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toxicology ch 11

QuestionAnswer
.Primary toxicity >1blood components are directly affected Cytoreductive or antimitotic agents
Secondary toxicity consequence of other tissue injury or systemic disturbances Affect nutrient supply (iron); clearance of toxins/metabolites (urea); production of growth factors (erythropoietin), granulocyte colony-stimulating factor (G-CSF)
Fetal hematopoiesis liver, spleen, bone marrow, thymus, lymph nodes
Adult hematopoiesis red bone marrow of axial skeleton & proximal limbs
The Erythrocyte 40% to 45% of blood volume, principal transport of oxygen & carbon dioxide; carrier and/or reservoir for drugs/toxins
CBC RBC count, H&H, mean corpuscular volume (MCV), reticulocyte count establish real anemia
Shift in plasma volume alters relative concentration of RBCs Can be confused w/ true anemia or erythrocytosis
2 mechanisms of anemia lower production or ­ destruction of erythrocytes destruction accompanied by ­ reticulocytes
Two processes contribute to ­ reticulocytes destruction accompanied by compensatory ­ in production during compensatory erythroid hyperplasia, reticulocytes released earlier in their life span
Heme synthesis incorporation of iron into porphyrin ring
.Iron deficiency anemia common; dietary deficiency or ­ blood loss = ¯ Hgb synthesis
Congenital thalassemia syndromes microcytosis, imbalance in α- & β-chain production; may be fatal
Sideroblastic anemia defect in synthesis of porphyrin ring; accumulated iron precipitates in perinuclear mitochondria of erythroblasts*
Megaloblastic anemia deficiency of folate &/or vitamin B12, cell cannot progress from G2 to prophase
Drug-induced aplastic anemia predictable or idiosyncratic rxn to xenobiotic; life-threatening disorder; characterized by peripheral blood pancytopenia, reticulocytopenia, bone marrow hypoplasia
Pure red cell aplasia syndrome caused by genetic defect, infection, immune-mediated injury, myelodysplasia, drugs, or other toxicants; peripheral smear relatively normal; marrow lacking RBC phenobarbital precursors*
Methemoglobinemia oxidation of heme iron to ferric state (Fe3+)
Microangiopathic Hemolytic Anemia Fibrin formation causes RBC fragmentation Schistocytes*
.Oxidative Hemolysis Most common defect: glucose-6-phosphate dehydrogenase (G-6-PD) deficiency ¯ repair ability = ­ ROS Often asymptomatic until RBCs exposed to oxidative stress
Nonoxidative Chemical-Induced Hemolysis Severe hemolysis, w/ anemia, jaundice, hemoglobinuria Arsine, lead, copper, chromium, venoms
Immune Hemolytic Anemia Mediated by interaction of IgG or IgM & RBC surface Ag
Myelotoxicity common w/ cytoreductive chemotherapy drugs (¯ mitosis, ­ DNA adducts)risk for toxic sequelae (i.e., infection); dose-related; monocytes recover 1st Effect ¯ by more specific treatments, cotreatments
Effects on Function in vivo effects rare Ethanol, glucocorticoids, radiographic contrast media impair/inhibit phagocytosis
.Idiosyncratic Toxic Neutropenia Affect on stem cells more severe Induces sudden agranulocytosis (¯ neutrophils); may cause aplastic anemia (bone marrow failure)
Mechanisms of Toxic Neutropenia .Immune-mediated neutropenia Xenobiotic acts as hapten (ab-ag rxn) or stimulates production of antineutrophil ab
Non-immune-mediated toxic neutropenia Genetic predisposition Direct damage: inhibition of granulopoiesis or neutrophil function
Secondary leukemia AML*/MDS (myelodysplastic syndromes) patients w/ hx of environmental, occupational, or therapeutic exposure to hematotoxins or radiation
Mechanisms of Toxic Leukemogenesis AML: dominant leukemia associated w/ toxicant exposure Cytogenetic abnormalities, i.e., loss of all or part of chromosomes 5 & 7
Created by: aceofspades08
 

 



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