Hematology I (SCIE2020) Harmening Chapter 5 PDF

Hematology I (SCIE2020) Harmening - Chapter 5 : Part B (5th Ed) Harmening - Chapter 4 : Part B (6th Ed) Evaluation of RBC Morphology + Intro to Platelet and WBC Morphology OBJEC...

Hematology I (SCIE2020) Harmening - Chapter 5 : Part B (5th Ed) Harmening - Chapter 4 : Part B (6th Ed) Evaluation of RBC Morphology + Intro to Platelet and WBC Morphology OBJECTIVES 4.7 Identify normal red blood cell morphology on a peripheral smear 4.12 Describe the characteristics of the following abnormal cells: 4.12.1 Target cells 4.12.2 Spherocytes 4.12.3 Ovalocytes 4.12.4 Elliptocytes 4.12.5 Stomatocytes 4.13 Identify the following cells on a peripheral smear: 4.13.1 Target cells 4.13.2 Spherocytes 4.13.3 Ovalocytes 4.13.4 Elliptocytes 4.13.5 Stomatocytes 4.14 List diseases that may show fragmented red cells and describe their pathophysiology 4.15 Describe the most common red blood cell inclusions and their composition, relating each inclusion to clinical conditions in which they may be found 4.16 Correlate pathophysiology of clinical conditions associated with abnormal appearance of red cells noted on the peripheral blood smear 4.18 Describe the Osmotic Fragility test for red blood cell osmotic fragility determination 4.19 State the expected Osmotic Fragility test result for spherocytes and target cells 4.20 Identify and describe the morphological alterations of size, shape, colour, and abnormal distribution patterns in erythrocytes 4.21 List any inclusions that may be found in erythrocytes Source: Harmening Figure 5-3 Normal and abnormal red blood cell morphology. Ovalocytes and Elliptocytes  This morphological abnormality is thought to be the result of a mechanical weakness or fragility of the membrane skeleton.  The pathogenesis of the formation of both these cells is unknown. It may be acquired or congenital.  Ovalocytes may be considered as more “egg- shaped” and have a greater tendency to vary in their hemoglobin content.  May appear as normochromic or hypochromic; normocytic or macrocytic.  Megaloblastic anemia is characterized by oval macrocytes (macro-ovalocytes) that and usually lack a central pallor. We will learn about this anemia later   Ovalocytes and Elliptocytes  Elliptocytes are “pencil”, “rod”, or “cigar”-shaped and hemoglobin appears to be concentrated on both ends of the cell.  Usually not hypochromic; usually exhibit a normal central pallor.  Hereditary elliptocytosis (HE) is an inherited condition with anywhere from 25% to 90% of all cells demonstrating the elliptical appearance.  The erythrocytes in HE, usually have a normal survival time; patients are typically asymptomatic and are diagnosed incidentally during testing for unrelated conditions.  In approximately 10% of cases where red cell survival time is shortened; patients' symptoms may vary from a mild to severe.  Mutations in the red cell membrane protein α-spectrin account for a majority of cases of HE, (with the remaining cases arising from mutations in β-spectrin or protein 4.1R).  Ovalocytes/elliptocytes may be possibly seen in association with several disorders, such as microcytic/hypochromic anemia.  Refer to Figure5-18 (next slide) for a description of pathologic processes associated with ovalocytes and elliptocytes. Source: Harmening Figure 5-18 Correlation of ovalocytes and elliptocytes to pathologic processes.  Ovalocytes/Elliptocytes Ovalocyte Elliptocyte 7 Source: Harmening Figure 5-16 Note the high percentage of elliptocytes in this blood smear from a patient with hereditary elliptocytosis. Note the oval macrocyte (micro-ovalocyte) at the arrow. Sickle Cells (Drepanocytes)  Depranocytes or sickle cells are typically crescent or sickle shaped with pointed projections at one or both ends of the cell.  These cells have been transformed by hemoglobin polymerization into rigid, inflexible cells no longer resembling the normal biconcave disc (see fig 5-19).  Patients may be homozygous or in some cases heterozygous for the presence of the abnormal hemoglobin, hemoglobin S (HbS).  In the homozygous patient, physiologic conditions of low oxygen tension (in vivo or in vitro) cause the abnormal hemoglobin to polymerize, forming tubules that line up in bundles to deform the cell.  The surface area of the transformed cell is much greater, and the normal elasticity of the cell is severely restricted.  These cells have lost their deformability and in many cases are unable to travel through the microvasculature of the tissues, which leads to oxygen depravation. Sickle Cells (Drepanocytes)  Most sickled cells possess the ability to revert to the discocyte shape when oxygenated; however, approximately 10% are incapable of reverting to their normal shape.  These irreversibly sickled cells are the result of repeated sickling episodes. On the peripheral smear, they appear as crescent-shaped cells with long projections.  Classically, sickled cells are best seen in wet preparations.  Many of the cells observed on the Wright–Giemsa stain are the oat cell- shaped form of the sickled cell. In this form, the projections are much less pronounced and the central area of the cell is fairly broad. This shape is considered reversible.  The more prominent pathologic conditions in which sickle cells may be observed are listed in figure 5-21. Source: Harmening Figure 5-20 Reversible, oat-shaped Source: Harmening Figure 5-19 Irreversibly sickle cell sickled cells Source: Harmening Figure 5-21 Correlation of sickle cells to pathologic processes Fragmented Cells (Schistocytes, Helmet Cells, Keratocytes) Fragmented Cells (Schistocytes, Helmet Cells, Keratocytes)  Schistocytes are split/cut/fragmented cells resulting from some form of trauma to the cell membrane. Fragmented Cells (Schistocytes, Helmet Cells, Keratocytes) There are certain triggering events in disease that lead to fragmentation, for example: alteration of normal fluid circulation.  Examples of fluid alterations are the development of fibrin strands, damaged endothelium, or a damaged heart valve prosthesis. The flow of blood in the circulation may actually sweep the erythrocytes through the fibrin strands, splitting the red cell. The shapes of these cells vary based on the shear forces and presentation of the red cells as they are cut by the fibrin.  Intrinsic defects of the red cell make it less deformable and, therefore, more likely to be fragmented as it traverses the microvasculature of the spleen. Examples such as antibody-altered red cells and red cells containing inclusions have significant alterations that increase their likelihood of being fragmented, consequently decreasing their survival time.  Schistocytes are the extreme form of red cell fragmentation (see fig 5-22).  Whole pieces of red cell membrane appear to be missing, and bizarre red cells are apparent.  Schistocytes may occur in patients with:  microangiopathic hemolytic anemia, disseminated intravascular coagulation (DIC), heart valve surgery, hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, in severe burn cases, as well as march hemoglobinuria (a form of hemoglobinuria seen in soldiers and long-distance runners). 17 Source: Harmening Figure 5-24 Correlation of fragmented cells to pathologic processes. HA = hemolytic anemia; DIC = disseminated intravascular coagulation; HUS = hemolytic uremic syndrome; TTP = thrombotic thrombocytopenic purpura.   The helmet cell also has distinctive projections, usually two, surrounding an empty area of the red cell membrane.  Helmet cells are seen in hematological conditions in which large inclusion bodies are formed (Heinz bodies, Howell–Jolly bodies).  Fragmentation occurs by the pitting Source Harmening Figure 5-23 Note the bite cell at the arrow. mechanism of the spleen.  This pitting mechanism removes the inclusion from the cell, giving the appearance of having taken a “bite out of the cell” and is sometimes referred to as a bite cell (see fig 5-23).  A helmet cell and a bite cell are, therefore, one and the same.  The helmet cells may also be seen in patients with pulmonary emboli, myeloid metaplasia and disseminated intravascular coagulation DIC.  All fragmented red cells are considered fragile and their survival time is diminished significantly to days, if not hours, owing to splenic sequestration.  Keratocytes are red cells that have been caught on fibrin strands in circulation, and rather than splitting, the cell hangs over the fibrin fusing two sides of the cell together, creating a vacuole. Once the cell escapes from the fibrin strand it appears in the peripheral blood as a red cell with a vacuole in one end resembling a blister and is called a blister cell. It also may be called a pocket-book cell (see fig 5-22).  Once the vacuole ruptures, the resulting cell appears to have two horns. This “horned” cell also resembles a helmet and is sometimes reported as such, but some references note it to be a keratocyte (Greek for keras, horn). The primary difference in the two cells is not in their appearance, but in their formation.  Note that all laboratories may not report fragmented red cells in the same manner  (i.e., all fragmented red cells reported as schistocytes) owing to the similarities in their origins. Follow the standard operating procedure for your institution.  Regardless of the specificity of the terminology used, it is imperative that the morphologists give a qualitative estimate of the abnormality seen in all fields. Especially in significant numbers, the appearance of fragmented red cells will provide physicians with important information on the condition of their patients.  Refer to fig 5-24 (next slide) for a flowchart correlation of the fragmented cells matched to the pathologic processes in which they may be observed.  Source: Harmening Figure 5-24 Correlation of fragmented cells to pathologic processes. HA = hemolytic anemia; DIC = disseminated intravascular coagulation; HUS = hemolytic uremic syndrome; TTP = thrombotic thrombocytopenic purpura. Burr Cells (Echinocytes)  Burr cells (echinocytes) are red cells with approximately 10-30 rounded spicules evenly placed over the surface of the red cells.  They are usually normochromic and normocytic.  They may be an artifact, usually as a result of specimen contamination, in which case they will appear in large numbers and will present with evenly dispersed smooth projections and may be referred to as crenated.  Note: the terms crenated cell and echinocyte may be used interchangeably by some technologists.  “True” burr cells occur in small numbers and appear irregularly sized with unevenly spaced spicules. Burr Cells (Echinocytes)  They may be seen in uremia, heart disease, cancer of the stomach, bleeding peptic ulcer, immediately following an injection of heparin, and possibly in patients with untreated hypothyroidism.  In general, they may occur in situations that cause a change in tonicity of the intravascular fluid (ex. dehydration).  Burr cells may be considered pathologic and should be reported. Acanthocytes (Thorn Cells, Spur Cells)  An acanthocyte is defined as a cell of normal or slightly reduced size, possessing 3-12 spicules of uneven length distributed along the periphery of the cell membrane.  The uneven projections of the acanthocyte are blunt rather than pointed, and the acanthocyte can easily be distinguished from the peripheral smear background because it appears to be saturated with hemoglobin. It appears essentially as a spherocyte with thorns.  The MCHC is, usually in the normal range (see fig 5- 25).  Specific mechanisms relating to the formation of acanthocytes are unknown.  Contain an excess of cholesterol and have an increased cholesterol-to-phospholipid ratio; consequently their surface area is increased. The lecithin content of acanthocytes is decreased.  The only inherited condition in which acanthocytes are seen in high numbers is the rare condition abetalipoproteinemia.  Most cases of acanthocytosis are acquired, such as the deficiency of lecithin-cholesterol acyltransferase (LCAT), which has been well documented in patients with severe hepatic disease.  This enzyme is synthesized by the liver and is directly responsible for esterifying free cholesterol; when this enzyme is deficient, cholesterol is increased in the plasma.  Acanthocytes may also be seen in myeloproliferative disorders, microangiopathic hemolytic anemia (MAHA), and autoimmune hemolytic anemias (AIHAs). We will learn about these later. Source: Harmening Figure 5-25 Note the acanthocytes on this peripheral smear. Source: Harmening Figure 5-26 Correlation of acanthocytes to pathologic processes.  Keep in mind that the red cell responds to this excess cholesterol in one of two ways, depending on the balance of other lipids in the membrane.  It may become a target cell or an acanthocyte.  Once an acanthocyte is formed, it is very liable to splenic sequestration and fragmentation, and the fluidity of the membrane is directly affected.  The most prominent pathologies in which acanthocytes may be observed are listed in fig 5-26 (previous slide). Source: Harmening Figure 5-22 Peripheral blood from a patient with renal disease. Note the presence of fragmented cells: A. burr cells; B. acanthocyte; C. blister/pocketbook cells; D. schistocyte. Teardrop Cells (Dacrocytes)  Teardrop cells appear in the peripheral circulation as tear- shaped or pear-shaped red cells (see fig 5-27).  The extent to which a portion of the red cells form tails is variable, and these cells may be normal, reduced, or increased in size.  The exact physiologic mechanism is unknown. Teardrop Cells (Dacrocytes)  As cells containing large inclusions attempt to pass through the microcirculation, the portion of the cells containing the inclusion cannot pass through and consequently gets pinched, leaving a tailed end.  The red cell is unable to maintain the discocyte shape once this has occurred.  Teardrop cells are often seen in idiopathic myelofibrosis (IMF).  May also be seen in patients with the thalassemia syndromes, in drug-induced Heinz body formation, in iron deficiency, and in conditions in which inclusion bodies are formed. Source: Harmening Figure 5-27 Teardrop cells (peripheral blood). Osmotic Fragility Test Osmotic Fragility Test Useful in confirmation of:  Hereditary spherocytosis  Thalassemia (alpha and beta) The Osmotic Fragility Test is used to measure the osmotic equilibrium of electrolytes is broken, causing the cell to “burst”  Whole blood is added to a series of graded hypotonic salt solutions  Water enters cell to maintain osmotic equilibrium  The red blood cells swell and become spherical  Critical volume is reached in which the cell contents leak out and cell may burst!  Hemoglobin is released (at “burst”) and hemoglobin can be measured with a spectrophotometer Osmotic Fragility Test Hereditary Spherocytosis  Spherocytes have increased osmotic fragility (aka. Cells are more prone to lysis and lyse at lower concentrations) Thalassemia  Thalassemic red cells have decreased osmotic fragility (aka. Cells are more resistant to lysis and lyse at higher concentrations) Erythrocyte (RBC) Osmotic Fragility Curve Red Cell Inclusions  Howell–Jolly Bodies  Howell–Jolly bodies are nuclear remnants containing DNA. They are 1 to 2 µm in size and may appear singly or doubly in an eccentric position on the periphery of the cell membrane. They are thought to develop in periods of accelerated or abnormal erythropoiesis. Figure 5-28 Howell–Jolly body.  They may be seen in both Romanowsky (i.e. Wright's, Giemsa), or supravitally stained peripheral smears.  A fragment of the chromosome becomes detached and is left floating in the cytoplasm after the nucleus has been extruded.  Howell–Jolly Bodies  Under ordinary circumstances, the spleen effectively pits these nondeformable bodies from the cell. However, during periods of erythroid stress, the pitting mechanism cannot keep pace with inclusion formation.  Howell–Jolly bodies may be seen after Figure 5-28 Howell–Jolly body. surgical splenectomy, congenital absence of the spleen, or splenic atrophy after multiple infarctions.  They may also possibly be seen in patients with thalassemic syndromes, sickle cell anemia as well as other hemolytic anemias, and in megaloblastic anemias. We will learn about these anemias. Howell Jolly Bodies 42  Basophilic Stippling  Red cells that contain ribosomes can potentially form stippled cells  Coarse, diffuse, or punctate basophilic stippling may occur and consist of ribonucleoprotein and mitochondrial remnants (fig 5-29).  These aggregates of ribosomes result from an alteration in the biosynthesis of hemoglobin.  Diffuse basophilic stippling appears as a fine blue dusting, Figure 5-29 Note the cells with red whereas coarse stippling is much more clearly outlined cell inclusions: basophilic stippling seen on a peripheral smear in a and easily distinguished. Punctate basophilic stippling is a patient with lead poisoning. mass of smaller forms and is very prominent and easily identifiable.  Basophilic Stippling  Stippling may be found in any condition showing defective or accelerated heme synthesis, such as alcoholism, thalassemia syndromes, megaloblastic anemias, and arsenic intoxication.  It is also considered a characteristic feature in the diagnosis of lead poisoning.  Basophilic stippling may be seen on a Figure 5-29 Note the cells with red cell inclusions: basophilic stippling Romanowsky or supravitally stained peripheral seen on a peripheral smear in a patient with lead poisoning. smear.  It is important for the technologist not to confuse stippling with Pappenheimer bodies. The primary differentiation factors are that basophilic stippling appears homogeneously over the cell, whereas Pappenheimer bodies tend to appear as clusters at the periphery of the cell. Basophilic Stippling 45  Pappenheimer Bodies and Siderotic Granules  Pappenheimer bodies (siderotic granules) are small, irregular magenta inclusions seen along the periphery of red cells. They usually appear in Source: Harmening Figure 5-30 Pappenheimer bodies (Wright stain). clusters, as if they have been gently placed on the red cell membrane.  Their presence on a Wright's or a supravital stained peripheral smear is presumptive evidence for the presence of iron. However, the Prussian blue stain is the confirmatory test for determining the presence of these inclusions.  Pappenheimer Bodies and Siderotic Granules  These bodies/granules in RBCs are nonheme iron, resulting from an excess of available iron throughout the body.  Even though Pappenheimers and siderotic granules are the same inclusion, they are designated differently depending on the stain Source: Figure 5-30 Pappenheimer bodies (Wright stain). used.  The inclusions are termed Pappenheimer bodies when seen in a Wright-stained smear (see fig 5-30) and siderotic granules when seen in Prussian Blue or other kinds of iron stain.  The explanation for the difference in terminology is that Romanowsky stains visualize Pappenheimer bodies by staining the protein matrix of the granule, whereas Prussian Blue stain is responsible for staining the iron portion of the granule. Remember!  Siderotic granules and Pappenheimer bodies are basically the same inclusion – iron. The differentiating factor is that on an iron stain (like Perl’s Prussian Blue) the inclusions are known as siderotic granules and on Wright's stain (like in a standard Hematology Lab) they are known as pappenheimer bodies. For us in lab, THEY ARE THE SAME THING! Pappenheimer Bodies (Romanowsky/Wright Stain) 49   Once the presence of siderotic granules has Siderocyte been confirmed by an iron stain, the cells in (when stained with iron stain such as PPB) which they are found are termed siderocytes.  Siderocytes containing a nucleus are described as sideroblasts and are commonly seen in sideroblastic anemias.  Sideroblasts exhibiting numerous siderotic Siderotic granules granules found within the mitochondria forming a ring around at least one-third of the nucleus, are referred to as ringed sideroblasts.  Siderocytes are seen in any condition in which there is iron overloading such as hemochromatosis. They may also be seen in the hemoglobinopathies (e.g., sickle cell anemia and thalassemia) and in patients following splenectomy. We will learn about these later.  Heinz Bodies  Heinz bodies are formed as a result of denatured or precipitated hemoglobin.  They are large (0.3 to 2 µm) inclusions that are rigid and severely distort the cell membrane.  Supravital stain - crystal violet or brilliant cresyl blue where the presence of Heinz bodies may be seen on the peripheral smear.  Heinz bodies cannot be visualized with Source: Harmening Figure 5-31 Heinz body prep; note the appearance of Heinz body inclusions. Romanowsky stains (see fig 5-31).  Heinz bodies may be seen in the α-thalassemic syndromes, glucose-6-phosphate dehydrogenase (G6PD) deficiency under oxidant stress, and in any of the unstable hemoglobin syndromes. They may also be seen in red cell injury resulting from certain chemicals. Heinz Bodies 52  Cabot Rings  The exact physiologic mechanism in Cabot ring formation is not known.  This structure may represent a part of the mitotic spindle, remnants of microtubules, or a fragment/remnant of the nuclear membrane.  Found in heavily stippled cells and may appear in a figure-of-eight (see Fig 5-32 and next slide).  Cabot rings may be found in megaloblastic anemias, Source: Harmening Figure 5-32 Note the appearance of a Cabot's ring in the cell at the homozygous thalassemia syndromes, and post- arrow. splenectomy. Cabot Rings 54 Hemoglobin CC Crystals  Hemoglobin (Hb) C crystals may be found in hemoglobin CC disease.  HbC disease is a mild chronic hemolytic anemia in which the patient is homozygous for the abnormal hemoglobin C.  HbCC crystals are formed by the crystallization of the abnormal hemoglobin into one end of the red cell membrane.  The crystal forms in a hexagonal shape with blunt ends, leaving the remainder of the cell with the appearance of being empty.  These crystals tend to stain dark red and are said to resemble a “bar of gold” and may be referred to as such (see next slide).  We will discuss later with hemoglobinopathies. Source: Harmening Figure 5-33 Note the hexagonal shaped crystal inclusions in a peripheral smear from a patient with HbC disease. These HbC crystals leave the remainder of the cellular cytoplasm to appear as “empty.” Hemoglobin SC Crystals  Hemoglobin SC (HbSC) crystals may be found on the peripheral smears of patients diagnosed with HbSC disease.  SC disease is a chronic hemolytic disorder punctuated by acute painful crisis and diverse chronic organ damage, secondary to the presence of both HbS and HbC.  The pathophysiology of the disease is exacerbated by the presence of both hemoglobins, as they tend to exhibit traits that are common to each such as sickling from HbS and crystallization from HbC.  The result of this combination is the formation of crystals with fingerlike blunt-pointed projections protruding from the cell membrane (see fig. 5-34).  We will discuss later with hemoglobinopathies. Some Summary Slides 59 Also, See Harmening 61 62  Summary of Some Inclusions Inclusions Composition Howell-Jolly body DNA in origin Basophilic stippling RNA remnants Siderotic granules/Pappenheimer bodies Iron Heinz bodies Denatured hemoglobin Howell–Jolly bodies, Pappenheimer bodies, and basophilic stippling may be seen in peripheral smears stained with both Romanowsky type stain (i.e., Wright's) and supravital stain (i.e., new methylene blue, brilliant cresyl blue) 63 64 Changes in Erythrocyte Shape Poikilocytosis - Major deviation in the shape of the RBC. Normally the odd one because as the cell ages small parts of the membrane become pinched off. Normally  5% variation. (See Harmening, p. 101) Spherocytes - Have a spherical form (round) instead of disc but the cell volume remains the same. There is no central area of pallor. Microspherocyte - microcytic and spherocytic. (See Harmening p. 103, fig.5-13; Anderson’s Atlas p. 40) Ovalocytes- Oval or egg-shaped Elliptocytes - the pronounced oval RBC found in the congenital disorder. (See Harmening p. 104, fig. 5-10; Anderson’s Atlas p. 37) Schistocytes - RBC fragments that assume a variety of shapes and sizes; smaller than a normal RBC; (See Harmening p. 106, 5-22(d); Anderson’s Atlas p. 39) Target Cell - (Platecyte, Leptocyte, Mexican hat or Codocyte) An abnormally thin (flat) cell with a central condensation of Hb and therefore resembles a ringed target. (See Harmening p. 102, fig.5-11; Anderson’s Atlas p. 30) Sickle Cells (Drepanocytes) - An erythrocyte that contains Hb S and undergoes bizarre shape changes if the oxygen tension or pH is reduced. Can be seen as mildly sickled, oat - shaped or holly leaf forms or severely sickled or crescent shaped. (See Harmening p. 105, fig. 5-19 and 5-20; Anderson’s Atlas p. 33) Stomatocytes - Have a central stoma or mouth which appears as an unstained central biconcave area more a slit than a circle. Frequently an artifact. Rarely a type of hereditary hemolytic anemia. (See Harmening p. 104, fig.5-15; Anderson’s Atlas p. 41) Crenation - Crenated cells are usually an artifact. They have regular smooth-tipped projections all around the periphery of the cell. It will affect all cells. Burr Cells (Echinocytes) - Usually a hormocytes; blunt, evenly spaced projections (10-30) at the periphery. Central pallor present. Seen in uremia and electrolyte imbalance. (See Harmening p. 106, fig. 5-22(A); Anderson’s Atlas p. 34) 65 ringed target. (See Harmening p. 102, fig.5-11; Anderson’s Atlas p. 30) Sickle Cells (Drepanocytes) - An erythrocyte that contains Hb S and undergoes bizarre shape changes if the oxygen tension or pH is reduced. Can be seen as mildly sickled, oat- shaped or holly leaf forms or severely sickled or crescent shaped. (See Harmening p. 105, fig. 5-19 and 5-20; Anderson’s Atlas p. 33) Stomatocytes - Have a central stoma or mouth which appears as an unstained central biconcave area more a slit than a circle. Frequently an artifact. Rarely a type of hereditary hemolytic anemia. (See Harmening p. 104, fig.5-15; Anderson’s Atlas p. 41) Changes in Erythrocyte Crenation - Crenated cells are usuallyShape an artifact. They have regular smooth-tipped projections all around the periphery of the cell. It will affect all cells. Poikilocytosis - Major deviation in the shape of the RBC. Normally the odd one because Burr Cells (Echinocytes) - Usually a hormocytes; blunt, evenly spaced projections (10-30) as theperiphery. at the cell ages small Central parts pallor of the present. membrane Seen become in uremia and pinched electrolyte off. Normally  5% variation. imbalance. (See Harmening, (See Harmening p.fig. p. 106, 101)5-22(A); Anderson’s Atlas p. 34) Acanthocytes - Look Spherocytes like spherocytes - Have a sphericalwith spiny(round) form irregularly sp projections instead of disc(2-10 butspicules); the cell volume remains most cells affected. A rare, underlying metabolic defect - abetalipoproteinemia. Cells the same. contain excessThere is no (See cholesterol. central area of Harmening pallor. p. 107, Microspherocyte fig. 5-25; Anderson’s Atlas-p.microcytic 29) and spherocytic. (See Harmening p. 103, fig.5-13; Anderson’s Atlas p. 40) Teardrop Cells (Dacrocytes) Pearshaped, withOval Ovalocytes- a tail.or Often formed if there are microcirculation problems. egg-shaped (See Harmening p. 108, fig 5-27; Anderson’s Atlas p. 31) Elliptocytes - the pronounced oval RBC found in the congenital disorder. (See Harmening Helmet p. 104,Cells (Bite Cells/Degmacytes) fig. 5-10; Anderson’s Atlas p. 37) Have 2 distinctive projections. Looks like a helmet. (See Harmening p. 106, fig.5-23; Schistocytes Anderson’s Atlas p.- RBC 32) fragments that assume a variety of shapes and sizes; smaller than a normal RBC; (See Harmening p. 106, 5-22(d); Anderson’s Atlas p. 39) Target Cell - (Platecyte, Leptocyte, Mexican hat or Codocyte) An abnormally thin (flat) cell with a central condensation of Hb and therefore resembles a ringed target. (See Harmening p. 102, fig.5-11; Anderson’s Atlas p. 30) Sickle Cells (Drepanocytes) - An erythrocyte that contains Hb S and undergoes bizarre shape changes if the oxygen tension or pH is reduced. Can be seen as mildly sickled, oat- shaped or holly leaf forms or severely sickled or crescent shaped. (See Harmening p. 105, fig. 5-19 and 5-20; Anderson’s Atlas p. 33) 66 Stomatocytes - Have a central stoma or mouth which appears as an unstained central  Erythrocyte Inclusions (See Harmening p. 108-111) Basophilic Stippling - Fine or coarse blue-black granules of uniform size and evenly distributed. Irregularly aggregates/clumps of basophilic RNA/clumped ribosomes; sometimes termed punctate basophilia (See Harmening p. 108 and fig. 5-29; Anderson’s Atlas p. 47; 2nd Ed p.45) Howell-Jolly Bodies – Usually fragments of nucleus (DNA); are derived either from (i) chromosomes that have become separated from the mitotic spindle in the process of abnormal cell division or (ii) from small nuclear fragments produced by nuclear fragmentation (karyorrhexis). (See Harmening p. 108 and fig. 5-28; Anderson’s Atlas p. 53; 2nd Ed.p.51) Cabot Rings - Red-violet oval, rings (or incomplete rings) or figure eight-shaped structures. Possibly nuclear remnants or part of the mitotic spindle. (See Harmening p. 110, fig 5-32; Anderson’s Atlas p. 48) Heinz Bodies - Denatured Hb, single or multiple, refractile, round, oval or irregular bodies. Not stained by Romanowsky stains. Only stained with supra-vital stains. (See Harmening p. 109, fig 5-31; Anderson’s Atlas p. 49; 2nd Ed.p.47) Siderocytes - Contain siderotic granules - iron containing structures, usually multiple, which stain bright blue with Perls’ Prussian blue (PBB) reactions. Pappenheimer bodies - Faint blue iron granules or rods found when stained on Wright- Giesma stained smears. They are usually peripherally located and are either single or in droplets. They are usually less than 1 µm. (See Harmening p. 109, fig. 5-30; Anderson’s Atlas p. 55; 2nd Ed p.53.) 67 LAB THIS WEEK Abnormal RBC Morphology – Part III (Poikilocytosis)   My Additional Notes Harmening Chapter 5  Part B  My Additional Notes Harmening Chapter 5  Part B