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155 Cards in this Set
- Front
- Back
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Forms a scaffold for blood clotting
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Fibrinogen
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Maintains osmotic pressure, carries lipophilic substances in blood
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Albumin
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New RBCs from bone marrow - complete hemoglobin synthesis and mature 1-2 days after entering
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Reticulocytes
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RBC proliferation is upregulated by this kidney hormone
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Erythropoietin
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Created when thrombopoietin is released by the liver and kidneys; function in blood clotting - 8 day lifespan
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Platelets
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65 - 75% of white blood cells in the blood - first to appear during bacterial infection
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Neutrophils
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An anti-parasitic agent; parasitic infections; can migrate across the blood-brain barrier
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Eosinophil
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Kidney-shaped nucleus
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Monocyte
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Are lymphocytes phagocytic
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NEVER!
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When activated by endothelial injury, aggregates with other platelets and interacts with fibrinogen to form hemostatic plug
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Platelets
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What occurs during the Primordial phase (3rd week in utero)
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Blood islands form in the mesoderm of the yolk sac
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What occurs during the Hepatosplenothymic phase (2rd month in utero)
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Hematopoietic cells invade the liver, spleen, and thymus
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What occurs during the Medullolymphatic phase (3rd month in utero)
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Blood formation shifts to bone marrow and lymphatic tissues
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When the bone marrow becomes the primary source of blood production
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5th month in utero
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Where are the megakaryocytes
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Only in marrow
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Where is bilirubin conjugated with glucuronic acid
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In the liver
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(derived from epithelium) most commonly metastasize via lymphatics
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Carcinomas
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(derived from mesoderm) most commonly metastasize via veins
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Sarcomas
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Lymph from both lower limbs and the abdominopelvic viscera collects in a large sac (sometimes multiple sacs) called
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Cisterna chyle
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2 models of Hematopoietic regulation
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Instructive and Stochatic Models
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Model of Hematopoietic regulation in which cytokines influence cell fate decisions
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Instructive Model
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Model of Hematopoietic regulation in which HSCs randomly committ to differentiate or self-renew
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Stochatic Model
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Provides ATP for regulation of intracellular cation concentration (Na, K, Ca, Mg)
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Emden-Meyerhof
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Two things that reduce oxidants in the Hexose-Monophosphate shunt
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NADPH and Glutathione
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Rapoport-Leubbering
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2,3 DPG to facilitate O2 release to the tissues
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Protects hemoglobin from oxidation
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Methemoglobin reductase
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The single most abundant intracellular protein
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Hemoglobin
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How many oxygen molecules can hemoglobin carry
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4
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3 Adult Hemoglobins
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A (alpha2/beta2), A2 (alpha2/delta2), F (alpha2/gamma2)
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An increase in the number of circulating red cells
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Erythrocytosis
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No increase in red cell mass but a decrease in plasma volume
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Relative erythrocytosis
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Cause of Absolute Erythrocytosis
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Hypoxia
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Red Blood Cell Mass =
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Production x Survival
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Any condition resulting from a significant decrease in total body red cell mass
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Anemia
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Not red cell mass, a count within a fixed volume - increases with hypoxemia
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Erythrocyte Count
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PCV or packed cell volume - total vol. of red cells relative to total vol. of whole blood in a sample
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Hematocrit
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When is your hematocrit the highest
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At birth
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Red cells are lysed and the free Hb reacted with potassium cyanide to form a stable pigment (cyanmethemoglobin) which is measured spectophotometrically
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Hemoglubin Concentration
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Age of Lowest Hb concentration
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2 months
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The mean volume of all RBCs; Hematocrit/RBC count =
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Mean Corpuscular Volume
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Hb/RBC count x 10
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Mean Corpuscular Hemoglobin - the average mass of each Hb
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Measures the average conc. of Hb in a given volume of packed red cells; Hb/HCT
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Mean Corpuscular Hemoglobin Concentration (MCHC)
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Red cell Distribution Width (RDW) measures
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The Variation in size
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Red cell Distribution Width (RDW) =
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Std of MCV x 100/ mean MCV
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Histologic stain that facilitates the differentiation of blood cell types
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Wright (Giemsa) Stain
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Nonspecific variation in RBC shape
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Poikilocytosis
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Nonspecific variation in RBC size
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Anisocytosis
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MCV > 100
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Macrocytosis
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These types of Macrocytes predominate in those with DNA defects
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Oval Macrocytes
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This type of macrocyte predominates in those with liver issues (think alcohol)
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Round Macrocytes
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MCV < 80 or <6 um
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Microcyte
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How do hypochromic RBCs look
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Increased central pallor (like more than 1/3 of the cell)
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Small RBC with 3-12 spikes and no central pallor
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Acanthocyte
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Associated pathology with lots of Acanthocytes
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Liver disease, abetalipoproteinemia
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Normal size RBC with 10-30 spikes with central pallor
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Echinocyte
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Most common cause of Echinocytes
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Artifact
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Schistocyte-Spur Cell
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Usually microcytic in size; irregularity of cell size and shape; small fragments lack any significant central pallor
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Resembles a pear: round with a single elongated or pointed extremity
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Teardrop Cell
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RBC type associated with bone marrow infiltration (myelofibrosis)
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Teardrop cell
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RBC deformed by polymerized Hb
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Sickle cell-Drepanocyte
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Spiculated RBCs (5)
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Acanthocyte, Echinocyte, Teardrop cell, Sickle cell, Schistocyte
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If more the 10% of your RBCs are rod shaped witih nearly parallel sides think
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Hereditary elliptocytosis (ovalocytosis)
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Round, thicker than normal, and without central pallor; often smaller than a RBC
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Spherocyte
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Intrinsic deficit of spectrin (high MCHC reflecting cell dehydration)
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Hereditary Spherocytosis
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Central pallor appears slit like, straight, or fish mouth
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Stomatocyte
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Increased surface membrane to volume ratio results in a central darker region within the area of central pallor
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Target cell
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Associated diseases with Target cells
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HbC, Asplenia, Liver disease, Thalassemia
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Immature RBC, larger, bluer (still red)
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Reticulocyte
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Numerous, evenly distributed blue-gray granules within the cytoplasm; maybe fine or coarse
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Basophilic Strippling
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Results from abnormal aggregates of ribosomes
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Basophilic Strippling
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Associated diseases with basophilic strippling
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Thalassemias, Anemia of chronic disease, Iron deficiency, Lead poisoning
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A DNA fragment produced when nuclear extrusion takes place; normally removed by spleen
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Howell-Jolly Body
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Iron containing particles visible on WG stain; abnormal sidersomes composed of both iron and protein matrix
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Pappenheimer body
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Blue granules, with irregular sharp edges; usually at periphery of cell; iron stain is positive and confirmatory
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Pappenheimer body
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How can you tell Howell-Jolly and Pappenheimer bodies apart?
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HJ - Iron negative; Pappenheimer - Iron positive
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Remnants of mitotic spindle; red-purple thread like rings
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Cabot Rings
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Linear arrangement of four of more RBCs - probably multiple myeloma or lymphoma
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Rouleaux
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Where does one obtain bone marrow from in both adults and children
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Iliac crest (posterior superior)
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Preferred for the cytology of marrow
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Aspirate
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For assessment of cellularity and architecture of marrow
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Biopsy
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Normochromic Normocytic (normal MCV, normal MCHC) anemias (5)
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Anemias of chronic disease, Immune Hemolytic anemia, Anemia of acute hemorrhage, Aplastic anemia, End organ failure (endocrinopathy, renal)
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Hypochromic, microcytic (low MCV, low MCHC) anemias (3)
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Iron deficiency anemia, Thalassemia, Anemia of chronic disease (long standing disease)
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Macrocytic, normochromic (increased MCV, normal MCHC) anemias (3)
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Vitamin B12/Folate deficiency, Refractory anemias/myelodysplastic syndrome (MDS), liver disease
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Normal red cell life span
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120 days
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What gives a reticulocyte its bluish coloration
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The RNA
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In anemia, reticulocytes are released into the blood (when)
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Prematurely
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Corrected Reticulocyte Count
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% observed Reticulocytes x Patient's Hct/45
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The maturity of a reticulocyte can be measured by what concentration
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RNA - younger ones have more RNA
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In Bone Marrow transplant patients, this is the first sign of successful engraftment
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An increased in Immature Reticulocyte fraction
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Deficiency in either heme or globin chain synthesis resulting in
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Hypochromic/microcytic anemia
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Deficiency in globin synthesis
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Thalassemia
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Deficiency in heme synthesis
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Iron deficiency
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Causes of Iron Deficiency Anemia in infants and children
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Inadequate intake, growth spurts with increased iron requirements
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Causes of Iron Deficiency Anemia in pre-menopausal women
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Menstrual blood loss, pregnancy with inadequate intake
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Causes of Iron Deficiency Anemia in adult men and post-menopausal women
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Blood loss due to tumor, peptic ulcer, gastrointestinal or genitourinary bleeding, malabsorption
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A nail disease that can be a sign of hypochromic anemia, especially iron-deficiency anemia
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Kiolonychia
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Bizarre eating practices due to the deficiency of iron
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PICA
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Toxic accumulation of iron
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Hemochromatosis
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Water soluble and can not be visualized by microscopy and does not stain with iron stains
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Ferritin
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Major storage form of iron, predominantely in bone marrow, spleen, and liver
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Ferritin
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The long term storage form of iron
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Hemosiderin
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Water insoluble, thus stains blue with iron stain
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Hemosiderin
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What is hemosiderin
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A heterogeneous iron-protein complex
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The carrier protein of iron; mediates iron exchange between tissues; recycled
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Transferrin
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How is iron absorbed
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Gastric acidity reduces all ferric (+3) to ferrous (+2) to be absorbed in the duodenum; then oxidized in blood to ferric form again and released to RBC precursor or stored (ferritin/hemosiderin)
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What happens to the Total Iron Binding Capacity in Iron Deficiency anemia
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Increased
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The iron concentration necessary to saturate the iron-binding sites of transferrin
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Total Iron Binding Capacity (TIBC)
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What happens to TIBC in IDA; in ACD?
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Iron Deficiency Anemia: increased; Anemia of chronic disease: decreased
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When insufficient iron is available for the developing RBC, there is an excess of this? that was destined to be converted to heme
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Free erythrocyte protoporphyrin
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A cost effective test that is increased in Iron Deficiency Anemia
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Zinc protoporphyrin
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A block in the incorporation of iron into the protoporphyrin ring to form heme
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Sideroblastic anemia
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Decreased erthrypoietic delta aminolevulinic acid synthetase (ALA synthase)
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Hereditary Sideroblastic Anemia
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A stem cell disorder; abnormality of mitochondrial Fe metabolism; 10% terminate in acute myelogenous leukemia
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Acquired Sideroblastic Anemia
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Plumbism
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Chronic lead poisoning
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Lead poisoning
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Lead inhibits ferrochelatase and ALA dehydratase; also inhibits RNA degradation=basophilic strippling
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Second only to IDA in frequency
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Anemia of Chronic Disease
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What happens in Anemia of Chronic disease
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Cytokines (hepcidin) release results in iron deprivation to proliferating cells
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In ACD, these inhibitory cytokines adversely impact erythropoiesis
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TNF-B, IL 1/6, INF-gamma, hepcidin
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Iron studies in ACD
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Increased ferritin; decreased serum iron; decreased % saturation; decreased TIBC; increased FEP or ZPP
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Type of anemia caused by decreased erythropoiesis; bone marrow shows erythroid hypoplasia
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Anemia in Chronic Renal Disease
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MCV > 100 fl
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Macrocytosis
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RNA continues to be translated and transcribed with resulting growth of the cytoplasm while nucleus lags behind. One or more cell divisions are skipped leading to larger than normal cells
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Oval Macrocytosis Megaloblastic
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Hyper segmented PMNs with oval macrocytosis megaloblastic
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Folate/B12 deficiency
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Hyposegmented PMNs with oval macrocytosis megaloblastic
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Myelodysplasia
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Consider in all infants with failure to thrive
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Megaloblastic anemia (B12/folate deficiency)
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Triad seen with Megaloblastic Anemia
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Oval macrocytes, Howell-jolly bodies, hypersegmented PMNs
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Active form of folate
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Tetrahydrofolate (THF)
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Vital in the metabolism of nucleotides and amino acids
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Tetrahydrofolate (THF)
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Folic acid deficiency causes:
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A block in the conversion of dUMP to dTMP resulting in defective DNA synthesis
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If folic acid is omitted from the diet, the liver has stores enough for
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3 to 6 months
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Necessary for synthesis of methionine, the central reaction in DNA synthesis
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Cobalamin (B12)
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Deficient Intrinsic Factor, due to destruction of parietal cells by autoantibodies
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Pernicious anemia (B12 deficiency)
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Most common cause of B12 deficiency
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Pernicious Anemia
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2 types of auto antibodies to Intrinsic Factor in Pernicious Anemia
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Blocking antibody (prevents formation of IF-B12 complexes) and Binding antibody (prevents absorption in the ileum)
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Metabolite elevated in both B12 and folate deficiency - costly
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Total Homocysteine
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Metabolite elevated in B12, normal in folate deficiency- costly
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Methylmalonic Acid
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Definitive test to destinguish between B12 malabsorption, dietary deficiency or absence of Intrinsic Factor
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Schilling Test
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An acute exacerbation of hemolysis due to activation of macrophages usually secondary to viral infection
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Hemolytic Crisis
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Impairment or cessation of BM red cell production (parvovirus B19!)
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Aplastic Crisis
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Antibody formation for foreign antigens (another individual's red cells)
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Alloimmune
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Most common form of Autoimmune Hemolytic Anemia
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Warm
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Warm Autoimmune Hemolytic Anemia is mediated by; Cold by
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IgG; IgM
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Seen in kids after viral infections; biphasic IgG Ab, fixes in cold, upon warming activates terminal C components with lysis. Anti P antigen
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Paroxysmal Cold Hemoglobinuria
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Seen in newborns due to Rh or other blood antigen incompatibility - mother's antibodies attach fetal RBCs
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Erythroblastosis fetalis
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Anti-Ig antibody added to patient's RBC agglutinate if RBCs are coated with Ig
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Direct Coombs test
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Normal RBCs added to patient's serum agglutinate if serum has anti-RBC surface Ig
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Indirect Coombs test
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Most common enzyme disorder
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Glucose-6-phosphate deficiency
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Deficient conversion of ADP to ATP
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Pyruvate Kinase Deficiency
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Deficiency in cytoskeleton spectrin protein
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Hereditary Spherocytosis
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Only cell to have elevated MCHC
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Spherocytes
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Defective spectrin chains with increased permeability to Na+
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Hereditary elliptocytosis
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In Paroxysmal nocturnal hemoglobinuria, two regulators for preventing complement amplification are missing on the RBC membrane
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CD55 (DAF) and CD59 (MIRL)
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Inhibits formation of C3 convertase
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CD 55 (DAF)
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Protects membrane from attack by C5 - C9 complex
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CD 59 (MIRL)
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Decreased vWF cleaving protease (ADAMTS13)
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Thrombotic thrombocytopenia purpura
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