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
State two long term risks pertaining to cyclophosphamide
- Increased risk of bladder cancer, leukaemia and lymphoma | - Risk of infertility, increasing with age
26
Why is sulphasalazine effective in acute and maintenance IBD treatment?
Poorly absorbed from the gut
27
What is the MoA of sulphasalazine?
Inhibits the release of IL-2 and inhibits T cell proliferation. Reduced chemotaxis and degranulation of neutrophils
28
State two adverse effects of sulphasalazine
N+V Hepatitis Myelosuppression
29
What are the two general MoAs of MAb's?
- Block substances | - Target specific cells
30
Give two examples of MAb's and their MoAs
- 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
Give an example of a fusion protein
Etanercept - Binds to TNFalpha
32
What is a risk in giving biologics that block TNFalpha? How can this risk be minimised?
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