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OCR Biology A Level Module 4 > 4.1.1 Communicable diseases, disease prevention and the immune system > Flashcards

4.1.1 Communicable diseases, disease prevention and the immune system Flashcards

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1
Q

What is keratinisation?

A

keratinocytes at the surface of the skin dry out and the cytoplasm is replaced by keratin

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2
Q

Describe the process of blood clotting

A
  • Collagen exposed = Ca2+ ions and clotting factors are released from platelets which activate an enzyme cascade
  • inactive thrombokinase = active thrombokinase
  • prothrombin = thrombin
  • soluble fibrinogen = fibrin
  • platelets are trapped causing a clot, scab forms seal
  • collagen deposited under and epidermis stem cells differentiate
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3
Q

What is involved in inflammation?

A
  • mast cells detect pathogen -> histamine -> vasodilation and make capillary walls more permeable to WBCs and proteins. Cytokines enhance phagocytosis
  • blood plasma and WBCs enter tissue fluid = OEDEMA
  • excess fluid drained = swelling of lymph nodes bc of lymphocyte production
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4
Q

What is the role of reflexes?

A

air expulsion to remove microorganisms in response to irritation

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5
Q

What is the role of mucous membanes?

A

goblet cells + glands secrete mucus to trap pathogens
stomach acid kills them
gut, ears, nose, airways

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6
Q

Describe the role of neutrophils in phagocytosis

A
  • large numbers, short lived
  • binds to opsonin attached to antigen on pathogen
  • phagosome formed from pseudopodia -> lysosomes fuse to form phagolysosome
  • hydrolytic enzymes released
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7
Q

Describe the role of macrophages in phagocytosis

A
  • monocytes in blood
  • don’t fully digest
  • antigen saved and moved to special protein complex
    becomes ANTIGEN PRESENTING CELL
  • increases chances that antigen will come into contact with lymphocytes
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8
Q

What is clonal selection?

A
  • activation of specific B/T lymphocytes
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9
Q

Describe the mode of action of B lymphocytes ( HUMOURAL)

A
  1. Antigen encountered
  2. Interleukins released from T-cells and macrophages causes clonal expansion
  3. Either differentiated into plasma cells to secrete antibodies (stimulated by monokines from macrophages)
  4. OR differentiated into B memory cells for immunological memory
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10
Q

Describe the mode of action of T lymphocytes ( CELL-MEDIATED)

A
  1. T-helper cells recognise APC or antigen
  2. Interleukins from T-cells and macophages causes clonal expansion
  3. This then causes differentiation into T-helper cells (release cytokines to stimulate T-cells, B-cells and phagocytosis)
  4. OR t-killer cells (interferon stimulates these) to attack cells
  5. OR T memory cells that remain in blood for long time after primary response
  6. OR t-regulator cells which shuts down immune response -> important in autoimmune disease
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11
Q

What is the difference between primary and secondary response?

A

PRIMARY: delay since it takes time to recognise antigens, perform phagocytosis and for the specific response to be generated due to clonal selection time etc

SECONDARY: much faster clonal selection due to the B + T memory cells that remain in the blood after primary response. Antibody production starts sooner and is much more rapid, AND the maximum concentration is higher
They remain in the blood for longer too

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12
Q

What is an autoimmune disease?

A
  • own body cells recognised as antigenic and are attacked by the immune system e.g. arthritis
  • genetic and environmental factors
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13
Q

Describe the general structure of an antibody

A

they are IMMUNOGLOBINS - complex proteins.

2 light chains and 2 heavy chains
variable region which binds to antigen
constant region which stays the same, may have binding site for phagocytosis
hinge region to allow flexibility
disulfide bridges

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14
Q

What is the role of opsonins?

A

bind to antigen and neutralise them, increase phagocytosis

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15
Q

What is the role of agglutinins?

A

cross-link pathogens by binding to 2 antigens, each on same type of pathogen. it is impeded from imovement. increases phagocytosis also

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16
Q

What is the role of anti-toxins?

A

bind to toxins, preventing them from entering cells

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17
Q

Role of cytokines in phagocytosis?

A

attract phagocytes

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18
Q

Outline how synthetic biology can be used in the provision of new medicines

A
  • genetic modification of organisms
  • to produce drug/ proteins/ vaccine
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19
Q

State when each of the 5 things happen:

  1. Antigen presentation
  2. Clonal expansion
  3. Clonal selection
  4. High T-helper cell activity
  5. Highest number of memory cells

A) 1st exposure to antigen
B) just after (rising antibody peak on graph)
C) as peak goes down
D) 2nd exposure to antigen
E) peak drifts off
F) line goes down more

A
  1. A only (only 1st exposure)
  2. B, D (occurs both times)
  3. A (only occurs the 1st response - already have appropriate cells selected for 2nd response)
  4. B, D (particularly helps with clonal expansion)
  5. E (highest possible antibody peak)
20
Q

What is a pathogen?

A

Microorganism that causes disease

21
Q

How do bacteria cause disease? Examples?

A

Damage cells and release toxins

TB, bacterial meningitis, ring rot.

22
Q

How do fungi cause disease? Examples?

A

Hyphae forming a mycelium -> grow under skin and release enzymes and spores = irritation.

Athlete’s foot, black sigatoka, ring worm

23
Q

How do viruses cause disease? Examples?

A

takes over genetic machinery + host cell eventually bursts

HIV/AIDS
influenza
tobacco mosaic

24
Q

How do protoctista cause disease? Examples?

A

Feed on cell contents

Malaria, blight

25
Q

Which factors affect transmission ?

A

Factors:
- hygiene e.g. hand washing, condoms
- treatment of water
-overcrowding
- poor ventilation
- poor health and diet
- homelessness
- living/working with migrants

26
Q

What is indirect transmission? What is an example? How does climate affect it?

A

using a VECTOR = another organism that may be used by pathogen to gain entry to primary host, or an intermediate

e.g. MOSQUITOES (Anopheles) for malaria.

Climate: mosquitoes, fungi, etc can reproduce more rapidly in warmer climates.

27
Q

How are plant pathogens transmitted?

A
  • Soil -> esp if roots are damaged
  • Fungi produce spores = airborne
  • Pathogens in leaves spread when they shed, or in seeds
  • Insect attack, and transfer of bacteria/spores
28
Q

What are some examples of passive plant defences?

A

Lignin -> almost completely indigestible
Stomatal closure
Tylose fills xylem vessels and prevents spread
Cellulose cell wall -> physical barrier
Waxy cuticle
Bark -> variety of chemical defences e.g. tannins
Callose -> prevents spread in sieve tubes/

Also many chemicals with antipathogenic properties present before.

29
Q

What are some examples of active plant defences?

A

Cell walls thickened, callose deposited, oxidative bursts.

Phenols : tannins in bark inhibit insect attack
Alkaloids: N containing compounds - inhibit herbivores
Terpenoids: antibacterial + antifungal properties
Hydrolytic Enzymes
Defensins: cysteine rich proteins with anti-microbial activity.

30
Q

What is a vaccination?

A

Deliberate exposure to antigenic material to stimulate an immune response

31
Q

What forms can a vaccination take?

A
  • Whole live microorganisms,weakened version of a pathogen, dead pathogen, antigens from a pathogen , toxoid
32
Q

What is a herd vaccination?

A
  • around 90% vaccinated. Disease can no longer spread = HERD IMMUNITY
33
Q

What is a ring vaccination?

A

vaccinating all near the new cases, also used to prevent spread of livestock disease

34
Q

Some pathogens can undergo —– -> may not be recognised by ——- cells. E.g. —— ——– may arise. Threats must be monitored so new —– can be identified and —– can be prepared.
To avoid——-, people at risk are immunised.
Worldwide research to determine which strains are likely to spread in a given year -> ——- programmes adapted.

A

mutations
memory
influenza
epidemics
strain
vaccines
pandemics
immunisation

35
Q

What are antibiotics?

A
  • Prevent bacteria/fungi growth
  • Most r derivatives of compound made by STREPTOMYCES bacteria
  • Over-use and misuse enabled resistance e.g. MRSA.
36
Q

What are the types of immunity?

A

Natural active: infection
Artificial active: vaccination
Natural passive: breast milk
Artificial passive: antibody injection

37
Q

Why do we need new drugs?

A
  • new diseases emerge
  • mutations
  • still many with no effective treatments
  • some antibiotics becoming less effective
38
Q

What is an example of accidental discovery?

A
  • Fungus penicillium grew on petri dish and released compounds that killed bacteria
39
Q

How do traditional remedies lead to medicines?

A
  • Plants/extracts now used in modern medicines
  • e.g. morphine from sap from unripe poppy seeds. Opium from poppies = anaesthetic.
  • Willow bark: relieve pain + fever. Active ingredient discovery -> add acetyl group -> reduces stomach bleeding -> led to aspirin and ibuprofen
  • therefore must maintain biodiversity
40
Q

How does wildlife and plant research lead to medicines?

A
  • monkeys, bears rub citrus oils as antiseptics
  • birds line nests with medicinal leaves
  • can get inspiration from this
  • research used to isolate active ingredient so similar molecules can be manufactured
41
Q

Why is research into mechanisms useful?

A
  • many diseases use membrane receptors e.g. HIV
  • if virus is blocked, pathogen cannot gain access
  • receptors are sequenced and modelling can determine shape once amino acid sequence is known
  • can find drug that mimics the receptor and binds to the virus
  • enzyme inhibitors can also be developed
42
Q

What is the use of synthetic biology and personalised medicine?

A

new molecules that mimic natural processes or use of natural molecules to produce new systems
sequence genes of person with a particular condition and develop specific drugs

43
Q

Using examples, explain how both genes and the environment can cause animals to vary in their specific immune responses (6)

A

Genes:
-inherit genes that code for immune cells and antibodies e.g. lymphocytes
- different alleles code for different versions of immune cells/ antibodies
- alleles code for many different variable regions
- MHC alleles
- mutation produces new alleles
- ref to autoimmune diseases such as lupus

Environment
- exposure to diff pathogens determines immune response e.g. measles produce memory cells
- vaccinations produce primary immune responses e.g. HPV by producing memory cells
- environmental influence on allergies
- poor diet can weaken immune system due to lack of vitamins
- epigenetic changes due to stress/chemicals
- autoimmune diseases with an environmental trigger such as AIDS

44
Q

Ash trees are an important part of the British landscape. In 2012, a fungal disease known as ash dieback arrived in UK from mainland Europe. Which of the following could explain how ash dieback could have reached the UK from mainland Europe?
1. Spores carried on wind
2. Young diseases trees imported from Europe and planted in UK
3. Contaminated soil from a previously infected crop

A) 1,2 and 3
B) Only 1 and 2
C) Only 2 and 3
D) Only 1

A

B

45
Q
A

OCR Biology A Level Module 4 (3 decks)

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