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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

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
What if the same antigen is encountered again?
- 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
Compare humoral-mediated immunity and cell-mediated immunity
**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
Compare secondary and primary response
**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
When might a secondary response take place?
- contact with pathogen for 2nd time - contact with pathogen for 1st time but after relevant vaccination
27
What is active and passive immunity?
Active: Form own antibodies + memory cells from exposure Passive: Get antibodies from mother via milk/placenta or injected with antibodies
28
What is natural and artificial immunity?
Natural: Exposure to pathogens through infection Artificial: Immune system stimulated by safe form of antigen
29
Explain differences between active and passive immunity
**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
Define vaccination
Deliberate exposure to harmless antigenic material which activates an immune response to allow production of antibodies + memory cells
31
What is herd immunity?
When a population has a high % vaccinated so disease can no longer spread - vaccinations in school
32
What is the difference between a pandemic and epidemic?
Pandemic: Disease spreads rapidly across multiple countries Epidemic: Disease spreads rapidly at a local or national level
33
Why are some diseases difficult to eradicate
- difficult to diagnose - not enough of pop vaccinated - boosters needed - migrants can carry diseases - can mutate frequently - antivax/concerns about side effects
34
What is an autoimmune disease?
- 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
What groups are considered more vulnerable and are given vacinations more regularly?
- elderly - children - pregnant women - compromised immune system - chronic diseases - health workers
35
What can cause auto-immune diseases?
- genetics - immune system responds to pathogen/microorganism abnormally - T regulator cells not working properly
35
Why are new medicines needed?
- new diseases emerge - some diseases still have no effective treatment - resistance to antibiotics - mutation/evolution of microorganism
36
Where are medicines sourced?
- plants + microorganisms - animals - extreme environments
37
Why may it be difficult to discover new drugs in the future?
- decrease in biodiversity due to habitat destruction - deforestation, pollution, fishing, industrialisation
38
What modern methods are scientists using to make drugs?
- 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
Give key aspects of pharmocogenetics
- 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
How do antibiotics work?
- disrupt cell wall - disrupt membranes - inhibit protein synthesis - inhibit DNA/RNA processes - disrupt metabolism
41
What are multodiscs and why are they used by hospitals?
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
How does antibiotic resistance occur?
- mutation for resistance occurs in bacteria - these bacteria survive and reproduce ( antibiotic = selection pressure) - allele passed to offspring - happens over many generations
43
Why is antibiotic resistance occurring in society?
- 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 (26 decks)

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