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Clinical 2 (Part B) > 17 - Osteoarthritis > Flashcards

17 - Osteoarthritis Flashcards

1
Q

Increased burden of disease due to ?? (2 things)

A
  • increasing age of population

- increasing obesity rates

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2
Q

Describe the burden of osteoarthritis

A
  • public health care system burden

- burden on QOL

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3
Q

Define OA

A

Joint pain that occurs for most days of the prior month plus radiographic changes in the symptomatic joint

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4
Q

What joints are affected?

A

impacts any joint, but typically is in the spine (cervical or lumbar), hands, hip and knees

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5
Q

What is primary OA?

A
  • idiopathic (unknown cause)

- often the elderly

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6
Q

What is secondary OA?

A
  • joint insults (trauma, infection)
  • rheumatoid arthritis
  • gout
  • congenital joint abnormalities
  • hematological genetic abnormalities (leukemia)
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7
Q

List 4 things that protect the joint

A

1) Synovial fluid - nourishment (physical protectant) - prevents friction
2) Ligaments and tendons - joint protection mechanism
3) Bone - shock absorbing effects
4) Cartilage - creates frictionless surface, impact-absorbing quality

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8
Q

What happens in OA?

A

There is an imbalance between repairing and synthesizing new cartilage.

*Imbalance between cartilage destruction and cartilage formation!

The remaining cartilage is softened and develops fibrillations and then you have exposure of the actual bone. Bones become more brittle and can have minor fractures. There are also changes to the synovium.

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9
Q

Is OA part of normal aging?

A

no way jose

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10
Q

What play a role in cartilage destruction?

A

IL-1 and metalloproteases

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11
Q

What is involved in the formation of osteophytes?

A

Local growth factors, especially TGF (transforming growth factor)

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12
Q

What is an osteophyte ?

A

a bony outgrowth associated with the degeneration of cartilage at joints

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13
Q

Risk factors for OA (list a few, more on slide 11)

A
  • age
  • obesity
  • nutrition
  • joint injury
  • physical activity
  • muscle weakness
  • women more at risk than men
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14
Q

Describe the diagnosis of OA

A

CLINICAL diagnosis:

-No further tests if: >45 yo + activity-related join pain + morning joint stiffness < 30 mins or non-existent

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15
Q

What are lab tests used for in OA?

A

to rule out other causes of symptoms (ex. gout or RA)

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16
Q

What are radiographs and joint aspiration useful for?

A

red, hot, swollen joints

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17
Q

List symptoms of OA

A
  • Stiffness: morning or after periods of inactivity that lasts less than 30 mins
  • Symptoms localized to the affected joint
  • Pain worse with activity (especially weight bearing) or prolonged use
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18
Q

List signs of OA

A
  • Often unilateral, occasionally symmetrical
  • Joints are not usually tender or inflamed
  • Joint instability may be present
  • No systemic symptoms
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19
Q

What is the pain in OA related to?

A
  • Not related to destruction of cartilage
  • From activation of nociceptive nerve endings within the joint by mechanical and chemical irritants
  • May be due to distension of the synovial capsule by increased joint fluid, micro fracture, periosteal irritation, or damage to ligaments, synovium or the meniscus
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20
Q

Describe the physical exam of OA

A
  • pain, stiffness, and limitation of both passive and active movement of the joint
  • crepitus, deformity, muscle atrophy, ligament tenderness in one or more of the affected joints
  • ligament and capsular laxity + muscle atrophy = joint instability (later leading to deformity)
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21
Q

Why don’t we X-ray everyone?

A

the results of an x-ray do not influence clinical management

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22
Q

What does an X-ray look for?

A
  • narrowing of joint space (due to loss of cartilage)
  • osteophytes
  • bone cysts
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23
Q

What types of nodes can be involved in OA?

A

1 - Heberden nodes

2 - Bouchard nodes

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24
Q

When will you refer ?

A
  • new onset of joint pain
  • duration of symptoms > 7-10 days
  • recent trauma
  • systemic symptoms
  • injury due to sports
  • local or diffuse muscle weakness
  • symptoms of burning, numbing, tingling
  • inflammation of joints
  • morning stiffness > 1 hr
  • drug-related
  • chronic liver disease or history of inflammatory arthritis
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25
Q

Who can we recommend products for?

A

patient with DIAGNOSIS of OA seeking self management

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26
Q

What do we first recommend?

A

Non-pharms (physiotherapist, exercise, weight loss)

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27
Q

After non-pharms, we start with ?

A

OTC recommendations

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28
Q

What pain scale is recommended for OA patients?

A 
WOMAC questionnaire (slide 22)
-determines severity of pain
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29
Q

Goals of therapy for OA ?

A
  • relieve or eliminate pain (and stiffness)
  • improve or restore joint function and mobility
  • improve muscle strength to protect cartilage, ligaments and joint capsule
  • prevent and reduce damage to the joint cartilage, bone, ligaments, muscles, and nerves
  • maximize QOL
  • educate the patient/caregiver to promote adherence
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30
Q

Treatment of OA:

If not enough pain relief from non-pharms, what do we try?

A

acetaminophen up to 1g QID

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31
Q

Treatment of OA:

If not enough pain relief from acetaminophen, what do we try?

A

-add topical diclofenac

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32
Q

Treatment of OA:

If not enough pain relief from adding topical diclofenac, assess risk factors for ___ events.

A

GI

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33
Q

Treatment of OA:

If they have no risk factors for GI events, try ?

A

low dose non-selective NSAID

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34
Q

Treatment of OA:

If they have 1-2 risk factors for GI events, try ?

A

low dose non-selective NSAID
+
gastroprotection

OR

low-dose Cox-2 inhibitor

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35
Q

Treatment of OA:

If they have multiple risk factors for GI events, try ?

A

alternative therapy (ex. local injections, duloxetine, opioids)

OR

low dose cox-2 inhibitor + gastroprotection

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36
Q

Treatment of OA:

If they’re on a low dose NSAID with or without gastroprotection, and not enough relief, what do we do?

A

try full-dose

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37
Q

Treatment of OA:

If they’re on a full dose NSAID with or without gastroprotection, and not enough relief, what do we do?

A

surgery

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38
Q

What are some risk factors for GI events?

A
  • ppl > 60
  • on high dose NSAID already
  • history of upper GI bleed
  • presence of H. pylori infection
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39
Q

For Hand OA:

What are some non-pharms?

A
  • assist devices
  • instruct on joint protection techniques
  • thermal modalities (hot/cold therapy)
  • splints
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40
Q

For Hand OA:

What are some charms?

A
  • topical capsaicin
  • topical NSAIDs
  • oral NSAIDs (including cox-2 selective inhibitors)
  • tramadol

*all conditional - no strong recommendations

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41
Q

For Hand OA:

Don’t use _______

A

acetaminophen

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42
Q

For Hand OA:

Patient > 75:

What are first line agents?

A 
-topical NSAIDs
or 
-topical capsaicin
and/or
-tramadol
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43
Q

For Hand OA:

Patient > 75:

What we do we try if first line agents are not effective?

A

combine therapy or two first line agents (i.e. topical NSAIDs and tramadol)

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44
Q

For Hand OA:

Patient < 75:

What are first line agents?

A
  • oral NSAIDS (if low CV and GI risk
  • topical NSAIDs
  • topical capsaicin and/or tramadol
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45
Q

For Hand OA:

Patient < 75:

What we do we try if first line agents are not effective?

A

combined therapy with two first line agents (i.e. oral NSAIDS and topical capsaicin or tramadol)

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46
Q

For Knee OA:

What are some strong non-pharms?

A
  • CV (aerobic) and/or resistance land-based exercise
  • aquatic exercise
  • lose weight (for those overweight)
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47
Q

For Knee OA:

What are some pharmacological agents?

A
  • acetaminophen
  • topical NSAIDs
  • oral NSAIDs
  • tramadol
  • intraarticular corticosteroid injections
48
Q

For Knee OA:

What do we recommend against?

A
  • chondroitin sulfate
  • glucosamine
  • topical capsaicin
49
Q

For Hip OA:

What are some non-pharms?

A
  • participate in CV and or resistance land based exercise
  • aquatic exercise
  • lose weight for those overweight

(same as knee OA)

50
Q

For Hip OA:

What are some pharmacological agents?

A
  • acetaminophen
  • intraarticular corticosteroid injections
  • oral NSAIDs
  • tramadol
51
Q

For Hip OA:

What do we recommend against?

A
  • chondroitin sulfate
  • glucosamine
  • topical capsaicin
52
Q

For Knee and Hip OA:

What is there no recommendation for ?

A
  • intraarticular hyaluronates
  • duloxetine
  • opioid analgesics
53
Q

For Knee and Hip OA:

What do we start with?

A

acetaminophen

54
Q

For Knee and Hip OA:

If acetaminophen isn’t effective, what do we try?

A
  • opioid analgesics
  • surgery
  • duloxetine (knee only)
  • intraarticular hyaluronates
55
Q

For Knee and Hip OA:

If acetaminophen is CI, what do we try? (alternative first line agents)

A

-topical NSAIDs (knee only), and/or
-intraarticular corticosteroids
and/or
-tramadol
and/or
-oral NSAIDs if <75 or low CV and GI risk

56
Q

For Knee and Hip OA:

If the alternative first line agents fail, what do we try?

A
  • opioid analgesics
  • surgery
  • duloxetine (knee only)
  • intraarticular hyaluronates
57
Q

Non-pharms for OA

A
  • exercise
  • weight loss
  • heat/cold therapy
  • massage
  • surgery
58
Q

Acetaminophen:

What dose do we use of regular release?

A

325-1000mg PO Q4-6 hours

Max 4g/day

59
Q

Acetaminophen:

What dose do we use of sustained release?

A

650mg PO q8h

Max 4g/day

60
Q

Acetaminophen:

How long should therapy be tried before assessing affect?

A

2 weeks

61
Q

Acetaminophen:

MOA?

A

inhibits PG synthesis through inhibition of COX-2 enzyme

62
Q

Acetaminophen:

Role in OA?

A

first line (except in hand)

first line for non-inflammatory OA

63
Q

Acetaminophen:

Efficacy?

A

-in mild, non-inflammatory OA, it is equivalent to NSAIDs

-less effective than NSAIDs in inflammatory/advanced OA
(acetaminophen < analgesic dose NSAID < anti-inflammatory dose NSAID)

64
Q

Acetaminophen:

Max dose for those > 75 yo

A

3.2g/day

65
Q

Acetaminophen:

Avoid ____

A

alcohol

66
Q

Acetaminophen:

Enhanced hepatotoxicity with _____

A

warfarin

67
Q

Capsaicin:

Dose

A

apply sparingly 3-4 times/day for 3-4 week period to achieve max therapeutic effect

68
Q

Capsaicin:

MOA

A

-capsaicin renders skin and joins insensitive to pain by depleting and preventing reaccumulation of substance P in peripheral sensory neurons so that local pain impulses cannot be transmitted to the brain

69
Q

Capsaicin:

Role in OA?

A

first line, esp for non-inflammatory OA

*not for hip bc we don’t use topical meds on hip

70
Q

Capsaicin:

SE?

A

tingling, burning or redness (in majority of patients)

71
Q

Topical diclofenac:

MOA

A

inhibits PG synthesis through Cox-1 and Cox-2 pathways

72
Q

Topical diclofenac:

Role in OA?

A
  • second line in OA due to safety

- can be used first line in there is an inflammatory component to the OA

73
Q

Topical diclofenac:

SE?

A

minimal bc of limited systemic bioavailability

74
Q

Which Cox enzyme is involved in gastroprotection?

A

Cox-1

  • Therefore if you inhibit it, you increase risk for GI effects
  • Cox-2 selective inhibitors are safer for ppl with GI risk
75
Q

What drug negates the gastroprotective effect of cox-2 selective inhibitors ?

A

ASA (bc it inhibits Cox-1 as that is the enzyme involved in platelet aggregation)

76
Q

What cox enzyme(s) are inhibited by corticosteroids?

A

cox-2

77
Q

What is Cox-1 involved in?

A
  • PGs
  • Thromboxanes

Involved in:

  • gastroprotection
  • platelet aggregation
  • renal function
78
Q

What is Cox-2 involved in?

A

-PGs

Involved in:
-pain, fever, renal function, tissue repair, reproduction, development

79
Q

If a patient requires NSAIDs and has a high GI risk with high CV risk (on ASA), what do we do?

A
  • avoid NSAID if possible
  • if can’t avoid NSAID, and have very high CV risk, use naproxen + PPI

-if can’t avoid NSAID, and have a very high GI risk, use cox-2 inhibitor + PPI

80
Q

If a patient requires NSAIDs and has a high GI risk with low CV risk, what do we do?

A

cox-2 inhibitor alone or topical NSAID
+
PPI

81
Q

If a patient requires NSAIDs and has a low GI risk with high CV risk (on ASA), what do we do?

A

naproxen + PPI

82
Q

If a patient requires NSAIDs and has a low GI risk with low CV risk, what do we do?

A

topical NSAID

83
Q

IA Steroids:

Methylprednisolone acetate (depo-medrol)

Dose?

A

10-20 mg per joint

20-80mg per large joint (knee, hip, shoulder)

84
Q

IA Steroids:

Triamcinolone acetone (Kenalog)

Dose?

A

5-15 mg per joint

10-40 mg per large joint (knee, hip, shoulder)

85
Q

IA Steroids:

MOA

A

anti-inflammatory properties for pain relief

86
Q

IA Steroids:

Role in OA?

A

alternative first line Tx for both knee and hip OA when pain control with acetaminophen or NSAIDs is suboptimal or offered concomitantly with oral analgesics

87
Q

IA Steroids:

Efficacy?

A
  • superior to placebo

- benefits only last 4-6 weeks tho

88
Q

IA Steroids:

Adverse effects?

A
  • hyperglycemia
  • edema
  • HTN
  • flushing
  • dyspepsia
  • hypercortisolism
89
Q

IA Hyaluronic acids:

Dose of sodium hyaluronate?

A
  • 1 injection into the involved joint

- may be given once only or weekly for 3-5 weeks

90
Q

IA Hyaluronic acids:

MOA

A

synovial fluid replacement/replenishment

91
Q

IA Hyaluronic acids:

Role in OA?

A

not routinely recommended

92
Q

IA Hyaluronic acids:

Efficacy?

A

limited efficacy and risks of serious events limit the routine use of these agents

93
Q

Duloxetine:

Dose

A

60mg once daily

max dose = 120 mg/day

94
Q

Duloxetine:

MOA

A

SNRI

95
Q

Duloxetine:

Role in OA?

A
  • adjunctive Tx in patients with a partial response to first-line analgesics
  • may be a preferred second-line med in patients with both neuropathic and MSK OA pain
96
Q

Duloxetine:

Efficacy?

A
  • demonstrated efficacy as add-on therapy when there has been less than optimal response to acetaminophen or oral NSAIDs
  • reduction in pain occurs at about 4 weeks after initiation
97
Q

Duloxetine:

Do not use with ?

A

potent CYP 1A2 inhibitors (fluvoxamine, cipro, ketoconazole) or MAOi

caution with other serotonergic drugs

98
Q

Duloxetine:

Common AE?

A

GI with n/v, constipation

99
Q

Duloxetine:

CI in ?

A

liver disease and severe renal impairment

100
Q

Tramadol:

Dose

A
  • 25 mg am, titrate dose in 25mg increments to reach maintenance of 50-100mg TID
  • max dose of 200-300 mg/day
101
Q

Tramadol:

MOA

A

analgesic with affinity for the mu-opioid receptor

102
Q

Tramadol:

Role in OA?

A
  • recommend as alternative first-line Tx of knee/hip pain in OA in patients who have failed Tylenol and topical NSAIDs, who are not appropriate candidates for oral NSAIDS and IA steroids
  • tramadol can be safe add on therapy to partially effective acetaminophen or oral NSAID therapy (modestly effective)
  • less data for monotherapy
103
Q

Tramadol:

Efficacy ?

A
  • demonstrated efficacy primarily as add on therapy when there has been less than optimal response to acetaminophen or oral NSAIDs
  • reduction in pain occurs at about 4 weeks after initiation
104
Q

Tramadol:

SE ?

A
  • n/v, dizziness, constipation, headache, somnolence

* do not use if CrCl < 30

105
Q

Risk factors for GI

A
  • age > 65
  • use of anticoagulants
  • use of steroids
  • history of PUD
  • high dose of NSAID
  • presence of H. pylori
106
Q

What NSAIDs are the worse for Cardiac conditions?

A

-diclofenac and high dose celecoxib

107
Q

What NSAIDs appear to be CV neutral?

A
  • low dose naproxen (<750mg/day)
  • ibuprofen (<1200mg/day)
  • celecoxib (<200mg/day)
108
Q

Any NSAID better than others for renal (AKI) ?

A

not likely

109
Q

How can we manage GI risk with NSAIDs?

A
  • PPI cotherapy
  • H. pylori treatment
  • Cox 2 inhibitors (celecoxib)
  • misoprostol cotherapy
110
Q

When do we monitor drug effect ?

A

Day 7, 14

111
Q

When do we monitor pain relief ?

A

Day 3, 7, 14, 28

112
Q

When do we monitor side effects ?

A

Day 3 and 7

113
Q

When do we monitor HTN ?

A

measure within 1 week of NSAID therapy

114
Q

When do we monitor renal function?

A

baseline, 1-2 weeks, then periodically (minimum annual) in those at risk

115
Q

When do we monitor hepatotoxicity ?

A

baseline and annual LFT in those at risk

Clinical 2 (Part B) (30 decks)

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