Topic 6.3 Immune response Flashcards

Mrs Richardson (25 cards)

1
Q

Inflammation

A
  • White blood cells are drawn to the infected area
  • They fight and eliminate the pathogen
  • Innate tissue repair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Symptoms of Inflammation

A

fever, heat and swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Fever

A
  • When infected by a pathogen, the hypothalamus raises your body temperature.
  • inhibits bacteria growth.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How inflammation works?

A
  • Mast cells and basophils release chemicals called histamines.
  • The histamines cause blood vessels to dilate causing local heat and redness.
  • This makes it harder for the pathogen to reproduce.
  • The dilated blood vessels also cause plasma, containing leukocytes and antibodies, to be forced out of the capillaries.
  • The antibodies disable the pathogens, therefore allowing phagocytes to destroy them.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Mast cells

A
  • Mast cells do not circulate in the bloodstream, they live in skin and mucosal tissues
  • When activated they release histamines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Phagocytes

A
  • They detect foreign antigens
  • The phagocyte engulfs the pathogen to form a phagosome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Basophils

A
  • They produce and release histamines
  • they circulate in the bloodstream and they are not phagocytic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Eosinophils

A
  • Particular type of phagocyte
  • They have the characteristic ‘lobed nucleus’ allowing it to morph shape in order to engulf pathogens
  • They also produce chemicals which are able to counteract the inflammatory histamines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Natural killer cell

A
  • Type of leukocyte that can recognise cells that are infected with as virus and cancer cells
  • They release proteins that induce programmed cells death by perforating the membrane of the damaged cell
  • This kills the infected/cancerous cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Primary response vs Secondary response

A
  • Primary is slower as you do not have the memory cells
  • Secondary has a rapid response of antibodies as you have memory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Artificial passive immunity

A

Gaining antibodies from an outside source
- Positives: immediate don’t need to wait for antibodies to be made
- Negative: Short term the person will not have long lasting protection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Passive immunity

A
  • When antibodies are introduced from an outside source
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Natural passive immunity

A
  • When an infant receives a mothers antibodies through the placenta or breast milk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Active immunity

A
  • Involves exposure to a pathogen/antigen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Natural active immunity

A

Through natural exposure eg. having a cold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Artificial active immunity

A

Through vaccination

17
Q

Vaccination

A
  • Vaccination aims to stimulate a primary immune response without actually causing the disease like a normal infection would
  • This allows people to safely develop memory cells against a pathogen
18
Q

Summary of Active immunity

A
  • Requires exposure to antigen (Through vaccine or infection)
  • Body makes own antibodies
  • Develops slowly
  • Long term because memory cells enable faster antibody production on re-infection
19
Q

Summary of passive immunity

A
  • Does Not require exposure to the antigen
  • The body is given antibodies made by someone else (eg. injection, across the placenta or in breast milk
    Immediate
  • Short term as antibodies are broken down and no memory cells are made
20
Q

Steps of phagocytosis

A
  • Pathogen comes along and phagocyte engulfs the pathogen
    That forms a phagosome
  • Binds with a lysosome containing digestive enzymes forming a Phagolysosome
  • That presents to antigen on the MHC
  • Cytokines are released
  • A T helper cell comes along and activates the B cells which divide and form plasma cells
  • The plasma cells release the antibodies and you will end up with memory B cells
21
Q

T killer cells (Cytotoxic/CD8+)

A
  • An antigen presenting cell eg. macrophage digests and engulfs the pathogen and presents it on its surface via MHC
  • Killer T cell with a complimentary T cell receptor binds to the MHC/antigen presenting cells
  • With the assistance of cytokines from an activated helper T cell the killer T cell becomes activated
  • Activated T killer cells and T killer memory cells are formed
  • Active T killer cells release perforin chemicals
  • These punch holes in the membranes of infected cells and cause them to burst (Cell lysis)
22
Q

Opsonins

A

Antibodies that bind with antigens to act as markers so that phagocytes can recognise foreign cells and destroy them

23
Q

Agglutinins

A

Antibodies that bind to antigens , causing foreign substances to clump together, which prevents them from entering cells and reproducing

24
Q

Lysins

A

Antibodies that bind to antigens and cause a foreign cell to rupture or disintegrate

25