u4 ao1 Flashcards

1
Q

first line of defence

A

the presence of physical, chemical, and microbiological barriers to keep pathogens out of the host organism

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2
Q

physical barriers (def and examples)

A

barriers that prevent of impede entry of pathogens

intact skin, cilia in the airways

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3
Q

chemical barriers (def and example)

A

Barriers that act to inhibit the growth or development of pathogens and/or act to destroy pathogens

stomach acid, antibacterial compounds in earwax

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4
Q

microbiological barriers

A

The presence of non-pathogenic bacteria (known as normal flora) in the body can prevent the growth or colonisation of pathogenic microorganisms as they compete for space and resources

bacteria on the skin, lower gastrointestinal tract

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5
Q

second line of defence

A

nonspecific response to injury and/or pathogens by a variety of cells and molecules

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6
Q

steps in the inflammatory response

A

Inflammation is initiated when damaged cells release cytokines to trigger nearby mast cells to release histamine

Histamine binds to blood vessels, resulting in vasodilation (widening of blood vessels) that increases blood flow, and increased permeability that makes the blood vessel more leaky

White blood cells, such as phagocytes, can easily leave the blood vessel and migrate to the site of inflammation. There is also an increase in fluid leaving blood vessels to the area of inflammation.

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7
Q

what are phagocytes

A

group of leukocytes responsible for the endocytosis and destruction of pathogens, foreign material, and cell debris

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8
Q

what are macrophages

A

a type of leukocyte found throughout the body that engages in phagocytosis and antigen presentation

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9
Q

what are neutrophils

A

Engages in phagocytosis of pathogens and foreign material, as well as the release of cytokines

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10
Q

antigen presenting cell

A

display antigens from consumed pathogens on their surface and interact with the adaptive immune system

Antigen-presenting cells are the specific immune cells which also express MHC Class II, using them to present the consumed antigens on their surface. These cells will then use their MHC Class II markers with the presented antigen to interact with the adaptive immune system

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11
Q

dendritic cells

A

a type of leukocyte
that engages in phagocytosis and antigen presentation

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12
Q

cytokines

A

a signalling molecule released by cells (typically in the immune system) which aids in communication between immune cells and helps protect against pathogens

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13
Q

eosinophils

A

a large granular leukocyte responsible for the release of toxic chemical mediators

contain toxic chemical mediators which destroy invading pathogens

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14
Q

natural killer cells

A

targets both abnormal and virally infected cells done by a killer inhibitory receptor and a killer activation receptor

killer inhibitory receptor – examines the surface of cells for MHC Class I markers

killer activation receptor – binds to certain molecules which appear on cells undergoing cellular stress (e.g. infected or cancerous cells).

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15
Q

mast cells

A

a type of leukocyte responsible for releasing histamine during allergic and inflammatory responses

Mast cells reside in connective tissues throughout the body. When they detect injury to surrounding cells or are stimulated by antigens or allergens, they become activated and degranulate, releasing histamine. Histamine has a number of effects on the body and is particularly important in the inflammatory response.

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16
Q

complement proteins

A

a number of different types of proteins found in the blood that opsonise, cause lysis, and attract phagocytes to invading pathogens

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17
Q

what can complement proteins do

A

opsonisation- stick on the surface of pathogens which makes it easier for phagocytes to recognise them as foreign

chemotaxis- gather near a pathogen and attract phagocytes which makes it more likely to be destroyed

lysis- complement proteins made a membrane attack complex (MAC) which create pore in the pathogen and destroy the pathogen by lysis (influx of fluid into the pathogen)

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18
Q

interferons

A

a cytokine released by virally infected cells that increases the viral resistance of neighbouring
uninfected cells

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19
Q

how are T cells made tolerant

A

T-cells only become activated when all parts of the epitope binds to the receptor

Epitopes recognised by T-cell receptors in the thymus consist of small self antigens held by a MHC protein

T-cells whose receptors bind these epitopes so tightly that they could attack the self cell are deleted by apoptosis.

The T-cells that survive this negative selection leave the thymus and migrate throughout the immune system to lymph nodes

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20
Q

how are B cells made tolerant

A

B cells are formed and mature in the bone marrow

Any cells that produce a receptor for antigen (BCR) that would bind self components too tightly undergo a process of receptor editing

They dip again into their pool of gene segments that encode the light and heavy chains of their BCR and try to make a new BCR that is not a threat (alternate splicing plays a big role here). If they fail, they commit suicide

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21
Q

what is the lymphatic system

A

a large network of vessels and tissues throughout
the body that form an important component of both the circulatory and immune systems

transportation of APC to secondary lymphoid tissues for antigen recognition
production of leukocytes, including lymphocytes in primary lymphoid tissues
removal of fluid from tissues around the body
absorption of fatty acids from around the body

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22
Q

what is the role of lymph nodes

A

a small secondary lymphoid tissue of the lymphatic system where antigen-presenting cells activate the adaptive immune system

23
Q

what are the primary lymphoid tissues

A

the place of creation and maturation of lymphocytes

bone marrow and thymus

24
Q

where are T/B-cells developed and where do T-cells go to mature

A

B and T cells are formed and mature in the bone marrow

T cells travel to the thymus to mature

25
Q

where do mature T/B cells reside

A

secondary lymphoid tissues which are the lymph nodes (tonsils) and the spleen

26
Q

what happens in secondary lymphoid tissues

A

maintenance of mature lymphocytes and ‘scans’ passing lymph for the presence of any pathogens or antigen-presenting cells.

27
Q

cell mediated

A

Antigen presenting cells (for example a dendritic cell but sub in cells if the question states one) carrying a target antigen on their MHC II binds to a complementary naïve T cell’s T cell receptor, triggering the release of cytokines.

The naïve T cell is activated and undergoes clonal expansion and differentiation into helper T and cytotoxic T cells (and memory T and suppressor T cells but this isn’t a major focus of your study design).

Helper T cells will regulate the action of other immune cells whilst cytotoxic T cells will travel to the area of infection, bind to affected cells displaying the target antigen and will trigger the death of target cells via apoptosis or perforin or granzymes.

28
Q

humoral response

A

The antigen binds to a complementary B cell receptor. This naïve B cell will also bind to a complementary Helper T cell via its MHC 2 and receive co-stimulation via cytokines from the helper T cell

The naïve B cell is activated and undergoes clonal expansion and differentiation into plasma B and memory B cells

Memory B cells will stay in the body in the event of future infections, whilst plasma B cells produce and release antibodies. These antibodies can bind to the target antigen and cause responses such as agglutination, opsonisation, neutralisation, immobilisation

29
Q

what are antibodies (function and longetivity)

A

quaternary structure released by plasma cells that bond to antigens on the surface of pathogens

30
Q

difference b/w antigen binding site and epitope

A

antigen binding site is where the antigen binds to while the epitope is the section of the antigen that actually binds to the antigen binding site

31
Q

B lymphocytes

A

a type of lymphocyte that plays an important role in humoral immunity and differentiates into plasma cells and B memory cells

32
Q

B memory cells

A

a differentiated B lymphocyte that is responsible for providing long-lasting immunological memory of an antigen

33
Q

Helper T

A

a type of differentiated T lymphocyte that supports the functioning of a number of different immune cells, including the cloning and differentiation of selected T and B cells

34
Q

cytotoxic T cells

A

a differentiated T lymphocyte that is responsible for the destruction of infected or abnormal cells

35
Q

how did European arrival negatively affected the immunity of Aboriginal and Torres Strait Islander peoples

A

major diseases in Europe bought to Australia from settlers were new in Indigenous populations, meaning there were no forms of immunity, natural or artificial, within indigenous populations.

No previous exposure to or knowledge of pathogens
Population density of groups forced into camps by colonisers
Decreased health and nutritional status of Aboriginal and Torres Strait Islander peoples due to disruption by colonisation
Intergroup social relationships

36
Q

why is there a gap in Indigenous and non-Indigenous health throughout history and in modern times

A

After European arrival, their access to food and water was restricted and denied, medicine practices were disrupted, and their relationship with Country and culture was irrevocably changed. They were also forced into camps at the edges of towns, where the opportunities for infection was heightened due to increased population densities.

All of these conditions led to a general decrease in the health status of Aboriginal and Torres Strait Islander people, making them more susceptible to disease and death.

However, it is difficult to accurately quantify the sheer impact that the Europeans had on the population and health status of Indigenous Australians.

37
Q

scientific strategies to identify pathogens

A

microscope,
letting them grow more to collect a bigger sample
antibodies/antigen detections
genetic sequencing

38
Q

social strategies to control spread of pathogen

A

Enforced quarantines

Public education on methods to limit the spread of the disease (hygiene and preventative methods to reduce risk of infection) or on proper use of medications (to avoid antibiotic resistance)

Government mandates (restrictions of public density limits and distancing, mask use)

Funding for research, testing, contact tracing and vaccination programs

39
Q

scientific strategies to control spread of pathogen

A

antibiotics, antivirals, fungicides

40
Q

what is R0

A

average amount of people that can be infected from one person

41
Q

what are different modes of transmission

A

Animal vectors
Airborne transmission
Droplet transmission
Direct physical contact transmission
Indirect physical contact transmission
Faecal-oral transmission

42
Q

what is an emerging diseases and why do diseases emerge

A

a disease caused by a newly identified or previously unknown agent
a disease that has existed but whose incidence in humans has increased in the past two decades, either locally or internationally.

43
Q

what is a re-emerging disease

A

disease which reappears after a significant decline in its incidence. Re-emerging diseases were once controlled but have increased to a level that causes significant health issues.

44
Q

why do diseases emerge/re-emerge

A

Mutations and evolution in pathogens
Globalisation and increased mobility of humans
Exposure of humans to animals
Increased population size and population density
Decreasing vaccination rates

45
Q

vaccination programs

A

a series of vaccinations designed to create long-term immunity to a disease

46
Q

different types of vaccinations and what they are

A

attenuated- live weak version of the pathogen (strongest)

inactive- killed pathogen (weaker)

subunit- the antigen of the pathogen only (weak)

mRNA (weak)

47
Q

draw graph of vaccination thing

A
48
Q

what is herd immunity

A

protection against a disease conferred to non-immune individuals when a high percentage of a population is immune to the same disease. Herd immunity is often achieved through high rates of vaccination

49
Q

what is immunotherapy

A

modifying the immune response by medical intervention

50
Q

monoclonal antibodies

A

Monoclonal antibodies are antibodies artificially derived from a single B cell clone (i.e. identical specific antibodies). They are most commonly made by
An animal (typically a mouse) is injected with an antigen and produces antigen-specific plasma cells
The plasma cells are removed and fused (hybridised) with tumour cells capable of endless divisions (immortal cell line)
The resulting hybridoma cell is capable of synthesising large quantities of monoclonal antibody

51
Q

what are the different types of immunity and examples

A

active natural - contracting a pathogen
active artificial - vaccine

natural passive- getting antibodies from an external source vie medical intervention
artificial passive- breastfeeding

52
Q

difference b/w pandemic and epidemic

A

The terms pandemic and epidemic both relate to the uncontrolled spread of infectious diseases, but they differ in geographic spread.

A pandemic affects a much larger geographical area compared with an epidemic. In an interconnected world, an epidemic can develop into a pandemic (but not vice versa).

For the World Health Organization (WHO) to declare an event as a pandemic, the infection must spread easily and sustainably among human populations in at least three countries in at least two different WHO regions.

53
Q

allergies

A

Upon initial exposure to the allergen, complementary B cells are activated and plasma B cells will release IgE.

IgE binds to mast cells to sensitise them

Upon re-exposure to the allergen, the allergen will bind and cross-link to the IgE on sensitised mast cells. This triggers the release of histamine and causes symptoms of inflammation