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

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

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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
AEs of Rituximab?
Risk of infection as B cells destroyed
26
How long does Rituximab take before positive effect? [1]
3 months after infusions
27
Describe MoA of Abatacept
**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
Tocilizumab targets which IL? [1] Describe MoA [2]
**Interleukin 6** Monoclonal antibody that binds to **IL-6 cytokine before it reaches target receptor**
29
What drug class is the first oral biological? [1]
JAK inhibitors
30
State three JAK inhibitors used to treat RA [3]
Tofacitinib, baricitinib and upadacitinib
31
Describe the MoA of JAK inhibitors
Targets **Janus kinase (JAK) pathways**: means that **multipe cytokines are blocked**
32
Describe the MoA of JAK inhibitors
**Targets Janus kinase (JAK) pathways**: means that **multipe cytokines are blocked**
33
State why biologicals, despire their efficacy are not used straight away for RA treatment? [2]
Due to the develop of **anti-drug antibodies** that will develop no matter what - **decrease** **efficacy**
34
Explain the mechanism of neutralising ADAs [2] & non-neutralising ADAs [2]
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 f**orm immune complexes around injection site** **reducing** drug **concentration** and **pharmacokinetics** Increased clearance
35
36
# RA Methotrexate and Rituximab would be First line treatment Second line treatment Third line treatment Fourth line treatment
**Third line treatment**
37
# RA Methotrexate and a 2nd line DMARD would be First line treatment Second line treatment Third line treatment Fourth line treatment
**First line treatment**
38
# RA Methotrexate & a TNF-inhibitor would be First line treatment Second line treatment Third line treatment Fourth line treatment
**Second line treatment**
39
Methotrexate inhibits which enzyme? [1]
**dihydrofolate reductase**
40
# RA Sulfasalazine is a prodrug for [1]
**5-ASA**
41
Hydroxychloroquine blocks: TLR7 TLR8 TLR9 TLR10 TLR11
**TLR9**
42
# RA Leflunomide inhibits which enzyme? [1] What is the effect of this? [2]
**Dihydroorotate dehydrogenase (DHODH)**: **stops** **pyrimidine** **synthesis** & therefore reduces pro-inflammatory cytokines: IL-1, TNF-A and IL-6; Blocks T cell proliferation
43
Which is the staple treatment for RA? Methotrexate Sulfasalazine Hydroxychloroquine Leflunomide Infliximab
Which is the staple treatment for RA? **Methotrexate** Sulfasalazine Hydroxychloroquine Leflunomide Infliximab
44
Which treatment for RA inhibits dihydrofolate reductase? Methotrexate Sulfasalazine Hydroxychloroquine Leflunomide Infliximab
Which treatment for RA inhibits dihydrofolate reductase? **Methotrexate** Sulfasalazine Hydroxychloroquine Leflunomide Infliximab
45
Which treatment for RA reduces purine synthesis? Methotrexate Sulfasalazine Hydroxychloroquine Leflunomide Infliximab
**Methotrexate**
46
Which treatment for RA reduces pyrimidine synthesis? Methotrexate Sulfasalazine Hydroxychloroquine Leflunomide Infliximab
**Leflunomide**
47
Which treatment for RA is safe for pregnant people? Methotrexate Sulfasalazine Hydroxychloroquine Leflunomide Infliximab
**Sulfasalazine**
48
Which treatment for RA is prodrug that operates in large intestine? Methotrexate Sulfasalazine Hydroxychloroquine Leflunomide Infliximab
Which treatment for RA is prodrug that operates in large intestine? Methotrexate **Sulfasalazine** Hydroxychloroquine Leflunomide Infliximab
49
Which treatment for RA that targets TLR-9? Methotrexate Sulfasalazine Hydroxychloroquine Leflunomide Infliximab
**Hydroxychloroquine**
50
Which treatment for RA that reduces dendritic cell activation? Methotrexate Sulfasalazine Hydroxychloroquine Leflunomide Infliximab
**Hydroxychloroquine**
51
Which is a treatment for RA that inhibits dihydro-orotate dehydrogenase? Methotrexate Sulfasalazine Hydroxychloroquine Leflunomide Infliximab
**Hydroxychloroquine**
52
Which treatment for RA requires folate to be given alongside? Methotrexate Sulfasalazine Hydroxychloroquine Leflunomide Infliximab
**Methotrexate**
53
Which treatment for RA is a tumor necrosis factor-alpha (TNF-alpha) inhibitor? Methotrexate Sulfasalazine Hydroxychloroquine Leflunomide Infliximab
**Infliximab**
54
Which treatment for RA is a monoclonal antibody? Methotrexate Sulfasalazine Hydroxychloroquine Leflunomide Infliximab
**Infliximab**
55
Which treatment for RA is an anti-CD20 monoclonal antibody? Etanercept Adalimumab Anakinra Rituximab Abatacept Tolizumab
**Rituximab**
56
Which treatment for RA causes B cell depletion? Etanercept Adalimumab Anakinra Rituximab Abatacept Tolizumab
**Rituximab**
57
Which treatment for RA leads to decreased T-cell proliferation and cytokine production? Etanercept Adalimumab Anakinra Rituximab Abatacept Tolizumab
**Abatacept**
58
Which treatment for RA is an IL-1 antagonist? Etanercept Adalimumab Anakinra Rituximab Abatacept Tolizumab
**Anakinra**
59
Which treatment for RA targets IL-6? Etanercept Adalimumab Anakinra Rituximab Abatacept Tolizumab
**Tolizumab**
60
Which treatment for RA targets upregulates CTLA-4, which switches T cell off? Etanercept Adalimumab Anakinra Rituximab Abatacept Tolizumab
**Tolizumab**

LOCO2 (58 decks)

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