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PHGY 209 > Blood Cells > Flashcards

Blood Cells Flashcards

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1
Q

Types of blood cells

A

Erythrocytes: RBC

Thrombocytes: Platelets

Leukocytes: WBC

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2
Q

RBC characteristics

A

Diameter: 7.2 micrometers
Lifespan: 120 days
Number: 5x10^6/microL (most common)

Bi-concave shape

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3
Q

Platelets Characteristics

A

Diameter: 2-3 micrometers
Lifespan: 7-8 days
Number 250,000-400,000/microL

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4
Q

WBC Characteristics

A

Diameter: 10-18 micrometers
Lifespan: hours or years
Number: 8,000-10,000/microL

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5
Q

What is Hematopoiesis

A

Formation of blood cells derived from multipotential (pluripotential) hematopoietic stem cells.

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6
Q

What is Erythopoiesis

A

Production of RBC

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7
Q

What is Thrombopoiesis

A

Production of Platelets

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8
Q

What is Leukopoiesis

A

Production of WBC

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9
Q

General Pattern of Hematopoiesis

A

Division:
Pluripotential stem cells replicates

Differentiation:
Stem cells commits to certain blood cell type

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10
Q

What are Cytokines

A

Proteins/peptides released by a cell that affect growth/development of another cell.

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11
Q

What are Hematopoietic Growth Factors

A

Cytokines influencing blood cell precursors

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12
Q

Prenatal Sites of Hematopoiesis

A

Yolk sac: first 3 months

Liver and spleen: after 1 month and up to 9 months

Bone marrow: After 3 months and for rest of life

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13
Q

Postnatal sites of Hematopoiesis

A

Axial skeleton: for whole life, in flat bones of skull, shoulder blades, sternum, vertebrae, ribs, pelvis

Distal Long bones: ends after 30 years
(in epiphysis of long bones)

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14
Q

Function of RBC

A

Transport respiratory gasses

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15
Q

Advantage of Biconcave shape in RBC

A

Allows Maximal surface area + minimal diffusion distance

increase permeability

high flexibility: can squeeze through capillaries

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16
Q

What is CBC

A

Complete blood count: RBC, WBC, platelet, Hematocrit, [Hb]

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17
Q

Cell size terms for RBC

A

Normocytic: 7 micrometers

Microcytic: smaller than 7 micrometers

Macrocytic: larger than 7 micrometers

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18
Q

Cell shape terms for RBC

A

Sickle Cell: irregular form, cannot travel correctly

Spherocyte: non biconcave, travel is harder, less flexible

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19
Q

How is # of RBC balanced

A

Rate of production = Rate of destruction of RBC = 2x10^6/s

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20
Q

RBC composition

A

Water
Lipids, proteins, ions
33% Hb

no organelles: no nucleus, no mitochondria

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21
Q

Roles of Enzymes in RBC

A

Glycolytic Enzymes: generate energy anaerobically (without O2)

Carbonic Anhydrase: CO2 transport

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22
Q

Structure of Hemoglobin

A

Four Heme chains and a Globin center

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23
Q

How many molecules of O2 can bind to a Hb molecule, and how many Fe2+

A

4 O2 molecules and 4 Fe2+ ions

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24
Q

Effect of Hb on O2 solubility

A

O2 alone in plasma has very low solubility : 0.3 ml O2/100 ml plasma

With Hb, solubility is high: 20 ml O2/100 ml blood

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25
Effect of O2 on blood color
Hb saturated with O2 = bright red O2 leaves Hb = dark red
26
Why have Hb in RBC instead of dissolved in plasma
Plasma viscosity would increase Plasma COP would increase Hb would be lost via kidney (same size as Albumin which is lost through kidneys)
27
Factors affecting binding/release of O2 to Hb
Temperature Ionic composition pH pCO2 intracellular enzyme concentration
28
Describe RBC precursor Proliferation
first 3-5 days, erythropoietin acts on Pluripotential hematopoietic stem cells division and differentiation occur cells decreases in size during last 24h cells are Reticulocytes with a nucleus but they lose it. Hb accumulates in cell
29
What is erythropoietin
Type of glycoprotein hormone/cytokine responsible for growth of RBC Produced by Kidney Released by stimulus from Hypoxia
30
Factors determining # of RBC
O2 requirements: training requires more RBC to have better O2 intake O2 Availability: At high altitude, O2 is more scarce, so more RBC to retain more O2
31
what is Hypoxia
Decreased RBC count from lack of O2 in environment or additional need for O2 in tissues
32
Explain negative feedback of Erythropoiesis
Kidney senses Hypoxia and releases Erythropoietin Erythropoietin reaches plasma and stimulates committed RBC precursors in Bone Marrow RBC # increases Oxygen levels in plasma increase Increased O2 is detected by kidney which stops further release of erythropoietin
33
Hormonal effects on erythropoietin
Testosterone: increases release of erythropoietin and sensitivity of RBC precursors to Erythropoietin (males have more RBC than females) Estrogen: opposite effect
34
Classification and Etiology of Anemia: Diminished Production, Abnormality at site of production (bone marrow) Aplastic (Hypoplastic anemia)
Etiology: unknown exposure to radiation chemicals or drugs Class. normocytic, normochromic
35
What happens to old RBC when they die
Recognized and removed by Macrophages in liver and spleen
36
What happens to RBC components when it is destroyed
Hb : Heme and Bilirubin pigment are sent to waste through liver and after to the intestinal tract Globin : goes back into amino acid pool Fe: Transferrin moves Fe for recycling and ferritin stores it in liver, spleen and gut
37
Characteristics of Bilirubin
Pigment giving yellow color to plasma Must be at 1mg/dL concentration If more it causes jaundice
38
Causes of jaundice
Excessive hemolysis: high digestion of RBC = more waste Liver damage: less Bilirubin goes to waste Higher concentration than 1mg/dL Bile duct obstruction: bilirubin does not reach intestinal tract and cannot be evacuated in feces (waste is sent to blood)
39
What is polycythemia
Production of RBC > Destruction RBC Ex: Ht = 70% instead of normal 45%
40
What is Anemia
Production of RBC < Destruction RBC Decrease in oxygen carrying capacity of blood Ex: Ht = 30% instead of normal 45% Hb content is lower
41
Relative polycythemia
Due to decreased plasma volume
42
Absolute Polycythemia
May be physiological or pathological
43
Physiological Polycythemia
Secondary effect due to high O2 needs or lower availability Indirect increase of RBC due to High altitude Increased physical activity Chronic lung disease Heavy smoking
44
Pathological Polycythemia
Direct cause of RBC increase Primary effect due to Tumors of cells producing EPO Unregulated RBC Production by bone marrow
45
Problems of polycythemia
Increases blood viscosity Slow blood flow leads to blood clots
46
Anemia : morphological
Shape: RBC are normocytic microcytic or macrocytic Color: hypochromic hyperchromic or normochromic
47
Classifications of Anemia
Morphological: shape and color + etiologic : diminished production, ineffective maturation, increased RBC destruction/ reduced survival
48
Classification and etiology of Anemia for diminished production from inadequate stimulus
Stimulation failure anemia etiology: renal disease (less EPO prod.) Class. Normocytic Normochromic
49
Classification and etiology of Anemia for diminished production from inadequate raw materials
Iron deficiency Anemia (most common) etiology: increased required Fe or inadequate supply of Fe Class. Microcytic, Hypochromic
50
What happens to Fe during RBC destruction
25 mg Fe/day is released 24 mg Fe/day is recycled 1 mg Fe/day is lost
51
Requirement difference of Fe in diet for males and females
males require 1mg Fe/day Females during menstruations require 2 mg Fe/day since 25mg Fe/month is lost in menstruations
52
Classification and etiology for anemia from ineffective maturation
Maturation failure anemia etiology: deficiencies of Vitamin B12 and folic acid (for DNA synthesis) inadequate supply of Fe Class. Macrocytic, Normochromic
53
Classification and etiology for anemia from Increased RBC destruction/reduced survival
Hemolytic Anemia, can be with jaundice Etiology: congenital, acquired (toxins, drugs, antibodies) Class. Abnormal RBC membrane structure: less flexible, fragile Abnormal enzyme systems Abnormal Hb structure = sickle cell
54
What is Hemorrhage
Blood loss external or internal
55
What is Hematoma
accumulation of blood inside tissues
56
What is Hemostasis
Arrest of bleeding after vascular injury
57
Overlapping mechanisms of Hemostasis
Primary Hemostasis Secondary Hemostasis
58
What is primary Hemostasis
Within few seconds Platelets respond to block bleedings Vascular response: vasoconstriction
59
What is secondary Hemostasis
Takes a few minutes Clot formation by coagulation factors activated by thrombin
60
Hemostasis general steps
Vasoconstriction Platelet Plug formation Blood Clot Formation
61
What is vasoconstriction
Smooth muscle cells of vessel wall contract when injury happens opposed endothelial cells stick together, so less blood can go through
62
What is Platelet response
Platelet group to the site of damaged blood vessel and plug (White Thrombus)
63
Platelet Structure
2-4 micrometer diameter, no nucleus contains many granules with factors for vasoconstriction, platelet aggregation, clotting, growth, microtubules, mitochondria, sER live 7-10 days produced at every site of Hematopoiesis
64
Hematopoiesis of Platelets
Pluripotential cells become Myeloid stem cell Thrombopoietin from liver Differentiates into Megakaryocyte
65
Steps of Platelet Plug Formation (4)
Adhesion Activation and release of Cytokines Aggregation Consolidation (white thrombus formed)
66
Platelet functions
Release vasoconstricting agents/cytokines forma platelet plug (white thrombus) Release clotting factors Participate in clot retraction Maintenance of endothelial integrity
67
What is clotting
After injury to blood vessel, sequential activation and interaction of a group of plasma proteins/clotting factors in presence of Ca++ and phospholipid agents
68
Clotting Pathways
Extrinsic pathway Intrinsic pathway both depend on Ca++, phospholipids and protein factors both make prothrombinase pathway: male thrombin
69
Extrinsic pathway
takes 15-20 secs Tissue phospholipids, plasma factors and Ca++ produce Thrombin Thrombin activates fibrinogen which results in fibrin being created (Red thrombus)
70
Intrinsic Pathway
takes 3-6 min damage to blood vessel activates plasma factors, Ca++ and PF3 to do prothrombinase Thrombin is produced and it activates fibrinogen => fibrin => blood clot
71
Positive feedback in prothrombinase
extrinsic pathway produces small amount of thrombin Thrombin activates intrinsic pathway and more thrombin is produced
72
What regulates clotting
Inhibitors of platelet adhesion Anticoagulants (block reactions of coagulation scheme)
73
What is Thrombolysis
Clot lysis is the destruction of clot of prevention from adhesion
74
How does Clot Lysis happen
Intrinsic/extrinsic proactivators activate Plasminogen activator Plasminogen is activated and becomes plasmin Plasmin blocks Fibrin from becoming fragments to clot
75
What are inhibitors of platelet adhesion
Aspirin prevent platelets from closing blood vessels. used to prevent heart attacks: blood clots inside vessels
76
Anticoagulant Drugs do what
Interfere with clot formation Coumarin blocks synthesis of Prothrombin Heparin inhibits thrombin activation
77
Thrombolytic drugs do what
Promote clot Lysis

PHGY 209 (9 decks)

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