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Pharm II-Exam 3 > Rheumatology > Flashcards

Rheumatology Flashcards

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?

A

Stomatitis

21
Q

Methotrexate ADE’s

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?

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

A

Inhibits pyrimidine synthesis=decrease in lymphocytes and modulation of inflammation

24
Q

Leflunomide toxicities

A
  1. GI
  2. Hair loss
  3. Liver
  4. bone marrow
25
Q

Leflunomide CI

A
  1. Liver dz

2. Teratogenic

26
Q

Hydroxychloroquine clinical application

A
  1. Mild RA

2. Adjunct in combo DMARD therapy in more progressive dz

27
Q

Hydroxychloroquine ADE’s

A
  1. Lacks myelosuppressive*
  2. Hepatic and renal toxicities
  3. Ocular: Decrease in night or peripheral vision
28
Q

Sulfasalazine MOA

A

Prodrug cleaved in colon to:

  1. Sulfapyridine (active anti rheumatic) AND
  2. 5-aminosalycylic acid
29
Q

What can effect the absorption of Sulfasalazine?

A

Decreased w/ abx

Binds iron supplements

30
Q

Sulfasalazine ADE’s

A
  1. Elevated hepatic enzymes

2. Skin color change to yellow-orange

31
Q

Minocycline clinical applications

A

Low dz activity and w/o features of poor prognosis

No effect on erosion progression

32
Q

What CANT be given during Tofacitinib (JAK inhibitor) treatment?

A

Live vaccines

33
Q

Gold salts ADE

A

Myelosuppression

34
Q

Azathioprine ADE

A

Leukopenia

Hepatoxicity

35
Q

Cyclosporine ADE

A

Nephrotoxicity

36
Q

Cyclophosphamide ADE

A

Gastritis

37
Q

Define Biologic agents

A

Genetically engineered protein molecules block the pro inflammatory cytokines

38
Q

CI to Biologic TNF-α

A

CHF

39
Q

Biologic TNF-α ADE’s

A
  1. MS-like illness or exacerbate MS

2. Increased risk of lymphoproliferative CA

40
Q

what kind of TNF-α is Etanercept?

A

Fusion protein

Binds to TNF, makes it biologically inactive

41
Q

what kind of TNF-α is Inflixmab?

A

Chimeric AB combining portions of mouse and human IgG1

Binds to TNF

42
Q

What do pt’s need to be also taking while on Inflixmab? Why?

A

Methotrexate to prevent AB response to foreign protein

43
Q

Lis the other Biologic DMARD TNF-α’s

A
  1. Adalimumab
  2. Golimumab
  3. Certolizumab
44
Q

What is Anakinra? What does it block?

A

Non-TNF

Blocks IL-1

45
Q

Anakinra ADE

A

HTN

46
Q

What does Tocilizumab block?

A

IL-6

47
Q

Tocilizumab ADE’s

A
  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
Q

Rituximab MOA

A

Binds to B cells=depletion of peripheral B cells

49
Q

Abatecept MOA

A

Binds to CD80/86 on T cells to prevent full activation of T-cells

Pharm II-Exam 3 (4 decks)

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