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28 Cards in this Set
- Front
- Back
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What are the normal ranges for RBC count?
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adult males: 4.6-6.2 mil
adult females: 4.2 - 5.4 mil high count = polycythemia low count = anemia |
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What are the functions of RBC?
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transport O2 to tissues, remove CO2
maintenance of pH homeostasis (globin) contribution of blood viscosity lower blood oncotic P by keeping Hb inside cells |
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What are some of the Hb reactions?
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Oxyhemoglobin: Hb + O2 (O2 attaches to Fe in heme)
Reduced Hb: (deoxyHb) -combines with H+ and acts as buffer Methemoglobin (MetHb): -iron oxidized from Fe2+ to Fe3+ -incapable of carrying oxygen --> cyanosis carboxyhemoglobin: Hb + CO -CO has 200x more affinity for Hb than O2 causes CO poisoning |
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What is Erythropoiesis?
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first precursor is proerythroblast - no hemoglobin and has organelles
further differentiation has 3 features: -decreased size and nuclear extrusion -loss of organelles; ribosomes account for blue cytoplasmic basophilia (blue staining) -increase in Hb content marks increased eosinophilia (pink staining) |
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What are the stages of Erythropoiesis?
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3-5 cell divisons between proerythroblast --> mature erythrocyte
from first cell to release of reticulocytes = 7 days formation in order: -proerthyroblast -basophilic erythroblast -polychromatophilic erythroblasts (mitosis stops after this stage) -orthochromatophilic erythroblast (normoblasts) -reticulocytes -erythrocytes |
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What are essentials in the production of erythrocytes?
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erythropoietin (produced in kidneys that stimulates mRNA for globin)
iron folic acid vitamin B12 |
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What are reticulocytes?
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immature red blood cells, shed nucleus but retain nuclear material
contain few mitochondria and golgi complex enter blood and within 1-2 days develop into mature RBC supravital staining - cannot be seen in stained blood but by basic dyes show blue precipitate due to RNA remnants |
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What are the functional changes going from proerythroblast --> RBC?
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appearance of Hb:
-stem cells and proerythroblasts have no Hb -some Hb is present in early erythroblasts -late erythroblasts are saturated with Hb Degeneration of the nucleus: -starts in late erythroblast stage -disappears by the reticulocyte stage cell organelles: -reticulocytes contain remnants of DNA and cell organelles progressive decrease in cell size only mature RBC and reticulocytes present in blood |
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What are characteristics of reticulocyte and erythropoiesis rates?
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normal reticulocyte count: 1 % (2-6 % in newborns)
increase in reticulocyte = increase in RBC production (hypoxia, hemorrhage, stress, therapy of anemia) lower reticulocyte count = lower erythropoiesis (low EPO production, lower ability of bone marrow to respond to EPO, nutritional anemia) |
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What happens in hypoxia?
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1. stimulates EPO production by 90 % kidney and 10 % liver
2. this then increases production of hematopoietic stem cells 3. increased RBC proudction liver is an important source of EPO in the fetus, but less sensitive to hypoxia than kidneys |
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How do Vitamin B12 and Folic Acid control Erythropoiesis?
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increase synthesis of DNA causing rapid proliferation of erythroblastic cells
B12: -required for action of folic acid on erythropoiesis -in GI Tract binds with IF -B12+IF --> binding to mucosal receptors in intestine transporting it across the intestinal mucosa -release of blood freed of IF -binding to plasma globulins --> red bone marrow or storage in liver (3-4 year reserve) |
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What are some outside factors affecting control of erythropoiesis?
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testosterone - stimulates release of EPO
adrenal cortical steroids and ACTH: -stimulate EPO in physiological concentrations -large doses are inhibitory |
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How are RBC destroyed?
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site of destruction:
-circulating blood -macrophage system (spleen and liver) Senescent RBC: -lower metabolic rate, increase fragility leading to rupture of membrane when RBC passes through tight spots of circulation (ex. red pulp of spleen) |
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What are the stages of Hb metabolism?
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Prehepatic:
-removal of Hb (macrophaged) -conversion of hem into biliverdin & CO --> bilirubin --> blood plasma -in plasma water insoluble bilirubin combines with albumin to form water soluble complex --> liver Hepatic: -bilirubin + glucuronic acid (replacing albumin) --> bilirubin mono or bi-glucoronide (water soluble) and secretion of conjugated bilirubin into bile Posthepatic: -takes place in GI and kidneys -formation of urobilinogen from bilirubin -converts stercobilinogen --> oxidation and excretion in feces as stercobilin -this is absorbed by small intestine and excreted by kidneys as urobilinogen |
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How is iron metabolized in blood?
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1. dissociation of Fe from heme --> plasma --> binding to transferrin, transport into blood
2. detachment from transferrin and storage in liver, muscles, and macrophages attached to ferritin or hemosiderin 3. release from storage sites and transport into blood by transferrin 4. transport into RBC precurso by endocytosis leading to heme synthesis |
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What happens in iron overload?
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under normal conditions, no free iron. bound to:
-plasma proteins (transferrin) -intracellular proteins (ferritin, hemosiderin, Hb, myoglobin, cyt C) increased reabsorption of dietary iron in GI leads to iron overload: -saturation of transferrin leading to increased plasma level of free iron -this increased deposition of iron in tissues leads to increased iron storage in ass. with hemosiderin-insoluble complex diseases of liver, heart, endocrine pancreas, gonads |
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What is Anemia?
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deficiency of blood due to low RBC count or low Hb quantity in RBC
results in: -hypoxia -increase in pulse and respiratory rates -lower exercise and cold tolerance -higher fatigue -lower blood viscosity |
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What is Nutritional Anemia?
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1. Iron deficiency - microlytic hypochromic anemia
-due to chronic hemorrhage (ulcer, tumor, excess menstruation) or increase iron demands (pregnancy) -low RBC and Htc -RBC small and pale 2. Deficiency of B12, Folic Acid, or IF - Megaloblastic anemia -maturation failure: decreased rate of erythroblast proliferation, more precursor cells (megaloblasts), low fragility to plasma membrane decreasing life span |
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What is Hemorrhagic anemia?
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abnormal blood loss
replacement of lost fluid within 1-3 days causing dilution of RBC normocytic |
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What is Aplastic Anemia?
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suppression or destruction of bone marrow
normocytic |
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What is Hemolytic Anemia?
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high rate of RBC destruction:
-hereditary spherocytosis: spherical cells -sickle cell: sickle shape thalassemias: -hereditary -low amount of globin -cells are microcytic and hypochromic |
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What is Sickle Cell disease?
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inherited disease
high prevalence in malaria belt causes formation of HbS instead of HbA -HbS precipitates into long crystals when oxygen tension is low (hypoxia) |
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What is Polycythemia?
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Increased RBC, Htc, and Hb
reasons: -hypoxic erythropoietic drive (high altitudes) -hemoconcentration (dehydration) -polycythemia vera or erythemia resutls in: -increase blood viscosity -lower venous return -increase BP |
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What is agglutination, agglutinogens, and agglutinins?
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agglutination - clumping of incompatible RBC (AG) and plasma (AB)
agglutinogens - RBC AG agglutinins - Plasma AB |
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What are Antibodies?
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present in plasma
react with agglutinogen A or B -anti A AB = alpha -anti B AB = beta are gamma globulins (IgM and IgG origin: -absent immediately after birth possible combinations: -alpha, beta, alpha and beta, neither alpha or beta (o) |
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What happens in blood transfusion?
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transfusion of small amount of donor blood
-dilution of agglutinogens of donor blood by plasma of recipient --> low concentration of donor's agglutinins in recipients blood --> donor's agglutinins do not agglutinate recipients RBC in incompatible blood transfusion agglutinins in plasma of recipient can react with agglutiongens in RBC of donor causing agglutination and hemolysis. |
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What is meant by universal donors and recipients?
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donor = group O
-has no immunocompetent agglutinogens and are not agglutinated by any agglutinins universal recipients = AB -contains no agglutins and is unable to agglutinate donor cells |
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What is Rh factor and how prevalent is it in society?
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Rh is an antigen present in RBC membrane - transmembrane proteins
Population: -85 % caucasians -90 % african americans -99 % asians -100 % africans |
