Autoimmune hemolytic anemia (aiha)
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Autoimmune hemolytic anemia (AIHA) is caused by antibodies against a person's own red blood cells, leading to their premature destruction and anemia. There are two main types - warm AIHA caused by IgG antibodies active at body temperature, and cold AIHA caused by IgM antibodies. Symptoms include jaundice and fatigue from anemia. Diagnosis involves blood tests showing low red blood cell counts and the presence of antibodies coating red blood cells. Treatment focuses on immunosuppression with corticosteroids or other drugs to reduce antibody levels and blood transfusions to manage anemia.
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Auto immune hemolytic anemia
Autoimmune hemolytic anemia is caused by antibodies that bind to and prematurely destroy red blood cells. It is classified into warm and cold types based on antibody characteristics and mechanisms of hemolysis. Workup involves a Coombs test to detect antibodies coating red blood cells via direct or indirect agglutination. Treatment depends on type but may include steroids, splenectomy, cold protection, or rituximab.
Approach to Autoimmune Hemolytic Anemia
This document discusses different types of autoimmune hemolytic anemias (AIHA). It begins by defining autoimmunity and describing the main types of AIHA - warm, cold agglutinin disease, and paroxysmal cold hemoglobinuria. For each type, it covers characteristics, pathophysiology, clinical findings, laboratory evaluation, therapy and key differences. Warm AIHA is the most common and can be primary or associated with other diseases. Cold agglutinin disease usually affects the elderly and involves cold agglutinins while paroxysmal cold hemoglobinuria is typically post-viral and involves Donath-Landsteiner antibodies. Therapy depends on severity and underlying cause but may include corticosteroids
Paroxysmal Nocturnal Hemoglobinuria
PNH is a rare acquired hemolytic disorder caused by a somatic mutation in the PIG-A gene, resulting in a deficiency of glycosylphosphatidylinositol (GPI)-anchored proteins on the surface of blood cells. This renders the cells susceptible to complement-mediated lysis. PNH is characterized by hemolytic anemia, thrombophilia, and bone marrow failure. Diagnosis is made through flow cytometry to detect the absence of GPI-anchored proteins CD55 and CD59 on red blood cells. Treatment involves blood transfusions, anticoagulation therapy, and complement inhibition with eculizumab which significantly reduces hemolysis.
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Megaloblastic anemia
Megaloblastic anemia is a type of macrocytic anemia caused by a failure of DNA synthesis, resulting in asynchronous maturation of red blood cell nuclei and cytoplasm. The most common causes of megaloblastic anemia are vitamin B12 and folic acid deficiencies. Treatment involves treating the underlying deficiency, with vitamin B12 therapy for B12 deficiency and oral folic acid supplementation for folic acid deficiency. Response to treatment is monitored through improvement of hematological markers and symptoms over 1-8 weeks.
Aiha
This document summarizes autoimmune hemolytic anemia (AIHA), including its classification, diagnostic tests, findings, and treatment approaches. It discusses the main types of AIHA - warm AIHA, cold AIHA, and drug-induced AIHA. Warm AIHA is the most common type, often idiopathic but sometimes secondary to other conditions. Diagnostic tests for AIHA include a positive direct antiglobulin test and findings such as low haptoglobin and high LDH. Treatment depends on the AIHA type but may include corticosteroids, rituximab, splenectomy or other immunosuppressants. Cold AIHA and drug-induced AIHA have their own characteristic serological and
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This document discusses hemolytic anemias caused by extracorpuscular defects. It describes immune and non-immune mechanisms that can destroy red blood cells, including autoimmune disorders, drug reactions, alloimmune responses to blood transfusions or pregnancy, infections, and membrane defects. The main types of immune hemolytic anemias are autoimmune (warm or cold antibody types), alloimmune (due to blood transfusions or pregnancy), and drug-induced. Workup may include blood tests to detect anemia, spherocytes, a positive direct Coombs test, and the thermal amplitude of any detected antibodies. Management depends on the underlying cause.
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Auto immune hemolytic anemia
Autoimmune hemolytic anemia is caused by antibodies that bind to and prematurely destroy red blood cells. It is classified into warm and cold types based on antibody characteristics and mechanisms of hemolysis. Workup involves a Coombs test to detect antibodies coating red blood cells via direct or indirect agglutination. Treatment depends on type but may include steroids, splenectomy, cold protection, or rituximab.
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Paroxysmal Nocturnal Hemoglobinuria
PNH is a rare acquired hemolytic disorder caused by a somatic mutation in the PIG-A gene, resulting in a deficiency of glycosylphosphatidylinositol (GPI)-anchored proteins on the surface of blood cells. This renders the cells susceptible to complement-mediated lysis. PNH is characterized by hemolytic anemia, thrombophilia, and bone marrow failure. Diagnosis is made through flow cytometry to detect the absence of GPI-anchored proteins CD55 and CD59 on red blood cells. Treatment involves blood transfusions, anticoagulation therapy, and complement inhibition with eculizumab which significantly reduces hemolysis.
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This document summarizes autoimmune hemolytic anemia (AIHA), including its classification, diagnostic tests, findings, and treatment approaches. It discusses the main types of AIHA - warm AIHA, cold AIHA, and drug-induced AIHA. Warm AIHA is the most common type, often idiopathic but sometimes secondary to other conditions. Diagnostic tests for AIHA include a positive direct antiglobulin test and findings such as low haptoglobin and high LDH. Treatment depends on the AIHA type but may include corticosteroids, rituximab, splenectomy or other immunosuppressants. Cold AIHA and drug-induced AIHA have their own characteristic serological and
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1) In hemolytic anemia, the bone marrow compensates for red blood cell loss by increasing red blood cell production up to 10 times normal levels through increased erythropoietin production.
2) Signs of hemolysis include jaundice, dark urine, increased bilirubin in urine, increased LDH, low or absent haptoglobin, and an elevated reticulocyte count on peripheral blood smear.
3) Hemolysis can be intravascular or extravascular. Extravascular causes include splenomegaly while
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Autoimmune hemolytic anemia (AIHA) is a type of normochromic normocytic anemia that is caused by autoantibodies that are produced in the patient against his/her own blood cells, particularly against RBCs. As a result hemolysis occurs leading to anemia.
Autoantibodies are produced secondary to autoimmune diseases, lymphoproliferative disorder (LPDs), certain infections or immunodeficiency syndromes.
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immune hemolytic anemia
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1. Autoimmune hemolytic anemia (AIHA) is characterized by the abnormal production of antibodies that destroy red blood cells, leading to anemia.
2. There are three main types of AIHA - warm, cold, and mixed - defined by the temperature at which antibodies cause hemolysis.
3. Warm AIHA is the most common type and causes hemolysis at normal body temperatures, while cold AIHA antibodies are only active at low temperatures below 37°C.
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This document discusses warm autoimmune hemolytic anemia (WAIHA) and cold autoimmune hemolytic anemia (CAIHA). WAIHA accounts for 70% of autoimmune hemolytic anemias and is caused by IgG antibodies binding to red blood cells at 37°C or above, causing extravascular hemolysis. CAIHA is caused by IgM antibodies binding to red blood cells below 37°C, causing intravascular hemolysis and symptoms in cold areas like fingers and toes. Both result in a positive direct Coombs test and can be idiopathic or secondary to infections, lymphoproliferative disorders, or drugs.
Autoimmune haemolytic anaemia
Autoimmune haemolytic anaemia is caused by abnormalities of the immune system where antibodies attack a person's own red blood cells. There are two main types: warm antibody haemolytic anaemia, which is the most common type, and cold agglutinin disease. Warm antibody haemolytic anaemia can be primary or secondary to other conditions and causes haemolysis mainly in the spleen. Cold agglutinin disease is caused by antibodies that react at low temperatures and causes haemolysis in the liver and spleen. Symptoms are due to anaemia and may include fatigue, jaundice, and dark urine. Diagnosis involves blood tests showing anaemia and antibodies on the direct antiglobulin test. Treatment depends on the severity but may include
Hemolytic anemia
1. Hemolytic anemia results from the premature destruction of red blood cells, either intravascularly or extravascularly. It can be classified as acquired or hereditary.
2. Acquired hemolytic anemias are caused by extrinsic factors like antibodies, infections, toxins, or mechanical trauma. Hereditary hemolytic anemias result from intrinsic red blood cell defects.
3. Common causes of acquired hemolytic anemia include autoimmune hemolytic anemia, microangiopathic hemolysis, paroxysmal nocturnal hemoglobinuria, and isoimmune hemolytic anemia from blood transfusions. Hereditary forms often involve defects in the red blood cell membrane or interior
Hemolytic anemia
1) Autoimmune hemolytic anemia (AIHA) is caused by antibodies that target a person's own red blood cells. There are warm and cold types classified by the temperature at which the autoantibodies react.
2) Warm AIHA is caused by IgG antibodies that react at 37°C and cause intravascular hemolysis. Cold agglutinin disease (CAD) and paroxysmal cold hemoglobinuria (PCH) are caused by IgM or IgG antibodies that react at cold temperatures and cause extravascular or intravascular hemolysis.
3) Treatment depends on the type and severity of AIHA. Supportive care includes transfusion and keeping patients warm. Corticosteroids
ACQUIRED HEMOLYTIC ANEMIA.ppt
This document discusses various types of acquired hemolytic anemias, including immune and non-immune causes. It covers autoimmune hemolytic anemia, distinguishing between warm and cold types. It also discusses alloimmune hemolytic anemias like hemolytic disease of the newborn. Non-immune causes discussed include red cell fragmentation syndromes, infections, chemicals/physical agents, and acquired membrane disorders. Aplastic anemia is also summarized, covering etiology, pathogenesis, clinical features, and differential diagnosis.
Type 2.pptx
Type II hypersensitivity reactions involve antibody-mediated destruction of cells through three main mechanisms: complement-mediated cell lysis, antibody-dependent cell-mediated cytotoxicity (ADCC), and target cell dysfunction. Complement-mediated lysis results from membrane attack complex formation following complement activation by antigen-antibody complexes. ADCC occurs when antibodies bind to cell surfaces and recruit natural killer cells to induce apoptosis. Target cell dysfunction involves antibodies altering cell surface receptors and physiology rather than directly killing cells, as seen in Graves' disease and myasthenia gravis. Examples provided include autoimmune hemolytic anemia, hemolytic disease of the newborn, Goodpasture syndrome, and drug-induced thrombocytopenia.
anaemia.pptx
Normocytic anemias can be caused by increased red blood cell destruction (hemolytic) or decreased red blood cell production (aplastic). Hemolytic anemias are characterized by an increased reticulocyte count as the bone marrow attempts to compensate for the loss of red blood cells. The document describes various causes of hemolytic anemia including intrinsic red blood cell defects from genetic disorders like sickle cell disease or enzyme deficiencies, as well as extrinsic causes such as autoimmune disorders or infections. Aplastic anemia is discussed as an example of normocytic anemia caused by bone marrow failure shown by pancytopenia and a low or normal reticulocyte count.
Immune mediated haemolytic anemia in dogs
Immune-mediated hemolytic anemia (IMHA) is a life-threatening blood disorder in dogs where the immune system destroys the animal's own red blood cells. It can be either primary (idiopathic) or secondary to underlying causes like infection or vaccination. Diagnosis involves identifying anemia, signs of hemolysis, a positive direct Coombs' test, and ruling out other potential causes. Treatment focuses on immunosuppression using glucocorticoids and other drugs, intensive supportive care, and addressing any underlying triggers. Prognosis is guarded as mortality rates are high, especially early on, though long-term remission is possible with aggressive therapy.
Extracorpuscular hemolytic anemia
This document provides an overview of approaches to diagnosing and classifying extracorpuscular hemolytic anemia. It discusses that hemolytic anemia can be immune-mediated or non-immune, and describes approaches to determining the etiology, including evaluating for autoimmune causes through tests like the direct antiglobulin test or determining underlying alloantibodies. Clinical manifestations and laboratory findings of hemolytic anemia are also summarized.
Hemolytic anemia (1)
Hemolytic anemia is a condition where red blood cells are destroyed and removed from circulation prematurely. There are many causes of hemolytic anemia including inherited disorders like sickle cell anemia and enzyme deficiencies, immune mediated destruction of red blood cells, infections, toxins and mechanical trauma. Hemolytic anemias can be classified based on location of hemolysis (intravascular or extravascular), source of defect (intracorpuscular or extracorpuscular), and mode of onset (hereditary or acquired). Common symptoms include paleness, fatigue, fever and signs of hemoglobin in urine, blood or stool.
Medicine 5th year, 8th lecture/part one (Dr. Sabir)
This document discusses hemolytic anemias, which are characterized by decreased red blood cell lifespan. It describes the classification, clinical features, laboratory findings, and specific types of hemolytic anemias including congenital defects like hereditary spherocytosis and enzyme deficiencies like G6PD deficiency. It also covers immune-mediated hemolytic anemias such as warm antibody-mediated and cold antibody-mediated types.
Child with pallor & jaundice (hemolytic anemia)
This document discusses causes of pallor and jaundice in a child, including hereditary spherocytosis, glucose-6-phosphate dehydrogenase deficiency, sickle cell anemia, thalassemia, and autoimmune hemolytic anemia. It provides details on the mechanisms, clinical presentations, investigations, and management of each condition. Hereditary spherocytosis is caused by a red blood cell membrane defect, resulting in destruction in the spleen. Thalassemia and sickle cell anemia are hemoglobinopathies caused by genetic defects in hemoglobin production or structure. Autoimmune hemolytic anemia occurs when antibodies destroy red blood cells. Distinguishing features, treatments including transfusions, splenectomy, and
Haemolytic disorders
This document discusses hemolytic disorders and provides details on various types. It begins with definitions of hemolytic disorder and hemolytic anemia. It then covers topics like hemopoiesis, regulation of hemopoiesis, the red blood cell, pathophysiology of hemolysis, classification of hemolytic anemias, clinical presentation, laboratory evaluation, red blood cell morphology, immune hemolytic anemia, drug and toxin induced hemolytic anemia, hereditary hemolytic disorders like G6PD deficiency and sickle cell disease, and traumatic hemolysis. In summary, it provides a comprehensive overview of the causes, pathophysiology, clinical features and laboratory findings of different hemolytic disorders.
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Autoimmune hemolytic anemia (aiha)
- 2. What is AIHA? When the increased destruction of erythrocytes due to the presence of anti-bodies against them,with or without complement on RBCs membrane. As premature cell destruction will lead to anemia 2ndry to the hemolysed RBCs, and the bone marrow will not be able to compensate the destructed RBCs by another healthy RBCs.
- 3. Symptoms. Onset typically show In secondary AIHA, symptoms of primary illness may overshadow Jaundice Splenomegaly ~20%
- 4. Classification of AIHA. Primary Secondary (RBCs auto antibodies are present (AIHA occurring in association And cause HA. with another systemic illness But no evidence often called secondary AIHA. Underlying systemic illness.
- 5. AIHA Subtypes Classification based on optimal RBC-autoantibody reactivity temperatures. Warm and Cold AIHA more predominant. Warm is IgG (Opsinization) autoantibodies that bind optimally at 37°C. Cold is IgM (Complement) that strongly agglutinates at 4°C.
- 7. Warm AIHA (wAIHA) 1 in 80,000 Predominant type found in children. wAIHA – mononucleosis, HIV, and chronic lymphocytic lymphoma. Optimal temperature of 37°C. Usually associated with IgG (Also IgA and IgM). IgG bind to the RBCs at 37’C,lead to extravascular hemolysis in the spleen IL-10 and IL-12 play a role in this process.
- 8. Cold AIHA (cAIHA) Maximal activity of in vitro RBC binding at temp. between 0’C and 30’C. Almost always caused by IgM antibody with specificity for antigen of system on RBCs. Antibodies are usually found in infection mononucleosis. This hemolysis is complement-dependent manner.
- 9. Diagnosis. CBC(decrease HB level) Jaundice and abnormally dark urine Direct antiglobulin test (DAT) or Coombs test (positive) Heptoglobin will be decrease Indirect bilirubin will increase Bone marrow aspiration if you suspect AIHA secondary to leukemia or lymphoma Increased sensitivity fcRBC-bound Ig detection
- 10. Treatment. 1. Immunotherapy – the treatment of disease by inducing, enhancing, or suppressing an immune response Classified as suppression immunotherapy if the immunotherapy reduces or suppresses the immune response 2. Corticosteroid in IgG mediated AIHA, Corticosteroid will interfere with Fc receptor which are responsible for RBC destruction… 3. pulse dose dexamethasone can be effective in warm AIHA…
- 11. THANK YOU
Editor's Notes
- Decrease RBCs production so decrease blood flow and increase RBCs destruction
- Splenomegaly= enlargement of the spleen
- igG Inhibition of B cell activation Mononucleosis= enlarged lymphnodes and swollen spleen may last for a few weeks longer CLL= type of bloodcancer
- In chronic cold agglutinin disease, the patient is more symptomatic during the colder months.
- Cbc= complete blood count