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anatomy and physiology > test 11 immune systems test > Flashcards

test 11 immune systems test Flashcards

1
Q

what are antibodies

A

small y-shaped proteins

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2
Q

antibodies are the same i ___- except

A

sam in structure except the two tips of y, which have heavily variable structures

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3
Q

the tips of the y have nearly

A

nearly infinite shapes and can recongnzie practically every molecule

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4
Q

the stem of the y is called he

A

Fc region

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5
Q

the branches of the y are called

A

the Fab regions

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6
Q

pathogens are broken down by phagocytes into

A

shreds called antigens

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7
Q

antigens are sensed by

A

antigen binding sites on antibodies

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8
Q

what are antibodies also called

A

immunoglobulins (Ig)

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9
Q

the five types of immunoglobulins

A

IgG, IgM, IgD, IgA, IgE

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10
Q

the most common type of immunoglobulin

A

igG

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11
Q

what are B cells

A

a specific type of white blood cells

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12
Q

what is the primary purpose of B cells

A

is to create antibodies

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13
Q

Each B cell creates just

A

just one specific antibody through V(D)J recombination

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14
Q

what happens once a B cell’s antibody has recognized a pathogen and “treated” the body

A

the B cell turns into a memory B cell

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15
Q

where to memory B cells go

A

travels to a lymph node and lies dormant until the next time that same antigen is spotted

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16
Q

what happens the next time the same antigen is spotted

A

the dormant cell rapidly creates antibodies, faster than the last time the body saw this antigen

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17
Q

the same time the antigen is spotted the body is

A

the body is quickly cured (often even before you feel sick)

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18
Q

B cells thing is the principle in which

A

vaccination works

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19
Q

what are T cells

A

another type of white blood cells

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20
Q

T cells are produced by

A

the thymus

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21
Q

why are T cells called T cells

A

because they are produced by the thymus

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22
Q

where is the thymus

A

just superior to the heart

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23
Q

like B cells, T cells are also

A

antigen specific

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24
Q

T cells have special receptors on their membranes called

A

TCRs

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25
Q

TCRs

A

T cell receptors

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26
Q

what do TCRs do

A

look for digested pieces of stuff that macrophages and dendritic cells have broken apart in phagocytosis

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27
Q

if the digested stuff found by the T cells is bad…

A

the T cell will trigger some events from the different types of T cells

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28
Q

Some T cells are

A

cytotoxic T cells, helper T cell, regulatory T cells

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29
Q

what will cytotoxic T cells do when triggered

A

they will hunt down and kill cells that contain a certain antigen

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30
Q

what will helper T cells do when triggered

A

begin producing cytokines that will attract B cells, cytotoxic T cells and macrophages and cause white blood cells hematopoiesis

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31
Q

what will regulatory T cells do when triggered

A

shit down other T cells at the end of a immune response

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32
Q

each antigen has smaller regions called

A

epitopes

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33
Q

epitopes can be recongnized by what

A

the variable sequence, or paratope of antibodies can recognize

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34
Q

do most pathogens have many epitopes

A

yes

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35
Q

why do most pathogens have many epitopes

A

so they can recognized by many antibodies

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36
Q

what is the primary purpose of antibody binding

A

to promote opsonization

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37
Q

what are the 4 ** other mechanisms that help fight pathogens

A
  • neutralization
  • agglutination
  • precipitation
  • complement activation
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38
Q

the Fab region (s) of an antibody bind to

A

the antigen

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39
Q

what happens after the Fab region (s) of an antibody binds to the antigen

A

the Fc region dangles off

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40
Q

many phagocytes have special receptors called

A

opsonin receptors

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41
Q

what do opsonin receptors do

A

increases the chemical attraction between themselves and dangling Fc regions

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42
Q

opsonization makes marked antigens

A

more “delicious-looking” to phagocytes

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43
Q

what is neutralization

A

refers to when an antibody physically blocks the antigen from having its effect

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44
Q

one example of antibody neutralization

A

is bacterium corynebacterium diphtheriae

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45
Q

what does bacterium corynebacterium diphtheriae do

A

secrets a small protein called diphtheria toxin

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46
Q

the diphtheria toxin can

A

enter cells and break the eEF-2 protein

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47
Q

what is the eEF-2 protein

A

a vital part of protein synthesis in human cells

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48
Q

diphtheria toxin is

A

an antigen that has an antibody

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49
Q

what the antibody for diphtheria do

A

blocks diphtheria toxin from binding to receptors and entering the cell

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50
Q

the antibody for diphtheria causes eEF-2

A

it is never turned off, meaning that the immune system is neutralized by antibodies

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51
Q

what is agglutination

A

the clumping together of molcules

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52
Q

some antibodies will cause bacteria to

A

to stick together in large groups

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53
Q

what can agglutination do

A
  • antibodies can cause microbes to stick together

- makes it easier for phagocytes to engulf them

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54
Q

agglutination plays a major role in

A

blood types

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55
Q

types of blood people can have

A

type A, B, AB , O

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56
Q

what does type A blood have

A

have A antigen of RBCs and b antibody in blood

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57
Q

what does type B blood have

A

have B antigen of RMCs and A antibody in blood

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58
Q

what does type AB blood have

A

have A and B antigen on RBCs and no antibodies in blood

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59
Q

what does type O blood

A

have neither A nor B antigen on RBCs, both antibodies in blood

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60
Q

what happens if a person gains a transfusion of blood with an antigen they have antibodies for

A

the antibodies will cause RBCs to agglutinate and then lyse

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61
Q

what happens when RBCs agglutinate and then lyse

A

free hemoglobin clogs the kidneys and makes them shut down

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62
Q

some antigens, usually ____ are soluble

A

usually harmful pieces of virus, are soluble

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63
Q

what can soluble antigens do

A

“hide” across the body by dissolving in serum

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64
Q

antibodies can bind to soluble antigens and

A

force them out of solution and cause them to form a solid precipitate

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65
Q

when antibodies cause soluble antigens to form a solid precipitate

A

makes the antigens easier targets for phagocytosis

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66
Q

in order for precipitation to work you need

A

roughly equal parts of antigens and antibodies are required for this to work

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67
Q

precipitation is often coupled with

A

coupled agglutination

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68
Q

complement pathway

A

a shared component of the innate and adaptive immune system

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69
Q

complement pathway can be turned off and on using

A

by the presence of PAMPs or by a signal from antigen-antibody complexes

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70
Q

in short, cytokines released because of ________

A

because of PAMPSor antigen-antibody complexes will leads to a cascade

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71
Q

cytokines released because of PAMPS or antigen-antibodies will lead to what cascade

A

a cascade that makes many different proteins together and forms a giant pore in a pathogen’s membrane, killing it

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72
Q

what are autoimmune diseases

A

a broad class of diseases where the body attacks itself

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73
Q

what happens when there is an autoimmune disease

A

antibodies in the body mistake “self” cells for “nonself” cells and begins attacking them

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74
Q

autoimmune disease usually causes one of which 3 thing

A
  • tissue damage
  • increased tissue growth
  • altered tissue function
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75
Q

the immune responses

A

primary and secondary

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76
Q

primary immune response

A

the first time the body sees an infection and it takes a while to “gather the troops”

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77
Q

secondary immune response

A

each subsequent response, it happens much faster and much stronger

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78
Q

what do vaccines do

A

expose the body to PAthogen without getting you sick

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79
Q

to do a vaccine a bacterium or virus has to be specially prepared by …

A

attenuated
killed/inactivated
subunit

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80
Q

attenuated vaccination

A

bacterium/virus is alive, but has been genetically modified in such a way that its “bad” genes have been removed

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81
Q

killed/inactivated vaccination

A

bacterium/virus is grow in the la and then killed by adding heat or formaldehyde. dead specimens are injected

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82
Q

subunit vaccination

A

bacterium/virus is grown in lab. only one part )is placed into vaccine and injected

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83
Q

which parts are usually injected in subunit vaccination

A

(usually a capsid in . viruses and a membrane or wall component in bacteria- just a single epitope

84
Q

examples of attenuated vaccines

A

MMR,Measles, Mumps, Rubella

85
Q

Pros of attenuanted vaccines

A
  • only a small dose
  • no booster required
  • gives strongest immunity
86
Q

cons of attenuated vaccine

A
  • must be refrigerated
  • miniscule risk of mutation to regain pathogenicity
  • may cause adverse reaction
87
Q

examples of killed/inactivated vaccines

A

polio

88
Q

pros of killed/inactivated vaccine

A
  • no risk of mutation to regain pathogenicity

- does not need to be refrigerated

89
Q

cons of killed/inactivated vaccines

A
  • much larger doses required
  • often needs “booster” shots
  • may cause adverse reaction (less likely than attenuated”
90
Q

subunit vaccine example

A

Heb B

91
Q

pros of subunit vaccine

A
  • no risk of mutation to regain pathogenicity
  • does not need to be refrigerated
  • not likely to overwhelm immune system and cause adverse reaction
92
Q

cons of subunit vaccine

A
  • gives weakest immunity because only one or a few epitopes recognized
  • much larger doses required
  • often requires boosters
93
Q

which is the only disease we’ve eradicated

A

smallpox

94
Q

vaccines also provide what

A

active immunity

95
Q

what s active immunity

A

vaccines cause you body to make memory B cells that recognize antigens and spring into action the next time you encounter them

96
Q

active immunity generally lasts

A

for life

97
Q

other medical treatments are designed around

A

passive immunity

98
Q

when is passive immunity

A

used in time-sensitive cases or when a patient has a weak immune system already

99
Q

examples of time sensitive cases

A

snakebites, tetanus

100
Q

what is passive immunity

A

involves inject neutralizing antibodies, harvested from a different host, into the patient

101
Q

passive immunity lasts…

A

days to months and is temporary

102
Q

the four types of immunity

A

active neutral, passive neutral, active artificial , passive artificial

103
Q

active neutral immunity

A

patient catches the disease, develops his/her own antibodies, and builds up memory B cells that will fight it the next time

104
Q

passive neutral immunity

A

infant patient drinks breastmilk receives mother’s antibodies, had temporary protection from many diseases

105
Q

active artificial

A

patient receives a vaccination of a attenuated or dead vaccine or a subunit, gains memory B cells without actually fighting

106
Q

passive artificial

A

patient receives injection of antibodies from donor organisms (horses,pigs) that neutralize antigens and give temporary immunity

107
Q

body’s main defense can be broken into what 2 parts

A

innate immune response, adaptive immune response

108
Q

innate immune response is

A

nonspecific had 2 parts

109
Q

2 parts of innate immune system

A
  • physical/chemical barriers to keep contaminants out

- responses like macrophages, inflammation, fever to keep microbes at bay

110
Q

adaptive immune response

A

how the body learns to specifically target and eliminate contaminants

111
Q

95% of infections

A

begin on the mucous membranes

112
Q

5% of infections

A

result from vector bites

113
Q

what does the skin normally act like

A

a solid barrier that stops bacteria from getting inside the body

114
Q

the outer layer of the skin is

A

coated in keratin

115
Q

what does keratin do in the skin

A

works with other lipids and proteins to form a tight seal, separating inside from out

116
Q

the outer cells of the skin are

A

continuously shedding and taking attached microbes with them

117
Q

what does the skin secrete

A

waxy,oily substance called sebum

118
Q

sebum gives the skin what pH

A

roughly 5.5, acidic compared to body pH

119
Q

body/ bloodstream pH

A

7.4

120
Q

the change in pH from sebum can

A

denature enzymes in bacteria, slowing their function

121
Q

aside from the skin, where else does the body use pH to denature bacterial enzyes

A

saliva, stomach, vagina,

122
Q

pH saliva

A

roughly neutral** check it

123
Q

pH stomach

A

varying pH of 2 after a meal, 3.5 closer to rest

124
Q

pH vagina

A

resting pH of 4

125
Q

what are some other physical barriers to keep microbes out

A

mucus, urination, defecatation, vomiting, tears, hairs, cilia

126
Q

where is mucus found

A

airway, esophagus, stomach, intestines, cervix in females

127
Q

what does mucus do to help be a physical barrier

A

microbes stick to it and are broken down by proteins and or expelled from the body

128
Q

what does urination, defecatation, vomiting and tears do

A

all wash microbes out of the body

129
Q

hairs in the ____ and cilia in the ___ stop

A

nose, windpipe, stop microbes from entering the lungs

130
Q

how does hair and bacteria stop cilia from entering the lungs

A

bacteria are pushed up and away from the lungs through the mucociliary elevator. extremely sensitive nerves in the air way ill force a cough reflex if a particle is detected

131
Q

lysozyme is found where

A

in tears, mucus , breast milk, saliva

132
Q

lysozyme break down what

A

peptidoglycan into smaller subunits, effectively killing the bacteria

133
Q

what is peptidoglycan

A

main component of bacteria cell walls

134
Q

the human body has many

A

bacteria living on it in mutualistic relationship

135
Q

bacteria living on humans in a mutualistic relation

A

collectively called normal flora

136
Q

what are some benefits that bacteria can cause for the body

A
  • create nutrients that the body can’t normally provide
  • competition for space and nutrients, making it hard for bad bacteria to thrive
  • creaet compounds that kill other bacteria
  • modify the pH of an area to make it inhospitable to other bacteria
137
Q

example of nutrients created by bacteria the body can’t normally provide

A

B12

138
Q

the human body has about how many human cells

A

10^13

139
Q

the human body has about how much bacteria

A

10^14

140
Q

phagocytes

A

white blood cells that eat and destroy foreign contaminants in phagocytosis

141
Q

types of phagocytes

A

neutrophils, dendritic cells, macrophages

142
Q

neutrophils

A

eat bacteria

143
Q

macrophages

A

eat everything that dosen’t have proper ID

144
Q

dendritic cells

A

eat surroundings that show PAMPs

145
Q

macrophages and dendritic cells

A

present digested gut sto surrounding cells, ecspecially T cells

146
Q

steps of phagocytosis 1-3

A
  1. chemotaxis and adherence of microbe to phagocyte
  2. ingestion of microbe by phagocyte
  3. formation of a phagosome
147
Q

steps of phagocytosis 4-7

A
  1. fusion of the phagosome with a lysosome to form phagolysosome
  2. digestion of ingested microbes by enzymes
  3. waste created with indigestible material
  4. digest waste materials
148
Q

the immune system looks for

A

certain microbe-associated patterns

149
Q

what patterns do the immune system look for

A

PAMPS

150
Q

PAMPs

A

pattern-associated molecular patterns

151
Q

examples of PAMPs

A 
peptidoglycan
LPS
Flagellin
Double-Stranded RNA
Glucans
152
Q

what is peptidoglycan (as a PAMP)

A

the main bacterial cell wall component

153
Q

why is peptidoglycan a special chemical

A

it surrounds the membranes of bacteria

154
Q

what is LPS

A

the main bacteria membrane component

155
Q

LPS

A

lipopolysaccharides

156
Q

LPS are long chains of..

A

sugars that attach to membranes of bacteria that have a thin peptidoglycan layers

157
Q

what is flagellin

A

a protein in bacteria flagella

158
Q

many bacteria indeed have

A

flagellum or multiple flagella

159
Q

what does flagellum do

A

help them move through the body

160
Q

the main protein in flagellum

A

flagellin, which is also recognized as a PAMP

161
Q

glucans

A

the major component of fungal cell walls

162
Q

PRRs

A

pattern recognition receptors

163
Q

what are PRRs

A

proteins found on the plasma membranes of macropahes

164
Q

what is the job or PRRs

A

to recognize PAMPS

165
Q

two main types of PRRs

A

phagocytosis receptors, TLRs

166
Q

phagocytosis receptors

A

PAMP binding that leads to the onset of phagocytosis

167
Q

phagocytosis receptors are only found

A

in pagocytes

168
Q

TLRs

A

Toll-like receptors

169
Q

toll-like receptors are

A

PAMP binding that leads to the activation of genes coding for cytokines

170
Q

what are cytokines

A

signalling proteins

171
Q

where are TLRs found

A

phagocytes, epithelial cells, and more

172
Q

are there many kinds of TLRs that each recognize specific microbial components yes

A

yes

173
Q

each TLR triggers

A

some release of cytokines that cause many things to happen

174
Q

cytokines are small______ produced by ____

A

proteins produced by white blood cells

175
Q

cytokines could be

A

autocrine, paracrine, endocrine

176
Q

autocrine cytokines

A

act on the blood cell that secretes them

177
Q

paracrine cytokines

A

act on nearby cells

178
Q

endocrine cytokines

A

travel long distances in the body

179
Q

cytokines can cause what different things to happen

A
  • vasodilation of blood vessels
  • up-regulation or down regulation of genes
  • white blood cell hematopoiesis
  • production of antibodies
  • apoptosis
  • inhibition of viral replication
180
Q

on important type of cytokines

A

chemokines

181
Q

what do chemokines do

A

attract molecules through chemical signals

182
Q

two main categories of chemokines

A

homeostatic , inflammatory

183
Q

homeostatic chemokines

A

attract various types of white blood cells to the area and invoke diapedesis

184
Q

what is diapedesis

A

jumping through the walls of a vessel into the infected tissue

185
Q

white blood cells are chemically attracted to

A

homeostatic chemokines

186
Q

inflammatory chemokines

A

initiate the inflammatory response by causing vasodilation, leading to more blood and red blood cells in the area

187
Q

inflammation can be

A

acute (quick onset) or chronic (long term)

188
Q

signs of inflammation

A

redness, heat, swelling, pain

189
Q

why are cytokines usually created

A

to recruit WBCs, which release more cytokines that recruit more WBCs in a positive feedback loop

190
Q

the body is supposed to keep the cytokine feedback loop

A

localized and shut it off at a certain point

191
Q

what happens if an infection gets too big

A

the body dosen’t shut down cytokines.. leading to a cytokine storm

192
Q

the result of a cytokine storm

A

widespread inflammation

193
Q

what can widespread inflammation lead to

A

ARDS

194
Q

what is ARDS

A

acute respiratory distress syndrome

195
Q

ARDS can lead to

A

death

196
Q

cytokine storms can also cause

A

damage to blood vessels when they dilate too much and for too long

197
Q

the damage of blood vessels in a cytokines storm can lead to

A

blood spilling in the extracellular space

198
Q

blood spilling in the extracellular space can cause

A

reddish splotches on the skin, and it will also lead to decreased oxygen levels which may lead to shock

199
Q

sepsis

A

when chemicals released into the bloodstream to fight infection trigger inflammatory responses throughout the body

200
Q

fevers are invoke by

A

pyrogens

201
Q

pyrogens can be classified as

A

endogenous or exogenous

202
Q

exogenous pyrogens

A

like LPS, come from outside and bind to PRRs, to trigger the release of endogenous pyrogens

203
Q

endogenous pyrogens

A

like interleukin-1 (IL-1) and (IL-) , are cytokines made by macropages in response to exogenous pyrogens

204
Q

where do endogenous pyrogens travel to

A

the hypothalamus in brain, which sends hormone signals across the body to increase temperature

205
Q

fevers help with

A
  • stop bacteria growth by denaturing

- increase the ability of certain macrophages to do their jobs by altering the membrane fluidity

anatomy and physiology (25 decks)

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