Exam 1 Flashcards

1
Q

What is the number one cause of death?

A

cardiovascular disease

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2
Q

What is the major underlying cause of cardiovascular disease?

A

ischemia

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3
Q

This is the underlying cause of cardiovascular ischemia.

A

atherosclerosis

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4
Q

This is the term for a traveling thrombus.

A

embolism

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5
Q

This is the term for a blood clot.

A

thrombus

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6
Q

This is formed by a platelet plug.

A

white thrombus

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7
Q

This is formed by fibrinogen or fibrin.

A

red thrombus

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8
Q

Along with atherosclerosis, this can also cause cardiovascular ischemis.

A

artery spasm

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9
Q

Abundant data links high blood cholesterol to _____________.

A

atherogenesis

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10
Q

Inflammatory mechanisms couple dyslipidemia to _________ formation.

A

atheroma

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11
Q

leukocyte recruitment and expression of pro inflammatory cytokines characterize early ___________.

A

atherogenesis

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12
Q

__________ pathways promote thrombosis.

A

inflammatory

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13
Q

__________ is responsible for MI and most strokes.

A

thrombosis

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14
Q

The _________ system can modulate inflammation.

A

nervous

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15
Q

_________ of the vagus nerve can inactivate TNF and cytokines.

A

stimulation

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16
Q

This is the most important example of special connective tissue.

A

blood cells

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17
Q

This is the prevention of blood loss.

A

hemostasis

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18
Q

Vascular _________ is associated with trauma.

A

constriction

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19
Q

Vascular constriction is associated with __________.

A

trauma

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20
Q

Platelets function as _______ cells.

A

whole

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21
Q

Platelets function as whole cells but CANNOT _________.

A

divide

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22
Q

What cells contain actin & myosin, enzymes & calcium, ADP & ATP, Thromboxane A2, serotonin, and growth factor?

A

platelets

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23
Q

Platelets cell membranes contain _________ that avoid the normal endothelium but adhere to damaged area.

A

glycoproteins

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24
Q

Phospholipids in the cell membrane of platelets contain this.

A

platelet factor 3 (thromboplastin)

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25
Q

This is the function of platelet factor 3 (thromboplastin).

A

initiates clotting

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26
Q

Irregular-shaped platelets are in the ______ form.

A

activated

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27
Q

Round, smooth platelets are in the ________ form.

A

inactivated

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28
Q

Vascular spasm, formation of platelet plug, blood coagulation, and fibrous tissue growth to seal are all mechanisms of _________.

A

hemostasis

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29
Q

Spasm is proportional to _________.

A

trauma

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30
Q

During platelet activation, contractile proteins contract causing ________ release.

A

granule

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31
Q

These are secreted in platelet activation.

A

ADP, Thromboxane A2 and serotonin

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32
Q

If Thromboxane A2 is blocked, can platelets be activated?

A

yes

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33
Q

This potentiates the release of granule contents (but is not essential for release to occur).

A

thromboxane A2

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34
Q

Thromboxane A2 is a vaso_________.

A

constrictor

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35
Q

Platelets are important in _______ ruptures.

A

minute

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36
Q

Lack of _______ is associated with small hemorrhagic areas under the skin and throughout internal tissues.

A

platelets

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37
Q

Platelets have a half-life of ______ days.

A

8-12

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38
Q

Platelets are eliminated primarily by ________ action.

A

macrophage

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39
Q

Greater than 1/2 of all macrophages are located in this organ.

A

spleen

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40
Q

This prevents platelet aggregation.

A

endothelium

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41
Q

Endothelium produces this.

A

PGI2 (prostacyclin)

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42
Q

PGI2 (prostacyclin) is a vaso________.

A

dilator

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43
Q

PGI2 (prostacyclin) stimulates platelet adenyl cyclase which ________ release of granules.

A

suppresses

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44
Q

Endothelium produces this factor for clotting.

A

8 (VIII)

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45
Q

These block both thromboxane A2 and prostacyclin production by blocking fatty acid cyclooxygenase which converts arachidonic acid to PGG2 and PGH2.

A

aspirin and ibuprofen

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46
Q

Why take aspirin to prevent heart attacks?

A

inhibit platelet activation

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47
Q

This converts arachidonic acid to PGG2 and PGH2.

A

fatty acid cyclooxygenase

48
Q

Blocking fatty acid cyclooxygenase blocks the production of these molecules.

A

thromboxane a2 and prostacyclin

49
Q

These prevent clots form forming.

A

anticoagulants

50
Q

Chelators, heparin and dicumarol are all types of __________.

A

anticoagulants

51
Q

This type of anticoagulant ties up calcium (citrate, oxylate).

A

chelators

52
Q

Chelators tye up _______.

A

calcium (citrate, oxylate)

53
Q

This anticoagulant complexes with Antithrombin III.

A

heparin

54
Q

This complexes with heparin.

A

antithrombin III

55
Q

Dicumarol causes inhibition of _______ dependent factors.

A

vitamin K

56
Q

This is the dissolving of clots that have already formed.

A

lysis

57
Q

This performs lysis of clots.

A

Plasmin

58
Q

This is the inactive form of plasmin which circulates in the blood.

A

plasminogen

59
Q

These are the factors inhibited by dicumarol.

A

2, 7, 9, 10

60
Q

These are other names for dicumarol.

A

cumadin, warfarin

61
Q

These cells synthesize factors 2, 7, 9, and 10.

A

hepatocytes

62
Q

These CANNOT dissolve already existing clots.

A

anticoagulants

63
Q

________ activators of plasminogen are found in the tissues, plasma and urine.

A

endogenous

64
Q

Endogenous activators of plasminogen are found in these locations.

A

tissues, plasma, urine

65
Q

_________ Activators of plasminogen are found in streptokinase, tPA (tissue plasminogen activator).

A

exogenous

66
Q

There is a ____ hour window associated with tPA for MI and stroke.

A

3

67
Q

Clots may be _______ by the proteolytic enzyme plasmin.

A

liquefied (fibrinolysis)

68
Q

This is a proteolytic enzyme that liquefies clots (performs fibrinolysis).

A

plasmin

69
Q

What form of plasmin circulates in the blood?

A

plasminogen

70
Q

Most of the frank tissue damage associated with infarction occurs upon _________.

A

reperfusion

71
Q

This type of injury is associated with the formation of highly reactive oxygen species with unpaired electrons = free radicals.

A

reperfusion

72
Q

Highly reactive oxygen species with unpaired electrons are called:

A

free radicals

73
Q

When pressure on tissues is relieved and again perfused with blood, these are generated.

A

free radicals

74
Q

This is an antioxidant that prevents reperfusion damage.

A

glutathione

75
Q

This is the ability to open up alternate routes of blood flow to compensate for a blocked vessel.

A

collateralization

76
Q

Angiogenesis, vasodilation, and the role of the SNS are all involved in:

A

collateralization

77
Q

The SNS may ________ collateralization via vasoconstriction.

A

impede

78
Q

The SNS may augment collateralization via the release of _____.

A

NPY

79
Q

The _______ mechanism of thrombosis is initiated by chemical factors released by damaged tissues.

A

extrinsic

80
Q

The _______ mechanism of thrombosis requires only components in blood and trauma to blood or exposure to collagen.

A

intrinsic

81
Q

This method of thrombosis does not need to be triggered by anything.

A

intrinsic

82
Q

The liver synthesizes ___ clotting factors.

A

5

83
Q

These are the clotting factors the liver synthesizes.

A

1, 2, 7, 9, 10

84
Q

This depresses liver formation of II, VII, IX, and X factors by blocking action of vitamin K.

A

coumarin (warfarin or cumadin)

85
Q

This is the only liver factor NOT depressed by coumarin (blocking action of vitamin k).

A

1 (I)

86
Q

This is a clotting disorder that is sex linked on the X chromosome, affecting almost males exclusively.

A

hemophilia

87
Q

85% of cases of hemophilia have a defect in this factor.

A

8 (VIII)

88
Q

15% of cases of hemophilia have a defect in this factor.

A

9 (IX)

89
Q

This is required for blood to clot.

A

calcium

90
Q

The key step in clotting is the conversion of:

A

fibrinogen to fibrin

91
Q

This is required for the key step in clotting and the conversion of fibrinogen to fibrin.

A

thrombin

92
Q

This is an autoimmune disorder where the body makes antibodies against phospholipids in cell membranes.

A

antiphospholipid antibody syndrome (APS)

93
Q

In Antiphospholipid antibody syndrome (APS), these are formed.

A

abnormal clots

94
Q

This is an amino acid in the blood that may irritate blood vessels promoting atherosclerosis.

A

homocysteine

95
Q

Homocysteine can also cause cholesterol to change into oxidized:

A

LDL

96
Q

Homocysteine makes the blood _____ likely to clot.

A

more

97
Q

High levels of homocysteine in the blood can be _______ by increasing intake of folic acid, B6 and B12.

A

reduced

98
Q

This is the main ion involved in depolarization.

A

sodium

99
Q

Heart muscle usually contains 1-2 ________ located nuclei.

A

centrally

100
Q

This is the natural pacemaker of the heart.

A

SA node

101
Q

Specialized excitatory and conductive muscle fibers (SA node, AV node, Purkinje fibers) contract _______ and have _____ fibrils.

A

weakly, few

102
Q

This is the term for many acting as one.

A

syncytium

103
Q

Syncytium is achieved due to the presence of these.

A

intercalated discs

104
Q

Intercalated discs have these to connect cardiac cells end to end.

A

gap junctions

105
Q

Duration of an action potential is _______ sec.

A

.2-.3

106
Q

Sodium channels are _______.

A

fast

107
Q

Ca++/Na+ channels are ________.

A

slow

108
Q

_________ has a sharp increase in permeability at the onset of depolarization.

A

sodium

109
Q

_______ permeability is increased during the plateau.

A

calcium

110
Q

_______ is increased during the resting polarized state.

A

potassium

111
Q

Ion flux is equal to:

A

current flow

112
Q

In excitable tissue, an action potential is a pulse-like change in ________ _________.

A

membrane permeability

113
Q

Typical cardiac muscle have both fast Na+ channels and slow Ca__/Na+ channels that open during ____________.

A

depolarization

114
Q

In specialized excitatory cells like the SA node, only _______ channels are operational during depolarization, increasing depolarization time.

A

slow

115
Q

This blocks fast Na+ channels, selectively changing a fast response into a slow response.

A

tetradotoxin