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Blood and Lymph Unit 1 > Hematology > Flashcards

Hematology Flashcards

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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
Hemoglobin 18 weeks - Birth
A2G2
26
1-5 Years onward
A2B2 and little A2D2 (2%)
27
Hgb Chesapeake
Increased affinity, red appearance, high RBC count
28
Hgb Zurich
Increases CO2 affinity, similar to smokers
29
Hgb Koln
mild anemia, reticulocytosis, splenomegaly
30
Methemoglobin
Hemoglobin binding ferric iron, usually 1% Caused by NADPH metHgb reductase deficiency or increased free radical exposure. Genetically: cytochrome b5 reductase deficiency
31
CO affinity for Hgb
250x higher, smokers 10-15% (normal 3%). Negative cooperativity
32
How does a pulse oximeter work?
DeoxyHgb absorbs 660nm; OxyHgb absorbs 940nm. Only pulsatile flow measured. CO heme absorbs 940, MetHgb absorbs both
33
Where does hepatopoiesis occur? | 0-3 months, 2-7 months, 7-9 months, Childhood, Adult
``` 0-3 months Yolk Sac 2-7 months Liver w/ some spleen 7-9 months Bone Marrow Childhood Most BM Adult Axial BM ```
34
HSCs and Progeitor Cells
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
35
Major Growth Factors
``` EPO Throbopoietin Granulocyte-Monocyte/Granulocyte/Monocyte CSFs IL-5 (Eosinophils) IL-3 (Basophils) ```
36
Blast Cell
large nucleus, immature cytoplasm (blue), large nucleolus
37
Erythropoiesis Timeframe
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
38
Granulopoiesis
3-5 days mitotic pool 5-7 day maturation 10 hour lifespan
39
Things to evaluate w/ marrow biopsy (6)
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.
40
Normal WBC results
4,500-10,500 WBCs/uL | 40-60% neutraphils, 1-4% eosinophils, 0.5-1% basophils, 2-8% monocytes, 20-40% lymphocytes
41
Major Central Lymphoid Organs
Bone Marrow and Thymus
42
Peripheral Lymphoid Organs
Lymph Nodes, Spleen, Peyer Patches, Tonsils
43
Blood-Lymph Circulation of Lymphocytes
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.
44
Immunogen
Antigen that elicits an immune response after binding an AB/TLR High affinity, multiple bound ABs, co-stimulation of other surface molecules important
45
Anemia of Chronic Disease Causes (4)
Neoplasms and Sepsis Chronic Inflammation/Infection Renal Issues Lead
46
Anemia of Chronic Disease Pathogenesis
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
EPO vs. Transfusion treatments for chronic anemia
EPO preferred for absolute deficiencies or EPO loss. | Transfusions indicated when heart damage possible.
48
B-12 and Folate Deficiencies (basis)
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
B12 sources/absorption
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
Folate sources/absorption
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
Bone Marrow Findings in B12/Folate Deficiency
Erythroid hyperplasia. Megaloblastic changes. Larger nuclei than anticipated based on maturity level.
52
Peripheral Blood Findings B12/Folate Deficiency
variable anemia, low reticulocyte count, macrocytosis, high bilirubin, and high LDH.
53
Causes of B12 anemia (3)
Autoimmune destruction of IF producing epithelial cells Lack of IF synthesis Malabsorption of B12
54
B12 deficiency timeline
Slow. High liver stores take long time to deplete w/ long half life for b12. Neruoabnormalities possible.
55
Causes of Folate Anemia (2)
Inadequate Dietary intake | Malabsorption (enterohepatic circulation disruption, alcohol consumption)
56
Folate Deficiency Timeline
Much faster than B12. Neuro abnormalities rare.
57
Diagnosing B12/Folate Deficiency
Both produce elevated plasma homocysteine. B12 also produces high methylmalonic acid levels.
58
Treatments for B12/Folate
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
Hemoglobin tetramers through development
0-4 Months: A2E2 and Z2E2 4-Birth: Fetal A2G2 After birth: A2B2 w/ 2% A2D2
60
Alpha Thalassemia usually caused by.....
Deletion on Chromosome 16
61
Beta Thalassemia usually caused by....
Point mutation on Chromosome 11
62
Clinical Signs of Thalassemia
Low Hgb, Low MCV, Low MCHC,
63
Alpha Thalassemia Trait
Silent: 1/4 deleted genes, no anemia, normal MCV Trait: 2/4 deleted, no/mild anemia, normal/low MCV NO transfusions needed
64
HgH Disease
3/4 alpha genes deleted, mod/severe anemia, low MCV, transfusions sometimes needed
65
Hydrops Fetalis
4/4 alpha genes deleted, incompatible with life
66
Thalassemia Smear Findings
microcytosis, target cells, polychromastia, normal RDW
67
Clinical manifestations of thalassemia
High bilirubin, AST, LDH from hemolysis, splenomegaly, expanded bone marrow, increased iron absorption, delayed growth, pulmonary HTN
68
Iron Valence States
Ferric 3+ and Ferrous 2+
69
Iron in Aquesous Solution Considerations
Forms insoluble salts unless protein bound
70
Where are Iron salts more soluble?
Low pH
71
How is body Iron balance controlled?
Absorption, no mechanism for excretion
72
How do you lose body iron?
exfoliation of skin/musosa, menstruation
73
Hemoglobin: 30-60; 60-90; 45-75; 10-10
Pneumonic for pO2 and % binding
74
Lifespans and daily production (RBCs, platelets, Neutrophils)
RBCs: 120 days; 175 bil/day Platelets: 7-10 days; 200bil/day Neutrophils: 7 hours; 70 bil/day
75
Hemoglobin E
Beta globin gene PM: 26 glu-lys. Unstable. Low MCHC
76
Hydroxyurea in Beta Thalassemia
Induces production of gamma chains, increases HbF
77
HgC Mutation
Beta6 Glu-Lys
78
HbD Punjab Mutation
Beta121 Glu-Gln
79
HbE Mutation
Beta26 Glu-Lys
80
HbO Arab Mutation
B121 Glu-Lys
81
HbS Mutation
Beta6 Glu-Val
82
Sickle Cell HbSS RBC Lifespan
20 days
83
Complications of chronic hemolytic anemia (4)
Aplastic Crises (Parvovirus B19) Growth delay Biliruibin Gallstones Vascular Occlusion
84
Effects of Vascular Occlusion in hemolytic anemia (8)
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
Sickle Cell Pain Crisis
Vaso-occlusion and temporary ischemia causing pain in the extremities, abdomen, chest
86
Complications w/ pain crises (vaso-occlusion) (5)
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
Treatments of Sickle Cell (3)
Bone Marrow Transplant: Curative Hydroxyurea: fetal hemoglobin production Transfusion Therapy: for severe acute circumstances
88
Hereditary Spherocytosis Cause
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
G-6-PD deficiency inheritance
Sex-linked Recessive
90
G-6-PD Pathology
Loss of G-6-PD creates inability to restore reduced GSH, increased oxidative damage to spectrin, reduced deformity, splenic trapping, macrophage hemolysis
91
Warm AB Autoimmune Hemolytic Anemia
IgG bind RBCs in warm areas of body, poor complement activation, Fc Receptor mediated macrophage hemolysis in spleen
92
Cold AB Autoimmune Hemolytic Anemia
IgG/IgM bind RBCs in cold ares of body, activate complement for intravascular hemolysis
93
Direct DAT/Coombs test
Tests for IgG/C3d/C4d on patient's RBCs by adding ABs against these components and testing agglutination
94
Indirect DAT/Coombs
Checks if patient's serum has IgG/complement that binds normal RBCs
95
Spleen Immunity Function
Creation of IgM, especially for encapsulated organisms
96
Complications of Splenectomy
Bacterial sepsis from S pneumoniae
97
Co-treatments w/ splenectomy
H influenza b, S pneumoniae vaccinations, and meningococcus vaccinations. Prophylactic ABX daily through childhood. See physician immediately w/ F
98
IgG Half Life
3 weeks
99
C1 Esterase Inhibitor
Suppresses basal complement activation from minimal concentration AG activation. Makes C1 unable to activate C4 and lead to cascade.
100
T Helper 1
Release lymphokines to attract macrophages
101
T Helper 17
Similar to TH1s but more powerful
102
T Helper 2
Stimulate macrophages to wall-off pathogens and start healing process
103
Follicular Helper T
After activation, move to B cell region of lymph node to promote B cell activation and class switching
104
Regulatory T Cell
Suppress activation/function of T helpers to stop immune response
105
Type I Immunopathology
Too much IgE, hypersensitivty
106
Type II Immunopathology
Antibodies that react to self or collateral damage to self from AG binding cells
107
Type III Immunopathology
Antibodies to soluble antigens, cause local damage through complement activation
108
Type IV Immunopathology
T-cell mediated damage to self (hepatitis, TB)
109
How many constant heavy chain segments in each type of AB?
3 for IgG, IgD, IgA | 4 for IgM and IgE
110
Unique physical characteristics of AB types
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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