17 - Osteoarthritis Flashcards
(115 cards)
1
Q
Increased burden of disease due to ?? (2 things)
A
- increasing age of population
- increasing obesity rates
2
Q
Describe the burden of osteoarthritis
A
- public health care system burden
- burden on QOL
3
Q
Define OA
A
Joint pain that occurs for most days of the prior month plus radiographic changes in the symptomatic joint
4
Q
What joints are affected?
A
impacts any joint, but typically is in the spine (cervical or lumbar), hands, hip and knees
5
Q
What is primary OA?
A
- idiopathic (unknown cause)
- often the elderly
6
Q
What is secondary OA?
A
- joint insults (trauma, infection)
- rheumatoid arthritis
- gout
- congenital joint abnormalities
- hematological genetic abnormalities (leukemia)
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
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.
9
Q
Is OA part of normal aging?
A
no way jose
10
Q
What play a role in cartilage destruction?
A
IL-1 and metalloproteases
11
Q
What is involved in the formation of osteophytes?
A
Local growth factors, especially TGF (transforming growth factor)
12
Q
What is an osteophyte ?
A
a bony outgrowth associated with the degeneration of cartilage at joints
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
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
15
Q
What are lab tests used for in OA?
A
to rule out other causes of symptoms (ex. gout or RA)
16
Q
What are radiographs and joint aspiration useful for?
A
red, hot, swollen joints
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
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
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
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)
21
Q
Why don’t we X-ray everyone?
A
the results of an x-ray do not influence clinical management
22
Q
What does an X-ray look for?
A
- narrowing of joint space (due to loss of cartilage)
- osteophytes
- bone cysts
23
Q
What types of nodes can be involved in OA?
A
1 - Heberden nodes
2 - Bouchard nodes
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
25
Who can we recommend products for?
patient with DIAGNOSIS of OA seeking self management
26
What do we first recommend?
Non-pharms (physiotherapist, exercise, weight loss)
27
After non-pharms, we start with ?
OTC recommendations
28
What pain scale is recommended for OA patients?
```
WOMAC questionnaire (slide 22)
-determines severity of pain
```
29
Goals of therapy for OA ?
- 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
30
Treatment of OA:
If not enough pain relief from non-pharms, what do we try?
acetaminophen up to 1g QID
31
Treatment of OA:
If not enough pain relief from acetaminophen, what do we try?
-add topical diclofenac
32
Treatment of OA:
If not enough pain relief from adding topical diclofenac, assess risk factors for ___ events.
GI
33
Treatment of OA:
If they have no risk factors for GI events, try ?
low dose non-selective NSAID
34
Treatment of OA:
If they have 1-2 risk factors for GI events, try ?
low dose non-selective NSAID
+
gastroprotection
OR
low-dose Cox-2 inhibitor
35
Treatment of OA:
If they have multiple risk factors for GI events, try ?
alternative therapy (ex. local injections, duloxetine, opioids)
OR
low dose cox-2 inhibitor + gastroprotection
36
Treatment of OA:
If they're on a low dose NSAID with or without gastroprotection, and not enough relief, what do we do?
try full-dose
37
Treatment of OA:
If they're on a full dose NSAID with or without gastroprotection, and not enough relief, what do we do?
surgery
38
What are some risk factors for GI events?
- ppl > 60
- on high dose NSAID already
- history of upper GI bleed
- presence of H. pylori infection
39
For Hand OA:
What are some non-pharms?
- assist devices
- instruct on joint protection techniques
- thermal modalities (hot/cold therapy)
- splints
40
For Hand OA:
What are some charms?
- topical capsaicin
- topical NSAIDs
- oral NSAIDs (including cox-2 selective inhibitors)
- tramadol
*all conditional - no strong recommendations
41
For Hand OA:
Don't use _______
acetaminophen
42
For Hand OA:
Patient > 75:
What are first line agents?
```
-topical NSAIDs
or
-topical capsaicin
and/or
-tramadol
```
43
For Hand OA:
Patient > 75:
What we do we try if first line agents are not effective?
combine therapy or two first line agents (i.e. topical NSAIDs and tramadol)
44
For Hand OA:
Patient < 75:
What are first line agents?
- oral NSAIDS (if low CV and GI risk
- topical NSAIDs
- topical capsaicin and/or tramadol
45
For Hand OA:
Patient < 75:
What we do we try if first line agents are not effective?
combined therapy with two first line agents (i.e. oral NSAIDS and topical capsaicin or tramadol)
46
For Knee OA:
What are some strong non-pharms?
- CV (aerobic) and/or resistance land-based exercise
- aquatic exercise
- lose weight (for those overweight)
47
For Knee OA:
What are some pharmacological agents?
- acetaminophen
- topical NSAIDs
- oral NSAIDs
- tramadol
- intraarticular corticosteroid injections
48
For Knee OA:
What do we recommend against?
- chondroitin sulfate
- glucosamine
- topical capsaicin
49
For Hip OA:
What are some non-pharms?
- participate in CV and or resistance land based exercise
- aquatic exercise
- lose weight for those overweight
(same as knee OA)
50
For Hip OA:
What are some pharmacological agents?
- acetaminophen
- intraarticular corticosteroid injections
- oral NSAIDs
- tramadol
51
For Hip OA:
What do we recommend against?
- chondroitin sulfate
- glucosamine
- topical capsaicin
52
For Knee and Hip OA:
What is there no recommendation for ?
- intraarticular hyaluronates
- duloxetine
- opioid analgesics
53
For Knee and Hip OA:
What do we start with?
acetaminophen
54
For Knee and Hip OA:
If acetaminophen isn't effective, what do we try?
- opioid analgesics
- surgery
- duloxetine (knee only)
- intraarticular hyaluronates
55
For Knee and Hip OA:
If acetaminophen is CI, what do we try? (alternative first line agents)
-topical NSAIDs (knee only), and/or
-intraarticular corticosteroids
and/or
-tramadol
and/or
-oral NSAIDs if <75 or low CV and GI risk
56
For Knee and Hip OA:
If the alternative first line agents fail, what do we try?
- opioid analgesics
- surgery
- duloxetine (knee only)
- intraarticular hyaluronates
57
Non-pharms for OA
- exercise
- weight loss
- heat/cold therapy
- massage
- surgery
58
Acetaminophen:
What dose do we use of regular release?
325-1000mg PO Q4-6 hours
Max 4g/day
59
Acetaminophen:
What dose do we use of sustained release?
650mg PO q8h
Max 4g/day
60
Acetaminophen:
How long should therapy be tried before assessing affect?
2 weeks
61
Acetaminophen:
MOA?
inhibits PG synthesis through inhibition of COX-2 enzyme
62
Acetaminophen:
Role in OA?
first line (except in hand)
first line for non-inflammatory OA
63
Acetaminophen:
Efficacy?
-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
Acetaminophen:
Max dose for those > 75 yo
3.2g/day
65
Acetaminophen:
Avoid ____
alcohol
66
Acetaminophen:
Enhanced hepatotoxicity with _____
warfarin
67
Capsaicin:
Dose
apply sparingly 3-4 times/day for 3-4 week period to achieve max therapeutic effect
68
Capsaicin:
MOA
-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
Capsaicin:
Role in OA?
first line, esp for non-inflammatory OA
*not for hip bc we don't use topical meds on hip
70
Capsaicin:
SE?
tingling, burning or redness (in majority of patients)
71
Topical diclofenac:
MOA
inhibits PG synthesis through Cox-1 and Cox-2 pathways
72
Topical diclofenac:
Role in OA?
- second line in OA due to safety
| - can be used first line in there is an inflammatory component to the OA
73
Topical diclofenac:
SE?
minimal bc of limited systemic bioavailability
74
Which Cox enzyme is involved in gastroprotection?
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
What drug negates the gastroprotective effect of cox-2 selective inhibitors ?
ASA (bc it inhibits Cox-1 as that is the enzyme involved in platelet aggregation)
76
What cox enzyme(s) are inhibited by corticosteroids?
cox-2
77
What is Cox-1 involved in?
- PGs
- Thromboxanes
Involved in:
- gastroprotection
- platelet aggregation
- renal function
78
What is Cox-2 involved in?
-PGs
Involved in:
-pain, fever, renal function, tissue repair, reproduction, development
79
If a patient requires NSAIDs and has a high GI risk with high CV risk (on ASA), what do we do?
- 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
If a patient requires NSAIDs and has a high GI risk with low CV risk, what do we do?
cox-2 inhibitor alone or topical NSAID
+
PPI
81
If a patient requires NSAIDs and has a low GI risk with high CV risk (on ASA), what do we do?
naproxen + PPI
82
If a patient requires NSAIDs and has a low GI risk with low CV risk, what do we do?
topical NSAID
83
IA Steroids:
Methylprednisolone acetate (depo-medrol)
Dose?
10-20 mg per joint
20-80mg per large joint (knee, hip, shoulder)
84
IA Steroids:
Triamcinolone acetone (Kenalog)
Dose?
5-15 mg per joint
10-40 mg per large joint (knee, hip, shoulder)
85
IA Steroids:
MOA
anti-inflammatory properties for pain relief
86
IA Steroids:
Role in OA?
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
IA Steroids:
Efficacy?
- superior to placebo
| - benefits only last 4-6 weeks tho
88
IA Steroids:
Adverse effects?
- hyperglycemia
- edema
- HTN
- flushing
- dyspepsia
- hypercortisolism
89
IA Hyaluronic acids:
Dose of sodium hyaluronate?
- 1 injection into the involved joint
| - may be given once only or weekly for 3-5 weeks
90
IA Hyaluronic acids:
MOA
synovial fluid replacement/replenishment
91
IA Hyaluronic acids:
Role in OA?
not routinely recommended
92
IA Hyaluronic acids:
Efficacy?
limited efficacy and risks of serious events limit the routine use of these agents
93
Duloxetine:
Dose
60mg once daily
max dose = 120 mg/day
94
Duloxetine:
MOA
SNRI
95
Duloxetine:
Role in OA?
- 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
Duloxetine:
Efficacy?
- 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
Duloxetine:
Do not use with ?
potent CYP 1A2 inhibitors (fluvoxamine, cipro, ketoconazole) or MAOi
caution with other serotonergic drugs
98
Duloxetine:
Common AE?
GI with n/v, constipation
99
Duloxetine:
CI in ?
liver disease and severe renal impairment
100
Tramadol:
Dose
- 25 mg am, titrate dose in 25mg increments to reach maintenance of 50-100mg TID
- max dose of 200-300 mg/day
101
Tramadol:
MOA
analgesic with affinity for the mu-opioid receptor
102
Tramadol:
Role in OA?
- 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
Tramadol:
Efficacy ?
- 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
Tramadol:
SE ?
- n/v, dizziness, constipation, headache, somnolence
| * do not use if CrCl < 30
105
Risk factors for GI
- age > 65
- use of anticoagulants
- use of steroids
- history of PUD
- high dose of NSAID
- presence of H. pylori
106
What NSAIDs are the worse for Cardiac conditions?
-diclofenac and high dose celecoxib
107
What NSAIDs appear to be CV neutral?
- low dose naproxen (<750mg/day)
- ibuprofen (<1200mg/day)
- celecoxib (<200mg/day)
108
Any NSAID better than others for renal (AKI) ?
not likely
109
How can we manage GI risk with NSAIDs?
- PPI cotherapy
- H. pylori treatment
- Cox 2 inhibitors (celecoxib)
- misoprostol cotherapy
110
When do we monitor drug effect ?
Day 7, 14
111
When do we monitor pain relief ?
Day 3, 7, 14, 28
112
When do we monitor side effects ?
Day 3 and 7
113
When do we monitor HTN ?
measure within 1 week of NSAID therapy
114
When do we monitor renal function?
baseline, 1-2 weeks, then periodically (minimum annual) in those at risk
115
When do we monitor hepatotoxicity ?
baseline and annual LFT in those at risk
