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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
What are the 4 "work horses" of RA?
1. Methotrexate 2. Leflunomide 3. Hydroxychloroquine 4. Sulfasalazine
26
MOA of which med? •inhibits pyrimidine synthesis--\> decrease in lymphocyte proliferation and modulation of inflammation
Leflunomide
27
What are the 2 contraindications for Leflunomide?
1. Liver disease 2. Teratogenic
28
What is the half life of Leflunomide (non-biologic DMARD\_?
14-16days | (long half life)
29
What are the 4 toxicities of Leflunomide (non-biologic DMARD)?
* GI * **_hair loss_** * liver * bone marrow toxicity
30
Mechanism of which med? •dampen antigen–antibody reactions at sites of inflammation
Hydroxychloroquine
31
Which non-biologic DMARD is used in **mild RA or as an adjuvant in combination DMARD therapy in more progressive disease**
Hydroxychloroquine
32
What are the 2 toxicities that Hydroxychloroquine lacks\>
–Lacks myelosuppressive –Lacks Hepatic and renal toxicities
33
Which med has **ocular** toxicities including: Visual changes including a decrease in night or peripheral vision
Hydroxychloroquine
34
Which med has the following toxicities? ## Footnote –Dermatologic-rash, alopecia, increased skin pigmentation –Neurologic-HA, vertigo, insomnia
Hydroxychloroquine
35
Sulfasalazine (nonbiologic DMARD) is a prodrug that is cleaved in the colon to what 2 things?
**Sulfapyridine** (active antirheumatic) and **5-aminosalicylic acid** | (this means that this is a prodrug dependent on bacteria in colon)
36
Sulfasalazine (nonbiologic DMARD) has rapid absorption where and has an onset in how many months?
Rapid absorption in **_GI tract_** Onset **_2 months_**
37
Which RA med has the following ADEs: * Elevated hepatic enzymes * May turn **skin to a yellow-orange color**—no clinical consequence (KNOW)
Sulfasalazine (nonbiologic DMARD)
38
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
Sulfasalazine
39
Absorption of Sulfasalazine can be decreased with what? (KNOW)
When **antibiotics** destroy colonic bacteria
40
Which med binds iron supplements and decreases absorption? (red)
Sulfazalazine
41
Which med can potentiate warfarin's effects- displace from protein binding?
**Sulfasalazine** (nonbiologic DMARD)
42
What are the names of the 2 JAK inhibitors used to tx OA?
1. Tofacitinib 2. Baricitinib ("JAK likes to eat Tofu at the Bar")
43
What is the use for the JAK inhibitors, Tofacitinib and Baricitinib?
moderate to severe RA who have failed or intolerance to methotrexate
44
**MOA of which RA 2 meds?** * **inhibition of JAK**- a tyrosine kinase * modulation and suppression of the immune system through **cytokine signal reduction**
JAK inhibitors: Tofacitinib and Baricitinib
45
ADEs of which 2 meds? * **serious infections** * **_lymphomas, and other malignancies_** * elevated plasma liver enzymes and lipids
JAK inhibitors: TOfacitinib and Baricitinib
46
Which two meds have been tested and treated for latent TB?
JAK inhibitor: Tofacitinib and Baricitinib
47
Should live vaccines be given during treatment with the JAK inhibitors: Tofacitinib and Baricitinib?
NO
48
Which 2 meds can cause **_Lymphomas or other malignancies_**? (KNOW)
JAK inhibitors: Tofacitinib and Baricitinib
49
**Azathioprine, cyclosporine and Clyclophosphamide** are other DMARDs used to tx RA. Match them to their ADEs: * \_\_\_\_\_= gastritis * \_\_\_\_\_= Leukopenia, hepatotoxicity * \_\_\_\_\_= nephrotoxicity
* **_Cyclophosphamide_** = gastritis * **_Azathioprine_** = Leukopenia, hepatotoxicity * **_Cyclosporine_** = nephrotoxicity \*Used less frequently today b/c of toxicity and/or lack of long term benefit\*
50
What is the 1 contraindication of the TNF-α biologic DMARDs? (KNOW)
CHF
51
The following are the ADEs of which group of biologic DMARDs? –**MS-like illness** or exacerbate MS –Increased risk of l**ymphoproliferative cancer**
**TNF-α Biologics** (limumab, Certolizumab, Entanercept, Golimumab, Infliximab)
52
Which TNF-α biologic DMARD? * Chimeric antibody combining portions of **mouse and human IgG1**
Infliximab
53
Which 4 vaccines can be given during RA therapy with Biologic DMARDs?
Killed vax: * Pneumococcal * IM influenza * Hep B Recombinant: * HPV
54
T/F: Live vaccines can be given to patients already on DMARD therapy, but NOT biologics
True
55
For patients **\> 50y/o** who will be starting a biologic or Tofacitinib, ACR recommends giving which vaccine?
Herpes Zoster vaccine
56
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
True
57
Which 2 biologics should be continued with Methotexate?
**Infliximab** (TNF-a) **Rituximab** (B cell)
58
Which BIologic DMARD causes **near complete depletion of peripheral B cells**?
Rituximab
59
Which med can turn your skin a yellow/orange color?
Sulfasalazine
60
MOA of methotrexate: Which enzyme does Methotrexate inhibit?
dihydrofolate reductase enzyme
61
What supplement is important to give with Methotrexate?
Folic acid

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