Module 4.1 Flashcards

Communicable diseases

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1
Q

Different types of pathogens

A

Viruses
Protoctista
Fungi
Bacteria

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2
Q

What type of pathogen is tuberculosis

A

Bacteria

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3
Q

What type of pathogen is ring rot

A

Bacteria
plants

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4
Q

What type of pathogen is HIV/AIDS

A

virus
humans

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5
Q

What type of pathogen is influenza

A

Virus
animals

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6
Q

What type of pathogen is tobacco mosaic virus

A

Virus
plants

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7
Q

What type of pathogen is malaria

A

Protoctista

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8
Q

What type of pathogen is potato/tomato late blight

A

Protoctista

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9
Q

What type of pathogen is black sigatoka

A

Fungi
Bananas

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10
Q

What type of pathogen is athlete’s foot

A

Fungi
Human

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11
Q

Means of direct transmission

A

Spores (in the air or on surfaces)
Droplets in the air
Direct contact physical contact (touching infected person, body fluids or contaminated surface)
Faecal-oral transmission (eating or drinking contaminated things)

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12
Q

What is a vector

A

Another organism that is used by a pathogen to gain entry to a primary host

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13
Q

What is indirect transmission

A

Transmission using a vector

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14
Q

What is direct transmission

A

Transmission that does not involve a vector

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15
Q

Primary non-specific defences against pathogens

A

Mucous membranes
Blood clotting
Wound repair
Inflammation
Expulsive reflexes
Skin

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16
Q

How mucous membranes help to prevent infection

A

Goblet cells secrete mucus
Pathogens get trapped in the mucus
Cilia waft the mucus with the pathogens in it upwards out of the lungs to the oesophagus to be swallowed to be killed in the acidic stomach

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17
Q

How blood clotting prevents infection

A

When blood vessels are damaged platelets release substances that via a cascade of events result in the formation of fibrin which forms a network trapping platelets and forming a clot
Creates a barrier to pathogens so they cannot enter the damaged tissue/blood and stops blood loss

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18
Q

How inflammation helps prevent infection

A

Mast cells detect the presence of pathogens and release histamine
Histamine makes capillaries more leaky so more tissue fluid can enter the infected area
Allows more WBCs mainly neutrophils to enter the area and begin to digest pathogens
Histamine also causes vasodilation of the arterioles leading to the infection site so more blood containing WBCs can enter the capillaries

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19
Q

How expulsive reflexes help prevent infection

A

Vomiting forces pathogens out of the stomach if they have been consumes
Sneezing and coughing forces pathogens out of the airways and helps to push the mucus containing pathogens out of the body/down the trachea

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20
Q

How skin prevents infection

A

Barrier to pathogens as the cells at the surface are no longer alive after being keratinised

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21
Q

How wound repair prevents infection

A

Closes the skin to create a complete barrier to infection
Scab dries and shrinks drawing sides of cut together
temporary seal created then skin is repaired

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22
Q

What are the types of phagocytes

A

Neutrophils and macrophages/antigen-presenting cells

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23
Q

Mode of action - neutrophils

A

Recognise foreign antigens on the pathogen
neutrophil binds to opsonin on the antigen of the pathogen
pseudopodia form extension of the plasma membrane around the pathogen
plasma membrane fuses around the pathogen placing it in a phagosome
Lysosomes fuse with the phagosome releasing their hydrolytic enzymes into the phagosome
Pathogen is digested
Products of digestion can be absorbed into the cell

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24
Q

Mode of action - macrophages/antigen presenting cells

A

Initiate the specific immune response
Same as neutrophil but antigens are not digested MHC/antigen complex is exposed on the surface of the cell
Antigen presenting cell is formed
Exposes the antigen so other cells of the immune system can recognise the antigen

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25
Q

What are opsonins

A

Protein molecules that attach to the antigens on the surface of a pathogen
Enhance the ability of phagocytic cells to bind to and engulf pathogens

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26
Q

Social factors affecting transmission

A

Overcrowding
poor ventilation
Poor health e.g. HIV makes it more likely to contract other diseases
Poor diet
Homelessness
Living or working with people who have migrated from an area where a disease is more common

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27
Q

Effect of warm climate on disease

A

Many bacteria, Protoctista and fungi grow and reproduce more rapidly in warm and humid condition so are more common in warmer climates
There is a greater variety of diseases found in warmer climates so plants and animals in these climates are more likely to become infected

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28
Q

Effect of cool climates on disease

A

Cooler climates may damage or kill pathogens or just reduce their ability to grow and reproduce making disease less common

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29
Q

Why is blood clotting needed

A

When the skin is not complete from lacerations and abrasion it opens the body to infection
If blood vessels are damages it could lead to excess blood loss

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30
Q

Why mucous membranes are needed

A

Exchange surfaces are very thin so are less protected

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31
Q

How to recognise neutrophils

A

Multilobed nucleus

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32
Q

How do macrophages travel in the body

A

Travel in the blood as monocytes
Settle in organs or lymph nodes then develop into macrophages and travel in lymph

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33
Q

How to recognise lymphocytes

A

Smaller with a large nucleus

34
Q

how antigen presentation helps

A

antigen-presenting cells move around the body and can come into specific cells that activate the full immune response (T and B lymphocytes)
there may only be one T and B lymphocyte with the correct recognition site for the antigen so the more antigen presenting cells there are the more chance there is the antigen will come into contact with them

35
Q

what cells are produced in the immune response

A

T helper cells
T killer cells
T memory cells
T regulator cells
plasma cells
B memory cells

36
Q

why is cell signalling important in the immune response

A

specific immune response involves coordinated action of a range of cells
to work together effectively the cells need to communicate

37
Q

What are interleukins

A

released by T cell and macrophages
stimulate clonal expansion and differentiation of B and T cells

38
Q

what are autoimmune disease

A

the immune system attacks a part of the body

39
Q

auto immune disease example

A

arthritis

40
Q

mode of action of T-help cells

A

have receptors on the plasma membrane which bind to specific antigens presented by macrophages
when bound they become activated

41
Q

role of T-helper cells

A

produce interleukins which also stimulates
activation of B cells (increase antibody production)
production of other types of T-cells
attracts and stimulates macrophage to ingest pathogens with antigen-antibody complexes

42
Q

mode of action B lymphocytes

A

have antibodies on plasma membrane
antigens bind to antibodies to activate B-cells

43
Q

role of B cells

A

once activated B-cells divide by mitosis to form B plasma cells

44
Q

role of plasma cells

A

produce large amounts of antibodies which they secrete by exocytosis
have large RER for protein synthesis (antibodies)

45
Q

role of T killer cells

A

when exposed to infected cells they release cytotoxins which enter the cytoplasm of target cells and trigger apoptosis

46
Q

what is clonal selection

A

the activation of the specific B and T lymphocytes when the specific antigen comes into contact with the receptors on their plasma membranes

47
Q

What is clonal expansion

A

Once the correct lymphocyte is activated they increase in number by mitotic divisions to become effective

48
Q

what are antigens

A

proteins or glycoproteins
stimulate immune response
body recognises antigens as foreign or self
foreign antigens stimulate antibody production

49
Q

how many polypeptide chains make up an antibody

A

4

50
Q

what are the 2 region of antibodies

A

constant region (same in all antibodies)
variable region (specific shape to be complimentary to antigen)

51
Q

role of the hinge region in antibodies

A

allows flexibility so molecule can grip more than one antigen

52
Q

what types of poly peptide chains are in an antibody

A

light chain and heavy chain

53
Q

what holds the polypeptides together in antibodies

A

disulfide bridges

54
Q

what are the ways antibodies work

A

Opsonins
Agglutinins
Anti-toxins

55
Q

how do opsonins work

A

bind to antigens on pathogens
then act as binding site for phagocytic cells to more easily bind and destroy the pathogen
or can neutralise pathogen by binding to antigen used to attach to host cell

56
Q

how do agglutinins work

A

as antibodies have 2 binding sites they can join separate pathogens
clumps the pathogens together
stops pathogens from entering cells
more easily engulfed by phagocytes

57
Q

how do anti-toxins work

A

renders toxins released by pathogens harmless

58
Q

what is the primary immune response

A

when and infecting agent is first detected and the immune system starts to produce antibodies but it takes a few days for the number of antibodies to ride to a level that can effectively combat the infection
once the pathogen is dealt with the number of antibodies drops rapidly

59
Q

what is the secondary immune response

A

if the body is infected a second time by the same pathogen B and T memory cells recognise the antigen and make the immune response much quicker
antibody production starts sooner and is much faster

60
Q

role of T memory cells

A

cells that remain in the blood to provide long term immunity

61
Q

role of B memory cells

A

cells that remain in the blood to provide long term immunity

62
Q

what are vaccinations

A

a way of stimulating the immune response to achieve immunity to a specific pathogen

63
Q

what is herd vaccination and herd immunity

A

using a vaccine to provide immunity to all or almost all of the population
once enough people are immune the disease can longer be spread through the population

64
Q

what is ring vaccination

A

when a new case of a disease is reported vaccines are given to all the people in the immediate vicinity of the new case to control the spread of disease

65
Q

why do vaccination programmes change

A

if a disease has been eradicated or reduced to very low levels that it is unlikely to spread the vaccination programme can be relaxed

66
Q

why do vaccines change

A

some pathogens can undergo genetic mutations which change their antigens meaning the vaccine has to change

67
Q

what is active immunity

A

the immune system is activated and produces its own antibodies

68
Q

what is passive immunity

A

when antibodies are supplied from another source e.g. mother to baby

69
Q

what is natural immunity

A

achieved through normal life processes

70
Q

what is artificial immunity

A

achieved through medical intervention

71
Q

what are the possible sources of new medicines

A

accidental discovery
traditional remedies
observation of wildlife
plants
research into disease causing mechanisms
personalised medicines

72
Q

plant medicine examples

A

morphine (unripe poppy seeds)
willow bark pain and fever relief

73
Q

microorganism medicine examples

A

penicillin

74
Q

personalised medicine

A

sequencing genes from individuals with a particular condition and developing drugs for that condition

75
Q

antibiotics benefits

A

less deaths from infection after wounds or surgery

76
Q

antibiotics risks

A

antibiotic resistance e.g. MRSA

77
Q

plant physical defences

A

cellulose cell wall
waxy cuticle
bark
lignin thickening of cell wall

78
Q

what is callose and how does it help plants

A

large polysaccharide deposited in the sieve tubes at the end of growing season around the sieve plates blocking the flow in the sieve tubes
can prevent a pathogen spreading around the plant

79
Q

chemical defences in plants

A

chemicals such as terpenoids, phenols and hydrolytic enzymes in the plant tissues have anti pathogenic properties

80
Q

why are chemical defences slow in plants

A

production of chemical requires a lot of energy so many are not produced until the plant detects an infection

81
Q

active plant defences

A

thickening and strengthening cell walls with additional cellulose
callose deposits near the invading pathogen
increase chemical production