U4O1 SAC: Flashcards

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1
Q

First Line of Defence:

A

a component of the innate immune system characterized by the presence of physical, chemical and microbiological barriers to keep pathogens out of the host organism

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2
Q

Types of First Lines of Defenses in Animals: Physical

A

Barriers that block or hinder pathogens from entering the organism

  • Intact skin
  • Mucous secretion
  • hairs(nose) that trap organisms
  • Cilia that sweep them away from the airways and into the throat where they are swallowed and destroyed
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3
Q

Types of First Lines of Defenses in Animals: Chemical

A

Barriers that work by producing chemical substances that make an environment unlivable for a pathogen

  • Presence of lysosome enzymes in tears and saliva destroy bacterial cell walls
  • Stomach Acid that destroys pathogens that have been consumed
  • Acidic sweat destroys pathogens growing on the body
  • Antibacterial compounds in earwax
  • Antibacterial proteins in semen
  • Low pH in the vagina
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4
Q

Second Line of Defence:

A

a component of the immune system characterized by the non-specific and immediate response to injury and pathogens by a variety of cells and molecules

- The backup plan for when pathogens slip past the first line of defence
- Composed of cellular and noncellular components All the cells involved are leukocytes
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5
Q

Natural Killer(NK) cells:

A

a large granulated leukocyte responsible for the recognition and destruction of damaged and or infected host cells

  • Achieved through the presence of receptors
  • releases granzymes and perforins to induce apoptosis
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6
Q

Types of NKC receptors: Killer Inhibitory Receptor

A
  • examines the surface of cells for MHC I markers
  • If the killer inhibitory receptor detects a sufficient number of MHC I markers, then it overrides the killer activation signal, preventing perforins being released and ultimately preventing cell death
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7
Q

Types of NKC receptors: Killer Activation Receptor

A
  • binds to certain molecules which appear on cells undergoing cellular stress
  • If the killer activation receptor is activated and the killer inhibitor receptor is unable to bind to sufficient MHC I markers, perforins are released forming a hole in the cell membrane
  • Granzymes are then released and enter the hole inducing cell apoptosis
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8
Q

Inflammatory Response:

A

a response designed to eliminate the effects of an injury, defend against potential pathogens, clear out cells that may be damaged or destroyed and initiate repair

- swelling - heat - pain - redness
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9
Q

Steps in the Inflammatory Response:

A
  1. Vasodilation
    • In response to an injury, Cytokines are released by immune cells
    • Mast cells degranulate releasing histamine
    • Histamine released travels to nearby blood vessels and binds to specific receptors
    • causing vasodilation which increases blood flow to the injury site causing swelling, redness and warmth
    • Gaps in blood vessels also form, increasing its permeability to cells of the immune system
  2. Phagocytosis:
    • Vasodilation increases permeability of blood vessels to allow for:
      ○ macrophages and neutrophils to enter the site of injury and phagocytose pathogens
      • Complement proteins to be attracted to pathogens and make it easier for phagocytes to destroy them
  3. Tissue Repair and Resolution
    - supporting connective tissue and functioning cells regenerate
    - inflammation ends when there is a release of molecules and mediators including anti-inflammatory cytokines that reverse the processes producing inflammation
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10
Q

Histamine:

A

a molecule released by mast cells which plays a key role in the inflammatory response

  • Causes vasodilation, increases permeability of blood vessels and act as a chemoattracter to phagocytes
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11
Q

Mast Cells:

A

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

- Reside in connective tissue
- When they detect an injury, they activate and degranulate(release contents), releasing histamine
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12
Q

Humoral Immunity:

A

an adaptive immune response in which extracellular pathogens are neutralised and destroyed by the secretion of specific antibodies produced by plasma cells

- Known as B cell immunity
- Primarily acts against extracellular pathogens
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13
Q

Humoral Immune Response:

A
    • A pathogen with an antigen that is complementary in shape to the antigen binding site on the receptor of a B cell interacts with that B cell.
    • When this occurs, the B cell is said to have been selected
      • Once a B cell has been selected, a T helper cell is selected through antigen presentation which also has a complementary receptor to the antigen
      • The complementary receptor to the antigen will recognise the selected B cell and secrete a number of different cytokines and interleukins
      • These cytokines cause the B cell to undergo clonal expansion through which many copies of the selected B cell are produced
      • The T helper cell also then stimulates the selected B cell via cytokines to undergo the process of differentiation
      • B cells are driven to differentiate into B memory cells and Plasma cells
      • After differentiating, plasma cells secrete antibodies into the blood in order to defend against the selected pathogen
        B memory cells reside in the body for a prolonged period of time and are responsible for immunological memory
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14
Q

Cell-mediated Immunity:

A

The adaptive immune response process which involves the destruction of infected or abnormal cells via clonal selection of a cytotoxic T Cell from a T cell

- Primarily acts against intracellular pathogens
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15
Q

Key Steps in Cell-Mediated Immunity:

A
    • As T Helper Cells are selected, antigen presenting cells arriving back at the lymph node comes upon a naive T Cell with a T receptor matching the antigen
    • The naive T cell becomes selected and is stimulated by cytokines, from the T Helper Cell, to help undergo the process of clonal expansion and differentiation
      • The new clones differentiate into cytotoxic T cells and T memory Cells(same as B memory Cells - immunological memory)
      • Majority of new clones differentiate into cytotoxic T cells however which leaves the lymph node to travel through the body and eventually reach the site of infection
      • The cytotoxic cells arriving at the infection site all have T cell receptors specific to the foreign antigen
      • Upon finding an abnormal cell presenting complementary foreign antigens on its MHC I , the cytotoxic T cell binds to the Antigen MHC I complex on the abnormal cell
      • secretes proteins such as cytotoxins which punch holes in the infected cells membrane and the contents ooze out - apoptosis
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16
Q

Natural Immunity:

A

protection against a disease formed without medical intervention

17
Q

Natural Active Immunity:

A

the person develops their own antibodies and memory cells

- Created when an individual's immune response encounters a pathogen and mounts a response
- creating antibodies and memory cells specific to it meaning the next time the same pathogen is encountered, it will be recognized and neutralised before it can cause disease
18
Q

Natural Passive Immunity:

A

antibodies created by an external source

  • when maternal antibodies cross the placenta into the foetus
19
Q

Artificial Immunity:

A

protection against a disease formed as a result of medical intervention

- Interacts with the immune system an can exist as many different types of molecules
20
Q

Artificial Active Immunity:

A

when an individuals own adaptive immune system develops antibodies and memory cells due to a medical intervention

- E.g. Vaccines
21
Q

Artificial Passive Immunity:

A

created when an individual acquires antibodies from an external source via a medical intervention

- E.g. People bitten by a snake are given antivenom containing antibodies to neutralise the venom
- Antibody treatments initially increase the number of antibodies, but over time they degrade until the immunity they created is gone
- Due to them not creating memory cells, a person given only antibodies will not develop immunological memory
22
Q

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

- Achieved through high vaccination rates(95%+)
23
Q

Infectious Disease:

A

an illness caused by a pathogen that can be transmitted between individuals

24
Q

Emerging Diseases:

A

an infectious disease that is new to the human population or that is rapidly increasing in incidence

25
Q

Re-Emerging Disease:

A

an infectious disease that was previously under control but that is now increasing in incidence

26
Q

Factors that contribute to the emergence and re-emergence of diseases:

A

Evolution of Causative Organism:
- Pathogens that cause disease can either evolve to infect humans or evolve to evade treatments by acquiring resistance

Globalisation and Travel:
- Diseases, due to our ability to travel globally quickly, can quickly spread to multiple countries

Increased Exposure of Humans to Animals:
- As the human population grows and climate change alters, humans come into contact with animals more often, therefore exposing the human race to more diseases originating from some type of animal reservoir

Increasing Human Population:
- Larger populations lead to increased population densities, therefore increasing the likelihood of a disease spreading and causing large scale health problems for a population

Changing Technology:
- New technology, such as the air conditioning systems, can be responsible for diseases as pathogens inhabit the system

Insufficient Vaccination of the Population:
- Previously managed diseases can re-emerge if population vaccination levels decrease stemming from the loss of herd immunity.

27
Q

Strategies for controlling Disease Transmission: Prevention:

A
  • Improving hygiene
    • Sterilising hands, surfaces and tools
    • Using PPE
    • Vaccinations
    • Lockdown of areas and movement restrictions
28
Q

Strategies for controlling Disease Transmission: Screening:

A
  • Routine testing for the presence of diseases in a population allowing governments to quickly see when a disease is on the rise
    • Observations of medication sales at pharmacies to look for changes that might indicate the prevalence of certain symptoms
29
Q

Strategies for controlling Disease Transmission: Quarantine and Isolation:

A
  • Once a person is ill or has the potential to be ill, they can be separated from healthy people to ensure they don’t spread diseases.
30
Q

Strategies for controlling Disease Transmission: Identification of the Pathogen:

A
  • If the pathogen can be detected and identified, appropriate responses can be initiated
31
Q

Strategies for controlling Disease Transmission: Identifying and controlling transmissions:

A
  • Once the pathogen is identified, appropriate steps can be taken to mitigate transmissions
    • E.g. Wearing masks if the pathogen is transmitted through respiratory droplets
32
Q

Strategies for controlling Disease Transmission: Treating Infected Individuals:

A
  • Antibiotics: medicines used to treat diseases caused by bacteria which target specific chemical pathways unique to bacteria without damaging patients cells
  • Antivirals: medicines that can be used to treat diseases caused by viruses which specifically interfere with viruses ability to attach to, replicate in and exit a hosts cell.
33
Q

Antibodies:

A

proteins produced by plasma cells during the Adaptive Immune Response that is specific to an antigen and combats a pathogen by binding to the antigens on the pathogens surface

- composed of 4 polypeptide chains(2 heavy and 2 light chains)
- Heavy chains are joined by a disulphide bond
- Each antibody is constructed with two regions; a constant and variable region
34
Q

Key Functions of Antibodies:

A

Neutralisation:
- Antibodies can block pathogens by blocking the site viruses use to enter the host cell

Agglutination:
- Antibodies bind with antigens from 2 different pathogens, forming an antigen-antibody complex making it easier for phagocytes to recognise and destroy pathogens

Immobilization:
- Antibodies can restrict the movement of pathogens around the body when forming large antigen-antibody complexes

Opsonisation:
- Antibodies can directly bind to the surface of pathogens, making it easier for phagocytosis to occur

Activation of Complement Proteins:
- Antibodies attach to the outside of pathogens, facilitating the formation of Membrane Attack Complexes