Immunosuppression and DMARDs Flashcards

1
Q

Name four corticosteroids

A
Dexamethasone
Prednisalone
Betamethasone
Hydrocortisone
Fludrocortisone
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2
Q

What is the MoA of corticosteroids?

A

Affect T cells, B cells, macrophages and NK cells - bazuka

Supresses the immune response

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3
Q

State four side effects of corticosteroids

A
  • Cushing’s syndrome
  • Osteoporosis
  • Reduced growth
  • Teratogenic
  • Immunosuppression
  • Cataracts
  • Obesity (central)
  • Suppressed HPA axis
  • Thin skin
  • Emotional disturbance
  • Raised BP
  • Oedema
  • Increased cholesterol
  • Diabetes
  • Striae
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4
Q

State three conditions that methotrexate is used for

A
  • RA (gold standard)
  • Haematological malignancy
  • Crohn’s
  • Psoriasis
  • Abortion
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5
Q

What is the MoA of methotrexate for non-malignant disease?

A

Not entirely sure, but it’s not folate-related

Maybe inhibits the production of adenosine, and therefore prevents the activation of T cells

Reduces joint damage in RA which is why it’s loved

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6
Q

What is the MoA of methotrexate for malignant disease?

A

Folic acid antagonist

Therefore methotrexate inhibits the synthesis of DNA, RNA and proteins, interfering with the S phase of the cell cycle

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7
Q

What are the three ways that methotrexate can be administered?

A

PO
IM
SC

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8
Q

How does the half-life of methotrexate metabolites affect dosing?

A

The active metabolites of methotrexate have very long half-lives

Therefore take once a week

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9
Q

Why should NSAIDs be avoided in pts on methotrexate?

A

Displaces methotrexate off of plasma proteins can can lead to toxicity

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10
Q

What is the treatment given to pts with methotrexate toxicity?

A

Folinic acid

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11
Q

Stae three adverse effects of methotrexate

A

Generally well-tolerated

  • Mucositis and marrow suppression (both respond well to folic acid supplements)
  • Hepatitis
  • Pneumonitis
  • Risk of infection
  • Teratogenic
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12
Q

Name two uses for azathioprine

A
  • Maintenance therapy for SLE and vasculitis
  • IBD
  • Atopic dermatitis
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13
Q

What is the MoA of azathioprine?

A

Antimetabolite to reduce DNA and RNA synthesis

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14
Q

How does the metabolism of azathioprine affect prescribing?

A

Metabolised by TPMT, therefore have to test the pt for TPMT deficiency

Deficiency in TPMT can make the pt prone to rapd marrow suppression.

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15
Q

State two adverse effects of azathioprine

A
  • Bone marrow suppression
  • Increased risk of malignancy
  • Increased risk of infection
  • Hepatitis
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16
Q

Name two calcineurin inhibitors

A

Ciclosporin

Tacrolimus

17
Q

State two uses for calcineurin inhibitors

A
  • Transplantation
  • Atopic dermatitis
  • Psoriasis
18
Q

What is the MoA of calcineurin inhibitors?

A

Prevents the production of IL-2 by T-helper cells.

Therefore prevents T cell stimulation by IL-2.

19
Q

State a use for mycophenolate mofetil

A
  • Primarily used in transplants

- Induce remission, and maintenance therapy in lupus nephritis and vasculitis

20
Q

What is the MoA of mycophenolate mofetil?

A

Prodrug

Impairs B and T cell proliferation by impairing guanosine synthesis

21
Q

State two adverse effects of mycophenolate mofetil

A

N+V
Diarrhoea
Myelosuppression
Increased risk of infection

22
Q

How can cyclophosphamide be used in rheumatology?

A

Works in 10 days, therefore can be used to induce remission then give MMF or azathioprine for maintenance

23
Q

What is the MoA of cyclophosphamide?

A

Prodrug converted to the active metabolite in the liver.

Alkylating agent

24
Q

What is acrolein, and how can pts taking cyclophosphamide be protected from it?

A

Bad metabolite that it toxic to the bladder epithellium.
Can cause haemorrhagic cystitis.

Give MENSA to mop up acrolein

25
Q

State two long term risks pertaining to cyclophosphamide

A
  • Increased risk of bladder cancer, leukaemia and lymphoma

- Risk of infertility, increasing with age

26
Q

Why is sulphasalazine effective in acute and maintenance IBD treatment?

A

Poorly absorbed from the gut

27
Q

What is the MoA of sulphasalazine?

A

Inhibits the release of IL-2 and inhibits T cell proliferation.

Reduced chemotaxis and degranulation of neutrophils

28
Q

State two adverse effects of sulphasalazine

A

N+V
Hepatitis
Myelosuppression

29
Q

What are the two general MoAs of MAb’s?

A
  • Block substances

- Target specific cells

30
Q

Give two examples of MAb’s and their MoAs

A
  • Adalimumab blocks TNFalpha to reduce inflammation, angiogenesis and joint destruction
  • Rituximab binds to CD20 on specific B cells to induce their apoptosis, leads to reduces Ab production, atigen presentation and cytokines.
31
Q

Give an example of a fusion protein

A

Etanercept - Binds to TNFalpha

32
Q

What is a risk in giving biologics that block TNFalpha? How can this risk be minimised?

A

TNFalpha is used to maintain granulomas.
TNFalpha blockers can cause the breakdown of granulomas, and therefore reactivation of TB

Before giving, screen for latent TB