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2 - Keiser A&P 2 > 0-1 chapter 18 - blood > Flashcards

0-1 chapter 18 - blood Flashcards

1
Q

circulatory system

A

consists of the heart, blood vessels and blood

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2
Q

cardiovascular system

A

refers only to the heart and blood vessels

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3
Q

hematology

A

the study of blood

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4
Q

functions of circulatory system

A

transport
protection
Regulation

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5
Q

transport

A

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

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6
Q

protection

A

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

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7
Q

regulation

A

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

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8
Q

Properties of Blood

A
  • adults have 4-6 L of blood

* a liquid connective tissue consisting of cells and extracellular matrix

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9
Q

plasma

A

matrix of blood

•a clear, light yellow fluid

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10
Q

formed elements

A

blood cells and cell fragments

•red blood cells, white blood cells, and platelets

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11
Q

seven kinds of formed elements

A

erythrocytes
platelets
leukocytes

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12
Q

erythrocytes

A

red blood cells (RBCs)

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13
Q

platelets

A

cell fragments from special cell in bone marrow

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14
Q

leukocytes-white blood cells (WBCs)

•five leukocyte types divided into two categories:

A

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

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15
Q

granulocytes

A

–neutrophils
–eosinophils
–basophils

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16
Q

agranulocytes

A

–lymphocytes

–monocytes

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17
Q

hematocrit

A

centrifuge blood to separate components

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18
Q

erythrocytes

A

are heaviest and settle first

•37% to 52% total volume

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19
Q

white blood cells and platelets

A
  • 1% total volume

* buffy coat

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20
Q

plasma

A
  • the remainder of volume
  • 47% -63%
  • complex mixture of water, proteins, nutrients, electrolytes, nitrogenous wastes, hormones, and gases
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21
Q

plasma

A

liquid portion of blood

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22
Q

serum

A

remaining fluid when blood clots and the solids are removed

•identical to plasma except for the absence of fibrinogen

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23
Q

3 major categories of plasma proteins

A

albumins
globulins
fibrinogen

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24
Q

albumins

A

smallest and most abundant

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

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25
Q

globulins

A
  • provide immune system functions

* alpha, beta and gamma globulins

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26
Q

fibrinogen

A

precursor of fibrin threads that help form blood clots

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27
Q

plasma proteins formed by

A

liver

–except globulins (produced by plasma cells)

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28
Q

Nonprotein Components of Plasma

A

nitrogenous compounds
nutrients
dissolved O2, CO2, and nitrogen
electrolytes

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29
Q

nitrogenous compounds

A 
–free amino acids
•from dietary protein or tissue breakdown
–nitrogenous wastes (urea)
•toxic end products of catabolism
•normally removed by the kidneys
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30
Q

nutrients

A

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

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31
Q

dissolved O2, CO2, and nitrogen

A

Nothing——————-

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32
Q

electrolytes

A

–Na+ makes up 90% of plasma cations

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33
Q

Properties of Blood

A

viscosity

osmolarity of blood

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34
Q

viscosity

A

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

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35
Q

osmolarity of blood

A

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.

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36
Q

hypoproteinemia

A

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

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37
Q

kwashiorkor

A

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

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38
Q

Hemopoiesis

A

the production of blood, especially its formed elements

adult production of 400 billion platelets, 200 billion RBCs and 10 billion WBCs every day

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39
Q

hemopoietic tissues

A

produce blood cells

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40
Q

yolk sac

A

produces stem cells for first blood cells

•colonize fetal bone marrow, liver, spleen and thymus

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41
Q

pluripotent stem cells (PPSC)

A

formerly called hemocytoblasts or hemopoietic stem cells

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42
Q

colony forming units

A

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

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43
Q

myeloid hemopoiesis

A

blood formation in the bone marrow

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44
Q

lymphoid hemopoiesis

A

blood formation in the lymphatic organs

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45
Q

Erythrocytes

two principal functions:

A

–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

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46
Q

Erythrocytes (RBCs)

A 
disc-shaped cell with thick rim
•lack mitochondria
–anaerobic fermentation to produce ATP
•lack of nucleus and DNA
–no protein synthesis or mitosis
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47
Q

blood type determined by

A

surface glycoprotein and glycolipids

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48
Q

cytoskeletal proteins

A

(spectrin and actin) give membrane durability and resilience

•stretch and bend as squeeze through small capillaries

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49
Q

gas transport

A

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

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50
Q

33% of cytoplasm is

A

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

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51
Q

carbonic anhydrase

A

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

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52
Q

Hemoglobin (Hb) Structure

A

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

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53
Q

heme groups

A

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

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54
Q

globins

A

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

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55
Q

RBC count and hemoglobin concentration indicate

A

amount of O2 blood can carry

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56
Q

hematocrit

A

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

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57
Q

hemoglobin concentration of whole blood

A

•men 13-18g/dL; women 12-16g/dL

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58
Q

RBC count

A

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

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59
Q

values are lower in women

A

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

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60
Q

Erythropoiesis

A

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

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60
Q

reticulocyte

A

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

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61
Q

iron

A

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

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62
Q

Nutritional Needs for Erythropoiesis

dietary iron

A

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

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63
Q

liver apoferritin binds to create

A

ferritin for storage

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64
Q

Nutritional Needs for Erythropoiesis

A

•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

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65
Q

Erythrocyte Homeostasis

A

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

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66
Q

stimuli for increasing erythropoiesis

A

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

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67
Q

Erythrocytes Death and Disposal

A 
•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
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68
Q

iron removed from heme

A

–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)

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69
Q

polycythemia

A

an excess of RBCs

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70
Q

primary polycythemia

A

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

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71
Q

secondary polycythemia

A

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

72
Q

dangers of polycythemia

A

increased blood volume, pressure, viscosity

•can lead to embolism, stroke or heart failure

73
Q

causes of anemia fall into three categories:

A

inadequate erythropoiesis or hemoglobin synthesis
hemorrhagic anemias
hemolytic anemias

74
Q

inadequate erythropoiesis or hemoglobin synthesis

A
  • 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
Q

hemorrhagic anemias

A

from bleeding

76
Q

hemolytic anemias

A

from RBC destruction

77
Q

pernicious anemia

A

inadequate vitamin B12from poor nutrition or lack of intrinsic factor

78
Q

hypoplastic anemia

A

slowing of erythropoiesis

79
Q

aplastic anemia

A

complete cessation of erythropoiesis

80
Q

anemia has three potential consequences:

A

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

81
Q

tissue hypoxia and necrosis

A
  • patient is lethargic
  • shortness of breath upon exertion
  • life threatening necrosis of brain, heart, or kidney
82
Q

blood osmolarity is reduced

A

producing tissue edema

83
Q

blood viscosity is low

A
  • heart races and pressure drops

* cardiac failure may ensue

84
Q

Sickle-Cell Disease

A

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
Q

Blood Types

A

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

86
Q

discovered blood types

A

Karl Landsteiner discovered blood types A, B and O in 1900

–won Nobel Prize

87
Q

antigens

A

–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
Q

agglutinogens

A

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

89
Q

antibodies

A

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
Q

agglutinins

A

antibodies in the plasma that bring about transfusion mismatch

91
Q

agglutination

A

–antibody molecule binding to antigens

–causes clumping of red blood cells

92
Q

RBC antigens called

A

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

93
Q

antibodies called

A

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

94
Q

ABO Group

A

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

95
Q

blood type A person has

A

A antigens

96
Q

blood type B person has

A

B antigens

97
Q

blood type AB has

A

both A and B antigens

98
Q

blood type O person has

A

neither antigen

99
Q

antibodies (agglutinins)

A

anti-A and anti-B

•appear 2-8 months after birth; at maximum concentration at 10 yr.

100
Q

agglutination

A

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

101
Q

transfusion reaction

A

–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
Q

universal donor

A

–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
Q

universal recipient

A

–Type AB –rarest blood type

–lacks plasma antibodies; no anti-A or B

104
Q

Rh Group

A

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
Q

Anti-D agglutinins

A

not normally present

–form in Rh-individuals exposed to Rh+blood

106
Q

Hemolytic Disease of Newborn

A

•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
Q

Rh antibodies attack

A

fetal blood

causing severe anemia and toxic brain syndrome

108
Q

Leukocytes

A

(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
Q

granules

A

–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
Q

granulocytes

A

neutrophils
eosinophils
basophils

111
Q

neutrophils

A

neutrophils(60-70%)-polymorphonuclear leukocytes

•barely-visible granules in cytoplasm; 3 to 5 lobed nucleus

112
Q

eosinophils

A

•large rosy-orange granules; bilobed nucleus

113
Q

basophils

A

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

114
Q

agranulocytes

A

lymphocytes

monocytes

115
Q

lymphocytes

A

(25-33%)

•variable amounts of bluish cytoplasm (scanty

116
Q

monocytes

A

(3-8%)

•largest WBC; ovoid, kidney-, or horseshoe-shaped nucleus

117
Q

Granulocyte Functions

neutrophils

A

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

118
Q

Granulocyte Functions

eosinophils

A

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
Q

Granulocyte Functions

basophils

A

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
Q

Agranulocyte Functions

lymphocytes

A

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
Q

Agranulocyte Functions

monocytes

A

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
Q

Complete Blood Count

A
  • Hematocrit
  • Hemoglobin concentration
  • Total count for RBCs, reticulocytes, WBCs, and platelets
  • Differential WBC count
  • RBC size and hemoglobin concentration per RBC
123
Q

leukopoiesis

A 
production of white blood cells
–pluripotent stem cells –(PPSCs)
•myeloblasts
•monoblasts
•lymphoblasts
124
Q

myeloblasts

A

neutrophils, eosinophils, basophils

125
Q

monoblasts

A

form monocytes

126
Q

lymphoblasts

A

give rise to all forms of lymphocytes

–T lymphocytes complete development in thymus

127
Q

red bone marrow

A

stores and releases granulocytes and monocytes

128
Q

circulating WBCs do not stay in bloodstream

A

–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
Q

leukopenia

A

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

130
Q

leukocytosis

A

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
Q

leukemia

A

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

132
Q

myeloid leukemia

A

uncontrolled granulocyte production

133
Q

lymphoid leukemia

A

uncontrolled lymphocyte or monocyte production

134
Q

acute leukemia

A

appears suddenly, progresses rapidly, death within month

135
Q

chronic leukemia

A

undetected for months, survival time three years

–effects -normal cell percentages disrupted; impaired clotting; opportunistic infections

136
Q

hemostasis

A

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

137
Q

three hemostatic mechanisms

A

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

138
Q

platelets

A

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

139
Q

normal platelet count

A

130,000 to 400,000 platelets/L

140
Q

platelets

functions

A

–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
Q

Thrombopoiesis

A 
Platelet Production
stem cells (that develop receptors for thrombopoietin)become megakaryoblasts
142
Q

megakaryoblasts

A

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

143
Q

megakaryocytes–live in

A

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
Q

vascular spasm

A

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
Q

Platelet Plug Formation

A

•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
Q

Coagulation

A

(clotting) –last and most effective defense against bleeding

–conversion of plasma protein fibrinogen into insoluble fibrin threads to form framework of clot

147
Q

procoagulants

A

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
Q

extrinsic pathway

A

factors released by damaged tissues begin cascade

calcium required for either pathway

149
Q

intrinsic pathway

A

factors found in blood begin cascade (platelet degranulation)

150
Q

extrinsic pathway

A

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

151
Q

intrinsic pathway

A

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

152
Q

Enzyme Amplification in Clotting

A 
Factor XII
Factor XI
Factor IX
Factor VIII
Factor X
Prothrombin activator
thrombin
fibrin
153
Q

rapid clotting

A

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

154
Q

Completion of Coagulation

A

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

155
Q

thrombin

A

converts fibrinogen into fibrin

156
Q

positive feedback

A

thrombin speeds up formation of prothrombin activator

157
Q

Fate of Blood Clots

A

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
Q

fibrinolysis

A

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
Q

Blood Clot Dissolution

A
  • positive feedback occurs

* plasmin promotes formation of fibrin

160
Q

platelet repulsion

A

platelets do not adhere to prostacyclin-coating

161
Q

thrombin dilution

A

–by rapidly flowing blood

•heart slowing in shock can result in clot formation

162
Q

natural anticoagulants

163
Q

heparin

A

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

164
Q

antithrombin

A

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

165
Q

Clotting Disorders

A

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

166
Q

hemophilia

A

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

167
Q

hemophilia A

A

missing factor VIII (83% of cases)

168
Q

hemophilia B

A

missing factor IX (15% of cases)

169
Q

hemophilia C

A

missing factor XI (autosomal)

170
Q

hematomas

A

masses of clotted blood in the tissues

171
Q

thrombosis

A

abnormal clotting in unbroken vessel

172
Q

thrombus

A

clot

•most likely to occur in leg veins of inactive people

173
Q

pulmonary embolism

A

clot may break free, travel from veins to lungs

174
Q

embolus

A

anything that can travel in the blood and block blood vessels

175
Q

infarction

A

(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
Q

Clinical Management of Clotting

goal

A

prevent formation of clots or dissolve existing clots

177
Q

preventing clots

A

–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
Q

dissolving clots that have already formed

A

–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

2 - Keiser A&P 2 (15 decks)

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