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PHAR 255 > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

1
Q

What is OA?

A

Chronic, progressive disorder characterized by the loss of articular cartilage in primarily hands, knees, hips and spine

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2
Q

True or False? The most common form of arthritis is OA

A

True

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3
Q

Peak age of onset of OA is?

A

50-60 years

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4
Q

The MOA of OA is not completely understood, but what is the primary and secondary etiology of it?

A

Primary - no identifiable factor
Secondary - other metabolic factors identified (i.e., hemachromatosis, acromegaly)

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5
Q

How is joint trauma a factor of OA? (3)

A
  1. Biochemical and mechanical changes –>
  2. Loss of functionality –>
  3. Changes in cartilage, joint capsule, subtracheal bone
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6
Q

Describe the pathogenesis of OA (3)

A
  1. Imbalance between cartilage maintenance and destruction
  2. Role of inflammatory cytokines (TNF, IL-1)
  3. Role of matrix metalloprotease
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7
Q

Describe how the imbalance between cartilage maintenance and destruction can cause OA (3)

A
  1. Malfunction of chondrocyte (responsible for cartilage breakdown)
  2. End result is loss of proteoglycans and water
  3. Formation of osteophytes (bony outgrowths)
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8
Q

What are the 2 modifiable risk factors for OA?

A
  1. Obesity
  2. Joint trauma
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9
Q

What are the 4 non-modifiable risk factors for OA?

A
  1. Age
  2. Genetics
  3. Sex
  4. Joint misalignment/deformity
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10
Q

What are the clinical features of OA? (5 main ones)

A
  1. Gradual onset
  2. Initial absence of inflammation or joint swelling
  3. Mono-articular at first
  4. Pain and stiffness with activity
  5. No systemic symptoms
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11
Q

How many stages of pain are there in OA?

A

3

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12
Q

Describe stage 1 pain of OA

A

Predictable, sharp pain brought on by activity

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13
Q

Describe stage 2 pain of OA

A

Pain becomes more constant; episodes of stiffness

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14
Q

Describe stage 3 pain of OA

A

Constant dull/aching pain; chronic stiffness; episodes of intense, exhausting pain

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15
Q

With OA, pain tends to be worse at what time of day?
What other quality might this pain have?

A
  1. Tends to be worse later afternoon/early evening
  2. May have a neuropathic quality
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16
Q

What are the joints commonly affected in OA?

A
  1. Distal interphalangeal (DIP), proximal interphalangeal (PIP), joints of thumb
  2. Cervical and lumbar spine
  3. Hip, knee, meotarsophalangeal joint
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17
Q

What are 2 deformities seen with OA?

A
  1. Heberden’s nodes (at DIP)
  2. Bouchard’s nodes (at PIP)
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18
Q

OA is often diagnosed WITHOUT ___________ or ___ ______

A

radiography; lab tests

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19
Q

In general, OA is diagnosed if: (3)

A
  1. Persistent usage-related pain
  2. Age > 45 years
  3. Little early morning stiffness; more evening stiffness
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20
Q

Additional testing for OA diagnosis will be needed if there are these criteria: (3)

A
  1. Younger individuals
  2. Atypical signs or symptoms
  3. Weight loss
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21
Q

What are the 4 main components of OA diagnosis?

A
  1. History
  2. Physical exam
  3. Imaging
    - X-ray may be helpful for diagnostic clarification or monitoring
    - Does not necessarily correlate with pain
  4. Laboratory tests
    - To rule out other conditions mostly
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22
Q

What are the goals of OA treatment? (5)

A
  1. Focus on specific lifestyle changes
  2. Reduce pain
  3. Maintain or improve joint mobility
  4. Limit functional disability
  5. Improve self-management
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23
Q

What are the 4 pillars of treatment of OA?

A
  1. Patient education
  2. Rehabilitation
  3. Medications
  4. Referrals
    - Surgical
    - Non-surgical
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24
Q

True or False? OA can be cured

A

False - can only manage for the most part

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25
Q

In terms of patient education, what should we be telling patients about OA? (4)

A
  1. Explain nature of OA as a chronic disease process. Refer to resources
  2. Emphasize importance of exercise
  3. Emphasize importance of weight control
  4. Benefits, harms, costs, expectation of treatment options
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26
Q

What are some (4) aspects of OA rehabilitation?

A
  1. Exercise
  2. Relaxation, Mind/Body
  3. Other
    - Acupuncture (meh)
    - Thermal interventions
  4. Environmental changes/aids
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27
Q

What are some components of exercise that should be implemented for OA rehabilitation? (5)

A
  1. Introduction of at home or structured exercise is a key initial management strat
  2. Range of motion, strengthening, aerobic activity
  3. Land-based vs. aquatic based
  4. What is too much?
    - In general, pain in joint lasting >2 hours after exercise
  5. Physiotherapy
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28
Q

What are some examples of relaxation, mind/body that can be utilized for OA rehabilitation? (4)

A
  1. Tai Chi - knee and hip OA
  2. Yoga - knee OA
  3. Balance exercises - knee and hip OA
  4. Cognitive behavioural therapy (CBT) - knee, hip, and hand
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29
Q

What are some examples of environmental changes/aids involved in OA rehabilitation? (4)

A
  1. Raised toilet seats, home or work adaptations
  2. Supports, splints, braces
  3. Canes, walkers
  4. Supportive footwear, shock absorbing orthotics
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30
Q

What are 4 characteristics/principles of medication treatment of OA?

A
  1. Drug therapy is targeted at pain relief
  2. Treatment should be conservative and individualized
  3. Begin with monotherapy prn and add/substitute medications as needed
  4. PO, topical, intrarticular
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31
Q

What are the 8 medication OA treatment options?

A
  1. Acetaminophen
  2. Topical NSAIDs
  3. Other topicals (capsaicin, a535)
  4. Oral NSAIDs
  5. Opioids (traditional and tramadol)
  6. Duloxetine
  7. Injectable joint replacement fluid
  8. Injectable glucocorticoids
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32
Q

True or False? Non-pharmacological interventions are not really useful for OA

A

False - they remain the most effective, but underutilized interventions for OA

33
Q

What is the MOA of acetaminophen?

A

Acts within the CNS, prevents prostaglandin synthesis by blocking COX

34
Q

What is the dosing of acetaminophen in OA?

A
  1. Up to 1g QID (max 4g in 24h)
  2. Appropriate trial 2-3 weeks at maximum doses, then use lowest effective dose
35
Q

What are some safety concerns to keep in mind when using acetaminophen? (3)

A
  1. Does not cause liver disease at normal doses
  2. Risk from pts consuming from multiple sources
  3. Lowered doses prudent for patients with:
    - Liver disease
    - Malnutrition, low body weight, advanced age, especially with chronic dosing
36
Q

What are some (3) DIs to be aware of when using acetaminophen?

A
  1. Warfarin (at higher doses)
  2. Continued alcohol use
  3. Isoniazid
37
Q

What are 2 topical NSAIDs that might be used in OA?

A
  1. Diclofenac (1.5% solution, 1.16 & 2.32% gel, and compounded %)
  2. Ketoprofen compounded
38
Q

What is the MOA of topical NSAIDs for OA?

A

Thought to inhibit COX-2 near the site of action

39
Q

What are the characteristics of topical NSAIDs? i.e.,;
- How often applied?
- How long until they take effect?
- Efficacy?
- Safety?

A
  1. Applied BID (with diclo/voltaren ES) to QID (others)
  2. Analgesic effect in hours, full effect may take a couple of weeks
  3. 60% of patients achieve at least 50% pain reduction
  4. Safety issues, drug interactions unlikely
40
Q

What is the MOA of topical capsaicin for OA?

A

Depletes substance P and down-regulates nociceptive fibers

41
Q

What are the characteristics of topical capsaicin in OA? i.e.,;
- Efficacy
- How often to apply
- How long to use
- Safety (2)?

A
  1. Superior to placebo
  2. Apply to joint TID-QID
  3. Must be used consistently for 2-4 weeks to see improvement
  4. Initial burning and sensitivity
  5. Systemic effects are rare, case reports of severe burns
42
Q

What are the 2 topical capsaicin strengths?

A
  1. 0.025%
  2. 0.075%
43
Q

Where are topical NSAIDs typically used? (3)

A
  1. Knee
  2. Hand
  3. Foot
44
Q

Where is topical capsaicin used on the body?

A

Knee OA

45
Q

What is the MOA of topical methyl salicylate?

A

Acts as a topical counter irritant

46
Q

What are the characteristics of methyl salicylate for OA? i.e.,;
- How often to apply
- Efficacy (2)
- When to avoid?

A
  1. Apply TID-QID
  2. Little evidence to support use
  3. Not well studied in controlled environment
  4. Avoid in ASA allergic patients, potential warfarin interaction
47
Q

What is the MOA of oral NSAIDs?

A

Bind to COX and prevent the production of prostaglandins

48
Q

What are the characteristics of oral NSAIDs in OA? i.e.,;
- Efficacy
- Risks
- When to use

A
  1. More effective than acetaminophen
  2. Risk of GI/CV/renal toxicity
  3. Preferred if topical NSAID failed, multiple joints affected, or hip and spine OA
49
Q

What are the 4 concerns of using oral NSAIDs?

A
  1. CV - risk is with all; the effect is dose related
  2. GI - serious complications <1% per year; assess risk and consider prophylaxis
  3. Renal - risk is with all
  4. Drug interactions
50
Q

How should oral NSAIDs be used in OA? (2)

A
  1. Utilize low doses and slow escalation
  2. Switching may help if one failed
51
Q

What to monitor when on long-term oral NSAID therapy? (5)

A
  1. Blood pressure
  2. Electrolytes
  3. Renal function
  4. CBC
  5. INR in patients taking anticoagulants
52
Q

What is the MOA of opioids?

A

Bind to opioid receptors in CNS and PNS, alters perception and response to pain

53
Q

When are opioids used in OA? (3)

A

Only recommended in select pts/last-line therapy
- The evidence for efficacy suggests modest benefits at best
- Viable treatment option for severe pain or CI to other agents
- Smallest effective dose for shortest duration as possible

54
Q

What are the concerns (AEs) regarding opioid use in OA? (7)

A
  • Sedation
  • Nausea
  • Constipation
  • Respiratory depression
  • Tolerance
  • Increased risk of falls/fractures in elderly, confusion
55
Q

What is the MOA of tramadol?

A

Centrally acting analgesic that binds to mu-opioid receptors. Also inhibits reuptake of serotonin and NE

56
Q

What are the concerns regarding tramadol? (5)

A
  1. Similar to opioids
  2. Risk of serotonin syndrome
  3. Drugs that lower seizure threshold
  4. QT prolongation
  5. Requires 2D6 to metabolize
57
Q

What’s the dosing of tramadol?

A

Dose 1-2 tabs Q4-6h prn (max 8 tabs per day)

58
Q

What is the MOA of duloxetine in OA?

A

SNRI
- Utilized as a second-line agent, esp. if neuropathic pain

59
Q

What are the indications for duloxetine? (6)

A
  1. Depression
  2. Anxiety
  3. Neuropathic pain (DM)
  4. Fibromyalgia
  5. Chronic low back pain
  6. OA of the knee (off-label: OA of hip)
60
Q

How long until onset of effect of duloxetine for OA?

A

1-4 weeks

61
Q

What are the AEs of duloxetine? (8)

A
  1. Headache
  2. Dry mouth
  3. Constipation
  4. Sedation
  5. Fatigue
  6. Sweating
  7. Appetite loss
  8. BP and HR increases at high doses
62
Q

What are some warnings to be aware of when using duloxetine? (6)

A
  1. GI bleed risk
  2. CNS depression
  3. Fracture risk increase
  4. Orthostatic hypotension
  5. Serotonin syndrome
  6. Sexual dysfunction
63
Q

What are 3 CIs of duloxetine?

A
  1. Narrow angle glaucoma
  2. End-stage renal disease and hepatic impairment
  3. Seizure history
64
Q

What are 2 DIs seen with duloxetine?

A
  1. Risk of serotonin syndrome with SSRIs
  2. Clearance may be decreased by CYP1A2 or 2D6 inhibitors
65
Q

What is the MOA of injectable corticosteroids for OA?

A

Interrupts inflammatory cascade at several levels

66
Q

Where might injectable corticosteroids be used?

A

Can be considered in hip, knee, shoulder OA

67
Q

What is the efficacy of injectable corticosteroids? (2)

A
  1. Short-term relief, no long-term benefit (depends on how long it lasts for the pt)
  2. Pain reduced by an average of 1-2 points on 10 point scale
68
Q

What is the onset and duration of injectable corticosteroids?

A

Rapid onset, effects typically last 4-8 weeks

69
Q

What are 4 AEs associated with injectable corticosteroids?

A
  1. May accelerate cartilage degradation (esp. hand)
  2. Post-injection flare
  3. Local skin changes
  4. Infections
70
Q

What are 3 warnings for using injectable corticosteroids?

A
  1. Limited to 3-4 injections in one joint per year
  2. May worsen joint instability or weakness
  3. Minimize joint activity for 2-3 days
71
Q

What is the MOA of injectable joint fluid replacement?

A

Hyaluronic acid is a component of synovial fluid

72
Q

Where might injectable joint fluid replacement be used?

A

Indicated for knee OA; other types off-label

73
Q

What is the efficacy of hyaluronic acid?

A

Uncertain benefit, costly

74
Q

What is the onset and duration of hyaluronic acid injection for OA? (2)

A
  1. Rapid in some; others require completed cycle
  2. May lost longer than intra-articular steroids
75
Q

What are the AEs of hyaluronic acid injection? (3)

A
  1. Arthralgia
  2. Injection site pain/reaction
  3. Post-injection flare
76
Q

Glucosamine and chondroitin for OA. Yay or nay?

A

Not recommended in treatment guidelines, BUT they’re pretty safe so worth a try

77
Q

What are 3 surgeries used in OA?

A
  1. Osteotomy (removal of bony tissue)
  2. Debridement (orthoscopic surgery)
  3. Joint replacement (arthoplasty)
78
Q

What are 4 other occupations to refer OA patient to?

A
  1. Dietician
    - Education on weight managment
  2. Physiotherapy or Occupational Therapy
    - Exercises and such
  3. Physician
    - Pain medication
  4. Rheumatologist or Internal Medicine specialist
    - Red flag conditions, unusual complications

PHAR 255 (14 decks)

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