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z - A Level Biology > 4.1.1: Communicable diseases > Flashcards

4.1.1: Communicable diseases Flashcards

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1
Q

Antibody

A

Y shaped glycoprotein made by B cells of immune system in response to the presence of an antigen.

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2
Q

Antigen

A

Identifying chemical on the surface of a cell that triggers an immune response.

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3
Q

Antigen-presenting cell (APC)

A

Cell that displays foreign antigens complexed with MHCs on their surfaces.

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4
Q

Antitoxin

A

Chemicals (antibodies) that bind to toxins produced by the pathogen so they no longer have an effect.

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5
Q

B lymphocyte

A

Lymphocytes that mature in the bone marrow.

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6
Q

Cytokine

A

Cell signalling molecules produced by mast cells in damaged tissues, attracting phagocytes to the site of infection.

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7
Q

Immunoglobulin

A

Y shaped glycoproteins that form antibodies.

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8
Q

Macrophages

A

Form of phagocyte, made in the bone marrow, which travel in the blood as monocytes.

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9
Q

Memory cell

A

B and T lymphocytes that provide immunological memory.

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10
Q

Monocytes

A

Form in which macrophages travel in the blood.

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11
Q

Neutrophils

A

Most common form of phagocyte. Has a multilobed nucleus and is produced in the bone marrow.

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12
Q

Two main types of phagocyte

A
  • Neutrophil

* Macrophage

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13
Q

Opsonin

A

Chemicals that bind to pathogens, tagging them so that phagocytes can recognise them more easily.

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14
Q

Phagocyte

A

Cell that engulfs a pathogen.

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15
Q

Phagocytosis

A

Process in which a phagocyte engulfs a pathogen.

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16
Q

Plasma cell

A

Type of B lymphocyte which releases antibodies into circulation.

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17
Q

Primary response

A

Production of antibodies the first time a pathogen is encountered.

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18
Q

Secondary response

A

Production of antibodies the second time a pathogen is encountered.

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19
Q

T helper cell

A

T lymphocytes with CD4 receptors on cell surface membrane which bind to antigens on APCs and produce interleukins.

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20
Q

T killer cell

A

T lymphocytes that destroy pathogens carrying a specific antigen using perforin; cytotoxic T cells.

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21
Q

T memory cell

A

T lymphocytes that form part of immunological memory.

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22
Q

T regulatory cell

A

T lymphocytes that suppress immune system, stopping the response after a pathogen has been destroyed, thereby preventing an autoimmune response.

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23
Q

Variable region

A

Region on an antibody which has a shape complementary to that of a specific antigen.

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24
Q

Histamine

A

Chemicals produced by mast cells in damaged tissues that make blood vessels dilate and their walls leaky.

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25
Q

Transmission of animal diseases - direct methods

A
  • Contact (e.g. skin to skin, bodily fluids)
  • Inoculation (puncture wounds, bites, sex)
  • Ingestion (contaminated food)
26
Q

Transmission of animal diseases - indirect methods

A
  • Fomites
  • Droplet inhalation
  • Vectors (e.g. water, mosquitos)
27
Q

Factors that increase the transmission of plant diseases

A
  • Choice of plant species (resistant strain?)
  • Overcrowding or monoculture
  • Poor availability of mineral ions
  • Damp, warm conditions
  • Farming practices (disinfecting equipment, crop rotation)
  • Import/export control
  • Climate change (animal vectors in new areas)
28
Q

B effector cell

A

Divides to form plasma cell clones.

29
Q

B memory cell

A

B lymphocyte that provides immunological memory; programmed to remember a specific antigen and allow a rapid response upon reinfection.

30
Q

Secondary non-specific defenses (examples)

A

Phagocytes

31
Q

Natural active immunity

A

Antigens enter body naturally, immune response occurs (e.g. infection) –> LONG TERM

32
Q

Natural passive immunity

A

Antibodies pass from foetus/baby to mother –> do not produce antibodies of own –> SHORT TERM

33
Q

Artificial passive immunity

A

Antibodies introduced in an immune serum –> SHORT TERM –> no memory cell formation

34
Q

Herd vaccination

A

Vaccinate 80%+ of population

35
Q

Ring vaccination

A

Vaccinate people in immediate vicinty

First response to new outbreak

36
Q

Vaccinations process

A

1) Attentuated version of pathogen
2) Recognised by immune system –> formation of memory cells
3) Recognised quickly next time encountered

37
Q

Artificial active

A

Antigens introduced artificially –> VACCINE

38
Q

Sources of medicines

A

Plants and fungi
Synthesise drug design using computer programmes
Genome analysis can help find targets
Synthetic biology –> genetically engineer bacteria to produce drugs/animals in milk

39
Q

Why are new drugs needed?

A

Many diseases have no effective treatment
New diseases emerging
Antibiotic resistance
Reduce side effects

40
Q

Example of autoimmune disease

A

Lupus, Rheumatoid arthritis

41
Q

Disulfide bridge for

A

shape maintenance

42
Q

Hinge region

A

Gives flexibility, enables agglutination

43
Q

Constant region

A

Bind to phagocytes

44
Q

Variable region

A

Bind to antigen or toxin

45
Q

Primary non-specific defences in animals

A
  • Skin (keratinocytes)
  • Mucous membranes (cilia, goblet cells)
  • Stomach acid
  • Tears (contain lysozymes and antibodies)
  • Blood clotting and scab formation
  • Inflammation
46
Q

Why does blood clotting occur (context of communicable diseases)?

A

• Acts to prevent entry of microorganisms into a wound

47
Q

How does blood clotting occur?

A

• When platelets contact collagen (in skin or wall of damaged vessels) they secrete:
⟶ Thromboplastin: enzyme that triggers cascade of reactions resulting in a clot
⟶ Serotonin: makes smooth muscle in vessel walls contract to reduce blood flow

48
Q

How does inflammation occur?

A

• Mast cells release
⟶ Histamines: dilate blood vessels causing localised heat and swelling; make blood vessels more leaky causing swelling –> allows phagocytes to enter tissues, heat prevents pathogen reproduction
⟶ Cytokines which attract white blood cells

49
Q

How do cytokines work?

A
  • Cell signalling molecules which act over short distances at v. low concentrations
  • Bind to specific membrane bound receptors on phagocytes and attract them to the site of infection
  • Can cause release of second messengers inside the cell, which can alter gene expression
50
Q

How do opsonins work?

A

They bind to pathogens to make them more easily recognisable to phagocytes, e.g. antibodies

51
Q

What are agglutinins and what do they do?

A

Agglutinins: chemicals (antibodies) that cause pathogens to clump together so they are easier for phagocytes to engulf and digest.

52
Q

Two types of plant defences against pathogens

A
  • Chemical defences

* Physical defences

53
Q

How do plant physical defences work?

A

• Produce high levels of polysaccharide callose (which has 𝛽-1,3 linkages and 𝛽-1,5 linkages between glucose monomers)

1) Callose is synthesised and deposited between the cell wall and cell membrane in cells next to the infected cells. These callose papillae act as barriers, preventing pathogens entering cells around the site of infection
2) Large amounts of callose continue to be deposited in cell walls. Lignin is added, making the barrier even stronger.
3) Callose blocks the sieve plates in the phloem, sealing off the infected part of the plant.
4) Callose is deposited in the plasmodesmata between infected cells and their neighbours, sealing off healthy cells and helping prevent the pathogen from spreading.

54
Q

Examples of plant defensive chemicals

A
  • Insect repellants e.g. pine reson and citronella
  • Insecticides e.g. pyrethrins made by chrysanthemums which act as insect neurotoxins; caffeine = toxic to insects and fungi
  • Antibacterial compounds: e.g. antibiotics like phenols, antiseptics, lysosomes containing enzymes that break down bacterial cell walls.
  • Antifungal compounds: phenols; chitinases = enzymes that break down the chitin fungal cell wall.
  • General toxins: e.g. chemicals that are broken down into cyanide.
55
Q

What is cell-mediated immunity?

A

Cells have been changed from the inside e.g. viral infection, cancer cells.

56
Q

What is humoral immunity?

A

Antigens have been found outside cells e.g. bacteria, fungi, APCs

57
Q

Cell-mediated immunity (process)

A

1) Phagocyte becomes APC
2) Receptors on T-helper cells fit antigens on APC
3) T-helper cells fit antigens on APC
4) Cloned T cells:
• develop into T memory cells
• produce interleukins –> stimulate phagocytosis
• produce interleukins –> stimulate B cells to divide
• develop into T killer cells that destroy infected cells

58
Q

Humoral immunity (process)

A

1) B cell with complementary antibody engulfs pathogen , becomes APC
2) Activated T-helper cells bind to B cell APC. THIS IS CLONAL SELECTION
3) Activated T-helper cells produce interleukins two activate B cells
4) CLONAL EXPANSION: activated B cells divide by mitosis to form clones of B plasma and B memory cells
5) Cloned plasma cells produce antibodies (Primary immune response)
6) If body infected by same pathogen again, B memory cells divide rapidly to form plasma cell clones.

59
Q

What is clonal selection?

A

the B cell with the correct antibody is selected for cloning.

60
Q

What is clonal expansion?

A

activated B cells divide by mitosis to form clones of B plasma and B memory cells.

z - A Level Biology (25 decks)

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