Chapter 20 Flashcards
Erythropoetin, EPO, promotes the survival of early erythroid progenitor cells via inhibition of the default apoptosis pathway. This, EPO rescues stem cells that are otherwise fated to undergo programmed cell death.
Erythropoetin, EPO, promotes the survival of early erythroid progenitor cells via inhibition of the default apoptosis pathway. This, EPO rescues stem cells that are otherwise fated to undergo programmed cell death.
Mean corpuscular volume, MCV, is the index used to measure the volume of a red blood cell. It categorizes RBCs by size.
Normal size RBC = normocytic
Smaller size RBC = microcytic
Larger cells are referred to as macrocytic.
Mean corpuscular volume, MCV, is the index used to measure the volume of a red blood cell. It categorizes RBCs by size.
Normal size RBC = normocytic
Smaller size RBC = microcytic
Larger cells are referred to as macrocytic.
Mean corpuscular hemoglobin concentration measures hemoglobin content.
Mean corpuscular hemoglobin concentration measures hemoglobin content.
Macrocytic anemia may be caused by impaired DNA synthesis due to a deficiency of folic acid, B9, or vitamin B12.
This results in abnormal nuclear development, ineffective erythrocyte maturation, and macrocytic anemia.
Folic acid deficiency is most commonly due to inadequate dietary intake, which often develops in patients with poorly balanced diets, like alcoholics.
Macrocytic anemia may be caused by impaired DNA synthesis due to a deficiency of folic acid, B9, or vitamin B12.
This results in abnormal nuclear development, ineffective erythrocyte maturation, and macrocytic anemia.
Folic acid deficiency is most commonly due to inadequate dietary intake, which often develops in patients with poorly balanced diets, like alcoholics.
Possible causes of macrocytic anemia include liver disease, hypothyroidism, and primary bone marrow disease.
Possible causes of macrocytic anemia include liver disease, hypothyroidism, and primary bone marrow disease.
Chronic disease and renal disease cause normochromic, normocytic anemia.
Chronic disease and renal disease cause normochromic, normocytic anemia.
Iron deficiency and thalassemia are microcytic anemias.
Iron deficiency and thalassemia are microcytic anemias.
Pernicious anemoa is an autoimmune disorder in which patients develop antibodies against gastric parietal cells and intrinsic factor. Parietal cell antibodies lead to atrophic gastritis with achlorhydria (low gastric acid).
Deficiency of vitamin B12 or B9 results in megaloblastic anemia. Peripheral blood smear shows macrocytosis and hypersegmentation of neutrophils.
Megaloblastic maturation, characterized by cellular enlargement with asynchronous maturation between the nucleus and cytoplasm, is noted in bone marrow precursors from all lineages. Although the bone marrow tends to be hypercellular, the blood demonstrates pancytopenia (low RBC, WBC, & platelets) because of ineffective hematopoesis.
Neurologic symtoms develop in vitamin B12 deficiency, secondary to degeneration of the posterior and lateral columns of the spinal cord.
Pernicious anemoa is an autoimmune disorder in which patients develop antibodies against gastric parietal cells and intrinsic factor. Parietal cell antibodies lead to atrophic gastritis with achlorhydria (low gastric acid).
Deficiency of vitamin B12 or B9 results in megaloblastic anemia. Peripheral blood smear shows macrocytosis and hypersegmentation of neutrophils.
Megaloblastic maturation, characterized by cellular enlargement with asynchronous maturation between the nucleus and cytoplasm, is noted in bone marrow precursors from all lineages. Although the bone marrow tends to be hypercellular, the blood demonstrates pancytopenia (low RBC, WBC, & platelets) because of ineffective hematopoesis.
Neurologic symtoms develop in vitamin B12 deficiency, secondary to degeneration of the posterior and lateral columns of the spinal cord.
Megaloblastic anemias are cause by impaired DNA synthesis of either vitamin B12 or folic acid (B9). In the face of defective DNA synthesis, nuclear development is impaired, whereas cytoplasmic maturation proceeds normally.
This is called nuclear to cytoplasmic asynchrony, and results in the formation of megaloblasts. Because the magaloblastic precursors do not mature enough to be released into the blood, they undergo intramedullary destruction.
Megaloblastic anemias are cause by impaired DNA synthesis of either vitamin B12 or folic acid (B9). In the face of defective DNA synthesis, nuclear development is impaired, whereas cytoplasmic maturation proceeds normally.
This is called nuclear to cytoplasmic asynchrony, and results in the formation of megaloblasts. Because the magaloblastic precursors do not mature enough to be released into the blood, they undergo intramedullary destruction.
Aplastic anemia is a disorder of pluripotential stem cells that leads to bone marrow failiure. The disorder features hypocellular bone marrow and pancytopenia (low RBC, WBC, & platelets). Most cases are idiopathic.
The bone marrow in aplastic anemia shows variabley reduced cellularity, depending on the clinical stage of the disease. There is a decrease in the number of cells of myeloid, erythroid, and megakaryocitic lineages, with a relative increase in lymphocytes and plasma cells.
As the cellularity decreases, there is an increase in bone marrow fat.
Anemia, leukopenia, and thrombocytopenia characterize aplastic anemia. Patients with anemia present with weakness, fatigue, infection, and bleeding.
Aplastic anemia is a disorder of pluripotential stem cells that leads to bone marrow failiure. The disorder features hypocellular bone marrow and pancytopenia (low RBC, WBC, & platelets). Most cases are idiopathic.
The bone marrow in aplastic anemia shows variabley reduced cellularity, depending on the clinical stage of the disease. There is a decrease in the number of cells of myeloid, erythroid, and megakaryocitic lineages, with a relative increase in lymphocytes and plasma cells.
As the cellularity decreases, there is an increase in bone marrow fat.
Anemia, leukopenia, and thrombocytopenia characterize aplastic anemia. Patients with anemia present with weakness, fatigue, infection, and bleeding.
Myelofibrosis shows an increased connective tissue.
Myelofibrosis shows an increased connective tissue.
Microcytic, hypochromic, erythrocytes are characteristic of iron deficiency anemia casued by inadwquate uptake or, more often, excessive loss of iron.
Women who have menorrhagia (abnormally heavy and prolonged menstrual period at regular intervals), especially those who consume restricted diets, are especially prone to iron deficiency anemia.
Iron stores of the body are reduced, as evidenced by reduced levels of serum ferritin and low iron saturation.
Microcytic, hypochromic, erythrocytes are characteristic of iron deficiency anemia casued by inadwquate uptake or, more often, excessive loss of iron.
Women who have menorrhagia (abnormally heavy and prolonged menstrual period at regular intervals), especially those who consume restricted diets, are especially prone to iron deficiency anemia.
Iron stores of the body are reduced, as evidenced by reduced levels of serum ferritin and low iron saturation.
The presence of a peptic ulcer indicates GI bleeding as the cause of anemia. The resulting iron deficiency interferes with heme synthesis and thus leads to impaired hemoglobin production and anemia.
The presence of a peptic ulcer indicates GI bleeding as the cause of anemia. The resulting iron deficiency interferes with heme synthesis and thus leads to impaired hemoglobin production and anemia.
Defective globin chain synthesis and synthesis of structurally abnormal hemoglobin molecules are hemoglobinopathies.
Defective globin chain synthesis and synthesis of structurally abnormal hemoglobin molecules are hemoglobinopathies.
Poor utilization of iron stores reflects sideroblastic anemia and anemia of chronic disease.
Poor utilization of iron stores reflects sideroblastic anemia and anemia of chronic disease.
