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Physiology & Neurobiology 2275 > EXAM 2 - The Heart, Lymphatic and Immune System > Flashcards

EXAM 2 - The Heart, Lymphatic and Immune System Flashcards

1
Q

cardiac output

A

heart rate x stroke volume

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2
Q

blood pressure

A

cardiac output x peripheral resistance

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3
Q

cardiodynamic autonomic control: sympathetic

A

nerve from cardioacceleratory center (medulla) synapses in spinal cord

preganglionic axons release Ach onto ganglia

postganglionic axons synapse on SA node, AV node, and left ventricle and release NE

NE activates B1-adrenergic receptors coupled to Gsa GPCR

Gsa increases cAMP production and increases HR

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4
Q

where do the sympathetic postganglionic axons synapse on?

A

SA node, AV node, left ventricle

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5
Q

sympathetic synapse on heart

A

increase cAMP, increase HR

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6
Q

NE binding to Gsa

A

adenylate cyclase –> cAMP –> to PKA and HCN channels

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7
Q

effects of PKA

A

activates troponin

inactivates phospholamban

activates ryanodine receptors

activates L-type Ca2+ channels

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8
Q

effect of increasing troponin

A

increases contractile strength

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9
Q

effect of binding to HCN

A

increases heart rate

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10
Q

effect of decreasing phospholamban

A

phospholamban typically inactivates SERCA – by disinhibiting SERCA, Ca2+ gets pumped into SR quicker allowing for quicker repolarization –> quicker cardiac myocyte AP

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11
Q

effect of activating RyR

A

increases contractility due to Ca2+ eflux

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12
Q

effect of L-type Ca2+ activation

A

more depolarized plateau phase to permit contraction

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13
Q

hydrostatic pressure near heart in arteries

A

high; 80-120 mmHg

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14
Q

hydrostatic pressure in capillaries

A

low (15-25)

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15
Q

hydrostatic pressure in veins

A

0-20

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16
Q

parallel circulatory systems

A

pulmonary circulation
systemic circulation

two pumps for two loops

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17
Q

coronary arteries

A

arise from coronary sinus in aorta and delivers oxygenated blood to cardiac muscle tissue itself

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18
Q

cardiac veins

A

drain into coronary sinus and opens into right atrium

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19
Q

arteries and arteriole functions

A

distribution

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20
Q

arteries and arteriole constraints

A

distribution vessels must be able to handle pressure during contraction and store pressure during diastole

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21
Q

capillary function

A

exchange

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22
Q

capillary constraints

A

exchange vessels must permit bidirectional flow of substances

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23
Q

vein functions

A

collection

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24
Q

vein constraints

A

collection vessels must be able to deal with low pressure upon returning to the heart

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25
Q

path of circulation

A

arteries carry blood away from heart

branch into arterioles

branch into capillaries

capillaries do exchange

later rejoin into venules

venules deposit into veins

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26
Q

which vessels do not have elastic fibers

A

veins, capillaries

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27
Q

which vessels do not have smooth muscle

A

capillaries, veins

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28
Q

which vessel has the greatest wall thickness

A

aorta, artery

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29
Q

which vessel has the thinnest thickness?

A

vein,,capillary (smallest is venule)

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30
Q

arteries

A

hold 13%

elastic
muscular
arterioles

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31
Q

elastic arteries

A

conducting

buffer changes in pressure

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32
Q

muscular arteries

A

distributing

most common

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33
Q

arterioles

A

resistance
small diameter
no externa
can affect BP

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34
Q

veins

A

hold 64%; volume reservoir

venules
medium diamater
large

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35
Q

venules

A

collect blood from capillary to deposit into veins

no media

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36
Q

medium diameter veins

A 
return blood
expand easily (high compliance)
valves
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37
Q

large veins

A

return blood back to the heart

thin 3 layers

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38
Q

capillaries

A

hold 9%
microcirculation

large SA

continuous
fenestrated
sinusoid

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39
Q

thoroughfare channels

A

provide direct flow b/w arterioles and venules (capillary)

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40
Q

metarterioles

A

precap sphincters to regulate blood flow

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41
Q

arteriovenous anastomaoes

A

alternative blood pathway

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42
Q

continuous capillaries

A

exchange of small molecules in most tissues

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43
Q

fenestrated capillaries

A

fenestrations in endothelium that allow peptide exchange

hypothalamus, kidney, intestine, pituitary

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44
Q

sinusoid capillaries

A

allow exchange of large proteins

larger diameter, large sinuses

liver, bone marrow, spleen

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45
Q

B1 AR

A

NE binds to this, adenylate cyclase, cAMP PKA etc etc etc

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46
Q

B2 AR

A

epi binds to this, increases cAMP and inhibits MLC in smooth muscle

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47
Q

M3 cholinergic

A

Ach binds to this and decreases cAMP to relax smooth muscle

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48
Q

A1 AR

A

gq coupled; NE binds to this and increases IP3 for more contraction in smooth muscle

also binds:
angiotensin
endothelin
thromboxane

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49
Q

NO smooth muscle

A

endothelial gets NO from blood flow, it diffuses into smooth muscle

guanylate cyclase to cGMP to PKG

  • inhibit IP3 (dilation)
  • stimulate MLC phosphatase; decreases MLC (dilation)
  • stimulates K+ channel; ends contraction
  • inhibits L-type Ca2+; decreases contraction
  • stimulates pump to get rid of Ca2+
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50
Q

compliance

A

how easily a heart chamber or blood vessel expands when filled with blood (pressure)

51
Q

veins

A

high compliance

low elasticity

52
Q

arteries

A

low compliance

high elasticity

53
Q

LARGE volume change but small pressure change

A

veins

54
Q

LARGE pressure change but small volume change

A

artery

55
Q

venous blood reserve

A

central reflexes can decrease compliance of veins to supply more blood to the arterial circulation as needed

56
Q

structures for venous circulation

A

skeletal pump
valves
respiratory pump

57
Q

skeletal pump

A

veins pass through here and when muscles contract they press on veins and blood moves

58
Q

respiratory pump

A

drop in pressure in chest cavity during inhalation reduces pressure on the veins and allows blood to flow back up to the heart

59
Q

flow =

A

(change in) pressure / resistance

60
Q

change in pressure =

A

P artery - P venous

61
Q

systemic circulatory pressure > total peripheral resistance

A

flow

62
Q

why is the flow in the capillaries not zero?

A

the systemic circulatory pressure is greater than the total peripheral resistance

63
Q

resistance is proportional to

A

length
viscosity
turbulence

64
Q

resistance is inversely proportional to

A

radius

65
Q

vascular networks

A

parallel vessel circuits

vessel series

66
Q

parallel vessel circuits

A

lower resistance (capillaries)

67
Q

vessel series

A

high resistance

68
Q

flow =

A

velocity x area

69
Q

if flow is constatn

A

velocity = 1/area

70
Q

poisseuille’s law

A

predicts blood flow rate in a vessel

viscosity and length dictate this

71
Q

filtration

A

removal of solutes from blood to deliver to tissues

72
Q

driivng force of filtration

A

hydrostatic pressure forces fluid OUT of the capillaries

73
Q

reabsorption

A

wastes and water into capillaries

74
Q

driving force of reabsorption

A

oncotic pressure brings fluid BACK into the capillaries

75
Q

net filtration pressure =

A

net hydrostatic pressure (NHP) - net colloid oncotic pressure (NCOP)

76
Q

sigma for NFP

A

adjustment for pressure; reflection coefficient

1 < s < 0

high: low protein permeability, concentration is important
low: high permeability, more even and less important

77
Q

filtration > reabsorption

A

net leakage of fluid

78
Q

Kf

A

filtration rate

79
Q

high Kf

A

high water permeability

80
Q

low Kf

A

low water permeability

81
Q

lymphoid tissues

A

nodules, tonsils, adenoids, MALT

82
Q

tonsils

A

germinal centers for B cell proliferation

83
Q

lymph organs

A

nodes, thymus, spleen ; immune function site

84
Q

first line of defense

A

prevention of infection

85
Q

second line of defense

A

targeted destruction of pathogens

86
Q

third line of defense

A

specific targeting of pathogens (immunomemory)

87
Q

bacteria protists parasites fungi

A

living cells with biochem machinery needed

88
Q

control points nonspecific defenses

A

point of entry
disruption of life cycle
interfere w toxins

89
Q

point of entry control point

A

block receptor binding

90
Q

disruption of life cycle control point

A

slow growth of pathogen until immune system can destroy it

91
Q

interfere w toxins

A

block toxin release

92
Q

physical / chemical barriers

A

1st

skin and linings

protective chemicals (acidity, lysozyme, antimicrobial peptides)

mucous membranes (traps particles and organisms, transports)

93
Q

phagocytes

A

2nd

microphages: neutrophils, eosinophils

macrophages

94
Q

macrophages

A

monocytes (bone marrow and blood)

langerhaans cells (skin and mucosa)

osteoclasts (bone)

microglia (CNS)

red pulp (spleen)

95
Q

immunological surveillance

A

2nd

monitor cells for abnormal markers (AB and complement proteins)

attack and kill abnormal cells (pathogens and self cells w bad marker)

96
Q

interferons

A

2nd

small proteins released in response to viral infection

97
Q

complement system

A

2nd

3 pathways for protease cleavage but end at MAC

98
Q

MAC

A

pokes holes in membranes to kill pathogens

99
Q

inflammatory response

A

2nd

increased flow of plasma and leukocytes to tissue

elevated phagocytosis, activated hemostasis, activation of complement, response termination

100
Q

fever / pyrogenesis

A

pathogen inactivation

elevate body temp

increased leukocyte movability, increased phagocytosis, increased T cell proliferation, increased interferon activity, DECREASE endotoxins

can damage cell

101
Q

naturally acquired passive immunity

A

transfer of maternal antibodies across placenta

102
Q

induced passive immunity

A

administration of AB to combat infection (booster shot)

103
Q

induced active immunmity

A

develops after admin of antigen to prevent disease (vaccines)

104
Q

naturally acquired active immunity

A

develops after exposure to antigens in environment

105
Q

humoral response

A

B cells + MHCII + CD4 on Th

neutralization
agglutination
opsinization

106
Q

cell mediated response

A

Tc regulate and kill infected cells + nucleated cells + MCH1 + CD8

107
Q

BCR

A

Fab and Fc portion can be secreted as AB

108
Q

TCR

A

alpha and beta chains never secreted; CD3

109
Q

somatic recombination

A

in bone marrow when making WBC

germline DNA – SR – DJ rearranged – SR – VJ and VDJ joined – transcription

110
Q

IgM

A

all areas in response to infection

secreted as pentamer

111
Q

IgA

A

mucosa linings, dimer, fight off microbes in body secretions

112
Q

IgG3

A

blood plasma placenta to fetus

signals macrophage in infection

113
Q

IgD

A

least prevalent

114
Q

IgE

A

epithelia, mast cells histamine, inflammation

115
Q

primary diversification (during development)

A

somatic recombination
junctional diversity
combinatorial diversity

116
Q

junctional diversity

A

VDJ and VJ shuffling: nucleotides randomly insert

117
Q

combinatorial diversity

A

different heavy and light chains can pair

118
Q

secondary diversification (after activation, B cells)

A

somatic hypermutation

isotype switching

119
Q

somatic hypermutation

A

selects for AB that binds tighter to pathogen

120
Q

isotype switching

A

constant region switch

121
Q

MCH1

A

1 bound domain, short

122
Q

MCHII

A

2 domains, medium

123
Q

anergic

A

no response need antigen and sitmulatory proteins

Physiology & Neurobiology 2275 (6 decks)

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