week 10 mariel

• Major blood components

  • Plasma/water content of blood (55%) = proteins, albumins, globulins, fibrinogen, electrolytes, waste products
  • Cellular (40-45%) = Erythrocytes , Leukocytes, & Thrombocytes
• Hematopoiesis


  Complex process of the formation and maturation of blood cells
• Bone marrow


  • Site of hematopoiesis
  • Pelvis, Sternum, Vertebrae, Ribs
  • Embryonic site would be liver and spleen
• Stem cell


  A component in our bone marrow. We are able to reproduce different cellular components in our blood.
• Types of blood cells

  • Lymphoid - T or B Lymphocytes
  • Myeloid - erythrocytes, leukocytes, and platelets

  
• Erythrocytes/Red blood cells


  • Biconcave, a very thin membrane that allows diffusion, consists primarily of hemoglobin
  • Life span is 120 days
• Erythropoiesis


  1. Process of formation of red blood cells

  2. Kidneys are responsible for helping to develop erythropoiesis, because kidneys can detect low levels of oxygen
• Erythropoietin


  Stimulates differentiation of the primitive myeloid stem cell into erythroblasts, kidney stimulates production of erythropoietin/rbc when it detects low levels of oxygen
• Types of leukocytes


  • Granulocytes - Neutrophils, Eosinophils, Basophils
  • Agranulocytes - Monocytes, Lymphocytes
• Thrombocytes

  Plays an essential role in control of bleeding. Clotting factor (Injury → release of endothelin → vasoconstriction (1st defense in terms of bleeding) in the area of the injury → stimulation of von wille brand factor → attracts platelets in the site of injury → clot formation temporary plug → clotting cascade; you will not bleed to death)
• Anemia


  Reduction in the number of RBC and/or hemoglobin concentration compared with normal values for age
• Safe value/range of hemoglobin across all life span is 10g/dl and above
• Much older child or adolescence= 10g/dl
• Children age 6-10 years old = 11.2-14.5g/dl
• Full grown adult = should be at least 11g/dl
• Main causes of anemia

  • Hypoproliferative - inadequate production
  • Hemolytic- Increase destruction of rbc
  • Hemorrhage- excessive loss
• Iron deficiency anemia

  Inadequate supply or loss of serum iron
• At birth a full term has: 300 mg iron is needed at birth to 5-6 months of life
• Clinical manifestations of IDA

  • Pallor (pale because lack of rbc)
  • Fatigue (tired because not enough oxygen)
  • Dizziness
  • Glossitis
  • Tachycardia (compensatory mechanism)
  • Koilonychia (spoon-shaped nail)
  • Angular stomatitis
• Diagnostics for IDA


  • RBC count is small (microcytic/hypochromic)
  • Mean Corpuscular Volume (MCV) is decreased
• Therapeutic management for IDA

  • Dietary management; Iron-fortified food/milk substitute for breastmilk, importance of correct complementary feeding
  • Administration of ferrous iron (more readily absorbed than ferric iron) can be oral/liquid/parenteral
  • Blood transfusion in severe cases (packed RBC not whole blood to avoid circulatory overload)
• Nursing management for oral iron

  • Give before meals, can be given after meals but potency is reduced by 50%
  • Take with Vitamin C rich juice to enhance absorption by reducing to its most soluble form
  • Do not give antacids or dairy products. It diminishes absorption
• Nursing management for liquid iron

  • Administer via straw to prevent teeth staining
  • Do oral care before and after administration
  • Instruct that dark colored stool is normal
  • Increase fluid intake to avoid constipation
• Nursing management for parenteral iron

  • Use the Z-track method in administration IM injection to avoid leakage, and staining the skin, and avoid massaging the injection site. maintain z-track for 5 minutes after administration
  • If it is done through ID or SQ it can lead to staining of the skin and might harm those tissues
  • Provide health teaching (diet and medications)
  • Do skin and oral care after administration and bed rest
• Sickle cell anemia


  • Presence of abnormally shaped elongated rbc
  • Inheritance - which causes the hemoglobin molecule to be defective
  • Exposure to low oxygen tension, dehydration, and temperature elevation by this sickle hemoglobin (Hbs) causes it to become crystal like and lose its original round, biconcave, and pliable structure
• Clinical manifestations of sickle cell anemia

  • S/sx of anemia
  • Jaundice (elevated bilirubin level)
  • Enlargement of bones (face and skull)
  • Tachycardia
  • Cardiac murmurs
  • Cardiomegaly
  • Dysrhythmia
  • Splenomegaly (since it is elongated; usually stuck in the entrance of the spleen = pooling of rbc/blood = can add up to the jaundice of the patient)
• Diagnostics for sickle cell anemia

  • Blood smear- sickled rbc
  • Sickle cell turbidity test (blood mixed with special solution - POSITIVE = turbid or cloudy, NEGATIVE = clear)
  • Hemoglobin electrophoresis – determines abnormal shaped RBC
• Types of sickle cell crises

  • Sequestration crisis- splenomegaly; pooling of large quantities of blood in the spleen
  • Aplastic crisis- diminished RBC production usually triggered by infection (parvovirus)
  • Hyperhemolytic crisis- accelerated RBC destruction resulting to jaundice and reticulocytosis
• Therapeutic management for sickle cell anemia

  • Hydroxyurea - increases concentration of HgbF. Helps rbc to become biconcave
  • Hematopoietic stem cell transplant- the only potential cure because the stem cell in our bone marrow will be replenish/renewed hence there is a chance that our body will be no longer produced a sickle cell rather, the body will now produce a normal biconcave RBC
  • Bed rest, hydration, electrolyte replacement, analgesia, blood transfusion/replacement therapy, antibiotics and vaccines (flu vaccine, pneumococcal vaccine, and meningococcal vaccine)
• Nursing management for sickle cell anemia

  • Minimize tissue deoxygenation
  • Hydration
  • Minimize crises
  • Promote supportive therapy
• Aplastic anemia


  • Rare type; bone marrow cannot produce different blood components resulting in pancytopenia (everything is defeated); everything will be below normal
  • Bone marrow hypoplasia/aplasia resulting to pancytopenia
  • Decrease or damage to marrow stem cell, damage in the microenvironment within the marrow, replacement of the marrow with fat since it is not working
• Etiology of aplastic anemia

  • Idiopathic
  • Congenital or acquired
  • Exposures to chemicals (benzene)
  • Viral infections
• Clinical manifestations of aplastic anemia

  • Infection
  • Anemia (fatigue, pallor, dyspnea)
  • Purpura (bruising)
  • Bleeding tendencies
• Bone marrow aspiration and biopsy (visible fatty marrow and few or no cells) is used for diagnosis of aplastic anemia
• Therapeutic management for aplastic anemia

  • Bone marrow transplant - younger than 60 years of age, healthy,compatible donor can be used
  • Peripheral stem cell transplantation
  • Immunosuppressive therapy
  • Blood transfusion, PRN
• Nursing management for aplastic anemia

  • Assess carefully for signs of bleeding and infection
  • Encourage frequent resting periods
  • Reverse or protective isolation
  • Good personal hygiene
  • Monitor VS especially temperature
  • Minimize bleeding (use soft bristle toothbrush, avoid injections, stool softener, nails should be short)
  • Immunosuppressive treatment (after transplantation)
  • Use ice pack to control bleeding (apply pressure)
• Beta-thalassemia


  • Body does not produce enough hemoglobin. Thalassemia comes from the Greek word '' thala/tala'' means ocean. In history most of the people who have thalassemia are those persons living near the ocean.
  • Classified according to the hemoglobin chain affected and the amount of the globin chain that is synthesized.
  • The two major categories are x-thalassemia and B-thalassemia. Thalassemia is seen in various population groups, such as Asians, Africans, and inhabitants of the Mediterranean and Middle Eastern regions, and the majority of births of affected individuals occur in these groups
• Clinical manifestations of B-thalassemia

  • Anemia (Before Diagnosis) - Pallor, Unexplained fever, Poor feeding, Enlarged spleen or liver
  • Progressive Anemia Signs of chronic hypoxia - Headache, Precordial and bone pain, Decreased exercise tolerance Listlessness, Anorexia
  • Other Features - Small stature, Delayed sexual maturation, Bronzed, freckled complexion (if not receiving chelation therapy)
  • Bone Changes (Older Children If Untreated) - Enlarged head, Prominent frontal and parietal bosses, Prominent malar eminences, Flat or depressed bridge of the nose, Enlarged maxilla, Protrusion of the lip and upper central incisors and eventual malocclusion Generalized osteoporosis
• Hemoglobin electrophoresis confirms the diagnosis of beta-thalassemia and is helpful in distinguishing the type and severity of the thalassemia because it analyzes the quantity and kind of hemoglobin variants found in the blood
• Therapeutic management for beta-thalassemia

  • Maintain 9.5g/dl hemoglobin; if below, have a packed rbc and BT at least 3x a week
  • Administration of Deferoxamine- (iron-chelating agent)