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PHGY 209 > Blood Cells > Flashcards

Blood Cells Flashcards

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
Q

Effect of O2 on blood color

A

Hb saturated with O2 = bright red

O2 leaves Hb = dark red

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26
Q

Why have Hb in RBC instead of dissolved in plasma

A

Plasma viscosity would increase

Plasma COP would increase

Hb would be lost via kidney (same size as Albumin which is lost through kidneys)

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27
Q

Factors affecting binding/release of O2 to Hb

A

Temperature
Ionic composition
pH
pCO2
intracellular enzyme concentration

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28
Q

Describe RBC precursor Proliferation

A

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

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29
Q

What is erythropoietin

A

Type of glycoprotein hormone/cytokine responsible for growth of RBC

Produced by Kidney

Released by stimulus from Hypoxia

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30
Q

Factors determining # of RBC

A

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

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31
Q

what is Hypoxia

A

Decreased RBC count from lack of O2 in environment or additional need for O2 in tissues

32
Q

Explain negative feedback of Erythropoiesis

A

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
Q

Hormonal effects on erythropoietin

A

Testosterone: increases release of erythropoietin and sensitivity of RBC precursors to Erythropoietin (males have more RBC than females)

Estrogen: opposite effect

34
Q

Classification and Etiology of Anemia: Diminished Production, Abnormality at site of production (bone marrow)

Aplastic (Hypoplastic anemia)

A

Etiology: unknown exposure to radiation chemicals or drugs

Class. normocytic, normochromic

35
Q

What happens to old RBC when they die

A

Recognized and removed by Macrophages in liver and spleen

36
Q

What happens to RBC components when it is destroyed

A

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
Q

Characteristics of Bilirubin

A

Pigment giving yellow color to plasma

Must be at 1mg/dL concentration

If more it causes jaundice

38
Q

Causes of jaundice

A

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
Q

What is polycythemia

A

Production of RBC > Destruction RBC

Ex: Ht = 70% instead of normal 45%

40
Q

What is Anemia

A

Production of RBC < Destruction RBC

Decrease in oxygen carrying capacity of blood

Ex: Ht = 30% instead of normal 45%

Hb content is lower

41
Q

Relative polycythemia

A

Due to decreased plasma volume

42
Q

Absolute Polycythemia

A

May be physiological or pathological

43
Q

Physiological Polycythemia

A

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
Q

Pathological Polycythemia

A

Direct cause of RBC increase

Primary effect due to
Tumors of cells producing EPO
Unregulated RBC Production by bone marrow

45
Q

Problems of polycythemia

A

Increases blood viscosity

Slow blood flow leads to blood clots

46
Q

Anemia : morphological

A

Shape: RBC are normocytic microcytic or macrocytic

Color: hypochromic hyperchromic or normochromic

47
Q

Classifications of Anemia

A

Morphological: shape and color
+
etiologic :
diminished production,
ineffective maturation,
increased RBC destruction/ reduced survival

48
Q

Classification and etiology of Anemia for diminished production from inadequate stimulus

A

Stimulation failure anemia

etiology: renal disease (less EPO prod.)

Class. Normocytic Normochromic

49
Q

Classification and etiology of Anemia for diminished production from inadequate raw materials

A

Iron deficiency Anemia (most common)

etiology: increased required Fe or inadequate supply of Fe

Class. Microcytic, Hypochromic

50
Q

What happens to Fe during RBC destruction

A

25 mg Fe/day is released
24 mg Fe/day is recycled
1 mg Fe/day is lost

51
Q

Requirement difference of Fe in diet for males and females

A

males require 1mg Fe/day
Females during menstruations require 2 mg Fe/day since 25mg Fe/month is lost in menstruations

52
Q

Classification and etiology for anemia from ineffective maturation

A

Maturation failure anemia

etiology: deficiencies of Vitamin B12 and folic acid (for DNA synthesis)
inadequate supply of Fe

Class. Macrocytic, Normochromic

53
Q

Classification and etiology for anemia from Increased RBC destruction/reduced survival

A

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
Q

What is Hemorrhage

A

Blood loss
external or internal

55
Q

What is Hematoma

A

accumulation of blood inside tissues

56
Q

What is Hemostasis

A

Arrest of bleeding after vascular injury

57
Q

Overlapping mechanisms of Hemostasis

A

Primary Hemostasis
Secondary Hemostasis

58
Q

What is primary Hemostasis

A

Within few seconds

Platelets respond to block bleedings
Vascular response: vasoconstriction

59
Q

What is secondary Hemostasis

A

Takes a few minutes
Clot formation
by coagulation factors activated by thrombin

60
Q

Hemostasis general steps

A

Vasoconstriction
Platelet Plug formation
Blood Clot Formation

61
Q

What is vasoconstriction

A

Smooth muscle cells of vessel wall contract when injury happens

opposed endothelial cells stick together, so less blood can go through

62
Q

What is Platelet response

A

Platelet group to the site of damaged blood vessel and plug
(White Thrombus)

63
Q

Platelet Structure

A

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
Q

Hematopoiesis of Platelets

A

Pluripotential cells become Myeloid stem cell

Thrombopoietin from liver Differentiates into Megakaryocyte

65
Q

Steps of Platelet Plug Formation (4)

A

Adhesion

Activation and release of Cytokines

Aggregation

Consolidation (white thrombus formed)

66
Q

Platelet functions

A

Release vasoconstricting agents/cytokines

forma platelet plug (white thrombus)

Release clotting factors

Participate in clot retraction

Maintenance of endothelial integrity

67
Q

What is clotting

A

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
Q

Clotting Pathways

A

Extrinsic pathway

Intrinsic pathway

both depend on Ca++, phospholipids and protein factors

both make prothrombinase pathway: male thrombin

69
Q

Extrinsic pathway

A

takes 15-20 secs
Tissue phospholipids, plasma factors and Ca++ produce Thrombin

Thrombin activates fibrinogen which results in fibrin being created (Red thrombus)

70
Q

Intrinsic Pathway

A

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
Q

Positive feedback in prothrombinase

A

extrinsic pathway produces small amount of thrombin

Thrombin activates intrinsic pathway and more thrombin is produced

72
Q

What regulates clotting

A

Inhibitors of platelet adhesion

Anticoagulants (block reactions of coagulation scheme)

73
Q

What is Thrombolysis

A

Clot lysis is the destruction of clot of prevention from adhesion

74
Q

How does Clot Lysis happen

A

Intrinsic/extrinsic proactivators activate Plasminogen activator

Plasminogen is activated and becomes plasmin

Plasmin blocks Fibrin from becoming fragments to clot

75
Q

What are inhibitors of platelet adhesion

A

Aspirin prevent platelets from closing blood vessels.
used to prevent heart attacks: blood clots inside vessels

76
Q

Anticoagulant Drugs do what

A

Interfere with clot formation

Coumarin blocks synthesis of Prothrombin
Heparin inhibits thrombin activation

77
Q

Thrombolytic drugs do what

A

Promote clot Lysis

PHGY 209 (5 decks)

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