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

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Presentation transcript:

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

Variation in Normal

Crookston collection

Rubriblast

Prorubricyte

Prorubricyte

Rubricyte

Metarubricyte Metarubricyte

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

RBC Erythrocyte

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.

Prorubricyte (Basophilic Normoblast)

Prorubricyte or Basophilic Normoblast The cytoplasm is intensely basophilic Maslak, P. ASH Image Bank 2005;2005:101351 Copyright ©2005 American Society of Hematology. Copyright restrictions may apply.

Rubricyte (Polychromatophilic Normoblast)

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

Metarubricyte

Metarubricyte, nucleus ejected

Polychromasia

Review of poikilocytes shape

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.

Normal v IDA Maturation

Iron Deficiency Anemia (IDA)

IDA Unit of Minn, Hematography case 2

IDA

Iron deficient Crookston collection. 33

Hypochromic RBCs

Hypochromic, Microcytic

IDA, treated Note 2 populations of cells

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.

B12 or Folate Deficient Normal

Normocytic v. Macrocytic

Normal v B12/Folate Deficiency Maturation

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

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

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.

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

B12/Folate

Hypersegmented PMN

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

Pernicious Anemia

Megaloblastic Anemia Megaloblastic Anemia, Peripheral Blood Smear

Hypochromic/Microcytic Normochromic/Normocytic Macrocytic(/Normochromic)

Macrocytic, Microcytic Normocytic

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

Hereditary Spherocytosis Unit of Minn, Hematography case 8

Normal v. Spherocytosis

Spherocytosis Atlas of Hematology, Nagoya Unit

Spherocytes Crookston collection.

Normal v Ovalocyte

Hereditary Ovalocytosis Crookston collection.

Eliptocytosis

Hereditary Stomatocytosis

Stomatocytosis

Cut by Fibrin Strands

RBC Fragmentation Crookston collection

Fragmented red blood cells resulting from physical trauma Crookston collection

Helmet Cells

Membrane damaged RBCs

Schistocytes

Burr Cells (Echinocytes)

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

Disseminated Intravascular Coagulation Atlas of Hematology, Nagoya Univ

Acanthocytes & Burr Cells

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

Acanthocytes

Uremia

Anemia of Renal Disease Burr cells in kidney disease, uremia

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.

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.

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

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

Microangiopathic Hemolytic Anemia (MAHA)

TTP Univ of Minn, Hematography case 5

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.

Burr Cells (Crenated Cells) Thorn Cells Acanthocytes Burr Cells (Crenated Cells)

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 0671264 1993: 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 11. Mono: increased monocytes 12. EOS increased eosinophils 13. 75% EOS: increased eosinophils 14. Schisto Acantho: Many schistocytes and acanthocytes 15. 09009291992: ?? Mystery slide. What do you see

END

http://www.clt.astate.edu/wwilliam/hem_i_erythrocytes_morphology_and__physiology.htm

Temple Unit School of Medicine

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 Copyright ©2005 American Society of Hematology. Copyright restrictions may apply.