M4C12 - Communicable diseases Flashcards

1
Q

What diseases are caused by bacteria?

A

Tuberculosis, ring rot (potatoes, tomatoes)

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2
Q

What diseases are caused by viruses?

A

HIV/AIDS, influenza, tobacco mosaic virus.

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3
Q

What diseases are caused by protoctista?

A

Malaria (plasmodium protist), potato/tomato late blight.

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4
Q

What diseases are caused by fungi?

A

Black sigatoka (bananas), athletes foot.

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5
Q

Give some examples of direct transmission

A

-Exchange of bodily fluids
-Direct skin contact
-Ingestion

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6
Q

Give some examples of indirect transmission

A

-Inanimate objects - bedding/socks
-Droplet effect - cough/sneeze

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7
Q

How do vectors affect transmission (plants and animals)

A

Climate change - leads to new vectors and diseases, increased rainfall and wind aids animal vectors.

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8
Q

How do spores affect transmission (plants)

A

Build-up of spores and pathogens in soil due to damp, warm conditions.
Climate change aids spread of spores.

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9
Q

How do living conditions affect transmission (plants and animals)

A

Overcrowding - increases likelihood of contact, poor nutrition, poor disposal of waste, poor mineral nutrition reduces resistance.

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10
Q

Give some chemical defences in plants in response to pathogens

A

-Antibacterial compounds e.g. PHENOLS
-Hydrolytic enzymes e.g. CHITINASE.

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11
Q

Give some physical defences in plants to protect against pathogens

A

Waxy cuticle, tree bark, cellulose cell walls.

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12
Q

What is callose and how does it limit the spread of pathogens

A

-callose is synthesised and deposited between the cell walls and the cell membrane in cells next to the infected cells.
-These callose papillae act as barriers, preventing the pathogens entering the plant cells around the site or infection.
-Large amounts of callose continue to be deposited in cell walls after the initial infection. Lignin is added, making the mechanical barrier to invasion even thicker and stronger.

Plants seal off diseased tissue and sacrifice it. Meristems mean they can grow more.

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13
Q

Give some non-specific primary defences in animals

A

Tears, skin, mucus

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14
Q

Explain the process of blood clotting

A

-Platelets come into contact with collagen on skin or wall of damaged blood vessel, they adhere and begin secreting several substances such as:
-Thromboplastin - enzyme that triggers a reaction that produces fibrin which forms a clot.
-After the scab hardens, epidermal cells below the scab start to regrow as well as the blood vessels.

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15
Q

Explain the process of inflammation

A

-Mast cells detect the presence of pathogen in tissue and release histamine.
-Histamine causes vasodilation
-Histamine causes capillary walls to become more permeable to white blood cells.
-Tissue fluid production increases
-Excess tissue fluid drains into the lymph vessels, carrying pathogens to lymphocytes.
-Lymphocytes initiate the specific immune response.

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16
Q

Explain mucus membranes and expulsive reflexes as a defence:

A

-Goblet cells secrete mucous which traps pathogens and cilia sweep them out.
-These trapped pathogens can be removed via expulsive reflexes e.g. coughing, sneezing, vomiting.

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17
Q

Explain the structure and mode of action of neutrophils

A

Structure - Have a multi-lobed nucleus.
Function- Perform phagocytosis

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18
Q

Explain the structure and mode of action of macrophages

A

structure - larger cells made in bone marrow, travel in blood as monocytes, develop into macrophages in lymph nodes.
Function - Antigen presentation (capture antigens and present to T lymphocytes).

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19
Q

What is the role of cytokines?

A

Cell signalling molecules that attract phagocytes to site of infection.

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20
Q

What is the role of opsonins?

A

Bind to pathogens and increase recognition by phagocytes

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21
Q

Explain the role of phagosomes and lysosomes?

A

Phagocyte engulfs the pathogen and encloses it in a vacuole called a phagosome.
Phagosome combines with a lysosome to form a phagolysosome.
Enzymes (lysins) from the lysosome digest and destroy the pathogen.

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22
Q

Explain process of phagocytosis

A

-Receptors on cell membrane of a phagocyte recognise antibody molecules known as opsonins, which are bound to pathogens and enhance phagocytosis.
-Once engulfed by a phagocyte, a pathogen is contained in a vacuole called a phagosome.
-Organelles called lysosomes produce enzymes that digest the pathogen.
-Indigestible material is discharged from the cell by exocytosis.

23
Q

Explain the primary immune response involving T lymphocytes:

A

-Antigens are presented on surface of macrophage
-Macrophage searches for T-helper cell with complementary receptor to antigen. Antigen binds to T-helper cell receptor.
-Stimulated T-helper cell secretes interleukins which stimulate T-cells to divide by mitosis.
-T cells develop into killer T cell, T memory cells or produce interleukins to stimulate clonal expansion of B lymphocytes.

24
Q

Explain the primary immune response involving B lymphocytes:

A

-The activated T helper cell binds to a B-cell which is presenting antigens (clonal selection)
-Interleukins produced by the T helper cell activate the B lymphocytes.
-Activated B cell divides by mitosis (clonal expansion) and differentiates into plasma cells which secrete antibodies specific to one antigen.

25
Q

Explain what happens in the secondary immune response:

A

Memory cells (Memory helper T cells and Memory killer T cells) (differentiated B lymphocytes) direct a secondary immune response.
-T cells and antibodies are produced more quickly as there is no wait for clonal selection, and for a longer period than during the primary response.

26
Q

Describe the structure and function of antibodies

A

-An antibody is a Y shaped protein with a contant and variable region.

-The variable region is of a complementary shape to a specific pathogenic antigen which allows it to bind to the antigen and neutralise the antigen. The variable region varies between antibodies so different antibodies can bind to different antigens.

-The constant region region of the antibody is the same for all antibodies, allows phagocytes to bind to the antibody.

-Antibodies also have a hinge region which increases their flexibility.

27
Q

What is the role of the disulphide bond in antibodies?

A

Hold polypeptides/light chain and heavy chain together.

28
Q

What is the role of agglutins?

A

Clump pathogens together which stops pathogens reproducing and helps phagocytosis of pathogens.

29
Q

How do antibodies work?

A

-Bind to antigens on pathogens
-Antigen is a binding site to bind host cells and it will be blocked by the antibody.
-This is called neutralisation.

29
Q

What is an antitoxin?

A

An antibody with the ability to neutralise a specific toxin.

30
Q

What is Natural immunity?

A

Gained during normal course of your life. Infection by pathogens stimulating the immune response.

31
Q

What is Active immunity?

A

Gained by deliberate exposure to antigens or antibodies.

32
Q

Give an example of Natural Passive immunity:

A

Antibodies provided by the placenta or breast milk. Baby therefore initially immune to disease that mother has already encountered. Useful during first few weeks.

33
Q

Give an example of Artificial Passive immunity:

A

Immunity provided by injecting antibodies made by another individual e.g. tetanus injections.

34
Q

Give an example of Natural
Active immunity:

A

Immunity provided by antibodies made in the immune system as a result of infection by pathogen. The person suffers the disease once but then is immune e.g. chicken pox.

35
Q

Give an example of Artificial
Active immunity:

A

Immunity provided by antibodies made in the immune system as a result of vaccination. The person is injected with a weakened pathogen in order to activate immunity e.g. TB jab.

36
Q

What is an autoimmune disease?

A

An abnormal immune response against tissues normally in the body.

37
Q

What is arthritis and how is it treated?

A

Autoimmune disease - attacks the joints especially the hands, wrists, ankles and feet.
No cure but treated with steroids, anti-inflammatory drugs.

38
Q

How can you treat autoimmune diseases?

A

Nonsteroidal anti-inflammatory drugs and immunosuppressants.

39
Q

Describe the principle of vaccination

A

-Antigens or inactive pathogens are injected into the body
-B-lymphocytes detect the antigens and multiply. They produce antibodies (via plasma cells) and memory.
-The antibodies gradually disappear, but the memory cells remain for many years.
-When pathogens with the same antigen infect the body, the memory cells immediately make antibodies.

40
Q

What is an epidemic?

A

When a communicable disease spreads rapidly to a lot of people at a local or national level.

41
Q

What is Herd immunity?

A

Vaccinate most people in population. This stops infection spreading within population as there is a lack of people to pass infection on to.

42
Q

What is ring vaccination?

A

Vaccinate all people around a victim. This contains the spread of the disease within a ring. Involves spotting and reporting victims and then isolating them. Then trace contacts of victim and isolate and vaccinate them.

43
Q

Why can’t malaria be prevented by vaccintaion? (global issues)

A

The plasmodium protist is very evasive, it spends time inside the erythrocytes so it is protected by self antigens from the immune system, and within an infected individual its antigens reshuffle.

44
Q

Why can’t HIV be prevented by vaccination? (global issues)

A

It enters macrophages and T helper cells, so it has disabled the immune system itself.

45
Q

Name 2 medicines and their sources:

A

Penicillin - penicillium mould
Aspirin - Based on compounds from willow bark.

46
Q

Why is it important to protect biodiversity?

A

Because only a fraction of life on earth has been destroyed and reduced biodiversity creates the risk that a plant, animal, or micro-organism that can provide a life-saving drug is destroyed.

47
Q

What is a personalised medicine?

A

A combination of drugs that work with your individual combination of genetic and disease.

48
Q

How do antibiotics work?

A

Interfere with the metabolism of the bacteria without affecting the metabolism of the human cells (selective toxicity)

49
Q

What is antibiotic resistance and how is it developed?

A

Genetic mutations may occur in bacteria which makes it resistant to an antibiotic. When the antibiotic is used, it leads to natural selection of the bacteria with the mutation resulting in a resistant strain of bacteria. The resistant bacteria survive and reproduce. The resistant gene is passed onto offspring.

50
Q

What is MRSA?

A

A group of gram positive bacteria that are resistant to antibiotics such as methicillin and oxacillin (derivatives of penicillin. They usually cause skin and joint infections.

51
Q

What type of pathogen causes scarlet fever?

52
Q

Why don’t antibiotics work on viruses?

A

Because they don’t have a cell wall that antibiotics can attack like bacteria does