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Flashcards in Rheumatology Deck (49)
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1

What is the MC type of OA?

Primary=Idiopathic

2

Define Secondary OA

associated with a known cause

3

What is the primary objective of medication therapy in OA?

Pain Relief

4

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

Acetaminophen

5

CI to NSAIDs

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

6

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

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

7

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

Naproxen

8

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

Topical NSAIDs= Ketoprofen

9

What is activated in the pathogenesis of RA?

1. Macrophages
2. T-cells
3. Fibroblast

10

Effects of activated macrophages, T-cells and fibroblast

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

11

What is drug therapy targeting in RA?
Overall goal of drug treatment?

IL-1
IL-6
IL-17

*Control inflammation!="Treat to Target"

12

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

DMARDs: Methotrexate

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

13

When should NSAIDs and corticosteroids be considered in RA treatment?

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

14

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

Oral agents as monotherapy

15

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

Combination therapy and biologics to suppress inflammation:
1. Methotrexate-hydroxychloroquine
2. Methotrexate-leflunomide
3. Methotrexate-sulfasalazine

16

What does ACR recommend/endorse?

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

17

List the ANti-TNF drugs

1. Etanercept
2. Infliximab
3. Adalimumab
4. Certolizumab
5. Golimumab

18

Methotrexate MOA

Anti-inflammatory properties:
1. Inhibits cytokine production
2. Inhibits purine biosynthesis
3. stimulate release of adenosine

19

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

Folic acid
Folic acid antagonist

20

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

Stomatitis

21

Methotrexate ADE's

1. GI: N/V/D
2. Hepatic: elevated liver enzymes
3. Hem: Thrombocytopenia
4. Pulm: pulmonary fibrosis and pneumonitis

22

Who is Methotrexate CI?

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

23

Leflunomide MOA

Inhibits pyrimidine synthesis=decrease in lymphocytes and modulation of inflammation

24

Leflunomide toxicities

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