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Biomedicine II CNM (2024) > 15. Immune System > Flashcards

15. Immune System Flashcards

1
Q

What are the 3 lines of defence in the body?

A

First line of defense = physical barrier created by skin and mucous membrane.

Second line of defense = non-specific immune responses such as some immune cells, proteins, fever and inflammation.

Third line of defense = specific / adaptive immune response

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2
Q

Describe the key differences between the ‘innate immunity’ and the ‘specific / adaptive immunity’.

A

Innate immunity refers to a natural non-specific immune response that targets anything deemed as foreign.

Specific immunity is targeted again specific pathogens.

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3
Q

What are pathogens and how might they enter the body?

A

An infectious agent that can cause disease in a host.

Entering through:
- a break in the skin
- respiratory system
- digestive system
- reproductive systems
- eyes

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4
Q

What is an antigen and what are the 2 types?

A

A substance that can be recognised by leukocytes.

  1. Foreign antigen (eg microbes, food, drugs)
  2. Self-antigen (present on cell membrane of own cells as an identity card)
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5
Q

What are antibodies?

A

Proteins that are produced in response too and that combine with these specific antigens.

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6
Q

List the 4 ways in which skin provides defense against pathogens.

A

1- Physical barrier with layers of tightly-packed epithelial cells.
2- Epidermis consists of dead cells that shed removing microbes.
3- Sweat removes microbes and contains IgA
4- Sebum contains fatty acids inhibiting microbe growth

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7
Q

List 5 ways in which mucous membranes provide defense against pathogens.

A

1- Saliva, tears and mucus secretion wash away microbes & contain anti-microbial substances
2- Mucus traps microbes & foreign particles
3- Cilia propel foreign substances back up and out
4- Tears & saliva contain IgA & lysozyme to break
5- Hairs filter air in the nose
6- Acidity of vagina, urinary tract, and stomach make it inhabitable.
7- Excretion of urine & faeces expel microbes
8. Vomiting and diarrhoea are rapid forms of expulsion

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8
Q

Explain how the micro ciliary escalator contributes to immune defence.

A

Mucus traps microbes and foreign particles.
Cilia propel the foreign substance towards the pharynx where they can be swallowed.

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9
Q

Describe how the Microflora contribute to immune defence

A

Microflora out compete pathogens for attachment sites on the epithelial cell surfaces and for essential nutrients.

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10
Q

Describe how the Gastric acid contribute to immune defence

A

The acidity destroys bacteria

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11
Q

Describe how the vagina contribute to immune defence

A

Acidity makes it unfavourable for microbes to inhabit

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12
Q

What are the types of second line of defence? (7)

A

Complement system
Transferrins
Phagocytes
Natural killer cells
Inflammation
Cytokines
Fever

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13
Q

What are transferrins

A

Part of the second line of defence.

Iron-binding proteins in the blood - act to inhibit the growth of certain bacteria by reducing the amount of iron available. Bacteria could otherwise use the iron for their growth.

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14
Q

What is the complement system and where are they produced?

A

Part of the second line of defence - made up of over 30 proteins produced in the liver.

When activated these proteins act in a cascade/amplified way.

Identified by a letter and number. Normally a C (eg C3, C4)

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15
Q

How do complement proteins destroy microbes?

A
  1. Promoting phagocytosis
    Fragment C3b coats a microbe in a process called opsonisation. This promotes attachment of phagocytes.
  2. Contributing to inflammation
    C3a & C5a bind to mast cells and cause them to release histamines.
  3. Causing cytolysis
    Destroying (bursting) microbes
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16
Q

What are cytokines?

A

Small protein hormones secreted by leukocytes that stimulate or inhibit normal cell functions.

Part of the second line of defence. They are the bridge between the second and third line of defence.

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17
Q

Describe 3 types of cytokines

A
  1. Interleukins - act as mediators between leukocytes. Mostly produced by T-helper cells
  2. Interferons - produced by viral-infected cells, defusing to uninfected neighbouring cells and preventing cell replication
  3. Tumour necrosis factor (TNF) - promotes accumulation of neutrophils and macrophages and causes cell death
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18
Q

Name two phagocytic cells

A

Macrophages
Neutrophils

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19
Q

Describe the role of phagocytes

A

Part of the second line of defence

Phagocytes are attracted to sites of inflammation by chemotaxis.

Non-specific in their targets. They engulf and digest foreign materials.

Macrophages are antigen-presenting cells.

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20
Q

List 3 fixed macrophages found in specific tissues

A
  • Histiocytes (connective tissue)
  • Kupffer cells (liver)
  • Alveolar macrophages (lungs)
  • Microglia (nervous tissue)
  • Langerhans cells (skin)
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21
Q

Describe the 5 stages of phagocytosis

A

1) Chemotaxis: Release of chemicals by microbes, leukocytes damaged tissue and by activated complement that attract phagocytes.

2) Adherence: Attachment of phagocytes to target

3) Ingestion: Cell membrane extends projection that engulf the microbe.

4) Digestion: Ingested structure merges with lysosomes to form phagolysosomes. Lysosomes & enzymes digest

5) Excretion: Indigestible material is excreted.

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22
Q

Describe Natural Killer cells

A

Part of the second line of defence.

Non-specific lymphocytes in the blood, lymph nodes, spleen and bone marrow.

Attach anything that they don’t recognise including abnormal body cells.

Release granules containing perforin which inserts into the cell membrane and creates a channel for tissue fluid to flow into the cell causing cytolysis.

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23
Q

What is inflammation and what can cause is?

A

A non-specific defensive response to tissue damage caused by pathogens, abrasions, chemicals, cell distortion or disturbance, and extreme temperatures

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24
Q

What are the cardinal signs of inflammation?

A

Redness
Heat
Pain
Swelling
Loss of function

(Same signs regardless of cause and location)

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25
Q

What are the 3 basic stages of inflammation?

A
  1. Vasodilation and increased permeability.
    Vasodilation allows additional blood to the area brining oxygen, nutrients and immune cells, and removes toxins and dead cells.
    Increased permeability permits movement of immune cells.
    Together create redness, swelling, heat.
  2. Emigration of phagocytes:
  3. Tissue repair
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26
Q

Name the 4 chemical mediators involved in inflammation.

What are they released by and what are their function?

A
  1. Histamines
    - released by mast cells and basophils
    - cause vasodilation and increased permeability
  2. Leukotriens
    - released by mast cells
    - attract phagocytes
  3. Kinnins
    - induce vasodilation and increased permeability as well as attract phagocytes
  4. Prostaglandins
    - lipids released by damaged cells
    - enhance effects of histamine and kinnins
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27
Q

What are the 4 outcomes of inflammation?

A
  1. Resolution
  2. Chronic inflammation
  3. Granuloma
  4. Fibrosis
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28
Q

How does a non specific fever occur?

A

Commonly occurs in infection and inflammation

Many bacterial toxins elevate body temp which triggers the release of fever-causing cytokines from macrophages such as interleukin-1

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29
Q

What’s the purpose of a fever?

A
  • Makes interferons more effective
  • Inhibits growth of some microbes
  • Speeds up the reactions that aid repair
30
Q

Where do lymphocytes form and develop?

A

They form in the bone marrow.

B-lymphocytes stay to mature in the bone marrow.
T-lymphocytes migrate to the thymus to develop there.

31
Q

What’s the broad function of lymphocytes?

A

An adaptive/specific immunity, whereby they learn to respond to foreign antigens.

Each T- & B-lymphocyte is specific for a particular antigen. They both produce immune memory for previously encountered antigens.

32
Q

What is the benefit of immune memory?

A

Produces a much quicker and more effective attack with the next encounter of the antigen.

33
Q

What are the cell-surface proteins call that are required for the immune system to recognise cells that are healthy body cells versus those that are ‘non-self’?

A

Major Histocompatibility Complex (MHC)
(Class I & Class II)

34
Q

Describe a Class I MHC

A

A cell-surface protein used to display the identity of the cell so the immune system can determine healthy body cells from abnormal/infected cells.

Located on all body cells except erythrocytes.

When the body is cancerous or invaded by a pathogen, it produces abnormal proteins which combine with the MHC-I flagging it to leukocytes.

35
Q

Describe a Class II MHC

A

Located only on the cell membrane of antigen-presenting cells
(Macrophages and B-lymphocytes)

MHC-II displays the foreign antigen having ingested the foreign cell. These are used to communicate with T-helper cells

36
Q

Briefly describe the 4 types of T-lymphocytes

A

T-Helper cells aka CD4
- mediate the immune response
- increase immune cell activity
- release cytokines

Cytotoxic cells aka CD8
- directly attach invading antigens
- release perforin to burst cells

Memory T-cells
- store memory for future exposure

Regulatory T-cells
- turn off the immune response to prevent excessive reaction

37
Q

Explain what self-tolerance and self-recognition are in relation to T-cells.

A

Self-recognition - ability to recognise self-antigens
Self-tolerence - lacks reactivity to fragments of self-antigen.

NB a loss of self-tolerance leads to autoimmunity

38
Q

What are the 2 types of adaptive immunity?

A

Cell-mediated immunity
- by T-cells - cytotoxic t-cells directly attach invading antigens

Antibody-mediated immunity
- by B-cells secreting antibodies. This defence is mostly against extracellular pathogens.

39
Q

Describe what happens during antigen presentation

A

Through the action of phagocytosis, macrophages use lysosomes to break down the antigen into fragments and combines some of these fragments with MHC molecule.

MHC binds with T-helper cell causing release of cytokine - interleukin-2

Triggers T-lymphocyte proliferation & stimulates B-lymphocyte clonal selection

40
Q

What cells are produced during T-cell proliferation (clonal selection)?

A

Cytotoxic T-lymphocytes
Memory T-lymphocytes
Helper T-lymphocytes

41
Q

What cells are produced during B-cell clonal selection?

A

Plasma cells that secrete antibodies
Memory B-cells

42
Q

Describe the structure of an antibody

A

Contain 4 polypeptide chains
Generally 2 antigen-binding sites
Form antibody-antigen complexes once they bind with their specific antigen.

43
Q

What are the 5 ways an antibody can inactivate an antigen.

A

1) Neutralising - neutralises bacteria toxins or prevent viral attachment
2) Immobilising
3) Agglutinating and precipitating - use both their binding sites to cause clumping of cells
4) Activating complement
5) Enhancing phagocytosis

44
Q

What is the location and function of IgG antibodies?

A

Location: blood, lymph and intestines

Function: protects against bacteria and viruses

45
Q

What is the location and function of IgA antibodies?

A

Location: Sweat, tears, saliva, breast milk

Function: localised protection of mucous membrane

46
Q

What is the location and function of IgM antibodies?

A

Location: blood and lumph

Function: Main class of antibodies for early immune response

47
Q

What is the location and function of IgE antibodies

A

Location: blood

Function: Allergic reactions - binds to mast cells

48
Q

What are the primary and secondary immune responses?

A

Primary = first exposure
Slow response
IgM antibodies followed by IgG

Secondary = subsequent exposure
Much faster response due to memory
Much most IgG

49
Q

What is a hypersensitive immune reaction?

A

Refers to an excessive immune response produced by the normal immune system.

50
Q

What is Type I hypersensitivity and give an example?

A

Known as an allergy.
Mediated by IgE antibodies that bind to mast cells.
Onset is immediate/rapid

E.g. hayfever

51
Q

What is Type II hypersensitivity and give an example?

A

Antibodies react with self-antigens resulting in destruction of the body’s own cells.

IgG antibodies produced.

E.g. Haemolytic disease of the newborn

52
Q

What is Type III hypersensitivity and give an example?

A

Antigen-antibody complexes deposit in tissue such as joints, skin, kidneys and eyes. These activate the complement system.

IgG, IgM and IgA mediated.

E.g. Rheumatoid arthritis

53
Q

What is Type IV hypersensitivity and give an example?

A

Cell-mediated
Over-reaction of T-cells to an antigen damaging normal tissue.

E.g. allergen contact dermatitis.

54
Q

List FOUR common allergens.

A
  • Certain foods
  • Animal dander
  • Mites
  • Dust
  • Chemicals / detergents / perfumes / soaps
    -Latex
  • Pollen
55
Q

Describe the pathophysiology of an ‘allergy’.

A

Initial exposure causes sensitisation - a slow response.

The body produces IgE specifically for that allergen

Subsequent exposure is an exaggerated immune response. The full immune response has been developed.

56
Q

Explain the key difference between a ‘food intolerance’ and a ‘food allergy’.

A

Food allergy effects 2% of adults - it is an iGe-mediated immune response.

Food intolerance effects far more people. Symptoms are triggered by the food due to lacking enzymes and other digestive factors needed to deal with the food.

57
Q

Define auto-immunity.

A

A breakdown of mechanisms responsible for self-tolerance

58
Q

What is Systemic lupus erythematous (SLE)?

A

A chronic inflammatory, autoimmune, multi-system disorder in which autoantibodies are formed again nuclear antigens.

59
Q

Describe the pathophysiology of Systemic lupus erythematous (SLE)

A

B-cell activation, increasing IgG levels against components of cell nuclei.

Impaired immune regulatory mechanisms - inability to remove immune complexes from tissue causing complement activation and inflammation.

Impaired T-cell regulation.

60
Q

Name two causes of SLE

A
  • Higher oestrogen levels
  • Low vitamin D levels
  • Chronic bacterial infections and viral infections
  • Smoking
61
Q

List two triggers of SLE

A
  • Oral contraceptive pill
  • HRT
  • Stress
  • UV light
  • Pesticides
62
Q

State TWO characteristic signs / symptoms of SLE

A
  • Butterfly rash on the face
  • Photosensitivity
  • Vasculitis
  • Raynard’s syndrome
  • Joint pain
63
Q

Name ONE unique blood test used to identify SLE.

A

Anti-nuclear antibodies (ANAs)

64
Q

What is Rheumatoid arthritis (RA)

A

Chronic, systemic inflammation of many tissues, primarily the synovium.

65
Q

Describe the pathophysiology of Rheumatoid arthritis (RA)

A

Rheumatoid Factor (RF) auto-antibodies attack IgG antibodies creating an immune complex.

Complex activated complement proteins that lead to inflammation and complexes depositing in joints.

66
Q

What gene is associated with Rheumatoid arthritis (RA)

A

HLA - DR4/DR1

67
Q

Name THREE signs / symptoms of RA.

A
  • Symmetrical /bilateral arthritis of small joints
  • Morning stiffness
  • Deformity of joints
  • General malaise and fatigue
68
Q

What is Ankylosing spondylitis (AS)

A

Systemic autoimmune disease associated with chronic inflammation of the spine and sacroiliac joints, often leading to spinal fusion.

69
Q

What gene is associated with Ankylosing spondylitis (AS)

A

HLA-B27

70
Q

List TWO bacterial causes/triggers of AS.

A

Salmonella
Shingella

71
Q

List TWO signs / symptoms of AS.

A
  • Lower back symptoms often improve with activity
  • Kyphotic spine
  • Hip and heel pain
  • Acute iritis

Biomedicine II CNM (2024) (6 decks)

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