NR 507: MIDTERM REVIEW (A GUARANTEED)
Hematology
Hematopoiesis: -process of blood cell production
-Constant throughout life to replace RBCs that grow old and die, are killed by
disease, or are lost through bleeding
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NR 507: MIDTERM REVIEW (A GUARANTEED)
Hematology
Hematopoiesis: -process of blood cell production
-Constant throughout life to replace RBCs that grow old and die, are killed by
disease, or are lost through bleeding
-Occurs in liver and spleen of fetus
-Occurs in bone marrow after birth
-2 stages: 1. Proliferation (mitotic division)
2. Maturation (differentiation)
-Bone marrow: red (hematopoietic/active) & yellow (fatty/inactive)
Hematopoietic stem cells (HSCs)- all blood cells are created from HSCs
-signaled to undergo differentiation (by cytokines and chemokines, growth
factors) to form RBC, WBC, & platelets
· Lymphoid: T cell (T-lymphocyte) & B cell (B-lymphocyte)
· Myeloid: Monocyte & Granulocytes (WBCs)
· Erythrocyte (RBC)
· Megakaryocyte (Platelets)
Mesenchymal stem cells-develop into osteoclasts, fibroblasts, & adipocytes
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Erythropoietin: -hormone that stimulates erythrocyte production
-Secreted by the kidneys in response to tissue hypoxia
Erythrocyte: -most abundant cells in the body
-primarily responsible for tissue oxygenation
-mature erythrocytes lack a nucleus and mitochondria, cannot synthesize protein
or carry out oxidative reactions. Cannot divide *anaerobic metabolism only
-life span: 100-120 days
-contains hemoglobin molecules
o Stages: (7-day process)
· Hemocytoblast (stem cell) binds with erythropoietin
· Proerythroblast- committed to morph into RBC
· Erythroblast- ribosome synthesis (2 phases)
· Normoblast- Hgb accumulation & nucleus ejection
· Reticulocyte –(immature RBC) released into circulation, no nucleus, ribosome,
or mitochondria
· RBC (after it has been in bone marrow 1-2 days)
Hemoglobin: oxygen carrying protein of the erythrocyte
-hemoglobin packed blood cells pick up oxygen in the lungs and exchange it for
carbon dioxide in the tissues
-composed of 2 pairs of polypeptide chains (globins) & 4 colorful iron complexes
(hemes)
-can carry up to 4 molecules of oxygen
Oxyheoglobin- binding of oxygen to Fe in heme molecule, RED
Deoxyhemoglobin- reduced hemoglobin, after it releases the oxygen to the
tissues, BLUE
Risk factors and causes for developing any type of anemia:
-blood loss (acute or chronic)
-impaired erythrocyte production
-increased erythrocyte destruction
-a combination of these factors
Iron Deficiency Anemia- Microcytic-Hypochromic Anemia
-most common nutritional disorder
-occurs when iron stores are depleted reduced hemoglobin synthesis
-more common in toddlers, adolescent girls and, women of childbearing age
-causes:
· Dietary deficiency
· Impaired absorption
· Increased requirement
· Chronic blood loss
Thalassemia-Microcytic-Hypochromic
-inherited autosomal recessive disorder
-impaired synthesis of one of the two chains of adult hemoglobin (alpha or beta)
-common among Mediterranean descent
-can be minor or major, can be asymptomatic or lethal (Cooley’s)
Sickle Cell Anemia-Normocytic-normochromic/Hemolytic
-inherited autosomal recessive disorder
-presence of atypical hemoglobin-Hemoglobin S
-amino acid change on the beta-globin chain (glutamine replaced for valine)-
distort erythrocytes into sickle shape= cannot properly carry O2.
-vaso-occlusive crisis (pain), aplastic crisis (anemia), sequestration crisis (blood
pooling in spleen), hyperhemolytic crisis ( accelerated RBC destruction)
- Stress, hypoxia, anxiety, fever, cold, dehydration = lower O2 binding
-↑ risk of CVA, splenic damage, or kidney damage. Most people with sickle cell
will become asplenic by adulthood.
Hemolytic Anemia-
-premature destruction of erythrocytes
-majority occur within phagocyctes in lymphoid tissue
-congenital (sickle cell or thalassemia) acquired (transfusion reaction, infection,
autoimmune)
-causes elevated erythropoietin to induce accelerated production of erythrocytes
and in increase in the products of hemoglobin catabolism
-transfusion with incorrect blood type: intravascular hemolysis by activation of
complement system; extravascular hemolysis by phagocytosis of antibody-coated
erythrocytes in spleen
Pernicious Anemia-Macrocytic
-vitamin B deficiency
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