Lesson 3: Defence against disease Flashcards

1
Q

What are pathogens?

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 - physical 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 healthy 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 are the differences between innate and adaptive immune systems?

A

Innate:
* present from birth
* provides rapid
* non-specific defences against pathogens.
* Mediated by phagocytes.
Adaptive:
* Develops during our lives
* slower
* specific
* mediated by lymphocytes

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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

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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25
What immunity are T lymphocytes involved in?
cell-mediated immunity
26
What response are B lymphocytes involved in?
humoral response
27
What are the types of T cells/lymphocytes?
T helper cells T killer cells T regulator cells T memory cells
28
What are the functions of T killer cells?
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.
29
What are the function(s) of T regulator cells?
suppress the immune system after pathogens have been destroyed
30
What are the function(s) of T memory cells?
provide a rapid response if the body is re-infected by the same pathogen.
31
What are antibodies?
Y-shaped proteins that bind to a specific antigen that has triggered an immune response.
32
What is the structure of antibodies?
2 heavy chains bonded to 2 light chains through disulphide bridges
33
What mechanism do antibodies bind to antigens with?
lock and key
34
What is the binding site on antibodies called?
variable region
35
What is the function of hinge regions on antibodies?
allows flexibility, meaning two antigens can bind at once.
36
What is formed when an antibody binds to an antigen?
antigen-antibody complex
37
What are the 3 ways antibodies can defend against pathogens?
opsonin agglutinins anti-toxins
38
What is the opsonins method?
bind to and ‘tag’ pathogens, making them recognisable to phagocytes.
39
What is the agglutinins method?
causes pathogens to clump together
40
What is the anti-toxins method?
binds to toxins and making them harmless.
41
Which response requires the production of antibodies, humoral or cellular?
humoral
42
Stages of humoral response
* 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.
43
How is HIV transmitted?
* unprotected sex * blood transfusions * breastfeeding
44
What are the effects of HIV?
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.
45
What is one way of determining the progression of HIV?
measure the helper T-cell count
46
What are antibiotics?
drugs used to treat bacterial infections.
47
What are the two types of antibiotics?
Bactericidal Bacteriostatic
48
How do bacteriostatic antibiotics work?
slow the growth or reproduction of bacteria.
49
How do bactericidal antibiotics work?
kill bacterial cells
50
What can antibiotics target in bacteria?
protein synthesis membrane integrity cell wall
51
What is antibiotic resistance?
bacteria with resistance to antibiotics due to genetic mutation
52
What are the steps of achieving antibiotic resistance?
* 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.
53
What is the issue with antibiotic resistance?
resistance is developing faster than new antibiotics
54
How to prevent antibiotic resistance?
* Practise good hygiene * Take antibiotics only when needed * Make sure to complete the full course of antibiotics.
55
What are zoonotic diseases?
disease that can spread from non-human vertebrate animals to humans.
56
What are spillover events?
when pathogens which are found in other animals cross to humans.
57
How are the chances of spillover events increased?
Consumption of their meat Poaching Deforestation
58
How do vaccines work?
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.
59
What is the difference in immune response between the first and second vaccination?
second immune response is larger and stronger than first
60
What is herd immunity?
when a significant number of people in the population have been vaccinated, giving protection to those that do not have immunity.
61
What factors need to be considered when evaluating data related to the COVID-19 pandemic?
* Data sources * Data types * Data collection * Data representation * Data limitation
62
How are T helper cells activated?
when it binds to a complementary antigen
63
What paths can a T-helper cell take after activation?
* More helper T-cells are produced * Produces interleukins which activates the B-cells specific to the same antigen * Produces interleukins which activates killer T-cells specific to the same antigen