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hematology exam 2
erythrocyte, hemoglobin,
| Question | Answer |
|---|---|
| mature eryhrocytes | biconcave, central pallor (1/3 cell) specialized cell-33% hemoglobin & carries O2 |
| what is the lifespan of erythrocytes? | 120 day life span |
| how is the erythrocyte removed | removed by phagocytosis -by macrophages -removal triggered by the increasing rigidity of cell membrane as it ages |
| erythopoiesis | production of erythrocytes, differentiation of hematopoetic stem cell (HSC) to the formation of mature erythrocytes |
| Heme | pigment portion of hemoglobin, synthesized as erythrocyte matures, responsible of oxygen transport to tissues and CO2 from tissues |
| vital substances to erythrocyte and hemoglobin production: | amino acids, iron, vitamin b12 b6, folic acid, erythropoietin |
| erythropoietin | produced by kidneys, glycoprotein hormone-cross placenta, stimulates erythropoiesis in fetus |
| erythropoietin secretion | stimulated by low tissue oxygen levels, results in production of hemoglobin containing erythrocytes, forms a feedback loop |
| RBC production | hypoxia due to decreased RBC count decreased O2 levels, kidney releases erythropoietin, erythropoietin stimulates red bone marrow, enhanced erythropoiesis increases RBC count, increases O2 carrying ability of blood |
| erythropoietin function | causes committed erythoid cell to differentiate into proerythroblasts-major function, shorten time for each maturation step, early release of reticulocytes into blood |
| erythropoietin interacts with other stimulating factors | interleukin 3 to promote megakaryocyte production |
| drug Procrit | erythropoietin is found in procrit which is administered to stimulate RBC production |
| erythropoietin disorders include | polycythemia- increased erythrocyte concentration (erythrocytosis) |
| primary polycythemia | excessive erythropoietin production, common cause neoplasm |
| secondary polycythemia | caused by tissue hypoxia |
| relative polycythemia | increased RBCs not a result of increase erythropoietin |
| erythrocyte development | matures from stem cell to nucleated cell stage in 4-5 days |
| reticulocyte | in bone marrow for 2.5 days in blood for 1 day |
| erythrocyte maturation process-nucleus | undergo a mass decrease and becomes smaller, condenses/progresses from staining red to staining dark blue, move from loose, delicate strands to more coarse/clumped, erythrocyte=anucleate cell |
| CFU-GEMM | colony-forming unit granulocyte-erythrocyte-monocyte-megakaryocyte |
| BFU-E | burst-forming unit-erythrocyte, not actively proliferative stored in BFU-E cell pool influence by erythropoietin to form CFU-E |
| CFU-E | colony forming unit-erythrocytes uni-potiential, contain high concentration of erythropoeitin receptors in cell membrane-forms into pronormoblast progress onto through stages to mature erythrocyte |
| rubriblasts (pronormoblast) | 12-19 micrometers, n:c ratio-10:1, large round nucleus, 0-2 nucleoli. fine chromatin pattern, cytoplasm basophilic (blue), no granules present, located in bone marrow, stage last slightly longer than 24hrs |
| prorubricyte (basophilic normoblast) | 12-17 micrometers, slightly smaller than rubiblasts, 6:1 N:C ratio, clumped nuclear chromatin (coarse), nucleoli present then disappears, cytoplasm-basophilic deeper (richer blue), located in bone marrow, longer 24hr |
| rubricyte (polychromatic normoblast) | 11-15 micrometers, 4:1 N:C ratio, nucleus stains deep red-purple, no nucleoli, hemoglobin appears, chromatin clumpy-condensed, cytoplasm-pink w/blue (gray appearance), in bone marrow, longer 24hrs |
| chromatin | complex DNA and proteins that forms chromosomes within nucleus of eukaryotic cells |
| Metarubricyte (orthochromic normoblast) | 8-12 micrometers, 2:1 N:C ratio, chromatin-completely dense (pyknotic), cytoplasm-reddish pink (acidophilic)-high concentration of hemoglobin LAST STAGE TO HAVE NUCLEUS, bone marrow, last 48hrs |
| reticulocyte | 7-10micrometers, immature erythrocyte-extruded nucleus, cytoplasm-polychromatic (remaining RNA), partly in bone marrow for 2 days and partly in blood |
| reticulocytes-erythrocytes | reticulocytes form into erythrocytes-cytoplasmic RNA is catabolized, ribosomes dissolve, hemoglobin full occupies cell normally-amount of reticulocytes in circulation=number in bone marrow |
| reticulocytes if erythropoietin is released | increased # of young reticulocytes are released into circulation, stress shift reticulocytes, occurs in bleeding/infection |
| to stain retics | use of supravital stain=new methylene blue, precipitates the RNA into a mesh on the cell |
| normal values for reticulocytes | 0.5-1.5 % in adults 2.5-6.5% in children |
| mature erythrocyte | 6-8micrometer, biconcave disc, central pallor (1/3 of cell), no nucleus, membrane is a lipid bilayer made of phospholipids, cytoplasm stains salmon pink/red |
| defective nuclear maturation-megaloblastic maturation | nuclear maturation lags behind cytoplasmic maturation, characterized by erythrocytes increased cellular cytoplasm and overall size, seen in B12/folic acid deficiencies anemia |
| hemoglobin discovered | discovered by Felix Seyler-1862 1st protein whose structure described by x-ray crystallography, main component of erythrocytes each RBC contains 300 million hemoglobin molecules |
| hemoglobin main functions | transport oxygen in the body return CO2 to the lungs |
| chemical composition of hemoglobin | normal adult hemoglobin-Hgb A contains: 4heme group, 4 polypeptide chains-2 alpha (141 amino acids) 2 beta chains(146 amino acids) configuration-4 chains coiled into 8 helices, forms egg shaped molecule with central cavity |
| synthesis of hemoglobin | occurs during erythrocyte maturation process, begins in basophilic normoblasts (prorubicyte) not visible until polychromatic normoblast (rubicyte) |
| formation of heme from Porphyrin | occurs in most red blood cells except mature RBCs-red bone marrow/liver heme colored compound-composed of 4 pyrrole rings connected to form larger tetrapyrrole ring |
| heme begins with synthesis of porphyrin | succinyl coenzyme A (CoA) condenses with glycine to form adipic acid-unstable is decarboxylated to delta-aminolevulinic acid (delta-ALA) 2 delta-ALA condense to form porphobilinogen PBG |
| heme begins with synthesis of porphyrin | 4 molecule of PBG condense into uroporphyogen I or III converts to protoporphyrinogen to protoprophyrin, 4 iron molecules are chelated to protophyrin to form heme-expelled from mitochondria to cytoplasm-binds to globin chains |
| role of iron | delivered to cell membrane of an immature cell by transferrin (Fe3+-ferric ion) Fe3+ affixes to cell membrane transferrin is released and Fe3+ is reduced Fe2+ iron crosses membrane and forms heme in mitochondria |
| hepcedin | peptide hormone produced in liver, coordinates iron acquisition with iron utilization and storage, main regulator of intestinal iron absorption influencing iron availability for erythropoiesis |
| globin structure | genetically controlled, polypeptides chains form globin molecule are formed in ribosomes normal hemoglobin=2 alpha chains and 2 beta chains |
| hemoglobin formation-globins | synthesized on ribosomes, attached to Golgi apparatus in cytoplasm and stay there |
| hemoglobin formation-heme | made in mitochondrion exported back outside into the cytoplasm |
| hemoglobin formation | heme and globin attach in the cytoplasm |
| hemoglobin structure | globin formation strongly tied protoporphyrin formation decreased globins formation-extra iron in cytoplasm=ferritin aggregrates decreased prophyrin formation-iron encrusts mitochondria and around nucleus-sideroblast |
| disorders of heme synthesis | inherited-rare autosomal recessive conditions acquired-inhibition of heme synthesis at various points and of various enzymes |
| porphyria | disease of heme metabolism, leads to excessive accumulation and excretion of porphyrins and precursor in bilary or renal systems-clinical presentation, source enzyme deficiency site of enzyme deficiency. wine red color in urine-Erhlich's reagent |
| genetic defect of iron | low levels of enzyme that promote iron absorption and recycling |
| iron overload | primary disorders increase iron absorption from diet, secondary disorders chronic disease |
| sideroblastic anemia | mitochondria iron overloading in erythroid precursors in the marrow |
| hereditary hemochromatosis | genetic error of metabolism, inappropriate increased absorption of iron, results in progressive iron overload and excessive accumulation in organs |
| function of hemoglobin | oxygen binding and disassociation binding of O2 molecules 2,3 DPG carbon dioxide transportation-indirect erythrocyte mechanism, direct erythrocyte mechanism transport in solution |
| oxygen binding | first molecule of oxygen is bound to heme molecule the structure of hemoglobin changes to promote binding of more oxygen |
| oxygen binding and disassociation | binding 1 O2 molecule increases affinity for more O2 , 1st oxygen bind alpha chain=change in structure, 2nd oxygen bind alpha chain and cause another change that aligns chains, =expelling 2,3 DPG and ability of beta chains to bind O2 |
| role of 2,3 DPG (2.3 diphosphoglycerate) | oxygen affinity for hemoglobin regulated by concentration of phosphates primarily 2.3 DPG -diminishes molecules binding affinity for oxygen, allows release of oxygen to tissues |
| role of 2.3 DPG | at tissue sites-heme groups unload oxygen, beta chain pulls apart available for 2,3DPG and form salt bridges in lungs-oxygen intake=breaking of salt bridges beta chains pulling apart repelling 2,3DPG, heme group able to bond to oxygen |
| oxygen disassociation | P50-value assigned as partial pressure of oxygen required to saturate half of hemoglobin when deoxyhemoglobin concentration=oxyhemoglobin concentration at constant pH and temp= partial pressure-26.52mmHg, pH=7.4 temp=37.5degree C |
| affinity to oxygen | shift to left-increased affinity to oxygen binding shift to right-decreased affinity to oxygen binding |
| hemoglobin F | fetal hemoglobin increased affinity for oxygen, may result in the formation of methemoglobin in adults, results in left shift in the oxygen dissociation curve |
| carbon dioxide transport | a function of hemoglobin, carried by 3 different mechanism-indirect erythrocyte mechanism, direct erythrocyte mechanism, transport in solution |
| indirect erythrocyte mechanism | CO2 diffuse into RBC is converted to carbonic acid-accepted by alkaline deoxyhemoglobin, bicarbonate ion diffuse back into plasma in exchange for CL -diffuses into cell=chloride shift, bicarbonate carried back to lungs-converted back to CO2 and water |
| direct erythrocyte mechanism | 1/4 CO2 transport, deoxyhemoglobin directly bind CO2 on globin chains, forms carbaminohemoglobin form salt bridges stablize molecule and decrease affinity oxygen |
| fetal hemoglobin F | globin chains contains 2 alpha and 2 gamma chains made in liver, hemoglobin in fetus and newborns, appears at 5th week of gestation and last for few months after birth=60-80% by 6 months Hgb F is totally replaced by HgbA1, normal adults <2% of hgb F |
| Hemoglobin A | 95-97% of adult hbg, appears 5th week of gestation, 2alpha 2beta chains |
| hemoglobin A2 | 2alpha and 2 delta chains, delta chains differ from beta chains by 10 amino acids 2-3% hemoglobin in normal adults |
| glycosylated (hemoglobin A1) | subfraction of normal hbg A, includes A1a, A1b, A1c, formed during maturation of erythrocyte and found pts who are hyperglycemic, slow irreversible process is dependant on pts blood glucose level-monitor glycemic control normal 3-6% A1 |
| variant forms of hemoglobin | differs from normal hemoglobin by molecule that replaces the oxygen-carboxyhemoglobin, sulfhemoglobin, methemeglobin |
| carboxyhemoglobin | binding carbon monoxide with hemoglobin-has capacity to bind to CO at same proportion as oxygen, affinity for CO is 210x greater than the affinity for oxygen, binding CO forms carboxyhemoglobin (stable) hemoglobin unable to bind O2 normal 1-3% |
| carboxyhemoglobin | caused by carbon monoxide poisioning-10%judgment impaired, 15-30%acute poisoning 40%resulting unconsciousness/death measured spectrophotoically and compared with oxyhemoglobin absorbance |
| sulfhemoglobin | combination of hemoglobin with sulfur, forms irreversible change in polypeptide chains-formed w/in cell it remains cell until the cell is removed from circulation, cant bind O2 can bind CO to form carboxysulfhemoglobin, |
| carboxysulfhemoglobin | can result in denaturation and precipitation of hemoglobin called Heinz bodies, normal adults <1% elevation=cyanosis |
| methemoglobin | Hgb M disease- metabolic disorder/ structural defect in Hgb molecule, usually produce asymptomatic cyanosis, >2% methemoglobin causes" acquired toxins and genetic enzyme deficiency |
| analysis of hemoglobin | electrophoresis-separation based on charge, denaturation procedures-kleihauer-betke, fetal Hgb acid resists denaturation where adult dosnt, chromatography-based on affinity for solid phase |
| membrane characteristics of erythrocyte | soft pliable=protein-lipid bilayer structure, 40%lipid-cholesterol/phosolipids 52%protein-glycoproteins |
| deformability | ability to change shapes in order to fit through blood vessels, changes depending on ATP level in cell and intracellular ca ion concentration |
| membrane characteristics RBC | contains antigens, composed of oligosaccharides and glycoproteins, they distinguish blood types on outside and within the membrane |
| cytoplasmic characteristics of RBC | contained within cytoplasm=hemoglobin, potassium and sodium ions (K+ higher concentration) glucose, enzymes and no mitochondria |
| cytoplasmic enzymes | efficient cell metabolism must be long lasting, used to provide energy to-maintain hemoglobin iron in active ferrous state Fe2+, drive Na/K pump, reduce state on membranes, preserve integrity of membrane |
| hemolytic anemia | will result with cytoplasmic enzyme dificiencies |
| pyruvate kinase deficiency | most common enzyme deficiency, involved in embden meyerhof pathway |
| glucose-6-dehydrognease deficiency | render the cell venerable to denaturation of hemoglobin |
| erythrocyte metabolic activities | limited ability to metabolize fatty acid/amino acids. generate energy through the breakdown of glucose through:-embden meyerhof glycolitic pathway, hexose monophospate shunt, methemoglobin reductase pathway and luebering rapaport pathway |
| Embden-Meyerhof pathway | major source of cellular energy, breakdown glucose to generate 2 ATP=phosphates necessary for shape and flexibility of membrane, maintenance of membrane lipids, energy for Na/K+ pump and Ca flux |
| decreases in embden-meyerhof pathway | yields a decrease in ATP production =in vivo(living organism)-premature cell death, in vitro (lab)-loss of viability in stored blood products |
| oxidative pathway/hexose monophosphate shunt | oxidative breakdown of glucose-NADH is reduced to NADHP,required for reduction of glucose to form glutathione, shunt defective-decreased amount of glutathione is produced, oxidation of RBC and dentaturation, heinz bodies seen |
| methemeglobin reductase pathway | Fe2+-reduce state of Fe capable of bounding hemoglobin, Fe3+-oxisized state, cant bind to Hbg, pathway prevents oxidation of heme Fe, requires reducing action of NADH, w/out process=synthesis of methmohemoglobin rise 20 40% of total Hbg |
| luebering-rapoport pathway | important in oxygen-carrying capacity of erythrocyte, regulates oxygen affinity of Hbg, capable of regulating oxygen transport during conditions of hypoxia and disorders of acid-base balance |
| life span of RBC | adults-120 days fetus-60-70 days premature infants 35-50days |
| aging process of RBC | membrane becomes less flexible, concentration of cellular Hbg increase, enzyme activity decreases-particularyly in Glycolysis |
| extravascular hemolysis | most frequent method of RBC catabolism, occurs in spleen, inherently stressful environment for cell, blood flow=sluggish, pH=low promoting oxidation, glucose levels=low decreasing ATP formation, leave spleen rbcs need to be flexible to fit splenic sieve |
| extravascular hemolysis | membrane systems fails, selective permeablility of membrane is lost water enters cells, loses its discoidal shape=spherical, are trapped, then engulfed by macrophages in sinusoidal lining |
| when phagocytize Hbg molecule is disassembled | iron-transported by transferring to bone marrow=new RBC, globin-catabolized by liver into amino acids=amino acid pool, porphryin ring is broken=alpha carbon leaves as CO-tetrapyrrole is carried by plasma alb to liver conjugated & excreted in bile |
| intravascular hemolysis | <10% RBC breakdown, w/in lumen of blood vessels, lysis=mechanical or traumatic cause, Hbg released into blood stream-disassociates into Alpha beta dimmers-bind to haptoglobin, haptoglobin-Hbg complexes are removed from circulation by hepatic cell of live |
| intravascular hemolysis part 2 | haptoglobin levels are depleted-Hbg is excreted in urine, Hbg not bound or excreted in urine=oxidized form methemoglobin, heme is released and transported by hemopexin and removed by liver |
| Hbg content | normal values dependent on age and sex, measured by spectrophotometric-cyanmethmoglobin reaction, dacie's and drabkins, acid hematin-HCL added to form acid hematin, alkaline hematin-NaOH |
| hematocrit | packed red cell volume/crit, % of total volume of blood that is occupied by packed RBC, normal values vary based on age and sex, expressed in % |
| hematocrit elevations | pathological polycythemia, physiological polycythemia, shock associated with surgery burns traumas and dehydration |
| hematocrit decreases | anemia, hydration, pregnancy, cardiac decompensation poor circulation |
| rule of three | mathematic caluclation used to verify the validity of RBC count Hgb and hematocrit values RBC*3=Hgb, Hgb*3=Hematocrit, 5*3=15-Hgb 15*3=45-hematocrit |
| RBC indices | set of mathematical calculation that define size and hgb content of erythrocytes needs measurement of Hgb hematocrit and Rbc if an error of 5% or > occurs in any of the 3 parameters=invalid indices |
| mean corpuscular volume MCV | average volume of erythrocytes in given blood sample hematocrit*10/RBC, expressed in femtoliter (fL), determining if RBC are-microcytic-<80fL, normocytic-80-100fL, or macrocytic->100fL |
| Mean corpuscular hemoglobin MCH | the amount of hgb (weight) in average erythrocyte in blood sample mch=hgb*10/rbc, picograms (pg), considered less important in determining anemia microcytic-<27pg, normocytic-27-32pg, macrocytic->32pg |
| mean corpuscular hemoglobin concentration MCHC | absolute value expresses the concentration of hemoglobin in terms of average weight in average RBC MCHC=hgb*100/hematocrit %, IDA-<31%, normal31-37%,hyperchromic>37% |
| red cell distribution width RDW | variability in size of circulation erythrocytes and is indicated as coefficient of variation of RBC size, normal RBC 80-100fL in blood, uses MCV RBC count and histogram distribution, RDW=SD/mean RBC size*100 |
| RDW clinical conditions in RBC routinely elevated/decreased are usually caused by | ineffective RBC production-iron deficiency b12 and folate deficiency, increased RBC devastation, alteration of erythropoiesis |
| reticc | determine if red blood cells are being created in bone marrow at an appropriate rate, RBC stained with supra vital stain and retic are counted, retic=#retics/1000*100 %, corrected reticc calculated to adjust reticc to hct CRC=%retic*(pt HCT/normal HCT) |
| erythrocyte sedimentation rate ESR | nonspecific screening test used for monitoring inflammatory disorders differentiation between various diseases, 1hr test, measures distances RBC settle in unclotted blood toward bottom a specially marked test tube |
| rate the RBC fall is | directly proportional to erythrocyte mass indirectly proportional to plasma viscosity |
| discocytes | mature normal erythrocytes |
| variation from normal erythrocytes | size, shape, alteration in color, inclusions, alteration of distibution |
| grading of morphology | method of enumerating the amount of morphological changes seen in pt sample, multiple grading scales, must verify with lab as which scale is being used, 0-25% cells=few/slight 1+, 26-50% moderate 2+, 51-75% many 3+, >75% marked 4+ |
| macrocytes | larger than normal RBC->8.2micrometer, defect in nuclear maturation or stimulated erythropoiesis, causes a premature release of retic |
| microcytes | smaller than normal RBC <6.2micrometer, many times there will also be decrease in Hgb synthesis =hypochromic cells |
| poikilocytosis | many shapes, caused by chemical/physical alteration of either the cellular membrane or physical contents of cell |
| acanthocytes | multiple thorny, spike like projections irregularly distributed, increase in cholesterol:lecthin ration cell membrane, found in rare hereditary disorder, change=irreversible |
| blister cells | RBC containing: 1 or more vacuoles, significant thinning of outer border of cell membrane, caused by: damage to membrane or removal of inclusion by spleen also known as Pyknocytes |
| burr cells Echinocytes | RBCs with 1 or more knobby projections, crenated RBC-short scalloped projections equally distributed around cell membrane, caused by expansion of outer edge of lipid bilayer change=irreversible |
| elliptocytes | narrow/elongated RBC/ rod shaped loss of membrane integrity due to abnormality of proteins in cell membrane |
| helment cells | schizocytes-larger scooped out part, result of rupture of blister cell, formed from pseudovacuoles near membrane, removal of an inclusion |
| schistocytes | fragments of erythrocytes small and irregular, causes:mechanical damage, impact hemolysis, severe burns |
| drepanocytes or sickle cells | resemble crescents with one end of cell being pointed, caused by polarization of variant Hgb |
| spherocytes | round RBC that have lost biconcave shape, very compact and round caused by loss of membrane w/out equal loss of hgb |
| stomatocytes | RBCs with slit like opening-mouth due to expansion of inner level of lipid bilayer of cell membrane |
| codocytes target cells | bulls eye, thinner than normal membrane, due to: increased membrane to RBC volume ratio, membrane excess, seen in thallasemia and hemoglobinopathies |
| dacryocytes teardrop cells | smaller than normal RBC shape of teardrop due to membrane damage of RBC in crowded bone marrow, membrane damage at time of exit of bone marrow |
| hypochromic color | central pallor exceed 1/3 of cell - cell is dark in overall appearance |
| hyperchromic | central pallor less than 1/3 cell cell is dark overall appearance |
| polychromasia | non-nucleated RBC that stains blue-orange lacks full hgb immature reticulocyte polychromatic cells with netting |
| basophilic erythrocyte | stains blue-gray, no pink color |
| basophilic stippling | tiny round dark blue granules, made up of ribosomes and RNA associated with erythropoiesis lead poisoning and severe anemias |
| cabot rings | ring shaped loop shaped inclusions, remnants of microtubles of mitotic spindles, seen in lead poisoning and pernicious anemia |
| crystals | rodlike or angular opague structures found in abnormalities in Hgb C and A, use brilliant cresyl blue stain to see H |
| Heinz bodies | denatured Hbg visible with brilliant cresyl blue or crystal violet stain, seen in hemolytic anemia G6PD defieiencies and hemolytic anemias |
| howell jolly bodies | round solid staining inclusion-dark blue, made from remnants of DNA small with only 1/2 per cell, seen in mature RBC occur during increased erythropoiesis spleen cant keep up with pitting RBCs of DNA-pernicious anemia/hemolytic anemia |
| pappenheimer bodies | no normally seen in peripheral blood smears, siderotic granules-purple dots=iron inclusion, aggregates of mitochondria ribosomes and Fe particles, seen stained Prussian blue stain, iron loading diseases, hyposplenism |
| aggultination | clumping of red blood cells indicates reaction with antibodies with the rbc antigens |
| rouleaux | arranging cells like stacks of coins occurs in presence of cryoglobulins or excessive proteins |
| malaria | disease caused by blood parasite asexual phase of reproduction of parasite takes place in RBC schizongony can be seen in RBCs |
| malaria P.vivax | enlarged RBCs that stain pale, contain fine red/pink granules call schuffner dots or granules |
| p. falciparum | gameocytes phase seen in RBC has crescent shaped structures may see dark red or pink rods known as maurers dots |
| P, malariae | all stages seen in RBCs usually contains one ring and one chromatin dot arent enlarged may have dust fine pink dots known as ziemanns strippling |
| p ovales | alls stages seen in RBC infected RBCs appear oval enlarged and pale contains only one ring and one chromatin dot |
| babeosis | tick borne intra erythrocytic protozoan parasite babesia microti, intro-erythrocytic rings and merozoites arranged in tetrads rbc fragments and hemolytic anemia |
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