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Blood and Lymph > Basics of Hematology > Flashcards

Basics of Hematology Flashcards

1
Q

Hematopoiesis

A

Formation of blood cellular components

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2
Q

Erythropoiesis

A

Process by which RBCs are produced

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3
Q

Hemostasis

A

The arrest of stopping of bleeding

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4
Q

Thrombosis

A

Formation of a blood clot inside a blood vessel that obstructs the flow of blood

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5
Q

What are the 5 types of WBCs in blood?

A

Lymphocytes, Neutrophils, Monocytes, Eosinophils, Basophils

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6
Q

Platelets (what, where, how)

A

Small cell fragments produced from MEGAKARYOCYTES found in the bone marrow. Reponsible for hemostatis, which results from interaction between platelets, endothelium, and blood coagulation factors

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7
Q

Hematocrit

A

RBC/Total

Expressed as a percentage

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8
Q

What is plasma composed of?

A

Proteins, Lipids, Salts, Carbohydrates

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9
Q

What is the Buffy Coat?

A

Composed of WBCs and Platelets. Between RBC (bottom) and Plasma (top) when a vile of blood is spun down

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10
Q

RBC metabolism

A

No mitochrondria, so dependent of anaerobic metabolism. Reduction through glutathione pathway. Dependent on NADPH through pentose phosphate shunt

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11
Q

Hemolysis

A

RBC destruction

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12
Q

Normal RBC morphology

A

Circular, biconcave disc-shaped. Mean size 7.5um. Lacks nuclei. Eosinophilic cytoplasm. Central area of pallor, less that 1/3 the diameter of the cell

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13
Q

Causes of Abnormal RBC Count

A

Anemia: Decreased RBC due to blood loss, destruction, or insufficient erythropoiesis
Erythrocytosis/Polycythemia: Increased RBC due to reactive changes (smoking), thalassemia, or primary marrow neoplasm

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14
Q

Causes of Abnormal Hemoglobin Concentraion

A

Anemia: Decreased due to blood loss, destruction, or insufficient erythropoiesis
Erythrocytosis/Polycythemia: Increased RBC due to reactive changes (smoking), thalassemia, or primary marrow neoplasm

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15
Q

Causes of Abnormal Hematocrit

A

Decreased due to anemia of fluid overload

Increased due to erythrocytosis/polycyhemia or dehydration

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16
Q

Mean Corpuscular Volume (MCV)

A

Mean size of RBC

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17
Q

Causes of Abnormal MCV values

A

Low for Microcytosis, iron deficiency anemia or thalassemia

High for Macrocytosis, megaloblastic anemia

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18
Q

Mean Cell Hemoglobin (MCH)

A

Mean quantity of hemoglobin in a single red cell

parallels MCV. If MCV goes up or down, MCH goes up or down

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19
Q

Causes of Abnormal MCH values

A

Low MCH: Hypochromatic, iron deficiency anemia

High MCH: Hyperchromatic, megaloblastic anemia

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20
Q

Red Cell Distribution Width (RDW)

A

Measure of the variability in size of red cells. The wider the cell histogram, the higher the RDW.

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21
Q

Causes of Abnormal RDW values

A

Increased in anemia and disease with RBC destruction (ie schistocytosis)

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22
Q

Neutrophil

A

A granular WBC. The most common type of WBC. Primary role in inflammation and destroy pathogens via phagocytosis

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23
Q

Neutropenia

A

Decreased absolute neutrophil count

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24
Q

Causes of Neutropenia

A

Infections, Drugs, Ionizing radiation, Marrow diseases, Bone marrow infiltration by tumors, Autoimmune disease, Congenital neutropenia

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25
Q

Neutrophilia

A

Increased in absolute neutrophil count

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26
Q

Causes of Neutrophilia

A

Physiologic (neonates, exercise, emotion, pregnancy, lactation), Acute inflammation (infections, surgery, infarcts, autoimmune), Malignancies, Drugs (adrenaline, corticosteroids, lithium)

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27
Q

Eosinophil

A

A WBC with lobed nucleus and cytoplasmic granules. Contribute tot he destruction of parasites and to allergic reactions by releasing chemical mediators (ie histamine)

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28
Q

Eosinopenia (and causes)

A

Decrease in eosinophils. Caused by drugs (corticotrapin, corticosteroids, epinephrine, histamine) or Acute inflammation or Infection

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29
Q

Eosinophilia (and causes)

A

Increase in eosinophils. Caused by: Infections (parasites or fungi), Allergic disorders, Leukemias, Churg-Strauss syndrome, Malignancies

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30
Q

Basophil

A

One type of granulocytic WBC. Essential to the innate immune response of inflammation because they release histamine. Usually two nuclear lobes

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31
Q

Basopenia (and causes)

A

Decreased Basophil count. Caused by Acute Hypersensitivity reactions, Autoimmune, Cushings Syndrome, Pregnancy, Drugs (progesterone, corticosteroids, corticotrophin)

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32
Q

Basophila (and causes)

A

Increased basophil count. Caused by Mastocytosis, CML, basophilic Leukemia, Eosinophilic Leukemia, pH-positive acute Leukemia

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33
Q

Monocyte

A

Mononuclear, phagocytic WBC. Derived from myeloid stem cells. They circulate the blood for 24 hours and then move to tissues where they mature into macrophages

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34
Q

Monocytopenia (and causes)

A

Decreased monoctye count. Caused by aplastic anemia, Cyclic neutropenia, Hemodialysis, Severe Thermal Injuries AIDS, Hairy cell Leukemia

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35
Q

Monocytosis (and causes)

A

Increased monocyte count. Caused by Marrow diseases, Hodgkin’s disease, Carcinoma, Multiple Myeloma, Being an Infant

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36
Q

Lymphocyte

A

WBC, mostly found in lymph nodes and spleen. Mostly small, but can be large if reactive. Condensed chromatin.

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37
Q

Lymphopenia (and causes)

A

Decreased Lymphocyte count. Caused by DiGeorge syndrome, Severe combined Immunodeficiency, HIV, malaria, TB, Cushings Syndrome, Hodgkins disease

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38
Q

Lymphocytosis (and causes)

A

Increased Lymphocyte count. Caused by certain viral infections (EBV, CMC, primary HIV infection, Chickenpox, Smallpox, MMR). Occurs naturally in infants and young children. Also occurs after a splenectomy

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39
Q

Thrombocytopenia (and causes)

A

Decreased platelet count. Caused by Peripheral destruction, Sequestration of spleen, Inadequate production

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40
Q

Thrombocytosis (and causes)

A

Increased platelet count. Caused by Primary marrow neoplasm, inflammation, surgery, splenectomy, iron deficiency anemia, hemorrhage

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41
Q

Morphology and Parameters of Iron Deficiency Anemia

A

Small RBC, Larger central pale area, Target cells.
Increase in RDW
Decrease RBC, HGB, HCT, MCV, MCH, MCHC

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42
Q

Spheroctyes

A

Abnormal RBC

Spherical, No central pallor. Due to decreased cell membrane. Increase MCHC

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43
Q

Bite cells

A

Abnormal RBC

Bite-like defect due to removal of Heinz body in spleen. Associated with G6PD deficiency

44
Q

Schistocytes

A

Abnormal RBC
Fragmented RBC, helmet cells
Seen in burns, mechanical heart cells

45
Q

Target cells

A

Abnormal RBC
Central hemoglobin, target shape.
Seen in Thalassemia, Hemoglobin C, Iron deficiency, Liver disease

46
Q

Basophilic Stippling

A

Morphology of evenly dispersed find blue granules that are composed of aggregated ribosomes (rRNA). Caused by lead poisoning, thalassemia, sideroblastic anemia, or Infection

47
Q

Howell-Jolly Bodies

A

Morphology of a single, dense, blue dot containing nuclear DNA remnant. Caused by splenectomy, Fungal, Megaloblastic anemia

48
Q

Heinz Body

A

Denatured/oxidized hemoglobin attached to inner cell membrane. Stained with supravital dye. Caused by G6PD deficiency and associated with Bite Cells

49
Q

Dohle Body

A

Abnormal WBC inclusion
Pale blue inclusion at the periphery of cytoplasm, contains condensed RNA. Caused by Infection, Inflammation, Burns or Pregnancy

50
Q

Toxic Granulation (Hypergranularity)

A

Increase in numbers and prominence of 10 granules. Due to rapid cell division. Often associated with Dohle Bodies. Caused by bacterial infection or marrow recovery

51
Q

Hypersegmented Neutrophils

A

More than 5 nuclear lobes. Associated with Megaloblastic Anemia

52
Q

What is the Wright-Giemsa Stain

A

Used to stain peripheral blood smear. Basic elements are orange-red (hemoglobin, basic proteins and some cytoplasmic granules). Acidic elements are stained purple-blue (DNA, RNA, Basophil granules, Cytoplasm of mature Lymphoctyes and Monocytes)

53
Q

What are the types of WBC are normally found in peripheral blood

A

Lymphocytes (T-cells, B-cells, NK cells)
Granulocytes (neutrophils, eosinophils, basophils)
Monocytes

54
Q

What WBC types fluctuate with age?

A

Neutrophils, Monocytes, Lymphocytes (most abundant WBC in childrent up to 8)

55
Q

Reticulocytes

A

Young, anucleated RBCs that retain some RNA, ribosomes and other organelles that enable ongoing production of hemoglobin. Retained in marrow for 3-4 days, then circulate for 1-2 days before maturing

56
Q

Where does hematopoiesis occur throughout life?

A

Fetal- Yolksac until 3months gestation, then Liver/spleen
Birth- Bone marrow
Child- localized to axial skeleton
Adult- vertebrae, pelvis, sternum, ribs, skull

57
Q

What does Myeloid mean?

A

Pertaining to, derived from, or resembling bone marrow

ie Granulocytes, RBC, Platelets, Monocytes, Lymphocytes

58
Q

The progression of a Stem Cell

A

Stem Cell&raquo_space; Progenitor&raquo_space; Precursor&raquo_space; Mature Cell

59
Q

What are the Hematopoietic Growth Factors (HGFs)

A

Erythropoietin (Epo)
Interleukin-3 (IL-3)
Granulocyte colony-stimulating factor (G-CSF)
Granuloctye-macrophage colony-stimulating factor (GM-CSF)
Macrophage colony-stimulating factor (M-CSF)

60
Q

Where are Hematopoietic Growth Factors produced, and what do they do?

A

HGFs regulate proliferation, differentiation, and maturation of stem cells, progenitor cell, and precursor cells. HGFs enhance survival and functional activities of mature blood cells. They interact with specific cell-surface receptors that regulate gene expression.
HGFs are produced by activated T and B-lymphocytes, macrophages, fibroblasts and endothelial cells

61
Q

What is cellularity?

A

The portion of the marrow that is hematopoietically active (red marrow). If 1/2 the marros is occupied by hematopoietic cells and 1/2 by fat, the cellularity is 50%

62
Q

How does bone marrow cellularity change with age?

A

Cellularity decreases with age. After age 50, cellularity is equal to ~100-age of patient

63
Q

Granulocytic precursors (Basophil, Neutrophil, Eosinophil)

A

Myeloblast > Promyeloctye > Myelocyte > Metamyelocyte > Band form > Mature cell
Look at pictures to identify

64
Q

Erythroid precursors

A

Pronormoblast > Basophilic erythroblast > Polychromatophilic erythrobast > Orthochromatic erythrobast/Normoblast > Reticulocyte > Erythrocyte
Look at pictures to identify

65
Q

What is the link between Erythropoiesis and Hemoglobin level?

A

The rate of erythropoiesis determines the hemoglobin level

66
Q

What initiates erythropoiesis?

A

Hypoxia stimulates Erythropoietin, a hormone produced by the kidneys. Erythropoietin activates stem cells of marrow to differentiate into pronormoblasts, Increases rate of mitosis and maturation, Increases rate of hemoglobin production, Increases rate of reticulocyte release into peripheral

67
Q

How can you distinguish the different types of Granulocytes in peripheral smear?

A

Neutrophils- pink granules
Eosinophils - red granules
Basophils - dark purple granules

68
Q

Auer Rods

A

Rod-shaped structures present in the cytoplasm of myelobasts (granulocytes), but are ONLY seen in abnormal conditions (ie Leukemia)

69
Q

Mast Cells

A

Large tissue cell resembling a basophil. Covered with IgE. Present throughout body in connective tissue, concentrated in mucus membranes of respiratory and digestive tracts

70
Q

Where do T- Lymphocytes reside?

A

Early T-lymphoid progenitor cells migrate to the THYMUS where they mature. Some go back to reside in marrow

71
Q

Where do B-Lymphocytes mature?

A

Maturation takes place in the BONE MARROW

72
Q

Define Neutropenia and its clinical consequences

A

Neutropenia is the decrease in the absolute neutrophil count (bands and segs) below accepted norm. Varies wtih age, race, ethnicity and altitude. Neutropenia in blood may reflect a decrease in the marrow meyloid pools. This increases risk of infection!

73
Q

What are the two major causes of neutropenia?

A
  1. Decreased bone marrow production

2. Increased turnover of neutrophils

74
Q

Examples of Decreased Bone Marrow Production Neutropenia

A

Kostmann Syndrome, Shwachman Diamond Syndrome, Cyclic Neutropenia

75
Q

Examples of Increased Turnover Neutropenia

A

Drug induced (ie chemotheraphy), Viral infection, Nutritional deficiences (folate, B12, copper and protein calorie malnutrition, which causes ineffective myelopoiesis)

76
Q

Kostmann Syndrome

A

Severe peripheral neutropenia and decrease in myeloid production. High infection risk. Often develop Myeloid Leukemia or Myelodysplastic Syndrome. Monocytosis, eosinophilia, myeloid hypoplasia. Recurrent infections within first months of life. Elastase gene mutation (ELA-1) or HAX-1 gene mutation

77
Q

Shwachman Diamond Syndrome

A

Neutropenia, pancreatic insufficiency with fat malabsorption, bony abnormalities and growth delay. Inheritance is AUTOSOMAL DOMINANT. Defect in nurse cells in marrow.

78
Q

Cyclic Neutropenia

A

Severe peripheral neutropenia for 5-7 days with 15-25 day cycle. Recurrent fevers, pharyngitis, gingivitis, mouth ulcers. Other times in cycle no increased risk of infection.

79
Q

Examples of Increased Turnover Neutropenia

A

IMMUNE: Chronic benign neutropenia of childhood, Autoimmune neutropenia, Alloimmune neutropenia.
NON-IMMUNE: Infection, Splenomegaly/hypersplenism, Pseudoneutropenia

80
Q

Chronic benign neutropenia

A

Production of antibodies that cross react with neutrophils. No increased risk for infection and neutropenia resolves after 6-54 months (av, 20 months)

81
Q

Autoimmune Neutropenia

A

Antibodies to specific determinants on the neutrophil, in association with LUPUS, Evan’s Syndrome or Felty’s Syndrome. Antibodies to RBCs, platelets or coagulation

82
Q

Alloimmune Neutropenia

A

Passive transfer of antibody from mother’s circulation attacking baby’s cells. Accumulation of IgG antibodies by fetus provides pool of antibodies which bind the infant’s neutrophils. Lasts weeks to months

83
Q

Treatments for Neutropenia

A

G-CSF dose of 3-5ug/kg to help normalize production, increase neutrophil counts and prevent infection. For antibody syndromes, IV gamma globulin may be used.

84
Q

Leukocytosis

A

An increase in the total WBC, caused by infection, inflammation, non-specific physiologic stress or malignancy

85
Q

Define the term “Left Shift”

A

Change in WBC that results in an increase in the number of bands and segs

86
Q

Eosiniphilia (and causes)

A

Absolute count of Eosinophils >350ul. Caused by allergies/allergic disorders (asthma), Parasite infections and Drug reactions (usually allergic)

87
Q

Basophilia (and causes)

A

An increase in peripheral basophils. Caused by drug/food hypersensitivity, hives, infection (RA, flu, TB), and myeloproliferative diseases like CML

88
Q

Normal functions of Neutrophils

A

First response of host. Rolling, Adhesion to enothelial cells, Diapedesis through cell junctions, and chemotaxis to wound

89
Q

Organelles/Biochemistry of Neutrophil Rolling/Adherence

A

Plasma membrane associated receptors. Granules containing stores of receptors. Actin cytoskeleton and accessory proteins. Abnormalities results in inability to accumulate neutrophils, recurrent infections and poor wound healing

90
Q

Organelles/Biochemistry of Neutrophil Chemotaxis

A

Plasma membrane, actin cytoskeleton and accessory proteins, granules. Glycolysis for energy. Abnormalities in Fc receptors cause primary ingestion defects

91
Q

Organelles/Biochemistry of Neutrophil Ingestion

A

Plasma membrane. Actin cytoskeleton. Glycolysis.

92
Q

Organelles/Biochemistry of Neutrophil Degranulation/Killing

A

Plasma membrane. Actin cytoskeleton. Azurophilic and specific granules. Glycolysis. Abnormalites lead to deficient neutrophil function and altered morphology

93
Q

Leukocytes Adhesion Deficiency I

A

Autosomal recessive CD18 deficiency, lack of CD11b/CD18 expression. Recurrent soft tissue infections. Poor wound healing. Caused by NEUTROPHILIA and DECREASED ADHERENCE

94
Q

Chronic Granulomatous Disease (CGD)

A

Defects in 1 of 4 oxidase components. Sex linked recessive or autosomal recessive. Recurrent purulent infections with catalase positive bacteria and fungi involving skin and mucus membranes. Deep infections of organs as well. NEUTROPHILIA. Defect in OXIDASE ENZYME system.

95
Q

Chekiak Higashi Syndrome

A

Formation of giant, leaky granules. Autosomal recessive CHS gene. Oculocutaneous albanism, Recurrent enfection of skin, mucus membranes and respiratory tract. hepatosplenomegaly, Neurodegeneration. NEUTROPENIA. Giant granules in all leukocytes

96
Q

Myeloper-oxidase Deficiency

A

Autosomal-recessive Post-translational modification defect in processing protein. Generally healthy, but increased fungal infections when associated with diabetes. DEFICIENCY of MYELOPEROXIDASE. Defect in killing CANDIDA

97
Q

Defects in Phagocytic Function

A

Very high rates of bacterial and fungal infections, especially with atypical microorganisms. Infections with catalase positive organisms in patients with CGD. Peridontal disease in children. Recurrent infection in areas of body that are in contact with the microbial world

98
Q

Defects in Compliment

A

Similar bacterial infections as might be seen with antibody deficiency (H. influenza, S. pneumonia). Terminal complement deficiencies (C5-C9) see problems with Neisseria organisms

99
Q

Screening for Phagocytes

A

CBC with dif, morphology, Bactericidal activity, Chemotaxis assay, Expression of CD11b/CD18, NBT dye reduction or DHR oxidation

100
Q

Confirmatory tests for Phagocytes

A

Adherence to inert surface or endothelial cells (CD11b/18 measurements). Reponse to chemoattractants, Ingestion of labeled particles or bacteria, Bactericidal/candidicidal activity (O2, H202 production)

101
Q

Screening for Complement

A

C3, CH50, Quantitative lgs, Lymphocyte numbers

102
Q

Confirmatory tests for Complement

A

Measure specific complement components in the alternative or classical pathway. Perform a detailed evaluation of the adaptive immune response.

103
Q

Management of innate immune disorders

A

Anticipate infections, Broad spectrum antibiotics (switch to specific antibiotics after dx), G-CSF at 3ug/kg/day, Transplantation with hematopoetic stem cells

104
Q

NADPH Oxidase System

A

Membrane bound enzyme complex. Latent in neutrophils until activated to assemble by respiratory burst. The system generates superoxide by transferring electrons from NADPH inside the cell across the membrane and coupling to molecular oxygen to produce superoxide. Superoxide can be made in phagosomes which contain bacteria/fungi. Can spontanteously form H202 that will then generate ROS

105
Q

Diagnostic tests for NADPH oxidase defect

A

Nitro blue tetrazolim chloride- Defect = no blue. More blue with more production of ROS
DHR test: whole blood stained with DHR, incubated and stimulated to produce superoxide, which reduces DHR

Blood and Lymph (3 decks)

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