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A+P 2 > Chapter 21 (Lecture) > Flashcards

Chapter 21 (Lecture) Flashcards

1
Q

ability of the body to resist many agents (both living and nonliving) that can cause disease; resistance to disease

A

immunity

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2
Q
  • first line of defense: surface barriers such as intact skin and mucosae
  • second line of defense (internal): antimicrobial proteins, phagocytes, fever, NK cells, and other cells; hallmark is inflammation
  • NO MEMORY
A

innate (nonspecific) immune system

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3
Q
  • takes considerably longer to mount
  • humoral immunity
  • cellular immunity
  • MEMORY; each response is unique, and second exposure is quicker
A

adaptive (specific) defense system

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4
Q
  • a functional system rather than an organ system in an anatomical sense
  • structures are a diverse array of molecules plus trilions of immune cells (especially lymphocytes) that inhabit lymphoid tissues and circulate in bodily fluids
A

immune system

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5
Q

harmful or disease-causing microorganisms

A

pathogens

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6
Q

benefits of keratin

A

resistant to most weak acids, alkalis and bacterial enzymes

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7
Q

protective chemicals of the innate immune system

A
  • acid (acid mantle)
  • enzymes
  • mucin
  • defensins
  • lipids, sebum and dermicidin
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8
Q

protective mechanism: normally acidic pH inhibits bacterial growth; cleanses the lower urinary tract as it flushes from the body

A

urine

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9
Q

protective mechanism: continuously lubricate and cleans eyes (tears) and oral cavity (saliva): contain lysozyme, an enzyme that destroys microorganism

A

tears, saliva

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10
Q

protective mechanism: inhibits growth of most bacterai and fungi in female reproductive tract

A

acid mantle of the vagina

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11
Q

protective mechanism: contains concentrated hydrochloric acid and protein-digesting enzymes that destroy pathogens in the stomach

A

gastric juice

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12
Q

protective mechanism: propel debris-laden mucus away from nasal cavity and lower respiratory passages

A

cilia

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13
Q

protective mechanism: filter and trap microorganisms in respiratory and digestive tracts

A

nasal hairs

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14
Q

protective mechanism: traps microorgansim in respiratory and digestive tracts

A

mucus

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15
Q

protective mechanism: skin secretions (sweat and sebum) make epidermal surface acidic, which inhibits bacterial growth; also contain various bactericidal chemcials

A

acid mantle of skin

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16
Q

vesicle formed as a result of phagocytosis

A

phagosome

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17
Q
  • phagocytes
  • about 126B/day produced
  • usually the first WBC to make it to an infection
  • 1 time use
A

neutrophils

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18
Q

made up of dead neutrophils, microbes, pathogens

A

pus

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19
Q
  • monocytes in blood, this in tissue
  • leave blood and increase in numbers at site of infection
  • cleanup crew
  • dendritic cells, microglia, alveolar, hepatic
A

macrophages

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20
Q
  • mobile
  • release factors that attract more WBCs
A

basophils

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21
Q
  • immobile
  • are found near sites of possible pathogen influx
  • release chemotaxic factors
  • can also phagocytize bacteria
A

mast cells

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22
Q

factors that attract more WBCs

A

chemotaxic factors

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23
Q

act as moderators of inflammatory response and kill parasites by releasing enzymes all over them

A

eosinophils

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24
Q
  • B cells and T cells
  • Natural Killer Cells (NKC)
A

lymphocytes

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25
Q

recognize tumor and cancerous cells in general

A

NKC (natural killer cells)

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26
Q
  • prevents the spread of damaging agents to nearby tissues
  • disposes of cell debris and pathogens
  • sets the stage for the repair process
A

inflammatory process

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27
Q

cardinal signs of inflammation

A
  • redness
  • heat
  • swelling
  • pain
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28
Q
  • happens after first exposure, involves the creation of killer T cells and memory cells
  • usually takes about 3-7 days, and you will feel sick during this time
A

primary response

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29
Q

occurs upon a repeated exposure to the same antigen or a similar formand the memory clels recognize it and the response is faster and of greater magnitude

A

secondary response

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30
Q

long-lived and require less activation to respond than do other APCs

A

memory T cells

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31
Q
  • production is regulated by helper T cells and antigen presenting cells
  • once activated, proliferate and produce Killer Ts and memory T cells
A

cytotoxic T cells

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32
Q

effects of cytotoxic T cells

A
  • cause cells to lyse (contact killing) by releasing perforins
  • cause the release of cytokines that attract cells such as macrophages and WBCs (inflammatory response)
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33
Q

caused by the release of histamines, prostaglandins, etc. from the injured tissues

A

vasodilation

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34
Q

allows protein rich fluid to seep into the injured region from the blood vessels

A

vascular permeability

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35
Q

which factors cause edema in the injured area

A

vasodilation and vascular permeability

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36
Q

steps of phagocyte mobilization

A
  1. leukocytosis
  2. margination
  3. diapedesis
  4. chemotaxis
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37
Q

follows chemical signals to injured site

A

chemotaxis

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38
Q

true or false:

inflammatory response can be localized or systemic in nature

A

true

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39
Q

functions of antimicrobial proteins

A
  • preventing entrance to cell
  • vasodilation
  • increased permeability
  • attracting WBCs
  • increasing phagocytosis
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40
Q
  • protects body against viral attack
  • mobilize NK cells
  • can be released by lymphocytes to cause widespread immune mobilization
A

interferon

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41
Q

virus infected cells produce interferon which

A

stimulates neighboring cells to produce antiviral proteins

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42
Q

A group of bloodborne proteins, which, when activated, enhance the inflammatory and immune responses and may lead to cell lysis.

A

complement system

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43
Q

classical complement pathway is stimulated by

A

antibodies

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44
Q

alternate complement pathway is stimulated by

A

factors C3 which break down into different compounds

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45
Q

complement works in which response

A

both the innate and adaptive resopnses

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46
Q

a systemic response that involves the release of pyrogens

A

fever

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47
Q

events of phagocytosis

A
  1. phagocyte adheres to pathogens or debris (using receptors)
  2. phagocyte forms pseudopods that eventually engulf the particles, forming a phagosome
  3. lysosome fuses with the phagocytic vesicle, forming a phagolysosome
  4. toxic compounds and lysosomal enzymes destroy pathogens
  5. sometimes exocytosis of the vesicle removes indigestible and residual material
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48
Q
  • wander throughout the tissue spaces in search of cellular debris or “foreign invaders”
A

free macrophages

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49
Q

such as stellate macrophages in the liver, are permenant residents of particular organs

A

fixed macrophages

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50
Q

when neutrophils enter blood from the bone marrow

A

leukocytosis

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51
Q

neutrophils cling to the capillary wall

A

margination

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52
Q

neutrophils flatten and squeeze out of capillaries

A

diapedesis

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53
Q

steps of interferon release/production

A
  1. virus enters cell
  2. interferon genes switch on
  3. cell produces interferon molecules
  4. interferon binding stimulates cell to turn on genes for antiviral proteins
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54
Q
  • antigen-antibody complex
  • C1, C4, C2 complex
A

classical pathway of complement system

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55
Q

coats pathogen surfaces, which enhances phagocytosis

A

opsonization

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56
Q

steps to contact killing

A
  1. cytotoxic t cell binds tightly to the target cell when it identifies foreign antigen on MHC I proteins
  2. Tc releases perforin and granzyme molecules from the granules by exocytosis
  3. perforin molecules insert into the target cell membrane, polymerize, and form transmembrane pores similar to thsoe produced by complement activation
  4. granzymes enter the target cell via the pores. once inside, the proteases degreade cellular contents, stimulating apoptosis
  5. Tc detaches and searches for another prey
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57
Q

steps TH cells use to help in humoral immunity

A
  1. TH cells binds with the self-nonself complexes of a B cell that has encountered its antigen and is displaying it on MHC II on its surface
  2. TH cell releases interleukins as a co-stimulatory signals to complete B cell activation
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58
Q

steps of TH cells in cell-mediated immunity

A
  1. previously activated TH cell binds dendritic cell
  2. TH cell stimulates dendritic cell to express co-stimulatory molecules needed to activate CD8 cell
  3. dendritic cell can now activate CD8 cel with the help of IL2 secreted by TH cell
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59
Q

steps to the activation of T cells

A
  • dendritic cells engulfs an exogenous antigen, processes it,, and displays its fragments on class II MHC protein
  • immunocompetent CD4 cell recognizes antigen-MHC complex. both T-Cell Receptor and CD4 protein bind to antigen-MHC complex
  • CD4 cells are activated, proliferate, and become memory and effector cells
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60
Q
  • fixes complement, often first produced
  • powerful agglutinogen
A

IgM

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61
Q

secreted into tears and colostrum, protects body surfaces

A

IgA

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62
Q

binding site on B-cells

A

IgD

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63
Q

activates complement, found in plasma

A

IgG

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64
Q

binds to mast cells and basophils, stimulates inflammation

A

IgE

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65
Q

types of active immunity

A
  • naturally acquired
  • artificially acquired
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66
Q

types of passive immunity

A
  • naturally acquired
  • artificially acquired
67
Q

types of humoral immunity

A
  • active
  • passive
68
Q

immunity that comes from infection; contact w/ pathogen

A

naturally acquired active immunity

69
Q

acquired from vaccines; dead or attenuated pathogens

A

artificially acquired active immunity

70
Q

comes from antibiodies passed from mother to fetus via placenta; or to infant in her milk

A

naturally acquired passive immunity

71
Q

acquired from injection of immune serum (gamma globulin)

A

artificially acquired passive immunity

72
Q

why can B-cells act as APCs

A

their receptors are antibodies

73
Q
  • dendritic cells, macrophages, activated B lymphocytes
  • engulf antigens and produce fragments on their surface attached to MHC complexes
A

antigen presenting cells

74
Q
  • spontaneous activation
  • stabilizing factors B, D, and P
  • no inhibitors on pathogen surface
A

alternative complement pathway

75
Q
  • secreted by macrophages and neutrophils exposed to foreign substances
  • stimulates the hypothalamus to make prostaglandin E
A

pyrogens (IL1)

76
Q

what is the role of prostaglandin E

A

raises the set point for the body’s internal temperature

77
Q

how do NSAIDs reduce fever

A

by inhibiting PGE synthesis

78
Q

benefits of fever/pyrexia

A
  • promotes interferon activity
  • elevate metabolic rate to promote healing
  • inhibit reproduction of pathogens
79
Q

anything above what internal temperature will cause delirium and higher temperature cause irreversible damage

A

105

80
Q
  • found in macrophages, B cells, and monocytes
  • processed antigens will cause costimulation to occur
A

MHC II

81
Q

found in nucleated cells, causes red flag to be raised if they display a foreign antigen

A

MHC I

82
Q
  • displayed by all body cells, usually by MHC I complexes
A

self antigens

83
Q
  • region on the surface of an antigen that is immunogenic
  • simple antigens may have only one or two of these
  • more complex ones may have hundreds that bind and activate different types of antibody
A

antigenic determinants/epitopes

84
Q

usually polymers that are not deemed reactive by the body

A

implants

85
Q
  • both immunogenic and reactive
  • viruses, bacteria, fungi, etc
A

complete antigens

86
Q

haptens, pet dander, poison ivy, cosmetics, perfumes

A

haptens

87
Q

reactive, but not immunogenic so they only cause a reaction if they bind to other proteins in our body

A

haptens

88
Q
  • any molecule that triggers an immune response
  • usually have a fairly high molecular weight
  • complex molecules that are unique to individuals (proteins, polysaccharides, glycoproteins, glycolipids)
  • body usually only attacks “non-self”
A

antigens

Ag, antigen generating

89
Q
  • antigen-specific
  • systemic
  • memory
  • two major components: humoral and cell-mediated immunity
A

adaptive response

90
Q

which lymphocytes are responsible for humoral immunity

A

b cells

91
Q

which lymphocytes are responsible for cell-mediated immunity

A

T cells

92
Q

produced from lymphoblast precursors in red bone marrow

A

lymphocytes

93
Q

reach maturity in the bone marrow before being released

A

B cells

94
Q

immature T-cells migrate where before maturation

A

thymus

95
Q
  • created in red bone marrow, but soon leave
  • mature in thymus gland–undergo positive and negative selection
  • after selection they colonize lymphatic tissue and organs everywhere in the body
A

T-cells

96
Q

if they do not react to foreign antigens or if they DO react to self antigens they are culled from the population

A

negative selection

97
Q

if they react to foreign antigen, but not to self antigen

A

positive selection

98
Q
  • mature in bone marrow
  • undergo a similar type of seletion as T cells
  • once they are mature they colonize many of the same tissues as T cells
A

B cells

99
Q

overall goal of any cell that acts as an APC

A

interact the antigen and then stimulate the two arms of the specific immune response

100
Q

true or false:

T cells can detect antigens on their own

A

false

101
Q

the process wherein the MHC II complex of an APC binds with a helper T cell and this stimulaates the release of cytokines between the two cells which causes the helper T cells to either:
* proliferate and produce more helper T cells
* stimulate B or T cells

A

costimulation

102
Q
  • most effective agianst intracellular microorganisms such as viruses, fungi, bacteria, and parasites
  • activation regulated by antigen-presenting cells and helper T-cells
A

T-cells

103
Q

types of T cells

A
  • cytotoxic
  • helper
  • memory
104
Q

killer, CD8, or T8 t-cells

A

cytotoxic T cells

105
Q

CD4 T-cells, activate CD8 cells and also stimulate antibody mechanisms

A

helper T cells

106
Q

come from cytotoxic cells and remember the pathogens

A

memory T cells

107
Q
  • have receptors on their surface for an antigen
  • when they are challenged by an antigen, activates specific receptors and begins stimulating them to divide
A

naive B cells

108
Q

rapidly creates plasma cells and memory cells

A

clonal selection of B cells

109
Q

secrete antibodies at rates up to 2000/s for 4-7 days

A

plasma cells

110
Q

long lived and retain the imprint of the antigen so they can respond almost immediately to future attacks

A

memory cells

111
Q

effects of antibodies

A
  • neutralization
  • agglutination
  • precipitation
  • complement
112
Q

antibody can bind directly to the antigenic determinant and interfere with or deactivate the antigen

A

neutralization

113
Q

antibody can combine with the antigenic determinants on two antigens rendering them ineffective adn making them more susceptible to phagocytosis

A

agglutination

114
Q

small water soluble antigens are settled out of solution and are then engulfed

A

precipitation

115
Q

antibodies can activate the complement cascade, and release factors which induce the inflammatory response and cell lysis

A

complement

116
Q

variable regions of the antibody

A

heavy and light chains

117
Q

regions of the antibody that bind and activate the complement

A

constant regions

118
Q

what are B cells most effective against

A

extracellular bacteria, parasites, and viruses

119
Q

B cells respond to invasion by producing antibodies that are specialized globulins known as

A

immunoglobulins (Ig)

120
Q

antibodies are injected from another source

A

passive immunity

w

121
Q

individuals will produce their own antibodies

A

active immunity

122
Q

individual is exposed and develops antibodies and memory cells

A

active natural immunity

123
Q
  • vaccination; antigen is introduced in altered form
  • memory cells formed
A

active artificial immunity

124
Q
  • passed from mother to newborn through placenta/milk (IgA)
  • effects wear off in a few months as the child’s own immune develops
A

passive natural immunity

125
Q
  • antibodies taken from another source are given via a vaccination
  • quick fix as body will produce no antibodies naturally
A

passive artificial immunity

126
Q

steps to fever onset

A
  • hypothalamic thermmostat is reset to higher set point
  • onset: body temp rises
  • stadium: body temp oscillates around new set point
  • infection ends, set point returns to normal
  • defervescence: body temp returns to normal
127
Q

steps to lymphocyte maturation

A
  1. lymphocytes destined to become T cells migrate (in blood) to the thymus and develop immunocompetence there. b cells develop immunocompetence in red bone marrow
  2. immunocompetent but still naive lymphocytes leave the thymus and bone marrow. “seed” the lymph nodes, spleen, and other lymphoid tissues where they encounter their antigen
  3. antigen-activated immunocompetent lymphocytes (effector cells and memory cells) circulate continuously in the bloodstream and lymph and throughout the lymphoid organs of the body
128
Q

steps to endogenous protein processing and display

A
  1. endogenous antigen is degraded by protease
  2. endogenous antigen peptides enter ER via a transport protein
  3. endogenous antigen peptide is loaded onto class I MHC protein
  4. loaded MHC protein migrates in vesicle to the plasma membrane, whete it displays the antigenic peptid
129
Q

steps to exogenous protein processing and display

A

1a. class II MHC synthesized in ER
1b. extracellular antigen is phagocytized
2a. class II MHC is exported from ER in vesicle
2b. phagolysosome degrades antigen
3. vesicle fuses with phagolysosome, invariant chain is removed, and antigen is loaded
4. vesicle with loaded MHC migrates to the plasma membrane

130
Q

MHC II display can cause

A

costimulation

131
Q

fluid containing clotting factors and antibodies

A

exudate

132
Q
  • a lipid-based chemical messenger synthesized by most tissue cells; acts locally as a paracrine
  • produced from arachidonic acid
A

prostaglandins

133
Q

vasodilation of local arterioles cause

A

local hyperemia

134
Q

increased blood flow due to vasodilation of blood vessels entering the injured area

A

hyperemia

135
Q

which minerals needed for bacterial reproduction do both the liver and spleen sequester during a fever

A

iron and zinc

136
Q

when collagen fibers are laid down to a wall of a sac of pus, what structure is formed

A

abscess

137
Q

mechanism of complement proteins

A

foorming pores in the membranes of target cells

138
Q

function of neutrophils

A

phagocytes, will migrate to the site of an infection within a few hours

139
Q

fever inducing molecules are secreted by leukocytes and macrophages

A

pyrogens

140
Q

which defense cells are common antigen presenting cells (APCs)

A

macrophages

141
Q

caused by excess tissue fluid in the injured area; helps to dilute harmful substances and brings in excess oxygen

A

edema

142
Q

nonspecific defense cels specialize in attack cancer cells and virus-infected cells

A

natural killer cells

143
Q

enzyme in saliva and lacrimal fluids that destroys bacteria

A

lysozyme

144
Q

a process of coating a pathogen to enhance phagocytosis

A

opsonization

145
Q

fluid that seeps from the capillary contains clotting factors and antibodies during inflammation

A

exudate

146
Q

when a localized area exhibits increased capillary filtration, hyperemia, and swelling, it is indication that

A

inflammation is occurring

147
Q

an increase in the number of white blood cells that are in circulation

A

leukocytosis

148
Q

process in which neutrophils squeeze through walls of capillaries into the tissues

A

diapedesis

149
Q

a person may harbor pathogens walled off in … for years without displaying any symptoms

A

granulomas

150
Q

first line of defense against pathogens

A

skin and mucous membranes

151
Q

which of the following is the most specific internal defense against disease

a. inflammation
b. NK cells
c. T cells
d. phagocytes

A

T cells

T cells are a part of the adaptive (specific) defenses against disease. They are involved in cell-mediated immunity as they defend the body against specific pathogens.

152
Q

brings more leukocytes to the site of infection

A

inflammation

152
Q

true or false:

virus-infected cells secrete interferons to “warn” other cells of the presence of virus and these other cells and inhibit viral replication

A

true

153
Q

role of interferons in defense against disease

A

protects cells that have not yet been infected by viruses

154
Q
  • requires that circulating antibodies are bound to antigens
  • an example of overlap between innate and adaptive immune function
  • will result in enhanced inflammation, opsonization as well as formation of MAC proteins
A

classical activation of complement system

155
Q
  • sets the stage for repair processes
  • prevents the spread of injurious agents to nearby tissue
  • disposes of cellular debris and pathologies
A

functions of the inflammatory process

156
Q

redness and heat of an inflamed area are due to local hyperemia caused by

A

vasodilation

157
Q

unless they are attached to protein carriers, haptens have … but not …

A

reactivity but not immunogenicity

158
Q

how do vaccines work

A

by priming the adaptive immunity with a relatively harmless primary exposure

artificially acquired active immunity

159
Q

results when naive lymphocytes are activated

A

primary response

160
Q

result of activating memory cells

A

secondary response

161
Q

A class I MHC protein presents an antigen. What type of cell is likely presenting and to what type of cell would it be presented?

A

Any nucleated cell would present antigens to a CD8 cell.

162
Q

Which lymphocytes act as the bridge between the cellular and humoral responses?

A

helper T cells

163
Q

What types of antigen do mature T cells normally not recognize?

A

self antigens

A+P 2 (21 decks)

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