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Blood and Lymph Unit 1 > Hematology > Flashcards

Hematology Flashcards

1
Q

Leukemia vs. Lymphoma

A

Leukemia: malignancy in the marrow
Lymphoma: malignancy outside of the marrow, usually WBCs in a secondary lymph organ

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2
Q

Acute vs. Chronic Leukemia

A

Acute involves immature cells, more rapid

Chronic involves more mature cells

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3
Q

Measured components of CBC (8)

A

WBC, RBC, Hemoglobin, Hematocrit, Platelet Count, Mean Corpuscular Volume, Differential, Mean Platelet Volume

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4
Q

Calculated Components (6)

A

Hematocrit, Mean Corpuscular Volume, Mean Corpuscular Hemoglobin, Mean Corpuscular Hemoglobin Concentration, Red Cell Distribution Width, Absolute Leukocyte Counts

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5
Q

Transcription Factor most common in innate immunity

A

NFk-B

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6
Q

Cytokine vs. Chemokine

A

Cytokine: general small protein signaling molecule
Chemokine: cytokine that promotes chemotaxis

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7
Q

Purpose of innate immune system

A

Start inflammation quickly, Rubor/Calor/Tumor/Dolar

Signals adaptive immune system through dendritic cells

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8
Q

Reticulocyte Count
Absolute Reticulocyte
Reticulocyte Index

A

Count: counting on slide, 0.4-1.7% of total cells
Absolute: Percentage x RBCs. >50,000/uL is elevated
Index: fold increase beyond baseline, countx(pt/normHgb)x1/stress factor, 1-2 is normal

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9
Q

Anemia General Symptoms and Signs

A

Symptoms: SOB, Tachy, dizziness, fatigue, claudication, angina, pallor
Signs: tachycardia, tachypnea, dyspnea, pallor

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10
Q

Iron Distribution

A

65% Hemoglobin, 6% myoglobin, 25% ferritin/hemosiderin,

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11
Q

Iron Absorption

A

Iron from food made soluble in gastric pH

Gastroferrin binds elemental or heme-bound iron

Ferric iron is transported into cells through DMT1 transporter and DCYTB converts ferric (3+) iron to ferrous (2+) iron.
Either bound to ferritin in cell or exported via ferroportin and converted to ferric through hephaestin

Hepicidin inhibits ferroportin. AAs and VitC improve absorption. Erythropoiesis improves absorption.

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12
Q

Iron Transport

A

Transferrin binds 2 moles ferric iron and delivers to bone marrow. Interacts w/ transferrin R, clathrin-mediated pinocytosis.
pH in endosome causes iron dissociation and it enters cytoplasm through DMT1.

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13
Q

Development of Iron Deficiency

A

See reduced Hemoglobin, RBC production, cell rigidity.
Causes: failure to absorb or inability to keep up w/ production demands.
1. Iron depletion in ferritin stores, absorption increases, functions are normal
2. Serum iron reduced, iron binding affinity increases, iron loading is impaired, normal RBC production.
3. Low serum iron, increased transferrin, reduced erythropoiesis,
Signs: microcytosis, hypochromia, increased protoporphyrin

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14
Q

Symptoms of Iron Deficiency

A

Pallor, Fatigue, Loss of Exercise Tolerance, Irritability,

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15
Q

Effects of Iron Deficiency

A

Heart, Liver, Endocrine disorders

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16
Q

Treatments of iron deficiency

A

Phlebotomy, Chelators

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17
Q

Hemoglobin only binds __ Iron

A

Ferrous (2+)

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18
Q

P50 Oxygen in body

A

27mmHg

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19
Q

pH and oxygen affinity

A

decreases as pH decreases

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20
Q

[CO2] and oxygen affinity

A

decreases as CO2 increases

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21
Q

Temperature and oxygen affinity

A

decreases as temperature increases

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22
Q

2-3BPG

A

Binds between beta chains, stabilizes T conformation.

Affinity decreases as enzyme increases

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23
Q

Myoglobin vs. Hemoglobin oxygen dissociation curves

A

Myoglobin is monomer, no cooperativity, hyperbolic dissociation curve hyperbolic w/ high affinity at low concentration.
Poor O2 transporter b/c dissociation only occurs at very low O2 but effective in very low O2 environment of cell.

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24
Q

Hemoglobin 4-14 weeks

A

Z2E2 and A2E2

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25
Q

Hemoglobin 18 weeks - Birth

A

A2G2

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26
Q

1-5 Years onward

A

A2B2 and little A2D2 (2%)

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27
Q

Hgb Chesapeake

A

Increased affinity, red appearance, high RBC count

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28
Q

Hgb Zurich

A

Increases CO2 affinity, similar to smokers

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29
Q

Hgb Koln

A

mild anemia, reticulocytosis, splenomegaly

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30
Q

Methemoglobin

A

Hemoglobin binding ferric iron, usually 1%
Caused by NADPH metHgb reductase deficiency or increased free radical exposure.
Genetically: cytochrome b5 reductase deficiency

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31
Q

CO affinity for Hgb

A

250x higher, smokers 10-15% (normal 3%). Negative cooperativity

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32
Q

How does a pulse oximeter work?

A

DeoxyHgb absorbs 660nm; OxyHgb absorbs 940nm. Only pulsatile flow measured. CO heme absorbs 940, MetHgb absorbs both

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33
Q

Where does hepatopoiesis occur?

0-3 months, 2-7 months, 7-9 months, Childhood, Adult

A 
0-3 months Yolk Sac
2-7 months Liver w/ some spleen
7-9 months Bone Marrow
Childhood Most BM
Adult Axial BM
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34
Q

HSCs and Progeitor Cells

A

HSCs self renew and become colony stimulating units
Progenitors: limited self renewal, limited to 1-2 lineages w/in set
Precursors: dedicated to 1 lineage

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35
Q

Major Growth Factors

A 
EPO
Throbopoietin
Granulocyte-Monocyte/Granulocyte/Monocyte CSFs
IL-5 (Eosinophils)
IL-3 (Basophils)
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36
Q

Blast Cell

A

large nucleus, immature cytoplasm (blue), large nucleolus

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37
Q

Erythropoiesis Timeframe

A

2-7 days maturation in BM w/ 3-5 days of division.
Reticulocytes 1 day BM and 2-3 days in periphery
120 day lifespan

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38
Q

Granulopoiesis

A

3-5 days mitotic pool
5-7 day maturation
10 hour lifespan

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39
Q

Things to evaluate w/ marrow biopsy (6)

A

Cellularity (100-age)
Myeloid-Erythroid ratio: 3:1
Maturation: heterogenous appearance
Reasonable # of megakaryocytes
Proper iron amount in macrophages (Prussian Blue)
Lesions: no fibrosis, tumors, granulomas, etc.

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40
Q

Normal WBC results

A

4,500-10,500 WBCs/uL

40-60% neutraphils, 1-4% eosinophils, 0.5-1% basophils, 2-8% monocytes, 20-40% lymphocytes

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41
Q

Major Central Lymphoid Organs

A

Bone Marrow and Thymus

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42
Q

Peripheral Lymphoid Organs

A

Lymph Nodes, Spleen, Peyer Patches, Tonsils

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43
Q

Blood-Lymph Circulation of Lymphocytes

A

Extravasate in post-capillary venules at high cuboidal endothelial cells. Either stay in lymph node or enter lymph and return to system circulation via at SVC.

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44
Q

Immunogen

A

Antigen that elicits an immune response after binding an AB/TLR
High affinity, multiple bound ABs, co-stimulation of other surface molecules important

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45
Q

Anemia of Chronic Disease Causes (4)

A

Neoplasms and Sepsis
Chronic Inflammation/Infection
Renal Issues
Lead

46
Q

Anemia of Chronic Disease Pathogenesis

A

TNF from neoplasms/sepsis reduces erythropoiesis, iron stores, and INF-beta which collectively reduce erythropoiesis.
Inflammation/Infection produces IL-1 which reduces erythropoietin and iron metabolism. Also produces INF-gamma which suppresses erythropoiesis.
Renal is lack of erythropoiesis
Lead inhibits protoporphyrin ring synthesis and iron addition to rings

47
Q

EPO vs. Transfusion treatments for chronic anemia

A

EPO preferred for absolute deficiencies or EPO loss.

Transfusions indicated when heart damage possible.

48
Q

B-12 and Folate Deficiencies (basis)

A

Both important co-factors for hematopoiesis, covert methionine to homocysteine which creates tetrahydrofolate for DNA synthesis. Decreases cause RBCs to decrease in size, arrest in size, and get destroyed.

49
Q

B12 sources/absorption

A

Meat, Eggs, Milk. It is released in acidic gastric environment and binds Intrinsic Factor from GI cells, absorbed in terminal ileum and released from IF, binds transcobalamin binding protein II that transports it to liver for storage or bone marrow for use.

50
Q

Folate sources/absorption

A

Folate is in many foods, absorbed in jejunum, hydrolyzed, reduced, and methylated before distribution to tissue or stored in liver. Biliary secretion and enterohepatic circulation provides constant supply for tissue.

51
Q

Bone Marrow Findings in B12/Folate Deficiency

A

Erythroid hyperplasia. Megaloblastic changes. Larger nuclei than anticipated based on maturity level.

52
Q

Peripheral Blood Findings B12/Folate Deficiency

A

variable anemia, low reticulocyte count, macrocytosis, high bilirubin, and high LDH.

53
Q

Causes of B12 anemia (3)

A

Autoimmune destruction of IF producing epithelial cells
Lack of IF synthesis
Malabsorption of B12

54
Q

B12 deficiency timeline

A

Slow. High liver stores take long time to deplete w/ long half life for b12. Neruoabnormalities possible.

55
Q

Causes of Folate Anemia (2)

A

Inadequate Dietary intake

Malabsorption (enterohepatic circulation disruption, alcohol consumption)

56
Q

Folate Deficiency Timeline

A

Much faster than B12. Neuro abnormalities rare.

57
Q

Diagnosing B12/Folate Deficiency

A

Both produce elevated plasma homocysteine. B12 also produces high methylmalonic acid levels.

58
Q

Treatments for B12/Folate

A

Cobalamin deficiency treated w/ IM or SC daily for 2 weeks with monthly doses for life.
If absorption is not an issue, can be given PO
Folate given orally or parenternally

59
Q

Hemoglobin tetramers through development

A

0-4 Months: A2E2 and Z2E2
4-Birth: Fetal A2G2
After birth: A2B2 w/ 2% A2D2

60
Q

Alpha Thalassemia usually caused by…..

A

Deletion on Chromosome 16

61
Q

Beta Thalassemia usually caused by….

A

Point mutation on Chromosome 11

62
Q

Clinical Signs of Thalassemia

A

Low Hgb, Low MCV, Low MCHC,

63
Q

Alpha Thalassemia Trait

A

Silent: 1/4 deleted genes, no anemia, normal MCV
Trait: 2/4 deleted, no/mild anemia, normal/low MCV
NO transfusions needed

64
Q

HgH Disease

A

3/4 alpha genes deleted, mod/severe anemia, low MCV, transfusions sometimes needed

65
Q

Hydrops Fetalis

A

4/4 alpha genes deleted, incompatible with life

66
Q

Thalassemia Smear Findings

A

microcytosis, target cells, polychromastia, normal RDW

67
Q

Clinical manifestations of thalassemia

A

High bilirubin, AST, LDH from hemolysis, splenomegaly, expanded bone marrow, increased iron absorption, delayed growth, pulmonary HTN

68
Q

Iron Valence States

A

Ferric 3+ and Ferrous 2+

69
Q

Iron in Aquesous Solution Considerations

A

Forms insoluble salts unless protein bound

70
Q

Where are Iron salts more soluble?

A

Low pH

71
Q

How is body Iron balance controlled?

A

Absorption, no mechanism for excretion

72
Q

How do you lose body iron?

A

exfoliation of skin/musosa, menstruation

73
Q

Hemoglobin: 30-60; 60-90; 45-75; 10-10

A

Pneumonic for pO2 and % binding

74
Q

Lifespans and daily production (RBCs, platelets, Neutrophils)

A

RBCs: 120 days; 175 bil/day
Platelets: 7-10 days; 200bil/day
Neutrophils: 7 hours; 70 bil/day

75
Q

Hemoglobin E

A

Beta globin gene PM: 26 glu-lys. Unstable. Low MCHC

76
Q

Hydroxyurea in Beta Thalassemia

A

Induces production of gamma chains, increases HbF

77
Q

HgC Mutation

A

Beta6 Glu-Lys

78
Q

HbD Punjab Mutation

A

Beta121 Glu-Gln

79
Q

HbE Mutation

A

Beta26 Glu-Lys

80
Q

HbO Arab Mutation

A

B121 Glu-Lys

81
Q

HbS Mutation

A

Beta6 Glu-Val

82
Q

Sickle Cell HbSS RBC Lifespan

A

20 days

83
Q

Complications of chronic hemolytic anemia (4)

A

Aplastic Crises (Parvovirus B19)
Growth delay
Biliruibin Gallstones
Vascular Occlusion

84
Q

Effects of Vascular Occlusion in hemolytic anemia (8)

A

Spleen: sequestration and auto-infarction
CNS: large vessel occlusion stroke when young hemorrhagic stroke when older from damage
Lung: occlusion and damage, pulmonary HTN
Kidney: dehydration 2’ to damage, glomerulus damage
Retina: detachment and blindness from hemorrhage
Avascular necrosis in joints
Skin ulcers

85
Q

Sickle Cell Pain Crisis

A

Vaso-occlusion and temporary ischemia causing pain in the extremities, abdomen, chest

86
Q

Complications w/ pain crises (vaso-occlusion) (5)

A

Hand-Foot Syndrome
Acute Chest Syndrome (deoxygenation, pulmonary edema)
Multi-organ failure syndrome
Priapsim (sustained painful erections 2’ to trapped RBCs)
Bone Infarction: necrotic injury

87
Q

Treatments of Sickle Cell (3)

A

Bone Marrow Transplant: Curative
Hydroxyurea: fetal hemoglobin production
Transfusion Therapy: for severe acute circumstances

88
Q

Hereditary Spherocytosis Cause

A

Defect in spectrin ankyrin, or band 3 that weakens cytoskeleton and destabilizes lipid bilayer. Decreased deformability leads to entrapment in spleen and extravascular hemolysis via macrophages.

89
Q

G-6-PD deficiency inheritance

A

Sex-linked Recessive

90
Q

G-6-PD Pathology

A

Loss of G-6-PD creates inability to restore reduced GSH, increased oxidative damage to spectrin, reduced deformity, splenic trapping, macrophage hemolysis

91
Q

Warm AB Autoimmune Hemolytic Anemia

A

IgG bind RBCs in warm areas of body, poor complement activation, Fc Receptor mediated macrophage hemolysis in spleen

92
Q

Cold AB Autoimmune Hemolytic Anemia

A

IgG/IgM bind RBCs in cold ares of body, activate complement for intravascular hemolysis

93
Q

Direct DAT/Coombs test

A

Tests for IgG/C3d/C4d on patient’s RBCs by adding ABs against these components and testing agglutination

94
Q

Indirect DAT/Coombs

A

Checks if patient’s serum has IgG/complement that binds normal RBCs

95
Q

Spleen Immunity Function

A

Creation of IgM, especially for encapsulated organisms

96
Q

Complications of Splenectomy

A

Bacterial sepsis from S pneumoniae

97
Q

Co-treatments w/ splenectomy

A

H influenza b, S pneumoniae vaccinations, and meningococcus vaccinations. Prophylactic ABX daily through childhood. See physician immediately w/ F

98
Q

IgG Half Life

A

3 weeks

99
Q

C1 Esterase Inhibitor

A

Suppresses basal complement activation from minimal concentration AG activation. Makes C1 unable to activate C4 and lead to cascade.

100
Q

T Helper 1

A

Release lymphokines to attract macrophages

101
Q

T Helper 17

A

Similar to TH1s but more powerful

102
Q

T Helper 2

A

Stimulate macrophages to wall-off pathogens and start healing process

103
Q

Follicular Helper T

A

After activation, move to B cell region of lymph node to promote B cell activation and class switching

104
Q

Regulatory T Cell

A

Suppress activation/function of T helpers to stop immune response

105
Q

Type I Immunopathology

A

Too much IgE, hypersensitivty

106
Q

Type II Immunopathology

A

Antibodies that react to self or collateral damage to self from AG binding cells

107
Q

Type III Immunopathology

A

Antibodies to soluble antigens, cause local damage through complement activation

108
Q

Type IV Immunopathology

A

T-cell mediated damage to self (hepatitis, TB)

109
Q

How many constant heavy chain segments in each type of AB?

A

3 for IgG, IgD, IgA

4 for IgM and IgE

110
Q

Unique physical characteristics of AB types

A

IgD: big hinge region
IgM: pentamer, 1 J chain
IgE: lots of sugars associated
IgA: secretory component, 1 J chain

Blood and Lymph Unit 1 (1 decks)

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