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LOCO2 > Disease Modifying Anti-rheumatics (DMARD) (+ 25qs) > Flashcards

Disease Modifying Anti-rheumatics (DMARD) (+ 25qs) Flashcards

1
Q

OA - fill in about colexcicb

A
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2
Q

State the treatment pyramid for RA:

Pain management: [2]

First line disease treament (Mild RA): [2]

Second line disease treatment (moderate RA) [2]

Second line disease management: (severe RA) [2]

A

Pain management: NSAID & Opioids

First line: Methotrexate & 2nd line DMARD

Second line disease treatment (moderate RA) Methotrexate & TNF-inhibitor

Second line disease management: (severe RA) Methotrexate & Rituximab

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3
Q

If have a flair of RA which drug might be used as adjunct therapy? [1]

A

Oral corticosteroid pulse (e.g. prednisilone)

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4
Q

How may you start DMARD treatment if have severe RA? [2]

A

Start with high dose and taper down once under control

OR

Add prednisilone

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5
Q

State 3 reasons why may not prescribe methotrexate [3]

A

Liver damage (methotrexate metabolised in liver)
Pregnant
Co-morbidities

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6
Q

State two factors that DMARDs improve [2]

What does DMARD not improve? [1]

A

Improves:
* early improves number of swollen
* improves radiographic progression

No effect:
* the patients fatigue severity

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7
Q

Explain MoA of methotrexate [4]

How is it administered? [1]

A

Oral dose (can change to subcut. or IM)

MoA:
* Folic acid antagonist which will limits DNA and RNA synthesis by inhibiting dihydrofolate reductase and thymidylate synthetase
* Causes a reduction in purine synthesis
* Induce ROS
* Causes activation of apoptosis
* Inhibits pro-inflam cytokines IL-1 & NF-kB

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8
Q

State three side effects of methotrexate [2]

A

Can cause liver problems
Can affect blood count
Hair

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9
Q

Describe MoA of Sulfasalazine [5]

A

Mode of action in RA not well understood:
* Metabolised in the colon by gut bacteria to 5-ASA
* 5-ASA stays in large intestine lamina propria and has local anti-inflammatory actions
* Supresses generation of superoxide radicals and cytokine production by inflammatory cells
* IL8 decreased in synovial fluid and decreased production of IgM and IgG, and decreased angiogenesis
* Inhibits IL-1 and TNF-a

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10
Q

Describe the MoA of Hydroxychloroquine [2]

A
  • Accumulates in lysosomes increasing the pH decreasing protein modifications
  • Blocks Toll-like receptor 9 which recognises DNA containing immune complexes decreases activation of dendritic cells: less autoantobodies produced
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11
Q

Describe MoA of Leflunomide [3]

A

Pro-drug: gets metabolised in liver

Inhibits dihydroorotate dehydrogenase (DHODH) and therefore stops pyrimidine biosynthesis

Reduces pro-inflammatory cytokines: IL-1, TNF-A and IL-6

Blocks T cell proliferation

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12
Q

leflunomide has a similar mechanism of action to

Etanercept
Infliximab
Methotrexate
Sulfasalazine
Hydroxychloroquine

A

Methotrexate

Both block block on RNA and DNA synthesis via different, synergestic pathways

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13
Q

State which of the following blocks pyrimidine or purine synthesis:

Methotrexate
Leflunomide

A

Methotrexate: stops purine synthesis
Leflunomide: stops pyrimidine synthesis

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14
Q

Name two TNF-a blockers for RA [2]

A

Etanercept
Infliximab

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15
Q

Explain MoA of Etanercept:

What is etanercept a fusion protein for? [1]

What is etanercept Fc for? [1]

A

When TNF-a is released: finds receptors on cells, activates and causes signal transduction

Etanercept is a fusion protein human TNF receptor 2 and Fc human IgG.

Etanercept binds to TNF-a before TNF-a can get to cell and cause inflammatory, signalling

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16
Q

Describe MoA of Infliximab [1]

A

Monoclonal antibody against TNFα

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17
Q

Which of the following acts quicker:

Infliximab
Etanercept

A

Infliximab
Etanercept

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18
Q

Infliximab often prescribed alongside which drug? [1]

A

Infliximab and methotrexate

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19
Q

Name another TNF-inhibitor used in RA [1]

A

Adalimumab

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20
Q

Name a Human recombinant IL-1 receptor antagonist to treat RA

A

Anakinra

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21
Q

Describe efficacy of IL-1 antagonists c.f TNF-alpha blockers

A

IL-1 receptors antagonists are not as effective in RA as TNF-alpha blockers

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22
Q

Despite good efficacy, why is Anakina not as commonly prescribed for RA? [1]

A

Requires subcut daily injections

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23
Q

Describe MoA of Anakinra [1]

A

Monoclonal antibody that is a IL-1 antagonist

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24
Q

Describe MoA of Rituximab

A

Monoclonal antibody that targets CD20 on B cells

Means B cell can’t become activated

Destroys normal and malignant B cells

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25
Q

AEs of Rituximab?

A

Risk of infection as B cells destroyed

26
Q

How long does Rituximab take before positive effect? [1]

A

3 months after infusions

27
Q

Describe MoA of Abatacept

A

Blocks T cell activation which thus means macrophages and B cells cannot be activated.

Competes with CD28 binding to CD80/86 by upregulating CTLA-4, which switches T cell off

Reduces production of TH17 cells
Thus reducing inflammation

28
Q

Tocilizumab targets which IL? [1]

Describe MoA [2]

A

Interleukin 6

Monoclonal antibody that binds to IL-6 cytokine before it reaches target receptor

29
Q

What drug class is the first oral biological? [1]

A

JAK inhibitors

30
Q

State three JAK inhibitors used to treat RA [3]

A

Tofacitinib, baricitinib and upadacitinib

31
Q

Describe the MoA of JAK inhibitors

A

Targets Janus kinase (JAK) pathways: means that multipe cytokines are blocked

32
Q

Describe the MoA of JAK inhibitors

A

Targets Janus kinase (JAK) pathways: means that multipe cytokines are blocked

33
Q

State why biologicals, despire their efficacy are not used straight away for RA treatment? [2]

A

Due to the develop of anti-drug antibodies that will develop no matter what - decrease efficacy

34
Q

Explain the mechanism of neutralising ADAs [2] & non-neutralising ADAs [2]

A

Because they are chimeric / humanised antigens you get anti-drug antibodies:

Neutralising ADA
* Directly interferes with the biological drugs ability to work
* Bind to the antibody/biological directly and stop it being able to bind to TNF-alpha, IL-1, etc

Non-neutralising ADA
* May form immune complexes around injection site reducing drug concentration and pharmacokinetics
Increased clearance

35
Q
A
36
Q

RA

Methotrexate and Rituximab would be

First line treatment
Second line treatment
Third line treatment
Fourth line treatment

A

Third line treatment

37
Q

RA

Methotrexate and a 2nd line DMARD would be

First line treatment
Second line treatment
Third line treatment
Fourth line treatment

A

First line treatment

38
Q

RA

Methotrexate & a TNF-inhibitor would be

First line treatment
Second line treatment
Third line treatment
Fourth line treatment

A

Second line treatment

39
Q

Methotrexate inhibits which enzyme? [1]

A

dihydrofolate reductase

40
Q

RA

Sulfasalazine is a prodrug for [1]

A

5-ASA

41
Q

Hydroxychloroquine blocks:

TLR7
TLR8
TLR9
TLR10
TLR11

A

TLR9

42
Q

RA

Leflunomide inhibits which enzyme? [1]

What is the effect of this? [2]

A

Dihydroorotate dehydrogenase (DHODH): stops pyrimidine synthesis & therefore reduces pro-inflammatory cytokines: IL-1, TNF-A and IL-6; Blocks T cell proliferation

43
Q

Which is the staple treatment for RA?

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab

A

Which is the staple treatment for RA?

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab

44
Q

Which treatment for RA inhibits dihydrofolate reductase?

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab

A

Which treatment for RA inhibits dihydrofolate reductase?

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab

45
Q

Which treatment for RA reduces purine synthesis?

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab

A

Methotrexate

46
Q

Which treatment for RA reduces pyrimidine synthesis?

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab

A

Leflunomide

47
Q

Which treatment for RA is safe for pregnant people?

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab

A

Sulfasalazine

48
Q

Which treatment for RA is prodrug that operates in large intestine?

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab

A

Which treatment for RA is prodrug that operates in large intestine?

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab

49
Q

Which treatment for RA that targets TLR-9?

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab

A

Hydroxychloroquine

50
Q

Which treatment for RA that reduces dendritic cell activation?

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab

A

Hydroxychloroquine

51
Q

Which is a treatment for RA that inhibits dihydro-orotate dehydrogenase?

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab

A

Hydroxychloroquine

52
Q

Which treatment for RA requires folate to be given alongside?

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab

A

Methotrexate

53
Q

Which treatment for RA is a tumor necrosis factor-alpha (TNF-alpha) inhibitor?

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab

A

Infliximab

54
Q

Which treatment for RA is a monoclonal antibody?

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide
Infliximab

A

Infliximab

55
Q

Which treatment for RA is an anti-CD20 monoclonal antibody?

Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab

A

Rituximab

56
Q

Which treatment for RA causes B cell depletion?

Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab

A

Rituximab

57
Q

Which treatment for RA leads to decreased T-cell proliferation and cytokine production?

Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab

A

Abatacept

58
Q

Which treatment for RA is an IL-1 antagonist?

Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab

A

Anakinra

59
Q

Which treatment for RA targets IL-6?

Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab

A

Tolizumab

60
Q

Which treatment for RA targets upregulates CTLA-4, which switches T cell off?

Etanercept
Adalimumab
Anakinra
Rituximab
Abatacept
Tolizumab

A

Tolizumab

LOCO2 (58 decks)

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