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Physio > Cardio Lec 1-3 > Flashcards

Cardio Lec 1-3 Flashcards

1
Q

Function of the valves

A

prevent back flow of blood

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2
Q

When do valves close

A

when arterial pressure is > than ventricle

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3
Q

Systole refers to

A

contraction

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4
Q

Diastole referes to

A

relaxation

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5
Q

End systolic volume

A

amount of blood remaining in ventricle at end of systole

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6
Q

End diastolic volume

A

amount of blood in ventricles before they contract

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7
Q

What blood actually gets ejected

A

end systolic & end diastolic

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8
Q

Stroke volume

A

amount of blood that gets ejected

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9
Q

Functions of the circulatory system

A

transportation, regulation of hormones & temp, protection

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10
Q

RBC’s transport __ & remove __

A

O2; CO2

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11
Q

Blood carries __ to distant sites

A

hormones

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12
Q

Cardiovascular system refers to

A

heart + blood vessels

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13
Q

4 chambered dual pump

A

heart

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14
Q

The atria ___ blood, ventricles __ blood

A

receive; pump blood to lungs & body

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15
Q

Which has a greater workload? atria or ventricles?

A

ventricles

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16
Q

Which has a greater workload? left or right ventricle?

A

left b/c pumps blood to systemic side

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17
Q

Amount of cardiac output per min?

A

5L/min

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18
Q

Arteries move blood __, veins ___

A

away; return blood to heart

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19
Q

T/F: All veins carry dO2 blood & all arteries carry O2 blood

A

F

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20
Q

Largest artery

A

Aorta

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21
Q

Arteries –>

A

arterioles –> capillaries

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22
Q

Capillaries are

A

site of gas exchange; THIN-walled

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23
Q

How does gas exchange occur in capillaries?

A

O2 delivered to tissues, CO2 picked up

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24
Q

Capillaries –>

A

venules –> veins

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25
Q

Largest veins

A

IVC + SVC

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26
Q

Components of blood

A

plasma + formed elements

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27
Q

Plasma is the ___ portion, the formed elements are the ___ portion

A

fluid; cellular

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28
Q

The Buffy coat contains

A

WBC’s + platelets

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29
Q

Plasma vol. is regulated tightly by

A

osmoreceptors

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30
Q

When blood osmolarity increases, it indicated possible

A

dehydration

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31
Q

What is the purpose of RBC’s donut shape?

A

increased surface area for a higher diffusion rate

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32
Q

Characteristics of erythrocytes

A

flexible (to squeeze thru small caps), donut shaped, anucleated, 120 day lifespan, no mitochondria, anaerobic resp

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33
Q

Why is it advantageous for erythrocytes to have no mitochondria (means they are anaerobic)

A

b/c they would use the O2 that they are transporting

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34
Q

Each RBC has ___ of Hb molecules

A

a lot

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35
Q

How many chains in each Hb?

A

4; 2 alpha + 2 beta

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36
Q

Heme

A

iron recycled from old RBC’s

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37
Q

Iron deficiency =

A

anemia

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38
Q

Characteristics of Hb

A

each has heme at center; contains iron which binds to O2

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39
Q

Heme is carried by

A

transferrin

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40
Q

Dietary needs of iron are __, but __

A

small; essential

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41
Q

Anemia causes

A

low Hb or low RBC count; blood loss or iron def

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42
Q

Symptoms of anemia

A

tired, pale, weak, SHORT BREATH (would be trying to get more O2), FAST HR (heart trying to deliver what blood you do have to tissues)

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43
Q

Pernicious anemia

A

lack of intrinsic factor (B12 injection)

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44
Q

Aplastic anemia

A

destruction of bone barrow (chemo could cause)

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45
Q

Polycythemia

A

elevated RBC’s

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46
Q

When does polycythemia lead to viscosity issues

A

only in severe cases

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47
Q

T/F: Polycythemia is usually not detrimental; it is an adaptation

A

T

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48
Q

Sickle-cell anemia is due to

A

a genetic mutation in Hb

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49
Q

Characteristics of leukocytes

A

contain nuclei & mitochondria; are motile

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50
Q

Why do leukocytes need to be motile?

A

to be able to move outside of bloodstream to fight pathogens

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51
Q

Diapedesis

A

ability to squeeze through capillary walls

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52
Q

Extravasation

A

exit from vascular system & enter into tissues

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53
Q

Types of leukocytes

A

granulocytes: basophils, eosinophils, neutrophils
agranulocytes: lymphocytes, monocytes

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54
Q

Normal hematocrit count

A

males: 40-54%
females: 37-47%

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55
Q

Normal Hb count

A

males: 14-17
females: 12-16

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56
Q

Platelets

A

smallest formed elements; cell fragments of megakaryocytes

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57
Q

Platelets form

A

platelet plug for CLOTTING

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58
Q

Characteristics of platelets

A

anucleated, move around, short lifespan

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59
Q

Platelets get destroyed by the

A

spleen & liver

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60
Q

Hematopoiesis

A

blood cell formation

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61
Q

Leukopoiesis

A

WBC production

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62
Q

Process of leukopoiesis

A

totipotent cells give rise to blood cell precursor

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63
Q

Myeloblasts –>
Lymphoblasts –>
Monoblasts –>

A

granulocytes
lymphocytes
monocytes

64
Q

Erythropoiesis

A

RBC production

65
Q

Erythropoiesis regulated by

A

erythropoietin

66
Q

Erythropoietin secreted by

A

kidneys in response to hypoxia

67
Q

T/F: People w/ asthma, w/ blood loss, at a high altitude, w/ a lung disorder, or doing strenuous exercise can all be hypoxic

A

T

68
Q

T/F: RBC’s have a limited lifespan & require continual replacement

A

T

69
Q

T/F: People with emphysema usually have elevated levels of Hb

A

T

70
Q

Clinical relevance of having elevated levels of reticulocytes

A

it indicates recent blood loss b/c it indicated that RBC synthesis has been stimulated to a large degree

71
Q

Process of EPO

A

hemocytoblast (stem cell) –> EPO binds receptors proerythroblasts –> erythroblast –> normoblast –> nucleus lost –> reticulocyte –> erythrocyte (then released into blood)

72
Q

Antigens

A

molecules capable of eliciting an immune response

73
Q

When we recognize antigens as cells it’s b/c we recognize those cells as ___

A

foreign

74
Q

Antigens are important b/c they produce

A

antibodies

75
Q

When you produce antibodies against your own cells

A

auto-immune disorder

76
Q

A blood binds __; produces __

A

a-antigen; anti-b abs

77
Q

B blood binds __; produces __

A

b-antigen; anti-a abs

78
Q

AB blood binds __; produces __

A

a & b-antigens; neither

79
Q

O blood binds __; produces __

A

no antigens; anti-a & anti-b abs

80
Q

Why are abs produced when we have no prior exposure to them?

A

they are produced in response to intestinal bacteria that has antigens that look similar to blood surface antigens –> they cross react

81
Q

Universal donor

A

O (b/c they have no antigens)

82
Q

Universal recipient

A

AB (b/c they don’t produce A or B antibodies)

83
Q

Most common type of blood

A

O

84
Q

Least common type of blood

A

AB

85
Q

What happens if someone w/ A receives B?

A

transfusion reaction –> agglutination –> clot vessels (ischemia) –> cells targeted for destruction by immune system –> donor cells lyse & free Hb released –> free Hb can block kidney tubules –> death from renal failure

86
Q

Transfusion reaction

A

mismatched blood; donor’s blood is agglutinated by recipients abs

87
Q

T/F: Plasma contains abs

A

T

88
Q

Why does agglutination occur?

A

each ab molecule contains many binding sites

89
Q

How is blood typing done?

A

drop of blood is placed in different ab solutions

90
Q

Clumping =

A

positive reaction (antigens of that type present)

91
Q

Anyone w/ d-antigens is

A

Rh+

92
Q

Anyone w/o d-antigens is

A

Rh-

93
Q

O+ means

A

type O AND Rh+ (has d-antigen)

94
Q

O- means

A

type O AND Rh- (lacks d-antigen)

95
Q

AB- means

A

has AB only

96
Q

AB+ means

A

has Ab & D

97
Q

T/F: Anti-d abs are not present until exposure

A

T

98
Q

Why is it an issue for an Rh- mother to be carrying an Rh+ baby?

A

1st preg = no issue b/c no prior exposure to d-abs; will be exposed during birth and mom will create d-abs
2nd preg = issue b/c mom now has d-abs that will attack baby’s blood –> baby born w/ severe anemia

99
Q

How is erythroblastosis fetalis prevented?

A

RhoGAM prior to birth

100
Q

What does RhoGam do?

A

antibody that effectively HIDES baby’s antigens from mom’s immune system so she wont make abs against it

101
Q

Blood is

A

a liquid that has the ability to turn into a gel-like semi-solid substance is response to injury

102
Q

T/F: People with clotting disorders bruise easily & badly

A

T

103
Q

T/F: Inappropriate clot formation is as bad as no clot formation

A

T

104
Q

Are platelets normally repelled from vessel walls & eachother

A

yes

105
Q

What is the purpose of a vascular spasm when there is injury to the vessel

A

to slow down bleeding

106
Q

Vonwillebran factor

A

factor that bridges the interaction between platelets & collagen strands to be able to form a platelet plug

107
Q

Vonwillebran’s disease

A

lack factor so platelets CAN’T adhere to exposed collagen –> platelet form doesn’t form as well

108
Q

What is released when platelets are ‘activated’

A

serotonin, thromboxane, ADP

109
Q

What is the function of serotonin here

A

to further stimulate the vascular spasm that slows down blood loss

110
Q

What is the function of ADP & thromboxane here

A

to recruit more platelets & make platelets sticky

111
Q

The platelet plug is a ___ fix

A

temporary; until stable clot forms

112
Q

NSAID’S act as ___ drugs

A

anti-platelet

113
Q

How are NSAID’S anti-platelet drugs

A

b/c they inhibit cyclooxygenase which is required for the production of thromboxane –> if you can’t make tx, you can’t aggregate platelets as well –> can’t form platelet plug as well

114
Q

What does the clotting cascade do?

A

convert fibrinogen –> fibrin & ensure that fibrin strands deposit on platelet plug

115
Q

Serum

A

plasma w/o clotting factors/fibrinogen

116
Q

In order to form a clot, you must form __

A

fibrin

117
Q

Extrinsic pathway is activated by

A

chemicals released when tissue is damaged

118
Q

Intrinsic pathway is activated by

A

platelet activation

119
Q

Both the extrinsic & intrinsic pathways are activated as a result of

A

a damaged vessel

120
Q

Both the intrinsic & extrinsic pathways are produced in what form?

A

inactive that can activate quickly

121
Q

If someone can’t activate platelets, would they still be able to clot?

A

yes, but not so well

122
Q

If someone can’t activate 1 of 2 clotting factors, can they still clot?

A

yes, bc they give you some redundancy in case something goes wrong

123
Q

What begins the common pathway?

A

activation of factor x

124
Q

Common pathway

A

activates prothrombin –> activates thrombin –> activates fibrinogen –> becomes fibrin

125
Q

What activates factor x?

A

both the intrinsic & extrinsic pathways

126
Q

Antithrombin inhibits ___

A

thrombin

127
Q

What happens if you don’t produce thrombin & why?

A

you don’t clot as well bc you won’t be as good to produce fibrin

128
Q

When else can the body think there is damage to a vessel?

A

when a vessel ruptures due to atherosclerosis

129
Q

Which pathway is quicker to reach the common pathway?

A

extrinsic

130
Q

Can long-term antibiotic therapy cause a problem with clotting?

A

yes bc bacteria make vit K

131
Q

A defect in factor viii linked to royal families in Europe

A

Hemophilia A

132
Q

Which factors are vit K dependent?

A

2, 7, 9, 10

133
Q

All clot busting drugs cause activation of ___

A

plasmin

134
Q

Anticoagulant that activates antithrombin & works quickly

A

Heparin

135
Q

Anticoagulant that inhibits vit K & takes days to work

A

Coumadin

136
Q

Process of vessel repair

A

plasminogen (inactive) –> plasmin (active) –> plasmin digests fibrin promoting clot brkdwn

137
Q

Clotting cascade

A

damage to vessel –> vessel spasms –> exposed collagen recruits platelets to area –> platelets become activated –> serotonin release (further spasm) –> ADP & TX released (more platelets to area to stick together) –> platelet plug formed

138
Q

Right side of the heart pumps blood to the

A

lungs

139
Q

Left side of the heart pumps blood to the

A

body

140
Q

T/F: Right heart generates greater pressure

A

F; left

141
Q

As compared to the left heart, what percentage of blood is pumped through the right heart

A

100% (the same)

142
Q

When should AV valves open?

A

atrial press > ventricular

143
Q

When should AV valves shut?

A

when ventricles contract

144
Q

When should semilunar valves open?

A

ventricular press > arterial pressure

145
Q

When should semilunar valves shut?

A

arterial pressure > ventricular pressure

146
Q

The cardiac cycle refers to

A

the repeating pattern of contraction & relaxation

147
Q

First the ___ contract, THEN the ___ contract

A

atria; ventricles

148
Q

80% of blood that ventricles receive from atria occurs

A

passively

149
Q

20% of blood that ventricles receive from atria occurs

A

when atria finally contract

150
Q

EDV refers to

A

blood in ventricles at the end of ventricular diastole/amount of blood when filled

151
Q

ESV refers to

A

little bit of blood that remains after the ejection phase

152
Q

Stroke vol

A

amount of blood ejected from the ventricles in one systole

153
Q

SV =

A

EDV - ESV

154
Q

If EDV = 100 mls & ESV = 20 mls, what is the SV?

A

80 mls

155
Q

Ventricles contract once filled –>

A

ventricular press > atrial press –> av valves shut –> ventricular press > aortic press –> aortic semilun. valves open –> blood moves up aorta (begins ejection phase)

156
Q

SV is usually about

A

70 mls

157
Q

Which valves open during the isovolumetric contraction phase?

A

none

Physio (14 decks)

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