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35 Cards in this Set
- Front
- Back
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Differentiate Hemolytic Disease and Hemolytic Anemia |
Hemolytic disease is a condition in which there is increased hemolysis. Hemolytic anemia is when erythropoiesis cannot compensate for increased hemolysis |
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Describe the Defect/Disorder/Etiology of Hereditary Spherocytosis |
Autosomal dominant Deficiency or abnormality or membrane proteins decreased surface area to volume ratio cells become rigid Extravascular hemolysis |
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Describe the Defect/Disorder/Etiology of Hereditary Elliptocytosis |
Autosomal dominant Deficiency of membrane cytoskeletal proteins extravascular hemolysis |
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Describe the Defect/Disorder/Etiology of Hereditary Acanthocytosis (Abetalipoproteinemia) |
Deficiency of abetalipoproteinemia Sphingomyelin/lecithin ratio is increased extravascular hemolysis |
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Describe the Defect/Disorder/Etiology of Hereditary Stomatocytosis |
Increase passive permeability of Na+ & K+ which causes a net swelling of the cell. Intravascular hemolysis |
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Describe the Defect/Disorder/Etiology of Glucose 6 Phosphate Dehydrogenase Deficiency |
Most Common Decreased G6PD causing decrease NADPH causing decreased amount of glutathione resulting in increased methemoglobin due to oxidizing agents (food, meds, infxns) Intravascular hemolysis |
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Describe the Defect/Disorder/Etiology of Pyruvate Kinase Deficiency |
Causes a chronic anemia Decreased ATP production and therefore hemolysis due to failure of ATP dependent rxns Extravascular hemolysis |
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Describe the Defect/Disorder/Etiology of Sickle Cell Trait |
Hemoglobin A 55-85% Hemoglobin S 20-45% Heterozygous A and S on chromosome 11 Resistance to Plasmodium falciparum (malaria) Extravascular hemolysis |
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Describe the Defect/Disorder/Etiology of Sickle Cell Anemia |
Hemoglobin A 0% Hemoglobin S 80-100% Hemoglobin F 0-20% Homozygous on chromosome 11 Prone to infxn Extravascular hemolysis |
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Describe the Defect/Disorder/Etiology of Alpha Thalassemia |
Inherited Alpha gene deletion on chromosome 16, reduced alpha chains Single gene deletion results in 'silent carrier' Trans deletion - one gene deleted from each parent Cis deletion - two genes deleted from one parent (neither is very serious) Hb H disease - deletion of 3 of 4 alpha genes Chronic moderate to severe microcytic anemia Hydrops fetalis - deletion of all four alpha genes results in stillbirth Extravascular hemolysis |
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Describe the Defect/Disorder/Etiology of Beta Thalassemia Minor |
Inherited beta gene mutation of chromosome 11 heterozygous Extravascular hemolysis |
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Describe the Defect/Disorder/Etiology of Beta Thalassemia major |
Inherited serious lifelong anemia affects both beta chains, decreased production of of beta chains homozygous 4 genetic variants Inadequate erythropoiesis or increased hemolysis extravascular hemolysis |
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Describe the Defect/Disorder/Etiology of Paroxysmal Nocturnal Hemoglobinuria |
Rare stem cell disorder decreased production of phospholipids decreased membrane proteins that inhibit the action of complement, resulting in an increased sensitivity to complement increased sensitivity to complement and hemolysis Intravascular hemolysis |
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Describe the Defect/Disorder/Etiology of Immune Hemolytic Anemias due to alloantibodies |
Antibodies formed from foreign antigen stimulation attack foreign RBCs Occurs in Pregnancy, Transfusions, Organ Transplants
Includes Hemolytic disease of the newborn and Transfusion Reactions |
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Describe the Defect/Disorder/Etiology of Auto Immune Hemolytic Anemias: Warm, Cold |
Warm (70% of AIHAs) RBC sensitized by anti-IgG Cold: RBC sensitized by anti-IgM |
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Describe the Defect/Disorder/Etiology of Immune Hemolytic Anemias due to complement activation |
i.e. Paroxysmal Nocturnal Hemoglobinuria Due to complement binding Intravascular hemolysis |
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Describe the Defect/Disorder/Etiology of Hemolytic Anemias due to Mechanical and Chemical Trauma |
hemolysis due to excessive physical abuse March hemoglobinuria - hemoglobinuria and hemoglobinemia present after exercise Severe burns - hemolysis from heat. microangiopathic hemolytic anemias - hemolysis from intravascular lesions (DIC, artherosclerosis) Chemical - caused by oxidation or interference with cellular enzymes |
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Describe the Defect/Disorder/Etiology of Hemolytic Anemias due to infections and parasites |
Bartonella bacilliformis - intra-erythrocyte bacillus. caused severe hemolysis Clostridium perfringens - produces a toxin that hydrolyzes components of RBC membrane Malaria - Plasmodium falciparum, P. vivax, P. malariae, P. ovale. infected cells are either removed phagocytically or burst when parasite reaches maturity Babesiosis - resemble Plasmodium, but smaller rings |
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Describe the Lab findings in Hereditary Spherocytosis |
Microspherocytes polychromasia increased osmotic fragility Auto hemolysis increased corrected with glucose or ATP increased MCHC |
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Describe the Lab findings in Hereditary Elliptocytosis |
enlarged spleen hyperbilirubinemia 25-95% elliptocytes spherocytes and polychromasia |
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Describe the Lab findings of Hereditary Acanthocytosis |
Acanthocytes low ESR Osmotic fragility is normal Mechanical fragility increased cholesterol and triglycerides also usually decreased |
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Describe the Lab findings of Hereditary Stomatocytosis |
10-30% stomatocytes no spherocytes autohemolysis increased partly corrected with ATP and glucose Osmotic fragility increased |
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Describe the Lab findings of G6PD deficiency |
bite cells and other schistocytes heinz bodies Polychromasia Decreased haptoglobin Autohemolysis corrected with glucose enzyme assay |
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Describe the lab findings of Pyruvate Kinase Deficiency |
Increased 2, 3 BPG Enlarged spleen Autohemolysis corrected with ATP but not glucose no characteristic morphology enzyme assay |
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Describe the lab findings of Sickle Cell Trait |
Asymptomatic usually May see hypochromic/microcytic anemia target cells decreased oxygen - sickle cell crisis hemoglobin electrophoresis |
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Describe the lab findings of Sickle Cell Anemia |
Sickle cells Target cells Howell Jolly Bodies Basophilic stippling NRBC Polychromasia Osmotic fragility decreased Hemoglobin electrophoresis |
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Describe the Lab findings of Alpha Thalassemias |
Hemoglobin H inclusions seen with supravital stain Microcytes, Hypochromasia Polychromasia Hydrops fetalis produces Hemoglobin Barts |
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Describe the lab findings of Beta Thalassemia Minor |
Asymptomatic Little to no anemia |
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Describe the lab findings of Beta Thalassemia Major |
Decreased Hgb A, incerased Hgb F and A2 RBC normal or increased Microcytic/Hypochromic Retic increased Polychromasia Target cells Ovalocytes NRBCs Basophillic stippling
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Describe the lab findings of Paroxysmal Nocturnal Hemoglobinuria |
Blood acidosis No spherocytes Hamms test positive Hemolysis occurs upon waking up due to pH changes |
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Describe the lab findings of Immune Hemolytic Anemias due to alloantibodies |
HDN: Mild - mild anemia moderate- anemia, polychromasia, howell jolly bodies, basophillic stippling, spherocytes, NRBCs, decreased plt count. may have increased WBC count. Dat positive Hyperbilirubinemia Severe - intrauterine death |
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Describe the lab findings of Auto Immune Hemolytic Anemias (warm & cold) |
Hemolytic picture |
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Describe the lab findings of Immune Hemolytic Anemias due to complement activations |
Dat positive Donath Landsteiner positive |
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Describe the lab findings of hemolysis due to Mechanical and Chemical Trauma |
Mechanical - Hemolytic picture Chemical - Heinz bodies and bite cells |
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Describe the lab findings of hemolysis due to Infections and Parasites |
1 parasite seen is diagnostic |
