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biology module 4 > disease and immunity > Flashcards

disease and immunity Flashcards

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1
Q

what causes communicable disease

A

pathogens

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2
Q

what are pathogens

A

infective organisms

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3
Q

what are the 4 types of pathogens

A

bacteria, virus, fungi, Protoctista

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4
Q

are bacteria prokaryotes or eukaryotes

A

prokaryotes

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5
Q

bacteria being prokaryotes means that they have - cell structure to -

A

very different, the eukaryotic cells they infect

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6
Q

how do we classify bacteria

A

by their shape or cell wall

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7
Q

what shape is a bacilli bacteria

A

rod

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8
Q

what shape is a cocci bacteria

A

spherical

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9
Q

what shape is a vibrios bacteria

A

comma shaped

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10
Q

what shape is a spirilla bacteria

A

spiral

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11
Q

what shape is a spirochaetes bacteria

A

corkscrew

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12
Q

what do we use to see the cell wall of bacteria

A

gram staining

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13
Q

gram positive bacteria look

A

purple

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14
Q

gram negative bacteria look

A

red

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15
Q

why is gram staining useful

A

it can allow us to tell how the bacteria would react to antibiotics

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16
Q

are viruses living

A

no

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17
Q

viruses are bigger/smaller than bacteria

A

smaller

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18
Q

once viruses invade living cells, what do they do?

A

take over the biochemistry of the host cell to make more viruses

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19
Q

how are viruses successful pathogens

A

they reproduce rapidly and adapt to the environment of their host

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20
Q

what are bacteriophages

A

viruses that attack bacteria

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21
Q

all natural viruses are…

A

pathogens

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22
Q

Protoctista are prokaryotic/eukaryotic

A

eukaryotic

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23
Q

are all Protoctista pathogens

A

no

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24
Q

many protoctista move between hosts through

A

vectors

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25
Q

fungal diseases are typically worse in

A

plants

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26
Q

fungi are prokaryotic/eukaryotic

A

eukaryotic

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27
Q

many fungi are saprophytes meaning that

A

they feed off of dead and decaying matter

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28
Q

what is produced when fungi reproduce

A

spores

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29
Q

which pathogens directly damage their host cells

A

viruses, Protoctista, fungi

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30
Q

which pathogens produce damaging toxins

A

bacteria, fungi

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31
Q

how do viruses damage their host cells

A

they insert their DNA into the host cell’s DNA, then burst out of the cell and destroy it

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32
Q

how do Protoctista damage their host cells

A

they take over cells and break them open, using the cell contents for reproduction

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33
Q

how do fungi directly damage their host cells

A

they digest living cells and break them down for food

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34
Q

how do bacteria damage their host cells

A

they produce poisonous toxins, which either break down cell surface membranes, inactivate enzymes or interfere with genetic material to prevent mitosis

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35
Q

how do fungi indirectly damage their host cells

A

they produce toxins which affect the host cells

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36
Q

direct transmission of pathogens occurs as pathogens

A

move directly from one host to another

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37
Q

the 3 methods of direct transmission of pathogens are

A
  • direct contact
  • inoculation
  • ingestion
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38
Q

what is direct contact (examples)

A

kissing, exchange of bodily fluids, skin to skin contact and microorganisms

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39
Q

what is inoculation (examples)

A

sex, animal bites, shared needles, puncture wounds

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40
Q

what is ingestion (examples)

A

contaminated food or drink, pathogens on the hands

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41
Q

what re the 3 modes of indirect pathogen transmission

A
  • fomites
  • inhalation
  • vectors
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42
Q

what are fomites

A

where the pathogen travels through inanimate objects such as bedding

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43
Q

what is inhalation

A

small droplets of saliva or mucus containing pathogens may be breathed in

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44
Q

what are vectors

A

things which carry pathogens from host to host, such as insects or water

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45
Q

direct transmission of pathogens in plants is where

A

leaves or other plant parts touch

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46
Q

indirect transmission of pathogens in plants is

A

soil contamination or vectors

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47
Q

animal bacteria disease-

A

tuberculosis

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48
Q

what does tuberculosis do

A

destroys lung tissue and suppresses the immune system

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49
Q

how can we prevent tuberculosis

A

vaccines

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50
Q

how can we cure tuberculosis

A

antibiotics

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51
Q

plant bacteria disease-

A

ringrot

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52
Q

what does ringrot do

A

destroys leaves, tubers and fruit of potatoes, tomatoes and aubergines

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53
Q

animal virus disease-

A

HIV

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54
Q

what does HIV do

A

targets t helper cells and destroys the immune system

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55
Q

can we prevent or cure HIV

A

no

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56
Q

plant virus disease-

A

tobacco mosaic virus

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57
Q

what does tobacco mosaic virus do

A

damages leaves, flowers, fruits and stunts growth of plants

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58
Q

plant fungus disease-

A

black sigatoka

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59
Q

what plants get black sigatoka

A

bananas

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60
Q

what does black sigatoka do

A

destroys banana leaves and turns them black

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61
Q

plant protoctista disease-

A

late blight

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62
Q

what cause late blight

A

the protoctista oomycete

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63
Q

what does late blight do

A

destroys leaves, tubers and fruit

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64
Q

animal fungus disease-

A

athlete’s foot

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65
Q

what does athlete’s foot do

A

fungi grow on the moist, warm skin between toes

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66
Q

how can we cure athlete’s foot

A

anti-fungal creams

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67
Q

animal protoctista disease-

A

malaria

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68
Q

what causes malaria

A

a Protoctista called plasmodium

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69
Q

how is malaria spread

A

through the vector of mosquitoes

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70
Q

what does malaria do

A

Protoctista invade the liver, red blood cells and brain

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71
Q

how can we cure malaria

A

we can’t

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72
Q

how do we control malaria

A

by controlling mosquito populations

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73
Q

what are the 2 ways which plants recognise pathogens

A

chemicals are released when the cell wall is attacked, receptors in the cells respond to molecules from the pathogens

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74
Q

what happens when plant cells recognise pathogens

A

genes on the nucleus are switched on, sending alarm signals to unaffected cells and triggering responses

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75
Q

what is a plants physical defence

A
  • callose is synthesised and deposited between cell walls and surface membranes in cells next to the infected ones, and in phloem sieve plates and plasmodesmata; the callose papillae act as barrier to prevent the spread of the infection.
  • Lignin is added to the cell wall, making the barrier thicker
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76
Q

what are the plants chemical defences

A
  • insect repellents
  • insecticides
  • antibitotics, antiseptics, lysosomes
  • antifungal compounds
  • anti-oomycetes
  • general toxins
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77
Q

what are all the human non-specific primary defences

A
  • skin
  • mucous membranes
  • lysozymes in tears and urine and stomach acid
  • expulsive refluxes
  • blood clotting and wound repair
  • inflammatory response
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78
Q

how does our skin protect us

A

it is impermeable to most pathogens, and has a flora of healthy microorganisms to outcompete pathogens, and sebum to inhibit pathogen growth

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79
Q

how do mucous membranes act as a primary defence

A

they line body tracts, and secrete sticky mucus to trap microorganisms, contains phagocytes and lysozymes to destroy bacterial and fungal cell walls

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80
Q

how do lysozymes in tears and urine act as a primary defence

A

destroy bacterial and fungal cell walls

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81
Q

how do expulsive reflexes protect us

A

they expel pathogens

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82
Q

why is blood clotting used as a primary defence

A

it creates a scab so that pathogens can’t enter through wounds

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83
Q

when is blood clotting triggered

A

when platelets come into contact with a broken vessel wall, they adhere to it and secrete substances

84
Q

platelets secrete

A

thromboplastin

85
Q

what does thromboplastin work with

A

ca 2+ ions

86
Q

thromboplastin and ca2+ ions catalyse the

A

conversion of prothrombin into thrombin

87
Q

thrombin catalyses the

A

conversion of fibrinogen into fibrin

88
Q

fibrin forms a

A

mesh over a wound, creating a clot

89
Q

serotonin is secreted by plasma, which has the effect of

A

smooth muscle walls of the blood vessel contracting, so narrowing and reducing blood supply to a cut area

90
Q

what characterises inflammation

A

pain, swelling, redness, heat

91
Q

what is activated in damaged tissue

A

mast cells

92
Q

what is secreted when mast cells are damaged

A

histamines and cytokines

93
Q

what do histamines do in the inflammatory response

A
  • make blood vessels dilate, increasing heat and redness so pathogens can’t reproduce
  • make blood vessels leakier to create more tissue fluid
94
Q

what do cytokines do in the inflammatory response

A

attract phagocytes

95
Q

what is the animal secondary non-specific response

A

phagocytosis, cytokines being released

96
Q

what do cytokines do in the secondary non-specific response

A

the stimulate the hypothalamus to raise body temperature so pathogens can’t reproduce

97
Q

what are the steps of phagocytosis:

A
  • pathogen produces chemicals which attract phagocytes
  • phagocytes recognise non-human proteins on the pathogen
  • the phagocyte engulfs the pathogen and encloses it in a vacuole called the phagosome
  • the phagosome combines with a lysosome to form a phagolysosome
  • enzymes from the lysosome digest the pathogen
98
Q

what attracts phagocytes to pathogens

A

the chemicals pathogens produce

99
Q

how do phagocytes identify pathogens

A

they recognise non human proteins on the pathogen

100
Q

what does a phagocyte do after identifying a pathogen

A

engulf it and encloses it into the phagosome

101
Q

what is a phagaosome

A

a vacuole in the phagocyte which encloses pathogens

102
Q

what happens after a phagosome engulfs a pathogen

A

it combines with a lysosome to form a phagolysosome

103
Q

what is a phagolysosome

A

a phagosome combined with a lysosome

104
Q

what happens after a phagolysosome has formed

A

enzymes from the lysosome digest the pathogen

105
Q

what are phagocytes

A

specialised cells in the blood and tissue which carry out phagocytosis

106
Q

where are phagocytes produced

A

the bone marrow

107
Q

what organelles do phagocytes contain lots of

A

lysosomes, ribosomes and RER

108
Q

phagocytes migrate around the body towards

A

signals from cytokines

109
Q

what are the 3 types of phagocytes

A
  • neutrophils
  • macrophages
  • dendritic cells
110
Q

which types of phagocytes are APCs

A

macrophages, dendritic cells

111
Q

which type of phagocyte is most common

A

neutrophils

112
Q

when do neutrophils join tissue fluid

A

during infections

113
Q

a large number of neutrophils are made during infection, then

A

they die and make up pus

114
Q

what do neutrophils do

A

engulf and digest pathogens

115
Q

what do macrophages do

A

engulf and digest pathogens

116
Q

are neutrophils or macrophages larger

A

macrophages

117
Q

where do we find macrophages

A

in the organs and lymph

118
Q

macrophages are long/ short lived

A

long

119
Q

macrophages can become

A

APCs

120
Q

after digesting a pathogen, macrophages and dendritic cells can combine with

A

antigens from the pathogen surface membrane

121
Q

macrophages and dendritic cells take antigens from the pathogen surface membrane and combine them with

A

special glycoproteins in the cytoplasm called major histocompatibility complex (MHC)

122
Q

what is a major histocompatibility complex

A

special glycoproteins in the cytoplasm which combine with antigens from the pathogen surface membrane

123
Q

what does the MHC do

A

moves the pathogen antigens to the surface membrane of dendritic cells and macrophages to create APCs

124
Q

what do APCs do

A

stimulate other cells from the specific immune response

125
Q

dendritic cells have long processes- what are these

A

arm like structures

126
Q

why do dendritic cells have processes

A

to increase surface area to interact with pathogens

127
Q

where are dendritic cells found

A

entry points such as skin, digestive tract and mucous membranes

128
Q

are dendritic cells APCs

A

yes

129
Q

where do dendritic cells go after phagocytosis

A

lymph nodes

130
Q

phagocytes release cytokines, which here act as

A

cell signalling molecules to attract other phagocytes and trigger the specific immune response

131
Q

what do opsonins do

A

bind to pathogens and tag them to make identifying them easier

132
Q

what is an antigen

A

a molecule on the cell surface membrane which is usually a protein or a glycoprotein

133
Q

which cells have antigens

A

all of them

134
Q

what is another name for antibodies

A

immunoglobulins

135
Q

what shape are antibodies

A

y shaped

136
Q

what molecules are antibodies

A

globular glycoproteins

137
Q

what hold light chains together

A

disulfide bridges

138
Q

which mechanism allows antibodies to bind to antigens

A

lock and key

139
Q

what is the binding site

A

an area of 110 amino acids on the heavy and light chains

140
Q

what do amino acids in the binding site do

A

give antibodies their shape and specificity

141
Q

what is the binding site part of

A

the variable region

142
Q

purpose of the hinge region

A

provide the molecule with flexibility and allow it to bind to 2 separate pathogens

143
Q

an antibody in an antibody-antigen complex acts as

A

an opsonin

144
Q

can pathogens invade host cells when part of an antibody-antigen complex

A

no

145
Q

antibodies act as -, clumping pathogens together

A

agglutinins

146
Q

antibodies act as antitoxins, meaning that

A

they neutralise toxins produced by pathogens

147
Q

why are secondary responses so much fastere

A

T memory cells

148
Q

in humoral immunity, the body responds to pathogens found

A

outside of cells

149
Q

humoral immunity step 1

A

a pathogen enters the body and multiplies

150
Q

humoral immunity step 2

A

lymphocytes come into contact with the pathogen in one of 3 ways

  • encountering the pathogen
  • encountering APCs
  • encountering infected cells displaying the antigen of the pathogen
151
Q

3 ways lymphocytes can come into contact with pathigens

A
  • encountering the pathogen
  • encountering APCs
  • encountering infected cells displaying the antigen of the pathogen
152
Q

humoral immunity step 3

A

clonal selection, where correct T and B cells bind with pathogenic antigens

153
Q

humoral immunity step 4

A

clonal expansion or proliferation, when the correct lymphocytes divide rapidly by mitosis

154
Q

humoral immunity step 5

A

the cells differentiate into particular types of B or T cells

155
Q

4 types of T cells

A
  • killer
  • memory
  • helper
  • regulator
156
Q

T killer cells function

A

attack infected host cells

157
Q

T memory cells function

A

stay in the blood for future infections

158
Q

T helper cells function

A

release cytokines to stimulate B cells to divide and stimulate phagocytosis

159
Q

T regulator cells function

A

stop immune response after pathogen is removed and prevent T cells from attacking own tissue

160
Q

what do b cells differentiate into

A
  • plasma cells

- B memory cells

161
Q

plasma cells function

A

blood clotting, make antibodies

162
Q

B memory cells function

A

stay in the blood for future infections

163
Q

in cell-mediated immunity, what respond

A

T lymphocytes

164
Q

in cell-mediated immunity what do T lymphocytes respond to

A

cells of organisms changed in some way

165
Q

examples of in cell-mediated immunity

A

viruses and cancers

166
Q

what do macrophages release

A

monokines

167
Q

what do monokines do

A

attract neutrophils by chemotaxis, stimulate b cells to differentiate and release antibodies

168
Q

what to T cells, B cells and macrophages release

A

interleukins

169
Q

why do T cells, B cells and macrophages release interleukins

A

to stimulate proliferation and differentiation of T and B cells

170
Q

many cells release interferon, which

A

inhibits virus replication and stimulates T killer cells

171
Q

in cell-mediated immunity, macrophages

A

engulf and digest pathogens, then become APCs

172
Q

in cell-mediated immunity, interleukins are released, causing

A

T cells to divide rapidly

173
Q

in cell-mediated immunity, cloned T cells may

A
  • develop into memory cells
  • stimulate phagocytosis
  • stimulate B cells to divide
  • stimulate development of specific T killer cells
174
Q

active natural immunity example

A

being infected

175
Q

passive natural immunity example

A

breastfeeding, antibodies passing across placenta

176
Q

active artificial immunity example

A

vaccination

177
Q

passive artificial immunity example

A

injecting antibodies or antitoxins

178
Q

name 4 autoimmune diseases

A

multiple sclerosis, type 1 diabetes, arthritis, lupus

179
Q

multiple sclerosis tissues affected

A

myelin sheath

180
Q

multiple sclerosis symptoms

A

fatigue, limited mobility, numbness and tingling, muscle spasms

181
Q

multiple sclerosis treatments

A
  • disease-modifying therapies
  • stem cell transplant
  • physiotherapy
182
Q

type 1 diabetes tissue affceted

A

insulin-secreting cells in the pancreas

183
Q

type 1 diabetes symptoms

A

feeling thirsty, sweet-smelling breath, weight loss, cuts don’t heal

184
Q

type 1 diabetes treatments

A

insulin injections, pancreas transplants, immunosuppressant drugs

185
Q

arthritis tissue affected

A

joints

186
Q

arthritis symptoms

A

joint pain, inflammation, restricted movement

187
Q

arthritis treatments

A

anti-inflammatory drugs, steroids, immunosuppressant drugs

188
Q

lupus tissue affected

A

skin and joints, all organs

189
Q

lupus symptoms

A

fatigue, fever, joint pain, butterfly rash

190
Q

lupus treatments

A

anti-inflammatory drugs, steroids, immunosuppressant drugs

191
Q

what are autoimmune diseases

A

where the T regulator cells don’t function well, so white blood cells attack human tissue

192
Q

where do we source medicine (3)

A

computer programmes, plants, microorganisms

193
Q

where is penicillin from

A

mould

194
Q

where is aspirin from

A

willow bark

195
Q

people have different genes, and therefore different

A

enzymes

196
Q

people having different enzymes means

A

they react differently to different medicines

197
Q

by testing someone’s genome, we can see

A

which drugs will be most effective for them

198
Q

what is personalised medicine

A

testing someone’s genome and using it to prescribe them to most effective medicine possible

199
Q

example of personalised medicine

A

Herceptin

200
Q

Herceptin use

A

treat breast cancer

201
Q

why do we use synthetic biology

A

some drugs are too expensive or difficult to mass produce

202
Q

how do we create synthetic drugs

A

genetic engineering to develop bacteria to produce drugs

203
Q

example of microorganism synthetic drugs

A

E.coli can be used to produce a precursor for an antimalarial drug

204
Q

how can mammals be used in synthetic drugs

A

they can be genetically modified to produce drugs in their milk

205
Q

example of mammal synthetic drugs

A

goats can produce human antithrombin used in blood clotting

206
Q

nanotechnology uses

A

tiny synthetic particles to deliver drugs to specific cells

207
Q

when do we use nanotechnology

A

to deliver drugs to kill cancer cells without harming healthy cells

biology module 4 (1 decks)

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