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biology A-LEVEL > DISEASES AND IMMUNITY: Module 4 > Flashcards

DISEASES AND IMMUNITY: Module 4 Flashcards

1
Q

what is a pathogen

A

an organism which causes diseases

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2
Q

infectious (communicable) diseases

A

caused by pathogens
spread between people, infecting each other

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3
Q

non infectious (non-communicable) diseases

A

are not caused by pathogens
they cannot be spread person to person
usually happen due to genetics or lifestyle

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4
Q

4 types of pathogens

A

bacteria
viruses
protoctists
fungi

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5
Q

2 example of bacterial diseases in humans

A

myobacterium tuberculosis
bacterial meningitis

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6
Q

an example of a bacterial disease affecting plants

A

ring rot

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7
Q

treatment for bacterial disease
and how do they work

A

antibiotics
break down bacterial cell wall (peptidoglycan)

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8
Q

2 viruses affecting humans

A

Human immunodeficiency virus (HIV)
covid-19

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9
Q

virus affecting plant

A

tobacco mosaic virus (TMV)

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10
Q

protoctist disease in humans

A

plasmodium causes malaria

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11
Q

protoctist disease affecting plants

A

blight

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12
Q

fungal disease affecting humans

A

ringworm
athletes foot

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13
Q

fungal diseases affecting plants

A

black sigatoka

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14
Q

ways of transmitting communicable diseases

A

droplet transmission like sneezing
vectors like anopheles mosquitoes
fungal spores in wind

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15
Q

what factors affect transmissions of diseases

A

social factors: HIV underdiagnosed
living conditions: TB spread fast in overcrowding
climate: vectors live in different climates like mosquitoes in warmer ones

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16
Q

how does our body openings (e.g. eyes) act as a defensive barrier

A

cavities lined w mucus membrane
with lysozyme enzymes which kills bacteria by damaging their cell walls making them burst

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17
Q

how does our skin act as a defensive barrier

A

physical barrier preventing pathogens from entering
but when cut or wounded, wound clotted by platelets

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18
Q

how does our breathing system have defensive barriers

A

goblet cells secrete mucus
trapping pathogens
sweeping them by cilia to stomach acid

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19
Q

how does our stomach have defensive barriers

A

stomach acid is acidic
denaturing proteins and killing pathogens

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20
Q

how does our intestines have defense mechanisms

A

has its own helpful and harmless bacteria
which compete with other pathogens

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21
Q

how does inflammation help as a non specific response

A

damaged tissues triggers release of histamines
vasodilation happens near area
increased blood flow causes the redness
more blood flow delivers nutrients for repair

22
Q

expulsive reflexes

A

coughing / sneezing
expels or removes harmful pathogens from body

23
Q

plant physical defences

A

waxy cuticle on surface traps pathogens, not letting them enter leaf

cell wall prevents pathogens entering plant cell

pathogens enter plants: triggers callose (polysaccharide) to be released between cell wall and plasma membrane, so pathogens cant enter

24
Q

plant chemical defences

A

some plant produce antimicrobial compounds that kill pathogens
plants have tannins which stops vectors as they bind to saliva to deactivate insect enzymes

25
what do pathogens have on their surface
specific antigens
26
3 types of phagocytes
macrophage monocyte neutrophils
27
how to tell apart phagocytes
neutrophils have multi lobed nucleus and are usually smaller macrophages have kidney shaped nucleus and are larger
28
specific immune response: step 1 with phagocytes until APC formed
- opsonin coats pathogen - phagocyte recognises foreign pathogen and engulfs it (endocytosis) - inside phagocyte it vesicles into a phagosome that lysosomes fuse to form phagolysosome - hydrolytic enzymes digest pathogen - pathogen removed from cell (exocytosis) - phagocyte keeps some antigens from pathogen to present on its surface (becomes antigen presenting cell)
29
Specific immune response: step 2 T lymphocytes and their role
- T lymphocyte has specific receptor binding to the antigen presenting cell - this activates T cell (clonal selection) causing mitosis of T cells (clonal expansion) - T helper cells releases cytokines (interleukin) to activate B lymphocytes - T killer cells destroy cells infected by pathogen - T regulartory cells suppress immune response to protect host cells - T memory remains in bloodstream for a quicker secondary response incase of reinfection
30
specific immune response: step 3 B lymphocytes and their role
- cytokines from T helper trigger B lymphocytes - B lymphocytes with antibody on surface specific to the antigen from pathogen are activated - they divide by mitosis and differentiate into plasma cells and B memory - plasma cells release many antibodies into plasma specific to pathogen antigen - B memory remains in bloodstream to divide in case of reinfection
31
antibody structure
- quaternary protein (two heavy, two light chains) - polypeptides held together by disulfide bonds - they have a variable region that is different between antibodies as it has specific antigen binding site - constant region is the same for all antibodies - hinge region allows flexibility of antibody
32
3 roles of antibodies
- neutralisation (anti-toxin) - agglutination - opsonisation
33
neutralisation; antibody
neutralises toxins to make them harmless so u feel less ill
34
agglutination; antibody
clumps pathogens to be engulfed by phagocytes easier and to make them too big to invade host cells
35
opsonisation; antibody
coats and marks pathogen for phagocytosis
36
why is your secondary immune response quick
- T and B memory cells from initial infection remain - divide by mitosis to mass produce cells - to fight off disease
37
active immunity:
when your body makes its own antibodies
38
natural active immunity
getting sick
39
active artificial immunity
vaccination using weakened pathogen
40
passive immunity
you get antibodies from elsewhere
41
natural passive immunity
breastmilk
42
artificial passive
antibody injection
43
autoimmune diseases how and tell me two
persons immune system fails to distinguish self antigens and foreign antigens effectively attacking and killing normal cells - lupus - rheumatoid arthiritis
44
vaccines
- dead or weakened (atenuated) pathogen injected into host - to trigger less harmful specific immune response - producing T and B memory cells for the disease in case of infection
45
why cant antibiotics help viruses
viruses have no cell structure (no cell walls) so antibiotics cannot work
46
why dont antibiotics harm host cells
animal cells have no cell wall to be targeted by antibiotics
47
antibiotic resistance explained
- a random mutation in pathogenic bacteria - protects the bacteria from antibiotics - bacteria survive and reproduce more bacteria with antibiotic-resistance characteristic
48
what is causing antibiotic resistance to be widespread
over-prescription not completing the course
49
Why should biodiversity be protected in terms of diseases and immunity
many medicinal drugs from plants have not yet been discovered so you would not want these undiscovered species of plants to go extinct
50
personalised medicine
medicine being tailored to your genetics to make the treatment more effective

biology A-LEVEL (24 decks)

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