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Pharmacology > Antirheumatic Drugs > Flashcards

Antirheumatic Drugs Flashcards

1
Q

Analgesia for osetoarthritis includes:

A

APAP
NSAIDs
COX-2 inhibitors

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2
Q

IF inflammation is present in osteoarthritis what should be prescribed?

A

NSAIDs
COX-2 inhibitors
Intra-articular corticosteroids

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3
Q

What drug is not effective in RA?

A

APAP, no effect on inflammatory component

Non-acetylated salicylates also less effective than traditional NSAIDs

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4
Q

Why is ASA rarely used in RA?

A

AE of high doses needed to achieve anti-inflamm effects

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5
Q

Which drugs are used for symptomatic therapy of RA and which to prevent/slow disease progression?

A

Symptomatic- NSAIDs, corticosteroids(systemic, intra-articular)
Prevent/slow- DMARDs (disease modifying antirheumatic drugs)

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6
Q

How are corticosteroids used in RA?

A
  • Life threatening complications of RA, like vasculitis
  • Bridge time to onset of action of DMARDs
  • Pulse for acute flare ups
  • Intra-articular therapy for very acute inflammation
  • *Do not use longterm d/t SE
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7
Q

Long term AE of corticosteroids:

A 
Hyperglycemia 
Catatracts 
Glaucoma 
Aspetic necrosis of weight bearing joints
Osteoporosis
Cushing's syndrome
Adrenal suppresion 
Sodium and water retention 
CNS side effects (high doses)
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8
Q

When dosing corticosteroids, the ______ does possible should be used.

A

Lowest

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9
Q

Patients will need to be tapered after being on corticosteroids for how long and why?

A

> 2wks

prevent withdrawal secondary to adrenal suppression

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10
Q

Coricosteroids include:

A 
Cortisone
Hydrocortisone
Prednisone 
Prednisolone 
Methylprednisolone
Triamcinolone
Dexamethasone 
Betamethasone
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11
Q

Which corticosteroids should be avoided in patients with CHF and HTN and why?

A

(in order of most to lease mineralcorticoid activity)
Cortisone
Hydrocort
Prednisone
Prednisolone
These have higher mineralcorticoid activity and cause more sodium and water retention

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12
Q

When should DMARDs be started?

A

As soon as RA is diagnosed to prevent/slow progression of joint destruction and deformities

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13
Q

Conventional DMARDs include:

A 
Hydroxychloroquine (Plaquenil, Quineprox)
Methotrexate
Azathioprine (Imuran, AZA)
Gold 
Penicillamine 
Sulfasalazine 
Leflunomide 
Minocycline 
Cyclophosphamide
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14
Q

Biologic DMARDs include:

A 
Etanercept (Enbrel)
Infliximab (Remicade)
Adalimumab (Humira)
Certolizumab pegol (Cimzia)
Golimumab (Simponi)
Tocilizumab (Acetmra)
Rituximab (Rituxan)
Abatacept (Orencia)
Anakinra (Kineret)
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15
Q

How long does it typically take DMARDs to elicit a response?

A

3-6months

use NSAIDs or corticosteroid to manage s/s, NSAIDs often continued even once DMARDs begin to work

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16
Q

What should be monitored to assess efficacy of DMARDs?

A

ROM

ADLs

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17
Q

Which DMARDs, which used to be the standard of care, are seldom used d/t their high incidence of toxicity?

A

Gold (oral or IV) and Penicillamine

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18
Q

S/s of toxicity of Gold or Penicillamine?

A

Myelosuppresion, proteinuria, stomatitis rash, altered taste perception (penicillamine), visual changes (gold)

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19
Q

Azathioprine, a conventional DMARD, is also used for ______ ______.

A

Crohns Disease (rarely used for RA)

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20
Q

Azathioprine is a prodrug for what and what does it do?

A

Mercaptopurine

Immunosuppressant

21
Q

S/s of azathioprine toxicity are:

A

Mylosuppression, hepatotoxicity, rash, infection

reserved for aggressive disease or serious complications like vasculitis

22
Q

Hydroxychloroquine (PO), a conventional DMARD, is also used as an ______ ______ .

A

Anti-malarial drug

23
Q

Hydroxychloroquine is most commonly used for what type of RA and may take up to how long before a clinical effect is seen?

A

Used for mild RA

May take 6mos

24
Q

Toxicity of Hydroxychloroquine includes what s/s:

A

Usually well tolerated, some GI upset

Retinopathy is rare but ophthalmology exams are recommended q6-12mos

25
Q

Sulfasalazine (PO) is used for what type of RA and what other diseases?

A

Mild RA

Crohns Disease and ulcerative colitis (more often used for these)

26
Q

What is Sulfasalazine’s MOA:

A

Cleaved by intestinal bac to sulfapyridine(active metabolite) and 5-ASA.
It can bind to iron and decrease absorption, significant in patients taking abx d/t decreased gut flora conversion to active form may be reduced

27
Q

AE of Sulfasalazine:

A

GI upset
Rash
Bodily fluid can turn yellow-orange

28
Q

Leflunomide’s (PO), a conventional DMARD, MOA:

A

Inhibitor of pyrimidine synthesis= altered lymphocyte activation and decreased inflamm response

29
Q

Leflunomide’s is contraindicated in what type of patients?

A 
Pregnant women (may d/c in potential fathers)
Category X/teratogenic
30
Q

Toxicties of Leflunomide include:

A

Hepatotoxicity
Reversible alopecia
GI distress

31
Q

In case of toxicity or patients wishing to stop Leflunomide what can be given to lower drug levels?

A

Cholestyramine

otherwise half life of active met= 2wks and could take months

32
Q

Methotrexate, a conventional DMARD, is available:

A

PO, IM, SubQ

33
Q

MOA of Methotrexate:

A

Folate antagonist= purine biosynthesis inhibition cytokine production inhibition, adenosine production stimulation =anti-inflammatory effect
(patients need folic acid replacement)

34
Q

Advantages of Methotrexate:

A

Well tolerated
Cheapest DMARD
Symptomatic relief in 1 month

35
Q

Toxicities of Methotrexate include:

A

GI upset
Megaloblastic anemia (treat with folic acid)
Hepatoxicity

36
Q

What are biologic DMARDs?

A

Genetically developed proteins

37
Q

Advantage of biologic DMARDs:

A

No routine laboratory monitoring

38
Q

Disadvantages of biologic DMARDs:

A

Risk of infections and malignancy
Temporarily suspend treatment if inf. occurs
TB skin test prior to use
Very expensive
IV, subQ with common injection site reactions

39
Q

Etanercept, infliximab, adalimumab, certolizumab, pegol, golimumab are all biologic DMARDs that are also:

A

TNF-a Blockers

Downregulate or antagonize tumor necrosis factor-a = cytokine mediator of RA

40
Q

Many of the TNF-a blockers are used in combination with:

A

Methotrexate or other DMARDs

41
Q

What black box warning do TNF-a blockers carry with them?

A

Serious risk of infection (invasive fungal infections, reactivated of TB, etc)
Lymphoma and other malignancies in children and adolescents

42
Q

What is Rituximab’s MOA:

A

Depletes B cells which have been shown to be responsible for inflammation in RA

43
Q

When is Rituximab used?

A

When patients fail traditional DMARDs and anti-TNF agents

44
Q

What are the black box warnings associated with Rituximab?

A
  • Fatal infusion reactions (prevent with methylpred, APAP, and antihistamines
  • severe mucocutaneous reactions
  • PML (progressive multifocal leukoencephalopathy)
45
Q

What is Abatacept, a biologic DMARD, MOA:

A

Inhibits T cell activation

used when patients fail traditional DMARDs and anti-TNF agents

46
Q

What is Anakinra, a biologic DMARD, MOA:

A

Antagonizes IL-1 receptors (pro-inflam cytokine)
(used when patients fail traditional DMARDs and anti-TNF agents; may be used in combo with traditional DMARDs but never combined wtih anti-TNF drugs d/t increased risk of infection

47
Q

What is Tocilizumab, a biologic DMARD, MOA:

A

Inhibits IL-6 (inflam. cytokines)

Used when patients fail anti-TNF

48
Q

What black box warning does Tocilizumab carry?

A

Serious risk of infections (fungal inf., reactivation of latent TB, opportunistic infections)

49
Q

What type of supplements might a patient on sulfasalazine need to take?

A

Iron

Pharmacology (48 decks)

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