis. Hypersegmented Neutrophils: In peripheral blood smears, an increased number of neutrophils with more than five lobes are often observed. CLINICAL MANIFESTATIONS Fatigue and Weakness: Due to reduced oxygen- carrying capacity of larger but functionally immature RBCs. Pallor: Resulting from anemia. Neurological Symptoms: In severe cases, vitamin B12 deficiency can lead to neurological symptoms, including numbness, tingling, and difficulty walking. LABORATORY FINDINGS Low Serum Vitamin B12 Levels: Confirming the deficiency. Peripheral Blood Smear: Macrocytosis and hypersegmented neutrophils. TREATMENT Vitamin B12 Supplementation: Typically administered by injection for efficient absorption. Addressing Underlying Causes: Treating conditions causing malabsorption or dietary deficiencies. HEMOLYTIC ANEMIA Hemolytic anemia is a condition characterized by the premature destruction of red blood cells (hemolysis), leading to a decrease in the overall number of circulating red blood cells. This can occur due to intrinsic abnormalities in the red blood cells themselves (intrinsic hemolytic anemia) or as a result of external factors affecting the red blood cells (extrinsic hemolytic anemia).  PATHOPHYSIOLOGY 1. Intrinsic Hemolytic Anemia: A. Hereditary Hemolytic Anemias: Sickle Cell Anemia: Genetic Mutation: Inherited mutation in the HBB gene, leading to the production of abnormal hemoglobin (HbS). Hemoglobin Polymerization: HbS molecules can polymerize under certain conditions, causing RBCs to assume a sickle shape, leading to hemolysis. Thalassemia: Genetic Mutation: Inherited mutations affecting the synthesis of alpha or beta globin chains of hemoglobin. Imbalanced Hemoglobin Chains: Reduced synthesis of one type of globin chain leads to an imbalance, causing hemolysis. 2. Extrinsic Hemolytic Anemia: A. Immune Hemolytic Anemias: Autoimmune Hemolytic Anemia (AIHA): Autoantibodies: The immune system produces antibodies that target and destroy the body's own red blood cells. Coating of RBCs: Antibodies bind to the surface of RBCs, marking them for destruction by macrophages in the spleen or liver. Drug-Induced Hemolytic Anemia: Hapten Mechanism: Drugs can bind to RBCs, creating a complex that triggers an immune response. Immune-Mediated Destruction: The immune system recognizes the drug-bound RBCs as foreign and destroys them. B. Mechanical Hemolytic Anemias: Microangiopathic Hemolytic Anemia (MAHA): Vascular Injury: Conditions such as thrombotic microangiopathies (e.g., thrombotic thrombocytopenic purpura) cause damage to RBCs as they pass through narrowed blood vessels. Shearing Forces: RBCs are mechanically damaged, leading to hemolysis. C. Infections: Malaria: Rupture of Infected RBCs: Release of merozoites from infected RBCs leads to hemolysis. PATHOLOGICAL CONSEQUENCES A. Hemolysis: Premature Destruction: RBCs are broken down before the end of their normal lifespan (120 days). Release of Hemoglobin: Hemoglobin is released into the bloodstream. B. Compensatory Mechanisms: Erythropoiesis Acceleration: The bone marrow attempts to compensate by producing new RBCs at an increased rate. Reticulocytosis: Increased release of reticulocytes (immature RBCs) into the bloodstream. CLINICAL MANIFESTATIONS Anemia Symptoms: Fatigue, weakness, pallor. Splenomegaly: Enlargement of the spleen as it works to clear damaged RBCs. LABORATORY FINDINGS Increased Reticulocyte Count: Reflects the compensatory response. Peripheral Blood Smear: May reveal characteristic changes depending on the underlying cause. TREATMENT Addressing Underlying Cause: Depending on the specific etiology (e.g., immunosuppression, splenectomy). Blood Transfusion: In severe cases to manage anemia. APLASTIC ANEMIA Aplastic anemia is a rare but serious disorder characterized by a failure of the bone marrow to produce an adequate number of blood cells, including red blood cells (RBCs), white blood cells (WBCs), and platelets. The underlying pathophysiology involves damage to the hematopoietic stem cells and the bone marrow microenvironment. PATHOPHYSIOLOGY 1. Hematopoietic Stem Cell Injury: Immune-Mediated Destruction: The most common cause of aplastic anemia is an immune-mediated attack on hematopoietic stem cells. T lymphocytes, activated by an unknown trigger, attack and destroy the hematopoietic stem and progenitor cells in the bone marrow. This immune response disrupts the normal process of blood cell production. 2. Cytotoxic Injury: Exposure to Toxins and Drugs: Certain drugs, chemicals, and toxins can directly damage the bone marrow. Examples include chemotherapeutic agents, radiation, and some environmental toxins. The cytotoxic effect impairs the replication and function of hematopoietic cells. 3. Genetic Predisposition: Inherited Aplastic Anemias: Rare genetic disorders can predispose individuals to aplastic anemia. Examples include Fanconi anemia, dyskeratosis congenita, and Shwachman-Diamond syndrome. These conditions often involve mutations affecting DNA repair mechanisms. PATHOLOGICAL CONSEQUENCES A. Decreased Production of Blood Cells: Red Blood Cells (RBCs): Reduced production leads to anemia, characterized by a decrease in hemoglobin levels and impaired oxygen-carrying capacity. Anemia manifests as fatigue, weakness, pallor, and shortness of breath. White Blood Cells (WBCs): Neutropenia occurs due to a decrease in neutrophils, increasing the risk of infections. Infections may be severe and life-threatening. Platelets: Thrombocytopenia results in a reduced number of platelets. Increased risk of bleeding, bruising, and petechiae due to impaired blood clotting. B. Compensatory Mechanisms: Reticulocytopenia: As the bone marrow fails to produce sufficient blood cells, the number of reticulocytes (immature RBCs) in the peripheral blood decreases. CLINICAL MANIFESTATIONS Fatigue, Weakness, Pallor: Due to anemia. Frequent Infections: Resulting from neutropenia. Bleeding and Bruising: Associated with thrombocytopenia. LABORATORY FINDINGS Peripheral Blood Smear: Reveals pancytopenia, showing reduced numbers of RBCs, WBCs, and platelets. Hypocellular bone marrow with decreased cellularity. Bone Marrow Biopsy: Confirms the hypocellular nature of the bone marrow. May reveal fatty infiltration in place of normal hematopoietic cells. TREATMENT Hematopoietic Stem Cell Transplant (HSCT): Allogeneic HSCT is a potentially curative option for younger patients with a suitable donor. Autologous HSCT or immunosuppressive therapy may be considered in certain cases. Immunosuppressive Therapy: Anti-thymocyte globulin (ATG) combined with cyclosporine can suppress the immune response and improve blood cell production