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Immunology Flashcards

1
Q

What is vaccination?

A

Deliberate administration of antigens to produce immunological memory

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2
Q

When are long lived T and B cells generated?

A

Adaptive immune response

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3
Q

Where do long lived plasma cells reside?

A

Bone marrow

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4
Q

In immunological memory, how does IgG clear infection before symptoms occur?

A

Direct neutralisation of bacteria
Rapid mobilisation of phagocytes and complement
IgA blocks bacterial binding to mucous membranes

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5
Q

What are naïve B and T cells?

A

Mature but not yet activated (induce a strong response in 14-21 days)

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6
Q

What can naïve B and T cells become?

A

Effector or memory cells

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7
Q

What have memory B cells already undergone?

A

Ig class switching and hypermutation

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8
Q

What is immunisation?

A

The process through which an individual develops immunological memory to a disease

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9
Q

What is active immunisation?

A

Protection by the persons own immune system- usually permanent

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10
Q

What is passive immunisation?

A

Protection transferred by another person or animal- temporary

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11
Q

What are the two types of active vaccination?

A

Live attenuated vaccines or inactive vaccines e.g. killed, subunit or toxoid

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12
Q

What are some features of inactivated vaccines?

A

Do not multiply, not as effective, antibody based (not T cell), will diminish with time, multiple doses

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13
Q

What can under-inactivation cause?

A

Pathogens or toxins within the body

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14
Q

What can over-activation cause?

A

Ruins conformation of the antigen so there can be no antibody binding

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15
Q

What are some features of a live attenuated vaccine?

A

Similar to natural infection, organism must replicate, needs 1 dose

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16
Q

What is the advantage of inactivated vaccines over live attenuated ones?

A

Generally safer and easier to store

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17
Q

What is the most common example of natural passive immunisation?

A

Through transfer of maternal antibodies in placenta and maternal antibodies through breast milk

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18
Q

What antibody is transferred across the placenta?

A

IgG

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19
Q

What are examples of therapeutic passive immunisation?

A

Human immunoglobulin or monoclonal antibodies

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20
Q

What makes some organisms difficult to create vaccinations for?

A

Chronic/latent disease or rapidly evolving infections

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21
Q

What are some new approach vaccinations?

A

Mucosal vaccines, intranasal vaccine and preventative vaccines against cancer causing viruses

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22
Q

What is primary immunodeficiency?

A

Inherited abnormalities associated with a failure of development of components of the immune system

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23
Q

What are the hallmarks of immunodeficiency?

A

Serious, persistent, unusual, recurrent infections

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24
Q

What is classed as recurrent infection?

A

2 major or 1 major and recurrent minor infections in one year

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25
Q

What are typical features of immunodeficiency in general?

A

Weight loss, failure to thrive, severe skin rash, chronic diarrhoea, mouth ulcers, autoimmune disease, family history

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26
Q

What is more common, primary or secondary immunodeficiency?

A

Secondary

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27
Q

What are causes of secondary immunodeficiency?

A

Physiological, infections, treatment, malignancy, nutritional disorders

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28
Q

What do defects of phagocyte production usually cause?

A

Failure to produce neutrophils or a failure of their maturation

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29
Q

What is Kostmann Syndrome?

A

Rare autosomal recessive disorder of severe chronic neutropenia

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30
Q

What are signs of Kostmann Syndrome?

A

Infections after birth, fever, irritability, ulcers, failure to thrive

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31
Q

What is the supportive treatment for Kostmann Syndrome?

A

Prophylactic antibiotics and antifungals

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32
Q

What is the definitive treatment for Kostmann Syndrome?

A

Stem cell transplant, granulocyte colony stimulating factor

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33
Q

What is leukocyte adhesion deficiency?

A

Genetic defect in leukocyte integrins to cause a failure of neutrophil adhesion and migration

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34
Q

What does leukocyte adhesion deficiency show?

A

Leukocytosis (high WCC) and localised bacterial infections

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35
Q

What are opsonins?

A

Binding enhancers for phagocytosis

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36
Q

What do opsonin defects cause?

A

Defective phagocytosis but not significant disease

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37
Q

In general, how are phagocyte deficiencies treated?

A

Oral/IV antibiotics, surgical drainage of abscess, bone marrow transplant

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38
Q

What is chronic granulomatous disease?

A

Failure of oxidative killing mechanisms. It is x-linked deficiency of NADPH oxidase

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39
Q

What does CGD result in?

A

Excessive inflammation and granuloma formation, recurrent deep bacterial and fungal infections, failure to thrive, lymphadenopathy, hepatosplenomegaly

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40
Q

What is the prophylactic treatment for CGD?

A

Prophylactic antibiotics and antifungals

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41
Q

What is the definitive treatment for CGD?

A

Stem cell transplant, gene therapy

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42
Q

What are organisms which can hide from the immune system in cells?

A

Salmonella, chlamydia, rickettsia

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43
Q

Where is it common for organisms to hide in the body?

A

Macrophages

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44
Q

What is reticular dysgenesis?

A

Failure to produce neutrophils, lymphocytes, monocytes/macrophages, platelets

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45
Q

How is reticular dysgenesis treated?

A

Only by stem cell transplant

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46
Q

What is SCID?

A

Failure to produce lymphocytes in the thymus

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47
Q

When are signs of SCID?

A

Unwell by 3 months, persistent diarrhoea, failure to thrive, infections of all types, family history

48
Q

What is the commonest form of SCID?

A

X-linked mutation in the IL2 receptor which results in the inability to produce cytokines

49
Q

What is the clinical presentation of SCID?

A

Low/absent T cells, normal/increased B cells, poorly developed lymphoid tissues

50
Q

How is SCID treated?

A

Prophylactic antibiotics, stem cell transplant, gene therapy

51
Q

What is DiGeorge syndrome?

A

Defect of the 3rd/4th pharyngeal pouch so there is failure of thymus development which results in T cell immunodeficiency

52
Q

What are physical signs of DiGeorge syndrome?

A

Low set ears, high forehead, cleft palate, small mouth

53
Q

What are clinical signs of DiGeorge syndrome?

A

Hypocalcaemia, T cell lymphopenia, congenital heart disease, recurrent bacterial and viral infections, frequent fungal infection

54
Q

What is the treatment for DiGeorge syndrome?

A

Prophylactic antibodies and treatment of infection and immunoglobulin replacement

55
Q

What is the good thing about DiGeorge syndrome?

A

T cell function improves with age

56
Q

What do antibody deficiencies present as?

A

Recurrent bacterial infections

57
Q

What is Bruton’s X-linked Hypergammaglobulinaemia?

A

Failure to produce mature B cells

58
Q

What is selective IgA deficiency?

A

A genetic component which only affects about 1/3rd of sufferers

59
Q

What is CVID?

A

Lots of different diseases, low IgG/IgA/IgE

60
Q

How does CVID present?

A

Recurrent bacterial infections associated with autoimmune disorder

61
Q

What type of hypersensitivity reactions are allergic responses?

A

Type 1

62
Q

What is an allergic response?

A

IgE mediated antibody response to an external antigen

63
Q

What antibodies do non-atopic episodes involve?

A

IgG and IgA

64
Q

Allergen specific T cells are activated by allergen derived peptides in allergic reactions. What does this cause?

A

Differentiation of CD4+ T cells into effector Th2 cells which produce cytokines

65
Q

Which interleukins does Th2 produce to synthesise IgE by B cells?

A

IL4, 13 and 5

66
Q

What does the production of IgE during allergic responses result in?

A

Eosinophil and mast cell recruitment to the site of allergen

67
Q

Abnormal response to allergens is the normal response to what?

A

Helminth infection

68
Q

Mast cells release preformed substances. What are these?

A

Histamine, heparin and tryptase

69
Q

Mast cells synthesise molecules on demand. What are these?

A

Leukotrienes, prostaglandins and cytokines

70
Q

What do mast cells express receptors for?

A

The Fc region of the IgE antibody

71
Q

When do clinical features of allergic responses occur?

A

Within minutes

72
Q

What are clinical features of allergic responses?

A

Urticaria, angioedema, asthma, allergic rhinitis, conjunctivitis and anaphylaxis

73
Q

In extrinsic asthma, what does the release of histamine and other inflammatory mediators result in?

A

Muscle spasm (bronchodilation and wheeze), mucosal inflammation and inflammatory cell infiltrate (secretions)

74
Q

What do non-allergic responses occur as a result of?

A

Spontaneous mast cell degranulation

75
Q

What can non-allergic responses occur as a result of?

A

Drugs, thyroid disease, idiopathic, physical urticaria

76
Q

What is the management of type 1 hypersensitivity reactions?

A

Allergen avoidance, block/prevent mast cell activation, anti-inflammatory agents, management of anaphylaxis, immunotherapy

77
Q

What drugs block mast cell activation?

A

Sodium cromoglicate

78
Q

What drugs prevent mast cell activation?

A

Antihistamines, leukotriene receptor antagonists

79
Q

What are anti-inflammatory agents?

A

Corticosteroids

80
Q

What is given to manage anaphylaxis?

A

Adrenaline

81
Q

What do type II hypersensitivity reactions involve?

A

Direct cell killing

82
Q

What are type II hypersensitivity reactions triggered by?

A

Antibody binding to an antigen on the cell surface or extracellular matrix

83
Q

What is the result of type II hypersensitivity reactions?

A

Cell lysis or inflammatory reactions at the site of antibody deposition

84
Q

When the antibody binds to a cell surface antigen, what does this result in?

A

Activation of complement for cell lysis and opsonisation

85
Q

What antibodies are involved in type II hypersensitivity reactions and why?

A

IgG and IgM as they activate complement

86
Q

Complement activation results in the activation of C3. What does this cause?

A

Chemotaxis, solubilisation of immune complexes, direct killing of bacteria and opsonisation

87
Q

What type of bacteria does complement generally kill and how?

A

Directly encapsulated bacteria through the membrane attack complex

88
Q

What complement proteins are involved in type II hypersensitivity reactions?

A

C3a and C5a

89
Q

How does direct cell killing take place in type II hypersensitivity reactions?

A

Through B cells producing antibodies directed against the cell membrane protein

90
Q

What other immune system components are involved in type II hypersensitivity reactions?

A

Eosinophils and natural killer cells

91
Q

What are clinical examples of type II hypersensitivity reactions?

A

Blood cells (transfusion reactions), Goodpasture’s syndrome, myasthenia gravis, binding of antibodies to TSH receptor

92
Q

How are type II hypersensitivity reactions managed?

A

Removal of the pathogenic antibody (blood removed by cell separator) or immunosuppression

93
Q

What are type III hypersensitivity reactions?

A

Immune complex mediated

94
Q

What is the key feature of type III hypersensitivity reactions?

A

Antibodies binding to soluble antigens

95
Q

What triggers type III reactions and what happens to these?

A

Excess antigens- antibody binds to them to form small immune complexes

96
Q

Where are the immune complexes of type III reactions found?

A

Trapped in blood vessels, joints and glomeruli

97
Q

What is activated in type III reactions?

A

Complement

98
Q

What is the result of type III reactions?

A

Antibody mediated phagocytosis and infiltration and activation of neutrophils and macrophages to result in tissue damage

99
Q

A clinical example of type III reactions is farmer’s lung. What happens here?

A

Inhaled fungal particles are deposited which stimulates antibody binding

100
Q

What does immune complexes in the walls of the alveoli and bronchioles result in?

A

Leukocyte accumulation and activation

101
Q

What are symptoms of leukocyte accumulation in the lungs?

A

Wheezing and malaise 4-8 hours after antigen exposure. Can also be dyspnoea, pyrexia and a dry cough

102
Q

What are other examples of type III hypersensitivity reactions?

A

Acute hypersensitivity pneumonitis, systemic lupus erythematosus

103
Q

What is the difference between types II and III reactions?

A

Type II is localised and type III is systemic

104
Q

How do you test for type III reactions?

A

Test for specific IgG antibodies

105
Q

How do you manage type III reactions?

A

Allergen avoidance, steroids, immunosuppression

106
Q

What are type IV reactions?

A

Delayed hypersensitivity

107
Q

What are autoimmune examples of type IV reactions?

A

Type 1 diabetes, psoriasis, rheumatoid arthritis

108
Q

What are non-autoimmune examples of type IV reactions?

A

Nickel hypersensitivity, TB, leprosy, sarcoidosis, cellular rejection of organ transplant

109
Q

What differentiates type IV reactions?

A

T cell mediated

110
Q

In type IV hypersensitivity reactions, what is generated on initial sensation to an antigen?

A

Effector Th1 cells

111
Q

What happens on subsequent exposure to antigens in type IV reactions?

A

Activation of Th1 cells, recruitment of macrophages, lymphocytes and neutrophils to cause persistent inflammation

112
Q

What do Th1 cells activate in type IV reactions?

A

Interferon gamma cytokines

113
Q

What is poison ivy an example of?

A

Type IV reaction

114
Q

What is sarcoidosis?

A

Multi-system granulomatous disease

115
Q

What type of immune response is involved in sarcoidosis?

A

Non specific response involving T cells and macrophages

116
Q

What does sarcoidosis result in?

A

Persistent production of activated cytokines

Respiratory (16 decks)

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