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PHARM > Rheumatoid Arthritis and DMARDs > Flashcards

Rheumatoid Arthritis and DMARDs Flashcards

1
Q

How do you treat osteoarthritis?

A

acetaminophen

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2
Q

describe osteoarthritis:

A

associated with age, immune system is NOT involved, treatment is acetaminophen, not an NSAID, good for analgesic purposes

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3
Q

T/F. Rheumatoid arthritis is an autoimmune disease.

A

TRUE, with immune system drug targets.

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4
Q

First approach of treatment for RA:

A

physical therapy; rest and splitting to prevent muscular atrophy

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5
Q

Second approach for treatment of RA:

A

drugs; to relieve symptoms, MINIMIZE TISSUE DESTRUCTION CAUSED BY INFLAMMATION

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6
Q

T/F. Aggressive treatment very early to halt disease progression is now common.

A

TRUE.

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7
Q

What does DMARDs stand for?

A

Disease-Modifying Anti-Rheumatic Drugs: slowing or stopping disease progression

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8
Q

Third approach to treatment of RA:

A

surgery if drugs inadequate

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9
Q

Three groups that help treat RA:

A

NSAIDs and GCs, “Traditional” DMARDs, and Biologic Response Modifies or Biologics

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10
Q

Group of drugs that is generally a broad immune-toxic mechanism:

A

Traditional DMARDs

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11
Q

What does traditional mean?

A

oral

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12
Q

Group of drugs that target individual specific signaling molecules:

A

Biologic Response Modifiers or Biologics

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13
Q

Protein or peptide drugs:

A

Biologic response modifiers

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14
Q

Small molecule drugs, brand and can do all types of things:

A

Traditional DMARDs (and oral)

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15
Q

NSAID used for RA:

A

Naproxen.

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16
Q

Why is NSAID never mono therapy?

A

It provides just a bandaid, but does not fix problem, not sufficient enough; only provides initial relief

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17
Q

GC stands for:

A

glucocorticoids

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18
Q

What is a glucocorticoid?

A

anti-inflammatory steroids

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19
Q

What is the most commonly used GC?

A

Prednisone

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20
Q

Characteristics of Prednisone:

A

highly effective, but long term toxicity effects; not used as a mono therapy, rapid acting bridge agent

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21
Q

Traditional DMARDs:

A

methotrexate, hydroxychloroquine, sulfasalazine, triple drug therapy, leflunomide, minocycline

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22
Q

Biologic DMARDs

A

ANTI-TNF drugs, etanercept, infliximab

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23
Q

The first choice DMARDs drug for initial therapy of RA and used in early stages of RA (but can be used in late stages too:

A

Methotrexate, also called MTX

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24
Q

Do we use Methotrexate with other drugs?

A

Yes, very often. Also use in more than 50% of RA patients

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25
Q

Dose of methotrexate?

A

once per week, mat take up to 4-6 weeks to see effects

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26
Q

Structure and mechanism of methotrexate:

A

FOLIC ACID analog; folate transporters.

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27
Q

Does methotrexate have a long half life in the cell than plasma?

A

Yes, much longer than plasma half-life.

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28
Q

What is mechanism 1 of methotrexate?

A

acts as anti-metabolite (anti-folate) to inhibit PURINE and PYRIMIDINE synthesis; inhibits DHFR and FH4; anti-cancer mechanism

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29
Q

What is mechanism 2 of methotrexate?

A

inhibits enzyme AICAR; inhibits purine synthesis; increase anti-inflammatory mediate ADENOSINE outside cells; doesn’t just slow but REVERSES; MAJOR MECHANISM in RA

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30
Q

What is mechanism 3 of methotrexate?

A

reduce pyrimidine synthesis, inhibits proliferation of inflammatory cells

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31
Q

Overall the mechanisms for methotrexate rely on what?

A

rapid immune cell proliferation depends on purines and pyramids; methotrexate inhibits both, but increases adenosine (anti-inflammatory)

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32
Q

Side effects of methotrexate:

A

minor GI problems, rare hepatotoxicity with high doses, elevation of liver enzyme levels at high doses, USE ONCE A WEEK to avoid high doses, avoid alcohol, avoid patients with liver failure

33
Q

Many side effects of methotrexate or due to what?

A

induced folate deficiency

34
Q

How can you reduce folate deficiency?

A

REPLACEMENT FOLIC ACID DAILY (1-3 mg)

35
Q

What are CONTRAINDICATIONS of methotrexate?

A

renal insufficiency; pregnancy or those planning for pregnancy (teratogenic), nursing mothers, abortifacient with misoprostol

36
Q

What is a less common complication but signs need to be watched when administering MTX?

A

increased infections, including upper respiratory, TB, fungal

37
Q

Anti-malarial drug that is anti-inflammatory:

A

hydroxychloroquine

38
Q

What drugs do we use hydroxychloroquine with?

A

MTX, sulfasalazine

39
Q

How is hydroxychloroquine thought to work?

A

altering cellular pH

40
Q

T/F. hydroxychloroquine has a slow onset and very long half-life (45 days). And skin is reservoir.

A

TRUE.

41
Q

Side effects of hydroxychloroquine:

A

Retinal damage (melanin contains tissues such as eye), decreased blood glucose, increased risk of hypoglycemia in diabetics; NO adverse effects in pregnancy/breast feeding

42
Q

is another traditional DMARD and immune-suppressive drug, it has poorly defined mechanisms but is thought to:

A

inhibition of multiple immune cells and cytokines

43
Q

What drugs do we give Sulfasalazine with?

A

Hydroxychloroquine and/or MTX

44
Q

Where is Sulfasalazine metabolized and what is it metabolized to?

A

metabolized in gut; metabolized to salicylate and sulfapyridine

45
Q

Sulfasalazine is known to have anti-inflammatory effects where?

A

In the bowel

46
Q

Common side effects of Sulfasalazine:

A

GI issues, anorexia, headache, skin irritation

47
Q

Most significant concerns with Sulfasalazine:

A

blood dycrasias; reduce folate absorption; do not use in those with sulfa or CELEBREX allergy (cross-reactivity)

48
Q

Another name for Triple drug therapy:

A

Nebraska therapy (UNMC)

49
Q

Process of triple drug therapy:

A

start with MTX weekly, then try hydroxychloroquine plus Sulfasalazine daily; then try all three in combo; can add NSAIDs or prednisone

50
Q

Inhibits digydro-orotate dehydrogenase which inhibits pyrite synthesis; also inhibits tyrosine kinases at higher doses:

A

Leflunomide

51
Q

What is overall effect of Leflunomide?

A

INHIBIT T-CELL proliferation, reduces antibody production by B-Cells

52
Q

T/F. Leflunomide is a pro-drug.

A

TRUE

53
Q

Why does Leflunomide have an extremely long effective half-life with significant consequences?

A

due to repeated entero-heptatic recirculation; active agent can remain in body long after last administration

54
Q

Side effects of Leflunomide:

A

diarrhea, and hair loss (alopecia), carcinogenic and teratogenic, CONTRAINDICATED before and during pregnancy, cholestyramine WASHOUT if needed prior to stopping birth control

55
Q

Well established tetracycline antibiotic that inhibits collagenase; specific action to decrease collagen degradation component of RA:

A

minocycline

56
Q

minocycline administration and use:

A

oral, once or twice a day. use in early disease progression

57
Q

Side effects of minocycline:

A

dizziness and hyper pigmentation

58
Q

Biologic DMARDs:

A

newer drugs that are peptides or proteins (NOT small molecules)

59
Q

How to biologic DMARDs act?

A

all are immuno-suppresive but act by targeting INDIVIDUAL SPECIFIC MEDIATORS; target mediators early in inflammation signaling cascades

60
Q

What types of drugs prevent auto-antibody production and release and subsequent inflammation?

A

biologic DMARDs

61
Q

T/F. Biologic DMARD block signaling molecules.

A

TRUE, these signaling factors drive inflammation and damage to synovial cells and structures

62
Q

Difference between murine, chimeric, and humanized:

A

0%, 65%, 90%

63
Q

What does “mib” and “nib” stand for?

A

Mib = protease/proteosome inhibitors; nib = (inhibit) kinase inhibitors

64
Q

T/F. All of the biologics are more effective when used in combination with methotrexate/

A

TRUE.

65
Q

Side effects for biologics:

A

increased risk of infections, blood dycrasias, increased cancer incidence (non-Hodgkins, non-melanoma skin), GI problems, headache, skin rash, cough

66
Q

Examples of Anti-Tumore Necrosis Factor drugs (ANTI-TNF):

A

EtanerCEPT, InflixiMAB

67
Q

Which of the biologics is most commonly used?

A

Anti-TNFs

68
Q

What does TNF-alpha do?

A

upstream regulator of many other immune and inflammatory cytokines; TNF receptors p55 and p75

69
Q

One of the first anti-TNF drugs:

A

Etanercept

70
Q

The soluble p75 subunit of the TNF reCEPTor used as a drug:

A

Etanercept

71
Q

Mechanism by which Etanercept works:

A

bings to and prevents TNF from binding to its cellular receptor

72
Q

Administration and use of Etanercept:

A

given weekly, shortest duration, used in combo with MTX

73
Q

Side effects of Etanercept:

A

headaches, sinus issues, allergies, PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY (PML) (rare untreatable viral infection of CNS); black box warning for lymphomas

74
Q

T/F. Etanercept is not a protein.

A

FALSE, it IS a protein.

75
Q

A Monoclonal AntiBody against TNF (not part of the receptor), a mouse-human chimera (xi), bings to TNF:

A

InfliXImab

76
Q

Another anti-TNF drug that is monoclonal antibody against TNF:

A

InfliXImab

77
Q

Administration and use of InfliXImab:

A

IV, every 4-8 weeks, after initial loading dose; ALWAYS COMBINED WITH MTX or other t-DMARDs

78
Q

Side effects of InfliXImab:

A

similar to Etanercept; can cause HYPOTENSION (do not use in heart failure patients)

PHARM (18 decks)

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