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43 Cards in this Set

  • Front
  • Back

Red Cell Production

Define as dynamic process that originates from pluripotent stem cells, appealing due to their adaptability, they respond to programmed chemical environment, committed RBC cell line, and Erythroblast. Largest living cell from bone marrow.

Red Cell Changing During Maturation

Occurs in a period of 5 days, each precursor cell goes through three successive divisions. Cells sized reduced, nucleus is baseball around. Nuclear: cytoplasm ratio decreases. Nuclear chromatin becomes more condensed and cytoplasm color changes from blue to pink/salon as hemoglobin synthesized. Mature red blood cells is a nucleated.

Erythrocytes

clusters in specific areas during maturation. Easily identified in the blond marrow aspirated by certain morphologic clues, extremely round nuclear material along with basophilic cytoplasma

Mature vs Immature RBCs

Size : Immature Large Mature Small


Cytoplasm Color: Blue // Salmon


Nuclear Shape: Baseball Round //


Nucleus: Yes /// No


N:C Ratio: High /// Low

American Society of Clinical Pathologist


ASCP - Rubriblast


ASCP - Prorubricyte


ASCP- Rubricyte


ASCP - Metarubricyte

The College of American Pathologist


CAP - Pronormoblast


CAP - Basophilic normoblast


CAP - Polychromatophilic normoblast


CAP- Orthochromic normoblast

6 Maturation Stages

1. Pronormoblast 2. Basophilic normoblast. 3. Polychromatophilic normoblast. 4. Orthochromic normoblast, 5. Reticulocyte, 6. Erthrocyte

Pronormoblast

18-20 nm


N:C 8:1


Nuclear chromatin , round nucleus, densely packed chromatin, evenly distributed fine textures with deep violet color

Basophilic normoblast

16 nm


N:C 6:1


Nuclear Chromatin : Round nucleus, crystalline chromatin appearance, red-purple color


Cytoplasm: Cornflower blue with indistinct area of clearing


Polychromatophilic Normoblast (first stage of hemoglobin synthesis)

13nm


N;C 4:1


Nuclear Chromatin: condensed, moderately compacted


Cytoplasm: Color mixture, blue layers with traces of orange-red, hemoglobin synthesized


Orthochromatic normoblast (most nRBCs seem in blood at this stage, Hgb synthesis still occurring)

8nm


N:C 1:1


Nuclear chromatin: dense, velvet-appearing homogeneous chromatin


Cytoplasm: increased volume with orange -red color shades with slight blue tone


Reticulocyte (need supra vital stain to visualize)

8nm


Remnant of RNA visualized as reticulum, filamentous structure in chains or as a single dotted structure in new methylene blue stain. Seen in Wrights stain as large bluish cells, polychromatophilic macrocytes

Mature red cells (biconcave disk)

6-8nm


Disk shaped cell filled with hemoglobin


Has an area of central pallet of 1to3nm

Structures of Red Cell Membrane

Can travel more than 300 milks through peripheral circulation. Navigate through circulatory system due to cell flexibility and trilaminar structure : outer glycolipds/glycoproteins. Central: cholesterol and phospholipds, Inner: cytoskeleton. Made up of integral and peripheral proteins 50% proteins,m 40 % lipids, and 10 % carbohydrates. The lipid factor serves as barrier to most water soluble molecules. Cholesterol makes up 25% of lipid fraction.

RBCs conditions for 130 days survival

Deformable , hemoglobin structure and function must be adequate and the red blood cell must maintain osmotic balance and permeability

Integral Proteins: Peripheral Proteins

Transport (active and Passive) Active uses ATP


Provide structures for many antigens (400)


Contains 60 % carbohydrates


Contains most of the membrane sialic acid which imparts a peripheral protein net negative charge to cell surface



Cytoskeleton: Peripheral Proteins

Responsible for deformability , deformability and elasticity are crucial to red blood cells. Can stretch 117% of its surface. Spectrin and ankryin are responsible for flexibly of cells.

Transport Mechanism

Diffuse freely through special channels aquaphorins : water, chloride , bicarbonate

Red Cell Metabolism

The mature red blood cells is non nucleated, no nucleus or mitochondria for metabolizing fatty or amino acids. its derives all is energy from the breakdown of glucose.

4 ways of Red Cell Metabolism

1. Embden Meyerhof (anaerobic)


2. Pentose phosphogluconate pathway (hexose monophospate shunt)


3. Methemoglobin reductase


4. Rapaport luebering pathway

Quantify abnormalities Anisocytois

Variation in size

Quantify abnormalities Poikilocytosis

Variation in shape

Quantify abnormalities Hemoglobin

Content or distribution

Variation Red Cell Size

Normal 6-8nm/MCV 80-100fl


Macrocytic >9nm/MCV>100fl


Microcytic<6nm/MCV<80fl

2 Types of Microcytic Anemias

Iron deficiency anemia - deficient iron intake or defective iron absorption.


Thalassemia 0 decreased or absent globin synthesis, missing or diminished alpha or beta chains are lead to impaired configuration with microcytic cells having increased central pallor : hypochromia

Hemoglobin

Heme - form from having four iron atoms surrounded by the protoporphyrin and two paris of globin chains are assembled onto the molecule with the heme structure lodged in the pockets of globin chains. Iron is need to the four heme , since iron needs to be absurd from the bloodstream and its transferred to the pronormoblast of the bone marrow for incorporation into the hem structures.

Iron overload disorder (sideroblastic)

shows dimorphic cell population, microcytes mixed with macrocytes, showing normal hemoglobin levels and some showing hypochromia.

Anemia of chronic inflammation

10% of individuals with this anemia due to renal failure or thyroid dysfunction having microcytic RBCS in peripheral smell. Iron delivery to reticuloendothelia system is imparied

Macrocytic Anemia

Nuclear synthesis depends on vitamin b12 and folic acid. Macrocytic RBC are produced in the absence of these elements. B12 deficiency, pernicious anemia, folic acid deficiency. alcoholism and liver disease give rise to increased MCV.

Variation in Red Cell Color

Polychromasia: gray/blue color. bone marrow is responding to anemic stress. When therapy started due to iron deficiency or megaloblastic anemia. when bone marrow is being stimulated as a result of a chronic hematologic condition such as thalassemia or sick cell disorders.

Hypochromia

hemoglobin synthesis is impaired, its a gradual process, all microcytic cells are hypo chromic. hypo chromic of varying degree can be seen in iron deficiency anemia, thalassemic conditions, sideroblastic process.

Variations in red cell morphology

due to decrease red blood cell production, increased destructions, defective splenic functions


Spherocytes

Compacted RBCs with reduced central pallor, due to inherited spectrin abnormality, aging red blood cells loose pieces of membrane during senescence and autoimmune diseases


MCHC .36%, near normal MCV, increased osmotic fragility

Sickle Cells

Reversible half moon shaped, irreversible crescent shaped and pointed projections,, sickle hemoglobin (Hgb S) Hypoxia

Ovalocytes and Elliptocytes Defines

Ovalocytes - egg shaped, appear macrocytic, hypo chromic, normochromic, seen in thalassemic syndromes.


Elliptocyes : cigar shaped, abnormal spectrin and band 4.1

Elliptocytes

Present in iron deficient and idiopathic myelofibrosis


Target Cells

Bull eye shaped cells, due to artifact and hemoglobin and red cell surface membrane. Seen in IDA, Hgb C disease, Liver disease , post splenectomy. As cholesterol increases in plasma, the RBC surface expands resulting to increase surface area. Target cells appears hypo chromic, hemoglobin along the edges of the cell and thin layer of hemoglobin located centrally or as a thick band


Acanthocytes

Small sized cell with uneven thorn like spicules form RBC membrane. Spicules ranges 3-9. Observed in liver disease, autoimmune hemolytic anemia, and mcleod syndrome (loss of muscle mass, missing killing proteins.

Stomactocyte

Elongated areas of central pallor site, several chemical agents are responsible : phenothiazine and chlorpromazine. Can be seen in Rh null phenotype, hereditary stomatocytosis and some alcoholic conditions


Burr Cells (echinocyte)

Cells crenated with regular spaced spikes, seen in conditions of uremia or dehydrations. also when smears are forced to dry though repeated waving in the air


Bite cells (helmet)

Cells with portion of membrane removed. heinz bodies rich cells (pitted in spleen)

Fragmented (schistocyte)

Pieces of red blood cell membranes have ben sheared and hemoglobin leaks through membranes, causing anemia


due to DIC or TTP, seen in burn patients , heart value surgery patients, causes formation of large inclusions (heinz bodies) and predispositions of thrombi

Inclusions

Cytoplasm of all normal red blood cells free of debris, granules, or other structures, inclusions are results of distinctive conditions


Types of Inclusions

Howell Jolly Bodies - dan remnants, seen when erythropoiesis is rushed, conditions splenectomy, hyposplenism, megablastic anemia, hemolytic and pernicious anemia.


Papenheimer Bodies/siderblastic granules- iron loading processes, prussian staining, wright stain, conditions : splenectomy megablastic anemia, hemoglobinopathies


Basophilic Stippling : RnA and mitochondria remnants , accelerated erythropoiesis conditions are lead intoxication, thalassemia and abnormal heme synthesis


Heinz Bodies: denature Hgb, located toward periphery of red blood cel membrane. bite cells is evidence that heinz bodies formed and removed by spleen. not using wright stain but cresyl blue stain to see. conditions unstable Hgb, Hgb Zurich, hemoglobinopathies, g6pd deficiency.