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Physio 2 > after midterm 2 > Flashcards

after midterm 2 Flashcards

1
Q

what is the main function of the immune system

A

protects us from infectious agents and harmful substances

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2
Q

example of innate immunity (non specific internal defences)

A

physiologic responses (inflammation, fever)

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3
Q

how are antibodies released in adaptive immunity

A

plasma cells synthesize and release them

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4
Q

what are bacteria

A

single celled prokaryotes

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5
Q

varied types of bacteria

A

spherical
rodlike
coiled

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6
Q

some bacteria are _____ while others are ____

A

harmless
virulent

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7
Q

what do virulent bacteria do

A

contain pili, capsule, or release toxins or damaging enzymes

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8
Q

examples of virulent bacteria

A

tetanus
strep

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9
Q

what is a virus

A

piece of DNA or RNA in a protein shell

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10
Q

what must a virus enter in order to reproduce

A

a cell

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11
Q

examples of viruses

A

cold, ebola, chicken pox

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12
Q

what is fungi

A

eukaryotic cells with membrane and cell wall

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13
Q

examples of fungi

A

mold, yeast, multicellular fungi that produce spores

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14
Q

what do fungi release and what does this do

A

release proteolytic enzymes which induces inflammation

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15
Q

what can fungi infect

A

mucosal linings (ex: yeast infection) or cause internal infections (ex: histoplasmosis - lung infection)

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16
Q

what are protozoans

A

eukaryotic cells without a cell wall

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17
Q

how are protozoans ingested

A

by drinking infected water

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18
Q

protozoan disease examples

A

malaria
trichomoniasis

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19
Q

what are multicellular parasites

A

nonmicroscopic parasites that take nourishment from host
ex: tapeworm

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20
Q

what are prions

A

fragments of infectious proteins
-neither cells nor viruses

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21
Q

what do prions do

A

cause disease in nervous tissue
(ex: mad cow disease - spreads from cows to humans by consuming infected meat)

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22
Q

primary location of:
T & B lymphocytes
macrophages
dendritic cells
NK cells

A

lymphatic tissue

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23
Q

primary location of alveolar macrophages

A

select organs

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24
Q

primary location of dendritic cells

A

skin and mucosal membranes

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25
Q

primary location of mast cells

A

connective tissue throughout body

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26
Q

what are cytokines and what type of immunity produces them

A

small proteins that regulate immune activity
-produced by both innate and adaptive

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27
Q

explain how cytokines work

A
  1. chemical messengers are released from one cell that bind to receptors of target cells
  2. they can act on the cell that:
    -released it
    -on local cells
    -on distant cells after going through blood
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28
Q

effects of cytokines

A
  1. signalling cells
  2. controlling development and behaviour of immune cells
  3. regulates inflammatory response
  4. destroys cells
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29
Q

how do adaptive and innate immunity differ

A
  1. cells involved
  2. specificity of cell response
  3. mechanisms of eliminating harmful substances
  4. response time
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30
Q

innate immunity

A

present at birth (passed on from mom)
-protects against different substances
-responds right away to potentially harmful agents

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31
Q

adaptive immunity

A

acquired immediately
-response to antigen involves specific T & B lymphocytes
-takes a few days

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32
Q

characteristics of inmate immunity

A
  1. stops potentially harmful substances from entering
  2. responds to a range of harmful substances
  3. first line of defense is skin and mucosal membrane
  4. second line of defence involved internal processes
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33
Q

what % of our blood is immune cells

A

less than 1 %

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34
Q

cells of innate immunity

A

basophil and mast cell
natural killer cell
eosinophils

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35
Q

basophil and mast cell

A

proinflammatory chemical secreting cells

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36
Q

NK cell

A

apoptosis-initiating cells (get rid of dead cells)

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37
Q

eosinophils

A

parasite destroying cells

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38
Q

antimicrobial proteins

A

molecules that function against microbes

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39
Q

interferons

A

class of cytokines that nonspecifically interfere w spread of intracellular pathogens

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40
Q

how to interferons work

A
  1. IFN-alpha and beta are produced by leukocytes and virus infected cells which then bind to neighbouring cells to prevent their function
  2. trigger synthesis of enzymes that destroy viral nucleic acids, inhibit synthesis or viral proteins
  3. stimulate NK cells to destroy virus infected cells
  4. IFN-g produces by T lymphocytes and NK cells
  5. stimulates macrophages to destroy virus infected cells
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41
Q

what is the complement system

A

group of over 30 plasma proteins
-work along with complement antibodies
- synthesized by liver, constantly released in inactive form
-complement activation follows pathogen entry

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42
Q

effects of activated complement

A

inflammation:
enhanced by complement
-activates mast cells and basophils; attracts neutrophils and macrophages
opsonization:
complement protein binds to pathogen
-enhances likelihood of phagocytosis of pathogenic cell
cytolysis:
complement triggers splitting of target cell
-complement proteins form MAC that creates channel in target cells membrane
elimination of immune complexes:
complement links antigen-antibody complexes to erythrocytes
-cells move to liver and spleen where complexes are stripped off

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43
Q

cardinal signs of inflammation

A
  1. redness from increased blood flow
  2. heat from increased blood flow and increased metabolic activity within the area
  3. swelling from increase I fluid loss from capillaries
  4. pain from stimulant of pain receptors
  5. loss of function from pain and swelling in severe cases
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44
Q

duration if acute inflammation

A

8-10 days

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45
Q

what is a fever

A

abnormal body temp elevation (1 degree or more above 37 degrees c

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46
Q

what does a fever result from

A

release of pyrogens form immune cells or infectious agents

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47
Q

events of a fever

A
  1. pyrogens circulate through blood and target hypothalamus
  2. hypothalamus releases prostaglandin E2
  3. hypothalamus raises temp set point leading to fever
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48
Q

3 fever stages

A
  1. onset
  2. stadium
  3. defervescence
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49
Q

onset stage of fever

A

temp starts to rise
-hypothalamus stimulates dermis blood vessels to constrict (less heat loss)
-shivering of muscle generates more heat

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50
Q

stadium stage of fever

A

elevated temp is maintained
-metabolic rate increases to promote elimination of harmful substances
-liver and spleen bind zinc and iron thereby slowing microbial reproduction

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51
Q

defervescence stage of fever

A

when temp returns to normal
-hypothalamus no longer stimulates by pyrogens
-prostaglandin release decreases
-hypothalamus stimulates mechanisms to release heat (sweat)

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52
Q

benefits of fever

A
  1. inhibits reproduction of bacteria and viruses
  2. promotes interferon activity
  3. increases activity of adaptive immunity
  4. accelerates tissue repair
  5. increases CAMs on endothelium of capillaries in lymph nodes
  6. recommended to leave a low fever untreated
53
Q

risks of a high fever

A

dangerous is its 103F in children or lower in adults
-seizure
- irreversible brain damage
-death

54
Q

what are the two branches of adaptive immunity

A

cell mediated immunity
humeral immunity

55
Q

why are pathogens detected by lymphocytes

A

bc they contain antigens

56
Q

what is an antigen

A

substance that binds a t lymphocyte or antibody
-usually a protein or large polysaccharide

57
Q

examples of antigens

A

protein capsid of viruses
cell wall of bacteria or fungi
bacterial toxins
abnormal protein or tumour antigens

58
Q

foreign antigens

A

differ from human body molecules
-binds immune components

59
Q

self antigens

A

body own molecules
-dont bind immune components

60
Q

antigenic determinant

A

specific site on antigen recognized by immune system

61
Q

immunogen

A

antigen that induces an immune response

62
Q

immunogenicity

A

ability to trigger response

63
Q

haptens

A

small foreign molecules that induce immune response when attached to carrier molecule in host

64
Q

example of a hapten

A

toxin in poison ive

65
Q

what are the antigen receptors of both T & B lymphocytes

A

T: TCR (T cell receptor)
B: BCR (B cell receptor)

66
Q

lymphocyte contact w antigen

A
  • B lymphocytes make direct contact w antigen
  • T lymphocytes have antigen presented by some other cell
67
Q

T lymphocyte subtypes

A

helper t lymphocytes are CD4+ cells
cytotoxic t lymphocytes are CD8+ cells
memory T cells and regulatory T cells

68
Q

helper t lymphocytes do what

A

assist in cell mediated, humeral, and innate immunity

69
Q

cytotoxic t lymphocytes

A

release chemicals that destroy other cells

70
Q

antigen presentation

A

cells display antigen on plasma membrane so T cells can recognize it

71
Q

which two categories of cells present antigens

A

all nucleated cells of body
antigen presenting cells

72
Q

what is major histocompatibility complex (MHC)

A

a group of transmembrane proteins

73
Q

where is MHC I found

A

on all nucleated cells

74
Q

where is MHC II found

A

on antigen presenting cells (APC’s) in addition to MHC I

75
Q

pulmonary ventilation

A

movement of gases between atmosphere and alveoli

76
Q

pulmonary gas exchange

A

exchange of gases between alveoli and blood

77
Q

gas transport

A

transport of gases in blood b/w lungs and systemic cells

78
Q

tissue gas exchange

A

exchange of respiratory gases b/w blood and the systemic cells

79
Q

Boyles gas law

A

relationship of volume and pressure
-at constant temp, pressure of a gas decreases if volume of the container increases and vice versa
-p1 and v1 represent initial conditions and p2 and v2 the changed conditions

80
Q

atmospheric pressure

A

pressure of air in environment

81
Q

alveolar volume

A

collective volume of alveoli

82
Q

intrapulmonary pressure

A

pressure in alveoli
-fluctuates w breathing

83
Q

intrapleural pressure

A

pressure in pleural cavity
-fluctuates w breathing

84
Q

how does air flow in during inspiration

A

thoracic vol increases, thoracic pressure decreases

85
Q

how does air flow out during expiration

A

thoracic volume decreases, thoracic pressure increases

86
Q

quiet inspiration steps

A
  1. diaphragm and external intercostals contract increasing thoracic volume
  2. diaphragm movement accounts for 2/3 of volume change; external intercostal movement account for 1/3
  3. intrapleural vol increases, so intrapleural pressure decreases
  4. lungs pulled by pleurae, so lung vol increases and intrapulmonary pressure decreases
  5. because intrapulmonary pressure is less than atmospheric pressure, air flows in until these pressures are equal
87
Q

quiet expiration steps

A
  1. diaphragm and external intercostals relax decreasing thoracic vol
  2. pleural cavity vol decreases, so intrapleural pressure increases
  3. elastic recoil pulls lungs inward, so alveolar vol decreases and intrapulmonary pressure increases
  4. since intrapulmonary pressure is greater than atmospheric pressure, air flows out until these pressures are equal
88
Q

forced breathing

A

-requires contraction of additional mm
-causes greater changes in thoracic cavity volume and intrapulmonary pressure
-more air moves into and out of the lungs
-significant chest volume changes are apparent

89
Q

2 groups of medulla respiratory centre

A

ventral rest group (ant medulla)
dorsal resp group (post medulla)

90
Q

irritant receptors

A

in air passageways stimulated by particulate matter

91
Q

baroreceptors

A

in pleurae and bronchioles respond to stretch

92
Q

proprioceptors of mm and joints are stimulates by what

A

body movements

93
Q

physiology of quiet breathing

A

-inspiration begins when VRG inspiratory neurons fire spontaneously
-signals are sent from VRG to nerve pathways exciting skeletal muscles for about 2 secs
-quiet expiration occurs when VRG is inhibited
-signals no longer sent to inspiratory mm for 3 seconds

94
Q

reflexes that alter breathing rate and depth

A

-chemoreceptors alter breathing by sending signals to DRG which are then relayed to VRG
-ventilation increases in response to central chemoreceptors detecting increase in blood H or PCO2 and peripheral chemoreceptors detecting increase in blood H or PCO2
-increased ventilation expels more CO2 returning conditions to normal
-ventilation decreases if chemoreceptors detect decreases in H or PCO2

95
Q

minute ventilation

A

-process of moving air into and out of lungs
-amount of air moved b/w atmosphere and alveoli in 1 min

96
Q

tidal vol

A

amount of air per breath

97
Q

resp rate

A

number of breaths per min

98
Q

tidal vol x respiration rate = ?

A

minute ventilation

99
Q

anatomic dead space: conducting zone space

A

no exchange of respiratory gases

100
Q

alveolar ventilation

A

amount of air reaching alveoli per min
(tidal volume - anatomic dead space) x resp rate = alveolar ventilation

101
Q

physiologic dead space

A

-normal anatomic dead space + any loss of alveoli
-some disorders decrease number of alveoli participating in age exchange
-anatomic dead space = physiologic dead space in healthy individual where loss of alveoli is minimal

102
Q

low FEV causes what

A

problem w air escaping lungs, esp at high velocities

103
Q

low FVC causes what

A

problem w air escaping at all points

104
Q

low FEV causes what

A

lung damage

105
Q

low FVC causes what

A

low compliance

106
Q

partial pressure

A

pressure exerted by each gas within a mixture of gases measured in mm Hg

107
Q

daltons law

A

total pressure in a mix of gases is equal to the sum of the individual partial pressures

108
Q

reasons partial pressures in alveoli differ from atmospheric partial pressures

A
  1. air from environment mixes w air remaining in anatomic dead space
  2. O2 diffuses out of alveoli into blood; CO2 diffuses from blood into alveoli
  3. more water vapor is present in alveoli than in atmosphere
109
Q

partial pressure gradients

A

gradient exits the partial pressure for a gas is higher in one region of the respiratory system than another

110
Q

alveolar gas exchange

A

b/w blood in pulmonary capillaries and alveoli

111
Q

systemic gas exchange

A

b/w blood in systemic capillaries and systemic cells

112
Q

ventilation perfusion coupling

A

ability of bronchioles to regulate airflow and arterioles to regulate blood flow

113
Q

what does bloods ability to transport depend on

A

-solubility coefficient of O2
-presence of hemoglobin

114
Q

CO2 3 means of transport

A
  1. CO2 dissolved in plasm
  2. CO2 attached to amine group of global portion of hemoglobin
  3. bicarbonate dissolved in plasma
115
Q

what does hemoglobin transports

A

-O2 attached to iron
-carbon dioxide bound to the global
-H ions bound to the global

116
Q

hemoglobin and binding of O2

A

each hemoglobin can bind up to four O2 molecules

117
Q

cooperative binding effect

A

each O2 that binds causes a change in hemoglobin making it easier for next O2 to bind

118
Q

as Po2 (mm Hg) increases, so does what

A

percent o2 saturation of hemoglobin

119
Q

altitude sickness

A

-adverse physiologic effects from a decrease in alveolar pO2 and low O2 saturation
-symptoms of headache, nausea, pulmonary oedema, and cerebral edema

120
Q

O2 reserve

A

O2 remaining bound to hemoglobin after passing through systemic circulation

121
Q

CO2 binding to hemoglobin

A

binding causes release of more O2 from hemoglobin

122
Q

H binding to hemoglobin

A

-H ion binds to hemoglobin and causes a conformational change
-causes decreased affinity for O2 and o2 release

123
Q

components of the urinary system

A

kidneys, ureters, bladder, urethra

124
Q

kidney function

A

filter blood, remove waste products and convert filtrate into pee

125
Q

function of ureters

A

transports urine from kidneys to bladder

126
Q

bladder function

A

expandable muscular sac stress much as 1L urine

127
Q

urethra function

A

eliminates pee

128
Q

processes that occur as filtrate is converted to urine

A

-elimination of metabolic wastes
-regulation of ion levels
-regulation of acid base balance
-regulation oc BP
-elimination of biologically active molecules

Physio 2 (3 decks)

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