disease prevention Flashcards

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1
Q

what is a first line defence mechanism

A

physical and chemical defence that prevent the entry of pathogens

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2
Q

what are examples of first line defence mechanisms

A
skin 
mucous membranes 
chemicals such as lysozyme 
sebum 
hydrochloric acid
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3
Q

what is an expulsive reflex

A

coughing and sneezing, which expel irritants that may include pathogen from the upper part of the gas exchange system, including the throat and nasal passage

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4
Q

what are the four main ways in which animal defend themselves against infectious diseases

A

=physical - tissues provide barriers that pathogens cannot pass through unaided
=cellular - cells alert the body to the presence of pathogens, produce substances that provide protection and ingest and digest pathogens
=chemical - substances secreted by the body provide inhospitable envrionment’s for pathogens, trap them, cause them to burst, stop them reproducing and stop them entering cells
=harmless bacteria and fungi - such harmless organisms
that live on us and inside the alimentary canal and urinogenital system compete with pathogenic organism

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5
Q

what is the second line of defence

A

phagocytic cells and antimicrobial proteins that act against any type of invading microorganism that has breached the first line of defence

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6
Q

what is a non-specific defence

A

present from birth, these defences do not distinguish between different pathogens, and they give the same response each time a particular pathogen enters the body. They usually act very quickly but are not always highly effective.

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7
Q

what is inflammation

A

A local response to tissue damage and infection, involving the release of chemical signalling molecules and resulting in increased blood flow and movement of phagocytes into the infected tissues.

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8
Q

what is cytokines

A

Small protein molecules that act as cell signalling compounds. Many of them are involved in stimulating events that occur in response. Interleukins are included in the group of compounds known as cytokines

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9
Q

throughout the body, mast cells respond to tissue damage by secreting histamine. This cell-signalling compound stimulates a range of ways :

A
  • blood flow through capillaries increases as a result of vasodilation
  • capillaries become increasingly ‘leaky’, so that fluid enters the tissues, leading to swelling
  • phagocytes leave the blood, enter the tissues and engulf the tissues material
  • some plasma proteins leave the blood
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10
Q

what is a neutrophils

A

a short lived phagocytic cell, produced in the bone marrow, that circulates in the blood. Of all white blood cells, 60-70% are neutrophils. They have lobed nuclei and granular cytoplasm

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11
Q

what is a monocyte

A

a larger cell than neutrophil that circulates in the blood and leaves to remain as a long-lived macrophage in tissues such as the lungs

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12
Q

what is a macrophage

A

a large, lung lived phagocytic cell that remains in tissues. Macrophages process pathogens and present antigens to T lymphocytes

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13
Q

what is a dendritic cell

A

a large phagocytic cell with lengthy extensions that give a large surface area to interact with pathogens and with lymphocytes

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14
Q

wound healing involves the following stages

A
  • the formation of new blood vessels
  • the production of collagen
  • the formation of granulation tissue that fills the wound, allowing further changes to occur underneath
  • the formation of new epithelial cells by division of stem cells that migrate over the new tissue
  • wound contraction. by contractile cells
  • death of unwanted cells
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15
Q

what are phagocytes

A

are cells that carry out phagocytosis to engulf pathogens and other foreign material.
There are three main types of phagocytes, neutrophil, monocytes/macrophages and dendritic cells

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16
Q

when do the numbers of neutrophils massively increase

A

during infection,
The neutrophils poor out the bone marrow, circulate in the blood and then leave through capillary walls into damaged tissue.
Neutrophils do not live long after engulfing and digesting bacteria
During lung infection neutrophils ;eave the alveolar capillaries and digest their way through the lining of alveolar to reach bacteria

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17
Q

what is the 3rd line of defence

A

a response to invading pathogens in which lymphocytes and antibodies act against specific pathogens

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18
Q

what is an immune response

A

The sequence of events that occurs as the specific immune system responds to a foreign antigen; this may involve activation of the cloning of B cells that have receptors specific to the antigen, or specific T cells as well.

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19
Q

what is a b lymphocyte

A

Type of white blood cell that matures in bone marrow; when B cells respond they become plasma cells

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20
Q

what is a T lymphocyte

A

type of white blood cell that matures in the thymus gland. When T cells respond during an immune response, they do not make and release antibodies

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21
Q

what do active T cells do

A

do not make antibodies, instead they work in a variety of other ways, depending on the type of cell surface proteins that they have

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22
Q

what do active B cell do

A

make and release antibodies

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23
Q

what do mature B cells have

A

receptors that have exactly the same specificity as the antibody molecules that they are ‘programmed’ to secrete. each B cell has a differently shaped B cell receptor (BCR), similarly each T cell has T cell receptors that identify its specificity.
This allows them to have a huge variation in BCR’s and TRC’s allows lymphocytes to recognise the molecules on the surface of invading microorganisms

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24
Q

what is a clone

A

a group pf genetically identical cells.
In the immune system, there are clones of B cells and clones of T cells. Each clone has its own unique cell surface receptor complementary to a specific antigen

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25
Q

what do each group of identical B cells an each group of indentical T cells form

A

small clones

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26
Q

when does the immune response happen

A

once the B cells and T cell detect the presence of their antigen in the body

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27
Q

what is the first stage of the immune response

A

Antigen presenting

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28
Q

the multiple interactions on antigens and BCR’s is sufficient enough to

A

activate the B cell to divide and differentiate into plasma cells

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29
Q

what is a plasma cell

A

an activated B cell that makes and releases antibodies during an immune response

30
Q

some of the activated B cells form plasma cells which make many

A

ribosomes and the membrane necessary for rough endoplasmic reticulum

31
Q

what is a t helper cell

A

type of T cell that coordinated an immune response by stimulating the response of B cells and T killer cells by producing chemical signals such as interleukins

32
Q

central to the immune response are

A

T helper cells that respond to antigens presented by macrophages, this stimulates both T cells and B cells

33
Q

what are the stages in an immune response involving helper T cells

A

1) antigen presentation - APC’s in the lymph nodes engulf pathogens by endocytosis and then ‘cut them up’. These macrophages process antigens from the surface of the pathogen and put them into special proteins within their own cell surface membrane
2) clonal selection - T cells with receptors complementary in shape to the antigens bind to the macrophage. These small groups of specific T cells are clones that are selected by the macrophage. The APC secretes molecules of interleukin 1 to stimulate the selected t helper cells
3) clonal expansion - because every few T cells have the capability of destroying the invading pathogen, the cells in the clones divide by mitosis to form much larger clones. THC release interleukin 2 to stimulate BC to divide & differentiate into plasma cells.
4) antibody production - the stimulated B cells form plasma cells, which secrete the appropriate antibody

34
Q

what is clonal selection

A

the process during immune responses when specific clones of B cells and/or T cells interact with antigens displayed by APC’s

35
Q

what is clonal expansion

A

the division by mitosis of small groups of identical B cells and T cells during an immune response. This gives rise to effector cells (e.g. plasma cells) and to memory cells

36
Q

what is a t killer cell

A

Type of T cell that kills infected host cells

37
Q

what is a T regulator cell

A

type of T cell that stops immune response and prevents T cells attacking that body’s own cells and tissues.

38
Q

once T killer cells are activated by the binding of Antigens, T killer cells do what

A

fix to the surface of the infected cells and secrete performs, which are perforins inserted into the cell surface membranes of infected cells
Perforins form channels through membranes so that toxins such as hydrogen peroxide etc can enter the infected host cells. The host cell dies. §

39
Q

the immune response cannot be allowed to continue unchecked, so

A

another group of TC, the T regulator cells, down-regulate the immune response.
The t regulator cells shut down the immune response once the pathogens have been removed from the body, they also prevent the T cells from attacking the uninfected hosts

40
Q

what is the primary immune response

A

the first time a pathogen is detected in the body, the response by the lymphocytes is known which is known as the primary immune response
which is when we are feeling ill, then t killer cells are produced which help to remove the infectious agent, and we recover

41
Q

what is the secondary immune response to an antigen occurs

A

much faster than the PIR, and there are rarely any symptoms of the infection

42
Q

anitbodies are what type of protein

A

plasma proteins, known as immunoglobulins.

43
Q

what is the structure of an antibody

A

constant region (bottom strand, heavy polypeptide region)
variable region (light polypeptide chain)
hing region where the strand splits
antigen-binding sites (pathogens)
Receptor binding sites (phagocytes)
It is a Y shape

44
Q

within each class of antibody, the antibodies function in different ways in defence; some of these are

A

antitoxins
agglutination
opsonins

45
Q

what is an antitoxin

A

antitoxins combing with toxins secreted by bacteria (e.g. tetanus) to render them harmless

46
Q

what is agglutination

A

bind of two identical antigens on two or more pathogens, causing them to clump together. This makes it more difficult for them to spread and easier for phagocytes to engulf them. The largest class of antibody, with ten antigen-binding sites, is more effective at this than the antibody class with just two antigen binding sites.

47
Q

what is opsonins

A

‘coat’ pathogens to facilitate phagocytosis. Phagocytes have receptors for the constant regions of antibodies. By attaching to bacteria, these antibodies ‘mark’ them for destruction by phagocytes. Opsonisation is often compared to ‘sugaring’ pills to make them easier to swallow

48
Q

what are the different types of immunity

A

natural active immunity
natural passive immunity
artificial natural immunity
artificial passive immunity

49
Q

what is natural active immunity

A

occurs when you are infected
- i.e. occurs when the person is exposed to a live pathogen, develops the disease, and becomes immune as a result of the primary immune response

50
Q

what is natural passive immunity

A

occurs when antibodies cross the placenta during pregnancy; it also occurs when a child is breastfed by its mother. Breast milk is rich in IgA antibodies, but only against the diseases the mother has had

51
Q

what is artificial active immunity

A

is the result of being given a vaccine that contains one or more antigen

52
Q

what is artificial passive

A

occurs when antibodies are injected into a person to give them instant immunity. People who are likely to have tenanus, rabies are often given antitoxins by injection as a precaution. in each case, the antitoxin is neutralises the toxins released by each of the pathogens and prevents the damage that the toxin can cause

53
Q

explain why people who have suffered from server burns are at an increased risk of infectious disease

A

people with server burns will have lost the protection by the skin. This makes easier for pathogens to enter the body

54
Q

describe the role of phagosomes and lysosomes in defence

A

phagocyte engulf bacteria and viruses into a cavity formed by the plasma membrane. The membrane encloses the pathogens and fuses together to form a phagosome which traps the pathogens. Lysosomes contain lysozyme that breaks down the cell walls of bacteria and other hydrolytic enzymes that digest proteins, carbohydrates and nucleic acids. These enzymes become active when the lysosomes fuse with he phagosomes and their sonnets energy the phagosome where there is an acidic PH. intracellular digestion occurs to destroy the pathogens in what is correctly called phagolysosome

55
Q

Name two cell types that act as APC’s

A

macrophages, and dendritic cells

56
Q

distinguish between t helper cells and t killer cells

A

t helper cells secret interleukins to stimulate the activity if B cells and T killer cells. T killer cells search for infected cells and destroy them. T helper cells are not able to do this.

57
Q

what is an auto immune disease

A

when the body attacks itself using antibodies and T cell. that attack its cells. It occurs when the system attacks one or more self antigens, usually proteins.
about 5% of the uk have this disease
example are lupus, women are far more susceptible than men

58
Q

what has mass vaccination schemes given a rise to

A

herd immunity

-when as many people as possible are vaccinated, reducing the chance of transmission of the pathogen

59
Q

what is ring immunity

A

it is used to vaccinate people living or working near someone who is infected to prevent them staging the disease and spreading it

60
Q

what are problems with vaccinations

A

difficult to develop vaccines against diseases that are cause by eukaryotic organism, such as the malarial parasites plasmodium, because they have many genes that code for cell surface antigens.

61
Q

what are the three ways in which viruses can change their surface antigens

A

antigenic drift
antigenic shift
different strains of viruses invading the same cell

62
Q

what is antigenic shift

A

where there are major changes in the antigens within the same strain

63
Q

what is antigenic drift

A

where there are small changes In the structure and shape of the antigens within the same strain of virus

64
Q

how does penicillin work as an antibiotic

A

by inhibiting the bacterial enzyme traspeptidase, which catalyses the synthesis of murein, from which bacterial cells are made.

65
Q

disease outbreaks worldwide are carefully monitored in order to prevent

A

an epidemic

66
Q

if some people with a bacterial infection do not finish off all their antibiotics, when the feel better, or don’t take them properly what happens

A

some bacteria susceptible bacteria may survive, and if any mutations occur these may give resistance. The next time there is an infection of this strain of bacteria, the antibiotic may not work, because there are some resistant bacteria among those that have infected the body.

67
Q

bacteria can often develop resistance by acquiring genes that protect them from the effects of the antibiotic. The genes are often

A

easily spread from bacterium to bacterium - even from one species of bacterium to another.
An example is a gene that codes for the enzyme penicillinase. This breaks down penicillin, making it harmless

68
Q

new drugs are discovered and developed in several ways, by:

A
  • identifying likely compounds produced by organism such as fungi, actinobacteria, plants and animals
  • performing genetic analysis of organisms to search for likely genes that may code for potential drugs
  • finding molecules that fit into drug targets, such as receptor molecules for hormones and neurotransmitters at synapses
  • modifying existing drugs using computer modelling of the molecular structure of the drug and its target molecule
69
Q

some examples of potential new sources of new medicines are

A
  • marine antinobacteria have been discovered to be a source of rifamycins
  • calophyllum langierum, a rare tree from the rainforest in Malaysia, is the source of calanolide A - a drug that stops HIV entering the nuclei of healthy T helper cells
70
Q

what are 4 medicines derived from plants

A

Artemisinin - treatment of malaria (kills pathogen while inside RBC
galanthamine - treatment of Alzheimer’s (competitive inhibitor of enzyme in synapses that breaks down the chemical transmitter acetylcholine)
Teniposide - treats childhood leukaemia (slows growth of cancer cells by inhibiting enzymes involved in DNA replication)
Quinidine - treats fast heart rate, fibrillation (blocks channel proteins in cardiac muscle cells, so reducing conc. of impulses throughout the heart)

71
Q

most progress in personalised medicines has been made with drugs treating cancers. For example

A

trastuzumab is an antibody drug that interferes with a specific cell surface receptor and is used mainly to treat certain treats cancers

72
Q

what is synthetic biology

A

holds the potential for developing new drugs that require complex methods of synthesis that are difficult to achieve by purely chemical methods that may be very expensive.
- one of the best known applications of synthetic biology is genetically modifying e.coli and yeast for the commercial production of a precursor of the antimalarial drug artemisinin