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Biology > Disease - Module 4 > Flashcards

Disease - Module 4 Flashcards

1
Q

Process of phagocytosis
antigen presenting

1-6

A

1) Phagocyte attracted by chemicals produced by pathogen

2)phagocyte recognises pathogen as non-self and binds to it

3)phagocyte engulfs the pathogen to form phagosome - lysosome moves towards phagosome and combines with it, forming phagolysosome

4) In phagolysosome, enzymes break down the pathogen

5)digested pathogen absorbed by phagocyte - antigens combine with MHC in the cytoplasm

6)MHC/antigen complex is displayed on phagocyte membrane, making an antigen presenting cell

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2
Q

how do bacteria cause damage to host`?

A

Release Toxins which damage cell`

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3
Q

how do virusus damage the host?

A

Invade living cells, produce biochemical and structural changes in host cell. These can change cell functions or destroy the cell

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4
Q

How do protoctista enter host?

A

Parasites enter body through food or water contaminated by faeces of infected animal or person

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5
Q

how do Fungi damage host ?

A

IN plants, Fungi can digest plant tissue directly or through potent toxins

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6
Q

1)what is tuberculosis caused by?
2)Treatments

A

1)Bacteria
2)Antibodies, Improve living standards

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7
Q

1)what is Bacterial Meningitis caused by?
2)Treatments

A

1)Bacteria
2)Early antibiotics, Vaccines can prevent

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8
Q

1)what is HIV/AIDS caused by?
2)Treatments

A

1)Virus
2) Anti-retroviral drugs to slow down effects

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9
Q

1)what is Influenza caused by?
2)Treatments

A

1)Virus
2)Vaccine, antibiotics

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10
Q

1)what is Malaria caused by?
2)Treatments

A

1) Protoctista
2)Controlling mosquitos

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11
Q

1)what is Ring Worm caused by?
2)Treatments

A

1)Fungi
2)Antifungal creams

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12
Q

1)what is Ring Rot caused by?
2)Treatments

A

1) Gram positive bacteria
2)Wait for two years and destroy crops

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13
Q

1)what is Tobacco mosaic virus caused by?
2)Treatments

A

1) Virus
2)Resistant crop strains

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14
Q

1)what is Potato blight caused by?
2)Treatments

A

1) Protoctist
2)Resistant strains, careful management, chemical treatments

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15
Q

1)what is Black sigatoka caused by?
2)Treatments

A

1)Fungus
2) Resistant chains being developed, Fungicide

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16
Q

What signals the Production of Phytoalexins

A

-Pathogens can secrete cellulases to digest plant cell walls and enter the cells
-The products of cellulose hydrolysis are detected by receptors on the surface of the cell and signal to the cell that an attack is happening
*-The plant cell then produces phytoalexins as a defence mechanism

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17
Q

4 Roles of phytoalexins

A

-Disrupt cell membrane of bacteria
-stimulate ptoduction of chitinase to break down cell walls of fungal pathogens
-Disrupt metabolism of pathogen
-Delay reproduction of pathogen

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18
Q

4 Internal Plant defence

A

1) defensive chemicals give the alarm to other cells before they are attacked
2)Polysaccharides made to strengthen the cell walls (callose + lignin)
3)Signalling molecules alert nucleus to attack
4) phytoalexins

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19
Q

5 types of non-specific immune response

A

-Skin
-Mucous Membranes
-Lysozymes
-Expulsive Reflexes
-Blood clotting and wound repair

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20
Q

Skin in the non-specific immune response

A
  • covers body to prevent entry of pathogens
    -Healthy microbes live on skin and out compete pathogens
    -when we sweat, salt changes the PH and prevent microbes producing
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21
Q

Mucous Membranes in the non-specific immune response

A

-Line body tracts
-contain goblet cells which secrete sticky mucus
-mucus also contains phagocytes

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22
Q

Lysozymes in the non-specific immune response

A

-Found in blood, sweat and tears
-Catalyses the breakdown of microbial cell walls

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23
Q

Expulsive reflexes in non-specific immune response

A

-coughs and sneezes remove mucus (and trapped pathogens) from airways
-vomiting and diarrhoea remove pathogen from gut

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24
Q

Blood Clotting and wound repair in the non-specific immune response

basic

A

-Platelets adhere to collagen in the skin or cell wall of the damaged vessel
-This triggers the secretion of thromboplastin and seratonin

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25
Q

Inflammatory response​. Mast cells, Histamines and Cytokines

A

Localised response to pathogens resulting in inflammation​

Characterised by pain, heat, redness and swelling.​

Mast cells are activated in damaged tissues and release chemicals called histamine and cytokines​

Histamines​

Make the blood vessels dilate, causes localised heat and redness. Raised temperature helps prevent pathogens reproducing.​

Make blood vessel walls more permeable so blood plasma is forced out. This is then known as tissue fluid. This causes swelling and pain.​

Cytokines​

Signal white blood cells to the site.​

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26
Q

Process of blood clotting

A

-Platelets activated by damaged tissue
-release thromboplastin (enzyme)
-This catalyses reaction of prothrimbin into thrombin
-Ca 2+ ion needs to be present
-thrombin (enzyme) catalyses reaction of Fibrinogen into fibrin
-Fibrin forms the clot

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27
Q

Process Fever​

why is it useful

A

Normal body temperature is maintained by the hypothalamus in the brain.​

Cytokines stimulate the hypothalamus to raise the temperature of the body​

This is useful because:​

Most pathogens reproduce best at 37oC or lower. Higher temperatures inhibit pathogen reproduction.​

The specific immune system works faster at higher temperatures.

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28
Q

Phagosome

A

the vesicle a pathogen is engulfed by​

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29
Q

Neutrophil

A

a short-lived phagocytic cell which makes up 60-70% of phagocytes​

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30
Q

Macrophage

A

a large long-lived phagocytic cell found in tissue​

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31
Q

Monocyte

A

a macrophage when it is circulating in the blood​

32
Q

Cytokines

A

Chemicals act as cell signalling molecules ​

These signal other phagocytes that the body is under attack​

Stimulates phagocytes to move to the site of infection or inflammation​

Increase body temperature and stimulate the specific response​

33
Q

Opsonins

A

Chemicals that bind to pathogens so they can be more easily recognised by phagocytes​

Phagocytes have receptors on their cell membrane that bind to common opsonins​

34
Q

What is an antibody

A

-A protein molecule. Consists of four polypeptide chains
-groups pathogens together, easier for phagocytosis
-Protein produces in response to presance of antigen. Complimentary shape to antigen so binds

35
Q

Purpose of constant region on an antibody

A

Same in all antibodies. Allows binding to receptors on phagocytes

36
Q

What is an antigen

A

A foreign molecule that triggers an immune response. For example a protein or glycoprotein

37
Q

what is Agglutination (antibodies)

A

-Clumping
-Antibody binds to two separate pathogens, binding (+ grouping) them together
-Phagocyte binds to antibody
-Phagocyte engulfs the group of pathogens at same time
-phagocytosis happens more efficiently
- These antibodies are called agglutinins

38
Q

what is Neutralisation (antibodies)

A

-antibodies(antitoxins) bind to toxins
-phagocyte binds to antibodies
-toxins engulfed and destroyed
-Toxins destroyed more efficiently
- also stops toxins from attacking human cells, toxins are neutralised

39
Q

how do antibodies prevent pathogens binding to human cells

A

-Antibodies bind to Antigens on a pathogen
-This leaves no room for antigens on pathogens to bind to host cells , blocking them.
-This means pathogens can’t attach to then infect the host cells

40
Q

What is clonal selection

A

When a T lymphocyte binds to an antigen which has a complementary shape to its receptors

41
Q

What is the main way on which these T lymphocytes are exposed to invading antigens

A

Antigen presenting phagocyte presenting the antigens of the pathogens they engulf

42
Q

What happens once clonal selection has occurred?

A

Clonal expansion

43
Q

What is clonal expansion?

A

When the T lymphocyte with the receptor complimentary to the antigen divides by Mitosis to make clones of itself

44
Q

What are the 4 types of cells T lymphocytes can differentiate into?

A

T killer cells

T memory cells

T regulatory cells

T helper cells

45
Q

What do T killer cells do?

A

Attack and kill body cells infected with viruses

46
Q

What do T memory cells do?

A

Stay in blood for long time.
If same pathogen enters the body, they can go through clonal expansion and differentiate rapidly

47
Q

What do T regulatory cells do

A

Suppress immune system and help to prevent an autoimmune response

48
Q

What do T helper cells Do

A

Release interleukins (a type of cytokine) which stimulate the activation of B lymphocytes.

This is an example of cell signalling*

49
Q

How are B lymphocytes activated

(2 ways)

A

Interleukins released by T helper cells bind to receptors on cell surface of B lymphocyte, helping to activate the correct one.

They also go through clonal selection. They have antibodies on their surface and only one B lymphocyte will have. The complimentary antibody to invading antigen.

50
Q

What 3 types of cells do B lymphocytes differentiate into during clonal expansion?

A

B Plasma cells

B effector cells

B memory cells

51
Q

What do B Plasma cells do?

A

Produce antibodies

52
Q

What do B effector cells do?

A

Divide to form plasma cell clones

53
Q

What do B memory cells do?

A

Stays in blood for many years. If same antigen enters body, go through clonal expansion to rapidly produce B Plasma cells

54
Q

What is active immunity?

A

When your immune system makes antibodies after being stimulated by an antigen

55
Q

What is natural active immunity

A

When you become immune after catching a disease naturally

56
Q

What is artificial active immunity?

A

When you become immune after being given a vaccination

57
Q

What is passive immunity

A

Type of immunity you get by being given antibodies made by a different Organism.

Your own immune system is not producing any antibodies

58
Q

What is Natural passive immunity

A

A baby becoming immune due to antibodies passed from mother in placenta and breast milk

59
Q

What is artificial passive immunity

A

Becoming immune after being given an injection of antibodies from someone else

60
Q

What is an autoimmune disease

A

Natural immune system can’t tell difference between own and foreign antigens, attacking them

61
Q

3 examples of autoimmune diseases

A

Type 1 diabetes

Lupus

Rheumatoid arthritis

62
Q

What is a vaccine

A

A biological preparation that provides active acquired immunity to a particular infectious disease

63
Q

What is Herd immunity

A

Most people in community are vaccinated, disease becomes rare. Makes it less likely for unvaccinated people to get diseased

64
Q

What are the 2 ways in which vaccines can be taken

A

Nasally

Injection

65
Q

5 different manufacturing methods of vaccines

A

1) whole live organisms,
2)A harmless or attenuated version of pathogenic Organism
3)A dead pathogen
4)a preparation of the antigens from a pathogen
5)some harmless toxin (toxoid)

66
Q

3 problems with vaccines

A

Poor response

Antigenic variation

Antigenic concealment
-is occurs when the pathogen ‘hides’ from the immune system by living inside cells or when the pathogen coats their bodies in host proteins or by parasitising immune cells such as macrophages and T cells (eg.

67
Q

3 why do people have problems with vaccines

A

Poor response

Antigenic variation

Antigenic concealment

68
Q

Why was herd immunity used against smallpox successfully
1-6

A

1)smallpox doesn’t mutate, antigens remain
2)virus doesn’t infect animals, only transmitted through humans
3)easy to diagnose person with disease
4)vaccination used live strain, no booster needed
5)only one vaccine needed so cheap
6)vaccine could be freeze dried easy for transport and storage

69
Q

Chemical defences for plants

A

-Insect repellent
-neurotoxin for insects
-phenols- antiseptic for plants
-Antifungals = chitinase
Toxins- cyanide

70
Q

Physical barriers in plants

A

-callose between cell wall and cell membrane
-callose blocks sieve plates in phloem
–callose deposited in plasmodesmata of infected cells
-lignin added to callose deposits

71
Q

What is an antibiotic

A

Compounds that kill or inhibit the growth of bacteria by targeting prokaryotic metabolism or the structure of bacteria cells

72
Q

What 5 things to antibiotics target on bacteria

A

-metabolic enzymes
-cell wall synthesis (penicillins)
-Ribosome 70s
-cell membrane
-DNA synthesis

73
Q

How to prevent antibiotic resistance

A

-minimise use of antibiotics
-ensuring whole course of antibiotics is completed
-Good hygiene in hospital

74
Q

role of opsonins

A

opsonins
bind to / AW , pathogens / foreign cells / antigens , and
increase phagocytosis / recognition by phagocytes 

75
Q

Role of cytokines

A

cytokines
attract / AW , (named) phagocytes 

Biology (45 decks)

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