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05 > Non-Specific and Specific Immunological Responses , Infection and Fever > Flashcards

Non-Specific and Specific Immunological Responses , Infection and Fever Flashcards

1
Q

Define the innate immune system

A

A non specific response to foreign agents that also initiates the inflammatory response

Examples include:

  • skin
  • phagocytes
  • natural killer cells
  • stomach acid
  • mucous
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2
Q

Examples of physical and chemical barriers in the body

A
  • skin prevents the entry of pathogens
  • stomach acid’s low pH kills microbes
  • mucous traps dirt and microbes
  • tears and saliva contains antibacterial enzymes
  • ciliated respiratory epitheliums removes debris
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3
Q

Explain the internal defences of the body

A

Fighting pathogens that invade into the deeper tissues of the body

  • phagocytes such as NKC
  • Antimicrobial proteins such as complement proteins and interferons
  • fever and inflammatory response including mast cells, macrophages, and neutrophils

HOWEVER its has no memory

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4
Q

Define the process of Phagocytosis

A

Process where phagocytes engulfing other cells or particles

  • pathogens can be coated bu complement proteins or antibodies to enhance phagocytosis
  • phagocytes adhere to pathogen
  • Cytoplasmic extension surround pathogen engulfing it into a vesicles called a phagosome
  • a lysosome fuses with the phagosome to form a phagolysosome
  • pathogen is digested and microbial products are released from the cell
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5
Q

What are Natural Killer Cells?

A
  • Non phagocytic cells
  • Cytotoxic, granular lymphocyte

They attack cells that lack “self” cell surface receptor proteins and induce apoptosis in cancer cells and virus infected cells

  • Secrete interferons gamma that enhance the inflammatory response
  • Release perforin leading to osmotic cell lysis
  • Perforin is a pore forming cytolytic protein found in the granules of the cytotoxic T lymphocytes and NK cells. upon granulation, perforin binds to the target cell’s plasma membrane
  • a osmotic cell lysis occurs when a cell burst due to an osmotic imbalance that has caused excess water to diffuse in the cell
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6
Q

What are the Antimicrobial proteins involved in the immune response?

A
  • Interferons (interfere with viral replication) - produced by virus infected cells
  • Complement proteins (attack pathogen directly)

They

  • protect neighbouring cells
  • activate macrophages and NK cells
  • are used as a therapeutic agent in multiple sclerosis, lymphoma, leukaemia and hepatitis
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7
Q

Role of interferons

A
  • signals neighbouring cells to destroy RNA and reduce protein synthesis
  • signals neighbouring infected cells to undergo apoptosis
  • activates immune cells
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8
Q

Role of Complement Proteins

A
  • approx. 30 proteins that act in a sequences also known as the complement cascade

Complement proteins directly kill the bacteria or help destroy bacteria by attaching to them (opsonin coat), thus making macrophages and neutrophils to identify and engulf bacteria easier

Participates in specific immunity

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9
Q

How does complement proteins directly kill bacteria?

A

The complement proteins attach themselves to the surface of the bacterium creating holes in its cell wall and membrane. These holes allow fluid and salts to enter bacterium causing its to expand until it bursts or dies

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10
Q

Role of Histamine

A
  • Stimulates the vascular component of inflammation

- it is releases by mast cells and other WBCs

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11
Q

Roles of Nitrous Oxide

A
  • Promotes vasodilation

- Blocks platelet clumping and clot formation

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12
Q

Role of Aracodonic acid metabolites

A
  • From cell membrane phospholipids (cell damage)
  • Leukotrienes (C-4, D-4, E-4) maintain cellular and vascular inflammation
  • NSAIDS and steriods block prostaglandins and leukotrienes
  • Prostaglandins prolong the inflammatory process
  • PGD2, E2, F2 - vasodilation and increase capillary permeability
  • PG12 - vasodilation, inhibits platelet clumping
  • Thromboxane A2 - vasoconstriction and platelet clumping
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13
Q

Cytokines

A

messengers of the immune system

Cytokines can stimulate specific WBCs to become more effective killers and attract other WBCs to the site of infection

Some cytokines, called interferons, interfere with the reproduction of viruses

Participates in specific immunity

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14
Q

Function of Cytokines

A
  • Chemotactic factors attracts macrophates causing them to migrate into the site of infection
  • Macrophages activating factor causes the macrophages to destroy antigens by englufing them at a rapid rate
  • Lymphotoxin is a powerful poison that acts more directly, killing any cell or cytotoxic T cells
    (Sensitised T ceclls that release lymphotoxin are called Killer T cells
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15
Q

What is a tumour necrosis factor

A
  • multifunctional cytokine that works with interleukin playing a important role in diverse cellular events such as cell survival, proliferation, differentiation, and death
  • enhances the inflammatory response
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16
Q

Antigens and the Immune System

A
  • antigen is a substance capable of inducing a specific immune response

Immunity that occurs after exposure to an antigen either from a pathogen or a vaccination

  • Binding of antigen to lymphocytes antigen receptor will active the lymphocyte
  • It is important to recognise that bacteria or viruses are not themselves antigens bit that they contain antigens both on their surface and inside them
17
Q

Specific Immune System

A
  • Protects against pathogens and abnormal body cells (cancer)
  • Intensifies the inflammatory response
  • Activates complement
  • Is specific to one antigen
  • Humoral immunity (antibody mediated) - attack extracellular pathogens
  • Cellular immunity (cell-mediated) - attack intracellular pathogens
18
Q

Humoral Immunity

A
  • B lymphocytes become plasma cells when activated and produce antibodies
  • IL-1 stimulate helper T cells which causes IL-2 to cause cell division and activation of the B cells which mutates its own DNA to create antibodies, when successfully made, it clones many plasma cells that produces that particular antibody from that pathogen
19
Q

Second Stage of B cell Development

A
  • Occurs when the inactivated B cells bind to a specific antigen causing the B cell to become activated
  • this antigen antibody binding activates the B cell triggering a rapid series of mitotic divisions
  • this b cell produces clones some of which differentiate to become plasma cells and some that do not differentiate completely and remain in the lymphatic tissue as memory B cells
20
Q

Cell medicated immunity (T lymphocytes)

A
  • T lymphocytes are responsible for cellular immunity
  • T cells mature in the thymus before migrating to the lymph nodes and spleen

Antigen presentation stimulates the T cells to become either a helper t cells (stimulate b cells) or killer t cell

21
Q

Role of T cells

A
  • each t cell displays antigen receptor in its surface membrane
  • when encountering with antigen epitopes, it activates the t cells, causing it to divide repeatedly to form a clone of sensitised t cells
  • t cells target intracellular pathogens such as virus infected cells, bacteria, parasites as well as cancer cells
22
Q

Role of Helper T cells

A

Help to activate

  • Killer T cells and macrophages to attack infected cells
  • stimulate B cells to secrete antibodies

Become activated by interacting with antigen-presenting cells, such as macrophages

23
Q

Role of Killer T cells

A
  • Travels to the site where the antigen originally entered the body
  • binds to specific antigen
  • releases chemical messengers into the inflamed tissues called cytokines
24
Q

Inflammation

A
  • Protective tissue response to injury or destruction of tissues
  • Process of inflammation serves to destroy, dilute or wall of both injurious agent and tissues
25
Q

Five signs of inflammation

A

Swelling
- oedema due to increased vascular permeability and accumulation of exudate

Heat
- Increased blood supply to the area

Redness
- Due to vasodilation and increased blood xupply to area

Pain
- Due to increased pressure on nerve endings from swelling/oedema

Loss of function
- variable and is due to the inflammatory process and tissue damage

26
Q

Effects of Inflammation

A
  • initiates tissue repair
  • removes necrotic tissue
  • decreased spread of pathogen from the injury site
27
Q

Two components of acute inflammation

A
  • cellular e.g. neutrophils

- vascular e.g. increased capillary permeability

28
Q

Vascular component of acute inflammation

A

Initial vasoconstriction near site of injury followed by:

Vasodilation of arterioles and capillaries

  • increased blood flow to the area
  • increased hydrostatic pressure

Increased capillary permeability
- secondary to tight junction disruption in endothelial layer of blood vessels

29
Q

Cellular component of acute inflammation

A

Neutrophils and monocytes (phagocytes) are first to arrive at site of inflammation

Margination
- Phagocytes adhere to blood vessel walls

Emigration
- phagocytes slip out of the blood vessels through endothelial junctions

Phagocytosis —> degranulation (release of lysosomes) leads to death of the organism

30
Q

Systematic effects of inflammation

A

Fever due to:

  • effects of pyrogen from neutrophils and macrophages
  • effects of IL-1 on hypothalamus
  • increased temperature is harmful to some organisms
  • some organisms release endotoxins when killed

Leukocytosis due to:

  • stimulated by complement (C3a)
  • large released of store neutrophils
  • production of leukocytes by BM

Loss of appetite
Increased deep sleep
Weight loss
Weakness

31
Q

Sepsis to MOD

A

Sepsis - Systemic response to infection

Severe sepsis - sepsis associated with organ failure

Septic Shock - severe sepsis complicated by persistent hypotension

  • Multiple organ failure - altered organ function cannot maintain homeostasis with intervention
32
Q

Vaccines

A

Training the immune system to recognize and combat pathogens, either viruses or bacteria. To do this, certain molecules from the pathogen must be introduced into the body to trigger an immune response

05 (20 decks)

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