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bms 242 - core phys/pharm > Anti-inflammatories II > Flashcards

Anti-inflammatories II Flashcards

1
Q

What is rheumatoid arthritis?

A

Inflammation of the synovium of the joints

With autoimmune components

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2
Q

What are the risk factors of rheumatoid arthritis?

A

Smoking

Genetics

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3
Q

What are the symptoms of rheumatoid arthritis?

A
  • Swelling of the joints and pain
  • Poor sleep is associated
  • Can by symmetrical or not
  • Can spread to other parts of the body
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4
Q

What is the inflammatory reaction underlying rheumatoid arthritis?

A

1) Activation of TH1 (T-cells)
2) Leads to activation of MACROPHAGES, which infiltrate the area and secrete CYTOKINES
3) Leads to the recruitment activation of other cells at the area of inflammation
4) All the cells together cause erosion of the cartilage and bone - causing joint damage

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5
Q

What are the cytokines released by macrophages in the lead up to rheumatoid arthritis?

A

Pro-imflammatory cytokines:

1) IL-1
2) TNF-alpha

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6
Q

What are the cells recruited by cytokines in the lead up to rheumatoid arthritis?

A

1) Fibroblasts

2) Osteoclasts

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7
Q

What do fibroblasts do?

A

Try to resolve tissue damage BUT by doing so can cause damage - by lots of deposition of extracellular matrix proteins

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8
Q

What drugs can decrease the level of damage in rheumatoid arthritis?

Describe them

A

DMARDs:

1) Methotrexte
- Large structure
- Folic acid antagonist
- Cytotoxic and immunosuppressant activity

2) Sulfasalazine
- Has a sulphate group

3) Drugs with metal ions
- Free radical scavengers to reduce tissue damage

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9
Q

What are immunosuppresants?

A

Drugs which lower the bodys ability to reject transplanted tissues

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10
Q

What do imminosupressants do?

How?

A

Inhibit the induction phase of an inflammatory response:

  • Work directly at the level of the immune cells to suppress their activity and inhibit the transcription of proinflammatory cytokines
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11
Q

What is ciclosporin and what does it do?

A

An immunosupressant drug with helps to supress transplant rejection

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12
Q

What is the normal action in the cell, regarding cyclophilin and nf kappa b?

A

1) Cyclophillin usually binds to calcineurin
2) Calcineurin binds to Ca released in immune reactions - activating the calcineuin
3) Calcineurin (a phosphatase) removes phosphatase from nf kappa b (a transcription factor found in many cells)
4) Dephosphorylated nf kappa b can move into the nucleus and control the transcription proinflammatory cytokines

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13
Q

How does ciclosphorin work?

A

1) Binds to cyclophilin
2) Blocks the activation of calcineurin
3) Nf kappa b remains in the cytosol
4) Pro-inflammatory response is reduced and some cytokine production is inhibited

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14
Q

Which drugs repress transcription of pro-inflammatory mediators in immune cells?

A

Ciclosphorin

Glucocoricoids

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15
Q

How do glucocorticoids work?

A

Enter cells and translocate into the NUCLEUS - regulate at the level of transcription of pro-inflammatory mediators

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16
Q

What is a ‘cytokine’ and what can they do?

What are examples of cytokines?

A

ANY protein or polypeptide MEDIATORS which are synthesised or released by cells of the immune system during INFLAMMATION

They can act DIRECTLY on cells or AMPLIFY inflammation by inducing the formation of OTHER inflammatory mediators

Examples:
IL-1

IL-2

TNF-alpha

TGF-beta

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17
Q

How can new drugs be developed that are more effective than glucocoticoids or ciclosphorin?

What are these new drugs called?

A

Can be developed to target SPECIFIC cytokines

Biopharmaceuticals

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18
Q

How do biopharmaceuticals delivered?

A

They are INJECTED

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19
Q

What molecules are biopharmaceuticals?

A

Peptides

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20
Q

How do biopharmaceuticals work?

A

They are SPECIFICALLY directed to pro-inflammatory cytokines with high affinity

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21
Q

What is a type of biopharmaceutical and how does it work?

A

Humanised monoclonal antibodies:

  • Bind to TNF alpha released from macrophages
  • Preventing it from activating other cell types which cause tissue damage
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22
Q

Why is is important that the Fc region of a humanised monoclonal antibody is the equivalent to that of a human antibody?

A

To prevent rejection

So that they are treated like normal antibodies

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23
Q

Why mimic the soluble receptors made for cytokines by the body?

A

To bind up cytokines and prevent them from binding to their receptors

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24
Q

What causes asthma?

A

Chronic inflammation of the airways

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25
Q

Why do the symptoms of asthma become greater overime?

A
  • Airways become sensitised
  • Smooth muscle controlling the airways expand and become more sensitive to triggers

(Bronchial hyper-activity becomes greater overtime)

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26
Q

What are the treatments of asthma?

A

1) Salbutamol (bronchodilator)

2) Glucocorticoids (anti-inflammatory agent)

27
Q

What causes a resistance to salbutamol?

A

1) Overuse of inhalers causing de-sensitisation of the receptors
2) Polymorphisms in the Beta-2 adrenoreceptors causing a reduction in efficacy of salbutamol

28
Q

What is the pathology of asthma?

A

1) Atopic trigger (allergen)
2) Airways constricted upon exposure, due to immune cells accumulating in the airways

3) Stronger response several hours later - inflammatory response
- Cytokines released

29
Q

What can the 2nd stage of asthma lead to?

A

Irreversible damage to the airways

30
Q

What are 4 common sources of INHALED allergens?

A

1) Mold spores
2) Plant pollen
3) Faeces of dust mites
4) Animal fur

31
Q

What is hayfever classified as?

A

Asthma

32
Q

What kind of drugs are used to treat asthma and why?

A

Similar to drugs which are used to treat inflammation in other parts of the body

As asthma is classified as inflammation of the upper airways

33
Q

What determines what allergic disease you will have?

A

How the allergen gets into the body

34
Q

What ways can allergens get into the body?

A

1) Inhalation
2) Injection
3) Ingestation
4) Contact

35
Q

Examples of allergens which can be injected?

A

Venoms

Vaccines/drugs

36
Q

Examples of allergens which can be ingested?

A

Food

Orally administered drugs

37
Q

Examples of allergens which can be contacted?

A

Plant leaves (eg. stinging nettles)
Metals
Synthetic chemicals in industrial products

38
Q

How is it tested if you have an allergy?

Asthma?

A

Inject allergens underneath the skin

If have asthma - will also have a reaction to these allergens underneath the skin

39
Q

What is igE-mediated hypersensitivity?

A

Allergies

40
Q

What antibodies are produced against allergens?

A

igE class

41
Q

What are examples of allergies?

A

1) Asthma
2) Hayfever
3) Eczema
4) Hives
5) Food allergy
6) Systemic anaphylaxis

42
Q

What is the ‘scientific name’ for hayfever?

A

Allergic rhinitis

43
Q

Describe the igE-mediated response to allergens

A

1) Individual has compromised barriers combined with genetic predisposition
2) Allergen gets into the body and is recognised as foreign
3) Individual becomes sensitised (2-3 weeks) and has lots of igE to that particular allergen

4) IgE antibodies bind specifically and tightly to igE Fc receptors on:
- Mast cells (skin and mucus surfaces)
- Basophils (blood)
- Activated eosionophils (circulating immune cells

5) When RE-EXPOSED to an the same allergen:
- Cross-linking of IgE by allergen on mast cell surfaces
- Triggers the release of INFLAMMATORY mediators

44
Q

What are they key mediators in type 1 hypersensitivity reactions?

A

Mast cells

45
Q

What is the NORMAL function of mast cells?

A

To release granules when activated to fight PARASITIC INFECTIONS

46
Q

In hayfever, where are the mast cells activated?

A

UPPER airways

47
Q

In allergic asthma, where are the mast cells activated?

A

LOWER airways

48
Q

What is the ‘early-phase’ reactions of allergic asthma characterised by?

What causes this?

A

Characterised by:
- REVERSIBLE airway obstruction and inflammation

Caused by:

  • Increased number of mast cells in the bronchi
  • Release of HISTAMINE and PROSTANOIDS from these mast cells
49
Q

What percentage of patients with allergic asthma suffer from a ‘late-phase’ reaction?

A

50%

50
Q

What happens in the ‘late-phase” of allergic asthma?

A

1) Activation of mast cells causes recruitment and activation of further immune cells to the area - causes INFLAMMATION
2) These immune cells make DAMAGING mediators
3) Cytokines cause LEUKOCYE infiltration (esp. of eosinophils)

51
Q

What happens if the ‘late-phase’ of allergic asthma is not controlled?

A

Leads to chronic asthma and tissue damage

52
Q

What cells is asthma associated with?

How is this different to rheumatoid arthritis?

A

Overactivity of TH2 cells

In RA - TH1 cells involved

53
Q

What do TH2 cells do?

A

Activate cells that make the igE antibodies through the release of cytokines

54
Q

How is asthma treated and how is the late phase reaction controlled?

A

By controlling the synthesis of cytokines

For example, with glucocorticoids

55
Q

What are pro-inflammatory mediators?

A

Mediators which PROmote inflammation

56
Q

What are genetic factors which can alter the susceptibility to allergy?

A

IgE production
Gender
Age
Hyper-responsiveness

57
Q

What are environmental factors which can alter the susceptibility to allergy?

A

Nutrition
Pollutants
Family sizes

58
Q

What do inflammatory mediators cause to happen?

A

1) Smooth muscle contraction
2) Increased vascular permeability
3) Mucous secretion
4) Platelet aggregation
5) Stimulation of nerve endings
6) Recruitment and activation of eosinophils

59
Q

What is the pathology associated with inflammation of the airways? (characteristics)

A

1) Thickened basement membrane
2) Mucus with eosinophils
3) Infiltration of inflammatory cells
4) Odema (swelling)

60
Q

What are new therapies for treating asthma?

A

1) Humanises antibodies and soluble receptors to IgE and cytokines
2) PGD2 receptor antagonists
3) Inhibitors of immune cells and mast cell signalling

61
Q

What are humanised antibodies for soluble receptors for IgE?

A

Omalizumab

62
Q

What are humanised antibodies for soluble receptors for cytokines?

A

Biopharmaceuticals

63
Q

Do all DMARDs have the same action?

A

No

64
Q

What do DMARDs do?

A

Reduce symptoms of a disease AND slow disease progression

bms 242 - core phys/pharm (13 decks)

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