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Y5 - Immunology > Immunology Flashcards - Immune modulators > Flashcards

Immunology Flashcards - Immune modulators

1
Q

What methods are avilable to boost the immune response (3)?

A

Vaccination
Replacement of missing components
Cytokine therapy

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2
Q

What methods are avilable to suppress the immune response (3)?

A

Non-specific immunosuppression
Ab removal
Targeted dampening of immune response

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3
Q

What methods are avilable to deviating the immune response (1)?

A

Desentisation

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4
Q

What are the indications for bone marrow transplantation (2)?

A

Life threatening primary immunodeficiencies (e.g. SCID, Leukocyte adhesion deficiency)
Haematological malignancy

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5
Q

Is BM replacement in SCID curative?

A

Yes, potentially

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6
Q

What is normal human immunoglobulin? How is it made?

A

Pooled from donors, contains preformed IgG to a range of unspecified organisms

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7
Q

What is the half life of normal human immunoglobulin?

A

18 days

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8
Q

What are the indications for Ab replacement with normal human immunoglobulin?

A

Ab deficiency (Primary or secondary)

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9
Q

Which primary Ab deficiencies benefit from Ab replacement with normal human immunoglobulin (3)?

A

X-linked agammaglobulinaemia
X-linked hyper-IgM syndrome
Common variable immune deficiency

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10
Q

Which secondary Ab deficiencies benefit from Ab replacement with normal human immunoglobulin?

A 
Haematological malignancies (e.g. CLL, multiple myeloma)
After bone marrow transplantation
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11
Q

What are specific immunoglobulins used for?

A

Post exposure prophylaxis

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12
Q

How are specific immunoglobulins derived?

A

From plasma donors with high titres of IgG antibodies to specific pathogens e.g. Hep B, tetanus, Rabies, Varicella zoster

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13
Q

What are recombinant cytokines used for?

A

Boost immune response to cancer and specific pathogens

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14
Q

What is interferon alpha used for (6)?

A 
Hep B
Hep C
Kaposi's sarcoma
hairy cell leukaemia
CML
malignant myeloma
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15
Q

What is interferon beta used for (1)?

A

Relapsing MS

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16
Q

What is interferon gamma used for (1)?

A

Chronic granulomatous disease

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17
Q

What are the three types of reconbinant cytokines used as treatment?

A

interferon alpha, beta and gamma

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18
Q

What type of molecule are corticosteroids?

A

synthetic glucocorticoids

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19
Q

Name a corticosteroid

A

Prednisolone

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20
Q

What is the bodies daily glucocorticoid output in terms of prednisolone?

A

5-7.5mg

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21
Q

What are the immune effects of corticosteroids (3)?

A

Reduced prostaglandin synthesis
Inhibits phagocyte migration and function
Inhibits lymphocyte function and promotes apoptosis

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22
Q

What are the metabolic effects of corticosteroids (7)?

A 
Diabetes
Obesity
Lipid abnormalities
Osteoporosis
Moon face
Hirsutism
Adrenal suppression
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23
Q

What are the other side effects of corticosteroids (6)?

A 
Immune suppression
Cataracts
Glaucoma
Peptic ulceration
Pancreatitis
Avascular necrosis
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24
Q

How do corticosteroids affect phagocytes?

A

Inhibit migration into tissue by decreasing adhesion molecule expression and blocking migration signals
Decrease proteolytic enzyme release

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25
Q

How do corticosteroids affect lymphocytes?

A

Sequestration in lymphoid tissue CD4>CD8>B
Induction of apoptosis at high doses
Inhibition of cytokine gene expression
Decrease Ab production

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26
Q

How do corticosteroids decrease prostaglandin synthesis?

A

Inhibition of phospholipase A2

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27
Q

Name 4 anti-proliferative agents

A

Cyclophosphamide
Mycophenylate
Azathioprine
Methotrexate

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28
Q

How do cytotoxics work?

A

Inihibition of DNA synthesis

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29
Q

What is cyclophosphamide?

A

Anti-proliferative immunosuppressant / cytotoxic

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30
Q

What is the MoA of cyclophosphamide?

A

Alkylation of the guanine base of DNA, causing damage and preventing replication.

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31
Q

Which cells does cyclophosphamide affect most?

A

B cells > T cells, but all cells with high turnover at high doses

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32
Q

What are the major indications for cyclophosphamide?

A

Auto-immune diseases such as multisystem connective tissue disease or vasculitis with severe end organ involvement (e.g. wegeners granulomatosis, SLE)
Cancer

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33
Q

What are the side effects of cyclophosphamide (3)?

A

Toxicity to proliferating cells (BM depression, hair loss, sterility M»F)
Haemorrhagic cystitis
Complications of long term immunosuppression

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34
Q

What is azathioprine?

A

Anti-proliferative immunosuppressant / cytotoxic

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35
Q

What is the MoA of Azathioprine?

A

Metabolised to 6-mercaptopurine

This blocks de novo purine synthesis, preventing DNA replication

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36
Q

What cells does azathioprine affect?

A

T cells - activation and proliferation

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37
Q

What are the indications for Azathioprine (3)?

A

Transplantation
Auto-immune disease
Auto-inflammatory diseases (e.g. crohn’s, UC)

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38
Q

What are the side effects of azathioprine (3)?

A

Bone marrow suppression (esp leukocytes and platelets, and individuals who have TPMT polymorophisms)
Hepatotoxicity (uncommon)
Complications of long term immunosuppression

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39
Q

What is mycophenylate?

A

Anti-proliferative immunosuppressant / cytotoxic

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40
Q

What is the mechanism of action of mycophenylate?

A

Blocks de novo nucleotide synthesis, preventing DNA replication

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41
Q

Which cells does mycophenolate affect most?

A

T>B

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42
Q

What are the indications for mycophenylate (2)?

A

Used in transplantation as an alternative to azathioprine

Used in auto-immune disease and vasculitis as an alternative to cyclophosphamide

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43
Q

What are the side effects of mycophenylate (2)?

A

Bone marrow suppression (esp leukocytes and platelets)
Hepatotoxicity (uncommon)
Complications of long term immunosuppression (esp risk of herpes virus reactivation and progressive multifocal leukoencephalopathy)

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44
Q

What is the purpose of plasmapharesis?

A

Remove pathogenic Abs

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45
Q

What is the main limitation of plasmapharesis?

A

Rebound antibody production limits efficacy so need to give anti-proliferative too

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46
Q

What are the indications for plasmapharesis?

A

Severe Ab mediated disease: Goodpastures, severe acute myasthenia gravis, severe vascular rejection

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47
Q

Name 3 cell signalling inhibitors

A

Cyclosporin
Tacrolimus
Sirolimus

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48
Q

What is the MoA of cyclosporin?

A

Inhibits calcineurin, interrupting T cell signalling pathways and preventing IL2 release, therefore stopping T cell activation and proliferation

49
Q

What is the MoA of tacrolimus?

A

Inhibits calcineurin, interrupting T cell signalling pathways and preventing IL2 release, therefore stopping T cell activation and proliferation

50
Q

What are the side effects of cyclosporin?

A 
Dysmorphism +++
Nephrotoxic ++
HTN ++
Neurotoxic ++
Diabetogenic +
51
Q

What are the side effects of tacrolimus?

A

Diabetogenic +++
Nephrotoxic ++
HTN ++
Neurotoxic ++

52
Q

How do recombinant Abs work?

A

Target cell surface antigens

53
Q

What is the target of anti-thymocyte globulin?

A

T-cell surface molecules

54
Q

How does anti-thymocyte globulin work?

A

Depletes and modulates T cell function

55
Q

What are the indications for anti-thymocyte globulin?

A

Allogract rejection

56
Q

What are the side effects of anti-thymocyte globulin (4)?

A

Infusion reaction
Leukopenia
Infection
Malignancy

57
Q

What is the target of Basiliximab?

A

CD25, IL-2 receptor on T cells

58
Q

What is the MoA of basiliximab?

A

Binds to IL-2 receptor, stops T cell proliferation

59
Q

What are the indications for Basiliximab?

A

Prophylaxis of allograft rejection

60
Q

What are the s/e of basiliximab (2)?

A

Infusion reaction
Infection
?long term malignancy

61
Q

What is abatacept?

A

CTLA4-IG fusion protein

62
Q

What is the target for abatacept?

A

CD80 and CD86 receptors on antigen presenting cells

63
Q

What is the MoA of abatacept?

A

Prevents CD28 and CTLA4 proteins on T cells binding to APCs, preventing T cell activation

64
Q

What are the indications for abatacept?

A

Rheumatoid arthritis

65
Q

What are the s/e of abatacept?

A

Infusion reaction
Infection (TB, Hep B, Hep C)
?long term malignancy

66
Q

What is a cytokine storm?

A

Potentially fatal immune reaction - positive feedback loop of cytokines activating lymphocytes and macrophages causing cytokine release.

67
Q

What are the clinical features of a cytokine storm?

A

Vascular leak causing pulmonary oedema, cerebral oedema, cardiovascular collapse, poor peripheral perfusion and shock

68
Q

What is the target of rituximab?

A

CD20

69
Q

What is the MoA of rituximab?

A

Binds to CD20 on B cells, depleting mature B cells

70
Q

What are the indications for Rituximab?

A

Lymphoma
Rheumatoid arthritis
SLE

71
Q

What are the s/e of rituximab?

A

Infusion reaction
Infection (Progressive multifocal leukoencephalopathy)
Exacerbates CV disease

72
Q

What is the target of natalizumab?

A

alpha4 integrin on T cells

73
Q

What is the MoA of natalizumab?

A

Binds to alpha4 integrin, stopping VCAM1 and MadCAM1 binding and preventing T cell migration

74
Q

What are the indications of natalizumab?

A

Highly-active relapsing-remitting MS

Crohn’s

75
Q

What are the s/e of natalizumab?

A

Infusion reactions
Infection (progressive multifocal leukoencephalopathy
Hepatotoxicity
?long term malignancy

76
Q

What is the target for tocilizumab?

A

IL-6 receptor - membrane bound and soluble

77
Q

What is the MoA of tocilizumab?

A

Inhibits IL6 driven activation of neutrophils, macrophages, T and B cells.

78
Q

What are the indications of tocilizumab?

A

Castleman’s disease

Rheumatoid arthritis

79
Q

What are the s/e of tocilizumab?

A 
Infusion reactions
Infection
Hepatotoxic
Elevated lipids
?long term malignancy
80
Q

What is the action of anti-thymocyte globulin?

A

Bind cell surface antigens

81
Q

What is the action of basiliximab?

A

Bind cell surface antigens

82
Q

What is the action of abatacept?

A

Bind cell surface antigens

83
Q

What is the action of rituximab?

A

Bind cell surface antigens

84
Q

What is the action of natalizumab?

A

Bind cell surface antigens

85
Q

What is the action of tocilizumab?

A

Bind cell surface antigens

86
Q

Name 4 drugs that target TNFalpha

A

Infliximab
Adalimumab
Certolizumab
Golimumab

87
Q

What are the indications of anti-TNFalpha?

A

Rheumatoid arthritis
Ankylosing spondylitis
Psoriasis and psoriatic arthritis
Inflammatory bowel disease

88
Q

What are the s/e of anti-TNFalpha drugs (5)?

A 
Infusion / injection reactions
Infection (TB, Hep B, Hep C)
Lupus-like conditions
Demyelination
Malignancy
89
Q

What is etanercept?

A

Decoy TNF receptor

90
Q

What is the MoA of etanercept?

A

Binds TNFalpha and beta, preventing their physiological action

91
Q

What are the indications for etanercept?

A

Rheumatoid arthritis
Ankylosing spondylitis
Psoriasis and psoriatic arthritis

92
Q

What are the s/e of etanercept?

A 
Injection site reactions
Infection (TB, Hep B, Hep C)
Lupus-like conditions
Demyelination
Malignancy
93
Q

What is the target of ustekinumab?

A

p40 subunit of IL12 and IL23

94
Q

What is the MoA of ustekinumab?

A

Binds IL12 and IL23, preventing T cell and NK cell activation

95
Q

What are the indications for ustekinumab?

A

Psoriasis

96
Q

What are the s/e of ustekinumab?

A

Injection site reaction
Infection (TB)
?malignancy

97
Q

What is the action of ustekinumab?

A

Cytokine blockade

98
Q

What is the action of infliximab?

A

Cytokine blockade

99
Q

What is the action of adalimumab?

A

Cytokine blockade

100
Q

What is the action of certolizumab?

A

Cytokine blockade

101
Q

What is the action of golimumab?

A

Cytokine blockade

102
Q

What is the action of etanercept?

A

Cytokine blockade

103
Q

What is the action of denosumab?

A

Cytokine blockade

104
Q

What is the target of denosumab?

A

RankL

105
Q

What is the MoA of denosumab?

A

Prevents RANK activation on osteoclasts, stopping differentiation and function

106
Q

What are the indications of denosumab?

A

Osteoporosis

107
Q

What are the s/e of denosumab?

A

Injection site reactions
Infection
Avascular necrosis of the jaw

108
Q

What are the main side effects of immunosuppression?

A

Injection site reactions
Infusion reactions
Infection

109
Q

What are injection site reactions?

A

Mixed cellular infiltrates peaking at 48h. Often with CD8 cells.

110
Q

What are infusion reactions?

A

IgE mediated effects - urticaria, hypotension, tachycardia, wheeze
Also: headaches, fevers, myalgias
Cytokine storm

111
Q

How do you protect immunosuppressed PTs against infection?

A

Avoidance
Low threshold for treatment
Vaccination

112
Q

Which vaccines can you not use in an immunosuppressed PT?

A

BCG
Measles
Yellow fever
Polio (some)

113
Q

What causes progressive multifocal leukoencephalopathy?

A

John cunningham virus (JC virus)

114
Q

How does the JC virus cause PML?

A

infects and destroys oligodendrocytes

115
Q

Which cancers present in immunosuppressed PTs?

A

Lymphoma (EBV)

Non-melanoma skin cancers (HPV)

116
Q

What are the auto-immune s/e of immunosuppression (8)?

A 
SLE / lupus like syndromes
Anti-phospholipid syndromes
Vasculitis
Interstitial lung disease
Sarcoidosis
Uveitis
Autoimmune hepatitis
Demyelination
117
Q

How can we deviate normal immune responses?

A

Allergen desensitisation

118
Q

When is allergen desensitisation indicated?

A

Monoallergic disorders - bee, wasp venom, grass pollen, house mite dust

Y5 - Immunology (1 decks)

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