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PHGY 209 > Blood II > Flashcards

Blood II Flashcards

1
Q

RBC (erythrocytes)

A

5 x 10^6/μL
Diameter: 7.2 μm
Lifespan: 120 days

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2
Q

Platelets (Thrombocytes)

A

250,000-400,000/μL
Diameter: 2-3 μm
Lifespan: 7-8 days

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3
Q

WBC (Leukocytes)

A

8,000-10,000/μL
Diameter: 10-18 μm
Lifespan: hours - years

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4
Q

Hematopoiesis

A

All blood cells are derived from a common multi-potential, pluri-potential hematopoietic STEM cell

  1. Erythopoiesis (2 -3 x 10^6 RBCs produced per second)
  2. Thrombopoiesis
  3. Leukopoiesis
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5
Q

Hematopoietic Growth Factors

A

(HGFs)
influence the proliferation and differentiation of blood cell precursors

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6
Q

Cytokines

A

substances (proteins or peptides) released by one cell that affect the growth, development, and activity of another cell

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7
Q

Sites of Hematopoiesis

A

-3 months: Yolk Sac
-5 months: Liver and spleen
-Birth: Shifts to bone marrow
-Post Birth: Axial skeleton and Proximal epiphyses of long bones

(long bones stop as site by 30 y/o)

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8
Q

RBC Shape

A

“Bioconcave Disk” due to presence of “spectrin”
Spectrin: a fibrous protein forming a flexible network lined to cell membrane

  1. MAX surface area and MIN diffusion distance increase efficiency of O2 and CO2 diffusion
  2. Flexible in capillaries
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9
Q

Complete blood count (CBC)

A

RBC, WBC, platelet count, Hematocrit, Hb concentration

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10
Q

RBC size and Shape

A

Normocytic
Microcytic
Macrocytic

Sickle Cell (sickle shape)
Spherocyte (smaller and darker)

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11
Q

RBC count

A

Males: 5.1 –5.5 x 10^6/μL
Females: 4.5 -4.8 x 10^6/μL

~25 x 10^12 in 5L of blood

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12
Q

RBC Rate of production = RBC Rate of destruction

A

~2 x 10^6/second

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13
Q

RBC Enzyme Systems

A

Must make energy with no mitochondria

  1. Glycolytic Enzymes generates energy anaerobically
  2. Carbonic Anhydrase converts CO2 to bicarbonate which is easier to transport
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13
Q

RBC Components

A

Mostly water
33% Hemoglobin
Lipids, proteins, ions

Contain no organelles, nucleus, mitocondria

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14
Q

Hemoglobin - Oxygen complex

A

1 molecule of Hb binds to 4 O2

oxyhemoglobin = O2 + Hb (red in lungs)
deoxyhemoglobin = O2 released (dark blood in tissues)

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15
Q

Hemoglobin Structure

A

200-300 x 10^6 Hb molecules/RBC
MW = 64 kDa

Four subunits of chain with heme group
4 Heme - Iron (Fe) - O2 bonds

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16
Q

Hemoglobin Functions

A
  1. Transport O2 / CO2
  2. Increase O2 solubility in blood
  3. Acts as a buffer
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17
Q

Hemoglobin Values

A

Males: 16 g/100 ml blood
Females: 14 g/100 ml blood

O2 carrying capacity of blood: 20 ml O2/100 ml blood

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18
Q

Factors affecting ability of Hb to bind and release O2

A
  1. Temperature
  2. Ionic Composition
  3. pH
  4. pCO2 (partial pressure CO2)
  5. Intracellular enzyme concentration
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19
Q

Hematopoiesis Cell Lines

A

2 Cell lines
-Lymphoid stem cell (lymphocyte only)
-Myeloid stem cell (all others)

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20
Q

RBC Precursor Proliferation

A

(3-5 days)
1. Decrease in size (18 -> 7 μm)
2. Loss of nucleus and organelles
3. Accumulation of Hb

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21
Q

Erythropoiesis

A
  1. STEM Cell
  2. Myeloid cell line
  3. RBC Precursor Proliferation
  4. Reticulocyte
  5. Mature RBC
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22
Q

Reticulocyte

A

< 1 % of RBCS
Reflects the amount of effective erythropoiesis in bone marrow
24 hours

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23
Q

Factors determining # of RBCs

A
  1. O2 requirements
  2. O2 availability

RBC increases with decreased O2

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24
Q

Erythropoietin (EPO)

A

A glycoprotein hormone/cytokine produced mainly by the kidney

Stimulus for release is Hypoxia
-decreased RBC count
-decreased O2 availability
-increased tissue demand for O2

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25
Q

Regulation of Erythropoiesis

A
  1. Kidney senses hypoxia
  2. Kidney (renal cortex) releases EPO
  3. Increase EPO in plasma
  4. Stimulation of Bone Marrow
  5. Increased production of erythrocyte precursor
  6. Increased RBCs and oxygen in plasma

NEGATIVE FEEDBACK LOOP

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26
Q

Erythropoietin (EPO) acts on…

A

committed erythrocyte precursors

EPO stimulates proliferation and accelerates maturation of committed stem cell into mature RBC

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27
Q

Hormonal Effects on EPO

A

Testosterone increases release of EPO and sensitivity of RBC precursors to EPO

Estrogen has opposite effects

Males have more RBCs than females

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28
Q

Destruction of RBCs

A

Macrophages perform phagocytosis of old RBCs (120 days) and components are recycled

29
Q

RBC component recycling

A

Global: Amino acid pool
Iron: Binds to Transferrin and is moved to storage in liver, spleen, and gut
Hb: broken into Heme -> Bilirubin

30
Q

Bilirubin

A

Heme waste or yellow plasma pigment that passes through liver and intestinal tract to be excreted in feces
Backup of > 1mg/dL causes Jaundice

31
Q

Infant Jaundice

A

excess of RBCs are lysed and Bilirubin is released

32
Q

Jaundice Causes

A

Liver damage and bile duct obstruction block pathways of Bilirubin leading to a buildup in body

33
Q

RBC Dynamics

A

Production > Destruction = Polycythemia
Production < Destruction = Anemia

Measured by # of RBC, Hb, Ht

34
Q

Ht and abnormal RBC dynamics

A

We can not rely on Ht measurement as increased/decreased Ht can be due to dehydration/fluid retention and not polycythemia/anemia

35
Q

Polycythemia

A

(more RBCs)
> 18 g% Hb
> 6 x 106 RBCs/μL

increases blood viscosity and can slow flow into blood clots

36
Q

Relative Polycythemia

A

due to decreased plasma volume

37
Q

Absolute Polycythemia

A

Physiological: secondary effect due to higher O2 needs or lower O2 availability

Pathological: primary effect due to tumors producing EPO, unregulated RBC production

38
Q

Polycythemia vera

A

PATHOLOGICAL

-7 -8 x 10^6RBCs/μL
-Ht~70%
due to stem cell dysfunction

39
Q

Anemia

A

A decrease in the oxygen-carrying capacity of blood

  1. Decreased RBC Count
    Males: < 4 x 10^6/μL
    Females: < 3.2 x 10^6/μL
  2. Decreased Hb content
    Males: < 11 g%
    Females: < 9 g%
40
Q

Classification of Anemias

A

Microcytic (Shrunk)
Normocytic
Macrocytic (Enlarged)

Normochromic ~33% Hb
Hypochromic <33% Hb (Pale)
Hyperchromic >33% Hb (Too dark)

41
Q

Aplastic (Hypoplastic Anemia)

A

Diminished Production: Abnormality at site of production (bone marrow)

Normocytic, Normochromic

May be caused by exposure to chemicals, drugs, or radiation

42
Q

Stimulation Failure Anemia

A

Diminished Production: Inadequate stimulus

Normocytic, Normochromic

Renal disease causes less EPO production

43
Q

Iron Deficiency Anemia (Most common)

A

Diminished Production: Inadequate raw materials

Microcytic, Hypochromic

Increased requirement of Fe or inadequate supply of Fe

44
Q

Anemia Causes

A
  1. Diminished RBC production
  2. Ineffective RBC maturation
  3. Increased RBC destruction or reduced RBC survival (RBC survival disorders)
45
Q

Iron (Fe)

A

Total in Body: 4g
Hb: 65% Stored: 30% Myoglobin: 5% Enzymes: 1%

Daily Intake in diet: ~15 -20 mg
Daily absorb in gut:
Males: ~1 mg Fe/day
Females:~2 mg Fe/day

46
Q

Erythropoiesis and Iron

A

Normal erythropoiesis requires 25 mg Fe/day
Normal RBC destruction releases 25 mg Fe/day
1. 1 mg is lost
2. 24 mg are recycled

So males and females require intake of dietary iron to make up for losses (more for females)

47
Q

Maturation Failure Anemia

A

Ineffective Maturation: Deficiencies of Vitamin B12 and Folic Acid
(both required for DNA synthesis)

Macrocytic, Normochromic

48
Q

Intrinsic Factor Deficiency

A

Can lead to Maturation Failure Anemia / Pernicious Anemia

Intrinsic Factor is a glycoprotein needed to transport Vitamin B12

49
Q

Hemolytic Anemias

A

RBC survival disorders: may be accompanied by jaundice

Congenital or Acquired (toxins, drugs, antibodies)

  1. Abnormal RBC membrane structure
  2. Abnormal enzyme systems
  3. Abnormal Hb structure (Sickle Cell)
50
Q

Hemorrhage

A

Blood loss either externally or internally

Hematoma is accumulation of blood in the tissues

51
Q

Hemostasis

A

Arrest of bleeding following vascular injury
1. Vascular injury
2. Vasoconstriction
3. Platelet Plug formation
4. Blood clot formation

52
Q

Primary Hemostasis

A

Vascular Response
Platelet Response

53
Q

Secondary Hemostasis

A

Blood clot formation

54
Q

Vascular Response (vasoconstriction)

A

-Smooth muscle cells in vessel wall respond to injury by contracting
-Opposed endothelial cells stick together

55
Q

Platelet Structure

A

~ 2-4 μm diameter
-No nucleus
-Many granules containing factors for constriction, clotting, aggregation
-Many filaments, microtubules, mitochondria, sER

56
Q

Platelet Production

A
  1. Pluripotent stem cell
  2. Committed stem cell (Myeloid) stimulated by Thrombopoeitin (from liver)
  3. Megakaryocyte
  4. Megakaryocyte nucleus division into platelets
  5. Finger like projections release platelets into blood stream
57
Q

Platelet Plug formation

A
  1. Collagen exposure
  2. Platelets adhere to vessel via von Willebrand Factor
  3. Platelets release platelet factors
  4. Platelets aggregate
  5. Platelet plug formation
58
Q

Platelet factors

A

ADP
Thromboxane A2
Serotonin
PF3

59
Q

Platelet Functions

A
  1. Release vasoconstricting agents/ cytokines
  2. Form Platelet Plug(White Thrombus)
  3. Release Clotting Factors
  4. Participate in Clot Retraction
  5. Maintain Endothelial Integrity
60
Q

Petechia

A

small red/purple spots caused by bleeding into the skin due to lack of platelets

61
Q

Abnormal primary Hemostatic Response

A
  1. Failure of blood vessel constricting
  2. Platelet deficiencies
    (Numerical or Functional)

Aspirin inhibits synthesis and release of TXA2

62
Q

Clot formation

A

A function of plasma NOT RBCS
-Injury to vessel wall causes activation of plasma proteins and clotting factors
-Clotting factors act as enzymes or co-factors in the presence of Ca++ or phospholipid agents

63
Q

Intrinsic Pathway

A

3-6 mins
1. Damage to blood vessel
2. Interacting plasma factors
(Ca++ and PF3)
3. Prothrombinase cleaves Prothrombin into Thrombin
4. Thrombin cleaves Fibrinogen into Fibrin
5. Factor XIII cross links to form clot

64
Q

Extrinsic Pathway

A

15- 20 secs
1. Damage to tissue outside vessel
2. Interacting plasma factors
(Ca++ and Phospholipids)
3. Prothrombinase cleaves Prothrombin into Thrombin
4. Thrombin cleaves Fibrinogen into Fibrin
5. Factor XIII cross links to form clot

65
Q

Extrinsic Pathway and Intrinsic Pathway

A

-Extrinsic Pathway is closed after platelet plug formation
-Small amounts of THROMBIN generated in Extrinsic trigger strong positive feedback on Intrinsic generate larger quantities of THROMBIN

66
Q

Clotting Factor Deficiencies

A

Congenital: single factor hereditary deficiencies (Factor VIII, Hemophilia)
Acquired: multi-factor deficiencies (liver disease, Vitamin K deficiency)

Vitamin K is a cofactor in the synthesis of Prothrombin, VII, IX, X

67
Q

Clot Retraction

A

requires a contractile protein, thrombosthenin, released by platelets

Makes stable solid clot

68
Q

Clot lysis

A
  1. Intrinsic/Extrinsic proactivators trigger plasminogen activator
  2. Plasminogen Activator cleaves plasminogen into plasmin
  3. Plasmin cleaves fibrin into small fragments to destroy the clot
69
Q

Clotting Regulation

A

Inhibitors of platelet adhesion
Anticoagulants (Coumarin, Heparin)

70
Q

Thrombolytic Drugs

A

promote clot lysis
Tissue plasminogen activator
Streptokinase

PHGY 209 (4 decks)

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