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OCR Biology A Level > 4.1 Communicable Disease, Disease Prevention And The Immune System Part 2 > Flashcards

4.1 Communicable Disease, Disease Prevention And The Immune System Part 2 Flashcards

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1
Q

Define immune response

A

Specific response to an antigen which involves lymphocytes and antibody production

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2
Q

Give examples of non-specific immune response

A
  • macrophages engulf + digest pathogens in lymph node + present antigens
  • neutrophils engulf + digest pathogens in blood + around the body
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3
Q

Explain how macrophages are involvded in cell mediated response

A

Present antigens on their surface to activate T helper cell to start cell mediated immunity

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4
Q

Give key aspects of T helper cells and how they are involved in cell mediated immunity

A
  • made in bone marrow, mature in thymus gkand
  • specic receprots that bind to antigens on APCs
  • one activated release interlukins, stimulating T cells to divide by mitosis (develop into T-killer or T memory)
  • interlukins cause B-lymphocytes to divide by mitosis + stimulate process of phagocytosis
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5
Q

Give key aspects of T memory cells and how they are involved in cell mediated immunity

A
  • live for a long time
  • part of immunological memory
  • developed from cloned T cells
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5
Q

Give key aspects of B lymphocytes in humoral response

A
  • activated by T helper cells
  • divides by mitosis to form cloned B cells
  • makes lots of B memory cells (provide immunological memory)
  • makes plasma cells (which make antibodies)
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6
Q

Give key aspects of T killer cells and how they are involved in cell mediated immunity

A
  • specific receptors for antigens
  • release toxins (hydrogen peroxide) to kill infected cells + perforin to make holes in cell surface membranes
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7
Q

Give key aspects of T regulator cells

A
  • controls + regulates the immune system
  • stops immune system once pathogen is eliminated
  • prevents autoimmune disease
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7
Q

Give key aspects of T helper cells in humoral response

A
  • activates B lymphocytes at stat of humoral response
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8
Q

What is identification?

A

An antigen acts as an ID to tell your cells a pathogen if foreign

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9
Q

What is presentation?

A

Antigens presented on membranes by macrophages

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10
Q

What are distress signals?

A

Cells damaged by pathogens, so part of the pathogen is placed on the membrane to tell T lymphocyte to destroy it

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11
Q

What are cytokines?

A

Chemical messengers released by cells - cell signalling

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12
Q

What are interleukins?

A

Stimulate other T cells + B lymphocytes to divide rapidly by mitosis + stimulate phagocytosis

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13
Q

What is interferon

A

Stimulates T killer cells + inhibits virus replication

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14
Q

How does the interleukin cytokine work?

A

Has a specific shape which binds to complementary shaped receptors on B lymphocyte, which then activates mitosis of B lymphocyte

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15
Q

How do monokines work?

A

Macrophages release specific shaped monokines, which bind to other complementary receptors on B lymphocytes, activating cell activity (production of antibodies)

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16
Q

Give key aspects of T-lymphocytes

A
  • processed in the thymus
  • have receptors on their cell surface membrane
  • millions of different shapes with different shaped receptors for binding to different antigens
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17
Q

Explain the process of T-lymphocytes in cell mediated immunity

A
  1. Surface of T-helper cell with specific receptors bind to antigens on APC - clonal selection
  2. T helper cell divides by mitosis - clonal expansion
  3. Formed clones of activated T helper cells
18
Q

What do the clones of activated T helper cells do?

A

Release interleukins that:
- stimulate B cells to divide by mitosis
- stimulate phagocytosis
- stimulate the development of T killer cells

  • may develop into T killer cells
  • T killer cells release toxins that kill infected cells + release perforin
19
Q

What is the difference between clonal selection and clonal expansion?

A

Clonal selection: When receptors of a T or B lymphocyte bind to a specific antigen, selectively stimulating the proliferation of the cell by clonal expansion

Clonal expansion: When selected T or B lymphocytes divide by mitosis to make clones - mass proliferation of T/B lymphocytes

20
Q

Give key aspects of humoral immunity

A
  • involves B-lymphocytes (processed in bone marrow)
  • respond to antigens found outside cells (extracellular pathogens)
  • deals with antigens found in humors/body fluids
  • produces antibodies
  • relies on activated T helper cells made in cell-mediated immunity
21
Q

Give key aspects of B-lymphocytes

A
  • have antibodies on their cell-surface membrane
  • millions of different types of B-lymphocytes - each has a different antibody which binds to a different antigen
  • when an antigen on a pathogen enters the body, a B-lymphocyte with a complementary antibody will bind to engulf it
  • it then processes the antigen and presents it (has become an APC)
22
Q

Explain the process of humoral immunity

A
  1. T helper lymphocyte becomes activated by APC
  2. B-lymphocyte presents antigens from pathogens on its surface - forming a B cell APC
  3. Activated T-helper lymphocyte binds to antigens presented on B-cell APC (clonal selection)
  4. Interleukins produfced by activated T helper cells to activate B cells
  5. Activated B lymphocyte divides by mitosis to form a clone of B cells (Clonal expansion)
  6. Clone differentiates into plasma cells + B memory cells
  7. Plasma cells produce specific antibodies for specific antigens
  8. Memory B cells provide immunological memory
23
Q

What if the same antigen is encountered again?

A
  • the memory B cells will recognise the antigen on the pathogen with their antibody receptor
  • the memory cells divide rapidly making clones, which differentiate to form plasma cells - which make antibodies
  • memory b cells remain in the body for a long time - however eventually reduce - need for booster vaccines
  • secondary immune response
24
Q

Compare humoral-mediated immunity and cell-mediated immunity

A

Humoral
- antibody mediated
- B lymphocytes
- mode of action: antibody circulating in serum
- primary defense against extracellular pathogens

Cell-mediated
- cell mediated
- t lymphocytes
- mode of action: direct cell to cell contact or secreted soluble products
- primary defense against intracellular bacterua

25
Q

Compare secondary and primary response

A

Primary
- response takes longer
- smaller antibody conc in blood
- because of clonal selection + expansion

Secondary
- response is quicker
- larger antibody conc in blood
- due to immunological memory provided by memory cells

26
Q

When might a secondary response take place?

A
  • contact with pathogen for 2nd time
  • contact with pathogen for 1st time but after relevant vaccination
27
Q

What is active and passive immunity?

A

Active: Form own antibodies + memory cells from exposure
Passive: Get antibodies from mother via milk/placenta or injected with antibodies

28
Q

What is natural and artificial immunity?

A

Natural: Exposure to pathogens through infection
Artificial: Immune system stimulated by safe form of antigen

29
Q

Explain differences between active and passive immunity

A

Active
- exposed to antigen
- takes time to work
- long term protection
- memory cells made

Passive
- no contact with antigen
- immediate
- short term protection
- no memory cells

30
Q

Define vaccination

A

Deliberate exposure to harmless antigenic material which activates an immune response to allow production of antibodies + memory cells

31
Q

What is herd immunity?

A

When a population has a high % vaccinated so disease can no longer spread - vaccinations in school

32
Q

What is the difference between a pandemic and epidemic?

A

Pandemic: Disease spreads rapidly across multiple countries
Epidemic: Disease spreads rapidly at a local or national level

33
Q

Why are some diseases difficult to eradicate

A
  • difficult to diagnose
  • not enough of pop vaccinated
  • boosters needed
  • migrants can carry diseases
  • can mutate frequently
  • antivax/concerns about side effects
34
Q

What is an autoimmune disease?

A
  • immune system fails to recognise antigens as self
  • incorreclty identifies as non-self so antibodies made against cells
  • phagocytes/T killer cells attack + break down cells
34
Q

What groups are considered more vulnerable and are given vacinations more regularly?

A
  • elderly
  • children
  • pregnant women
  • compromised immune system
  • chronic diseases
  • health workers
35
Q

What can cause auto-immune diseases?

A
  • genetics
  • immune system responds to pathogen/microorganism abnormally
  • T regulator cells not working properly
35
Q

Why are new medicines needed?

A
  • new diseases emerge
  • some diseases still have no effective treatment
  • resistance to antibiotics
  • mutation/evolution of microorganism
36
Q

Where are medicines sourced?

A
  • plants + microorganisms
  • animals
  • extreme environments
37
Q

Why may it be difficult to discover new drugs in the future?

A
  • decrease in biodiversity due to habitat destruction
  • deforestation, pollution, fishing, industrialisation
38
Q

What modern methods are scientists using to make drugs?

A
  • computer programmes
  • design 3d models of molecules in bodies + antigens of pathogens
  • allowing models of potential drug molecules to be built to target particular area of a molecule
39
Q

Give key aspects of pharmocogenetics

A
  • combining knowledge of drug action with personal genetic material
  • doctors look at genome of patients + pathogen to increase chance of treatment working
  • personalised medicine
40
Q

How do antibiotics work?

A
  • disrupt cell wall
  • disrupt membranes
  • inhibit protein synthesis
  • inhibit DNA/RNA processes
  • disrupt metabolism
41
Q

What are multodiscs and why are they used by hospitals?

A

Discs which contain multiple antibiotics to test their effectiveness
- cheap
- quick to carry out tests
- compare antibiotics under same conditions
- allows early treatment of patient - don’t give patient antibiotic that doesn’t work
- prevent antibiotic resistance occuring

42
Q

How does antibiotic resistance occur?

A
  • mutation for resistance occurs in bacteria
  • these bacteria survive and reproduce ( antibiotic = selection pressure)
  • allele passed to offspring
  • happens over many generations
43
Q

Why is antibiotic resistance occurring in society?

A
  • widespread antibiotic use in the past (over prescribing, use of agriculture, used for viral infections)
  • people not finishing full course
  • natural selection - selection pressure of antibiotic
  • plasmids containing the antibiotic resistance genes shared by bacteria

OCR Biology A Level (20 decks)

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