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Infection&immunity > Edmead S1 > Flashcards

Edmead S1 Flashcards

1
Q

In the innate immune system cytokines are produced mainly by what?

A

Mononuclear phagocytes in response to infectious agents

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2
Q

Chemokines enhance extravasation- what is this?

A

The leakage of fluid out of its container

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3
Q

In the adaptive immune system- Th1 cells secrete what to stimulate macrophages and cytotoxic T cells causing tissue damage

A

IFN-gamma

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4
Q

In the adaptive immune system- Th2 cells released what type of cytokines and give an example

A

Anti inflammatory

IL-4

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5
Q

Which two cytokines increase leukocyte adhesion to endothelium

A

TNF

IL-1

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6
Q

Even though they are first line, why aren’t NSAIDs very good in RA?

A

Because they work by inhibiting COX so less prostaglandins and prostaglandin isn’t that important in chronic inflammation

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7
Q

Name 6 DMARDs

A 
Methotrexate 
Sulfasalazine 
Gold
Penicillamine
Hydroxychloroquine
Leflunomide
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8
Q

What’s the mechanism of action of methotrexate

A

Suppresses IL1 induced IL6 so decreased synovial cell proliferation and reduced reactive O2 species

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9
Q

What does lysosomotropic mean

A

Accumulates in lysosomes of cells in the body

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10
Q

Where are endogenous corticoids released from?

A

Adrenal cortex

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11
Q

Name a mineralocorticoid and what does it effect

A

Aldosterone

Affects water and electrolyte balance

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12
Q

Give two examples of glucocorticoids

A

Hydrocortisone and corticosterone

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13
Q

What do glucocorticoids affect?

A

Carbohydrate and protein metabolism

Anti inflammatory and immunosuppressive effects

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14
Q

Name a disease that results from deficiency in steroids

A

Addison’s disease

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15
Q

Name a syndrome that results from excess glucocorticoid

A

Crushings syndrome

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16
Q

Name a syndrome as a result of excess mineralocorticoid

A

Conns syndrome

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17
Q

What does the HPA axis stand for

A

Hypothalamic-pituitary-adrenal axis

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18
Q

In the HPA axis what’s the hormone released from the hypothalamus to the pituitary

A

Corticotrophin releasing hormone

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19
Q

In the HPA axis what’s the hormone released from the pituitary to the adrenals

A

Adrenocorticotrophic hormone

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20
Q

Name 3 key metabolic side effects of steroids

A

Osteoporosis
Diabetogenic-obesity
Mineralocorticoid effects (Na/H2O retention, hypertension, oedema, CV events)

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21
Q

What are TNF and IL-1 and what are they involved in?

A

Both proinflam cytokines involved in cell proliferation (both) and apoptosis (TNF)

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22
Q

What is TNF and IL-1’s primary beneficial function

A

Beneficial activation of innate immune system

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23
Q

Are TNF and IL-1 self induced?

A

Yeh they bind to receptor and up regulate

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24
Q

What are TNF and IL-1 produced by

A

LPS-activated monocytes/macrophages

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25
Q

How many forms of interleukin-1 are there?

A

2 forms
Alpha
Beta

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26
Q

Try or false: IL-1 alpha is the most common circulating form

A

False it’s mainly cytosolic or membrane bound

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27
Q

IL-1 is synthesised as what and by what?

A

As precursors and cleaved by interleukin-1 converting enzyme (ICE) also known as Caspase 1

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28
Q

What are ICE inhibitors and are they effective

A

Anti inflammatory agents

NO

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29
Q

What’s the main purpose of inflammation

A

Bring cells from blood to site of infection

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30
Q

What is thought to cause RA

A

Initiating antigen is unknown but disease often follows an infection

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31
Q

What initiates and sustains disease through recognition of autoantigen?

A

CD4+ Tcell

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32
Q

Give two examples of likely autoantigens in RA

A

Collagen and other cartilage components

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33
Q

Chronic inflammation is mediated largely by what?

A

CYTOKINES

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34
Q

What are cytokines?

A

Small proteins secreted by cells of the immune system

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35
Q

Cytokine function can be what three things

A

Autocrine
Paracrine
Endocrine

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36
Q

Give 4 key effects of cytokines

A

Induce T&B differentiation
Activation of macrophages
Cellular migration
Apoptosis

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37
Q

Chemokines enhance what?

A

Extravasation

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38
Q

TNF and IL-1 increase leukocyte adhesion to what?

A

Endothelium

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39
Q

Th1 cells secrete what to do what?

A

IFNg to stimulate macrophages and cytotoxic T cells causing tissue damage

40
Q

What do Th2 cells release and give an example

A

Anti inflammatory cytokines e.g IL4

41
Q

Give two examples of pro inflam cytokines

A

TNF

IL-1

42
Q

Give two examples of anti inflammatory cytokines

A

IL4

IL10

43
Q

What’s the TNF IL-1 cycle

A

TNF/IL-1 act on macrophages to stimulate Thelper to promote differentiation into Th1 which promotes more IFNg which feeds back on to macrophages to increase inflam

44
Q

Pain and swelling in RA is due to what

A

Infiltration of white blood cells

45
Q

What’s first line in treating RA

A

NSAIDs

46
Q

NSAIDs have 3As what are they

A

Analgesia
Anti inflam
Antipyretic

47
Q

How do NSAIDs work

A

Block cyclooxygenase which makes PG which causes pain and swelling

48
Q

What’s a key limitation of NSAIDs in RA

A

Target reducing PG but this isn’t a key problem in chronic inflammation

49
Q

What’s second line to treat RA

A

disease modifying rheumatic drugs DMARDs

50
Q

Are DMARDs slow acting?

A

Yes see effects after about 3-4 weeks

51
Q

What’s usually the first DMARD recommended?

A

Methotrexate

52
Q

How does methotrexate work?

A

It’s a folate antagonist- blocks DNA synthesis therefore blocks cell proliferation via inhibition of degydrofolate reductase

53
Q

What does IL-6 do and what potentially suppresses it via IL-1

A

IL-6 drives synovial cell proliferation and reduces reactive oxygen species
MTX might stop it

54
Q

What’s the problem with methotrexate

A

Targets enzyme which can actually change and become resistant or cells may use alternative pathway. Also toxic

55
Q

What’s sulphasalazine?

A

Is a DMARD acts as an antibiotic and anti rheumatic

56
Q

What’s penicillamine

A

DMARD prevents maturation of newly synthesised collagen- decreased joint swelling, RF, and concentration of acute phase proteins

57
Q

What’s a key side effect of penicillamine

A

Thrombocytopenia (low platelets)

58
Q

How does hydroxychloroquine work?

A

Stabilises lysosomes so reduces release of reactive oxygen species inhibits phospholipase A2 (PLA2)
Reduces cytokine transcription

59
Q

What’s Leflunomide

A

Newest DMARD targets enzymes involved in DNA synthesis and may suppress B cell activity and reduce RF

60
Q

What’s third line in RA

A

Steroids

61
Q

How do steroids work

A

Work in nucleus
Effect gene transcription
Block pro inflam cytokine production

62
Q

Why does the body rely on exogenous steroids when they’re given them?

A

Cos they suppress the endogenous steroids

63
Q

Can steroids work at all stages of the inflammatory response?

A

Yes

64
Q

Within the nucleus, steroids act on what to affect gene transcription

A

Proteins like AP-1 and NFkB that affect gene transcription

65
Q

Which form of IL-1 is the biggest problem that we want to target

A

Beta form

66
Q

Where is IL-1 synthesised?

A

In the micro tubules

67
Q

IL-1 increases synthesis of what?

A

COX-2 and iNOS

68
Q

IL-1 increases expression of what

A

VCAM and ICAM (selectins and adhesion molecules that enhance extravasation)

69
Q

How does C5a relate to IL-1

A

C5a increases IL-1 mRNA

70
Q

True or false:
Increase Tcells
Increase IFNg
Increase IL-1

A

TRUE

71
Q 
True or false: 
Increase CD40L
Increased BCells
Induces more IL-1b 
Increased extravasation
A

TRUE

72
Q

IL-1 receptors are members are member of what superfamily

A

Ig superfamily

73
Q

How many types of IL-1 receptor are there?

A

TWO:
Type 1 present on most cells (main receptor)
Type 2 mainly B cells, decoy receptor

74
Q

How many forms of TNF are there and which one is the main form?

A

Two forms

TNF alpha is main

75
Q

What type of receptor is the TNF receptor

A

Homotrimers

76
Q

What can cleave TNF from surface?

A

Metalloproteinases

77
Q

How many types of TNF. receptor are there and on which cells are they present?

A

TWO

all cells except RBC

78
Q

There are two TNF receptors.. Which one is responsible for cell growth AND cell death

A

TNFR 1

79
Q

How many receptors do you have to block in the TNF receptor in order to actually block it

A

At least two

80
Q

Almost all therapeutic antibodies we use are polyclonal. True or false?

A

FALSE it’s monoclonal

81
Q

What’s the drug name of anti ICAM

A

Enlinimab

82
Q

What was the problem with Enlinimab

A

Patients developed immune complexes which can block vessels

83
Q

Name the chimeric antibody

A

Inflixab (anti TNF)

84
Q

How do you minimise immunogenic reactions with infliximab?

A

Give with MTX if tolerated

85
Q

Name a humanised antibody

A

Certolizumab

86
Q

Name two fully humanised antibodies

A

Adalimumab

Golimumab

87
Q

What’s the problem with soluble receptors?

A

They are cleared very quickly so need repeat injections

88
Q

How can we extend circulatory lifecycle of antibodies

A

Dimerise two soluble receptors using PEG

89
Q

Give two examples of chimeric fusion proteins

A

Lenercept

Etanercept

90
Q

What’s anakinra?

A

Recombinant non glycosylation form of IL-1RA

Injected into joints via viral vector

91
Q

Name an anti-B cell therapy in RA

A

Rituximab

92
Q

How does Rituximab work?

A

B cell depleting monoclonal anti-CD20 antibody- causes B cell apoptosis

93
Q

Name an anti-T cell therapy in RA

A

Abatacept

94
Q

Name an IL-1 receptor antagonist

A

Anakinra

95
Q

Name a humanised monoclonal antibody against IL-6 receptor

A

Tocilizumab

96
Q

Name a janus kinase 3 inhihitor used in RA

A

Tofacitinib

Infection&immunity (9 decks)

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