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Parker Musculoskeletal Pharm > Non-biological DMARDs > Flashcards

Non-biological DMARDs Flashcards

1
Q

What is the standard initial tx of RA?

A

A non-bio DMARD (MTX), an NSAID, and a Corticosteroid.. Milder cases get Hydroxychloroquine over MTX

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2
Q

If initial tx fails, what do you do next?

A

Give a 1st line biologic (targeted) tx like a TNF-alpha blocker with or without MTX

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3
Q

What if the targeted tx fails?

A

Some docs try a different TNF-alpha blocker, others switch to a completely different targeted therapy

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4
Q

What is important for longer remission, less joint destruction, and a better QOL?

A

Early aggressive treatment

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5
Q

What did the AMPLE trial show?

A

Found that triple therapy with MTX, Sulfasalazine, and Hydroxychloroquinone is just as effective (and much CHEAPER) than using MTX with a biological agent

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6
Q

What did the TEAR trial show?

A

Showed that initiating tx with MTX as a monotherapy was just as effective as initiating tx with a double or triple therapy. You can always add drugs to the MTX if you need to and the pt will turn out just the same. Moral of the story: Start with MTX and go from there

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7
Q

MTX MOA?

A

Inhibits AICAR transformylase (involved in synthesis of inosine monophosphate) –> increased circulating adenosine!!

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8
Q

What does increased circulating adenosine do?

A

Decreases: lymphocyte proliferation, IL-1, INF-gamma, TNF, histamine release from basophils and chemotaxis of neutrophils
Increases: IL-4

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9
Q

What happens to MTX when it gets into the cell?

A

When it gets into the cell is undergoes polyglutamation –> intracellular retention

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10
Q

Where is MTX metabolized?

A

Liver- enterohepatic circulation increases half life

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11
Q

Where is MTX eliminated?

A

Kidney

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12
Q

ADEs of MTX?

A

Immunosuppression, skin rxn, GI toxicity in pts with ulcerative cholitis (esp w/ concurrent NSAID use), pulm fibrosis, blood dyscrasias, infection, bleeding

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13
Q

Contraindications of MTX?

A

Alcoholics, liver dz, pregnancy (cat X), HIV infection, vaccinations

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14
Q

How do you monitor MTX?

A

CBC, LFTs, Cr/BUN, serum uric acid, pregnancy test

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15
Q

Which MTX adverse effects were given their own heading in Sweatman’s document?

A
  1. Immunosuppression
  2. Pulmonary toxicity
  3. Child bearing age
  4. Vaccinations
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16
Q

When is sulfasalazine used?

A

When pt has inadequate response to NSAIDs

17
Q

What are the 2 metabolites of sulfasalazine and how is the drug metabolized into said metabolites?

A

Sulfasalazine is metabolized into sulfapyridine and mesalamine by colonic bacteria

18
Q

What is the active metabolite of Sulfasalazine and what does it do?

A

Mesalamine: it is anti-inflammatory by inhibiting PG and LT

19
Q

What is the fate of the other metabolite, sulfapyridine?

A

It is acetylated in the liver. Pts who are slow acetylators can have build up of sulfapyridine

20
Q

ADEs of Sulfasalazine?

A

Fatal blood dyscrasias. Also do not give to pts who are hypersensitive to salicylates or sulfonamides

21
Q

What is Leflunomide metabolized to? The active metabolite??

A

A77 1726

22
Q

What does A77 1726 do?

A

Inhibits dihydroorotate dehydrogenase (DHODH). DHODH is key in pyrimidine synthesis

23
Q

What does the inhibition of DHODH lead to?

A

Cell cycle arrest of B and T cells

24
Q

Is Leflunomide cytostatic or cytotoxic at clinical levels?

A

Cytostatic

25
Q

What metabolizes the Leflunomide to A77 1726? How is the drug eliminated?

A

CYPs metabolize it, eliminated by pooping

26
Q

ADEs of Leflunomide?

A

Hepatitis. Contraindicated in alcoholics, immunodef, bone marrow dysplasia, infection, pregnancy (cat X)

27
Q

How do you monitor Leflunomide?

A

CBC, LFTs, pregnancy test, serum electrolytes

28
Q

How do you monitor Sulfasalazine?

A

CBC, LFTs, Cr/BUN, Urinalysis

29
Q

Hydroxychloroquinone MOA?

A

Increases intracellular vacuole pH which alters:
1. protein degredation in lysosome
2. macromolecule assembly in endosome
3. protein modification by Golgi
MHC molecules aren’t assembled –> down regulation of immune response to foreign and self antigens

30
Q

What else is hydroxychloroquinone used for (probably more commonly)?

A

Malaria prophylaxis

31
Q

Metabolism/Elimination of Hydroxychloroquine?

A

Partial hepatic metabolism.. Followed by slow and extensive renal elimination

32
Q

ADEs of Hydroxychloroquine?

A
  1. CNS tox: neuropathy, seizures
  2. Hepatitis
  3. Blood dyscrasias
  4. Ocular disease (this seems unusual/unique.. Hmmm..)
33
Q

How do you monitor Hydroxychloroquine?

A

CBC and ophthalmic exam

Parker Musculoskeletal Pharm (3 decks)

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