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Red Blood Cell Disorders 1 - 3 - Coggle Diagram

- - - - What is EPO?
        
        molecule produced by pericytes from the renal system in response to stress such as hypoxia
- - - - Serum ferritin
      - Hemosiderin
      - Serum total iron-binding capacity
      - Serum iron
      - iron saturation
  - - - causes of macrocytic anemia
        
        Alcohol
        
        Alcohol has a direct toxic effect on erythroid precursors in the bone marrow, Alcohol interferes with folate absorption and metabolism, Chronic alcoholism damages the liver, leading to altered lipid metabolism this causes Increased cholesterol incorporation into RBC membranes leads to macrocytic, abnormally shaped RBCs (spur cells/acanthocytes)
        
        folate deficiency (Vit. B9)
        
        Pernicious Anemia
        
        imaging --> peripheral blood smear finding: Hypersegmented polymorphonuclear leukocytes
        
        cause: pernicious anemia caused by autoantibodies against intrinsic factor or the parietal cells where intrinsic factor is produced (in the stomach; GI) (B12 deficiency)
        
        MDS (Myelodysplastic Syndromes)
        
        a subset of this disorder is associated with sideroblastic anemia
        
        what is it: Clonal disorder causing dysplastic and ineffective hematopoiesis (bone marrow damage)
        
        Liver disease
        
        damages the liver, leading to altered lipid metabolism this causes Increased cholesterol incorporation into RBC membranes leads to macrocytic, abnormally shaped RBCs (spur cells/acanthocytes)
        
        Vitamin B12 (cobalamin)
        
        De-myelination & neuropathological symptoms
        
        Symptoms: include fatigue, glossitis, heartburn/gastritis, paresthesias, weakness, abnormal reflexes (either hyporeflexic or hyperreflexic), and an unsteady gait.
        Pernicious anemia is caused by autoantibodies that target intrinsic factor and gastric parietal cells, resulting in decreased or nonexistent intrinsic factor production. Intrinsic factor binds vitamin B12 in the stomach and is required to facilitate its uptake in the terminal ileum.
      - Types of Macrocytic Anemia
        
        Megaloblastic Macrocytic Anemia (due to defective DNA synthesis)
        
        Non-Megaloblastic Macrocytic Anemia (due to increased membrane surface area or reticulocytosis)
  - - - Subtypes of Microcytic Anemia
        
        Thalassemia
        
        Def: decreased or absent globin chain synthesis
        
        Beta-Thalassemia
        
        inc. Ferritin!! (nothing to hold iron)
        
        Target Cells! RBCs with a central density surrounded by a ring of pallor are seen in thalassemia!
        
        Alpha-thalassemia
        
        hemoglobin bart
        
        chronic disease
        
        iron deficiency
        
        spoon shaped fingernail
        
        Dec.. Reticulocyte count!! In iron deficiency anemia, low iron levels impair hemoglobin synthesis, leading to ineffective erythropoiesis and fewer reticulocytes being produced.
        
        High RDW!
        
        Red Cell Distribution Width) in a blood test measures the variation in size and volume of your red blood cells (RBCs)
        
        congenital sideroblastic anemia
        
        Defect in ALA
      - heme is required to make hemoglobin, and hemoglobin content is a major driver of RBC size. When heme synthesis is impaired, red blood cells can’t load enough hemoglobin, so they undergo extra cell divisions, becoming smaller (microcytic) & and paler (hypochromic)
  - - - Congenital Disorders
        
        Diamond-Blackfan Anemia
    - - low hemoglobin and hematocrit concentrations and manifests in vaso-occlusive crises.
- - - - G6PD Deficiency: G6PD deficiency is an X-linked deficiency of a central enzyme in the hexose monophosphate shunt pathway. G6PD deficiency makes RBCs sensitive to oxidative stress and subsequently causes a hemolytic anemia with exposure to oxidative stresses. Imaging: in a peripheral blood smear stained with crystal violet, precipitated hemoglobin appears as a small, round inclusion within the RBC (seen in this patient’s sample), known as a Heinz body.
      - Auto-immune hemolytic anemia: Spherocytes (RBCs lacking central pallor) and reticulocytes may appear on a peripheral blood smear.
    - - Paroxysmal Nocturnal Hemoglobinuria
        
        cola-colored”/ brown urine in the morning! can result in anemia along with thrombocytopenia and/or leukopenia (neither of which is seen in this patient). PNH is caused by an acquired defect in membrane proteins that ordinarily protect RBCs from destruction by complement.
      - Microangiopathic Hemolytic Anemia (MAHA) – Mechanical destruction (TTP, HUS, DIC, prosthetic heart valves
        
        Mechanical RBC destruction with MAHA can occur secondary to a mechanical heart valve or calcified/stenosis valves.
  - - - Where: Spleen, liver, lymph nodes (outside blood vessels)
        Mechanism: Macrophages eat up RBCs that are damaged or coated with antibodies.
    - - Paroxysmal Nocturnal Hemoglobinuria (Both but primarily intravascular)
      - Where: Inside blood vessels
        Mechanism: RBCs are destroyed directly in circulation (e.g., mechanical trauma, complement fixation).
  - - - Hereditary spherocytosis: in the setting of ingesting an oxidizing substance, such as a drug (eg, primaquine, dapsone) or fava beans, or a systemic infection (eg. Parvovirus B19). And look for round RBCs in imaging