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PHRM 825 Steroids Exam 2 > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

1
Q

what is pathogenesis?

A
  1. degenerative changes that occur in cartilage (a metabolically dynamic tissue) and
    the associated bone
  2. characterized by increased destruction and subsequent proliferation of cartilage
    and bone; regenerated articular surfaces do not possess the same qualities and
    architecture as the original joint.
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2
Q

what is incidence?

A
  • Observed more commonly in older patients
  • almost 85% of patients > 75 years
  • F > M
  • Joints most commonly affected:
  • Distal interphalangeal joint (DIP)
  • Hips
  • Knees
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2
Q

what is etiology?

A
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3
Q

what are the risk factors for OA?

A
  • Increasing age
    o Obesity
    o Congenital/anatomical defects
    o Muscle weakness
    o Female gender
    o Repetitive stress
    o Major joint trauma
    o Heredity
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4
Q

What are the clinical manifestations/ presentation of OA?

A

o pain
o pain worse with activity
o AM stiffness is brief (< 1 hour)
o crepitus
o inflammation is observed in more advanced disease / pain at rest
o asymmetric involvement
o muscle atrophy
o no systemic symptoms
o instability of weight bearing joints
o Herberden’s nodes
o Bouchard’s nodes

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5
Q

What are the goals/ desired outcome of therapy?

A

o Relief of pain and discomfort
o Maintain function and strength of joint

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6
Q

what is the non-pharmacologic treatment of OA?

A

▪ psychological support
▪ education
▪ rest
▪ physical activity / exercise
▪ heat / ice
▪ PT
▪ OT
▪ weight loss

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7
Q

what are the guidelines for hip/knee OA?

A
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8
Q

what are the guidelines for hand OA?

A
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9
Q

what are the monitoring parameters for patients with OA?

A
  • pain (pain at rest)
  • joint stability and function
  • risk of fall
  • ROM
  • X-rays
  • degree of disability
  • weight
  • ADRs from medications
  • compliance with non-drug
    measures
  • QOL issues
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10
Q

what is the purpose of joint replacement/ resurfacing surgery?

A
  • relieves pain
  • restores function to joint
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11
Q

what is the pipeline for medications in clinical trials?

A
  • intra-articular injections
  • disease modifying osteoarthritis drugs / biologics
  • nerve growth factor blocker
  • all-trans retinoic acid
  • fibroblast growth factors
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12
Q

Tell me all information related to Menthol/ camphor/ oil of wintergreen (mechanism of action/ adverse effects/ dose/ important notes).

A

topical counter irritant
* apply sparingly
* dose: aaa tid-qid
* avoid contact with eyes

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13
Q

Tell me all information related to capsaicin cream (mechanism of action/ adverse effects/ dose/ important notes).

A

mechanism of action: depletes substance p
* dose: aaa tid-qid
* wait 2 - 4 weeks to evaluate maximum effect
* educate patient about proper application procedures
* adverse effects: burning, stinging, and redness (leaves with continued use)

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14
Q

Tell me all information related to diclofenac gel (mechanism of action/ adverse effects/ dose/ important notes).

A

mechanism of action: local inhibition of COX-2 enzymes
* dose: 2-4g aa qid (16g max; 32g/body daily)
* not recommended in combination with systemic NSAID therapy
* adverse effects: pruritus, burning, pain, and rash

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15
Q

Tell me all information related to diclofenac solution (mechanism of action/ adverse effects/ dose/ important notes).

A
  • knee only
  • dose: 40drops to each knee qid (10 drops at a time
    –> two pumps (40mg) bid
  • adverse effect: local reaction
16
Q

Tell me all information related to tylenol (mechanism of action/ adverse effects/ dose/ important notes).

A
  • mechanism of action: inhibits synthesis of prostaglandins
  • dose: 1g q6h
  • Maximum dose per day: 3-4g per day
  • Patients at risk for hepatotoxicity:
    – heavy alcohol intake
    – pre-existing liver condition
17
Q

Tell me all information related to NSAIDs (mechanism of action/ adverse effects/ dose/ important notes).

A
  • mechanism of action: blocks prostaglandin synthesis by inhibition of COX enzymes
  • selection based on: cost, side effects, dosing convenience, other medical conditions,
    other medications, risk of bleeding, risk of PUD
  • dosing: analgesic dose vs. anti-inflammatory dose
    –> naproxen 200 or 440mg q8-12h
  • 1-2 week trial for pain and 2-4 week trial if inflammation exists
18
Q

Tell me all information related to tramadol (mechanism of action/ adverse effects/ dose/ important notes).

A

mechanism of action: affinity for µ receptor; inhibits norepinephrine and serotonin
* dose: 25-50mg q4-6 (titrate to 200-300mg/day)
* adverse effects/precautions: nausea, vomiting, dizziness, constipation

19
Q

Tell me all information related to duloxetine (mechanism of action/ adverse effects/ dose/ important notes).

A

adjunct to first line
* appropriate for neuropathic and musculoskeletal pain
* dose: 30mg/d day for 1 wk; max 60mg
* avoid with tramadol
* adverse effects: gi – nausea, vomiting, constipation

19
Q

Tell me all information related to glucosamine/ chondroitin (mechanism of action/ adverse effects/ dose/ important notes).

A

mechanism of action: stimulate proteoglycan synthesis from articular cartilage
* dose: 500mg tid (glucosamine); 400mg tid (chondroitin)
* slow onset
* adverse effects: gas, bloating, cramping, nausea, inc. bleeding with glucosamine
* concern about standardization of products
* some concern about use in patients with DM, HTN, hyperlipidemias due to increased
insulin resistance

20
Q

Tell me all information related to intra-articular corticosteroid injections (mechanism of action/ adverse effects/ dose/ important notes).

A
  • only used for isolated joints
  • no more often than every 4-6 months
  • peak pain relief in 7-10 days
21
Q

Tell me all information related to hyaluronate injections (mechanism of action/ adverse effects/ dose/ important notes).

A
  • mechanism of action: temporarily increase viscosity of joint
  • dose: injected once weekly x 3 - 5 weeks into joint (minor swelling)
  • maximum benefit in 8-12 weeks
22
Q

when are opioid analgesics used for OA?

A
  • used PRN for breakthrough pain
  • watch total dose of APAP very closely
  • dosing: start low and go slow; use SR or IR
  • adverse effects/precautions: nausea, constipation, dizziness, somnolence
23
Q

what are potential benefits for using a COX-2 inhibitor?

A

o once daily dosing
o lower incidence of severe GI bleeding

24
Q

what are the risks of using a COX-2 inhibitor?

A

o CV disease
o impact on renal function
o increased costs

25
Q

what combos could we consider for OA treatment?

A
  1. COX-2 Inhibitor Celebrex®
  2. Adding a PPI (NSAID + PPI Vimovo® (naproxen + esomeprazole))
  3. NSAID + misoprostol Arthrotec
    ® (diclofenac + Misoprostol)
  4. NSAID + H2 antagonist (Duexis® - ibuprofen + famotidine)
26
Q

what are the major adverse effects of NSAIDs?

A
  • GI upset
    o GI ulceration
    o bleeding
    o renal dysfunction
    o effects on BP
27
Q

how can we monitor NSAID therapy?

A

o blood pressure
o symptoms of edema or weight gain
o SCr
o Hgb/Hct
o signs of dehydration

28
Q

What patients at greatest risk for ADRs from NSAIDs?

A
  • dose dependent
    o age > 75
    o h/o GI bleed
    o h/o of PUD
    o anticoagulant therapy
    o antiplatelet therapy
    o glucocorticoids
    o patients with CHF, HTN, renal dysfunction, and dehydration are at increased risk
    of nephrotoxicity
    o increase risk of major cardiovascular events (MI, stroke)

PHRM 825 Steroids Exam 2 (8 decks)

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