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Pharm II-Exam 3 > Rheumatology > Flashcards

Rheumatology Flashcards

(49 cards)

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1
Q

What is the MC type of OA?

A

Primary=Idiopathic

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2
Q

Define Secondary OA

A

associated with a known cause

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3
Q

What is the primary objective of medication therapy in OA?

A

Pain Relief

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4
Q

Based on efficacy and safety, what is the initial pharmacologic recommendation in the treatment of OA?

A

Acetaminophen

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5
Q

CI to NSAIDs

A
  1. Renal patients
  2. Liver failure
  3. CHF
  4. Hx GI bleed
  5. Taking blood thinners
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6
Q

What can you consider to reduce GI toxicity with the use of NSAIDs?

A
  1. Nonacetylated salicylate: Choline magnesium trisalicylate
  2. COX-2 selective inhibitors
  3. Addition of Misoprostol or PPI
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7
Q

What can you consider to reduce CV risk with the use of NSAIDs?

A

Naproxen

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8
Q

What is recommended for pt’s older than 75 to reduce the risk of systemic toxicity?

A

Topical NSAIDs= Ketoprofen

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9
Q

What is activated in the pathogenesis of RA?

A
  1. Macrophages
  2. T-cells
  3. Fibroblast
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10
Q

Effects of activated macrophages, T-cells and fibroblast

A
  1. Tissue destruction
  2. Increased blood flow
  3. Cellular invasion of synovial tissue and joint fluid
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11
Q

What is drug therapy targeting in RA?

Overall goal of drug treatment?

A

IL-1
IL-6
IL-17

*Control inflammation!=”Treat to Target”

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12
Q

What is first line treatment in RA? When do you want to start drug treatment?

A

DMARDs: Methotrexate

Start w/in 3 months of dx! Early aggressive tx may prevent irreversible joint damage/disability

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13
Q

When should NSAIDs and corticosteroids be considered in RA treatment?

A

Adjunctive therapy early in course of treatment and as-needed if sx’s are not adequately controlled w/ DMARDs

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14
Q

Drug treatment in RA pt’s with less active dz and good prognostic indicators

A

Oral agents as monotherapy

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15
Q

Drug treatment in RA pt’s with high dz activity and/or poor prognostic indicators

A

Combination therapy and biologics to suppress inflammation:

  1. Methotrexate-hydroxychloroquine
  2. Methotrexate-leflunomide
  3. Methotrexate-sulfasalazine
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16
Q

What does ACR recommend/endorse?

A
  1. Triple combination:
    Methotrexate + hydroxychloroquine + sulfasalazine
  2. Use of Anti-TNF biologics in pt’s w/ early dz of high activity and presence of poor prognostic factors, regardless of previous DMARD use
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17
Q

List the ANti-TNF drugs

A
  1. Etanercept
  2. Infliximab
  3. Adalimumab
  4. Certolizumab
  5. Golimumab
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18
Q

Methotrexate MOA

A

Anti-inflammatory properties:

  1. Inhibits cytokine production
  2. Inhibits purine biosynthesis
  3. stimulate release of adenosine
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19
Q

What would you want to consider supplementing with in the use of Methotrexate? why?

A

Folic acid

Folic acid antagonist

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20
Q

What is the first ADE you often see in the use of Methotrexate?

21
Q

Methotrexate ADE’s

Study These Flashcards
A
  1. GI: N/V/D
  2. Hepatic: elevated liver enzymes
  3. Hem: Thrombocytopenia
  4. Pulm: pulmonary fibrosis and pneumonitis
22
Q

Who is Methotrexate CI?

Study These Flashcards
A
  1. Pregnant women
  2. Chronic liver dz
  3. Pleural or Peritoneal effusions
  4. Leukopenia, thrombocytopenia
  5. Immunodeficiency
  6. CrCl <40 ml/min
23
Q

Leflunomide MOA

Study These Flashcards
A

Inhibits pyrimidine synthesis=decrease in lymphocytes and modulation of inflammation

24
Q

Leflunomide toxicities

Study These Flashcards
A
  1. GI
  2. Hair loss
  3. Liver
  4. bone marrow
25
Leflunomide CI
1. Liver dz | 2. Teratogenic
26
Hydroxychloroquine clinical application
1. Mild RA | 2. Adjunct in combo DMARD therapy in more progressive dz
27
Hydroxychloroquine ADE's
1. Lacks myelosuppressive* 2. Hepatic and renal toxicities 3. Ocular: Decrease in night or peripheral vision
28
Sulfasalazine MOA
Prodrug cleaved in colon to: 1. Sulfapyridine (active anti rheumatic) AND 2. 5-aminosalycylic acid
29
What can effect the absorption of Sulfasalazine?
Decreased w/ abx | Binds iron supplements
30
Sulfasalazine ADE's
1. Elevated hepatic enzymes | 2. Skin color change to yellow-orange
31
Minocycline clinical applications
Low dz activity and w/o features of poor prognosis | No effect on erosion progression
32
What CANT be given during Tofacitinib (JAK inhibitor) treatment?
Live vaccines
33
Gold salts ADE
Myelosuppression
34
Azathioprine ADE
Leukopenia | Hepatoxicity
35
Cyclosporine ADE
Nephrotoxicity
36
Cyclophosphamide ADE
Gastritis
37
Define Biologic agents
Genetically engineered protein molecules block the pro inflammatory cytokines
38
CI to Biologic TNF-α
CHF
39
Biologic TNF-α ADE's
1. MS-like illness or exacerbate MS | 2. Increased risk of lymphoproliferative CA
40
what kind of TNF-α is Etanercept?
Fusion protein | Binds to TNF, makes it biologically inactive
41
what kind of TNF-α is Inflixmab?
Chimeric AB combining portions of mouse and human IgG1 | Binds to TNF
42
What do pt's need to be also taking while on Inflixmab? Why?
Methotrexate to prevent AB response to foreign protein
43
Lis the other Biologic DMARD TNF-α's
1. Adalimumab 2. Golimumab 3. Certolizumab
44
What is Anakinra? What does it block?
Non-TNF | Blocks IL-1
45
Anakinra ADE
HTN
46
What does Tocilizumab block?
IL-6
47
Tocilizumab ADE's
1. Increased infxn risk 2. Elevated plasma lipids 3. Elevated liver enzymes 4. GI perforation 5. Inducer of CYP450: Warfarin 6. Tested and Tx for TB
48
Rituximab MOA
Binds to B cells=depletion of peripheral B cells
49
Abatecept MOA
Binds to CD80/86 on T cells to prevent full activation of T-cells

Pharm II-Exam 3 (4 decks)

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