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Anatomy and Physiology II > Lesson 6 - The Circulatory System: Blood > Flashcards

Lesson 6 - The Circulatory System: Blood Flashcards

1
Q

leukocytes

A

WBC’s; blood cells that protect against infection and other diseases

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2
Q

what is the least abundant formed element?

A

white blood cells

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3
Q

how long do WBCs last in the bloodstream?

A

only a few hours in the blood before moving to tissues

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4
Q

leukocytes have a _____ nucleus

A

conspicuous

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5
Q

all WBCs have lysosomes called _____ _____

A

nonspecific granules

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6
Q

granulocytes have _____ _____

A

specific granules

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7
Q

specific granules

A

contain enzymes and other chemicals employed in defense against pathogens

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8
Q

granulocytes (3)

A

neutrophils
eosinophils
basophils

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9
Q

neutrophil

A

also called polymorphonuclear leukocytes (PMNs) because of the varied nuclear shapes

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10
Q

what WBC is the first to attack bacteria?

A

neutrophils

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11
Q

degranulations

A

occurs when lysosome granules fuse to endosomes containing phagocytized pathogen; occurs in neutrophils

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11
Q

what do neutrophils do in a bacterial infection? (2)

A

phagocytize bacteria and release antimicrobial chemicals to increase inflammation and attract other phagocytes to the are

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12
Q

what cell type numbers fluctuation greatly depending on the day/night cycle, seasonality, and with the phases of a menstrual cycle?

A

eosinophils

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13
Q

what cell type increases with parasitic infections?

A

eosinophils

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14
Q

when do numbers of eosinophils increase? (4)

A
  • parasitic infections
  • allergies
  • collagen diseases
  • diseases of the spleen and central nervous system
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15
Q

what types of things do eosinophils phagocytize? (3)

A
  • antigen-antibody complexes
  • allergens
  • inflammatory chemicals
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16
Q

what enzymes do eosinophils release? (2)

A
  • enzymes that weaken or destroy parasites such a worms
  • enzymes that counter the inflammatory effects of neutrophils and mast cells
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17
Q

what cell type increases with chickenpox, sinusitis, and diabetes?

A

basophils

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18
Q

what is histamine?

A

a vasodilator; dilates blood vessels and speeds flow of blood to an injured area

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19
Q

what is herapin?

A

an anticoagulant; prevents blood clotting and promotes the mobility of other WBCs in the area

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20
Q

both _____ and _____ increase local inflammation initiated by mast cells

A

histamine, heparin

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21
Q

basophils secrete _____ and _____

A

histamine, heparin

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22
Q

microphages (2)

A

neutrophils and eosinophils

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23
Q

what causes pus formation?

A

a mixture of dead neutrophils, cellular debris, and waste products during the immune response

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24
Q

agranulocytes

A

lack specific granules and include lymphocytes and monocytes

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25
Q

what things do lymphocytes destroy? (3)

A
  • cancer
  • foreign cells (?)
  • virally infected cells
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26
Q

lymphocytes present _____ to activate the immune response

A

antigens (APC)

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27
Q

visual appearance of a stained lymphocyte

A
  • variable amounts of bluish cytoplasm
  • ovid/round
  • uniform dark violet
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28
Q

visual appearance of a stained basophil

A

coarse, dark violet granules

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29
Q

when do lymphocyte numbers increase?

A

diverse infections and immune responses

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30
Q

what do lymphocytes do? (2)

A
  • coordinate actions of other immune cells
  • secrete antibodies and provide immune memory
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31
Q

when do monocyte numbers increase?

A

in viral infections and inflammation

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32
Q

what are monocytes called when the leave the bloodstream and enter tissues?

A

they transform into macrophages

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33
Q

what do monocytes do?

A

phagocytize pathogens and debris and act as antigen-presenting cells (APCs)

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34
Q

what do monocytes secrete?

A

substances that attract immune cells and fibroblasts to an injury site

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35
Q

what do fibroblasts produce?

A

scar tissue to seal off the injured area

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36
Q

leukopoiesis

A

production of white blood cells

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37
Q

what happens in the beginning of leukopoiesis?

A

hematopoietic stem cells differentiate into distinct types of colony-forming units

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38
Q

three types of CFUs

A
  1. myeloblasts
  2. monoblasts
  3. lymphoblasts
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39
Q

myeloblasts form (3)

A

neutrophil, eosinophils, and basophils

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40
Q

monoblasts form…

A

monocytes

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41
Q

lymphoblasts

A

forma ll types of lymphocytes

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42
Q

red bone marrow stores what type of WBCs? (2)

A

granulocytes and monocytes

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43
Q

when do monocytes complete development?

A

when they enter peripheral tissue and become macrophages

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44
Q

when do granulocytes leave the blood?

A

4-8 hours, live another 4-5 days in tissues

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45
Q

when do monocytes leave the blood?

A

leave in about 20 hours, enter tissues, become macrophages, and live for a few years

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46
Q

lymphocytes provide

A

long term immunity

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47
Q

how are lymphocytes recycled?

A

from blood to tissue fluid to lymph and back to blood

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48
Q

where do all WBCs (except T cells) develop?

A

in the bone marrow

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49
Q

hematopoietic stem cells produce WBC and _____

A

RBC

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50
Q

leukopenia

A

low WBC count, below 5,000 WBC/uL

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51
Q

causes of leukopenia (6)

A
  • radiation
  • poisons
  • infectious disease
  • cancer
  • autoimmune disorders
  • drugs that destroy/damage bone marrow cells
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52
Q

effects of leukopenia

A

elevated risk of infection

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53
Q

leukocytosis

A

high WBC count, about 10,000 WBC/uL

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54
Q

causes of leukocytosis (3)

A
  • infection
  • allergy
  • disease that increases WBC production
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55
Q

differential WBC count

A

identifies what percent of the total WBC count consists of each type of leukocyte

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56
Q

leukemia

A

cancer of hematopoietic tissue, usually producing a very high number of circulating leukocytes

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57
Q

effects of leukemia (3)

A

normal cell percentages disrupted, impaired clotting, and open to opportunistic infections

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58
Q

types of leukemia (4)

A
  • myeloid leukemia
  • lymphoid leukemia
  • acute leukemia
  • chronic leukemia
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59
Q

myeloid leukemia

A

uncontrolled granulocyte production

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60
Q

lymphoid leukemia

A

uncontrolled lymphocyte or monocyte production

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61
Q

acute leukemia (3)

not acute as is over soon

A

appears suddenly, progresses rapidly, death within months

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62
Q

chronic leukemia

A

undetected for months, survival time is three yearsc

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63
Q

complete blood count (CBC) (5)

A

profile of data on multiple blood values:
- hematocrit
- hemoglobin concentration
- total counts for RBCs, reticulocytes, WBCs, and platelets
- differential WBC count
- RBC size and hemoglobin per RBC

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64
Q

hemostasis

A

cessation of bleeding, involving platelets

65
Q

platelets

A

small fragments of megakaryocytes found in bone marrow

66
Q

thrombocytopenia

A

platelet deficiency

67
Q

causes of thrombocytopenia (4)

A
  • autoimmune disorders
  • bacteria in blood
  • medications
  • pregnancy
68
Q

signs of thrombocytopenia (3)

A

bleeding along the digestive tract, within skin, and sometimes in the CNS

69
Q

thrombocytosis

A

excessive platelets

70
Q

causes of thrombocytosis (3)

A

cancer, inflammation, infection

71
Q

what do platelets contain?

A

granules filled with platelet secretions

72
Q

what happens when platelets are activated?

A

they are capable of amoeboid movement

73
Q

platelets secrete… (3)

A
  • vasoconstrictors
  • procoagulants
  • growth factors
74
Q

procoagulants

A

clotting factors that promote clotting

75
Q

platelet growth factors do…

A

they stimulate mitosis to repair blood vessels

76
Q

_____ stick together to form _____ _____ to seal small breaks

A

platelets, platelet plugs

77
Q

what do platelets chemically attract? (2)

A

neutrophils and monocytes to sites of inflammations

78
Q

platelets do… (2)

A
  • initiation formation of clot dissolving enzyme
  • phagocytize and destroy bacteria
79
Q

thrombopoiesis

A

production of platelets

80
Q

what triggers hematopoietic stems cells in the bone marrow to become megakaryoblasts?

A

thrombopoietin

81
Q

_____ repeatedly replicate DNA without dividing

A

megakaryoblasts

82
Q

megakaryocytes

A

cytoplasm tendrils (proplatelets) protrude into blood sinusoids so as blood flows through it splits off fragments of the megakaryocytes forming platelets

83
Q

what are fragments of megakaryocytes called?

84
Q

the _____ recycles worn out platelets

85
Q

hemostasis involves three mechanisms (3)

A
  1. vascular spasm
  2. platelet plug formation
  3. blood clotting (coagulation)
86
Q

vascular spasm

A

starting stage of hemostasis
- immediate protection against blood loss causing constriction of a broken blood vessel

87
Q

causes of vascular spasm (3)

A
  • some nociceptors directly trigger constriction
  • smooth muscle injury
  • platelets release serotonin (vasoconstrictor)
88
Q

step one of vascular spasms

A

Endothelial cells in the lining of the blood vessel contract and exposes the basement membrane to blood – the basement membrane is usually not exposed to blood

89
Q

step two of vascular spasm

A

Endothelial cells release hormones called endothelins to stimulate smooth muscle contraction in blood vessel (promotes vascular spasms) and endothelial, smooth muscle, and fibroblast cell division

90
Q

step three of vascular spasm

A

Endothelial cells become “sticky” to seal off the breach in the vessel – allows platelets to attach later on

91
Q

how long does vascular spasm last?

A

up to 30 minutes

92
Q

when does platelet plug formation start?

A

about 15 seconds after vascular spasms has started

93
Q

broken blood vessels expose _____ and the _____ _____

A

collagen, basement membrane

94
Q

platelet plug formation: step 1

A

platelet pseudopods stick to damaged vessel and other platelets

95
Q

platelet plug formation: step 2

A

pseudopods contract, drawing together a platelet plug

96
Q

platelet plug formation: step 3

A

platelets undergo degranulation releasing ADP, Thromboxane A2, and serotonin

97
Q

platelet plug formation: step 4

A

continued via positive feedback cycle until the break in the vessel is sealed

98
Q

endothelium of intact vessels is very smooth and coated with _____

p

A

prostacyclin

99
Q

prostacyclin

A

a platelet repellent to prevent platelet adhesion at non-damaged areas

100
Q

degranulation

A

exocytosis of cytoplasmic granules and factors that promote hemostasis

101
Q

platelet secretions: ADP

what does it do?

A

attracts and degranulation more platelets

102
Q

platelet secretions: Thromboxane A2

A

an eicosanoid, promotes platelet aggregation, degranulation, and vasoconstriction

103
Q

platelet secretions: serotonin

A

a vasoconstrictor

104
Q

factors that limit the growth of the platelet plug include: (5)

A
  1. prostacyclin
  2. inhibitory compounds released by other WBCs
  3. circulating enzymes break down ADP
  4. negative feedback from serotonin
  5. development of blood clot isolates area
105
Q

prostacyclin

what cells release this?

A

released by endothelial cells to inhibit platelet aggregation

106
Q

high levels of serotonin block the action of _____

107
Q

coagulation

A

conversion of fibrinogen to fibrin threads to form the framework of a clot

108
Q

procoagulants use a _____ _____

A

reaction cascade

109
Q

reaction cascade

A

activate one factor and it will activate the next

110
Q

when does coagulation start?

A

about 30 seconds after vascular spasm has started

111
Q

where are procoagulants usually produced?

112
Q

two pathways of coagulation

A

extrinsic and intrinsic

113
Q

extrinsic mechanism for coagulation

involves?

A

involves the blood vessel components, where clotting factors from sources outside the body are released by damaged vessels and perivascular tissues

114
Q

how is the extrinsic mechanism of coagulation started?

A

tissue thromboplastin (factor III) from damaged tissues

115
Q

after factor II is initiated, where does it go>

A

cascades to factor 7, 5, and 10

116
Q

which coagulation pathway is faster?

A

extrinsic, it has fewer steps

117
Q

intrinsic mechanism

A

involves humoral (proenzymes) using only blotting factors found in blood itself

118
Q

what is the intrinsic mechanism of coagulation started?

A

contact with exposed collagen on ruptured vessel walls by platelets releasing factor 12

119
Q

what happens after factor 12 is released?

A

it cascades to factor 11, 9, 8, and 10

120
Q

both the intrinsic and extrinsic pathways of coagulation require?

121
Q

both the intrinsic and extrinsic pathways of coagulation converge on the triggering of?

A

factor 5 (X), the start of the common pathway

122
Q

the common pathway of coagulation (3)

A
  1. activation of factor 10 leads to production of prothrombin activator
  2. thrombin converts fibrinogen to fibrin
123
Q

factor 2

A

prothrombin

124
Q

fibrin molecules (monomers) bind to form

A

fibrin polymers

125
Q

factor _____ crosslinks fibrin polymer starts

126
Q

how does is the common pathway kept with positive feedback?

A

thrombin also forms prothrombin activator

127
Q

clot retraction

A

platelet pseudopods adhere to fibrin starts and contract, clot becomes come compact withing 30 minutes

128
Q

overall efficiency of coagulation can be measured with _____ _____ after a 1mm deep incision

A

bleeding time

129
Q

platelet-derived growth factor (PDGF) (2)

what secretes this? what does it do?

A

secreted by platelets and endothelial cells; mitotic stimulant for fibroblasts and smooth muscle to multiply and repair damaged vessels

130
Q

fibrinolysis

A

the dissolution of a clot, occurs after tissue repair is completed

131
Q

factor XII

A

catalyzes formation of enzyme kallikrein

132
Q

kallikrein

A

converts plasminogen into plasmin

133
Q

plasmin

A

a fibrin-dissolving enzyme that breaks up clots

134
Q

controls to prevents coagulation when it isn’t needed: platelet repulsion

A

platelets do not adhere to prostacyclin-coated endothelium

135
Q

controls to prevents coagulation when it isn’t needed: dilution (3)

A
  • small amounts of thrombin form spontaneously in plasma
  • thrombin is diluted by normal blood flow, preventing clotting
  • heart slowing in shock can result in clot formation
136
Q

controls to prevents coagulation when it isn’t needed: anticoagulants

what are they called?

A

antithrombin and heparin

137
Q

antithrombin

A

deactivated thrombin before it can act on fibrinogen

138
Q

heparin

what does it do?

A

interferes with formation of prothrombin activator

139
Q

where is antithrombin formed?

140
Q

where is heparin formed?

what type of cell?

A

basophils and mast cells

141
Q

hemophilia

A

a family of hereditary diseases characterized by deficiencies of one clotting factor or another

142
Q

what does hemophilia result in?

A

a failure for blood to clot

143
Q

hemophilia: physical exertion can cause what? (3)

A

intramuscular and joint hematomas (clotted blood in tissues) and cause severe pain and eventual joint immobility

144
Q

what level of clotting factor is enough to prevent symptoms of hemophilia?

A

half the normal level

145
Q

how are the most common types of hemophilia inherited?

A

sex-linked recessive traits

146
Q

classical hemophilia (hemophilia A)

A

missing factor VIII (83% of cases)

147
Q

hemophilia B

A

missing factor IX (15% of cases)

148
Q

thrombosis

A

abnormal formation of a clot in an unbroken vessel

149
Q

thrombus

A

an unwanted blood clot in a vessel

150
Q

where is a thrombus most likely to form, and in who?

A

the leg veins of inactive people

151
Q

embolus

A

a thrombus that has broken away from the vessel wall

152
Q

infarction

A

tissue death via loss of oxygen

153
Q

thromboembolism

A

traveling blood clots

154
Q

preventing unwanted clots (2)

A

use vitamin K antagonists such as coumarin, warfarin

155
Q

what do coumarin and warfarin do?

A

they’re vitamin K antagonists that prevent synthesis of clotting factors 2,7, 9, and 10 that require the vitamin

156
Q

dissolving unwanted clots that have already formed (3)

s.t.h.

A
  • streptokinase
  • tissue plasminogen activator
  • hementin
157
Q

streptokinase

A

enzyme made by streptococcus bacteria that is used to dissolve clots in coronary vessels

158
Q

tissue plasminogen activator (TPA)

A

converts plasminogen into clot-dissolving plasmin

159
Q

hementin

A

anticoagulant originating from a leech found in the Amazon

Anatomy and Physiology II (19 decks)

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