Rheumatoid Arthritis Flashcards
1
Q
Rheumatoid Arthritis
A
- chronic inflammatory autoimmune disorder
- may include rheumatoid nodules, vasculitis, eye inflammation, neurologic dysfunction, cardiopulmonary dz, lymphadenopathy
2
Q
Pathophys of RA
A
- chronic inflammation of synovial tissue –> proliferation –> pannus (inflamed synovium) –> erosion of bone/cartilage and joint destruction
- can develop joint damage as soon as 2 years after dz onset
3
Q
Clinical Presentation RA
A
- insidious onset
- prodromal sxs: fatigue, weakness, low grade fever
- symmetrical joint involvement, esp small joints of hands, wrists, feet
- dz waxes and wanes
4
Q
Joint Involvement in OA
A
-large joints, including hips, knees, neck, lower back
5
Q
Functional Classification of RA
A
1: completely able to perform usual ADLs
2: able to perform usual self-care and work, but not recreational activities
3: able to perform self-care, but not work or recreational activities
4: limited in ability to perform any ADLs
6
Q
Tx Goals
A
- reduce or eliminate pain
- protect articular structures
- control systemic complications
- prevent loss of joint functions
- improve or maintain QOL
7
Q
Non-Pharm Tx
A
- rest
- OT, PT
- pt education, pt support group
- weight reduction as needed
- surgery
8
Q
General Approach to Pharm Treatment
A
- start tx early and aggressively (>1 DMARD at effective doses)
- start DMARD therapy within 3 months of dx
9
Q
Medication Classes Commonly Used to Tx RA
A
- NSAIDs
- glucocorticoids
- nonbiologic and biologic DMARDs
10
Q
Factors that Affect Tx Decisions
A
- dz activity
- dz duration (early 24 mos)
- prognosis (poor = functional limitation, +Rh factor or anticyclic citrullinated peptide antibodies)
11
Q
NSAIDs for RA
A
- initial drug therapy for RA
- decrease joint inflammation and pain
- DO NOT prevent joint destruction or slow dz progression (should not be used alone)
12
Q
Corticosteroids for RA
A
- anti-inflammatory and immunosuppressive efects
- bridging therapy, continuous low dose (avoid), short term high dose bursts to control flare
13
Q
Corticosteroids AEs
A
- HTN, hyperglycemia, cataracts
- skin fragility
- fluid retention, weight gain, osteoporosis
14
Q
Methotrexate
A
- nonbiologic DMARD of choice
- often chosen as initial therapy
15
Q
Methotrexate MOA
A
-inhibits dihydrofolate reductase, purines and thymidylic acid, cytokines (decrease inflammation)
16
Q
Methotrexate AEs
A
- stomatitis, N/D
- possible alopecia
- elevated LFTs, liver toxicity risk is low
- thrombocytopenia, leukopenia
- rare pulm and lympho toxicity
17
Q
Methotrexate Relative CIs
A
- liver dz
- kidney impairment
- significant lung dz
- EtOH abuse
18
Q
Methotrexate CIs
A
-do not use in pregnant or nursing women
19
Q
Methotrexate Monitoring
A
LFT is necessary and CBC
20
Q
Methotrexate Clinical Response
A
1-2 months
21
Q
Methotrexate Interactions
A
- caffeine may decrease MTX effectiveness
- PPIs, NSAIDs, ASA may decrease renal clearance of MTX
22
Q
Leflunomide/Arava
A
-alternative option to MTX; as effective as MTX at reducing dz activity and progression
23
Q
Leflunomide/Arava MOA
A
-inhibits pyrimidine synthesis = anti-proliferative and anti-inflammatory effects
24
Q
Leflunomide/Arava AEs
A
- elevated liver enzymes, esp if combined with MTX
- hepatotoxicity
- pancytopenia
- agranulocytosis
- thrombocytopenia
- may interact w/ warfarin and increase INR
25
Leflunomide/Arava CIs
- liver dz
- viral hepatitis
- severe immunodeficiency
- obstructive biliary dz
- inadequate birth control (preg cat X)
- treatment with rifampin (increases leflunomide levels)
26
Leflunomide/Arava Monitoring
- ALT, platelet, WBC, hgb/hematocrit
| - baseline, monthly for 6 months then every 6-8 weeks
27
Leflunomide/Arava Half-Life
- undergoes enterohepatic recirculation
| - half life 14-16 days
28
Leflunomide/Arava Clinical Response
1-3 months
29
Minocycline
-recommended for mild dz only (early dz w/ low activity)
30
Minocycline MOA
- unclear
| - thought to have antimicrobial, anti-inflammatory, immunomodulatory and chondroprotective effects
31
Minocycline AEs
- photosensitivity, GI upset
- pseudotomor cerebri (benign intracranial HTN)
- abnormal pigmentation
- vertigo
- rare severe drug rxn (lupus-like)
32
Minocycline CIs
-do not use in kids <8, pregnant or nursing women 2ary to tooth discoloration
33
Minocycline Drug Interactions
- antacids (antacids decrease mino activity so dose separately)
- OCs
- anticoagulants
34
Minocycline Clinical Response
3-9 months
35
Hydroxychloroquine/Plaquenil
- often chosen as initial therapy for pts with milder or less active dz
- does not slow dz progression
36
Hydroxychloroquine/Plaquenil MOA
-inhibits movement of neutrophils and eosinophils
37
Hydroxychloroquine/Plaquenil AEs
- rash, diarrhea, abd. cramps
| - increased risk of retinal toxicity > 6 gm/kg
38
Hydroxychloroquine/Plaquenil Monitoring
- no lab monitoring needed
| - periodic ophthalmic exams for early detection of retinal toxicity
39
Hydroxychloroquine/Plaquenil Clinical Response
2-6 months
40
Sulfasalazine/Azulfidine
-helps slow dz progression in RA pts and may work more quickly than hydroxychloroquine
41
Sulfasalazine/Azulfidine MOA
-pro drug cleaved by colon bacteria to metabolites thought to have anti-RA activity
42
Sulfasalazine/Azulfidine AEs
- nausea, abd discomfort
| - mostly occur in first few months, can start with low dose
43
Sulfasalazine/Azulfidine Monitoring
- periodically for leukopenia
| - pts may notice yellow/orange color of urine or skin
44
Sulfasalazine/Azulfidine Clinical Response
1-3 months
45
Biologic DMARDs
- genetically engineered protein molecules
- much more expensive than other DMARDs
- all but 1 require parenteral administration
- risk of serious infections
46
MOA for Each Type of Biologic DMARD
- inhibit tumor necrosis factor alpha
- inhibit interleukin 1
- deplete peripheral beta cells
- inhibit full T cell activation
- block action of interleukin 6
47
Examples of TNF-alpha Inhibitors
- etanercept (Enbrel)
- adalimumab (Humira)
- infliximab (Remicade)
48
AEs of TNF-alpha Inhibitors
- some may exacerbate or cause CHF (etanercept from med sheet)
- do not use infliximab in pts with mod-severe HF and use others w/ caution in pts w/ HF
- risk of infections and lymphomas
49
Interleukin 1 Receptor Antagonist Name
anakinra (Kineret)
50
Interleukin 1 Receptor Antagonist AEs
-HA, local injection site rxn, infx
51
T-cell Activation Inhibitor Name
abatacept (Orencia)
52
T-cell Activation Inhibitor AEs
- HA, URTI, nasopharyngitis
- N most common
- acute infusion related reactions and hypersensitivity rare
- serious infection and malignancies
53
B-cell Depletion Drug Name
rituximab (Rituxan)
54
T-cell Activation Inhibitor Name AEs
-HTN, hyperglycemia, cataracts, skin fragility, fluid retention, weight gain, osteoporosis
55
IL-6 Blocking Drug Name
tocilizumba (Actemra)
56
IL-6 Blocker AEs
- URTI, HA, rhinitis
- HTN, increased LDL
- increased LFTs
57
Janus kinase selective inhibitor AEs
- risk of infxs and lymphomas
- GI perfs
- decreased lymphocytes/neutrophils/hgb
- LFT and lipid elevations
58
Combination Therapy
-single DMARD often inadequate for sxs control and preventing dz progression
59
List 4 less frequently used DMARDs.
- azathioprine
- cyclosporine
- D-penicillamine
- gold
60
What tx is recommended for low disease activity?
DMARD monotherapy
61
What tx is recommended for moderate disease activity without features of poor prognosis?
DMARD monotherapy
62
What tx is recommended for moderate disease activity WITH features of poor prognosis?
combination DMARD
63
What tx is recommended for high dz activity without features of poor prognosis?
- DMARD monotherapy OR
| - HCQ and MTX
64
What tx is recommended for high dz activity WITH features of poor prognosis?
- anti-TNF +/- MTX OR
| - combination DMARD therapy
