B4 - Disease Flashcards
(100 cards)
1
Q
Transmission:
How can being in a hot climate make transmission more likely?
A
increased heat provides more kinetic energy for chemical reactions and reproduction
2
Q
Transmission:
How can social factors such as poverty and developing countries make transmission more likely?
A
could result in poor sewage infrastructure, no fresh water/food, bad sanitation and overcrowded living. Medicines/vaccines might be less available.
3
Q
Types of Direct transmission in Animals?
A
- Direct contact
- Inoculation
- Ingestion
4
Q
Direct Transmission: how can direct contact be a form of transmission?
A
touching, kissing, contact with cuts in skin and sex
5
Q
Types of Indirect transmission in Animals?
A
- Vectors
- Droplets
6
Q
Direct Transmission: how can inoculation be a form of transmission?
A
touching, kissing, contact with cuts in skin and sex
7
Q
Direct Transmission: how can ingestion be a form of transmission?
A
drinking and eating contaminated things
8
Q
Indirect Transmission: how can a vector be a form of transmission?
A
animals that pass the pathogen to humans, e.g. mosquitoes’ malaria
9
Q
Indirect Transmission: how can droplets be a form of transmission?
A
pathogens transmitted in droplets of water.
e.g. saliva and mucus expelled when sneezing
10
Q
Indirect Transmission: how can fomites be a form of transmission?
A
dirty bedding, socks and cosmetics are examples of inanimate objects that can carry and transmit pathogens
11
Q
What modes of direct transmission are there in plants?
A
direct contact - between diff plants.
e.g. ring rot and tobacco mosaic virus
12
Q
what modes of indirect transmission are there in plants?
A
- contaminated soil
- vectors
13
Q
Indirect transmission: how is contaminated soil a form of transmission?
A
pathogens and their spores can remain in soil and infect roots of plants
14
Q
Indirect transmission: how are vectors a form of transmission?
A
wind, water, animals and humans can carry pathogens and spores from one plant to another
15
Q
Plant responses: how do plants prevent entry of diseases?
A
they have barriers such as bark or waxy cuticles
16
Q
Plant responses, what do plants have?
A
- barriers to prevent entry, e.g. bark/waxy cuticles
- antibacterial chemicals and proteins act as a defence against bacterial infections. Can repel insects (vectors) snd kill pathogens
- physical defences to prevent pathogens from spreading between cells, e.g. callose
17
Q
Animal responses; what is the primary line of defence?
A
It is non-specific
18
Q
Animal responses; how is the skin a primary line of defence?
A
- it is a physical barrier
- contains skin flora (healthy microorganisms), outcompete pathogens for space and resources on the skin
19
Q
Animal responses; how are blood clots a primary line of defence?
A
- blood clots will form if the skin is cut to form a new barrier
20
Q
Animal responses; how are mucous membranes a primary line of defence?
A
- line many body tracts
- mucus produced traps pathogens and the cilia sweep the mucus away from lung
21
Q
Animal responses; how are lysozymes a primary line of defence?
A
- hydrolytic enzyme which digest pathogens
22
Q
Animal responses; how are expulsive reflexes a primary line of defence?
A
- sneezing, coughing, vomiting
- mechanisms to force pathogens out of the body
23
Q
Animal responses; how is inflammation a primary line of defence?
A
- occurs in localised areas where damage to cells is detected.
- it causes the area to become red, hot, sore, itchy and swollen
- when cells are damaged, it triggers mast cells to release histamines and cytokines
24
Q
Animal responses; how are histamines a primary line of defence?
A
- cause blood vessels to dilate and therefore more blood is flowing to area
- the increased temp from blood can kill pathogens.
- make walls of blood vessels more permeable so more white blood cells can be delivered to the site of damage.
25
Animal responses; how are cytokines a primary line of defence?
- attract phagocytes, which can engulf and destroy pathogens
26
What is phagocytosis?
Phagocytes, travel in the blood and squeeze out of capillaries to engulf and digest pathogens. it is a non-specific response
27
What is the process of phagocytosis?
1. damaged cells and pathogens release cell signalling chemicals (cytokines) that attract the phagocytes to the site of infection
2. an opsonin protein can attach to pathogens to mark them and make it easier for neutrophils and macrophages to engulf them
3. phagocytes have receptors which can attach onto chemicals on the surge of pathogens
4. the phagocyte then engulfs the pathogen into a vesicle to create a phagosome
5. within the phagocytes, there are lysosomes which contain hydrolytic lysozyme
6. the lysosome fuses with the phagocytes to expose the pathogen to the lysozyme. The lysozyme hydrolyses the pathogen and any soluble useful molecules are absorbed into the cytoplasm of the phagocyte
7. the phagocytes will present the antigen if the digested pathogen on their surface (antigen-presenting cells)
28
what's the second line of defence?
It is specific and responds to antigens.
There are two types:
- B lymphocyte (B cells)
- T lymphocytes (T cells)
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where are B cell and T cells created?
Both created in bone marrow stem cells, but B cells mature in bone marrow whereas T cells mature in thymus
30
what are T cells reponsible for?
cell mediated repsonse
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how do T cells respond?
Receptors on T cells bind to antigens on antigen-presenting cells (APCs).
This will cause T cell to divide by mitosis (clonal expansion).
32
APCs are cells that present a non-self antigen on their surface.
What do these include?
- infected body cells presenting viral antigens on their surface
- a macrophage which has engulfed and destroyed a pathogen presenting the antigens on their surface
- cells of transplanted organ will have different shaped antigens on their surface compared to your self-cell antigens
- cancer cells will have abnormal-shaped self-antigens
33
what is the cell mediated response?
1. once a pathogen has been engulfed and destroyed by a phagocyte, the antigens are positioned on the cell surface. this is now called an APC
2. T helper cells have receptors on their surface which can attach to the antigens on APC
3. once attached, interleukins are produced which activates the T helper cells to divide by mitosis to replicate and make large numbers of clones
4. cloned T helper cells differentiate into diff cells
34
What are the different cells that T helper cells differentiate into?
- T helper cells and produce interleukins to activate B lymphocytes
- some produce interleukins to stimulate macrophages to perform more phagocytosis
- T memory cells for that shaped antigen
- T killer cells
- T regulator cells, which suppress the immune response to ensure the cell-mediated response only occurs when pathogens are detected.
35
What are T killer cells
can destroy abnormal or infected cells.
most common in viral infections because viruses infect body cells, body cells are sacrificed to prevent viral replication
36
How do T killer cells destroy cells?
release a protein, perforin, which embeds in the cell surface membrane and makes a pore so that any substances can enter or leave the cell and this causes death.
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What is the humeral response?
T helper cells stimulate the B cells by producing interleukins.
This initiates the humeral response, which involves antibodies.
38
What is an antibody?
- globular, quaternary proteins that have binding sites complementary in shape to antigens.
- they are made up of 4 polypeptide chains, 2 heavy polypeptide chains and 2 light polypeptide chains.
- its binding site is the variable region, where the antibody binds to a complementary-shaped antigen
- the rest of the antibody is the constant region
- when antigen and antibody bind its known as an antigen-antibody complex
39
What 3 ways do antibodies work in?
- agglutination
- marking pahtogens
- anti-toxins
40
Antibodies; what is agglutination?
the climbing together of pathogens to make it easier for phagocytes to locate and engulf them
41
Antibodies; how do they mark pathogens?
antibodies act as an opsonin when an antibody-antigen complex has been formed. The antibodies are marking the antigen making them more susceptible to phagocytosis
42
Antibodies; how do they work as anti-toxins?
can bind to toxins, preventing them from entering cells and causing harm. In this way, they act as anti-toxins
43
What's the process of the humeral response?
1. activated T helper cells bind to B cells with the complementary antibody to the antigen (clonal selection)
2. this B cell is activated by the release of interleukins from the T helper cell
3. B cells rapidly divide by mitosis to make clones which differentiate into memory B cells or plasma cells (clonal expansion)
4. the plasma cells produce antibodies. the antibodies attach to the antigens on the pathogen to help destroy them by agglutination and marking them for phagocytes
5. this is the primary immune response (first time body has encountered pathogen)
6. the B memory cells remain in blood after infection and can rapidly produce large amounts of antibodies if there is reinfection with the same pathogen
44
What are factors affecting the transmission of communicable diseases in *animals*?
1. overcrowded living and working areas
2. poor nutrition
3. a compromised immune system
4. poor disposal of waste, providing breeding sites for vectors
5. climate change - this can introduce new vectors and new diseases
6. culture and infrastructure - in many countries traditional medical practises can increase transmission
7. socioeconomic factors
45
Factors affecting the transmission of communicable disease in *plants*?
1. plant varieties of crops that are susceptible to disease
2. over-crowding increases the likelihood of contact
3. poor mineral nutrition reduces resistance of plants
4. damp, warm conditions increase the survival and spread of pathogens and spores
5. climate change - increased rainfall and wind promote the spread of diseases; changing conditions allow animal vectors to spread to new areas; drier conditions may reduce the spread of disease
46
How do plants recognise an attack?
Plants respond rapidly to pathogen attacks.
- receptors in cells respond to molecules from the pathogens, or to chemicals produced when the plant cell wall is attacked
- this stimulate the release of signalling molecules that appear to switch on genes in the nucleus.
- this triggers cellular responses, which include; producing defensive chemicals, sending alarm signals to unaffected cells to trigger their defences, and physically strengthening the cell walls
47
Physical defences: What does callose do in the initial attack?
- 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 of the infection
48
Physical Defences: second part to callose defence system
- 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
49
Physical Defences: third part to calls defence system
- callose blocks sieve plates in the phloem, sealing off the infected part and preventing the spread of pathogens
50
Plant Physical defences: forth part to callose defence system?
calls is deposited in the plasmodesmata between infected cells and their neighbours, sealing them off from the healthy cells and helping to prevent the pathogen spreading
51
Plant Chemical Defences: what type of chemical defence produces pine resin and citronella
insect repellent
52
Plant Chemical Defences: what type of chemical defence produces pyrethrins and caffeine
insecticides
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Plant Chemical Defences: what type of chemical defence produces of phenols
antibacterial compounds including antibiotics
54
Plant Chemical Defences: what type of chemical defence produces saponins
anti fungal compounds
55
Plant Chemical Defences: What type of chemical defence produces glucanases
anti-oomycetes
56
Plant Chemical Defences: What produces the type of chemical defence of cyanide
general toxins
57
Animal Non-specific defences: how does the skin act as a defence barrier
- covers the body and prevents the entry of pathogens
- has skin flora of healthy micro-organisms that outcompete pathogens for space on the body surface
- produces sebum, an oily substance that inhibits the growth of pathogens
58
Animal Non-specific defences: how do body tracts act as a defence barrier?
- e.g. airways of the gas exchange system are lined by mucous membranes that secrete mucus
- this traps microorganisms and contains lysosomes, that destroy bacterial and fungal cell walls.
- mucus also contains phagocytes, which remove the pathogen
59
Animal Non-specific defences: how do lysosomes act as a defence barrier?
- in tears, urine and stomach acid prevent pathogens getting into our bodies
- we have repulsive reflexes, coughs and sneeze eject pathogen mucus, whereas vomiting and diarrhoea expel the contents of the gut including any infective pathogens
60
Animal Non-specific defences: Why does blood clot and wound repairs when cutting yourself?
- The skin is breached and pathogens can enter the body.
- The blood clots rapidly to seal the wound
- When platelets come into contact with collagen in the skin or wall of damaged vessel, they adhere and begin secreting several substances.
- The clot dries out and forms a hard tough scab, keeping the pathogens out
- Epidermal cells below the scab start to get, sealing the wound permanently, while damaged blood vessels regrow
- Collagen fibres are deposited to give the new tissue strength
- once the new epidermis reaches normal thickness, the scab sloughs off and the wound is healed
61
Animal Non-specific defences: Wound repair - what is thromboplastin
an enzyme that triggers a cascade of reactions, resulting in the formation of a blood clot (or thrombus)
62
Animal Non-specific defences: Wound repair - what is serotonin
makes the smooth muscle in the walls of the blood vessels contract, so they narrow and reduce the supply of blood to the area
63
Animal Non-specific defences: What is inflammatory response?
A localised response to pathogens resulting in inflammation at the site of a wound. Inflammation is characterised by pain, heat, redness, and swelling of tissue
64
Animal Non-specific defences: Inflammatory response - what are mast cells
Mast cells are activated in damaged tissue and release chemicals called histamines and cytokines
65
Animal Non-specific defences: Inflammatory response - what are histamines
- Make the blood vessels dilate, causing localised heart and redness. The raised temp helps prevent pathogens reproducing.
- Make blood vessel walls more leaky so blood plasma is forced out, once forced out of the blood it is known as tissue fluid. Tissue fluid causes swelling (oedema) and pain.
66
Animal Non-specific defences: Inflammatory response - what are cytokines
They attract white blood cells (phagocytes) to the site. They dispose of pathogens by phagocytosis
67
Animal Non-specific defences: Fevers - how do cytokines stimulate temp?
- Normal body temperature of 37◦c and is maintained by the hypothalamus in the brain.
- When a pathogen invades the body, cytokines stimulate the hypothalamus to reset the thermostat and your temperature goes up.
68
Animal Non-specific defences: Fevers - how are cytokines stimulating hypothalamus a useful adaptation?
1. most pathogens reproduce best at or below 37○c. Higher temperatures inhibit pathogen reproduction
2. the specific immune system works faster at higher temperature
69
Animal Non-specific defences: Phagocytosis - what are phagocytes?
- are specialised white cells that engulf and destroy pathogens.
- build up at the site of an infection and attack pathogens (e.g. pus, cut or wound)
70
Animal Non-specific defences: Phagocytosis - what are the two main types of phagocytes?
1. neutrophils
2. macrophages
71
Animal Non-specific defences: Phagocytosis - what are the stages of phagocytosis?
1. Pathogens produce chemicals that attract phagocytes
2. Phagocytes recognise non-human proteins on the pathogen. This is a response not to a specific type of pathogen, but to a cell or organism that is non-self
3. The phagocyte engulfs the pathogen and encloses it in a vacuole called a phagosome
4. The phagosome combines with a lysosome to form a phagolysosome
5. Enzymes from the lysosome digest and destroy the pathogen
72
Animal Non-specific defences: Phagocytosis - what are opsonins
they are chemicals that bind to pathogens and ' tag' them so they can be more easily recognised by phagocytes. Phagocytes have receptors on their cell membranes that bind to common opsonins, and the phagocyte then engulfs the pathogen.
73
Specific Immune System: What are antibodies?
Antibodies are Y-shaped glycoproteins called immunoglobulins, which bind to a specific antigen on the pathogen or toxin that has triggered the immune response
74
Specific Immune System: What are antibodies made up of?
- Two identical long polypeptide chains called the heavy chains
- Two shorter identical chains called the light chains
- The chains are held together by disulphide bridges and there are also disulphide bridges within the polypeptide chains holding them in shape.
75
Specific Immune System: How to antibodies bind to antigens?
- with a protein based 'lock-and-key' mechanism similar to the complementarity between the active site of an enzyme and its substrate.
- the binding site is an area of 110 amino acids on both the heavy and light chains, known as the variable region.
- it is a different shape on each antibody and gives the antibody its specificity
- the rest of the antibody molecule is always the same, so its called the constant region.
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Specific Immune System: What is formed when an antibody binds to an antigen?
antigen-antibody complex
- the hinge region of the antibody provides the molecule with flexibility, allowing it to bind two separate antigens, one at each of its antigen-binding sites.
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Specific Immune System: How do antigens defend the body?
1. antibody of antigen-antibody complex acts as an opsonin so the complex is easily engulfed and digested by phagocytes
2. most pathogens can no longer effectively invade the host cells once they are part of an antigen-antibody complex
3. antibodies act as agglutinins causing pathogens carrying antigen-antibody complexes to clump together. This helps prevent them spreading through the body and makes it easier for phagocytes to engulf a number of pathogens at the same time
4. antibodies can act as anti-toxins, binding to the toxins produced by pathogens and making them harmless
78
Specific Immune System: Lymphocytes and the immune response - What are lymphocytes?
- B lymphocytes mature in the bone marrow
- T lymphocytes mature in the Thymus gland
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Specific Immune System: Lymphocytes and the immune response - What are the 4 main types of T lymphocytes?
1. T helper cells
2. T killer cells
3. T memory cells
4. T regulator cells
80
Specific Immune System: Lymphocytes and the immune response - What are T helper cells?
- Have CD4 receptors on their cell-surface membranes, which bind to the surface antigens on APC'S
- They produce interleukins, which are a type of cytokine
- Interleukins made by the T helper cells stimulate activity of B cells, which increase antibody production, stimulates production of other types of T cells and attracts and stimulates macrophages to ingest pathogens with antigen-antibody complexes.
81
Specific Immune System: Lymphocytes and the immune response - What are T killer cells?
- destroy the pathogen carrying the antigen
- Produce a chemical called perforin, which kills the pathogen by making holes in the cell membrane so its freely permeable
82
Specific Immune System: Lymphocytes and the immune response - What are T memory cells?
- live for a long time and are part of the immunological memory
- if they meet an antigen a second time they divide rapidly to form a huge number of clones of T killer cells that destroy the pathogen
83
Specific Immune System: Lymphocytes and the immune response - What are T regulator cells?
- cells suppress the immune system, acting to control and regulate it
- they stop the immune response once a pathogen has been eliminated, and make sure the body recognises self antigens and doesn't set up an autoimmune response
- interleukins are important in this control
84
Specific Immune System: Lymphocytes and the immune response - What are the 3 main types of B lymphocytes?
1. Plasma cells
2. B effector cells
3. B memory cells
85
Specific Immune System: Lymphocytes and the immune response - What are plasma cells?
- produce antibodies to a particular antigen and release them into the circulation
- an active plasma cell only lives for a few days but produces around 2000 antibodies per second while it is alive and active
86
Specific Immune System: Lymphocytes and the immune response - What are B effector cells?
divide to form the plasma cell clones
87
Specific Immune System: Lymphocytes and the immune response - What are B memory cells?
- live for a very long time and provide the immunological memory
- they are programmed to remember a specific antigen and enable the body to make a very rapid response when a pathogen carrying that antigen is encountered again.
88
Specific Immune System: Cell-mediated Immunity - What is cell-mediated immunity?
- T lymphocytes respond to the cells of an organism that have been changed in some way
89
Specific Immune System: Cell-mediated Immunity - What are the stages of the cell-mediated immunity?
1. In the non-specific defence system, macrophages engulf and digest pathogens in phagocytosis. They process the antigens from the surface of the pathogen to form antigen-presenting cells (APCs)
2. The receptors on some of the T helper cells fit the antigens. These T helper cells become activated and produce interleukins, which stimulate more T cells to divide rapidly by mitosis. They form clones of identical activated T helper cells that all carry the right antigen to bind to a particular pathogen
3. The clonded T cells may:
- develop into T memory cells, which give a rapid response if this pathogen invades the body again
- produce interleukins that stimulate phagocytosis
- produce interleukins that stimulate B cells to divide
- stimulate the development of a clone of T killer cells that are specific for the presented antigen and then destroy infected cells
90
Specific Immune System: Humoral Immunity - What is humoral immunity?
The body responds to antigens found outside the cells.
It produces antibodies that are soluble in the blood and tissue fluid and are not attached to cells.
91
Specific Immune System: Humoral Immunity - Response process?
1. Activated T helper cells bind to the B cell APC. This is **clonal selection** - the point at which the B cell with the correct antibody to overcome a particular antigen is selected for cloning
2. Interleukins produced by the activated T helper cells activate the B cells
3. The activated B cells divides by mitosis to give clones of plasma cells and B memory cells. This is clonal expansion.
4. Cloned plasma cells produce antibodies that fit the antigens on the surface of the pathogen, bind to the antigens and disable them, or act as opsonins or agglutinins. This is the **primary immune response**
5. Some cloned B cells develop into the b memory cells. If the body is infected by the same pathogen again, the B memory cells divide rapidly to form plasma cell clones. These produce the right antibody and wipe out the pathogen very quickly, before it can cause the symptoms of disease. This is the **secondary immune response**
92
Specific Immune System: Autoimmune diseases - what is the autoimmune disease?
When the immune system stops recognising 'self' cells and starts to attack healthy body tissue. Sometimes the immune stream responds abnormally to a mild pathogen or normal body microorganisms and in some cases the T regulator cells don't work effectively
93
Specific Immune System: Autoimmune diseases - How many autoimmune diseases are there and what can they cause?
- Around 8 different autoimmune diseases
- can cause chronic inflammation or complete breakdown and destruction of healthy tissue.
94
Specific Immune System: Autoimmune diseases - What can help treat it?
Immunosuppressant drugs, which prevent the immune system working, may be used as treatments but they deprive the body of its natural defences against communicable diseases.
95
Specific Immune System: Autoimmune diseases - What is Type 1 diabetes, what part of the body does it affect / what's the treatment?
- The insulin-secretiiing cells of the pancreas
- Insulin injections, pancreas transplants, immunosuppressant drugs
96
Specific Immune System: Autoimmune diseases - What is Rheumatoid Arthritis, body part it affects / treatment?
- Joints in wrists, hands, ankles and feet
- No cure, anti-inflammatory drugs, steroids, immunosuppressants, pain relief
97
Specific Immune System: Autoimmune diseases - What is Lupus, body part affected / treatment?
- Often affects skin and joints and causes fatigue / Can attack any organ in the body including kidneys, liver, lungs or brain
- No cure, anti-inflammatory drugs, steroids, immunosuppressants, various drugs
98
Preventing and Treating Disease: Non-communicable diseases - What are non-communicable disease?
Can't be passed from one person to another.
They include heart disease, types of cancer and many diseases of the nervous, endocrine and digestive system
99
Preventing and Treating Disease: Communicable diseases - what are communicable diseases?
Are caused by pathogens and can be passed from person to person.
When you come into contact with a foreign antigen, you need some form of immunity to prevent you getting the disease.
100
