Disease Flashcards

(57 cards)

1
Q

Virus

A

-Not alive.
-Cannot reproduce outside of cell.
-Capsid with protein sites to attach to host cells.
-Eg tobacco mosaic virus, HIV.

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2
Q

Fungi

A

-Eukaryotic.
-Chitin cell wall.
-Can be single or multicellular.
-Hyphae release digestive enzymes to surrounding tissue, causing decay.
-Eg black sigatoka, ring worm.

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3
Q

Bacteria

A

-Prokaryotic.
-Can reproduce rapidly.
-Peptidoglycan cell wall.
-Release toxic waste products or toxins.
-Divide by binary fission.
-Eg Ring rot, tuberculosis

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4
Q

Protists

A

-Eukaryotic.
-Singular or multicellular.
-Eg tomato blight, malaria (plasmodium).

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5
Q

Direct transmission

A

-Where a pathogen is passed from one organism to another without any stages.

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6
Q

Direct contact

A

-Skin to skin contact.
-Touching contaminated surfaces.
-Inoculation, where the skin is broken and microorganisms enter directly.

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7
Q

Transmission by spores

A

-Direct.
-Resistant stage of the pathogen that can be carried in the air or on surfaces in the soil.

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8
Q

Ingestion

A

-Where infected food or drink is consumed.

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9
Q

Indirect transmission

A

-When a pathogen is passed through an intermediate stage.

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10
Q

Fomites

A

-Inanimate objects with pathogens on.

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11
Q

Droplet infection

A

-Direct.
-Transfer of pathogens through sneezing or coughing.

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12
Q

Vectors

A

-Move to transfer pathogens to other places.
-Eg mosquitoes, wind, water

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13
Q

Factors increasing rate of transmission

A

-Overcrowding.
-Poor nutrition.
-Compromised immune system.
-Poor waste disposal and sanitation.
-Warm, damp conditions (more pathogens in warmer climates).
-Poor, crowded infrastructure.
-Increased rainfall or wind speed which can act as a vector.

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14
Q

Bodily barriers to stop infection

A

-Skin.
-Blood clotting.
-Mucous from goblet cells in epithelial layer traps pathogens.
-Coughs and sneezes expel pathogens.
-Inflammation increases blood flow by making capillaries more permeable, allowing more phagocytes onto tissues.
-Saliva contains lysosomes to destroy pathogens.
-Ear wax traps pathogens
-Stomach acid denatures enzymes in pathogens.
-Fever raises the body temperature, making enzymes in pathogens less effective.

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15
Q

Neutrophil

A

-Most common phagocyte.
-Multi lobed nucleus.
-Manufactured in the bone marrow, travel in blood and into tissue fluid.
-Large number of lysosomes to engulf and digest pathogens during phagocytosis.
-Short-lived.

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16
Q

Macrophage

A

-Largest phagocyte.
-Large nucleus.
-Manufactured in bone marrow, travel in blood as monocytes.
-Common in lymph nodes where they mature into macrophages.
-Engulfs but does not fully digest pathogens, antigen is moved to protein complex on the surface of the cell.
-Becomes an antigen presenting cell, allowing other cells of the immune system to recognise the antigen.

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17
Q

Antigen presentation

A

-Antigen of pathogen presented on macrophage (APC) and comes into contact with T and B lymphocytes that can complete the full immune response.
-APCs increase chance of contact between antigen and lymphocyte.

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18
Q

Clonal selection.

A

-Part of specific immune response.
-Receptors on T and B-Lymphocytes bind to antigen of antigen-presenting-cell and are activated.
-Leads to the production of antibodies and memory cells.
-This is stimulated and coordinated by a number of hormone-like-chemicals called cytokines.

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19
Q

T-Killer cells

A

-Formed from division of T-cells formed in clonal selection.
-Destroy complimentary pathogens by using perforins to punch holes in their membranes.

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20
Q

T-memory cells

A

-Formed from division of T-cells formed in clonal selection.
-Provides an immunological memory of specific pathogen.
-Can divide rapidly into many t-killer cells upon encountering the antigen a second time.

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21
Q

T-regulator cells

A

-Formed from division of T-cells formed in clonal selection.
-Suppress the immune system after the pathogen is destroyed.
-Prevent autoimmune response from T-killer cells.

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22
Q

T-helper cells

A

-Formed from division of T-cells formed in clonal selection.
-Release cytokines to stimulate B cells to develop, and stimulate phagocytosis.

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23
Q

B-memory cells

A

-Formed from division of B-cells in clonal expansion.
-Provide an immunological memory.
-Divide into many plasma cells upon second contact.

24
Q

Plasma cells

A

-Formed from division of B-lymphocytes.
-Circulate in blood.
-Divide to produce thousands of antibodies per second.
-Only live for a few days.
-Also known as B-effector cells.

25
Antibody structure
-Smaller variable region that is complementary to one specific antigen. -Larger constant region that allows phagocytes to recognise and bind to the antibody. -A smaller light chain and longer heavy chain, bonded within and between with disulphide bonds. -A hinge region that provides flexibility, allowing two variable regions to bind to more than one antigen.
26
Agglutination
-Due to their two binding sites, antibodies cause pathogens to stick together by attaching one site to two separate pathogens. When many antibodies do this they clump pathogens together. -Makes it easier for phagocytes to engulf pathogens. -Pathogens can also be physically impeded from carrying out some functions, such as entering cells.
27
Antitoxins
-Antibodies bind to molecules released by pathogenic cells. -Render toxic molecules harmless.
28
Neutralisation
-Antibodies bind to antigens used by pathogens for a specific purpose (eg attachment). This neutralises the antigen. -These are also opsonins.
29
Opsonisation
-Antibodies bind to the antigen of a pathogen and act as binding sites for phagocytic cells.
30
Natural immunity
-Gained by having the disease or other natural means.
31
Artificial immunity
-Gained by man made means such as vaccination.
32
Passive immunity
-Provided without an immune response (eg injection of antibodies, or those provided to babies via placenta or breast milk).
33
Active immunity
-Provided with an immune response.
34
Vaccination
-Either: -An injection of dead (typhoid) or inactive (measles) pathogens. -Or an injection of antigens from a pathogen (eg Hepatitis B). -Or toxoid, a harmless version of a toxin (eg tetatnus). -Exposes the body to antigenic material. Results in the production of B and T memory cells that prevent secondary infection.
35
Herd Immunity
-When a large number of people are vaccinated, meaning the pathogen is less likely to spread to unvaccinated people. -To immunise smallpox, 80-85% of the population were vaccinated.
36
Ring vaccination
-Where populations in the area surrounding an outbreak are vaccinated to contain the spread of disease.
37
Autoimmune disease
-Where the body fails to recognise a tissue or organ as self, and attacks itself. -Eg lupus, arthritis, type 1 diabetes. -Antibodies attack our own antigens. -Most have no cure, only immunosuppressant treatments.
38
Ways medicines are discovered
-Naturally occurring medicines in organisms such as fungus (penicillin), poppy seeds (morphine) or willow trees (aspirin). -Synthetised medicines from genetically modified organisms (usually bacteria) that reproduce to create more medicines. -Pharmacogenetics, in which an individuals genetics are used to determine the most effective drugs, and potentially in future manufacture personalised ones. -Research into disease causing mechanisms, such as binding sites on pathogens, and production of drugs that prevent binding to host cells.
39
Physical plant defences
-Thick cellulose cell wall. -Lignin thickening of cell walls. -Waxy cuticle prevents water with pathogens from collecting on the surface. -Guard cells which prevent pathogens entering via stomata. -These are known as passive plant defences as they are present before infection.
40
Chemical defences of plants
-Terpenoids have antibacterial and antifungal properties. -Alkaloids are bitter compounds that prevent damage to the plant from herbivores. -Phenols and tannins deactivate digestive enzymes in insects (also antibiotic and antifungal). -Defensins inhibit action of ion transport channels in plasma membrane of the pathogen. -Hydrolytic enzymes degrade bacterial cell walls. -Chitinase breaks down fungal cell walls.
41
Active plant defences.
-These are defences that occur after a pathogen is detected. -These include callose (phloem) and tylose (xylem) which are polysaccharides that are deposited into the vascular bundle to prevent flow across the plant. -Cell walls are thickened with additional cellulose. -Necrosis is deliberate cell death activated by injured cells to limit the pathogen's access to water and nutrients. Can create a canker in woody tissue, causing death of cambium tissue in the bark.
42
Cell-Mediated Response
-Response to cells infected by a pathogen, mainly viruses. -Macrophages engulf and digest pathogens, become APCs. -Followed by clonal selection and expansion of T-lymphocytes.
43
Clonal expansion
-Activated B or T cells divide via mitosis.
44
Monokines
-Released by macrophages, -Cause B cells to differentiate and release antibodies.
45
Interleukins
-Released by T helper cells and macrophages. -Cause B and T cell differentiation.
46
Humoral Immunity
-Response to pathogens in the blood stream, mostly bacteria and fungi. -Antibodies produced that are soluble in the blood, tissue fluid and lymph. -Bind to complementary antigens on pathogen's membrane.
47
Process of Humoral Immunity
-Macrophage engulfs pathogen outside of cell, becomes APC. -Bind to T-helper cell, releases cytokines that stimulate clonal expansion of B-cells. -Plasma cells produce large numbers of antibodies.
48
Process of blood clotting
-Damage to the skin can open the body to infection and lead to blood loss. -Blood clotting involves calcium ions and clotting factors (released from platelets and activated in an enzyme cascade). -Clot dries and forms a scab, which shrinks and draws the sides of a cut together. -Fibrous collagen in deposited under the scab. -Stem cells in the epidermis divide to form new cells which migrate to the edges of the cut and differentiate to form new skin. -New blood vessels grow, and the new tissues contract to draw the edges of a cut together.
49
Skin as a primary defence
-Acts as a physical barrier. -Outer layer (epidermis) consists of cells including keratinocytes. -These are produced at the base of the epidermis and migrate out to the surface of the skin. -These dry out and their cytoplasm is replaced by keratin (keratinisation). -When the cells reach the surface they are no longer alive. This layer of dead cells acts as a barrier to pathogens.
50
Inflammation
-Presence of microorganisms in the tissue is detected by mast cells. -These release a cell signalling substance called histamine. -This causes vasodilation and make the capillary walls more permeable to WBCs, which leave the blood and enter the tissue fluid. -Blood plasma also leaves, leading to an increased production of tissue fluid, which causes swelling (oedema). -Extra tissue fluid drains into lymphatic system, and pathogens come into contact with lymphocytes.
51
Antigens
-Chemical markers on cells' (outer) membranes. -Proteins or glycoproteins intrinsic to plasma membrane. -Allow body to recognise as self.
52
Opsonins
-Protein molecules that attach to antigens on the surface of a pathogen. -Non-specific, can attach to a wide variety of pathogenic cells. -Enhance the ability of phagocytic cells to bind and engulf the pathogen.
53
Cell signalling using cytokines
-Co-ordination of immune response requires communication between variants of T and B cells. -Uses cytokines (range of signalling chemicals complementary to surface receptors of target cells). -Macrophages release monokines to attract neutrophils (known as chemotaxis) or stimulate B cells to differentiate and release antibodies. -T cells and macrophages release interleukins which stimulate the clonal expansion and differentiation of B and T cells. -Many cells release interferon, which inhibits virus replication and stimulates T killer cells.
54
Antibodies
-Molecules that stimulate an immune response. -Bind to foreign antigens (usually proteins or glycoproteins in plasma membrane) that they are specific to. -Immunoglobins, complex proteins produced by plasma cells. -Different antibodies manufactured for every detected antigen.
55
Primary immune response
-Antibodies produced by immune system after infecting agent is first detected. -Takes a few days before number of antibodies rises to an effective level. -After pathogen is dealt with, number of antibodies drops significantly.
56
Secondary immune response
-Upon second infection by the same pathogen. -B and T memory cells circulating in the blood, recognise specific antigens, allowing a faster response. -Quick enough to prevent any symptoms being expressed, concentration rises much higher.
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Epidemic
-Mutation of a pathogen leads to memory cells losing effectiveness. This leads to an increase in transmission and cases. -In extreme events, particularly when pathogens mutate multiple times, an epidemic begins. -Examples include flu (1918), Hong Kong flu (1968) and swine flu (2009). -On a worldwide scale, this becomes a pandemic.