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P2 E2 Shea > Rheum- RA > Flashcards

Rheum- RA Flashcards

1
Q

Which group of meds is used in treatment of RA but not in the treatment of OA?

A

DMARDs

(Disease modifying antirheumatic drugs)

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2
Q

What are the 4 deformities of rheumatoid arthritis?

A
  1. Marked ulnar deviation
  2. Swan-neck deformity
  3. Active Synovitis
  4. Nodules
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3
Q

Goal of RA treatment:

  • Early aggressive treatment to prevent what 2 things
A

irreversible joint damage and disability

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4
Q

Which RA patients can be treated with oral agents as monotherapy?

A

Patients w/ less active disease and good prognostic indicators

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5
Q

Which RA patients are candidates for combination therapy and biologics to suppress inflammation

A

Patients with high disease activity and/or poor prognostic features

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6
Q

Within how many months of the diagnosis of RA should DMARDs be started?

A

3 months

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7
Q

Which 2 meds should be considered adjunctive therapy to DMARDS early in the course of treatment of RA?

A

NSAIDS and/or corticosteroids

(needed if sxs are not adequately controlled w/ DMARDs)

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8
Q

Which med is first line tx for RA?

A

DMARDs either as monotherapy or in combination

***Methotrexate (DMARD) often chosen

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9
Q

What is important to monitor in a pt taking methotrexate? How will you know if they are deficient?

A

folic acid

will get stomatitis (mouth sores) if deficient

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10
Q

RA treatment options:

What is used in Early disease of high activity and presence of poor prognostic factors

A

Biologics

(ACR endorses use of anti-TNF biologics regardless of DMARD use)

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11
Q

RA treatment options:

American College of Rheumatology (ACR) now endorses the use of _______ biologics in patients regardless of previous DMARD use

A

anti-TNF BIologics

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12
Q

Which 2 biologic agents have proven effective for patients who fail treatment with other DMARDs

A

Anti-TNF (TNFi) and non-TNF biologic agents (B cell inhibitors, IL-inhibitors, co-stimulation modifiers)

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13
Q

What are the 2 options if one DMARDs is ineffective or not adequately effective to induce response

A
  • combination therapy with two or more DMARDs
  • DMARD plus biologic agent may be used (ex: Methotrexate + Infliximab)
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14
Q

T/F: Methotrexate is less effective than biologic monotherapy

A

FALSE
Methotrexate is more effective

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15
Q

Why is Infliximab given in combo w/ Methotrexate?

A

to prevent development of infliximab antibodies that may reduce drug efficacy or induce allergic reactions.

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16
Q

Non Biologic RA combination treatment examples:

Initial combo therapy w/ either:

  • Methotrexate with _____
  • Sulfasalazine plus ______
  • Infliximab plus ______
A
  • Methotrexate with etanercept
  • Sulfasalazine plus prednisone
  • Infliximab plus methotrexate
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17
Q

For patients with moderate-to-high RA disease activity, ACR recommends dual DMARD combinations of:

  • methotrexate plus ________
  • methotrexate plus ________
  • methotrexate plus ________
A

Hydroxychloroquine

Leflunomide

Sulfasalazine

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18
Q

Non Biologic Combination Treatment Examples:

ACR recommends a triple combination of …..

A

Methotrexate, sulfasalazine, and hydroxychloroquine

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19
Q

Methotrexate:

Results as early as how long?

A

2-3 weeks

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20
Q

MOA of Methotrexate:

  • **Inhibits ______ production, inhibits _______biosynthesis, and may stimulate release of adenosine–leads to its antiinflammatory properties
  • Cytotoxic to rapidly dividing immune cells due to inhibition of dihydrofolate reductase
A

Inhibits cytokine** production, inhibits **purine biosynthesis

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21
Q

Which non-biologic DMARD is a folic acid antagonist- leading to deficiency? What could you give with it to reduce this adverse rxn?

A

Methotrexate

may be given w/ folic acid 1-5mg/week

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22
Q

What are the 6 contraindications of Methotrexate?

A
  • Pregnancy-teratogenic and nursing women
  • Chronic liver disease
  • Immunodeficiency
  • Pleural or peritoneal effusions
  • Leukopenia, thrombocytopenia,
  • CrCl <40ml/min
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23
Q

Toxicities of which med? Which may you see first?

–GI-N/V/D

–hematologic-thrombocytopenia

–pulmonary fibrosis and pneumonitis

–hepatic-elevated liver enzymes

–Stomatitis

A

Methotrexate

may see stomatitis first

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24
Q

If you have a patient take Methotrexate and they develop stomatits, what does this mean?

A

Folate deficiency

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25
Q

What are the 4 “work horses” of RA?

A
  1. Methotrexate
  2. Leflunomide
  3. Hydroxychloroquine
  4. Sulfasalazine
26
Q

MOA of which med?

•inhibits pyrimidine synthesis–> decrease in lymphocyte proliferation and modulation of inflammation

A

Leflunomide

27
Q

What are the 2 contraindications for Leflunomide?

A
  1. Liver disease
  2. Teratogenic
28
Q

What is the half life of Leflunomide (non-biologic DMARD_?

A

14-16days

(long half life)

29
Q

What are the 4 toxicities of Leflunomide (non-biologic DMARD)?

A
  • GI
  • hair loss
  • liver
  • bone marrow toxicity
30
Q

Mechanism of which med?

•dampen antigen–antibody reactions at sites of inflammation

A

Hydroxychloroquine

31
Q

Which non-biologic DMARD is used in mild RA or as an adjuvant in combination DMARD therapy in more progressive disease

A

Hydroxychloroquine

32
Q

What are the 2 toxicities that Hydroxychloroquine lacks>

A

–Lacks myelosuppressive

–Lacks Hepatic and renal toxicities

33
Q

Which med has ocular toxicities including:

Visual changes including a decrease in night or peripheral vision

A

Hydroxychloroquine

34
Q

Which med has the following toxicities?

–Dermatologic-rash, alopecia, increased skin pigmentation

–Neurologic-HA, vertigo, insomnia

A

Hydroxychloroquine

35
Q

Sulfasalazine (nonbiologic DMARD) is a prodrug that is cleaved in the colon to what 2 things?

A

Sulfapyridine (active antirheumatic) and 5-aminosalicylic acid

(this means that this is a prodrug dependent on bacteria in colon)

36
Q

Sulfasalazine (nonbiologic DMARD) has rapid absorption where and has an onset in how many months?

A

Rapid absorption in GI tract

Onset 2 months

37
Q

Which RA med has the following ADEs:

  • Elevated hepatic enzymes
  • May turn skin to a yellow-orange color—no clinical consequence

(KNOW)

A

Sulfasalazine (nonbiologic DMARD)

38
Q

Which nonbiologic DMARD has the following ADEs?

  • N/V/D, anorexia
  • Rash, urticaria, serum-sickness
  • leukopenia
  • Alopecia
  • Stomatitis
  • Elevated hepatic enzymes
  • May turn skin to a yellow-orange color
A

Sulfasalazine

39
Q

Absorption of Sulfasalazine can be decreased with what?

(KNOW)

A

When antibiotics destroy colonic bacteria

40
Q

Which med binds iron supplements and decreases absorption?

(red)

A

Sulfazalazine

41
Q

Which med can potentiate warfarin’s effects- displace from protein binding?

A

Sulfasalazine (nonbiologic DMARD)

42
Q

What are the names of the 2 JAK inhibitors used to tx OA?

A
  1. Tofacitinib
  2. Baricitinib

(“JAK likes to eat Tofu at the Bar”)

43
Q

What is the use for the JAK inhibitors, Tofacitinib and Baricitinib?

A

moderate to severe RA who have failed or intolerance to methotrexate

44
Q

MOA of which RA 2 meds?

  • inhibition of JAK- a tyrosine kinase
  • modulation and suppression of the immune system through cytokine signal reduction
A

JAK inhibitors: Tofacitinib and Baricitinib

45
Q

ADEs of which 2 meds?

  • serious infections
  • lymphomas, and other malignancies
  • elevated plasma liver enzymes and lipids
A

JAK inhibitors: TOfacitinib and Baricitinib

46
Q

Which two meds have been tested and treated for latent TB?

A

JAK inhibitor: Tofacitinib and Baricitinib

47
Q

Should live vaccines be given during treatment with the JAK inhibitors: Tofacitinib and Baricitinib?

48
Q

Which 2 meds can cause Lymphomas or other malignancies?

(KNOW)

A

JAK inhibitors: Tofacitinib and Baricitinib

49
Q

Azathioprine, cyclosporine and Clyclophosphamide are other DMARDs used to tx RA. Match them to their ADEs:

  • _____= gastritis
  • _____= Leukopenia, hepatotoxicity
  • _____= nephrotoxicity
A
  • Cyclophosphamide = gastritis
  • Azathioprine = Leukopenia, hepatotoxicity
  • Cyclosporine = nephrotoxicity

*Used less frequently today b/c of toxicity and/or lack of long term benefit*

50
Q

What is the 1 contraindication of the TNF-α biologic DMARDs?

(KNOW)

51
Q

The following are the ADEs of which group of biologic DMARDs?

–MS-like illness or exacerbate MS

–Increased risk of lymphoproliferative cancer

A

TNF-α Biologics

(limumab, Certolizumab, Entanercept, Golimumab, Infliximab)

52
Q

Which TNF-α biologic DMARD?

  • Chimeric antibody combining portions of mouse and human IgG1
A

Infliximab

53
Q

Which 4 vaccines can be given during RA therapy with Biologic DMARDs?

A

Killed vax:

  • Pneumococcal
  • IM influenza
  • Hep B

Recombinant:

  • HPV
54
Q

T/F: Live vaccines can be given to patients already on DMARD therapy, but NOT biologics

55
Q

For patients > 50y/o who will be starting a biologic or Tofacitinib, ACR recommends giving which vaccine?

A

Herpes Zoster vaccine

56
Q

T/F: After failure of anti-TNF agent, subsequent tx may include trialing an alternative anti-TNF agent or changing to a non-TNF biologic

57
Q

Which 2 biologics should be continued with Methotexate?

A

Infliximab (TNF-a)

Rituximab (B cell)

58
Q

Which BIologic DMARD causes near complete depletion of peripheral B cells?

59
Q

Which med can turn your skin a yellow/orange color?

A

Sulfasalazine

60
Q

MOA of methotrexate:

Which enzyme does Methotrexate inhibit?

A

dihydrofolate reductase enzyme

61
Q

What supplement is important to give with Methotrexate?

A

Folic acid

P2 E2 Shea (19 decks)

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