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105 Cards in this Set
- Front
- Back
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Major fxn of RBCs
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transport hemoglobin (which transports O2)
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Why do higher animals use RBCs instead of free hemoglobin in blood
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When free about 3% leaks through capillaries every time blood passes through
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Other fxns of RBCs
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carbonic anhydrase to catalyze CO2 and H2O to H2CO3; acid/base buffering
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Size and shape of RBCs
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biconcave disc ~7.7 um by 2.5 um/1 um
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average volume of RBC
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90-95 cubic um
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RBC concentration in blood of men
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5,200,000 +/- 300,000 per cubic mm
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RBC concentration in blood of women
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4,700,000 +/- 300,000 per cubic mm
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Hemoglobin concentration in RBCs
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up to 34 g/100 mL of cells (metabolic limit); normal levels always approach limit
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Hematocrit in blood
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40-45%
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whole blood hemoglobin concentration in men/women
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15 g per 100mL cells/14 g per 100mL cells
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Each gram of pure hemoglobin can bind how much oxygen
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1.34 mL oxygen
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RBC production during development
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yolk sac early, 2nd trimester liver (also spleen and lymph nodes), last month gestation exclusively in bone marrow
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When do long bone stop producing RBCs
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about 20 yrs old
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Where are RBCs produced after 20?
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membranous bones like vertebrae, sternum, ribs, and ilia
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Precursor of RBCs
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pluripotential hematopoietic stem cells (all cells of circulating blood derived from)
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Intermediate stage cells in differentiation
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commited stem cells
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commited stem cell that produces RBCs
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colony-forming unit-erythrocyte (CFU-E)
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Colony forming cells that from granulocytes and monocytes
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CFU-GM
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What are growth and reproduction of different stem cells produced by
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multiple proteins called growth inducers
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example of growth inducer
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interleukin-3; promotes growth and reproduction of all types of commited stem cells
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What promotes differentiation
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differentiation inducers
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What can cause formation of growth and differentiation inducers for RBCs
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exposure of blood to low O2 for a long time
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First cell that can be identified as a RBC precurser
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proerythroblast
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first generation cells of proerythroblast
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basophil erythroblasts; stain with basic dyes (little hemoglobin)
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What occurs as a RBC matures
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hemoglobin accumulates, nucleus condenses to small size and is absorbed/extruded from cell, ER reabsorbed, cytoplasmic organelle absorbed
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Characteristics of a reticulocyte
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small amount of basophilic material (golgi, mitochondria, etc remnants)
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At what stage does the cell diapedis into capillaries
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reticulocyte stage
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When does basophilic material dissappear from reticulocyte
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1-2 days; now called mature erythrocyte
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Concentration of reticulocytes normally in blood
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less than 1 percent
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2 reasons why RBC concentration closely monitered
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1) adequate number for O2 transport 2) cells do not impede blood flow
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Most essential regulator of RBC production
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tissue oxygenation
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What occurs in prolonged cardiac failure and many lung diseases
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RBC producation increased due to hypoxia increasing hematocrit and total blood volume
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What specific signal increases RBC producation
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erythropoietin (in low O2 states)
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Where is erythropoietin formed
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90% kidneys, rest mostly in liver
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Proposed cells that produce erythropoietin in kidney
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renal tubular epithelial cells in response to low O2
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What hormones can stimulate erythropoietin producation
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norepinephrine, ephinephrine, some prostaglandins
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What happens to RBC producation when kidneys removed/destroyed
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patient become anemic; remaining capability to stimulate RBC production can only produce 1/3 to 1/2 needed
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How quickly does erythropoietin reach max production
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within 24 hours
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How quickly do new RBCs enter circulation after erythropoietin stimulation
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about 5 days later
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what specifically does erythropoietin stimulate
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proerythrocytes from heatopoietic stem cells in bone marrow; also speeds up speed of RBC stages
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With large quantities of erythropoietin, how much can RBC synthesis increase
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10 times or more normal
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Essential vitamins for RBC production
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vit B12 and folic acid (needed for DNA synthesis)
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What do vit B12 and folic acid help form
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thymidine triphosphate; an essential building block of DNA
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What happens in absence of required vitamens
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failure of maturation and cell division; cells produced are larger than normal (macrocytes), oval instead of biconcave, have shorter life (but carry O2 normally)
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Pernicious anemia
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failure to absorb vit B12 for GI tract; atrophic gastic mucosa
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What helps absorb vit B12
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intrinsic factor produce by parietal cells in stomach
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How does intrinsic factor work
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combines with vit B12 and protects from digestion, binds to specific receptors on brush border in ileum, transported into blood by pinocytosis
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Where does vit B12 go once absorbed
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stored in liver, released as needed by bone marrow
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normal vit B12 usage per day and normal stroage
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1-3 ug required, 1000 times this is stored
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How long does it take for vit B12 deficiency to show up
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3-4 years of defective absorption to cause maturation failure anemia
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Where is folic acid found in diet (aka pteryoylglutamic acid)
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green vegies, some fruits, and meats (especially liver); easily destroyed during cooking
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sprue
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GI absorption abnormalities; can cause vit B12 and folic acid deficiency
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When is hemoglobin formed in RBCs
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begins in proerythroblast and continues through reticulocyte stage
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Step 1 of 5 hemoglobin synthesis
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succinyl-CoA formed in Kreb's cycle and binds with glycine to form a pyrrole molecule
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Step 2 of 5 hemoglobin synthesis
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4 pyrroles combine to form protoporphyrin IX
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Step 3 of 5 hemoglobin synthesis
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protoporphyrin IX combines with Fe++ to form the heme molecule
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Step 4 of 5 hemoglobin synthesis
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heme combines with a globin synthesized by ribosomes to form a subunit hemoglobin chain (alpha or beta)
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Step 5 of 5 hemoglobin synthesis
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2 alpha and 2 beta hemoglobin chains combine to form hemoglobin A (MW ~65,500)
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How many types of hemoglobin chains are there
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alpha, beta, gamma, and delta
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How many oxygens does a molecule of hemoglobin bind
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one O2 on 4 subunits = 8
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Abnormality in sickle cell anemia
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valine substituted for glutamic acid at one point in each of the beta chains
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What happens in low O2 in sickle cell anemia
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elongated crystals form making it nearly imossible for cells to pass through small capillaries = cells rupture
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How does O2 bind Fe++
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binds loosely with one of the coordination bonds of iron (not with 2 positive bonds of Fe++)
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What form is O2 released into tissues
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molecular oxygen (O2)
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What is iron critical for
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hemoglobin, myoglobin, cytochromes, cytochrome oxidase, peroxidase, catalase
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Total average quantity of iron in body and breakdown of location
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4-5 grams (65% in hemoglobin, 4% myoglobin, 1% variuos heme compounds for intracellular oxidation, 0.1% with transferrin in blood plasma, 15-30% stored)
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Where is iron stored
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liver and reticuloendothelial (bone marrow) parenchymal cells (mostly as ferritin)
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What happens to iron after absorption
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immediately combines with beta globulin (apotransferrin) to form transferrin
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How does iron reach targets/storage sites
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loosely bound in transferrin and can be released anywhere
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What does iron bind in cytoplasm
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apoferritin (MW 460,000) to form ferritin
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how does iron bind apoferritin
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can combine in clusters of iron radicals; ferritin contains variable amounts of Fe
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extremely insoluble form of iron storage
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hemosiderin; occurs when storage pool greater than what apoferritin can accomidate
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Unique characteristic of transferrin molecule
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binds strongly with receptors in cell membranes of erythroblasts in bone marrow; endocytosis
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hypochromatic anemia
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RBCs contain much less hemoglobin than normal; can occur when inadequate levels of transferrin available
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What happens to hemoglobin of expired RBCs
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ingested by monocyte-macrophage cells (put back into ferritin pool)
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Daily loss of Iron
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0.6 mg mostly into feces; 1.3 mg/day additional during menstration
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Where is iron absorbed
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all along small intestine
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How is Iron absorbed
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liver secretes apotransferrin into bile, it binds free iron = transferrin, binds receptors on membranes of intestinal epithilial cells, pinocytosis
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Rate of iron absorption
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VERY slow; max few miligrams per day
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How is total body iron regulated
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by rate of absorption
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Average circulation of RBCs
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120 days
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What do enzymes in RBCs do
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1) maintain membrane pliability 2) membrane transport ions 3) keep iron in ferrous form 4) prevent oxidation of proteins
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Size of trabeculae in red pulp of spleen compared with size of small capillaries
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3 um; 5-8 um
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macrophages in liver name
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kupffer cells
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What is hemoglobbin converted to by macrophages
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prophyrin portion converted to pigment bilirubin and released into blood
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Basic causes of anemia
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too few RBCs or too little hemoglobin in cells
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Chronic blood loss anemia
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RBCs produces are smaller and have too little hemoglobin; microcytic hypochromatic anemia
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Aplastic anemia
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Bone marrow not functioning; caused by radiation, chemicals, some drugs
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megaloblastic anemia
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lack of vit B12, folic acid, intrinsic factor; large RBCs with irregular shapes (megoblasts)
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hemolytic anemia
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RBCs fragile; many forms hereditary
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hereditary spherocytosis
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RBCs small and spherical
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Sickle cell
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hemoglobin S; 0.3-1 percent west african and american blacks
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erythroblastosis fetalis
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RH-pos feus attacked by RH-neg mom
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Main component of blood viscosity
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RBCs
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severe anemia blood viscosity
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half normal; causes decreases peripheral blood flow resistance; low O2 causes dilation of peripheral vessels; CO increased 3-4 times (offsets some effects of anemia)
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What occurs during exercise of anemic person
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extreme tissue hypoxia, acute cardiac failure
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Secondary polycythemia
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too little oxygen in breathed air, cardiac failure, etc
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how much does RBC count increase in secondary polycythemia
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6-7 million per mm cubed; 30% above normal
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physiologic polycythemia
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high altitutes of 14,000 to 17,000 ft
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Polycythemia vera (erythremia)
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pathologic; genetic aberration in hemocytoblastic cells (usually causes excess WBC and platlet formation too)
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what happens to blood viscosity in Polycythemia vera
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3+ times normal; blood volume increases, capillaries become plugged by viscous blood, vascular system become engorged
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CO in Polycythemia vera
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close to normal; viscosity decreases rate of return to heart, but increased blood volume increases return to heart; BP generally normal as well
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What occurs to BP in Polycythemia vera when compensation no longer occurs
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hypertension
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Color of skin in Polycythemia vera
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dependent on quantity of blood in skin subpapillary venous plexus; generally ruddy complexion with cyanotic tint
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Why does blue tint occur in Polycythemia vera
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blood stays in capillaries longer, therefore more oxygen dissociated, plus increased blood volume
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