1. Normal RBC
7 micron diameter. Round to slight oval. Biconcave disk. 1/3 central pallor.

4. Variation in Normal

7. Crookston collection

8. Rubriblast

9. Prorubricyte

10. Prorubricyte

11. Rubricyte

12. Metarubricyte
Metarubricyte

13. Reticulocyte
Ploychromatophilic RBC, Diffusely basophilic RBC, Shift Reticulocyte. 1. Color 2. Size 3. Lack of Central Pallor

14. RBC
Erythrocyte

15. Rubriblast or Pronormoblast (Proerythroblast)
Basophilic cytoplasm with large, indistinct nucleoli characterize the most immature recognizable cell in the erythroid series
Copyright ©2001 American Society of Hematology. Copyright restrictions may apply.

16. Prorubricyte (Basophilic Normoblast)

17. Prorubricyte or Basophilic Normoblast
The cytoplasm is intensely basophilic
Maslak, P. ASH Image Bank 2005;2005:101351
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18. Rubricyte (Polychromatophilic Normoblast)

19. Rubricyte or Polychromatophilic Normoblast
Maslak, P. ASH Image Bank 2004;2004:101152
Copyright ©2004 American Society of Hematology. Copyright restrictions may apply.

20. Metarubricyte

21. Metarubricyte, nucleus ejected

22. Polychromasia

25. Review of poikilocytes shape

28. Normochromic/Normocytic v. Hypochromic/Microcytic
Remember, microcytic/hypochromic erythrocytes may also be seen in anemia of chronic disease, in thalassemia and in the sideroblastic anemias. Blood loss is the most common cause of iron deficiency. Menstruation is the most likely reason in women ages 15 to 45 years. Iron deficiency anemia in adult men and postmenopausal women is most likely due to chronic gastrointestinal blood loss. Such losses are usually secondary to ulcerating lesions [peptic ulcer disease, mucosal trauma (hiatal hernias), drug ingestion (aspirin, nonsteroidal anti-inflammatory drugs, steroids, potassium), parasitic infections, inflammatory bowel disease and malignancy. Lack of dietary iron may cause anemia in infancy when the daily need for iron is not met by milk aloMalabsorption of iron is a rare cause of iron deficiency but is seen in patients who have had a partial gastrectomy or who have a malabsorption disorder.ne. This is why iron supplements are given to infants. Iron deficiency is a major cause of anemia in pregnancy.

29. Normal v IDA Maturation

30. Iron Deficiency Anemia (IDA)

31. IDA
Unit of Minn, Hematography case 2

32. IDA

33. Iron deficient
Crookston collection. 33

34. Hypochromic RBCs

35. Hypochromic, Microcytic

36. IDA, treated
Note 2 populations of cells

37. Anemia of Chronic Disease http://www. brainshark
Unit of Virginia, pathology. Anemia of chronic disease (ACD) is difficult to define as its etiology and pathogenesis is not clear. ACD is associated with an underlying disease (usually inflammation, infection, or malignancy), but is without apparent cause (not due to a lack of the nutrients iron, vitamin B 12, or folic acid). ACD resolves when the underlying disease resolves. ACD is the most common anemia in hospitalized patients. The anemia is usually mild (Hct = 30-40%), but may be lower. The Rocs of ACD are usually normochromic/normocytic, but, especially in time, may be mildly hypochromic/microcytic (mild decrease MCV and decrease MCHC). The primary mechanism for the pathogenesis of ACD is decreased red blood cell production. Why red blood cell production is decreased is unclear.

38. B12 or Folate Deficient
Normal

39. Normocytic v. Macrocytic

40. Normal v B12/Folate Deficiency Maturation

41. Folate Deficiency, Bone Marrow
Unit of Minn, Hematography case 14

42. Megaloblastic Anemia, Bone Marrow
Crookston collection. Abnormally large dysfunctional erythroblasts resulting from a B12 and folic acid deficiency.

43. Megaloblastic Anemia, Bone Marrow
Crookston collection. Megaloblasts viewed during different stages of development. Abnormally large dysfunctional erythroblasts resulting from a B12 and folic acid deficiency.

46. Macro Ovalocytes
Crookston collection. Abnormally large oval shaped erythrocytes, often associated with Megaloblastic Anemia.

47. B12/Folate

48. Hypersegmented PMN

49. B12/Folate Deficiency
Megaloblastic Anemia, Peripheral Blood Smear: Another view from the same case showing macroovalocytosis, hypersegmentation, thrombocytopenia.

50. Pernicious Anemia

51. Megaloblastic Anemia
Megaloblastic Anemia, Peripheral Blood Smear

52. Hypochromic/Microcytic Normochromic/Normocytic Macrocytic(/Normochromic)

53. Macrocytic, Microcytic Normocytic

54. Figure 2. Pathophysiology of hereditary spherocytosis
Gallagher, P. G. Hematology 2005;2005:13-18
Copyright ©2005 American Society of Hematology. Copyright restrictions may apply.

55. Hereditary Spherocytosis
Unit of Minn, Hematography case 8

56. Normal v. Spherocytosis

57. Spherocytosis
Atlas of Hematology, Nagoya Unit

58. Spherocytes
Crookston collection.

59. Normal v Ovalocyte

60. Hereditary Ovalocytosis
Crookston collection.

61. Eliptocytosis

62. Hereditary Stomatocytosis

63. Stomatocytosis

64. Cut by Fibrin Strands

65. RBC Fragmentation
Crookston collection

66. Fragmented red blood cells resulting from physical trauma
Crookston collection

67. Helmet Cells

68. Membrane damaged RBCs

69. Schistocytes

70. Burr Cells (Echinocytes)

71. ITP
Univ of Minn, Hematography ase 22 Immune thrombocytopenic purpura (ITP)

72. Disseminated Intravascular Coagulation
Atlas of Hematology, Nagoya Univ

73. Acanthocytes & Burr Cells

74. A-beta-lipoproteinemia
Crookston collection. A rare autosomal recessive condition that interferes with the proper digestion of fats.

75. Acanthocytes

77. Uremia

78. Anemia of Renal Disease
Burr cells in kidney disease, uremia

79. Hereditary Pyropoikilocytosis
Univ of Virginia Pathology. Severe hemolysis, bizarre poikilocytosis, and RBC fragmentation are the hallmarks of hereditary pyropoikilocytosis, a rare autosomal recessive disease. A structural abnormality of spectrin is present in which RBCs fragment when heated to only 45°C. Normal RBCs fragment at 49°C.

80. G6PD Deficiency
Univ of Minn, Hematography case 24 Glucose-6-phosphate dehydrogenase (G6PD) deficiency During times of oxidant stress the PBS usually shows spherocytes, schistocytes, and "bite" cells and "blister" cells where denatured hemoglobin (Heinz bodies) were removed in the spleen.

81. Heart Valve Replacement
Fragmentation Syndrome, heart valve: Schistocytes (fragmented cells). Mechnaical damage tocell membrane.

82. Hemolytic Disease of the Newborn
HDN of erythroblastosis fetalis. Most commonlhy caused by ABO incompatibility

83. Microangiopathic Hemolytic Anemia (MAHA)

84. TTP
Univ of Minn, Hematography case 5

85. Severe Burns
Univ of minn, Hematography case 21 The patient had been severely burned in a fire at his residence. He suffered 50% total burns with 35% third degree burns. He was immediately transferred to a specialized burn unit, but did not survive.

86. Burr Cells (Crenated Cells)
Thorn Cells Acanthocytes
Burr Cells (Crenated Cells)

87. 1. Ovalo (green label): normochromic/normocytic ovalocytes
1. Ovalo (green label): normochromic/normocytic ovalocytes. 80%+ are ovalocytes 2. H. Ovalo or Review Hered Ovalo: another case. normochromic/normocytic ovalocytes. 80%+ are ovalocytes 3. Hered Sphero: Many spherocytes 4. Hypo Micro: hypochromic microcytes, few hypochronic ovalocytes,occaisional hypochromic teardrop 5: IDA MCV 46 Hgb 3.8: hypochromic microcytes, hypochrmmic ovalocytes, hypochromic teardrops 6. B12/Folate : macrocycytic normochromic RBCs. Well filled with hgb. Few macrocytic ovalocytes, occ hyperseg PMN 7: H-J MCV 121: normochromic macrocytes. H-J bociesfew macrocytic target cells 8. B12/Folate: Many hpersegmented PMNs Normochromic macrocytes 9. NRBC: Many nucleated RBCs, mostly metarubricytes 10. ABO HDN: hemolytic disease of the newborn. Earlies stages of nrbc including prorubricyte and rubricyte Mono: increased monocytes 12. EOS increased eosinophils % EOS: increased eosinophils 14. Schisto Acantho: Many schistocytes and acanthocytes : ?? Mystery slide. What do you see

88. END

91. Temple Unit School of Medicine

92. Gallagher, P. G. Hematology 2005;2005:13-18
Figure 3. Peripheral blood smears in disorders of the erythrocyte membrane
Gallagher, P. G. Hematology 2005;2005:13-18
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