6.1 RBC & Disorders Flashcards
Red Blood Cells
Erythrocyte - Shape allows red blood cell to increase surface area for oxygen diffusion and change shape without rupturing.
Hemoglobin - Facilitates oxygen transportation
Erythropoiesis - Creation of red blood cells from bone marrow
Erythopoiesis
- Number of RBC is maintained by feedback mechanism called Erythropoietin, hormone produced in kidneys.
- From here it goes to Bone Marrow where it matures
- Erythropoietin is stimulated by decreased population of RBC, increased tissue oxygen consumption, decreased hemoglobin synthesis, hemorrhage.
- MAIN STIMULUS FOR RBC PRODUCTION IS HYPOXIA
Erythropoiesis phases
Stem Cell - Undifferentiated and may become erythroblast, myeloblast, lymphoblast.
Committed Cell - Immature erythrocyte with nucleus (Erythroblast)
Normoblast - Cell stuffed with hemoglobin and loses nucleus
Reticulocyte - Immature newly produced RBC. Increase in number reflects increase bone marrow activity
Mature RBC
Hemoglobin Synthesis
- Hemoglobin storage/synthesis begins in early erythroblast stage.
- Contains more than 250 million hemoglobin
- Lack of iron decreases hemoglobin in RBC
- Iron comes mainly from dietary intake (duodenum)
- Iron combines with apotransferrin to form transferrin
- Transferrin carried in plasma and stored as ferritin
- Transferrin can also be delivered to developing RBC’s in bone marrow and used for heme synthesis
Iron Cycle
- Most iron is contained and bound to Heme (red pigment in hemoglobin) in erythrocytes and muscle
- Remained is bound to ferritin/macrophages/hepatic parenchymal cells.
- When RBC’s are destroyed iron is recycled
- Iron absorption goes up when stores decrease, and excretion is accelerated when Iron is increased
Erythrocyte Life Cycle
- Released from bone marrow and enter blood stream
- RBC destroyed by splenic macrophages (phagocytic)
- Broken down into Heme and Globin molecule
- Heme releases iron and bilirubin for recycling
Bilirubin Cycle
- Aged RBC’s are destroyed in spleen via macrophages
- Iron is recycled to make new hemoglobin
- Transferrin (glycoprotein) makes recycle possible
- Bilirubin is produced in RBC breakdown and transported to the liver to be excreted in bile
- Failure of this process results in Jaundice
Anemia
- Decrease in total RBC’s in circulation or decrease in quality and quantity of hemoglobin
- Caused by impaired RBC production, acute/chronic blood loss, increased RBC Destruction
- Symptomatic Anemia (< 8 g/dL)
Anemia (cont)
Classification - Either by Etiology or Morphology
Etiology
Decreased/Defective production of erythrocytes or increased destruction of erythrocytes
Anemia Morphology (RBC Indices)
Mean Corpuscular Volume (MCV) - Size of cell
Mean Corpuscular Hemoglobin (MCH) - Quantity of hemoglobin in RBC
Mean Corpuscular Hemoglobin Concentration (MCHC)
Amount of hemoglobin per cell volume
Size
Macrocytic/Microcytic
Hemoglobin Content
Hyperchromic (Increased MCHC/Darker Color)
Hypochromic (Decreased MCHC/Paler Color)
Hematology Normal Ranges
Important
Check document
Manifestation of Anemia (Categories)
- Decreased oxygen transport resulting in compensatory mechanisms.
- Decrease in RBC indices and hemoglobin level
- Signs/Symptoms associated with pathologic process associated with anemia
Signs/Symptoms of Anemia
- Weakness
- Fainting
- Pallor
- Tachycardia
- Angina (Pressure/tightening/pain in chest)
- Heart failure
- Hemolytic (rupture) - Anemia
Iron Deficiency Anemia (Etiology/Pathophysiology)
- Most common type of Anemia
(Microcytic - Hypochromic)
Etiology
Decreased iron intake, Iron loss (Blood Loss), Increased bodily demands (pregnancy, infancy, adolescence)
Pathophysiology
- Deficiency in iron leading to hemoglobin and defect in oxygen carrying capacity
Iron Deficiency Anemia (Diagnostic Studies)
- Decreased hemoglobin and hematocrit
- Decrease in Ferratin (indicates iron stores)
- TIBC (Total Iron Binding Capacity) elevated
- Elevated serum transferrin (body’s attempt to harvest more iron from intestines)
- Tested via Endoscopy/colonoscopy to reveal marrow stores of hemoglobin
Iron Deficiency Anemia (Clinical Manifestations)
Microcytic/Hypochromic Anemia (Pale, Small RBC’s)
- Fatigue
- SOB
- Epithelial Atrophy
- Tachycardia
Iron Deficiency Anemia (Nursing Management)
- Treat source of blood loss
- Oral replacement of Iron
- IM Replacement (Not preferred, Z Track method)
- IV Replacement (Iron Sucrose or Iron Dextan)
Iron Deficiency Anemia (Nutritional Therapy/Patient Education)
Animal Protein - Heme Iron
Plant Protein - Non-Heme Iron
- Take oral iron with full meal and glass of water. Stool softeners because constipation may be an issue, stool becomes dark and tarry when taking iron, vitamin C helps body absorb iron, should not lie down for 1 hour after taking iron
Aplastic Anemia
- Rare (Failure of bone marrow to replace RBC)
Lack of all 3 Blood cells (WBCs, RBCs, Platelets)
Etiology - Radiation/chemotherapy, toxins, idiopathic
Most cases are idiopathic
Pathophysiology - Bone Marrow Hypocellularity
Aplastic Anemia (cont)
Clinical Manifestations
- Increased Infections, Fatigue, Pallor, Weakness, Petechia, Ecchymoses (bruising), bleeding
(Normocytic, Normochromic Anemia)
Management
- Blood transfusion, bone marrow stimulation medications, immunosuppressants, bone marrow transplant, stem cell transplant
Pernicious Anemia
- Macrocytic and Normochromic Anemia
- Lack of intrinsic factor from parietal cells to absorb vitamin B12. (B12 deficiency)
Clinical Manifestations - Typical Anemia, Nerve Demyelination, Difficulty Walking, jaundice, splenic enlargement, loss of appetite, abdominal pain.
Pernicious Anemia (cont)
Testing
- Serum Parietal and Intrinsic Factor Antibodies
- Gastric Biopsy (achlorhydria)
- Schilling Test - Urine excretion of B12 (Rarely Done)
Treatment
- Parental, sublingual, high oral dose of Vitamin B12
Folate Deficiency Anemia
- Macrocytic and Normochromic anemia with B12 deficiency
Pathogenesis
- Malabsorption of folate (occurs in upper small intestines)
Clinical Presentation
- Similar to Pernicious Anemia except neurologic manifestations are not seen. Fissures of lips (cheilosis) ulcers in buccal mucosa and tongue
Folate Deficiency Anemia (cont)
Diagnosis
- Folate and B12 Levels
Treatment
- Oral folate 1mg/day
Sickle Cell Anemia
- Presence of abnormal structure of globin chain
Normochromic (no iron deficiency and hemolytic)
Disorders
Sickle Cell Trait - Inherit Hgb A from one parent and Hgb S from another parent (Does not normally sickle)
Sickle Cell Disease - Inherit Hgb S from both parents
Sickle Cell Anemia (Pathogenesis)
- Caused by Autosomal Recessive Mutation
- Hypoxia, Acidosis, Dehydration, Cold Exposure can cause RBC’s to change their configuration
- Cells stretch into sickle shape, and become dense and rigid
- RBC’s are more prone to lysis
- Slows down blood flow
- Clot formations are common
- Patient experiences ischemia injuries
Sickle Cell Anemia (Clinical Presentation)
Acute - Hemolytic Anemia, Enlarged Spleen, Pulmonary Hypertension, DVT, Stroke Risk, Increased Risk of Infection
Chronic - Persistent Anemia, Avascular Necrosis, Organ Damage (Renal Ischemia/Renal Failure)
Sickle Cell Anemia
- Severity relates directly to proportion of HbS in RBC
Diagnosis - Newborn Screening (Sickledex) - Cannot distinguish sickle cell disease from sickle cell trait
- Presence of sickling in peripheral smear
- Hemoglobin electrophoresis and high performance liquid chromatography identifies different types of Hgb
Sickle Cell Anemia Treatment
- Correct precipitating factor
- Reverse hypoxemia
- Hydration
- Pain Medication
- Hydroxyurea - Medication that increases fetal hemoglobin (HbF) which reduces Hemoglobin S polymerization
Polycythemia
- Overproduction of RBC’s (erythrocytosis)
Polycythemia Vera
- Abnormality of stem cells in blood marrow
- Increased blood volume and viscosity (risk of thrombosis)
Diagnosis - Bone marrow biopsy
Treatment - Phlebotomy (removal of blood), Hydroxyurea, Pegylated INF (slow RBC production)
