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Alevel Biology > 4.1 > Flashcards

4.1 Flashcards

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1
Q

Pathogen

A

A microorganism that causes disease

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2
Q

Direct transmission

A

Passing a pathogen from host to host with no intermediary

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3
Q

Indirect transmission

A

Passing a pathogen from host to new host via a vector

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4
Q

Transmission

A

Passing a pathogen from an infected individual to an uninfected individual

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5
Q

Vector

A

An organism that carries a pathogen from one host to another

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6
Q

Callose

A

A large polysaccharide deposit that blocks old phloem sieve tubes

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7
Q

Inflammation

A

Swelling and redness of tissue cause by infection

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8
Q

Mucous membrane

A

Specialised epithelial tissue that is covered in mucus

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9
Q

Primary defence

A

Those that prevent pathogens entering the body

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10
Q

Antigen presenting cell

A

Cell that isolated the antigen form a pathogen and places it on the plasma membrane so that it can be recognised by other cells in the immune system

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11
Q

Clonal selection

A

Selection of a specific B or T cell that is specific to the antigen

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12
Q

Cytokines

A

Hormone like molecules used in cell signalling to stimulate the immune response

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13
Q

Neutrophils

A

A type of white blood cell that engulfs foreign matter and traps it in a large phagosome which fuses with lysosomes to digest the foreign matter

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14
Q

Opsonins

A

Proteins that bind to the antigen on a pathogen and then allow phagocytes to bind

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15
Q

Antibodies

A

Specific proteins released by plasma cells that can attach to pathogenic antigens

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16
Q

B memory cells

A

Cells that remain in the blood for a long time providing long term immunity

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17
Q

Clonal expansion

A

An increase in the number of cells by mitotic cell division

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18
Q

Interleukins

A

Signalling molecules that are used to communicate between different WBC

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19
Q

Plasma cells

A

Derived from the B lymphocytes, these r cells that manufacture antibodies

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20
Q

T helper cells

A

Cells that release signalling molecules to stimulate the immune response

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21
Q

T killer cells

A

Cells that attack and destroy our own body cells that are infected by a pathogen

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22
Q

T memory cells

A

Cells that remain in the blood for a long time providing long term immunity

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23
Q

T regulator cell

A

Cells that are involved with inhibiting or ending the immune response

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24
Q

What’s a pathogen

A

An organisms that causes disease

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25
Q

What is the organism that carries a pathogen called

A

A host

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26
Q

What is the hosts role for a pathogen

A

Creates a good habitat which the microorganism can live in

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27
Q

As a results of the host function what happens

A

Numerous types of microorganisms live in and on the body of another organism

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28
Q

How do pathogens live and what is its disadvantage

A

By taking nutrients from their host, but this can cause damage to the host

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29
Q

What kingdom does bacteria belong to

A

Prokaryotae

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30
Q

What are prokaryotae-bacteria cells like compared to eukaryotes

A

They are smaller but can reproduce rapidly in the right condition

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31
Q

In the right condition how many times can bacteria reproduce

A

Some can reproduce every 20mins in right condition

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32
Q

What happens once bacteria be enters host

A

They can multiply rapidly

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33
Q

How do bacteria presence in a host cause damage in animals

A

Causes disease by damaging cells or by releasing waste products/toxins harmful to the host

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34
Q

In plants how does bacteria cause damage

A

Bacteria often lives in vascular tissue and causes blackening and death of these tissues

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35
Q

Does fungi cause only one disease in plants and animals

A

Fungi causes a variety of diseases

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36
Q

how do fungal infections in animals work

A

Fungus lives in the skin of animals and where it’s hyphae which forms mycelium and grows under the skins surface

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37
Q

How does fungal infections spread

A

Fungus sends out special reproductive hyphae which grows to the surface on the skin to release spores causing redness and irritation

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38
Q

How to fungal infections spread in plants

A

Fungus often lives in vascular tissue where it gains nutrients, hyphae then releases extracellular enzymes like cellulase, to digest surrounding tissue which causes decay

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39
Q

What are symptoms of fungal infections in plants

A

Leaves often become mottled in colour (curled up and shrivelled) before dying, fruit storage organs like tubers (potatoes) will turn black and decay

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40
Q

How do viruses cause damage

A

They invade cells and take over genetic machinery and other organelles of a cell, they then cause the cells to manufacture more copies of the virus and host cells eventually burst which releases many new viruses which can infect healthy cells

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41
Q

What are protoctista

A

Diseases caused by animals like protoctists

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42
Q

How do protoctista cause harm to host

A

By entering host cells and feeding on the contents as they grow

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43
Q

How to the protoctista malaria cause harm

A

Malaria parasite (plasmodium) has immature forms that feed on haemoglobin inside RBC

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44
Q

What are the characteristics of tuberculosis

A

Affects many parts of the body, kills cells and tissues and lungs are usually attacked

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45
Q

What are symptoms of tuberculosis

A

Long lasting cough, weight loss, fever, night sweats

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46
Q

What organism causes disease tuberculosis and how do you cure it

A

Bacteria, treated by antibiotics for several months

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47
Q

What are characteristics of bacterial meningitis

A

Infections of meninges(membrane that surrounds brain and spinal cord), if membrane swells it causes damage to brain and nerves

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48
Q

What organism causes bacterial meningitis and how is it cured

A

Bacteria and cured by antibiotics

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49
Q

What are characteristics of ring rot (in plants)

A

Rings of decay in vascular tissue of a potato tuber or tomato as well as wilting of leaves

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50
Q

What organism causes ring rot and how do you treat it

A

Bacterium and remove infected plants

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51
Q

What are at or tons of bacterial meningitis

A

Seizures, headaches, drowsy, fever

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52
Q

What are symptoms of ring rot

A

Vascular wilt

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53
Q

What are characteristics of HIV/AIDS

A

Attacks cells in immune system and compromises immune response

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54
Q

What are symptoms of HIV/AIDS

A

Fever, rash, swollen glands

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55
Q

What organism causes HIV/ AIDS and how is it treated

A

Virus and can’t be treated but can live with it if you take antiretroviral drugs

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56
Q

What are characteristics influenza

A

Attacks respiratory system and causes muscle pain and headaches

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57
Q

What organism causes influenza and how is it cured

A

Virus and fluids and painkillers cure it

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58
Q

What are characteristics of tobacco mosaic virus

A

Causes mottling and discoloured leaves

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59
Q

What organism causes tobacco mosaic virus and how is it cured

A

Virus and cured by removing infected plants

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60
Q

What are characteristics of black Sigatoka (banana plants)

A

Causes leaf spots on banana plant, reducing yield

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61
Q

What organism causes black Sigatoka and how is it cured

A

Fungus and remove infected leaves and neighbouring leaves

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62
Q

What is characteristics of blight (tomato and potato)

A

Affects leaves and potato tuber and causes watery rot on leaves

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63
Q

What organism causes blight and how is it cured

A

Protocistan and removed infected ones and spray others with fungicide

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64
Q

What are characteristics of ringworm (cattle)

A

Growth of fungus in skin with spores causing erupting through skin to cause rash

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65
Q

What organism causes ringworm and how is it cured

A

Fungus and anti fungal cream

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66
Q

What are characteristics of athletes foot

A

Growth under the skin of feet, especially between toes

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67
Q

What organism causes athletes foot and how is it cured

A

Fungus and anti fungal cream

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68
Q

What are characteristics of malaria

A

Parasite in blood that causes headaches and fevers and may progress to coma and death

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69
Q

What organism causes malaria and how is it cured

A

Protoctistan and hard to treat

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70
Q

What happens after plants manufacture sugars in photosynthesis

A

They convert them to a wide variety of compounds like proteins and oils

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71
Q

What does sugars converting into proteins and oils in a plant mean for other organisms

A

They are a rich source of nutrients for many organisms like bacteria, fungi, protoctists, viruses, insects and vertebrates

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72
Q

Why is it bad for the plant that many organisms want to feed of them

A

Bacteria, fungi, protoctists and viruses may be pathogenic and insects and vertebrates may be vectors to help transmit these pathogens

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73
Q

Do plants have an immune system

A

They don’t have one like humans but they have developed a wide range of structural and chemical and protein based defences which can detect invading organisms and prevent them from causing extensive damage

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74
Q

What do plant defences include

A

Passive defences to prevent entry and active defences which are introduced when a pathogen detected

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75
Q

What is a passive defence in plants

A

Defences present before infection, their role is preventing entry and spread of pathogen, including physical and chemical barriers

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76
Q

What is the biggest physical and passive defence

A

Cellulose cell wall, acts as a physical barrier and contains a variety of chemical defences too activate when pathogen detected

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77
Q

How is lignin thickening of cell walls a little physical and passive defence

A

Lignin is waterproof and almost completely indigestible so pathogen will find it hard to enter it

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78
Q

How are waxy cuticles a passive and physical defence

A

They prevent water from collecting on cells surface, since pathogens collect in water and need water to survive lack of water is a passive defence

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79
Q

How is bark a passive and physical defence

A

Contains a variety of chemical defences that work against pathogenic organisms

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80
Q

How is stomata closure a physical and passive defence

A

Stomata are point of entry for pathogens, stomatal opening controlled by guard cells, when pathogenic organism detected, guard cells will close the stomata at that part of the plant

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81
Q

How is callose a physical and passive defence

A

It’s a large polysaccharide that is deposited in sieve tubes at the end of growing season, it’s deposited around sieve plates and blocks flow in sieve tubes which prevents pathogens spreading round the plant

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82
Q

How is tylose formation a passive and physical defence

A

Balloon like swellings or projections that fill xylem vessel, when tylose fully formed it plugs the vessel and vessel can no longer carry water, blocking xylem prevents spread of pathogens through heartwood (tylose also has high concentration of chemicals like terpenses-harmful to pathogens

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83
Q

What are some chemical defences plants have

A

Plant tissue contains variety of chemicals that have anti-pathogenic properties including terpenoids, phenols, alkaloids, hydrolytic enzymes

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84
Q

What chemical defences are passive (present before infection)

A

Terpenes and tylose and tannis in bark

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85
Q

Why are most chemicals not produced until plant detects infection

A

As they require lots of energy

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86
Q

What are active defences in plants

A

When pathogen attacks, specific chemicals in their cell wall can be detected by plant cells, these chemicals include specific proteins and glycolipids, plant responds by forfeiting defences already present which includes increasing physical defences and producing defensive chemicals

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87
Q

How can cell wall become an active defence

A

When pathogen detected cell wall thickens and strengthens with additional cellulose

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88
Q

How can deposition of callose become a active defence

A

Deposition of callose between plant cell wall and cell membrane near invading pathogen, callose deposits are polysaccharide polymers that impede cellular penetration at site of infection, it strengthens cell walls and blocks plasmodesmata

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89
Q

How are oxidative bursts a active defence

A

Oxidative bursts that produce highly reactive oxygen molecules capable of damaging the cells of invading organisms

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90
Q

What defence is an increase in production of chemicals

A

Active defence

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91
Q

What is the action of the active chemical defence terpenoids

A

Range of essential oils that have antibacterial and antifungal properties, may also create a scent like methanols and menthones produced by mint plant

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92
Q

What is the action of the active chemical defence phenols

A

Have antibiotic and antifungal properties. Tannis in bark inhibits attack by insects, these compounds bind to salivary proteins and digestive enzymes like trypsin and chymoteyspin, deactivating the enzymes. Insects that ingest high amounts of tannis don’t grow and die which helps prevent transmission of pathogens

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93
Q

What is the action of the active chemical defence alkaloids

A

Nitrogen-containing compounds like caffine, nicotine, cocaine, morphine, solanine. They give a bitter taste to inhibit herbivores feeding. They also act in a variety of metabolic reactions via inhibiting/activating enzyme action. Some alkaloids inhibit protein synthesis, if plant can reduce grazing by larger animals, it suffers less damage which can allow pathogens to enter plant

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94
Q

What is the action of the active chemical defence defensins (defensive proteins)

A

Small cysteine-rich proteins which broad anti-microbial activity, they appear to act upon molecules in plasma membrane of pathogens, possibly inhibiting action of ion transport channels

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95
Q

What is the action of the active chemical defence hydrolytic enzymes

A

Found in spaces between cells, include chicinease which breaks down chichin in fugal cell walls, glucanases which hydrolyse glycosidic bonds in glucans and lysosomes which are capable of degrading bacteria cells

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96
Q

What is necrosis

A

Deliberate cell suicide. A few cells sacrificed to save rest of the plant. By killing cells surrounding infection, the plant can limit pathogens access to water and nutrients, stopping it spread further around the plant

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97
Q

How is necrosis brought about by intracellular enzymes activated

A

By injury, these enzymes destroy damaged cells and produce brown spots on leaves or dieback

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98
Q

What is canker

A

Sunken necrotic lesion in the woody tissue like main stem or branch which causes death of cambium tissue in bark

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99
Q

How does plant defence overall work

A

Pathogen detected by plant cell wall receptors in cell membrane as when pathogen breaks down cell wall their bi-products recognised. So, a signalling molecule alerts nucleus of attack. Callose and lignin are then made to strengthen cell wall and defensive chemicals warn other cells before they’re attacked. Some defence molecules even directly attack the pathogen

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100
Q

What does pathogens life cycle involve

A

Living in or on other living things

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101
Q

What is the bi-product of a pathogens life cycle

A

It causes harm to their host

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102
Q

What does the pathogens life cycle involve in stages

A

Travelling from one host to another (transmission), entering the hosts tissue, reproducing and leaving hosts tissue

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103
Q

How are most pathogens transmitted

A

Pathogenic organisms can be transmitted between animals in many ways but most common is direct transmission

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104
Q

What is one method of direct transmission

A

Direct physical contact, like touching a person whose infected or touching contaminated surface or soil that harbours pathogens such as HIV, meningitis, ringworm and athletes foot

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105
Q

What factors effect direct transmission by direct physical contact

A

Hygiene-washing hand regularly, keeping surfaces clean, disinfecting cuts or abrasions, sterilising surgical instruments, using condoms during sexual intercourse

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106
Q

What is another way direct transmission can happen (faecal)

A

Faecal-oral transmission usually by eating food or drinking water contaminated by the pathogen like cholera and food poisoning

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107
Q

What factors effect direct transmission via faecal

A

Using human sewage to fertilise crops is common in some parts of the world, treatment of waste water And drinking water are important way to reduce risk. Washing all fresh food using treated water m, careful food prep and making sure food isn’t raw all reduce risk

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108
Q

What is another means of direct transmission (droplet)

A

Droplet infection-in which pathogens carried in tiny water droplets in the air like TB and influenza

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109
Q

What factors effect direct transmission by droplet infection

A

Catch it-bin it-kill it, cover mouth when coughing or sneezing, use a tissue and dispose of the tissue correctly

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110
Q

What is a means of direct transmission (spores)

A

Transmission by spores, which are a resistant stage of the pathogen. Can be carried by air or residue on surfaces or in soil like anthrax or tetanus

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111
Q

What factors effect direct transmission via spores

A

Use of mask and washing skin after contact with soil

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112
Q

What are 4 main ways of direct transmission

A

Direct physical contact, faecal contact, droplet infection, transmission by spores

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113
Q

What social factors also effect transmission (6)

A

Over-crowding(lots of people living in a house), poor ventilation, poor health (immunocompromised), poor diet, homelessness, living/working with people who have migrated from places where disease is more common

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114
Q

What is indirect transmission

A

Some pathogens are transmitted indirectly via a vector

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115
Q

What is a vector and give an example

A

Another organism that may be used by the pathogen to gain entry to primary host such as plasmodium parasite that causes malaria enters human host by bite from female mosquitoes

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116
Q

What is the life cycle of plasmodium (uses vector)

A

Person with malaria->gametes of plasmodium in blood->female mosquito sucks blood->plasmodium develops and migrated to mosquito salivary glands->uninfected person bitten->plasmodium migrates to liver->plasmodium migrates to blood-> person with malaria

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117
Q

How to plant pathogens spread

A

Also by direct and indirect means

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118
Q

How may pathogens in soil enter the plant

A

Will infect plants by entering the roots, especially if they have been damaged as a result of replant, burrowing animals or movement by storm

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119
Q

How does airborne transmission work in plants

A

Many fungi produce spores as a means of sexual or asexual reproduction, these spores are then carried by the wind and once pathogen inside plant in may affect vascular tissue

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120
Q

How may pathogens on leaves enter plant

A

Pathogens on leaves are distributed when leaves shed in autumn and carry pathogens back to soil where it can grow and infect other plants

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121
Q

How can pathogen effect plant when they enter the fruit and seed

A

Pathogen enters fruit or seed and is then distributed within seeds so many/all offspring are infected

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122
Q

How does indirect transmission in plants often occur

A

As a result of an insect attack

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123
Q

How do spores and bacteria enter plant by indirect transmission

A

Spores and bacteria become attached to burrowing insects which attack infected plant, when that nettle attacks another plant, pathogen is transmitted to uninfected plant so beetle acts as a vector

124
Q

Give an example of indirect transmission in plants

A

Fungus that causes Dutch elms disease is carried by a beetle

125
Q

What can many pathogens do in warm and moist conditions

A

Many protoctists, bacteria and fungi can grow and reproduce mor rapidly in warm and moist conditions so they tend to be more common in warmer climates

126
Q

What happens to pathogens in cool climates

A

Pathogens which live in warm climates may become damaged or even killed by winter weather as it reduces their ability to grow and reproduce

127
Q

What does it mean as pathogens thrive in warmer climates

A

Their is a greater variety or diseases to be found in warmer climates and animals or plants living in these regions are more likely to become infected

128
Q

What do pathogenic organisms need to do before causing harm

A

Enter the hosts body

129
Q

What has evolution done to hosts to make it harder for pathogenic organisms to enter the body

A

Evolution has adapted hosts to defend themselves against invasion

130
Q

What are primary defences

A

Mechanisms that have evolved to prevent entry of pathogenic organism, they are non-specific as they prevent entry of any pathogen

131
Q

What kind of defence is skin

A

Primary defence

132
Q

How is skin the main primary defence

A

Body covered by skin, outer layer of skin called epidermis and consists of layer of cells

133
Q

What are most of the cells in epidermis called

A

Keratinocytes

134
Q

What are keratinocytes

A

These are cells produced by mitosis at base of epidermis and then migrate out to surface of the skin

135
Q

What happen as keratinocytes migrate out to surface of skin

A

They dry out and cytoplasm is replaced by protein keratin which is a process called keratinisation and takes about 30days

136
Q

What happens by the time keratinocytes have reached the cells surface

A

They are no longer alive, keratinised layer of dead cells act as an effective barrier to pathogens and eventually dead cells slough off (dust)

137
Q

Skin only protects as long as…?

A

It’s complete

138
Q

What do abrasions and lacerations open the body to

A

Damaged skin opens body up to infection

139
Q

What happens when we cut ourselves to prevent infection

A

Body must prevent excess blood loss by forming a clot, this makes a temporary seal to prevent infection and to repair skin

140
Q

Why is blood clotting a complex process

A

As it is important to prevent clots forming in blood vessels, where they are not needed

141
Q

What is involved in blood clotting

A

Calcium ions and atleast 12 factors known as clotting factors

142
Q

Where are many clotting factors released from and what does this cause

A

Many clotting factors released from platelets and damaged tissue which activates an enzyme cascade

143
Q

What happens once a clot

Is formed

A

Clot will begin to dry out and form a scab, scab shrinks as it dries, drawing sides of cut together, making a temporary seal under which skin is repaired

144
Q

How is skin repaired under scab

A

First stage is deposition of fibrous collagen under the scab, stem cells in the epidermis then divide by mitosis to form new cells which migrate to end of cut and differentiates to form new skin, new blood vessels grow to supply oxygen and nutrients to new tissues, tissues contract to draw edges of cut together so repair can be completed, as new skin completed scab will be released

145
Q

What is the disadvantage of the exchange surfaces where oxygen and nutrients have to be exchanged to enter our blood

A

Exchange surface must be thinner so less well protected from pathogens

146
Q

What may air and food from our environment harbour and why is this a problem

A

May harbour microorganisms so the airway, lungs, digestive system are at risk of infection

147
Q

How are the lungs, airways, digestive system protected from infection

A

Mucous membrane

148
Q

What is a mucous membrane

A

Epithelial layers contain mucus secreting cells called goblet cells and their are also extra mucus-secreting glands under epithelium

149
Q

How does mucus membrane work in lungs

A

Mucus lines passages and traps pathogens that may be in the air, epithelium also has ciliated cells, cilia are tiny hair like organelles that move mucus to top of trachea where is can enter oesophagus, it’s swallowed and passes down digestive system where pathogen is killed by stomach acid which denatures pathogens enzymes

150
Q

Apart form airways, lungs where is mucous membrane also found

A

Gut, genital area, anus, ear, nose

151
Q

What is an adaptation of areas prone to attack by pathogen

A

They are sensitive, they respond to irritation that may be caused by presence of microorganisms or by the toxins they release-these reflexes include coughing, sneezing and vomiting

152
Q

How does coughing/sneezing protect against infection

A

Sudden expulsion of air will carry with it the microorganism causing the irritation

153
Q

What is a sign tissue is infected

A

Swelling and redness known as inflammation where tissue cells hot and painful

154
Q

What are mast cells

A

Presence of microorganisms in tissue is detected by specialised cells known as mast cells, they then release a cell signalling substance called histamine

155
Q

What does histamine do to surrounding tissue

A

Has a range of effects on surrounding tissue, which acts to help combat infection, the main effect is to cause vasodilatation and make capillaries walls more permeable to white blood cells and some proteins

156
Q

What happens once mast cells cause capillary walls to be more permeable

A

Blood plasma and phagocytic white blood cells leave blood and enter tissue fluid which leads to increased production of tissue fluid which causes swelling known as an oedema

157
Q

What happen to excess tissue fluid after oedema formed and what does this lead to

A

Excess tissue fluid drained into lymphatic system where lymphocytes are stored which can lead to pathogens coming into contact with lymphocytes and initiating specific immune response

158
Q

What are other less important primary defences

A

Eyes protected by antibodies and enzymes in tissue fluid, ear canal lined with wax to trap pathogens, female reproductive system protected by mucus plug in cervix and by maintaining relitavely acidic conditions in vagina

159
Q

What are the 5 main primary non specific defences

A

Skin, blood clotting, mucous membrane, coughing sneezing, inflammation

160
Q

What are secondary no specific defences used to combat

A

Pathogens that have entered the body

161
Q

When pathogen enters body how is it recognised as foreign

A

By the chemical markers on its outer membrane, makers called antigens

162
Q

What are antigens

A

Proteins or glycoproteins intrinsic to plasma membrane

163
Q

How are pathogens antigens recognised as foreign

A

Antigens are specific to an organism so it’s detected as foreign. Are own cells have antigens, but they are recognised as our own and don’t produce a response

164
Q

What are opsonins

A

Protein molecules that attach to the antigens on the surface of a pathogen-they are a type of antibody

165
Q

Are all opsonins specific and what does this mean

A

Some aren’t very specific so can attach to a variety of pathogenic cells

166
Q

What is role of opsonins

A

The role of opsonins is to enhance ability of phagocytic cells to bind and engulf the pathogen

167
Q

What is the first line of secondary non-specific defence

A

Phagocytosis

168
Q

What is phagocytosis

A

Specialised cells in blood and tissue fluid engulf and digest the pathogen

169
Q

What is the most common phagocyte and how do you recognise it

A

Neutrophil and recognise them by their multi-lobed nucleus

170
Q

Where are neutrophils manufactured

A

Bone marrow

171
Q

Where are neutrophils found

A

They travel in the blood and often squeezed out of blood into tissue fluid

172
Q

How long do neutrophils live and in what quantity

A

Short-lived but they will be released in large numbers as result of infection, die after engulfing a few pathogens

173
Q

What are features of neutrophils and function

A

Have many lysosomes and they engulf and digest pathogens, dead neutrophils may collect in an area of infection and form pus

174
Q

What are the 6 stages of phagocytosis

A

1.phagocytosis attracted by chemicals produced by pathogen 2.phagocyte recognises pathogen as foreign and binds to it 3.phagocyte engulfs pathogen to form a phagosome-lysosomes move to phagosome and combine forming phagolysosome 4.in phagolysosome digestive enzymes break down pathogen 5.digested pathogen absorbed by phagocyte-antigen combine with MHC in cytoplasm 6.MHC/antigen complex is displayed on phagocyte membrane, making an antigen presenting cell

175
Q

What are macrophages

A

Larger cells manufactured in bone marrow, they travel in blood as monocytes before settling in body’s tissue

176
Q

Where are many macrophages found

A

In lymphnodes where they mature into macrophages

177
Q

What are dendritic cells and where are they found

A

Type of macrophage and found in more peripheral tissues

178
Q

What do macrophages play an important role in

A

Initiating specific immune response to invading pathogens

179
Q

What happens when macrophage engulfs a pathogen

A

It doesn’t fully digest it, the antigen from the surface is saved and moved to a special complex on the surface of the cell and it becomes an antigen-presenting cell

180
Q

Why do macrophages expose the antigen on its surface

A

So that other cells of the immune system can recognise the antigen, the special protein complex ensures that the antigen-presenting cell isn’t mistaken for a foreign cell and attacked by other phagocytes

181
Q

What do antigen presenting cells do

A

Move around the body where it can come into contact with specific cells that can activate the full immune response, these are T lymphocytes and B lymphocytes, there may only be one T and one B cell with the correct recognition site for the antigen, so, the role of the antigen presenting cell is to increase the chance that the antigen will come into contact with them

182
Q

What is clonal selection

A

Activation of specific B and T cells

183
Q

What does clonal selection bring to play

A

A complex series of events that lead to production of antibodies that can combat the specific pathogen and memory cells that will provide long term immunity

184
Q

What is the whole series of specific immune response stimulated and coordinated by

A

Lots of hormone like chemicals called cytokines which stimulate the differentiation and activity of macrophages, B and T cells

185
Q

What are secondary non specific defences

A

Antigens and opsonins, phagocytes, phagocytosis, macrophages

186
Q

What does specific immune response involve

A

B lymphocytes (b cells) and T lymphocytes (t cells)

187
Q

What are T and B lymphocytes

A

White blood cells with large nucleus and specialised receptors on their plasma membrane

188
Q

What does the immune response produce and why

A

Antibodies as it is antibodies that neutralise foreign antigens

189
Q

What does immune response provide

A

Long term immunity from the disease, it produces immunological memory by the release of memory cells which circulate body for many years

190
Q

What 4 cell types do T lymphocytes develop into

A

T helper cells, T killer cells, T memory cells, T regulator cells

191
Q

What is a T helper cell

A

Releases cytokines- chemical messengers that stimulate B cells to develop and stimulate phagocytosis phagocytes

192
Q

What are T killer cells

A

Attack and kill host-body cells that display foreign antigens

193
Q

What are T memory cells

A

Provide long term immunity

194
Q

What are T regulator cells

A

Shut down immune response after pathogen has been successfully removed, so also involved in preventing autoimmunity

195
Q

What are 2 cell types B lymphocytes develop into

A

Plasma cells and B memory cells

196
Q

What are plasma cells

A

Circulate in the blood, manufacturing and releasing the antibodies

197
Q

What are B memory cells

A

Remain in the body for number of years and act as immunological memory

198
Q

What does specific immune response involve and what must be done to make it successful

A

Coordinated action of a range of cells- to work effectively they must communicate- known as cell signalling

199
Q

How is communication between cells achieved

A

The release of hormone like chemicals called cytokines

200
Q

Is their only one signalling molecule and what does this mean

A

There’s a huge range of signalling molecules, each performing a different role and in order to detect a signal, the target must have a cell surface receptor complementary in shape to shape of signalling molecule

201
Q

What are 3 examples of communication using cytokines

A

Macrophages release monokines, some attract neutrophils by chemotaxis and others stimulate B cells to differentiate and release antibodies. T cells and macrophages release interleukins which stimulate clonal expansion (proliferation) and differentiation of B and T cells. Many cells can release interferon, which inhibits virus replication and stimulates activity of T killer cells

202
Q

What is chrmotaxis

A

Movement of cells towards certain chemicals

203
Q

When does autoimmune disease occur

A

When immune system attacks a part of the body

204
Q

What are B and T cells normally specific to and what happens in case of autoimmune diseases

A

Normally T and B cells specific to our antigens are destroyed during early development of immune system, but autoimmune disease arises when antibodies start to attack our own antigens (possibly as antigens that aren’t usually exposed become exposed to attack)

205
Q

What are causes of autoimmune diseases

A

Unknown but seem to include both genetic and environmental factors

206
Q

What are examples of autoimmune diseases

A

Arthritis-painful inflammation of a joint, cause is uncertain but starts with antibodies attacking membranes around the joint. Lupus-can affect parts of the body causing swelling and pain, it may be associated with antibodies that attack certain proteins in the nucleus in cells and affected tissue

207
Q

What are antigens

A

Molecules that can stimulate an immune response - generate antibody response

208
Q

What molecules can act as an antigen

A

Almost any but they are usually proteins or glycoproteins in pathogens plasma membrane

209
Q

What will happen to a foreign antigen in human body

A

It will be detected by the immune system and will stimulate the production of antibodies

210
Q

What are antibodies specific to

A

Antibodies are specific to the antigen and antigen specific organism, so antibody specific to pathogen

211
Q

Why don’t our antigens stimulate an immune response

A

Our antigens are recognised by our immune system so don’t usually stimulate any response

212
Q

What are antibodies

A

Immunoglobulin- a complex protein produced by plasma cells in the immune system

213
Q

When are antibodies released

A

They are released in response to an infection

214
Q

How do antibodies work

A

They have a region with a complementary shape to that of particular antigen, they attach to antigens and render them harmless

215
Q

How many antibodies must our immune system manufacture

A

One type of antibody for every antigen detected

216
Q

What is antibodies structure

A

Y shaped with 2 distinct region, they consist of 4 polypeptide chains

217
Q

What are the 2 regions on an antibody

A

Variable region-had a shape specific to the shape of the antigen. Constant region- is the same in all antibodies, it may have a site for the easy binding of a phagocytic cell

218
Q

Detailed structure of antibody

A

Just underneath the variable region on Y fork is the light polypeptide chain, disulphide bridges hold polypeptides together, at the Y intersect there is a hinge region to allow flexibility so molecules can grip more than 1 antigen, bottom of Y is heavy polypeptide chain

219
Q

How do most antibodies work

A

By attaching to antigens on pathogens

220
Q

What are the 3 main groups of antigens

A

Opsonins, agglutinins, anti-toxins

221
Q

What are opsonins

A

A group of antibodies that bind to antigens on a pathogen, they then act as binding sites for phagocytic cells, so they can more easily bind and destroy the pathogen

222
Q

Are opsonins specific to antigens

A

Some opsonins aren’t very specific and stick to types of molecules that aren’t found in host cells (eg.peptidoglycan found in bacteria cell wall), others are produced as part of specific immune response and bind to very specific antigens, the pathogen may have another use of this antigen molecule (eg.it may be binding site used for attachment to host cell)

223
Q

What is neutralisation in opsonins

A

Opsonins bind to antigen and renders them useless

224
Q

What do opsonins do as well as assist in phagocytosis

A

Prevent the pathogen entering a host cell before it can be attacked by phagocytes

225
Q

What are agglutinins

A

Each antibody molecule has 2 identical binding sites, it can cross link pathogens by binding an antigen on one pathogen with one binding site and an antigen on another pathogen with its other binding site

226
Q

How does agglutinins destroy pathogens

A

When many antibodies perform the crosslinking they clump together (agglutinate) the pathogen

227
Q

What are the 2 advantages of agglutinins

A

They agglutinated pathogens are physically impeded from carrying out some functions like entering host cells. And agglutinated pathogens are readily engulfed by phagocytes(esp effective against viruses)

228
Q

What are anti-toxins

A

Some antibodies bind to molecules that are released by pathogenic cells, these molecules may be toxic and the action of anti-toxins renders them harmless

229
Q

What happens when infecting antigens first detected

A

The immune system starts to produce antibodies

230
Q

How long does it take for the number of antibodies in the blood to rise to a level that can successfully combat infection

A

A few days

231
Q

What is primary immune response

A

When antibody levels rise enough in the blood to combat an infection, once pathogen has been dealt with the number of antibodies in the blood drops rapidly

232
Q

Antibodies don’t stay in the blood but what happens if the same antigen is detected again

A

If body infected by same pathogen second time, antibodies must be made again but as a result of specific immune response there will be B and T memory cells circulating in the blood, these cells can recognise specific antigens and immune system can swing into action quicker, this time production of antibodies start sooner and is much faster (secondary immune response)

233
Q

What is good about secondary immune response

A

It is usually quick enough to prevent any symptoms being detected by host

234
Q

What do vaccinations provide

A

Provides immunity to specific diseases, this is created by deliberate exposure to antigenic material that has been rendered harmless - mostly injected but sometimes taken orally

235
Q

How does immune system treat antigenic material injected from vaccine

A

As a real disease, so immune system activated and manufactures antibodies and memory cells to give long term immunity

236
Q

What are the different forms antigenic material used in vaccines can take

A

Live, attenuated, dead, toxoid

237
Q

How does a whole/live virus work

A

Usually not as harmful as the one that causes disease but very similar antigens so antibodies produced will be affective against real disease (eg. Smallpox vaccine uses similar virus-cowpox)

238
Q

How does harmless/attenuated work

A

Weakened form of pathogenic organism such as measles and TB vaccine

239
Q

What is an example of a dead pathogen vaccine

A

Typhoid and cholera vaccine

240
Q

What is an example of vaccines where a preparation of the antigen from a pathogen

A

Hepatitis B vaccine

241
Q

What is a toxoid vaccine

A

A harmless version of a toxin like tetanus vaccine

242
Q

What is herd vaccination

A

Using vaccine to provide immunity to all/almost all of population at risk

243
Q

How does herd vaccination occur

A

Once enough people are immune, disease can no longer be spread through population and herd immunity is achieved

244
Q

What is needed for herd immunity to be effective

A

Almost all population must be vaccinated such as 80-85% of vaccines needed to eradicate small pox and 95% for measles

245
Q

In the UK there’s a vaccination programme to immune young children against what diseases

A

Diphtheria, tetanus, wooping cough, polio, meningitis, measles, mumps, rubella - vaccines given to most kids at appropriate age

246
Q

When is ring vaccination used

A

In new cases of a new disease being reported

247
Q

What is ring vaccination

A

When you vaccinate people in immediate vicinity of the new case/ cases which may mean vaccinating surrounding households or even a whole town/village

248
Q

Where is ring vaccination used worldwide

A

To control spread of livestock disease

249
Q

What happens once disease is eradicated or at low enough Kew it won’t spread

A

Vaccination program can become relaxed

250
Q

With what diseases has the vaccine programme relaxed

A

Smallpox and TB vaccine mostly stopped for UK kids

251
Q

What happens when pathogen undergo genetic mutations which change their antigens

A

Memory cells produced by vaccination don’t recognise new antigen and so pathogen may be transmitted and incidence of disease increases

252
Q

What is an example of a difficult disease to vaccinate against

A

Influenza as it is relatively unstable and regularly undergoes change in its antigens, when this happens epidemic may occur

253
Q

Why must threats from epidemics be monitored

A

So new strains of pathogen can be identified which enables health authorities to prepare from impending pandemic by stockpiling suitable vaccines and vaccinating those at risk from certain disease

254
Q

What is influenza and who does it affect

A

A killer disease cause by a virus, people over 65 and those with respiring tract conditions most at risk

255
Q

What occasionally happens with influenza that causes risk of epidemic and 3 examples

A

A new strain of flu virus arises that’s particularly virulent such as 1918 flu epidemic killed 40million worldwide, 1968/9 1 million died from Hong Kong flu and 2009-10 540 000 cases of swine flu in UK

256
Q

Ehh are worldwide numbers unknown for swine flu

A

Numbers unknown as strain was less virulent that expected so many cases were unreported

257
Q

Why are people at risk immunised

A

To avoid a pandemic

258
Q

What does the UK vaccination programme ensure for influenza

A

Over 65 and at risk are vaccinated and immunised- in 2013/14 75% over 65 immunised and 5% at risk we immunised

259
Q

What is newest development on influenza vaccine

A

Vaccine developed which can be taken by nasal spray and proposed to be given to all children in new few years

260
Q

What is so difficult about vaccinating flu

A

Strain of flu changes each year so immunisation programme has to change vaccine each year (worldwide research determines most likely strain)

261
Q

What are the 4 different ways immunity can be achieved

A

Natural, artificial, active, passive

262
Q

What is natural immunity

A

Achieved by normal life processes

263
Q

What is artificial immunity

A

Achieved through medicinal intervention

264
Q

What is active immunity

A

Achieved when immune system activated and makes its own antibodies

265
Q

What is passive immunity

A

Achieved when antibodies are supplied from another source

266
Q

What is active natural immunity

A

Immunity provided by antibodies made in immune system as result of infection, a person suffers once and then is immune like chickenpox

267
Q

What is natural passive immunisation

A

Antibodies provided via placenta or breast milk, this makes babies immune to diseases to which mother is immune to which is useful for first year of babies life when their immune system developing

268
Q

What is artificial active immunity

A

Immunity provided by antibodies made in immune system as result of vaccine, person injected with weakened, dead or similar pathogen or with antigens and this activates their immune system (immunity to TB or influenza)

269
Q

What is artificial passive immunity

A

Immunity provided by injection of antibodies made by another individual (hepatitis A and B), tetanus can also be treated this way when vaccine using toxoid hasn’t worked well

270
Q

How many different types of medicine are there in UK

A

6000

271
Q

Why are new drugs needed x3

A

New diseases emerging, still many diseases with no effective treatment, some antibiotic treatment became less effective

272
Q

How are new medicines discovered

A

Accidentally, observation of wildlife, plant research, personalised medicine, synthetic biology

273
Q

What is a famous accidental discovery of a drug

A

Antibiotic penicillin discovered by Fleming

274
Q

How does penicillin work

A

Fungus penicillin releases compounds that kill bacteria

275
Q

How did Fleming discover penicillin

A

Accident but he observed what he saw and explained what he saw, then Florey and Chain purified penicillin and demonstrated potential use of antibodies- shows importance of teamwork in science

276
Q

Are drugs a new discovery

A

No, many drugs have been used for centuries as people noted plants/extracts that have beneficial effect

277
Q

What did world health organisation calculate that the worlds population relies on traditional drugs

A

80%

278
Q

How many drugs are traditional medicine in India, China and Europe

A

India-7000 China- 5000 and in Europe many Morden drugs originated from traditional medicine

279
Q

Where does morphine originate form and when was it found

A

Sap from unrip poppyseed heads as long as Neolithic times

280
Q

What was used as anaesthetic in 12th century and from where and then in 19th century

A

Opium from poppies used and by 19th century both opium and morphine used

281
Q

How do opiate drugs, morphine and opium work as anaesthetic

A

They reduce nervous action in CNS, if nerves can’t carry impulses then no pain is felt

282
Q

What is medicinal use of willow bark and for how long

A

Reduce pain and fever- used for a long time

283
Q

After discovery of willow bark active ingredients what happened

A

A way was later found to reduce side effect of stomach bleeding by adding acetyl group which led to development of drugs aspirin and ibuprofen

284
Q

What animals make use of plants with medicinal properties and how

A

Monkeys, bears and other animals rub citrus oils on their coats as insecticides and antiseptics to prevent insect bite and infection and birds line their nest eight leaves to protect chicks from blood sucking mites

285
Q

What do scientists use traditional plant medicines and animal behaviour for

A

A starting point in search for new drugs

286
Q

How was aspirin developed

A

Research into plants used for traditional remedies enabled scientists to isolate active ingredient, this molecule can be analysed and similar molecules can then be manufactured

287
Q

In recent years where has discovery of natural drugs been focused on

A

Concentrated on tropical plants

288
Q

Why has natural drug research been focused on tropical plants

A

They have great diversity and there are hopes they may contain molecules that could form new medicinal drugs, but it’s important to remember there may be potential uses of wild and cultivated plants in the UK

289
Q

What is new chemical fingerprinting technology allowing scientists to do

A

Screen natural chemicals more effectively for their activity as potential medicines

290
Q

What are pharmaceutical companies research to do with disease causing mechanisms

A

Ways microorganisms cause disease

291
Q

How are pharmaceutical companies seeing how microorganisms cause disease

A

Looking at receptors on plasma membrane like HIV bonds to CD4 and CCR5 receptors on surface of T helper cells, so if binding between pathogen and receptor site can be blocked then disease causing pathogens can’t enter cell

292
Q

How can pharmaceuticals uses glycoprotein receptor molecules to determine how microorganisms cause disease

A

Glycoprotein receptor molecules can be isolated and sequenced- once the amino acid sequence is known, molecular modelling can be used to determine shape of receptor

293
Q

What is the next step in drug research

A

Finding a drug that mimics the shape of receptor and could be used to bind to virus itself which would block virus entering T helper cells- similarly drugs that inhibit action of certain enzymes can also be developed

294
Q

How does sequencing technology and molecular modelling have huge potential for future medicines

A

It’s possible to screen genomes of plants or microorganisms to identify potential medicinal compounds from DNA sequences

295
Q

What is personalised medicine

A

When fully developed sequencing technology and molecular modelling may be possible to sequence genes from individuals with certain condition and develop specific drugs for this condition

296
Q

What is 1 form of synthetic biology

A

Development of new molecules, especially enzymes that mimic biological systems

297
Q

What’s another form of synthetic biology

A

Used to design and construct new devices and systems that may be useful in research, healthcare or manufacturing (eg. Development of tomatoes containing pigment anthocyanin- pigment found in fruits like blueberries and has specific health benefits)

298
Q

What are anthocyanin

A

Antioxidants that help protect against coronary heart disease

299
Q

What are antibiotics

A

Compounds preventing growth of fungi or bacteria

300
Q

Is penicillin only antibiotic

A

No, since Flemings discovery many different compounds with antibiotic properties been discovered

301
Q

What are most in use antibiotics derivatives of

A

Compounds made by bacteria form genus streptomyces- antibiotics used widely to treat bacterial infection

302
Q

What happened before antibiotics

A

Many died from wound/surgery when they became infected

303
Q

When did antibiotics come widespread

A

In ww2 to prevent infection of wounds

304
Q

What has overuse/ misuse of antibiotics caused

A

Microorganisms to develop resistance and many currant antibiotics now have limited effectiveness, some bacteria became infamous for their multiple resistance to range of antibiotics

305
Q

What microorganisms have developed resistance to many antibiotics

A

Clostridium difficle and methicillin-resistance staphylococcus (MRSA)

Alevel Biology (25 decks)

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