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57 Cards in this Set
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- Back
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Chapter 32 RBC Anemia and Polycythemia
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Chapter 32
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acid base buffering in RBC
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by hemoglobin
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normal hematocrit
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40 to 45%
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early embryonic production of RBC
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yolk sack
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middle trimester production of RBC
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liver is primary
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last month of gestation production of RBC
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bone marrow
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areas that persistantly have red marrow throughout life
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vertebra sternum ribs and ilia
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CFU-E
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committed erythrocyre stem cell
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CFU GM
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committed granulocyte/monocyte stemcell
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LSC
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comitted lymphoid stem cell
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first cell in RBC series
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proerythroblast
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basophil erythroblasts
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follow proerythroblast stage
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stages of RBC synthesis (histo 10 better for this but phys uses different terms which are listed here)
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proerythroblast , basophil erythroblast , polychromatophil erythroblast, orthochromic erythroblast, reticulocyte, erythrocyte
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hemoglobin stains
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red/pink
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ribosomes stain
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purple
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diapedesis
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passage of mature blood cells throgh capilalry walls into blood stream
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reticulocytes persist in thr blood for about
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1-2 days until they fully mature
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when do RBC pass into bloodstream
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in reticulocyte phase
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most essential regulator of RBC production
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tissue oxygenation
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produces EPO
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kidneys
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how does renal hypoxia lead to EPO production
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increases levels of HIF-1 which is a transcription factor for the hypoxia response element which is a promotor of the EPO gene
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hormonal control of EPO
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NE/E and some prostaglandins can induce EPO
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maximal response to EPO occurs within
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24 hours
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new RBC begin to appear how long after EPO release (this was a test question last time)
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5 days later
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required for maturation of red blood cells
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B12 and folate
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lack of B12 or folate causes
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abnormal and diminished DNA and failure of division and maturation (leading to large cells)
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common cause of maturation failure anemia
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poor GI absorbtion due to atrophic gastritis and a lack of intrinsic factor
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describe how B12 is absorbed into bloodstream
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stomach parietal cells produce IF which binds tightly to B12 and protects it from digestion, where it is then taken up in ileum by pinocytosis
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B12 stored where
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liver , we usually have enough for 3-4 years of defective absorbtion before we see problems
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Folic acid deficiency can occur in what diseases
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sprue, also when food is overcooked folate can be broken down
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basics of hemoglobin formation
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succinyl coA and glycine form a pyrrole molecule. 4 pyrrole molecules form a protoporytphrin IX, combo of that with Fe++ creates a heme molecule , a heme plus a globin makes one subunit. 4 subunits (2a 2b) make normal hemoglobin A
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how many oxygen molecules can be carried by each hemoglobin molecule
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4 , one for each iron (Fe++)
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point mutation leading to sickle cell
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valine for glutamate in the beta chains
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when HBs is exposed to low O2 what happens
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elongate hemoglobin crystals precipitate and make cells sickle
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does oxygen bind tightly or loosely to hemoglobin
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loosely
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how much iron do we have in our bodies, where is it
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4-5 grams ~65% in hemoglobin , 4% myoglobin and 15-30 % stored in transferrin or ferritin
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binds to iron for transport in blood
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transferrin
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combines with iron in cell cytoplasm
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ferritin (apoferritin until it actualy has iron)
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insoluble storage iron formed when excess occurs
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hemosidren
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where is heme synthesized
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in mitochondria
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RBC lifespan
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120 days
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most important dietary forms of iro
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hemoglobin and myoglobin from meat
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how is iron acquired from gut
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liver secrets apotransferrin into bile, it picks up iron in gut and is absorbed into epithelial cells and onto the blood
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cytoplasmic RBC proteins designed to
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undergo glycolysis, maintain pliabilty of membrane, manitain ion transport, keep iron in Ferrous 2+ state
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traps old and injured RBC
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spleen
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phagocttizes released hemoglobin from destroyed RBC
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kupffer cells of liver and spleenic macrophages
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porphyrin portion of hemoglobin is converted into
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bilirubin
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after hemorrhage fluid portion of blood replaced in how long
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1-3 days
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how long after hemorrhage is hematocrit resored to normal
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3-6 weeks
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causes of bone marrow aplasia
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high dose raiation and chemotherapy
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tx for aplastic anemmia
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transfusions until a marrow transplant can occur
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megaloblastic anemia results from
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lack of B12 or folate , can be secondary to absorbative issues such as chronic atrophic gastritis or sprue
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hereditary spherocytosis causes this anemia
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hemolytic
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erythroblastosis fetalis
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Rh+ RBC in child are attached by antibodies from an Rh- mother , this usually occurs in the second pregnancy
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effect of anemia on heart
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increasesd flow and cardiac output to maintian normal oxygenation
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secondary polychyhemia occurs from
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high altitudes or failure of O2 delivery to tissues such as in the failing heart
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polycythemia vera
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see path 13
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