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Human Biology Y12 > response to infection > Flashcards

response to infection Flashcards

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1
Q

what happens if the body’s defence mechanisms against invading organisms are overcome?

A

the invaders may cause disease

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2
Q

infectious diseases

A

diseases that are spread from one person to another

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3
Q

pathogens

A

disease causing organisms

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4
Q

most common pathogens that affects the body

A

bacteria and viruses
+ fungi and animal parasites also affect the body (not main focus)

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5
Q

bacteria structural characteristics

A
  • cell wall
  • no nucleus (prokaryotes)
  • flagellum present
  • DNA in the form of plasmids
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6
Q

majority of bacteria is…

A

non-pathogenic

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7
Q

uses of bacteria

A
  • essential to life e.g. decomposition of organic material
  • industrial processes
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8
Q

location of bacteria

A

live in skin & inside intestines

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9
Q

effects of bacteria

A

producing toxins & inducing allergic responses

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10
Q

how to identify bacterium

A

grown on an agar player/growth medium in specific conditions → stained → viewed under microscope

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11
Q

viruses definition

A

microscopic infectious agents

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12
Q

virus structure

A

all contain genetic material in the form of DNA or RNA (but never both)
- consist of a protein sheath surrounding a core of nucleic acid
- some also have an external lipid envelope

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13
Q

reproduction of viruses

A

totally dependent on living cells for reproduction, infect a living cell and it’s DNA/RNA induces the cell to manufacture more virus particles, new virus particles leave the host cell → infect others, cells become damaged/changed or die

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14
Q

viruses: living or non-living?

A

not living things - cannot reproduce by themselves

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15
Q

why are symptoms from a virus affecting specific tissues?

A

viruses differ in the type of cell they invade, symptoms relate to the affected tissue

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16
Q

what happens when a virus infects bacteria?

A

bacteriophage is made

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17
Q

contagious disease

A

communicable disease may be spread by the transmission of pathogenic organism from one person to another

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18
Q

vectors

A

intermediate host of the pathogen that spread the infectious disease e.g. fleas, mosquitoes

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19
Q

ways of transmission of pathogens

A
  • transmission by contact
  • ingestion of food or drink
  • transfer of body fluids
  • infection by droplets
  • airborne transmission
  • transmission by vectors
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20
Q

transmission by contact w. examples

A
  • spread of pathogen by physical contact
  • direct = actually touching infected person
  • indirect = touching an object that has been touched by infected individual
  • e.g. skin infections, STIs
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21
Q

ingestion of food or drink w. examples

A
  • contaminated with pathogens
  • e.g. salmonella food poisoning, dysentery
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22
Q

transfer of body fluids w. examples

A
  • when blood or other fluids from an infected person comes into contact with mucous membranes (nose, throat, mouth, genitals, bloodstream) of another uninfected person
  • via a needle stuck; break in the skin
  • e.g. HIV, Hep B and C
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23
Q

infection by droplets w. examples

A
  • tiny droplets of moisture containing pathogenic organisms are admitted when breathing, talking, sneezing or coughing
  • may be breathed in by others; settle on food or utensils to be later ingested with food
  • e.g. Ebola, COVID-19, mumps, cold, flus
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24
Q

airborne transmission w. examples

A
  • moisture in exhaled droplets evaporate, most bacteria are killed, but viruses and some bacteria remain viable → cause infection when inhaled
  • particles are lighter → remain viable for greater distance than those transmitted by droplets
  • e.g. measles, chickenpox
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25
Q

transmission by vectors w. examples

A
  • animals such as insects, ticks or mites
  • some vectors transfer the pathogen directly
  • some may spread the pathogen to food or water → injected (e.g. houseflies)
  • Many vector-borne disease are spread by specific vector
  • e.g. malaria is spread by mosquitoes; lyme disease spread by ticks
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26
Q

non-specific defences

A

defence of the body that acts against all pathogens

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27
Q

specific defences

A

directed against a specific pathogen

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28
Q

external defence: skin

A
  • covers outside of the body
  • good at stopping entry of microorganisms (provided there are no cuts/abrasions)
  • special protection at openings in skin (mouth, eyes, anus)
  • normal bacteria occupy skin → pathogens find it difficult to establish
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28
Q

what do External defences do?

A

stop pathogens and foreign particles from entering

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29
Q

additional mechanisms of the skin

A

Sebum and sweat

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30
Q

sebum

A

oily, waxy secretion from sebaceous glands; kills pathogenic bacteria

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31
Q

sweat

A

liquid produced by sweat glands; contains salts and fatty acids that prevent growth of many micro-organisms

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32
Q

external defence: mucus

A

Mucous membranes secretes mucus = slippery, stringy substance
- Traps particles → inhibits entry of microorganisms to the organs of the body
- Eg, digestive, urinary and reproductive tracts

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33
Q

mucous membranes

A

epithelial tissue that secretes mucus and lines many body cavities

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34
Q

external defence: hair

A
  • Found in the nasal cavity and ears
  • Hairs + layer of mucus = trap up to 90% of particles inhaled when breathing
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35
Q

external defence: cilia

A
  • Cilia = hair like projections from a cell; beat rhythmically to move material across a tissue surface
  • Mucous membranes lining the nasal cavity and trachea have
    cilia
  • Beating of the cilia moves mucus (containing trapped particles and micro-organisms) towards the throat → coughed or swallowed
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36
Q

external defence: acids

A

Stomach juices are strongly acidic (HCI)
- Kills many of the bacteria taken in with food or those contained in mucus swallowed from nose or windpipe
- Vagina has acid secretions → reduce growth of microorganisms

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37
Q

external defence: lysozyme

A

lysozyme = enzyme that kills bacteria
- found in tears, saliva and perspiration

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38
Q

external defence: cerumen

A

cerumen = ear wax
- Protects the outer ear against infection by some bacteria
- Slightly acidic
- Contains lysozyme

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39
Q

external defence: movement of fluid

A

Eg. Urine flowing through urethra = cleansing action
- Prevents bacterial growth
- Helps stop bacteria reaching the bladder and kidneys

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40
Q

what are protective reflexes?

A

Involuntary reflexes that help protect the body from injury

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41
Q

examples of protective reflexes

A
  1. Sneezing
  2. Coughing
  3. Vomiting
  4. Diarrhoea
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42
Q

sneezing

A
  • Stimulus = irritation of the walls of the nasal cavity
  • Irritation = Fumes; dust particles
  • Forceful expulsion of air carries mucus, foreign particles and irritating gases out through nose and mouth
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43
Q

coughing

A
  • Stimulus = irritation of lower respiratory tract (bronchi and
    bronchioles)
  • Air is forced out of the lungs to try and remove the irritant
  • Air drives mucus and foreign matter up the trachea → throat
    and mouth
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44
Q

vomiting

A
  • Contraction of abdominal muscles and diaphragm expels stomach contents
  • Psychological stimuli, excessive stretching of stomach and bacterial toxins = induce vomiting
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45
Q

diarrhoea

A
  • Irritations cause increased contractions of the muscles of the wall of the intestines → irritant removed ASAP
  • Material doesn’t stay in the large intestine long enough for water to be absorbed
  • Irritants = bacteria, viruses or protozoans
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46
Q

what attacks organisms that overtake the external defences

A

Organisms that penetrate our external defences are attacked by phagocytes

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47
Q

phagocytes

A

Phagocytes = specialised WBC (leucocytes)

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48
Q

what do phagocytes do?

A

engulf and digest micro-organisms and cell debris
- Eliminates many pathogens before an infection has the chance to take hold

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49
Q

different types of cells that are phagocytic

A
  1. Monocytes and macrophages
  2. Neutrophils
  3. Dendritic cells
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50
Q

Monocytes

A

type of leucocyte found in the blood that migrates into damaged tissues (infected or inflamed) - form macrophages

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51
Q

Macrophages

A

large phagocytic cell; derived from monocyte

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52
Q

what do macrophages do?

A
  • Some move through tissues looking for and destroying pathogens
  • Some are fixed; only deal with pathogens that come to them
  • Important in removing microbes and dying cells through phagocytosis
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53
Q

neutrophils

A
  • Granulated leucocyte (granules visible in their cytoplasm)
  • Lobulated nucleus
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54
Q

lifespan of neutrophils

A
  • Short life span (die after a few days)
    • Dead cells = pus that forms after an infection
55
Q

what do neutrophils do?

A

First cells to move into the tissue to destroy the pathogen by phagocytosis (important in killing pathogens inside cells)

56
Q

dendritic cells

A
  • Characterised by projections from the cytoplasm
  • Different from macrophages and neutrophils = function goes beyond phagocytosis
  • Ability to detect, engulf and process foreign particles
    • Use info about ingested particles → assist with specific immunity
57
Q

what is inflammation?

A

response to damage to a tissue; involves swelling, heat, pain and redness in the affected area

58
Q

purpose of inflammation

A
  • Reduce the spread of pathogens, to destroy them and prevent entry of addition pathogens
  • Remove damaged tissue and cell debris
  • Begin repair of the damaged tissue
59
Q

four signs of inflammation

A
  • Redness
  • Swelling
  • Heat
  • Pain
60
Q

what is a complement system?

A

system of proteins produced by the liver that enhance the activity of antibodies and phagocytes

61
Q

what causes inflammatory repsonse?

A

damage to tissues

62
Q

what is inflammatory response assisted by?

A

assisted by proteins produced by liver cells and macrophages

63
Q

first step in inflammatory response

A

Mechanical damage or local chemical change → specialised leucocytes called mast cells to be activated by complement proteins
- Leads to release of histamine, heparin and other chemicals into the tissue fluid

64
Q

second step in inflammatory response

A

Histamine increases blood flow through the are due to vasodilation
- Walls of blood capillaries more permeable → more fluid moves through capillary walls into tissue
- Increased blood flow → heat and redness
- Escape of fluid → swelling

65
Q

third step in inflammatory response

A

Mast cells release heparin = prevents clotting in the immediate area of injury
- Clot of the fluid forms around damaged area
- Slows the spread of the pathogen into healthy tissues

66
Q

fifth step in inflammatory response

A

Abnormal conditions in the tissue stimulate pain receptors in inflamed area

67
Q

fourth step in inflammatory response

A

Complement system proteins and some chemicals released by the mast cells attract phagocytes (neutrophils) → consume micro-organisms and debris by phagocytosis

68
Q

sixth step in inflammatory response

A

Phagocytes are filled by bacteria, debris and dead cells = die
- Pus formed from dead phagocytes and tissue fluid

69
Q

seventh step in inflammatory response

A

New cells produced by mitosis → repair of damaged tissue
takes place

70
Q

fever

A

elevation of body temperature above 37C
Change due to resetting of body’s thermostat (controlled by the hypothalamus) to a level higher than normal

71
Q

what causes fever

A
  • Reaction due to pyrogens released by WBC during inflammatory response and act on hypothalamus
    • Pyrogens = substance that results in a fever
72
Q

what is pyrogen?

A

Produced by activated macrophages, dendritic and epithelial cells

73
Q

what happens at the start of a fever?

A
  • Body temp is still regulated in response to heat/cold with a fever → set point is at a higher level
  • Onset of fever is gradual - can be be rapid
  • Person’s thermoreceptors detect body temp → hypothalamus
    recognises it is lower than the new higher set point
    • Vasoconstriction in the skin and shivering occur
      • Conserve heat and increase heat production (increasing body temp)
74
Q

what happens when the fever breaks

A
  • When fever breaks (crisis) → body’s thermostat set to normal
    • Person feels hot and appears flushed → skin vasodilation and sweating (bring body temp down)
75
Q

how are fevers beneficial?

A
  • High body temp inhibits the growth of some bacteria and viruses
  • Heat speeds up the rate of chemical reactions → help body cells repair themselves more quickly during disease
  • May inhibit viral replication by allowing chemicals called interferons to operate more quickly
76
Q

dangerous effects of fever

A
  • If body temp goes too high → convulsions; brain damage
    • Death will occur © 44.4 - 45.5C
77
Q

what does lymphatic system consists of

A
  • Network of lymph capillaries joined to larger lymph vessels
  • Lymph nodes - located along the length of some lymph vessels
78
Q

function of lymphatic system

A

Important part of body’s internal defence against pathogenic organisms

79
Q

lymph nodes and phagocytosis

A
  • Lymph entering lymph nodes contain cell debris, foreign particles and microorganisms that have penetrated the body’s external defence
    • Some may be pathogenic
    • Larger particles (g. Bacteria) are trapped in meshwork of fibres as lymph flows through spaces
      in nodes
      • Macrophages ingest and destroy these by phagocytosis
80
Q

what happens when infections occur?

A

formation of lymphocytes
increases

81
Q

what is the immune system composed of?

A

Composed of cells and proteins that protect against foreign organisms,
range of alien chemicals, cancerous and other abnormal cells

82
Q

immune response

A

Homeostatic response that helps to deal with the invasion of micro-organisms and foreign substances enter the body → restore to normal conditions

83
Q

key cells involved in immune response

A
  • B-cells
  • T-cells
    • Produced in bone marrow
    • End up in lymphoid tissue
84
Q

where do B cells mature

A

born marrow then move to lymphoid tissue

85
Q

where do T cells mature

A

thymus then move to lymphoid tissue

86
Q

what do b cells develop into?

A

Develops into either plasma cell that produces antibodies or a memory cell

87
Q

what do T cells differentiate into?

A

Can differentiate into a no. of different kinds of cells that are involved
in cell-mediated immunity

88
Q

antibody mediated immunity

A

involves the production of special proteins called antibodies by B cells, which circulate around the body and attack invading agents

89
Q

cell mediated immunity

A

due to T cells and involves the formation of special lymphocytes that destroy invading agents

90
Q

antigens

A

Any substance capable of causing the formation of antibodies when introduced into the tissues → causing a specific immune response

91
Q

self-antigen

A

Molecules produced in person’s own body doesn’t cause IR

92
Q

non-self antigens

A

Foreign compounds that trigger IR by being recognised by receptors on B and T cells

93
Q

antibodies

A

Substance produced in response to a specific antigen; combines with the antigen to neutralise or destroy it

94
Q

what group of proteins do antibodies belong to?

A

immunoglobins

95
Q

what is it called when an antibody combines with an antigen?

A

antigen-antibody complex

96
Q

how is an antigen-antibody complex made

A
  • Antigen molecules have specific active sites with a particular shape
  • Antibody has the complementary shape > allowing two molecules to fit together like a key in a lock
  • Each antibody can combine with only one particular antigen
97
Q

Antigen presenting cells

A

Phagocytic cells that digest pathogens and present the antigen to lymphocytes; include dendritic cells and macrophages
they:
- Detect the presence of a non-self antigen
- Engulf the antigen
- Digest the pathogen, producing small fragments that move to the surface of the cell
- Present the antigen to the lymphocytes

98
Q

Primary response

A
  • First exposure to antigen
  • Slow response → days to build up large amounts of antibodies
  • Time for B-cells to multiply and differentiate > plasma cells and secrete
    antibodies
  • Declines after level of antibodies reached peak
99
Q

Secondary response

A
  • Second/subsequent exposure to same antigen
  • Response faster → memory cells recognise the antigen more quickly
  • Plasma cells are able to form quickly
  • Antibody levels in body plasma rising rapidly to higher level that lasts longer
  • Antigen has little opportunity to exert a noticeable effect on body = no illness
100
Q

killer T cells (cytotoxic)

A
  • migrate to the site of infection and deal with invading antigen
  • Attach to the invading cells → secrete chemical that will destroy antigen
  • Then go in search of more antigens
101
Q

helper T cells

A
  • Bind to antigen on antigen-presenting cells → stimulate secretion of
    cytokines that:
    • Attract lymphocytes to infection site → sensitised and activated → intensifies response
    • Attract macrophages to infection site → can destroy antigens by phagocytosis
    • Intensity phagocytic activity of macrophages
    • Promote the action of killer T-cells
102
Q

suppressor T cells

A
  • Act when the immune activity becomes excessive/infection dealt with successfully
  • Release substances that inhibit T and B cell activity > slowing down IR
103
Q

immunity

A

resistance to infection by invading micro-organisms

104
Q

natural immunity

A

occurs without any human intervention

105
Q

artificial immunity

A

produced by giving a person an antigen that triggers an IR; or giving them antibodies to an infecting antigen

106
Q

passive

A

When a person receives antibodies produced by someone else

  • Individuals body played no part in the production of antibodies
107
Q

active immunity

A

Results when the body is exposed to a foreign antigen > makes
antibodies in response to that antigen

This type of immunity lasts longer than passive > presence of
memory cells

108
Q

immunisation

A

programming the immune system to respond
rapidly to infecting microorganisms; developing immunity

109
Q

vaccination

A

artificial introduction of antigens of pathogenic
organisms

110
Q

vaccine

A

antigen preparation used in artificial immunisation

111
Q

Live-attenuated vaccines

A
  • Living attenuated microorganisms have reduced virulence (reduced ability to produce disease symptoms)
  • Immunised person doesn’t contract the disease; but manufactures antibodies against the antigen
112
Q

Inactivated vaccines

A
  • Contain dead microorganisms
  • Produce an immunity that is shorter lasting than immunisation using LA microorganisms
113
Q

Toxoid vaccines

A
  • Cases where bacteria produce their effects in humans by liberating toxins - not necessary to use the bacteria for immunisation
  • Toxins produced by the bacteria can be inactivated → when injected they don’t make the person ill
  • Inactivated toxins = toxoids
114
Q

Sub-unit vaccine

A

Fragment of organism can be used to provoke IR

115
Q

vaccines - Recombinant DNA

A
  • Insert certain DNA sequences from the pathogen into harmless bacterial cells
  • Chosen DNA sequence causes the production of antigens characteristic of the pathogen
  • Vaccination with harmless bacterium → immunity against pathogen
116
Q

vaccinations start at what age and why?

A
  • Vaccination starts after 6 weeks of age
    • Child’s blood contains antibodies from it’s mother via placenta and breast milk
    • If given earlier than weeks, antibodies from mother will eliminate antigens
    • 6 weeks gives newborn time for immune system to be activated
117
Q

booster reason

A
  • one injection of a vaccine isn’t enough to protect a person from particular disease
    • Antibody levels from the primary response following first dose will decline
    • Second vax (booster) needed to stimulate secondary response
      • Memory cells react quickly to second exposure → higher, longer lasting level of antibodies
118
Q

why should there be a time period between two vax shots?

A

Given too soon → antibodies present in blood will eliminate vaccine material before B-cells can be activated

119
Q

herd immunity

A

occurs when high proportion of ppl in a population are immunised that those who aren’t immune are protected

120
Q

social factors

A
  • Ethical concerns with the use of animals to produce vaccines
  • Ethical concerns with the use of human tissue to produce vaccines
  • Ethical concerns with informed consent
  • Ethical concerns with testing on animals
  • Availability
121
Q

Ethical concerns with the use of animals to produce vaccines

A

Viral vaccines require host tissue (as viruses can only be replicated in living cells)

122
Q

Ethical concerns with the use of human tissue to produce vaccines

A

Using human tissue avoids problems of cross-species infection from possible unknown viruses

123
Q

Ethical concerns with informed consent

A

Trialing vaccines in developing countries → use in populations with low standards of education → ppl aren’t fully aware of the risks → exploitation

124
Q

Ethical concerns with testing on animals

A
  • Prior to clinical trials in humans, vaccines tested on animals to identify potential
    problems
    • Legislation exists to limit the way animals can be used
    • Mice commonly uses
125
Q

Availability

A

Vaccines aren’t always readily available in all areas

126
Q

cultural beliefs

A

Religious beliefs
- Religious that rely on faith healing/healing through prayer
- Methods used to produce vaccines may contradict religious beliefs → non-participation in immunisation program

127
Q

Economic factors

A
  • Cost of vaccine
  • May be too expensive
  • Commercialisation
  • Interests of commercial vaccine production may affect it’s use
128
Q

antibiotics

A

Drugs used to fight infections of microorganisms eg. Bacteria

129
Q

why can’t antibiotics be used to treat viral infections?

A

Viruses are not living cells → do not metabolise

130
Q

types of antibiotics

A
  • Bactericidal antibiotics
    • Kill bacteria by
      • changing the structure of the cell wall or membrane
      • Disrupting action of essential enzymes
  • Bacteriostatic antibiotics
    • Stop bacteria from reproducing
      • Disrupting protein synthesis
131
Q

broad spectrum

A

Affects many types of bacteria

132
Q

narrow spectrum

A

Effective only against specific types of bacteria

133
Q

Antibiotic Resistance

A

Widespread use → some bacteria have evolved and become
resistant to antibiotics

  • Multiple drug resistance = resistance of some strains of bacteria to most available antibiotics
    • Caused by overuse of antibiotics in medicine and agriculture

How to slow this resistance

  • Developing new classes of antibiotics
  • Genetically engineer bacteria to disable antibiotic resistant genes
134
Q

Antivirals

A
  • Drugs used specifically to treat viral infections
  • No treatment for common ailments such as colds, chickenpox
  • The way viruses replicate makes it difficult to find drugs that will treat viral infections
    • Host cell produces new virus particles, any drug that interferes with the virus replication is likely to be toxic to the host
  • Research aimed at identifying viral proteins that can be disabled by specially designed chemicals
135
Q

Recombinant DNA and vaccines - Hep B vaccine

A
  • Gene for surface antigen on the virus is isolated → added to a plasmid
  • Plasmid introduced into a yeast cell
  • When yeast cell divides, new cells contain the plasmid with the gene for the antigen
  • Gene allows the yeast cells to produce the antigen protein which can be collected and purified

Human Biology Y12 (12 decks)

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