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OCR Biology A Level > 4.1 Communicable Disease, Disease Prevention And The Immune System > Flashcards

4.1 Communicable Disease, Disease Prevention And The Immune System Flashcards

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1
Q

Define health

A

The state of mental, physical and social wellbeing, not just the absence of disease

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2
Q

Define disease

A

Departure from health due to malfunction of mind or body that cause physical, mental or social symptoms

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3
Q

Explain what is meant when a disease is described as:
- infectious
- non-communicable
- deficiency
- inherited
- degenerative

A

Infectious: Diseases transmitted by a pathogenic organism
Non-communicable: Diseases not caused by pathogens
Deficiency: Diseases caused by a poor diet
Inherited: Diseases caused by a genetic fault passed from the parents
Degenerative: A gradual decline of bodily functions

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4
Q

What is a parasite?

A

An organism that lives inside or on a host that takes nutrition/energy from the host and often causes harm
- not all cause disease
- parasites gain nutrition/energy, a warm environment + protection from the outside environment

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5
Q

Give key details and examples of bacteria

A
  • prokayrotic
  • rapid asexual reproduction (20mins) by binary fission
  • cause disease by damaging cells or producing toxins
  • can be beneficial, neutral or pathogenic
  • no nucleus + membrane bound organelles
  • tuberculosis (TB), ring rot (potatoes, tomatoes)
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6
Q

Give key details and examples of virus

A
  • invade cells
  • take over genetic material and cell machinery
  • make viral copies of cells
  • host cells bursts and copies released killing cells causing diseases
  • not living
  • cold, flu, HIV/AIDS, TMV, influenza
  • 50x smaller than average bacteria
  • all pathogenic
  • some can attack bacteria
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7
Q

Give key details and examples of fungi

A
  • sends out reproductigve hyphae which produce spores
  • neutral or cause disease
  • affect animals but can cause devistation in plants
  • eukaryotic
  • don’t photosynhesise but digest food using extracellular enzymes
  • digest dead/decaying matter
  • can feed on living plants + animals
  • produce millions of spores that can travel rapidly + widely
  • athletes foot, black sigatoka
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8
Q

Give key details and examples of protoctista

A
  • generally single celled
  • eukaryotes
  • some are parasites
  • can enter cells + feed on contents
  • infect many mammals + birds
  • may need vectors
  • malaria, potato/tomato late blight
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9
Q

How do protoctista + fungi cause disease?

A

Protoctista: Don’t take over genetic material of cell, instead digest contents of cell when reproducing + break open cells

Fungi: Digest living cells + destroy them, also produce toxins

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10
Q

Name the two ways communicable diseases are transmitted

A

Direct + indirect

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11
Q

What is direct transmission and give examples

A

The pathogen is transferred directly from one individual to another
Direct contact: Kissing, exchanging bodily fluids, skin to skin contact, faeces
Innoculation: Animal bites, sharing needles
Ingestion: Contaminated food/drink

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12
Q

What is indirect transmission and give examples

A

The pathogen is transferred indirectly from one individual to another
Formites: Bedding, cosmetics
Droplet infection: Small droplets of saliva/mucus when coughing, sneezing + talking
Vectors: Animals + water transmitting diseases between hosts

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13
Q

How can the probability of transmission of a communicable disease be increased in animalss?

A
  • overcrowded living + working conditions
  • poor nutrition
  • comprimised immune system
  • poor waste disposal creates breeding sites for vectors
  • climate change heating areas, increasing areas vectors can survive
  • socioeconomic factors - lack of trained healthcare workers + insufficent public warnings related to disease
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14
Q

How are communicable plant pathogens transmitted indirectly?

A

Indirectly
Soil contamination: Infected plants leave pathogens inthe soil, infecting the next crop
Vectors: Wind, water, animals, humans carry pathogens between plants

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15
Q

What factors increase the transmission of a communicable diseases in plants?

A
  • planting plant varieties susceptible to disease
  • over-crowding
  • poor mineral nutrition
  • damp, warm conditions, which increases pathogen+vector reproduction
  • climate change heating areas, increasing areas vectors can survive
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16
Q

What physical defences do plants use to defend against pathogens?

A

Passive defense mechanisms: Present all the time. Some are physical, some are chemical which deter the growth of pathogens
Active defense mechanisms: Activated when a pathogen invades e.g. cells stimulating the synthesis of lignin + callose when bacteria + fungi attempt to penetrate cell walls

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17
Q

List examples of physical plant barriers to pathogens

A
  • tree bark
  • waxy cuticle over leaf epidermis
  • cellulose cell wall
  • stomata that close to stop pathogens entering
  • casparian strip in endodermis of the root
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18
Q

List examples of chemical plant barriers to pathogens

A

Plants produce chemicals that repel the vector or kill the pathogen. Used by humans to control insects, fungi + bacteria
- insect repellents: citronella from lemon grass
- insecticides: caffeine is toxic to insects + fungi
- antibacterial compounds: defensins (plant proteins that disrupt fungal/ bacterial cell membranes)
- antifungal compounds: chitinases (enzymes that hydrolyse chitin in fungal cell walls)
- anti-oomycetes: glucanases enzymes that break down polymers found in cell walls of oomycetes
- general toxins: chemicals that can be broken down to form cyanide, toxic to most living organis,s

19
Q

Give examples of other mechanisms in plant’s chemical defence

A

Secret compounds to support growth of microorganisms that compete with pathogens
Leaves secrete nutrients that support a community of microorganisms such as yeasts that are harmless to plant but complete successfuly with any pathogens
Sticky resins in bark that prevent the spread of pathogens

20
Q

How does cell signalling work in plants when a pathogen is present?

A
  1. Receptors respond to molecules from pathogen made when plant is attacked e.g. products made from cellulases produced when bacteria/fungus are digesting a pathway into cells binds to receptors onm cell surface
  2. Stimulates the release of signalling molecules
  3. Signalling molecules switch on genes in nucles
  4. Triggering cellular reponses: Defensive molecules directly attack pathogen, defensive chemicals alarm other cells, callose + lignin made
21
Q

Give an example of a defensive molecules that directly attack the pathogen and how it works

A

Procution of phytoalexins which:
- disrupt the cell surface membrane of bacteria
- stimulate secretion of chitinaes that break down fungi cell walls
- disrupt pathogen metabolism
- delay pathogen reproduction

22
Q

Give an example of defensive chemicals that alarm other cells of pathogens prescence

A

Salicyclic acid travels through plants to activate defense mechanisms in uninfected areas (sysem aquired resistance)
Ethylene is another signalling molecule that is secreted when plants are under attack, which vapourises to stimulate other leaves of the same plant and other plants in the immediate surroundings

23
Q

What is callose and how does it help plants fight pathogens?

A

Polysacchatride containing B-1,3 + B-1,6 glycosidic bonds released in large amounts when a plant is infected by a pathogen
1. Deposited between cell walls + cell surface membranes of cells next to infected cells to act as a barrier to prevent pathogens entering surroudning cells
2. Deposited in cell walls along with lignin to make barrier even thicker
3. Blocks sieve plates in phloem to seal of infected part preventing spread
4. Deposited in plasmodesmata to prevent spread between cells
5. Once deposited, it acts as a matrid where antimictobial compunds can be put

24
Q

Give key aspects of non-specific defenses

A
  • present from birth
  • don’t distinguish between different pathogens
  • give same responses each time a pathogen enters the body
  • act very quickly
  • not always highly effective
25
Q

Give examples of primary non-specific responses in the human body

A

Respiratory tract: Goblet cellls make mucus to trap pathogens + ciliated epithelium cells waft mucus
Eyes & ears: Ears contain lysozyme enzymes and antibodies which kill pathogens + ear wax traps pathogens
Skin: Keratinocytes (skin cells) are a physical barrier to microorganisms + sweat & sebum have an antibacterial effect
Genitals: Washing by urine + mucus + acidity

26
Q

Give key aspects of the skin as a non-specific defense

A
  • physical barrier covering the body which prevents pathogen entry
  • covered with ‘healthy’ microorganisms that outcompete pathogens for space on body surface
  • skin produces sebum (oily substance which prevents pathogen growth)
27
Q

Give key aspects of the mucous membrane as a non-specific defense

A
  • body tracts (airways of gas exchange system) lined with mucous membranes
  • goblet cells of these membranes secret sticky mucus
  • mucus traps microorganisms + contains lysozymes which destroy bacteria + fungal cell walls
  • mucus contains phagocytes which remove remaining pathogens
  • ciliated epithelial cells waft mucus out of the airway
28
Q

What are expulsive reflexes?

A

Coughs + sneezes that eject pathogen-laden mucus from the gas exchange system
Vomiting + diarrhoea expel contents of the gut + infective agents

29
Q

How are cuts in skin dealt with?

A
  • important to seal the wound so no pathoens enter
  • platelets come into contact with collagen in skin + adhere to it while secreting substances producing the coagulation cascade
  • cascade of events results in formation of fibrin which forms a network of rapped platelets forming a clot
  • clot dries out to form a tough scab preventing pathogen entry
  • epidermal cells below the scab grow, sealing the wound permanently, while blood vessels re-grow
  • collagen fibres deposited to give new tissue strength
  • once the new epidermis reaches normal thickness, the scab sloughs off - scab is healed
30
Q

Give key aspects of inflammation

A
  • localised response to pathogen, damage or irritant
  • characterised by pain, heat, redness + tissue swelling
  • involves mast cells becoming activated in damaged tissue
  • once activated mast cells release histamines + cytokines
  • examples of cell signalling using chemical mediators (histamines)
31
Q

Explain the process of cell signalling in inflammatory reponse

A
  • skin is damaged/presence of pathogen, so mast cells bind to pathogen/allergen
  • mast cells release histamine in local areas, not just in blood (not hormone but chemical mediator)
  • histamines bind to localised cells receptors and triggers
  • increased blood flow to area + makes capillaries more permeable to phagocytes
32
Q

How do phagocytes move in capillaries?

A
  • can alter shape + flexible
  • nucleus is narrow and lobed
  • capillary walls are more leaky
  • can fit through the gaps in capillary endothelium
33
Q

Break down secondary defenses inside the body

A

Non Specific
- phagocytosis

Specific
- cellular reponses (T- lymphocytes)
- humoral reponses (B- lymphocytes)

34
Q

Give key aspects of the two types of phagocyte

A

Both part of non-specific defences that have no antigen specific receptors - can digest a wide range of different pathogens

Neutrophils
- released when infected from bone marrow
- multi-lobed nucelus
- 70% of WBCs

Macrophages
- made in bone marrow but travel to lymph nodes
- more rounded nucelus
- 4% of WBCs
- important in non specific defense + specific immune system

35
Q

Explain key aspects of macrophage and monocytes and how you can tell the difference between them and a lymphocyte?

A

A monocyte can differentiate into a macrophage. Monocytes circulate in the blood and leaves to remain as a long-lived macrophage in tissues such as the lungs
- lymphocytes are smaller
- lymphocytes nucleus takes a bigger proportion of the cell

36
Q

Explain the steps of phagocyte action

A
  1. Phagocyte receptors (non-specific) bind to antigen on pathogen or to antibody constant region
  2. Pathogen identified by antigens (non-self)
  3. Pathogen englufed via phagocytosis
  4. Phagosome formed
  5. Lysosome fuses with phagosome to form phagolysosome
  6. Digestive enzymes (lysins) release onto pathogen
  7. Pathogen hydrolysed into amino acids + glucose
  8. Useful materials absorbed into cytoplasm
  9. Unwanted matyerials removed by exocytosis
37
Q

What extra step do macrophages do after phagocytosis?

A

Present antigens to other white blood cells involved in specific immune response (Antigen presenting cells)
Take longer for macrophages to engluf bacterium as the process is more complex

38
Q

What are cytokines and opsonins?

A

Cytokines: Cell signalling molecules that attract phagocytes to the site of infection
Opsonins: Chemicals that bind to pathogens and tag them, so they are more easily recognisable to phagocytes, which have receptors on their cell surface to bind to common opsonins (Antibodies are opsonins)

39
Q

What is a self antigen, a non-self antigen and antibody?

A

Non-self antigen: Protein/glycoprotein on surface of a pathogen that causes immune response (antibody production)
Self antigen: Protein/glycoprotein on cell surface membrane of body cell that allows immune system recognises the cell as self
Antibody: Y-shaped glycoprotein produced by B-lymphocytes. Specific antibodies bind to specific antigens on surface of other cells due to presence of variable region

40
Q

List key aspects of antibody structure

A
  • y-shaped glycoproteins (4 polypepties, 2 light/2 heavy) held together by disulphide bonds
  • constant region (same for all antibodies) allows for recogniton and binding to phagocytes
  • variable region allows for binding to specific antigen. Different on different antibodies + different primary structure. Allow for specific binding of antibodies to different antigens
  • variable region complementary to one antigen shape type
  • two variable regions allow for binding of multiple same antigens at the same time
  • hinge region allows flexibility of antiboy, as distance between binding sites vary. For agglutination
41
Q

List the regions of the antibody

A
  • variable region
  • cosntant region
  • two variable regions
  • hinge region
42
Q

What is neutralisation and agglutination?

A

Neutralisation - antibodies cover the pathogen binding site preventing pathogen binding to host cell + entering
Agglutination - large antibody binds many pathogens together so the group is too large to enter the host cell

43
Q

List other ways antibodies work

A
  • when an antibody-antigen complex is formed, it is made more easily englufed + digested by phagocytes (acts as an opsonin)
  • antibodies bind to toxins made by pathogens, rendering them harmless (anti-toxins)
  • antibodies act as lysins + destroy the pathogen
  • antibodies activate the complement cascade (complement proteins in blood interact with bacterial cell surface membrane to form holes in it)

OCR Biology A Level (20 decks)

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