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Flashcards in 0-1 chapter 18 - blood Deck (179):
1

circulatory system

consists of the heart, blood vessels and blood

2

cardiovascular system

refers only to the heart and blood vessels

3

hematology

the study of blood

4

functions of circulatory system

transport
protection
Regulation

5

transport

O2, CO2, nutrients, wastes, hormones, and stem cells

6

protection

•inflammation, limit spread of infection, destroy microorganisms and cancer cells, neutralize toxins, and initiates clotting

7

regulation

•fluid balance, stabilizes pH of ECF, and temperature control

8

Properties of Blood

•adults have 4-6 L of blood
•a liquid connective tissue consisting of cells and extracellular matrix

9

plasma

matrix of blood
•a clear, light yellow fluid

10

formed elements

blood cells and cell fragments
•red blood cells, white blood cells, and platelets

11

seven kinds of formed elements

erythrocytes
platelets
leukocytes

12

erythrocytes

red blood cells (RBCs)

13

platelets

cell fragments from special cell in bone marrow

14

leukocytes-white blood cells (WBCs)
•five leukocyte types divided into two categories:

white blood cells (WBCs)
•five leukocyte types divided into two categories
-granulocytes (with granules)
-agranulocytes (without granules)

15

granulocytes

–neutrophils
–eosinophils
–basophils

16

agranulocytes

–lymphocytes
–monocytes

17

hematocrit

centrifuge blood to separate components

18

erythrocytes

are heaviest and settle first
•37% to 52% total volume

19

white blood cells and platelets

•1% total volume
•buffy coat

20

plasma

•the remainder of volume
•47% -63%
•complex mixture of water, proteins, nutrients, electrolytes, nitrogenous wastes, hormones, and gases

21

plasma

liquid portion of blood

22

serum

remaining fluid when blood clots and the solids are removed
•identical to plasma except for the absence of fibrinogen

23

3 major categories of plasma proteins

albumins
globulins
fibrinogen

24

albumins

smallest and most abundant
•contributes to viscosity and osmolarity, influences blood pressure, flow and fluid balance

25

globulins

•provide immune system functions
•alpha, beta and gamma globulins

26

fibrinogen

precursor of fibrin threads that help form blood clots

27

plasma proteins formed by

liver
–except globulins (produced by plasma cells)

28

Nonprotein Components of Plasma

nitrogenous compounds
nutrients
dissolved O2, CO2, and nitrogen
electrolytes

29

nitrogenous compounds

–free amino acids
•from dietary protein or tissue breakdown
–nitrogenous wastes (urea)
•toxic end products of catabolism
•normally removed by the kidneys

30

nutrients

–glucose, vitamins, fats, cholesterol, phospholipids, and minerals

31

dissolved O2, CO2, and nitrogen

Nothing-------------------

32

electrolytes

–Na+ makes up 90% of plasma cations

33

Properties of Blood

viscosity
osmolarity of blood

34

viscosity

resistance of a fluid to flow, resulting from the cohesion of its particles
–whole blood 4.5 -5.5 times as viscous as water
–plasma is 2.0 times as viscous as water
•important in circulatory function

35

osmolarity of blood

the total molarity of those dissolved particles that cannot pass through the blood vessel wall
–if too high, blood absorbs too much water, increasing the blood pressure
–if too low, too much water stays in tissue, blood pressure drops and edema occurs
–optimum osmolarity is achieved by body’s regulation of sodium ions, proteins, and red blood cells.

36

hypoproteinemia

–deficiency of plasma proteins
•extreme starvation
•liver or kidney disease
•severe burns

37

kwashiorkor

–children with severe protein deficiency
•fed on cereals once weaned
–thin arms and legs
–swollen abdomen

38

Hemopoiesis

the production of blood, especially its formed elements
adult production of 400 billion platelets, 200 billion RBCs and 10 billion WBCs every day

39

hemopoietic tissues

produce blood cells

40

yolk sac

produces stem cells for first blood cells
•colonize fetal bone marrow, liver, spleen and thymus

41

pluripotent stem cells (PPSC)

formerly called hemocytoblasts or hemopoietic stem cells

42

colony forming units

specialized stem cells only producing one class of formed element of blood

43

myeloid hemopoiesis

blood formation in the bone marrow

44

lymphoid hemopoiesis

blood formation in the lymphatic organs

45

Erythrocytes

two principal functions:

–carry oxygen from lungs to cell tissues
–pick up carbon dioxide from tissues and bring to lungs
•insufficient RBCs may kill in few minutes due to lack of oxygen to tissues

46

Erythrocytes (RBCs)

disc-shaped cell with thick rim
•lack mitochondria
–anaerobic fermentation to produce ATP
•lack of nucleus and DNA
–no protein synthesis or mitosis

47

blood type determined by

surface glycoprotein and glycolipids

48

cytoskeletal proteins

(spectrin and actin) give membrane durability and resilience
•stretch and bend as squeeze through small capillaries

49

gas transport

major function
–increased surface area/volume ratio
•due to loss of organelles during maturation
•increases diffusion rate of substances

50

33% of cytoplasm is

hemoglobin (Hb)
•280 million hemoglobin molecules on one RBC
•O2delivery to tissue and CO2transport to lungs

51

carbonic anhydrase

(CAH) in cytoplasm
•produces carbonic acid from CO2and water
•important role in gas transport and pH balance

52

Hemoglobin (Hb) Structure

each Hb molecule consists of:
–four protein chains –globins
–four heme groups

53

heme groups

–nonprotein moiety that binds O2to ferrous ion (Fe2+) at its center

54

globins

four protein chains
–two alpha and two beta chains
–5% CO2 in blood is bound to globin moiety

55

RBC count and hemoglobin concentration indicate

amount of O2 blood can carry

56

hematocrit

(packed cell volume) –percentage of whole blood volume composed of red blood cells
•men 42-52% cells; women 37-48% cells

57

hemoglobin concentration of whole blood

•men 13-18g/dL; women 12-16g/dL

58

RBC count

men 4.6-6.2 million/L; women 4-2-5.4 million/L

59

values are lower in women

–androgens stimulate RBC production
–women have periodic menstrual losses
–hematocrit is inversely proportional to percentage of body fat

60

Erythropoiesis

Erythrocyte Production
•2.5 million RBCs are produced per second
•average lifespan of about 120 days
•development takes 3-5 days

60

reticulocyte

nucleus discarded to form a reticulocyte
–named for fine network of endoplasmic reticulum
–0.5 to 1.5% of circulating RBCs are reticulocytes

IMATURE RED BLOOD CELL

61

iron

key nutritional requirement
–lost daily through urine, feces, and bleeding
•men 0.9 mg/day and women 1.7 mg/day
–low absorption rate of iron requires consumption of 5-20 mg/day

62

Nutritional Needs for Erythropoiesis

dietary iron

ferric (Fe3+) and ferrous (Fe2+)
–stomach acid converts Fe3+to absorbable Fe2+
–gastroferritinbinds Fe2+and transports it to small intestine
–absorbed into blood and binds to transferrinfor transport to bone marrow, liver, and other tissues

63

liver apoferritin binds to create

ferritin for storage

64

Nutritional Needs for Erythropoiesis

•Vitamin B12and folic acid
–rapid cell division and DNA synthesis that occurs in erythropoiesis
•Vitamin C and copper
–cofactors for enzymes synthesizing hemoglobin
•copper is transported in the blood by an alpha globulin called ceruloplasmin

65

Erythrocyte Homeostasis

negative feedback control
–drop in RBC count causes kidney hypoxemia
–kidney production of erythropoietin stimulates bone marrow
–RBC count increases in 3 -4 days

66

stimuli for increasing erythropoiesis

–low levels O2 (hypoxemia)
–high altitude
–increase in exercise
–loss of lung tissue in emphysema

67

Erythrocytes Death and Disposal

•RBCs lyse in narrow channels in spleen
•macrophages in spleen
–digest membrane bits
–separate heme from globin
•globins hydrolyzed into amino acids
•ironr emoved from heme

68

iron removed from heme

–heme pigment converted to biliverdin (green)
–biliverdin converted to bilirubin(yellow)
–released into blood plasma (kidneys -yellow urine)
–liver removes bilirubin and secretes into bile
-concentrated in gall bladder: released into small intestine; bacteria create urobilinogen(brown feces)

69

polycythemia

an excess of RBCs

70

primary polycythemia

(polycythemia vera)
•cancer of erythropoietic cell line in red bone marrow
–RBC count as high as 11 million/L; hematocrit 80%

71

secondary polycythemia

from dehydration, emphysema, high altitude, or physical conditioning
–RBC count up to 8 million/L

72

dangers of polycythemia

increased blood volume, pressure, viscosity
•can lead to embolism, stroke or heart failure

73

causes of anemia fall into three categories:

inadequate erythropoiesis or hemoglobin synthesis
hemorrhagic anemias
hemolytic anemias

74

inadequate erythropoiesis or hemoglobin synthesis

•kidney failure and insufficient erythropoietin
•iron-deficiency anemia
•inadequate vitamin B12from poor nutrition or lack of intrinsic factor (pernicious anemia)
•hypoplastic anemia –slowing of erythropoiesis
•aplastic anemia -complete cessation of erythropoiesis

75

hemorrhagic anemias

from bleeding

76

hemolytic anemias

from RBC destruction

77

pernicious anemia

inadequate vitamin B12from poor nutrition or lack of intrinsic factor

78

hypoplastic anemia

slowing of erythropoiesis

79

aplastic anemia

complete cessation of erythropoiesis

80

anemia has three potential consequences:

tissue hypoxia and necrosis
blood osmolarity is reduced
blood viscosity is low

81

tissue hypoxia and necrosis

•patient is lethargic
•shortness of breath upon exertion
•life threatening necrosis of brain, heart, or kidney

82

blood osmolarity is reduced

producing tissue edema

83

blood viscosity is low

•heart races and pressure drops
•cardiac failure may ensue

84

Sickle-Cell Disease

hereditary hemoglobin defects that occur mostly among people of African descent
•caused by a recessive allele that modifies the structure of the hemoglobin molecule (HbS)

85

Blood Types

blood types and transfusion compatibility are a matter of interactions between plasma proteins and erythrocytes

86

discovered blood types

Karl Landsteiner discovered blood types A, B and O in 1900
–won Nobel Prize

87

antigens

–complex molecules on surface of cell membrane that are unique to the individual
•used to distinguish self from foreign
•foreign antigens generate an immune response

88

agglutinogens

antigens on the surface of the RBC that is the basis for blood typing

89

antibodies

proteins (gamma globulins) secreted by plasma cells
•part of immune response to foreign matter
•bind to antigens and mark them for destruction
•forms antigen-antibody complexes

90

agglutinins

antibodies in the plasma that bring about transfusion mismatch

91

agglutination

–antibody molecule binding to antigens
–causes clumping of red blood cells

92

RBC antigens called

agglutinogens
–called antigen A and B
–determined by carbohydrate moieties found on RBC surface

93

antibodies called

agglutinins
–found in plasma
–anti-A and anti-B

94

ABO Group

your ABO blood type is determined by presence or absence of antigens (agglutinogens) on RBCs
•most common -type O
•rarest -type AB

95

blood type A person has

A antigens

96

blood type B person has

B antigens

97

blood type AB has

both A and B antigens

98

blood type O person has

neither antigen

99

antibodies (agglutinins)

anti-A and anti-B
•appear 2-8 months after birth; at maximum concentration at 10 yr.

100

agglutination

each antibody can attach to several foreign antigens on several different RBCs at the same time

101

transfusion reaction

–agglutinated RBCs block small blood vessels, hemolyze, and release their hemoglobin over the next few hours or days
–Hb blocks kidney tubules and causes acute renal failure

102

universal donor

–Type O –most common blood type
–lacks RBC antigens
–donor’s plasma may have both antibodies against recipient’s RBCs (anti-A and anti-B)
•may give packed cells (minimal plasma)

103

universal recipient

–Type AB –rarest blood type
–lacks plasma antibodies; no anti-A or B

104

Rh Group

Rh (C,D,E) agglutinogens discovered in rhesus monkey in 1940
–Rh D is the most reactive and a patient is considered blood type Rh+if they have D antigen (agglutinogens) on RBCs
–Rh frequencies vary among ethnic groups

105

Anti-D agglutinins

not normally present
–form in Rh-individuals exposed to Rh+blood

106

Hemolytic Disease of Newborn

•occurs if Rh-mother has formed antibodies and is pregnant with second Rh+child
–Anti-D antibodies can cross placenta
•prevention
–RhoGAM given to pregnant Rh-women

107

Rh antibodies attack

fetal blood
causing severe anemia and toxic brain syndrome

108

Leukocytes

(WBCs)
•least abundant formed element
–5,000 to 10,000 WBCs/L
•protect against infectious microorganisms and other pathogens
•conspicuous nucleus
•spend only a few hours in the blood stream before migrating to connective tissue
•retain their organelles for protein synthesis

109

granules

–all WBCs have lysosomescalled nonspecific (azurophilic) granules –inconspicuous so cytoplasm looks clear
–granulocytes have specific granules that contain enzymes and other chemicals employed in defense against pathogens

110

granulocytes

neutrophils
eosinophils
basophils

111

neutrophils

neutrophils(60-70%)-polymorphonuclear leukocytes
•barely-visible granules in cytoplasm; 3 to 5 lobed nucleus

112

eosinophils

•large rosy-orange granules; bilobed nucleus

113

basophils

•large, abundant, violet granules (obscure a large S-shaped nucleus)

114

agranulocytes

lymphocytes
monocytes

115

lymphocytes

(25-33%)
•variable amounts of bluish cytoplasm (scanty

116

monocytes

(3-8%)
•largest WBC; ovoid, kidney-, or horseshoe-shaped nucleus

117

Granulocyte Functions

neutrophils

increased numbers in bacterial infections
–phagocytosis of bacteria
–release antimicrobial chemicals

118

Granulocyte Functions

eosinophils

increased numbers in parasitic infections, collagen diseases, allergies, diseases of spleen and CNS
–phagocytosis of antigen-antibody complexes, allergens, and inflammatory chemicals
–release enzymes to destroy large parasites

119

Granulocyte Functions

basophils

increased numbers in chicken pox, sinusitis, diabetes)
–secrete histamine(vasodilator) –speeds flow of blood to an injured area
–secrete heparin(anticoagulant) –promotes the mobility of other WBCs in the area

120

Agranulocyte Functions

lymphocytes

increased numbers in diverse infections and immune responses
–destroy cells (cancer, foreign, and virally infected cells)
–“present” antigens to activate other immune cells
–coordinate actions of other immune cells
–secrete antibodies and provide immune memory

121

Agranulocyte Functions

monocytes

increased numbers in viral infections and inflammation
–leave bloodstream and transform into macrophages
•phagocytize pathogens and debris
•“present” antigens to activate other immune cells -antigen presenting cells (APCs)

122

Complete Blood Count

•Hematocrit
•Hemoglobin concentration
•Total count for RBCs, reticulocytes, WBCs, and platelets
•Differential WBC count
•RBC size and hemoglobin concentration per RBC

123

leukopoiesis

production of white blood cells
–pluripotent stem cells –(PPSCs)
•myeloblasts
•monoblasts
•lymphoblasts

124

myeloblasts

neutrophils, eosinophils, basophils

125

monoblasts

form monocytes

126

lymphoblasts

give rise to all forms of lymphocytes
–T lymphocytes complete development in thymus

127

red bone marrow

stores and releases granulocytes and monocytes

128

circulating WBCs do not stay in bloodstream

–granulocytes leave in 8 hours and live 5 days longer
–monocytes leave in 20 hours, transform into macrophages and live for several years
–lymphocytes provide long-term immunity (decades) being continuously recycled from blood to tissue fluid to lymph and back to the blood

129

leukopenia

low WBC count below 5000/L
–causes: radiation, poisons, infectious disease
–effects: elevated risk of infection

130

leukocytosis

high WBC count above 10,000/L
–causes: infection, allergy and disease
–differential WBC count –identifies what percentage of the total WBC count consist of each type of leukocyte

131

leukemia

cancer of hemopoietic tissue that usually produces an extraordinary high number of circulating leukocytes and their precursors

132

myeloid leukemia

uncontrolled granulocyte production

133

lymphoid leukemia

uncontrolled lymphocyte or monocyte production

134

acute leukemia

appears suddenly, progresses rapidly, death within month

135

chronic leukemia

undetected for months, survival time three years
–effects -normal cell percentages disrupted; impaired clotting; opportunistic infections

136

hemostasis

the cessation of bleeding
–stopping potentially fatal leaks
–hemorrhage –excessive bleeding

137

three hemostatic mechanisms

–vascular spasm
–platelet plug formation
–blood clotting (coagulation)
•platelets play an important role in all three

138

platelets

small fragments of megakaryocytecells
–2-4 m diameter; contain “granules”
–complex internal structure and open canalicular system
–amoeboid movement and phagocytosis

139

normal platelet count

130,000 to 400,000 platelets/L

140

platelets

functions

–secrete vasoconstrictors that help reduce blood loss
–stick together to form platelet plugs to seal small breaks
–secrete procoagulants or clotting factors promote clotting
–initiate formation of clot-dissolving enzyme
–chemically attract neutrophils and monocytes to sites of inflammation
–phagocytize and destroy bacteria
–secrete growth factors that stimulate mitosis to repair blood vessels

141

Thrombopoiesis

Platelet Production
stem cells (that develop receptors for thrombopoietin)become megakaryoblasts

142

megakaryoblasts

–repeatedly replicate DNA without dividing
–forms gigantic cell called megakaryocyte with a multilobed nucleus
•100 m in diameter, remains in bone marrow

143

megakaryocytes–live in

live in bone marrow adjacent to blood sinusoids
–long tendrils of cytoplasm (proplatelets) protrude into the blood sinusoids –blood flow splits off fragments called platelets
–circulate freely for 10 days
–40% are stored in spleen

144

vascular spasm

prompt constriction of a broken vessel
–most immediate protection against blood loss
•causes:
–pain receptors
•some directly innervate blood vessels to constrict
–smooth muscle injury
–platelets release serotonin (vasoconstrictor)
•effects:
–prompt constriction of a broken vessel
•pain receptors -short duration (minutes)
•smooth muscle injury -longer duration
–provides time for other two clotting pathways

145

Platelet Plug Formation

•endothelium smooth, coated withprostacyclin –a platelet repellant
•platelet plug formation
–broken vessel exposes collagen
–plateletpseudopods stick to damaged vessel and other platelets -pseudopods contract and draw walls of vessel together forming a platelet plug
–platelets degranulate releasing a variety of substances
•serotonin is a vasoconstrictor
•ADP attracts and degranulates more platelets
•thromboxane A2, an eicosanoid, promotes platelet aggregation, degranulation and vasoconstriction
–positive feedback cycle is active until break in small vessel is sealed

146

Coagulation

(clotting) –last and most effective defense against bleeding
–conversion of plasma protein fibrinogen into insoluble fibrin threads to form framework of clot

147

procoagulants

clotting factors), usually produced by the liver, are present in plasma
–activate one factor and it will activate the next to form a reaction cascade

148

extrinsic pathway

factors released by damaged tissues begin cascade
calcium required for either pathway

149

intrinsic pathway

factors found in blood begin cascade (platelet degranulation)

150

extrinsic pathway

–initiated by release of tissue thromboplastin (factor III) from damaged tissue
–cascade to factor VII, V and X (fewer steps)

151

intrinsic pathway

initiated by platelets releasing Hageman factor (factor XII )
–cascade to factor XI to IX to VIII to X

152

Enzyme Amplification in Clotting

Factor XII
Factor XI
Factor IX
Factor VIII
Factor X
Prothrombin activator
thrombin
fibrin

153

rapid clotting

each activated cofactor activates many more molecules in next step of sequence

154

Completion of Coagulation

•activation of factor X
–leads to production of prothrombin activator
•prothrombin activator
–converts prothromb into thrombin

155

thrombin

converts fibrinogen into fibrin

156

positive feedback

thrombin speeds up formation of prothrombin activator

157

Fate of Blood Clots

clot retraction occurs within 30 minutes
•platelet-derived growth factor secreted by platelets and endothelial cells
–mitotic stimulant for fibroblasts and smooth muscle to multiply and repair damaged vessel

158

fibrinolysis

dissolution of a clot
–factor XII speeds up formation of kallikrein enzyme
–kallikrein converts plasminogen into plasmin, a fibrin-dissolving enzyme that breaks up the clot

159

Blood Clot Dissolution

•positive feedback occurs
•plasmin promotes formation of fibrin

160

platelet repulsion

platelets do not adhere to prostacyclin-coating

161

thrombin dilution

–by rapidly flowing blood
•heart slowing in shock can result in clot formation

162

natural anticoagulants

heparin

163

heparin

(from basophils and mast cells)interferes with formation of prothrombin activator

164

antithrombin

(from liver)deactivates thrombin before it can act on fibrinogen

165

Clotting Disorders

•deficiency of any clotting factor can shut down the coagulation cascade

166

hemophilia

family of hereditary diseases characterized by deficiencies of one factor or another
•sex-linked recessive (on X chromosome)

167

hemophilia A

missing factor VIII (83% of cases)

168

hemophilia B

missing factor IX (15% of cases)

169

hemophilia C

missing factor XI (autosomal)

170

hematomas

masses of clotted blood in the tissues

171

thrombosis

abnormal clotting in unbroken vessel

172

thrombus

clot
•most likely to occur in leg veins of inactive people

173

pulmonary embolism

clot may break free, travel from veins to lungs

174

embolus

anything that can travel in the blood and block blood vessels

175

infarction

(tissue death) may occur if clot blocks blood supply to an organ (MI or stroke)
–650,000 Americans die annually of thromboembolism –traveling blood clots

176

Clinical Management of Clotting

goal

prevent formation of clots or dissolve existing clots

177

preventing clots

–Vitamin K is required for formation of clotting factors
•coumarin (Coumadin) is a vitamin K antagonist
–aspirin suppresses thromboxane A2
–other anticoagulants discovered in animal research
•medicinal leeches used since 1884 (hirudin)
•snake venom from vipers (Arvin)

178

dissolving clots that have already formed

–streptokinase–enzyme make by streptococci bacteria
•used to dissolve clots in coronary vessels
•digests almost any protein
–tissue plasminogen activator (TPA) –works faster, is more specific, and now made by transgenic bacteria
–hementin–produced by giant Amazon leech