Immunomodulators and anti-inflammatories Flashcards

1
Q

Ciclosporin

A

Calcineurin inhibitor

Ciclosporin and tacrolimus form complexes with cytoplasmic immunophilins (cyclophilin and FKBP‑12, respectively), which block the action of calcineurin in activated T cells. This prevents production of interleukin‑2 and other cytokines, which normally stimulate T cell proliferation and differentiation.

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2
Q

Tacrolimus

A

Calcineurin inhibitor

Ciclosporin and tacrolimus form complexes with cytoplasmic immunophilins (cyclophilin and FKBP‑12, respectively), which block the action of calcineurin in activated T cells. This prevents production of interleukin‑2 and other cytokines, which normally stimulate T cell proliferation and differentiation.

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3
Q

Betamethasone

A

Corticosteroid

Corticosteroids regulate gene expression, which results in:

glucocorticoid effects, eg gluconeogenesis, proteolysis, lipolysis, suppression of inflammation and immune responses
mineralocorticoid effects, eg hypertension, sodium and water retention, potassium loss.

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4
Q

Dexamethasone

A

Corticosteroid

Corticosteroids regulate gene expression, which results in:

glucocorticoid effects, eg gluconeogenesis, proteolysis, lipolysis, suppression of inflammation and immune responses
mineralocorticoid effects, eg hypertension, sodium and water retention, potassium loss.

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5
Q

Hydrocortisone

A

Corticosteroid

Corticosteroids regulate gene expression, which results in:

glucocorticoid effects, eg gluconeogenesis, proteolysis, lipolysis, suppression of inflammation and immune responses
mineralocorticoid effects, eg hypertension, sodium and water retention, potassium loss.

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6
Q

Methylprednisolone

A

Corticosteroid

Corticosteroids regulate gene expression, which results in:

glucocorticoid effects, eg gluconeogenesis, proteolysis, lipolysis, suppression of inflammation and immune responses
mineralocorticoid effects, eg hypertension, sodium and water retention, potassium loss.

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7
Q

Prednisolone/prednisone

A

Corticosteroid

Corticosteroids regulate gene expression, which results in:

glucocorticoid effects, eg gluconeogenesis, proteolysis, lipolysis, suppression of inflammation and immune responses
mineralocorticoid effects, eg hypertension, sodium and water retention, potassium loss.

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8
Q

Triamcinolone

A

Corticosteroid

Corticosteroids regulate gene expression, which results in:

glucocorticoid effects, eg gluconeogenesis, proteolysis, lipolysis, suppression of inflammation and immune responses
mineralocorticoid effects, eg hypertension, sodium and water retention, potassium loss.

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9
Q

Antithymocyte globulins

A

Immunosuppressant antibodies

Polyclonal purified horse or rabbit antibodies against human lymphocytes that reduce the number of T lymphocytes in the circulation. Products may also contain small amounts of antibodies with cross-reactivity against other elements of blood.

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10
Q

Basiliximab

A

Binds to CD25 antigen on activated T lymphocytes, blocking the binding of interleukin‑2 and inhibiting T lymphocyte proliferation.

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11
Q

Baricitinib

A

Cytokine modulator

Inhibits Janus kinase (JAK) 1 and 2, suppressing immune response.

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12
Q

Tofacitinib

A

Cytokine modulator

Inhibits Janus kinase (JAK) 1, 2 and 3, suppressing immune response.

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13
Q

Upadacitinib

A

Cytokine modulator

Primarily inhibits Janus kinase (JAK) 1, suppressing immune response.

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14
Q

Everolimus

A

mTOR

Bind to the same intracellular protein (FKBP‑12) as tacrolimus; however, the protein-drug complex blocks the activity of mTOR kinase, preventing cell cycle progression and cytokine-induced T and B cell proliferation.

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15
Q

Sirolimus

A

mTOR

Bind to the same intracellular protein (FKBP‑12) as tacrolimus; however, the protein-drug complex blocks the activity of mTOR kinase, preventing cell cycle progression and cytokine-induced T and B cell proliferation.

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16
Q

Adalimumab

A

TNF-alpha antagonist

Bind to TNF alpha and inhibit its activity. TNF alpha is a cytokine involved in inflammatory and immune responses and in the pathogenesis of diseases such as psoriasis, rheumatoid and psoriatic arthritis, ankylosing spondylitis and inflammatory bowel disease.

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17
Q

Certolizumab

A

TNF-alpha antagonist

Bind to TNF alpha and inhibit its activity. TNF alpha is a cytokine involved in inflammatory and immune responses and in the pathogenesis of diseases such as psoriasis, rheumatoid and psoriatic arthritis, ankylosing spondylitis and inflammatory bowel disease.

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18
Q

Etanercept

A

TNF-alpha antagonist

Bind to TNF alpha and inhibit its activity. TNF alpha is a cytokine involved in inflammatory and immune responses and in the pathogenesis of diseases such as psoriasis, rheumatoid and psoriatic arthritis, ankylosing spondylitis and inflammatory bowel disease.

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19
Q

Golimumab

A

TNF-alpha antagonist

Bind to TNF alpha and inhibit its activity. TNF alpha is a cytokine involved in inflammatory and immune responses and in the pathogenesis of diseases such as psoriasis, rheumatoid and psoriatic arthritis, ankylosing spondylitis and inflammatory bowel disease.

20
Q

Infliximab

A

TNF-alpha antagonist

Bind to TNF alpha and inhibit its activity. TNF alpha is a cytokine involved in inflammatory and immune responses and in the pathogenesis of diseases such as psoriasis, rheumatoid and psoriatic arthritis, ankylosing spondylitis and inflammatory bowel disease.

21
Q

Abatacept

A

Cytokine modulator

Co-stimulation modulator; binds to CD80 and CD86 on antigen-presenting cells, which prevents full activation of CD28 T lymphocytes, thus reducing cytokine production and inflammation.

22
Q

Anakinra

A

Cytokine modulator

Recombinant form of human interleukin‑1 (IL‑1) receptor antagonist; it neutralises the activity of IL‑1, which is involved in acute inflammatory response.

23
Q

Auranofin

A

Gold salt

Exact mode of action is unclear; auranofin has anti-inflammatory and immunomodulating effects.

24
Q

Azathioprine

A

Immunomodulator

Purine antimetabolite. Azathioprine is metabolised, via mercaptopurine, to thioguanine nucleotides which interfere with purine synthesis, impairing lymphocyte proliferation, cellular immunity and antibody responses.

25
Q

Belimumab

A

Cytokine modulator

Inhibits B lymphocyte stimulator protein (which is over-expressed in systemic lupus erythematosus (SLE)); reduces B cell survival and differentiation into immunoglobulin-producing plasma cells.

26
Q

Hydroxychloroquine

A

Anti-inflammatory. May also have immunosuppressive effects.

27
Q

Leflunomide

A

Inhibits pyrimidine synthesis in leucocytes and other rapidly dividing cells by inhibiting activity of dihydro-orotate dehydrogenase. It has immunosuppressive, immunomodulating and antiproliferative properties. Also has uricosuric effects.

28
Q

Methotrexate

A

Mechanism of immunomodulatory effects in autoimmune diseases is unclear and may differ from its action as a folic acid antagonist in cancer treatment; it suppresses inflammation and immune responses.

29
Q

Mycophenolate

A

Mycophenolate mofetil and mycophenolate sodium are both converted to mycophenolic acid, which selectively suppresses lymphocyte proliferation and antibody formation by inhibiting inosine monophosphate dehydrogenase. Depletion of guanosine nucleotides (required for de novo purine synthesis in lymphocytes) results.

Acts on the immune system at a similar level to azathioprine but by a distinct and more lymphocyte-selective mode of action.

30
Q

Tocilizumab

A

Binds to and inhibits the activity of interleukin‑6 (IL‑6), a cytokine involved in the pathogenesis of inflammatory diseases such as rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA) and giant cell arteritis (GCA).

31
Q

Celecoxib

A

Selective COX-2 inhibitor NSAID

Have analgesic, antipyretic and anti-inflammatory actions. They inhibit synthesis of prostaglandins by inhibiting cyclo-oxygenase (COX) present as COX‑1 and COX‑2:

inhibition of COX‑1 results in impaired gastric cytoprotection and antiplatelet effects
inhibition of COX‑2 results in anti-inflammatory and analgesic action
reduction in glomerular filtration rate and renal blood flow occurs with both COX‑1 and COX‑2 inhibition.

32
Q

Diclofenac

A

Nonselective NSAID

Have analgesic, antipyretic and anti-inflammatory actions. They inhibit synthesis of prostaglandins by inhibiting cyclo-oxygenase (COX) present as COX‑1 and COX‑2:

inhibition of COX‑1 results in impaired gastric cytoprotection and antiplatelet effects
inhibition of COX‑2 results in anti-inflammatory and analgesic action
reduction in glomerular filtration rate and renal blood flow occurs with both COX‑1 and COX‑2 inhibition.

33
Q

Etoricoxib

A

Selective COX-2 inhibitor NSAID

Have analgesic, antipyretic and anti-inflammatory actions. They inhibit synthesis of prostaglandins by inhibiting cyclo-oxygenase (COX) present as COX‑1 and COX‑2:

inhibition of COX‑1 results in impaired gastric cytoprotection and antiplatelet effects
inhibition of COX‑2 results in anti-inflammatory and analgesic action
reduction in glomerular filtration rate and renal blood flow occurs with both COX‑1 and COX‑2 inhibition.

34
Q

Iburofen

A

Nonselective inhibitor NSAID

Have analgesic, antipyretic and anti-inflammatory actions. They inhibit synthesis of prostaglandins by inhibiting cyclo-oxygenase (COX) present as COX‑1 and COX‑2:

inhibition of COX‑1 results in impaired gastric cytoprotection and antiplatelet effects
inhibition of COX‑2 results in anti-inflammatory and analgesic action
reduction in glomerular filtration rate and renal blood flow occurs with both COX‑1 and COX‑2 inhibition.

35
Q

Indomethacin

A

Nonselective inhibitor NSAID

Have analgesic, antipyretic and anti-inflammatory actions. They inhibit synthesis of prostaglandins by inhibiting cyclo-oxygenase (COX) present as COX‑1 and COX‑2:

inhibition of COX‑1 results in impaired gastric cytoprotection and antiplatelet effects
inhibition of COX‑2 results in anti-inflammatory and analgesic action
reduction in glomerular filtration rate and renal blood flow occurs with both COX‑1 and COX‑2 inhibition.

36
Q

Ketoprofen

A

Nonselective inhibitor NSAID

Have analgesic, antipyretic and anti-inflammatory actions. They inhibit synthesis of prostaglandins by inhibiting cyclo-oxygenase (COX) present as COX‑1 and COX‑2:

inhibition of COX‑1 results in impaired gastric cytoprotection and antiplatelet effects
inhibition of COX‑2 results in anti-inflammatory and analgesic action
reduction in glomerular filtration rate and renal blood flow occurs with both COX‑1 and COX‑2 inhibition.

37
Q

Ketorolac

A

Nonselective inhibitor NSAID

Have analgesic, antipyretic and anti-inflammatory actions. They inhibit synthesis of prostaglandins by inhibiting cyclo-oxygenase (COX) present as COX‑1 and COX‑2:

inhibition of COX‑1 results in impaired gastric cytoprotection and antiplatelet effects
inhibition of COX‑2 results in anti-inflammatory and analgesic action
reduction in glomerular filtration rate and renal blood flow occurs with both COX‑1 and COX‑2 inhibition.

38
Q

Mefenamic acid

A

Nonselective inhibitor NSAID

Have analgesic, antipyretic and anti-inflammatory actions. They inhibit synthesis of prostaglandins by inhibiting cyclo-oxygenase (COX) present as COX‑1 and COX‑2:

inhibition of COX‑1 results in impaired gastric cytoprotection and antiplatelet effects
inhibition of COX‑2 results in anti-inflammatory and analgesic action
reduction in glomerular filtration rate and renal blood flow occurs with both COX‑1 and COX‑2 inhibition.

39
Q

Meloxicam

A

COX-2 selective inhibitor NSAID

Have analgesic, antipyretic and anti-inflammatory actions. They inhibit synthesis of prostaglandins by inhibiting cyclo-oxygenase (COX) present as COX‑1 and COX‑2:

inhibition of COX‑1 results in impaired gastric cytoprotection and antiplatelet effects
inhibition of COX‑2 results in anti-inflammatory and analgesic action
reduction in glomerular filtration rate and renal blood flow occurs with both COX‑1 and COX‑2 inhibition.

40
Q

Naproxen

A

Nonselective inhibitor NSAID

Have analgesic, antipyretic and anti-inflammatory actions. They inhibit synthesis of prostaglandins by inhibiting cyclo-oxygenase (COX) present as COX‑1 and COX‑2:

inhibition of COX‑1 results in impaired gastric cytoprotection and antiplatelet effects
inhibition of COX‑2 results in anti-inflammatory and analgesic action
reduction in glomerular filtration rate and renal blood flow occurs with both COX‑1 and COX‑2 inhibition.

41
Q

Parecoxib

A

COX-2 selective inhibitor NSAID

Have analgesic, antipyretic and anti-inflammatory actions. They inhibit synthesis of prostaglandins by inhibiting cyclo-oxygenase (COX) present as COX‑1 and COX‑2:

inhibition of COX‑1 results in impaired gastric cytoprotection and antiplatelet effects
inhibition of COX‑2 results in anti-inflammatory and analgesic action
reduction in glomerular filtration rate and renal blood flow occurs with both COX‑1 and COX‑2 inhibition.

42
Q

Piroxicam

A

Nonselective inhibitor NSAID

Have analgesic, antipyretic and anti-inflammatory actions. They inhibit synthesis of prostaglandins by inhibiting cyclo-oxygenase (COX) present as COX‑1 and COX‑2:

inhibition of COX‑1 results in impaired gastric cytoprotection and antiplatelet effects
inhibition of COX‑2 results in anti-inflammatory and analgesic action
reduction in glomerular filtration rate and renal blood flow occurs with both COX‑1 and COX‑2 inhibition.

43
Q

Allopurinol

A

Xanthine oxidase inhibitor

Inhibit xanthine oxidase which reduces production of uric acid, lowering serum urate concentration and allowing acute flares and crystal deposits to resolve if long-term serum urate <0.36 mmol/L.

44
Q

Febuxostat

A

Xanthine oxidase inhibitor

Inhibit xanthine oxidase which reduces production of uric acid, lowering serum urate concentration and allowing acute flares and crystal deposits to resolve if long-term serum urate <0.36 mmol/L.

45
Q

Colchicine

A

Reduces inflammation: inhibits neutrophil migration, chemotaxis, adhesion and phagocytosis in inflamed tissue, eg in gout it reduces inflammatory reaction to urate crystals.

46
Q

Probenecid

A

Increases renal excretion of uric acid by blocking its renal tubular reabsorption (uricosuric). Reduces the renal tubular excretion of some acidic drugs (eg penicillins), increasing their plasma concentration and prolonging their duration of action.