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biology topic 5 > Lesson 3: Defence against disease > Flashcards

Lesson 3: Defence against disease Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

What are pthogens?

A

organisms that cause disease

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2
Q

What are the different types of pathogens?

A
  • bacteria
  • fungi
  • protists
  • viruses
  • prions
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3
Q

How is bacteria harmful?

A

Produce toxins that damage body cells.

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4
Q

How is fungi harmful?

A

Digest living cells to destroy them. Some also produce toxins.

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5
Q

How is protist harmful?

A

Take over cells and break them open.

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6
Q

How are viruses harmful?

A

Use host cells to replicate before bursting out and destroying cells.

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7
Q

How are prions harmful?

A

causes degeneration of the nervous system

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8
Q

What color is gram positive bacteria after gram staining?

A

blue-purple

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9
Q

What color is gram negative bacteria after gram staining?

A

red

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10
Q

What are the two main defence mechanisms against pathogens?

A

non-specific and specific

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11
Q

What is non-specific defence?

A

response is the same for all pathogens

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12
Q

What is specific defence?

A

response is specific to each pathogen

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13
Q

What are some physical and chemical barriers against pathogens?

A

Skin - phyiscal barrier but also produces sebum which inhibits growth of pathogens

Mucous membranes - traps pathogens and uses lysozymes to destroy them.

Skin flora - large population of natural and helathy bacteria that outcompete pathogens for surface area.

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14
Q

How does blood clot?

A
  • Damaged cells release chemicals that stimulate platelets to adhere to damaged area.
  • damaged cells and platelets release chemicals called clotting factors that convert prothrombin (clotting protein) into thrombin.
  • Thrombin is an active enzyme that catalyses the conversion of soluble fibrinogen (another clotting protein) into insoluble fibrin which is a fibrous protein that forms a mesh-like network to stabilize the platelet plug.
  • More and more cellular debris becomes trapped in the fibrin mesh until stable clot is formed.
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15
Q

What is the difference between innate and adaptive immune systems?

A
  • Innate: present from birth, provides rapid, non-specific defences against pathogens. Mediated by phagocytes.
  • Adaptative: Develops during our lives, slower, specific and mediated by lymphocytes (antibodies)
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16
Q

What is the role of phagocytes?

A

engulf and destroy pathogens

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17
Q

What are the two main types of phagocytes?

A

neutrophils and macrophages

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18
Q

What are the stages of phagocytosis?

A

The pathogen releases chemicals that attract a phagocyte.
The phagocyte recognises the pathogen’s antigens as non-self. This causes the phagocyte to bind to the pathogen.
The phagocyte engulfs the pathogen.
The pathogen is now contained within a vacuole known as a ‘phagosome’.
The lysosome, containing lysozymes, fuses with the phagosome to form a phagolysosome.
The phagocyte presents the pathogen’s antigens on its surface to activate other cells in the immune system. The phagocyte is then referred to as an antigen-presenting cell (APC).

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19
Q

When is the adaptive immune system needed?

A

Innate immune system is unable to control an infection.

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20
Q

what are the two main types of lymphocytes?

A

B lymphocytes
T lymphocytes

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21
Q

Where do B lymphocytes mature?

A

bone marrow

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22
Q

Where do T lymphocytes mature?

A

thymus gland

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23
Q

What system plays a role in the immune response of the body?

A

lymphatic system

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24
Q
A
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25
Q

Where can you usually find lymphocytes after maturation?

A

Some of them remain in circulation while others are concentrated in the secondary lymphoid organs

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26
Q

What response are T lymphocytes involved in?

A

cellular response

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27
Q

What response are B lymphocytes involved in?

A

humoral response

28
Q

What are the types of T cells/lymphocytes

A

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

29
Q

What are the functions of T helper cells?

A
  • bind to complementary antigens on antigen-presenting cells
  • produce interleukins which stimulate B cells or phagocytes
  • form memory cells or T killer cells (stimulated by interleukins)
30
Q

What are the functions of T killer cells?

A

kill abnormal and foreign cells by producing a protein known as perforin which makes holes in the cell-surface membrane, causing it to become freely permeable and causing cell death.

31
Q

What are the function(s) of T regulator cells?

A

suppress the immune system after pathogens have been destroyed

32
Q

What are the function(s) of T memory cells?

A

provide a rapid response if the body is re-infected by the same pathogen.

33
Q

what are antibodies?

A

Y-shaped proteins that bind to a specific antigen that has triggered an immune response.

34
Q

What is the struture of antibodies?

A

2 heavy chains bonded to 2 light chains through disulphide bridges

35
Q

What mechanism do antibodies bind to antigens with?

A

lock and key

36
Q

What is the binding site on antibodies called?

A

variable region

37
Q

what is the function of hinge regions on antibodies?

A

allows flexibility, meaning two antigens can bind at once.

38
Q

What is formed when an antibody binds to an antigen?

A

antigen-antibody complex

39
Q

What are the 3 ways antibodies can defend against pathogens?

A

opsonin
agglutinins
anti-toxins

39
Q
A
40
Q

what is the opsonins method?

A

bind to and ‘tag’ pathogens, making them recognisible to phagocytes.

41
Q

what is the agglutinins method?

A

causes pathogens to clump together

42
Q

what is the anti-toxins method?

A

binds to toxins and making them harmless.

43
Q

Stages of cellular response

A
  • Macrophages engulf and digest pathogens, forming Antigen presenting cell (APCs).
  • The receptors of some T helper cells fit the pathogenic antigens now presented on the APCs. They produce interleukins, which stimulate more T cells to divide.
  • The cloned T cells may:
  • Develop into T memory cells (giving rapid response if this pathogen invades again)
  • Produce interleukins that stimulate phagocytosis
  • Produce interleukins that stimulate B cells to divide
  • Stimulate the development of cloned T killer cells that are specific to the presented antigen and then destroy infected cells
44
Q

which response requires the production of antibodies, humoral or cellular?

A

humoral

45
Q

stages of humoral response

A
  • Helper T-cells are stimulated by APCs and release interleukins.
  • Colonal selection - stimulates selected B cell to clone by mitosis
  • Clonal expansion - clones differentiate into plasma cells or memory cells
  • Primary immune response - plasma cells produce antibodies
  • Secondary immune response - memory cells circulate the blood and is ready to divide if body encounters the same pathogen.
46
Q

How is HIV transmitted?

A
  • unprotected sex
  • blood transfusions
  • breastfeeding
47
Q

what are the effects of HIV?

A

t-helper cells are killed which is used to activate B-cells which produce antibodies, therefore victims develop a weak immune system (AIDS stage) and die due to inability to fight off diseases.

48
Q

What is one way of determining the progression of HIV?

A

measure the helper T-cell count

49
Q

What are antibiotics?

A

drugs used to treat bacterial infections.

50
Q

What are the two types of antibtiotics?

A

Bactericidal
Bacteriostatic

51
Q

How do bacteriostatic antibiotics work?

A

slow the growth or reproduction of bacteria.

52
Q

How do bactericidal antibiotics work?

A

kill bacterial cells

53
Q

What can antibiotics target in bacteria?

A

protein synthesis
membrane integrity
cell wall

54
Q

what is antibiotic resistance?

A

bacteria with resistance ti antibiotics due to genetic mutation

55
Q

What are the steps of achieving antibiotic resistance?

A
  • Genetic mutations occur, making some bacteria resistant to an antibiotic.
  • When an infection is treated with antibiotics, resistant bacteria are able to survive.
  • Resistant bacteria reproduce, passing on the allele for antibiotic resistance to their offspring.
56
Q

what is the issue with antibiotic resistance?

A

resistance is developing faster than new antibiotics

57
Q

How to prevent antibiotic resistance?

A
  • Practise good hygiene
  • Take antibiotics only when needed
  • Make sure to complete the full course of antibiotics.
58
Q

what are zoonotic diseases?

A

disease that can spread from non-human vertebrate animals to humans.

59
Q

what are spillover events?

A

when pathogens which are found in other animals cross to humans.

60
Q

how are the chances of spillover events increased?

A

Consumption of their meat
Poaching
Deforestation

61
Q

how do vaccines work?

A

may contain any of the following:
* Dead or inactivated pathogens.
* Attenuated (weakened) pathogen strains.
* A harmless version of a toxin.
* Isolated antigens from a pathogen.
* Genetically engineered antigens.
This stimulates the primary immune response to produce antibodies against the pathogen.
Memory cells, capable of recognising these antigens, are produced.

62
Q

What is the the difference in immune response between the first and second vaccination?

refer to slide 87, lesson 3, topic 5

A

second immune response is larger and stronger than first

63
Q

what is herd immunity?

A

hen a significant number of people in the population have been vaccinated, giving protection to those that do not have immunity.

64
Q

what factors need to be considered when evaluating data related to the COVID-19 pandemic?

A
  • Data sources
  • Data types
  • Data collection
  • Data representation
  • Data limitation

biology topic 5 (3 decks)

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