Diseases 2 Flashcards

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1
Q

What do viruses consist of

A

Viruses consist of genetic material (DNA or RNA) wrapped in cuspids

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2
Q

How do viruses reproduces?

A

Reproduction of viruses:
-Virus attaches to host cell then passes through the membrane
-Copies itself using the enzymes of the host cells
-Virus particles leave host cells to infect others

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3
Q

Antibody structure

A

Antibody structure:
-Made up of 4 polypeptide chains (2 light/short, 2 heavy/large)
-Antigen binding site
-Hinge region
-Disulfide bridges between polypeptide chains
-Constant region

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4
Q

Hinge region of an antibody

A

The hinge region of an antibody -> flexible -> allows distance between two antigen binding sites to vary

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5
Q

Constant region of an antibody

A

Constant region of an antibody:
Same for every antibody

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6
Q

T helper cells

A

T helper cells has a surface molecule called CD4, which locks onto the MHC molecule on the macrophage

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7
Q

Activated T helper cells

A

Activated T helper cells produce chemicals called interleukins (type of cytokine) -> triggers the activated T helper cells to undergo mitosis + stimulates macrophages to carry out phagocytosis

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8
Q

Function of opsonins

A

Opsonins detect foreign chemicals -> sticks to them ->tagging it as foreign

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9
Q

Phagocytosis involving a neutrophil

A

Phagocytosis involving a neutrophil:
-Neutrophil is attracted by molecules produced by pathogens
-Receptors attach to opsonins + engulfs pathogens (pathogens are now in phagosome vacuole)
-Lysosome move to phagosome and fuses with it to form a phagolysosome
-Lysosome enzymes then break down and destroy the pathogen

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10
Q

Phagocytosis involving a macrophage

A

Phagocytosis involving a macrophage:
-Pathogen engulfed by phagosome
-Lysosome fuses
-Enzymes digest pathogens
-Glycoproteins (called the major histocompatibility complex/MHC) from cytoplasm move to the phagolysosome and bind to antigen molecules
-MHC binds to antigens -> forms an MHC-antigen complex
-Complex moves to cell surface membrane and antigens are presented to the exterior of the cell (this is where we say that the macrophage is acting as an antigen-presenting cell (APC)

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11
Q

APC

A

APC = Antigen presenting cell -> when the MHC-antigen complex is showing on the exterior of the cell

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12
Q

Cytokines

A

Cytokines: signal to phagocytes and other immune cells to move to site of the infection + can also cause inflammation and fevers

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13
Q

Process of blood clotting eg in the Arteries when a cut occurs

A

1) Damaged endothelium (cut skin)
2) Platelets exposed to the proteins outside the endothelium
3) Activates the platelets which triggers blood clotting
4) Forms plug over damaged area and platelets release chemicals (clotting factors including thromboplastin) which then acts on proteins

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14
Q

Chain of proteins involved in blood clotting from thromboplastin

A

Thromboplastin associated with calcium ions -> acts on blood protein prothrombin -> converts prothrombin into active enzyme Thrombin -> Frombin acts on soluble protein Fibronogen -> Forms insoluble protein Fibrin

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15
Q

Insoluble fibrin role in blood clotting

A

Insoluble fibrin forms a mesh which traps red blood cells -> forms blood clot/thrombus

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16
Q

Function of activated platelets releasing serotonin in blood clotting formation

A

Function of activated platelets releasing serotonin in blood clotting formation:
-Serotonin causes smooth muscle cells in blood vessels to contract
-Narrows blood vessel to reduce blood flow to the infected area

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17
Q

Why does infected area of skin when cut appear hot and red?

A

Heat and redness occur due to inflammation when the skin is damaged:
-Damaged tissue activates mast cells
-Activated mast cells release histamine
-Histamine causes nearby blood vessels to dilate (vasolidation) to increase blood supply to infected area which causes redness and heat (heat destroys pathogens)

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18
Q

Why do tissue swell (odeama) + feel painful when damaged?

A

-Histamine produced by activated mast cells makes vessel wall more permeable
-Allows more blood plasma to leave blood and form tissue fluid
-Nearby tissues swell and feel painful

19
Q

Specific immune responses

A

The two specific immune responses:
-The cellular/cell-mediated response involves the highly specialised cells that targets pathogens inside cells
-The humoral or antibody-mediated response targest pathogens in body fluids with antibodies

20
Q

Agglutination of antibodies

A

Agglutination: One antibody binds to two pathogens, causing them to clump together. This makes pathogens more easily engulfed by phagocytosis

21
Q

Neutralisation of pathogens and toxins

A

Antibodies can act as antitoxins, binding with toxins produced by pathogens

22
Q

Cell-mediated immunity response

A

Cell-mediated immunity response:
1). Macrophages engulf and digest pathogens by phagocytosis. They present the antigens on their surface (becoming antigen-presenting cells)
2). Specific T helper cell with receptor that fits the antigen on the macrophage will bind. The T helper cell will produce interleukins which stimulate more T cell to be produced
3). Cloned T cells may become more T helper cells (to produce more interleukins)/ Killer T cells / T memory cells to destroy infected pathogens

23
Q

T killer cells

A

T killer cells kill pathogens by producing a chemical called perforin, which makes holes in pathogens cell plasma membranes

24
Q

T memory cells

A

T memory cells act as the immunological memory, as they remain the blood for long periods of time. When a second infection occurs, they divide rapidly to form many killer T cells

25
Q

T regulator cells

A

T regulator cells prevent an autoimmune response by repressing the immune system after all the pathogens have been destroyed

26
Q

Humoral immunity response

A

Humoral immunity response:
1). T helper cells bind to the antigens on the presenting B cells (clonal selection)
2). Interleukins produced by the T helper cells activate the B cells
3). The B cells divide rapidly by mitosis to produce many different B cells (plasma and memory cells) (clonal expansion)
4). These cloned plasma cells produce specific complementary antibodies to bind to the pathogens antigen, disabling them, or causing agglutination or neutralisation

27
Q

Plasma cells as a B lymphocyte

A

Plasma cells produce specific antibodies to an invading antigen, only live for few days but reproduce rapidly

28
Q

B effector cells

A

B effector cells divide to form plasma cell clones

29
Q

B memory cells

A

B memory cells remain in blood for long periods of time, providing immunological memory

30
Q

Autoimmune response

A

Autoimmune response refers to when the immune system stops recognising ‘self’ antigens and attach healthy body tissues, some causing chronic inflammation to complete breakdown of tissues, immunosupressant drugs used

31
Q

What does vaccines involve?

A

Vaccines involve:
-Dead pathogens injected into bloodstream
-B memory cells remain in bloodstream and remember the antigen
-Vaccines involve clonal selection and expanision
-Lymphocytes release antibodies more quickly and efficiently

32
Q

Role of opsonins

A

Opsonins bind to pathogens and tag them, so to encourage phagocytosis

33
Q

Immunisation

A

Immunisation is the process of developing immunity

34
Q

How to find the volume of a neutrophil?

A

Volume of a neutrophil = 4/3 x pi x radius (cubed)

35
Q

Why are antibodies specific to nuclear proteins not made?

A

Antibodies specific to nuclear proteins are not made because proteins are normally hidden in the nucleus

36
Q

Natural sources of medicine

A

Natural sources of medicine: plants + microorganisms

37
Q

Type of immunity for vaccination of antibodies and vaccination of inactive pathogens

A

-Vaccination of antibodies = artificial passive immunity
-Vaccination of inactive pathogens = artificial active immunity

38
Q

Process that leads to the production of antibodies

A

Process that leads to the production of antibodies:
-Lymphocytes detect antigen on pathogen cell surface membrane
-Becomes activated and selected B cells divide by mitosis and differentiate into plasma cells
-Plasma cells release antibodies specific to antigen

39
Q

Role of T helper cells

A

T helper cells = stimulated by APCs -> releases cytokines/interleukins -> then stimulates B cell -> causes mitosis/clonal expansio

40
Q

Role of B memory cells

A

B memory cells: remain in the bloodstream after a primary infection in order to rapidly respond to a secondary infection as clonal selection is faster

41
Q

Neutrophil specialisations

A

Neutrophil specialisations:
-Well-developed cytoskeletons
-Many lysosomes
-Many mitochondria
-Lobed nucleus

42
Q

What is meant by ‘immunologically distinct toxins’?

A

Immunologically distinct toxins:
-Toxins produced by each strain different
-Each toxin has own 3D shape
-Toxins act as antigens to immune system
-Immune response occurs

43
Q

Example of primary defence mechanism against pathogens

A

Primary defence mechanism = immune system -> skin, tears, mucus, blood clotting

44
Q

Differences between humoral immune response and the cell-mediated immune response

A

Humoral immune response = involves B-lymphocytes, of which are activated by T cells that are attached to APC, stimulates B cells to divide into plasma cells

Cell-mediated response = involves T-lymphocytes, of which binds to receptor cells and activates other T cells to divide (eg into T killer cells, T regulator cells or T helper cells)