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Anatomy II > Immune System > Flashcards

Immune System Flashcards

1
Q

antigen

A

anything in out body that generates an immune response

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2
Q

pathogens

A

antigens that cause problems for our body

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3
Q

3 levels of immunity (informally)

A
  1. keep things out
  2. isolate thing to specific spot
  3. specifically kill those things
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4
Q

nonspecific immune system

A
  • our immune system going after ANYTHING that is a foreign substance
  • anything that prevents entry of foreign things into the body
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5
Q

innate immunity is another term for…

A

nonspecific immunity

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6
Q

t/f the immune system is an organ system

A

false!

it is a “functional system”

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7
Q

specific immune system

A
  • process of B and T lymphocytes going after only the specific pathogens that they are immunocompetent for
  • slower process
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8
Q

external body membranes are an examples of specific or nonspecific immunity?

A

nonspecific

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9
Q

which immune system is faster? specific or nonspecific

A

nonspecific

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10
Q

adaptive immunity is another term for…

A

specific immune system

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11
Q

superficial nonspecific defenses

A

nonspecific immunity mechanisms that occur outside of body

  • skin
  • mucous membranes
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12
Q

how does skin work in immunity?

A

prevents entry of foreign substances into body

there are layers of dead skin cells on outside of epidermis to help too

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13
Q

why does it matter for immunity that the epithelium (skin) is avascular?

A

that means the foreign substance has to get very deep into the body from skin to get into circulation

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14
Q

when does skin provide an entry path for antigens to get in??

A

when it is broken

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15
Q

what parts of body do mucous membranes cover that are considered “outside” of body?

A

GI tract

reproductive tract in females

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16
Q

how do mucous membranes work in immunity?

A
  • produces mucus
  • is barrier of epithelial tissue
  • may produce lysozyme and enzymes
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17
Q

how does mucus in mucous membranes help in immune response?

A

it can act as a trap

it may have an acidic pH which kills foreign things

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18
Q

skin-acid mantle

A

thin layer on skin that’s acidic, helps kill pathogens

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19
Q

how do digestive enzymes work in immunity?

A

enzymes denature the proteins of a foreign thing to shut it off

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20
Q

almost all internal nonspecific defenses will promote________

A

inflammatory response

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21
Q

internal nonspecific defenses

A
  • phagocytes (macrophages, neutrophils, eosinophils)
  • mast cells
  • natural killer cells
  • inflammation
  • antimicrobial proteins (interferon, complement system)
  • fever
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22
Q

major phagocytes in body

A

macrophages

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23
Q

2 types of macrophages? What does this mean?

A
  • fixed or free

- some in interstitial space, some in lymph, some in reticular bundles

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24
Q

how do neutrophils work as an internal nonspecific defense?

A

these cell don’t become phagocytic until they encounter something foreign

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25
Q

how do eosinophils work as an internal nonspecific defense?

A

they are phagocytic against parasitic worms

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26
Q

mast cells

A

type of internal nonspecific defense

binds, ingests, and destroys bacteria

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27
Q

NK cells are a type of _____

A

T cell

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28
Q

are NK cells specific or nonspecific?

A

nonspecific!

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29
Q

natural killer cells are able to kill _____; they tend to go after _____

A

anything

abnormal body cells

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30
Q

how do NK cells kill cells?

A

lysis

they have lytic chemicals to break cells down

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31
Q

how do lytic chemicals from NK cells break down cells?

A

the chemicals go through cell membranes and break down cell into pieces from the inside

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32
Q

t/f: NK cells do not need to be activated by foreign things to start working

A

true

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33
Q

cardinal signs of inflammation

A

redness
heat
swelling
pain

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34
Q

what causes inflammation?

A

skin’s barrier is broken

body tries to isolate anything that may have gotten into that spot

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35
Q

inflammation attracts _____ cells, which do what?

A

phagocytic cells; dispose of cellular debris and set the stage for repair

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36
Q

antimicrobial proteins

A

interferon

complement system

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37
Q

interferons

A
  • chemical secreted by infected cell that is a signal to start WBC production
  • protects neighboring cells from getting infected by same virus
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38
Q

complement system

A

group of over 20 different proteins floating (inactive) in bloodstream
activated when antigen is present –> causing inflammation and other cells to kill foreign things

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39
Q

what happens when complement system protein is activated

A

inflammation

other cells kill foreign thing

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40
Q

which internal nonspecific defenses are localized?

A 
phagocytes
mast cells
NK cells
inflammation
antimicrobial proteins
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41
Q

which internal nonspecific defenses are systemic?

A

fever

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42
Q

fever

A

elevated body temp

systemic response to infection (retards spread)

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43
Q

general (informal) process of phagocytes

A
  • antigen is surrounded by phagocytic cell
  • phagocyte engulfs antigen and puts it into a little vesicle
  • vesicle binds with another vesicle that contains enzymes
  • enzymes break down antigen
  • cell eliminates waste products
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44
Q

phagocytic mechanism (process)

A
  1. phagocyte recognizes pathogen’s carbohydrate surface marker
    this is enhanced via opsonization
  2. cytoplasmic extensions adhere to pathogen
  3. pathogen pulled inside cell (called phagosome) in vacuole
  4. lysosome binds with phagosome –> forming phagolysosome
  5. lysosomal enzymes digest pathogen
  6. residual body formed and then expelled
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45
Q

opsonization

A

antibodies bind to foreign markers on antigen –> mark it as foreign so macrophages know what to go after

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46
Q

what do macrophages create to adhere to pathogen?

A

cytoplasmic extensions

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47
Q

adhesion/adherence

A

when cytoplasmic extensions created by macrophage adhere to pathogen

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48
Q

name of vacuole that pulls pathogens into macrophage

A

phagosome

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49
Q

what is the waste called which is formed/expelled in phagocytic mechanism

A

residual body

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50
Q

t/f NK mechanism has a relatively long lag time

A

false!

it has no lag time

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51
Q

NK mechanism

A
  1. NK cells detect infected/cancerous cells based on lack of “self” markers or presence of certain sugars
  2. NK cells release perforins
  3. channels appear in target cells and nucleus disintegrates (lysis)
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52
Q

perforins

A 
class of cytolytic chemicals
break cell into pieces
released by NK cells
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53
Q

inflammatory mechanism

A
  1. toll-like receptors (TLRs) on surface of macrophages recognize pathogens
  2. TLRs release cytokines
  3. other cells release other inflammatory mediator chemicals
  4. vessels in injured area dilate and increase permeability
  5. hyperemia occurs
  6. exudate accumulates, causing edema
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54
Q

cytokines

A

“cell chemicals” (inflammatory chemicals)
released by TLRs in inflammatory response
promote inflammation and attract WBCs when they encounter antigen

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55
Q

inflammatory mediator chemicals

A

chemicals released by other cells (not TLRs) which aid in inflammation
ex incl histamines and prostaglandins (signaling molecules)

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56
Q

what stimulates other cells to release inflammatory mediator chemicals in the inflammation response?

A

TLRs

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57
Q

why might vessels leak plasma during the inflammation response?

A

because vessels in injured area increase permeability (and dilate)

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58
Q

hyperemia

A

accumulation of blood

leads to redness and heat

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59
Q

redness and heat are 2 characteristics of inflammation that are caused by what?

A

hyperemia

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60
Q

exudate

A

stuff exiting blood vessel in inflammation bc it is dilated

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61
Q

edema

A

swelling

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62
Q

why does edema cause pain?

A

edema signals nociceptors, which causes pain

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63
Q

swelling and pain are two characteristics of inflammation that are caused by what?

A

edema

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64
Q

advantages of exudate accumulation at site of infection

A
  • brings oxygen and nutrients to help tissue repair (to close breach)
  • brings clotting proteins and antibodies
  • dilutes harmful substances
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65
Q

how do exudates dilute harmful substances?

A

if you have a bunch of antigens clumped together, antigens in the middle are protected and survive (like body guards around celeb)
exudates dilute and separate the substances so they are easier to attack

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66
Q

results of inflammation (9)

A
  • injured cells release leukocytosis-inducing factors
  • causes neutrophil release by red bone marrow
  • loss of fluids slows blood flow locally
  • production of selections on endothelial cells
  • margination occurs
  • neutrophils escape capillaries
  • inflammatory chemicals act as chemotaxic agents
  • monocytes follow neutrophils
  • monocytes become macrophages after leaving capillaries
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67
Q

function of leukocytosis-inducing factors

A

stimulate production of WBCs (especially neutrophils)

promote leukocytosis

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68
Q

leukocytosis

A

abnormally high number of WBCs

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69
Q

how does loss of fluids slow blood flow locally?

A
  • diluted blood vessel allows more blood to accumulate

- as we pull fluid out of that blood, we have more formed elements accumulating, which slow blood flow

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70
Q

selectins

A
  • adhesion molecule specifically for neutrophils
  • product of inflammation
  • found on endothelial cells
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71
Q

margination

A

adherence of neutrophils along wall of blood vessel

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72
Q

how are neutrophils in the exudate?

A

because they escape capillaries

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73
Q

t/f inflammation promotes diapedesis

A

true!

neutrophils escape capillaries

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74
Q

monocytes follow _____

A

neutrophils

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75
Q

t/f more monocytes move to affected area in inflammation because we produce more

A

false!

monocytes are chemotaxically attracted to the area

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76
Q

monocytes become _____ after leaving capillaries

A

macrophages

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77
Q

monocytes produce ______ when they leave the capillaries and become macrophages

A

lytic chemicals (lysozymes)

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78
Q

interferon mechanism

A
  1. cells infected by virus release interferons
  2. IFNs diffuse to nearby cells
  3. PKR protein synthesis is stimulated
  4. PKR interferes with viral replication
  5. IFNs also activate macrophages and NK cells
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79
Q

while a virus-infected cell is dying, it secretes ______ to warn/protect nearby cells

A

interferon

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80
Q

protein that interferes with viral replication, so virus can no longer replicate

A

PKR

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81
Q

why do interferons activate macrophages and NK cells?

A

to kill the virus before it tries to replicate

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82
Q

role of PKR

A

interfere with viral replication

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83
Q

Complement System Mechanism I (Classical)

A
  1. antibodies bind to pathogens (which have been opsonified)
  2. complement proteins bind to antibody-pathogen complexes
  3. lysis, phagocytosis, and inflammation result (to destroy foreign thing)
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84
Q

what do complement proteins bind to in the antibody-pathogen complexes? antibodies or pathogens?

A

antibody

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85
Q

what destroys the antigen in complement system mech I?

A

complement proteins

86
Q

complement system mechanism II (Alternate)

A
  1. complement proteins bind to polysaccharide molecules on pathogens
  2. lysis, phagocytosis, and inflammation result
87
Q

which complement system uses antibodies?

A

mechanism I (classical)

88
Q

in complement system mechanism 2, when do complement proteins activate?

A

when they bind to polysaccharide molecules on pathogens

89
Q

fever mechanism

A
  1. leukocytes and macrophages exposed to pathogens secrete pyrogens
  2. pyrogens cause hypothalamus to raise body temp
90
Q

what part of body determines body temp?

A

hypothalamus

91
Q

pyrogens

A

chemical secreted by leukocytes and macrophages during fever that causes hypothalamus to raise body temp

92
Q

when is it good to take zinc?

A

if you have a viral infection

93
Q

when body temperature increases, that decreases the amount of stores of which minerals?

A

iron and zinc

94
Q

bacteria feed on which minerals to replicate?

A

iron and zinc

95
Q

does fever increase or decrease metabolic activity?

A

increases

96
Q

how do fevers work as immune response?

A
  • increase metabolic activity

- denature enzymes in antigen

97
Q

antigenic properties

A

antigenic determinants
immunogenicity
reactivity

98
Q

antigenic determinants promotes ___________ which promotes __________

A

immunogenicity; reactivity

99
Q

antigenic determinants

A

things on surface of antigen act activate immune system

stimulates specific immune response

100
Q

major histocompatibility complex

A

self markers

101
Q

self antigens

A

marker we produce that tells immune system we belong

not immunogenic to us, so does not activate immune system

102
Q

t/f our own self antigens do not activate our immune system

A

true

103
Q

characteristics of specific immunity

A
  • pathogen specific
  • not immediately active (lag time)
  • systemic
  • provides “memory”
104
Q

what does it mean that specific immunity provides memory?

A

when specific immune cells have been activated, they produce copies of themselves to activate quicker and better if exposed to same thing in the future

105
Q

specific immunity pathways

A

humoral

cell-mediated

106
Q

antibody-mediated response is another term for

A

humoral pathway

107
Q

humoral pathway

A
  • b lymphocytes in body become activated then produce antibodies, which float around in the body via the circulatory system
  • these antibodies are specific to certain antigenic properties
  • antibodies mark antigen for destruction
108
Q

antibodies work for _____ antigenic properties; antigens have ___ antigenic properties on it

A

only one; more than one

109
Q

cell mediated pathway

A
  • when our own body cells are infected/weird –> not saying ‘self’
  • t lymphocytes attack those directly and kill them by lysis
110
Q

all lymphocytes are produced by _______ in ___________

A

stem cells; red bone marrow

111
Q

t/f all lymphocytes are virtually identical when first formed, then differentiate

A

true

112
Q

t cells become immunocompetent where?

A

thymus

113
Q

b cells become immunocompetent where?

A

bone marrow

114
Q

where do immunocompetent cells mature?

A

in secondary lymph organs

115
Q

t/f lymphocytes are fully functional even before they are bound with an antigen

A

false

not fully mature yet

116
Q

why is there a time lag for specific immunity?

A

because the lymphocytes are not fully functional until they are bound to antigen

117
Q

antigen presenting cells (APC)

A

cells that engulf pathogen and present its fragments as antigens
still activate specific immune system even if their markers started out as “self” but got messed up

118
Q

antigen challenge

A

first encounter between a naive immunocompetent lymphocyte and antigen

119
Q

where does antigen challenge usually occur?

A

in secondary lymph tissue or organ

120
Q

naive immunocompetent lymphocyte

A

hasn’t ever encountered anything foreign yet

121
Q

when does primary humoral response happen?

A

the first time we encounter a foreign thing

122
Q

primary humoral response

A
  1. antigens bind with surface receptors on naive immunocompetent B lymphocyte
  2. clonal selection occurs
  3. most clones become plasma cells with produce antibodies
  4. some clone cells become memory cells
123
Q

which lasts longer: antibodies or memory cells?

A

memory cells

124
Q

clonal selection

A

b lymphocyte producing copies of itself by dividing

bc if there is one antigen floating around, there are probably more, so we need more receptors

125
Q

how long do plasma cells last?

A

4-5 days; then they die

126
Q

when does the secondary humoral response occur?

A

when we are exposed to the same antigen for a second time

127
Q

t/f secondary humoral response is the same mechanism as primary?

A

true

128
Q

how is the secondary humoral response different from the primary?

A

secondary response…..

  • is faster
  • lasts longer
  • is more effective
129
Q

why is the secondary humoral response more effective than the first?

A

because it is effectively producing lots of copies

130
Q

sources of humoral immunity

A

active
passive
natural
artificial

131
Q

active immunity

A

(becoming infected)
we produce our own antibodies
foreign substance got inside and we are acting on it

132
Q

passive immunity

A

getting antibodies are did not produce; comes from external source

133
Q

natural active immunity

A

we have been infected and produce antibodies

134
Q

natural passive immunity

A

how mom delivers antibodies to baby through breast milk or placenta

135
Q

artificial active immunity

A

vaccination

given a vaccine to activate production of antibodies by b lymphocytes

136
Q

artificial passive immunity

A

being given a shot of antibodies, injected into our bodies

137
Q

components of antibody structure

A
  • 2 identical heavy chains
  • 2 identical light chains
  • variable region
  • constant region
  • antigen binding site
138
Q

variable region of antibody

A

where light chains and heavy chains overlap

determines what it can bind to (varies)

139
Q

second humoral response is ______ to _______ x higher than primary

A

1000 to 10,000

140
Q

constant region of antibody

A

only heavy chains
always the same
determines how antigen gets destroyed

141
Q

antigen-binding site is determined by _______

A

variable region

142
Q

t/f type of antibody cannot change over course of infection

A

false! it can!

143
Q

monomers IgD, IgG, and IgE each have ___ binding sites

A

2

144
Q

classes of antibodies

A 
IgD
IgG
IgE
IgA
IgM
145
Q

IgD

A

receptors on surface of B lymphocytes

146
Q

IgG

A

most abundant antibody in blood
constant region binds with complement proteins, which destroy antigen
use complement system “classical pathway”
can cross placenta
produced late in primary or early in secondary response

147
Q

IgE

A 
bind to mast cells and basophils
not many in blood (only traces in plasma)
cause release of histamine
evoke inflammation 
activate immune system
activated during allergic reaction
located in mucosae
148
Q

IgA

A

dimer (2 monomers)
4 binding sites
in mucus
binds with antigen, prevents antigen from binding with other body cells

149
Q

IgM

A 
pentamer
10 binding sites
produced during primary response (first)
increased # IGM means recently infected
fix/activate complement protein
agglutination
150
Q

antibody functions

A
  • formation of antigen-antibody complex
  • provide site for binding of complement proteins
  • block sites on pathogens
  • cause clumping of antigen-containing cells
  • cause clumping of soluble antigen molecules
151
Q

neutralization

A

antibody function of blocking sites on pathogen so pathogen cannot bind

152
Q

monoclonal antibodies

A

commercially produced

used to be used in lab, then to treat cancer, now to treat covid patients

153
Q

cell mediated immune response

A
  1. t cell binds with antigen infected body cell
  2. co-stimulatory signals are present
  3. t cell is activated
  4. clones are produced
  5. some clones become memory cells
154
Q

when are co-stimulatory signals released?

A

due to binding of secondary sites

155
Q

t/f both helper t cells and cytotoxic t cells are active as part of specific immunity

A

true!

156
Q

t cell activators

A
  • class I MHC protein-linked antigens

- class II MHC protein-linked antigens

157
Q

endogenous

A

produced by the body/cell itself

158
Q

exogenous

A

produced by something other than own cell

159
Q

are class I MHC protein-linked antigens endogenous or exogenous?

A

endogenous

160
Q

are class II MHC protein-linked antigens endogenous or exogenous?

A

exogenous

161
Q

CD4 cells

A

helper t cells

162
Q

cancerous cells are examples of Class __ MHC protein-linked antigens

A

1

163
Q

bacterial infected macrophages are examples of class __ MHC protein-linked antigens

A

2

164
Q

____ are activated by class II MHC protein-linked antigens

A

CD4 (helper t cells)

165
Q

___ are activated by class I MHC protein-linked antigens

A

CD8 cells (cytotoxic t cells)

166
Q

what do CD8 cells do when activated by class I MHC protein-linked antigens

A

produce copies/memory cells and produce cytolytic chemicals

167
Q

antigen binding

A

t cell antigen receptors bind to antigen-MHC complex

168
Q

secondary binding produces ________

A

co-stimulators

169
Q

co-stimulators

A

t cell binding to other receptors on APC, cytokines, interleukins

170
Q

t/f each co-stimulator produces the same response

A

false! they all promote different response

171
Q

response of co stimulators

A

either facilitates or disables activation

slows down immune system or produces clones

172
Q

cytotoxic t cell functions

A

directly attack/kill our body’s infected cells

secrete lytic chemicals/perforins that cause cell lysis

173
Q

helper t cells

A

regulatory cells
class II
activate cytotoxic t cells to kill infected cells

174
Q

suppressor t cells

A

stops cloning
regulatory
releases chemicals that slow B and T cells from cloning

175
Q

CD8 cells

A

cytotoxic t cells

176
Q

types of immune disorders

A

immunodeficiencies
autoimmune diseases
hypersensitivities

177
Q

immunodeficiencies

A

any condition that causes immune cells to behave abnormally or don’t have enough

178
Q

autoimmune diseases

A

immune system attacks our own body cells

cannot accurately distinguish “self” cells

179
Q

hypersensitivities

A

responses to allergens

harmless to most, but activates immune system for some

180
Q

t/f you can be born with an immunodeficiency or acquire it

A

true

181
Q

severe combined immunodeficiency syndrome (SKIDS)

A

mutation in DNA that attacks lymphocytes, lacking specific immunity
congenital (genetic)

182
Q

AIDS

A

acquire something that kills T lymphocytes

die of another complication bc lacking lymphocytes

183
Q

signs of AIDS

A

lymph node swelling

184
Q

MS is what kind of immune disorder

A

autoimmune disease

185
Q

multiple sclerosis

A

immune cells attack white fiber in brain

lose neural connectivity

186
Q

myasthenia gravis is what kind of immune disorder?

A

autoimmune disease

187
Q

myasthenia gravis

A

immune system attacks neuromuscular junction

inhibits nervous muscle control

188
Q

graves’ disease is what kind of immune disorder?

A

autoimmune disease

189
Q

graves’ disease

A

immune system attacks thyroid gland

produce extra thyroid hormone

190
Q

signs of graves’ disease

A

bulging eyeball

191
Q

juvenile diabetes is what kind of immune disorder?

A

autoimmune disease

192
Q

juvenile diabetes

A

attacks pancreas

don’t produce sufficient insulin

193
Q

lupus is what kind of immune disorder?

A

autoimmune disease

194
Q

lupus

A

attacks tissue in kidneys, heart, lungs, skin

butterfly red marks/wolf bite

195
Q

rheumatoid arthritis is what kind of immune disorder?

A

autoimmune disease

196
Q

rheumatoid arthritis

A

attacks synovial joints

joint deformity, stiffness, pain

197
Q

cause of autoimmune diseases

A

unknown

maybe bacterial infection

198
Q

types of hypersensitivities

A

immediate, subacute, or delayed

199
Q

example of immediate/acute hypersensitivity

A

anaphylaxis

200
Q

immediate/acute hypersensitivity

A

happens within seconds of contact with allergen
first encounter (warning) causes sensitivity, not full blown allergic reaction
second encounter worse
this encounter could die

201
Q

anaphylaxis

A

body floods with histamine –> causes systemic vasodilation
usually get a warning
bp drops then death

202
Q

subacute hypersensitivity

A

a couple hours between exposure and response

203
Q

transfusion reaction is an example of which type of sensitivity?

A

subacute

204
Q

transfusion reaction

A

injected with wrong blood type

eventually… shiver; blue;die

205
Q

what happens when you are given the wrong blood type

A

after a few hours you get the shivers
hours later you turn blue
hours later you die

206
Q

delayed hypersensitivity

A

can take days from exposure to response

207
Q

poison ivy reaction is an example of which type of hypersensitivity

A

delayed

208
Q

t/f transplants have high likelihood of success

A

false

High probability of rejection of transplant because self is different than our self

209
Q

autograft

A

tissue from ourself

rejection risk is low

210
Q

isograft

A

tissue from identical twin, same MHC

rejection risk is low

211
Q

allograft

A

tissue from someone else

lower risk of rejection if you are more closely related to them

212
Q

xenograft

A

tissue from different species
generally rejected
use medication to shut off immune system for the transplant to establish

Anatomy II (17 decks)

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