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Flashcards in rheumatic drugs Deck (86)
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1

how would you define arthritis? if uncontrolled what two things does it lead to?

Described as a chronic, inflammatory, progressive condition that attacks synovial tissue lining joints
If uncontrolled leads to:
Joint destruction due to erosion or cartilage and bone
Joint deformities

2

arthritis Progresses from_____ to more ______ joints

periphery to more proximal joints

3

RA or OA? Autoimmune disease that causes INFLAMMATORY SYNOVITIS

RA

4

RA or OA? Degenerative disease that causes articular CARTILAGE LOSS & joint space narrowing

OA

5

RA vs OA: morning symptoms, symmetry + locations, and systemic or local symptoms?

RA: Morning symptoms > 1 hr (stiffness)
Symmetrical : Affects wrists, hands, feet
Systemic symptoms

OA: Morning symptoms < 1 hr (stiffness)
Asymmetrical: spine/hip
Localized symptoms

6

RA vs OA: which is more predominant in females? which in old people?

females: RA
old people: OA

7

lab findings in RA?

RA: Positive rheumatoid factor, anti-CCP antibody, and elevated ESR & CRP

**OA: normal lab findings

8

what is the onset for RA vs OA?

RA: rapid (weeks-months)
OA: progressive, longterm (years)

9

4 lab tests used to Dx RA vs OA?

Rheumatoid Factor (RF)
Anti-CCP
Erythrocyte Sedimentation Rate (ESR)
C-Reactive Protein (CRP)

10

of the classification criteria for RA, what score does on need to get dx? what is it based on?

6/10
(based on joint involvement, serology, acute phase reactants(CRP + ESR) and duration of symptoms)

11

goal of txt for RA? (3 things to include)

Goal of therapy is to control the inflammatory process so that disease remission occurs
This should lead to pain relief; maintenance of function; and improved quality of life

12

5 markers of txt for RA

1. Reduction in number of affected joints and in joint tenderness and swelling
2. Improvement in pain
3. Decreased amount of morning stiffness
4. Reduction in serologic markers such as RF (Rheumatoid Factor)
5. Improved quality of life

13

3 groups of drugs used to txt RA

1. anti-inflammatory : NSAIDs
2. anti-inflammatory/possible immunomodulatory: glucosteroids
3. DMARDS

14

what does DMARDS stand for? what 3 drug groups are included in this?

(disease modifying antirheumatic drugs)
Immunomodulators
Immunosuppressants
Biologic agents

15

do NSAIDs help modify the disease?

no, little effect on progression of bone/cartilage destruction, can preserve function

16

how long does it take for NSAIDs to work? analgesic vs anti-inflammatory effects

analgesic w/in hours
Anti-inflammatory effect occurs within 1-2 weeks of daily dosing

17

ADRs of NSAIDs

GI and cardiovascular

18

general MOA of glucocorticoids? (maybe weeds)

alter gene transcriptions - target downregulate COX and upregulate annexin 1 (pro-anti-inflammatory mediator)

19

glucocorticoids low dose vs high dose effects

Suppress inflammation at low doses and suppress immune system at high
Low dose <20mg prednisone/day
High dose> or= 40mg/day

20

what are glucocorticoids mostly used for regarding RA?

Often used as bridge therapy to provide anti-inflammatory effect while waiting for the DMARDs to take effect

21

4 general ADRs of steroids? (maybe weeds)

ADR: immune suppression, weight gain, insomnia, cushing

22

what do DMARDS work to do for RA?

Slow down the destruction from underlying disease, don’t stop it altogether
SLOW PROGRESSION

23

how long does it take DMARDS to work?

3 months of use before an effect is seen
*If no improvement by 3 months or target is not reached by 6 months-treatment needs to be modified

24

what kind of biologic agents may be used for RA? why?

inhibit tumor necrosis factor (TNF) & interleukin receptor antagonist
used in patients who don’t respond to first-line agents (methotrexate). Theyre better and more targetted BUT very expensive.

25

two main subgroups of DMARDS

1. conventional synthetic DMARDS(immunomodulating + immunosuppressing)
2. biologic DMARDS

26

what are the two immunomodulating csDMARDs?

Hydroxychloroquine (Plaquenil)*
Sulfasalazine (Azulfidine)*

27

what are the 3 immunosuppressive csDMARDs?

Methotrexate (Rheumatrex)*
Leflunomide (Arava)*
Azathioprine (Imuran) - not as commonly used

28

what are the TNFalpha biologic DMARDS?

Adalimumab (Humira)
Infliximab (Remicade)
Etanercept (Enbrel)
Golimumab (Simponi)
Certolizumab (Cimzia)

all "-umab" and Etanerecept

29

"other biologic DMARDs" (kinda weeds)

Abatacept (Orencia)
Rituximab (Rituxan)
Anakinra (Kineret)
Tocilizumab (Actemra)
Tofacitinib (Xeljanz)

30

3 serious ADRs of hydroxychloroquine

1. Cardiovascular: QT prolongation (not bad on its own but when in combo with other drugs that cause it- anti-pyschotics, macrolides)
2. Hematologic: Myelosuppression
3. Ophthalmic: Retinopathy