Pharm Chapter 16 - RA and OA

Question 1

What are some characteristics of RA?

Answer 1

•Diffuse pain (myalgia, arthritis)
•Morning stiffness lasting greater than one hour
Effects joints of: elbow, foot, hands/wrists, hip, knee, shoulder

Question 2

Factors contributing to RA

Answer 2

Genetics, smoking, viral insult or some situation that prompts a cascade of immunomodulators and destructive enzymes

Question 3

Prevalence of RA

Answer 3

3x more frequent in women

Question 4

Goals of RA drug therapy

Answer 4

• Decrease joint inflammation

* Arrest progression of disease

Question 5

What are the 3 categories of RA medications?

Answer 5

• NSAIDs
• Glucocorticoids
• DMARDs

Question 6

What does DMARDs stand for?

Answer 6

Disease Modifying Anit-Rheumatic Drugs

Question 7

NSAIDs

Answer 7

•Decrease inflammation
•Analgesic effect
•Specific choice is patient driven
MOA: COX inhibition thus blocking PGs and inflammatory mediators
AE: GI irritations and bleeds

Question 8

Glucocorticoids

Answer 8

•For acute exacerbations
•Reduce dose to smallest effective dose
•Can be injected directly into the joint (limit to 4 times per year)
MOA: Increase production of several anti-inflammatory proteins, Decrease production of pro-inflammatory substances
AE: Catabolic effects on supportive tissue, osteoporosis, muscle wasting, weakness, HBP, DM

Question 9

Types of DMARDs

Oral medications

Answer 9

Antimalarials
Azathioprine
Gold Salts
Leflunomide
Methotrexate
Penicillamine
TNF Inhibitors
Anakinra

Question 10

Antimalarials

Answer 10

Decrease T cell stimulation thus cause immunosuppression

AE: retinal toxicity

Question 11

Azathioprine

Answer 11

Immunosuppressant

One of the more toxic DMARDs (N/V limits its use)

Question 12

Gold Salts

Answer 12

Reserved for those who fail other therapies, PO preferred

AE: GI distress and blood dyscrasias

Question 13

Leflunomide

Answer 13

Slows bone erosions
Rapid onset, well tolerated
AE: GI distress, hair loss, liver toxicity

Question 14

Methotrexate

Answer 14

Oncology medication (at significantly higher doses)
One of the most effective DMARDs
Decreased bone erosion, reduced narrowing of the joint space
Decrease synovitis
DOC, superior effects, faster onset
Inhibition of folic acid blocks proliferation of lymphocytes in the inflammatory response
Monitoring liver function, PFTs

Question 15

Penicillamine

Answer 15

rarely used due to adverse effects – bloody urine, edema

Question 16

TNF Inhibitors

Answer 16

TNF is the key chemical mediator promoting joint inflammation and erosion in RA
Examples: Enbrel, Remicade, Humira: effect biologic response to TNF and destroy cells that secrete TNF
Risk of URTI, malignancy with these drugs

Question 17

OA Characteristics

Answer 17

• Mild synovitis and articular damage
• Primary OA - no seeming cause
• Secondary OA - some trauma or trigger

Question 18

Contributing factors to OA

Answer 18

• Intrinsic defect in joint cartilage

* Formation of bone cysts and protrusions

Question 19

OA Prevalence

Answer 19

• 50-80% of patients >65 yo have some form

* ~100% over 75 years

Question 20

Goals of OA drug therapy

Answer 20

1. Decrease pain

2. Improve active lifestyle

Question 21

Acetominophen

Answer 21

Drug of choise <4g per day

AE: less GI effects

Question 22

Intra-articular steroid injections

Answer 22

•No more than every 3 months

Question 23

Viscosupplementation

Answer 23

Injection of hyaluronan into the synovial fluid of arthritic joints. Restores normal viscosity of the synovial fluid, reducing joint stress. No effect for at least 4 weeks
Examples: Hyalgan, Synvisc, Supartz

Question 24

Glucosamine/Chondroitin

Answer 24

• Reasonable trial in patients with high rates of cartilage turnover

Question 25

Other therapies for OA

Answer 25

• Weight loss
• Low impact exercise
• PT
• Braces, orthotics, assistive devices **caution with glucocorticoids