Musculoskeletal: Rheumatic disease, suppressing drugs Flashcards

1
Q

Unlike NSAIDs, which are used only for symptom control, disease-modifying anti-rheumatic drugs (DAMRDs) can affect the progression of disease but may require how many months of treatment for a full therapeutic response?

A

2-6 months.

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2
Q

Methotrexate, sulfasalazine, intramuscular gold, and penicllamine are similar in efficacy - which may be better tolerated?

A

Methotrexate or sulfasalazine.

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3
Q

A combination of DMARDs (including methotrexate and at least one other DMARD) and a short-term corticosteroid, should be given to patients with newly diagnosed active RA, ideally within how long of the onset of peristent symptoms?

A

A combination of DMARDs (including methotrexate and at least one other DMARD) and a short-term corticosteroid, should be given to patients with newly diagnosed active rheumatoid arthritis, ideally within 3 months of the onset of persistent symptoms.

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4
Q

Gold and penicillamine are particularly useful in what form of rhuematism?

A

Palindromic rheumatism: a rare episodic form of inflammatory arthritis – meaning the joint pain and swelling come and go. Between attacks, the symptoms disappear and the affected joints go back to normal, with no lasting damage.

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5
Q

Systemic and discoid lupus erythematosus are sometimes treated with what?

A

Chloroquine or hydroxychloroquine sulfate.

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6
Q

After how long should a DMARD be replaced by a new one if it does not lead to an objective benefit?

A

6 months

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7
Q

Gold is given as what for active progressive rheumatoid arthritis? What route?

A

Gold is given as sodium aurothiomalate via deep intramuscular injection with the area then gently massaged.

A test dose must be given followed by doses at weekly intervals until there is definite evidence of remission.

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8
Q

In patients who do respond to deep intramuscular injections of sodium aurothiomalate the interval between injections is then gradually increased to what and how long is treatment continued for after complete remission?

A

Increased to 4 week intervals and continued for up to 5 years after complete remission.

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9
Q

How does gold (sodium aurothiomalate) work in RA?

A

Unknown, thought to be due to decreased T cell activation and inhibits proteolytic enzymes and can result in the destruction of synovial fibrolasts.

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10
Q

Penicillamine has a similar action to gold but more patients are able to continue treatment than with gold but side-effects are common.

Patients should be warned not to expect improvement for at least how long after treatment initiation?

A

6-12 weeks.

Pencillamine should be discontinued if there is no improvement within 1 year.

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11
Q

Sulfasalazine has a beneficial effect in suppressing the inflammatory activity of RA.

What abnormalities occur usually in the first 3 to 6 months of treatment and reversible on cessation of treatment?

A

Sulfasalazine causes haematological abnormalities usually in the first 3-6 months of treatment and are reversible on cessation of treatment:

Megaloblastic anaemia etc.

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12
Q

Certain antimalarials have a place in RA treatment, what are they?

A

Hydroxychloroquine sulfate.
Chloroquine.
(Mepacrine hydrochloride is sometimes used in discoid lupus erythematous)

They should NOT be used in psoriatic arthritis.

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13
Q

What drugs that affect immune response are used in RA? (5)

A
  1. Methotrexate
  2. Ciclosporin
  3. Cyclophosphamide
  4. Leflunomide
  5. Cytokine modulators (Adalimumab, certolizumab pegol, etanercept, golimumab, and infliximab)
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14
Q

Leflonumide acts on the immune system as a DMARD, its therapeutic effect starts after how long of treatment?

A

4-6 weeks, improvement may continue for a further 4-6 months.

Inhibits the mitochondrial enzyme dihydroorotate dehydrogenase (DHODH), which plays a key role in the de novo synthesis of uridine monophosphate (rUMP), which is required for the synthesis of DNA and RNA.

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15
Q

How does leflonimde work?

A

Inhibits DHODH, which plaus a key role in the de novo synthesis of uridine monophosphate (rUMP).

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16
Q

Ciclosporin is licensed for severe RA when?

A

Ciclosporin is licensed for severe RA when conventional second-line therapy is inappropriate or ineffective.

There is some evidence that ciclosporin may retard the rate or erosive progression and improve symptom control in those who respond only partially to methotrexate.

17
Q

Cyclophosphamide may be used for RA with severe systemic manifestations, it is toxic and what monitoring is needed?

A

Regular blood counts, including platelet counts.

18
Q

What are the main treatments for juvenile idiopathic arthritis?

A

Methotrexate, sulfasalazine can be used but should be avoided in systemic-onset juvenile idiopathic arthritis.

Gold and penicllamine are no longer used.

Cytokine modulators do have a role.

19
Q

Adalimumab, certolizumab, etanercept, golimumab and infliximab inhibit the activity of what?

A

TNF-a

20
Q

How does rituximab work?

A

It is an anti-lymphocyte monoclonal antibody which causes lysis of B lymphocytes

21
Q

Abatacept works how?

A

It prevents antigen-presenting cells from delivering the co-stimulatory signal to T cells.

22
Q

How does Anakinra work?

A

Anakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI)

23
Q

What is the mechanism of action of baricitinib?

A

Small molecule selective and reversible inhibitor of the Janus-associated tyrosine kinases JAK1 and JAK2.

24
Q

What is the mechanism of action ot tofacitinib? (slightly different to that of baricitinib)

A

Tofacitinib is a selective inhibitor of JAK1 and JAK3.

Baricitinib is a small molecule inhibitor of JAK1 and JAK2 which is reversible.

25
Q

How does belimumab work?

A

Belimumab is a human monoclonal antibody that inhibits B-cell activating factor (BAFF).

Used in SLE

26
Q

How does Sarilumab work?

A

Antibody that specifically binds to interleukin-6 receptors and blocks the activity of pro-inflammatory cytokines.

27
Q

How does secukinumab work?

A

Selectively binds to IL-17A and inhibits the release of proinflammatory cytokines and chemokines.

28
Q

How does tocilizumab work?

A

It is an antibody against IL-6R, IL-6 is a cytokine that plays an important role in immune response and is implicated in the pathogenesis of many diseases.

29
Q

How does ustekinumab work?

A

Works against IL-12 and IL-23

30
Q

Inhibits DHODH, which plaus a key role in the de novo synthesis of uridine monophosphate (rUMP).

A

Leflunomide

31
Q
TNF-a blocking agents 
A
C
E
G
I
A

Adalimumab, certolizumab, etanercept, golimumab and infliximab inhibit the activity of what?

32
Q

It is an anti-lymphocyte monoclonal antibody which causes lysis of B lymphocytes

A

Ritixumab

33
Q

It prevents antigen-presenting cells from delivering the co-stimulatory signal to T cells.

A

Abatacept

34
Q

blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI)

A

Ankinra

35
Q

Small molecule selective and reversible inhibitor of the Janus-associated tyrosine kinases JAK1 and JAK2.

A

Baricitinib

36
Q

selective inhibitor of JAK1 and JAK3.

A

tofacitinib

37
Q

a human monoclonal antibody that inhibits B-cell activating factor (BAFF).

A

Belumimab

38
Q

Antibody that specifically binds to interleukin-6 receptors and blocks the activity of pro-inflammatory cytokines.

A

Sarlimumab

39
Q

Selectively binds to IL-17A and inhibits the release of proinflammatory cytokines and chemokines.

A

Secukinumab