4.1.1 Disease and the Immune System Flashcards

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1
Q

What is a disease?

A
  • a condition that impairs the normal functioning of an organism
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2
Q

What is a pathogen?

A
  • a disease-causing organism

- can be bacteria, fungi, viruses and protoctista

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3
Q

What is a communicable disease

A
  • a disease that can be spread between organisms

- aka infection disease

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4
Q

What causes tuberculosis and what does it affect?

A
  • bacterium

- animals, typically animals and cattle

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5
Q

What causes bacterial meningitis and what does it affect?

A
  • bacterium

- humans

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6
Q

What causes ring rot and what does it affect?

A
  • bacterium

- potatoes, tomatoes

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7
Q

What causes HIV/AIDS and what does it affect?

A
  • virus

- humans

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8
Q

What causes influenza and what does it affect?

A
  • virus

- animals

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9
Q

What causes tobacco mosaic virus and what does it affect?

A
  • virus

- plants

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10
Q

What causes black sigatoka and what does it affect?

A
  • fungus

- banana plants

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11
Q

What causes ringworm and what does it affect?

A
  • fungus

- cattle

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12
Q

What causes athlete’s foot and what does it affect?

A
  • fungus

- humans

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13
Q

What causes potato/tomato late blight and what does it affect?

A
  • protoctist

- potatoes and tomatoes

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14
Q

What causes malaria and what does it affect?

A
  • protoctist

- animals

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15
Q

What is direct transmission?

A
  • when a disease is transmitted directly from one organism to another
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16
Q

give examples of direct transmission

A
  • direct physical contact
  • droplet infection
  • sexual intercourse
  • transmission by spores
  • faecal
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17
Q

What is indirect transmission?

A
  • when a disease is transmitted from one organism to another via an intermediate
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18
Q

Give examples of indirect transmission

A
  • intermediates such as
  • air
  • water
  • food
  • vector (another organism)
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19
Q

What three factors affect disease transmission?

A
  • overcrowding: living condition increase transmission of many communicable diseases
    e. g. TB is spread directly via droplet infection
  • climate:
    e. g. potato/tomato late blight is common during wet summers because spores need water to spread
    e. g. malaria because ideal for mosquito
  • humans, social factors:
    e. g. healthcare and education
  • poor ventilation
  • homelessness
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20
Q

Give examples of the primary non-specific defences to prevent pathogens entering an organism

A
  • skin
  • mucous membranes
  • blood clotting
  • inflammation
  • wound repair
  • expulsive reflexes
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21
Q

Explain how skin acts as a primary, non-specific defence

A
  • physical barrier, blocking pathogens from entering the body
  • acts as a chemical barrier by producing chemicals that are antimicrobial and can lower pH, inhibiting growth of pathogens
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22
Q

Explain how mucous membranes acts as a primary, non-specific defence

A
  • these protect body openings that are exposed to environment such as mouth, nostrils, ears, anus etc
  • goblet cells secrete mucous
  • mucus lines the passages and traps any pathogens
  • epithelium also has militated cells
  • they move the mucus to the top of the trachea, where it enter the oesophagus
  • it is swallowed and passes down the digestive system
  • this is killed by stomach and pathogen’s enzyme denatured
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23
Q

Explain how blood clotting acts as a primary, non-specific defence

A
  • a blood clot is a mesh of fibrin fibres
  • blood clots plug wounds to prevent pathogen entry and blood loss
  • they’re formed by a series of chemical reactions that take place when platelets are exposed to damaged blood vessels
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24
Q

Explain how inflammation acts as a primary, non-specific defence

A
  • include swelling, pain, heat and redness
  • can be triggered by tissue damage, as it releases molecules, increasing permeability of blood vessels, leaking fluid and causing swelling
  • molecules also cause vasodilation, which increases blood flow
  • makes area hot and brings white blood cells to the area to fight off any pathogens
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25
Q

Explain how wound repair acts as a primary, non-specific defence

A
  • surface is repaired outer layer of skin dividing and migrating to the edges of the wound
  • tissues below the wound then contract to being edges of the wound closer together
  • repaired using collagen fibres
  • scar formed when too many collagen fibres
26
Q

Explain how expulsive reflexes acts as a primary, non-specific defence

A
  • e.g. coughing and sneezing
  • attempts to expel foreign objects, including pathogens
  • occurs automatically
27
Q

Describe physical defences plants have

A
  • leaves and stems have a waxy cuticle, which provides a physical barrier against pathogen entry
  • may also stop water collecting on the lead, reduces risk of infection that are transferred between plants in water
  • plants are surrounded by cell wall
  • forms a physical barrier against pathogens that makes it past the waxy cuticle
  • plants produce a polysaccharide called callose
  • callose gets deposited between plant cell walls and plasma membranes during times of stress
  • callose deposition may make it harder for pathogens to enter cells
  • callose deposiition at the plasmodesmata may limit the spread of viruses between cells
28
Q

Describe chemical defences plants have

A
  • antimicrobial chemicals that kill pathogens or inhibit their growth
    e. g. saponins: destroy cell membranes of fungi and other pathogens
    e. g. phytoalexins: inhibit growth of fungi
  • other chemicals are toxic to insects: reduces the amount of insect-feeding on plants,
    reduces infection by plant viruses carried by insect vectors
29
Q

What are antigens?

A
  • antigens are molecules, usually proteins or polysaccharides, found on the surface of cells
30
Q

What is the difference between non-specific and specific immune responses?

A
  • non specific happens the same way for all microorganism

- specific is antigen specific, involving t and B lymphocytes

31
Q

What are the four main stages in the immune response?

A
  1. phagocytes engulf pathogens
  2. phagocytes activate T lymphocytes
  3. T lymphocytes activates B lymphocytes, which divide into plasma cells
  4. Plasma cells make more antibodies to a specific antigen
32
Q

Describe the first stage in the immune response

A
  • a phagocyte recognises the antigens on a pathogen
  • the cytoplasm of the phagocyte moves round the pathogen, engulfing it
  • this may be made easier by the presence of opsonins, molecules that attach to foreign antigens to aid phagocytosis
  • the pathogen is now contained in a phagosome, a type of vesicle in the cytoplasm of the phagocyte
  • a lysosome fuses with the phagosome, and the enzymes break down the pathogen
  • the phagosome then presents the pathogen’s antigens
  • it sticks the antigens on its surface to active other immune system cells
  • this is known as an antigen-presenting cell (APC)
33
Q

What is a phagocyte?

A
  • a phagocyte is a type of white blood cell that carries out phagocytosis (engulfment of pathogens)
  • found in blood and in tissues and carry out a non-specific immune response
34
Q

What are neutrophils?

A
  • a type of phagocyte
  • first white blood cells to respond to a pathogen inside the body
  • neutrophils move towards a wound in response to signals from cytokines, which are released by cells at the site of the wound
35
Q

Describe stage two of the immune response

A
  • a T lymphocyte is another type of white blood cell
  • surface is covered with receptors
  • receptors bind to antigens presented by APCs
  • each T lymphocyte has a a different receptor on its surface
  • when the receptor on the surface of a T lymphocyte meets a complementary antigen, it binds to it, so each T lymphocyte will bind to a different antigen
  • this activates the T lymphocyte, called clonal selection
  • then the T lymphocyte undergoes clonal expansion
36
Q

What are the different types of activated T lymphocytes (stage 2)?

A
  • T helper cells: release substances to activate B lymphocytes and T killer cells
  • T killer cells: attach to and kill cells that are infected with a virus
  • T regulatory cells: suppress the immune response from other white blood cells
  • some become memory cells
37
Q

Describe the third stage of the immune response

A
  • B lymphocytes are another type of blood cell
  • they’re covered with proteins called antibodies
  • antibodies bind to antigens to form an antigen-antibody complex
  • each B lymphocyte has a different shaped antibody on its surface
  • when the antibody on the surface meets a complementary shaped antigen, it binds to
  • together with substances from T helper cells activates the B lymphocyte
  • this is another example of clonal selection
  • the activated B lymphocytes divides, by mitosis into plasma cells and memory cells
  • this is called clonal expansion
38
Q

What is cell signalling (stage 3)?

A
  • how cells communicate
  • a cell may release a substance that binds to the receptors on another cell
  • really important in the immune response because it helps to activate all the different types of white blood cells needed
  • e.g. t helper cells release interleukins (a type of cytokine_ that bind to receptors of B lymphocytes
  • activates B lymphocytes
39
Q

Describe stage four of the immune response

A
  • plasma cells are clones of the B lymphocyte
  • they secrete loads of antibody’s specific to the antigen into the blood
  • this will from a lot of antigen-antibody complexes
40
Q

Describe the structure of an antibody

A
  • variable region: form the antigen binding sites
  • the shape of the variable region is complementary to a particular antigen. differs between antibodies

-hinge region: allows flexibility when the antibody binds to the antigen

  • constant regions: allow binding to the receptors on immune system cells. constant region is the same (same sequence of amino acids) in all antibody s
  • disulphide bridges hold the polypeptide chains of the protein together
41
Q

How do antibodies help clear infections

A
  • agglutinating pathogens: each antibody has two binding sites, so an antibody can bind to two pathogens at the same time, making the clumped together
  • phagocytes called agglutinins then bind to the antibodies and phagocytose a lot of pathogens all at once
  • neutralising toxins: toxins have different shapes. antibodies called anti-toxins can bind to the toxins produced by pathogens. this prevents the toxins from affecting human cells, so the toxins are neutralised. the toxin-antibody complexes are also phagocytose
  • preventing the pathogen binding to human cells: antibodies may block the cell surface receptors that the pathogens need to bind to the host cells. meaning the pathogen can’t attach to or infect host cells
42
Q

Describe why the primary response is slow

A
  • when a pathogen enters the body for the first time, the antigens on its surface activate the immune system. this is the primary response
  • the primary response is slow because there aren’t many B lymphocytes that can make the antibody needed to bind to it
  • eventually the body will produce enough to overcome the infection, but showing symptoms of disease
  • after exposure, both B and T lymphocytes produce memory cells, which remain in the body for a long time
  • Memory T lymphocytes remember the specific antigen and will recognise it
  • Memory B lymphocytes remember the specific antibodies needed to bind to the antigen
  • the person is now immune
43
Q

Describe the secondary response

A
  • if the same pathogen enters again, immune system will produce a quicker, stronger immune response
  • known as secondary response
  • clonal selection happens faster
  • memory B lymphocytes are activated and divide into plasma cells that produce the right antibody to the antigen
  • memory T lymphocytes are activated and divide into the correct type of T lymphocytes to kill the cell carrying antigen
  • secondary response often begins before any symptoms are shown
44
Q

What is active immunity?

A
  • when your immune system makes its own antibodies after being stimulated by an antigen
45
Q

What are the two different types of active immunity?

A
  • natural: when you become immune after catching a disease

- artificial; when you become immune after vaccination

46
Q

What is passive immunity?

A
  • the type of immunity from being given antibodies made by a different organism
  • immune system doesn’t produce antibodies of its own
47
Q

What are the two types of passive immunity?

A
  • natural: when a baby becomes immune due to the antibodies received from mother through placenta and breast milk
  • artificial: when you become immune after being injected with antibodies from someone else
48
Q

which type of immunity require exposure to antigen?

A
  • active
49
Q

which type of immunity takes a while to develop?

A
  • active
50
Q

which type of immunity has long-term protection?

A
  • active
51
Q

Which type of immunity produces memory cells?

A
  • active
52
Q

What is an autoimmune disease?

A
  • when an organism’s immune system isn’t able to recognise self-antigens
  • immune system treats the self-antigens as foreign antigens and launches an immune response on its own tissues
53
Q

give examples of autoimmune diseases

A
  • lupus: immune system attacking cells in the connective tissues. damages tissues and causes painful inflammation. affects skin, joints, organs
  • rheumatoid arthritisL caused by the immune system attacking joints.
54
Q

How do vaccines control disease and prevent epidemics?-

A
  • vaccines avoid you suffering symptoms from the disease as the B lymphocytes usually have to divide to deal with pathogen
  • vaccines contain antigens that cause your body to produce memory cells against a particular pathogen, without cause disease. you become immune without symptoms
  • disease becomes rare if most people in a community are vaccinated. herd immunity. prevents epidemics
  • vaccines always contain antigens that may be free, or attached to a dead or attenuated pathogen
  • booster vaccines may be given later on to make sure memory cells are produced
55
Q

Is vaccination the same as immunisation?

A
  • no
  • vaccination is the administration of antigens into the body
  • immunisation is the process by which you develop immunity
  • vaccination causes immunisation
56
Q

Give examples of routine vaccines

A
  • MMR

- meningitis C

57
Q

Why do vaccination programmes change?

A
  • flu vaccine changes every year because antigens on the influenza virus change regularly, forming new strains
  • memory cells produced from vaccination with one strain will not recognise other strain with different antigens
  • the are immunologically distinct
  • a different vaccine has to be made every year
  • labs such as WHO and CDC collect samples of different strains to test for effectiveness
  • new vaccines developed and choose most effective
  • governments choose
58
Q

what are antibiotics and why are they useful?

A
  • antibiotics are chemicals that kill or inhibit the growth of bacteria
  • used by humans to treat bacterial infections
  • useful because they can target bacterial cells without damaging human body cells
59
Q

Describe antibiotic resistance and why it is a problem

A
  • there is genetic mutation in a population of bacteria
  • genetic mutations make some bacteria naturally resistant to an antibiotic
  • the bacterium is more adapted for survival and so it lives longer and reproduces
  • this leads to the allele for antibiotic resistance being passed onto offspring
  • antibiotic resistance spreads and becomes more common over time
  • a problem because you can’t get rid of them with antibiotics
  • increased use of antibiotics means antibiotic resistance is increasing
  • superbugs are becoming more common meaning we are less able to treat potentially life threatening bacteria infection
60
Q

Give examples of antibiotic-resistant bacteria

A
  • MRSA (meticillin resistant staphylococcus aureus): causes serious wound infections and is resistant to several antibiotics, including meticillin
  • clostridium difficile: infects digestive system. c. difficile produces a toxin, causes fever diarrhoea and cramps
61
Q

Descrive sources of medicine

A
  • natural compounds: plants, animals and microorganisms
  • only a small population of organism have been investigated so far, so perhaps many more antibiotics
  • we need to protect sources of drugs by maintaining biodiversity, or it could die before studied
  • using new technique to look at already studied organisms
62
Q

What is the future of medicine?

A
  • personalised medicine:
  • genes determine how body responds to drugs. different people respond different, making it more effective for some than others.
  • personalised medicine is tailored to an individual’s DNA. doctors may be able to predict how you will respond to different drugs and prescribe most effective
  • hope more effective drugs

synthetic biology:

  • using technology to design and make artificial proteins, cells and microorganisms
  • e.g. engineering bacteria to destroy cancer cells