NR 507: MIDTERM REVIEW
Hematology
Hematopoiesis: - The process of blood cell production
-Constant through life to replace Red Blood Cells that grow old and die, are killed by disease, or are
lost due to 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 formRBC, 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 thetissues, 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)-distorterythrocytes 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 willbecome
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
-Autoimmune gastritis-impaired intrinsic factor (transporter needed for vitamin B12
absorption)
Hematology
Hematopoiesis: - The process of blood cell production
-Constant through life to replace Red Blood Cells that grow old and die, are killed by disease, or are
lost due to 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 formRBC, 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
<clip_image001.png>
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 thetissues, 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)-distorterythrocytes 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 willbecome
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
-Autoimmune gastritis-impaired intrinsic factor (transporter needed for vitamin B12
absorption)
