IC16: Management of Osteoarthritis

Question 1

List 5 categories of knee pain differentials and provide examples

Answer 1

1. Inflammatory- RA, psoriatic arthritis, gout,, pseudogout, spondyloarthritis
2. Infection- septic arthritis, osteomyelitis
3. Degenerative- osteoarthritis
4. Soft tissue rheumatism- tendonitis, bursitis
5. Trauma- fractures, disclocation, ligament injury, patella problems
6. Tumor/malignancy

Question 2

List 3 knee pain red flags that require urgent referral

Answer 2

1. Infection
2. Trauma
3. Malignancy-related causes

Question 3

Describe the prevelance of OA in relation to age and gender

Answer 3

1) < 50yo: men > women (possibly sports related & other injuries)
2) > 70yo: women > men (esp OA in hands)

Question 4

List at least 4 risk factors of OA

Answer 4

**1. Joint injury **(sports, surgery)
**2. Obesity **(incr load on weight bearing joints/metabolic OA related to obesity)
3. Ageing (changes in ECM: thinning, decr joint hydration & incr brittleness)
4. Anatomic factors (varus alignment - bow legged ; valgus alignment aka knocked knee)
5. Genetic predisposition
6. Gender
7. Occupation

Question 5

Desribe the pathophyisiology of OA

Answer 5

1. Articular cartilage damage
2. Incr chondrocyte activity to remove/repair damge
3. Aberrant chondrocyte fxn causes more breakdown
4. Cartilage loss & apoptosis of chondrocyte
5. Formation of fibrillations in carilage & cartilage shards
6. Cartilage shards cause inflammatory & pathologic changes in joint capsule & synovium, leading to effusion & synovial thickening

Question 6

How does OA cause pain?

Answer 6

1. Activation of nociceptive nerve endings within joint by mechanical & chemical irritant
2. Distension of synovial capsule from incr joint fluid, microfracture, periosteal irritation, or dmg to ligament, synovium or meniscus

Question 7

What are osteophytes & what is their function?

Answer 7

• Osteophytes aka bony spurs are bony lumps that grow on the bones or around the joints
• Function: A compensatory structure formed tos stabilise osteoarthritic joint

Question 8

List the clinical presentations of OA

Answer 8

1. Pain, swelling, erythematous & warmth
2. Morning stiffness **< 30min **
3. Limited joint movement
4. Functional limitation/instability (eg. difficulty climbing stairs, leaving hse)
5. Asymmertrical polyarthritis (weight bearing joints): Hand, knee, hip

Question 9

how does OA joint involvement differ from that in RA?

Answer 9

OA: More DIP involvement than RA (RA more towards metacarpal & wrist)

Question 10

Is the onset of OA pain gradual or acute?

Answer 10

Insidious (gradual); slow progression over years

Question 11

How is pain affected with joint use and rest?

Answer 11

Worse with joint use, relieved by rest

Question 12

List and state the 3 stages of OA

Answer 12

Stage 1: Predictable sharp with with mechanical insult - limits high impat activities & modest effect on function
Stage 2: Pain becomes more constant, with unpredictable episodes of stiffness, daily activities start to be affected
Stage 3: Constant dull/aching pain punctuated by episodes of oten unpredictable intense, exchausting pain - cause severe limitations in function

Question 13

Is radiographic imaging necessary for the diagnosis of OA?

Answer 13

No. Radiographic changes (degeneration) may not be observed until severe disease

Question 14

When is additional testing required for a OA diagnosis?

Answer 14

1. Younger patients
2. Presence of atypical S/Sx that suggest alternative/additional diagnosis:
* a) Hx of recent trauma,
* b) rapidly worsening sx or deformity,
* c) concerns of infxn or malignancy (unusual site of involvement, marked pain at rest, unintended weight loss)

Question 15

Compare & contrast between OA, RA & gout
- No. of joints
- Location
- Symmetry
- Pain characteristics
- Associated s/s
- Deformities in advance disease
- Diagnostic labs performed

Answer 15

Refer to IC16 OA, slide 16

Question 16

State the Goals of Tx for OA

Answer 16

1. Relieve pain (& inflammation if any) - pharmacological
2. Improve/preserve ROM & joint function (nonpharm)
3. Improve QoL

Question 17

State the mainstay treatment for OA

Answer 17

Nonpharmacological mgmt eg. exercise

Question 18

State 3 nonpharmacological treatments for OA

Answer 18

1. Excerise
2. Weight management (improve QoL, physical fxn, reduce pain by reducing load on weight bearing joints)
3. Information & support (engage & empower pt)

Question 19

State the type of exercise that can be provided for OA treatment

Answer 19

1. Exercise- can reduce pain & improve physical function

Types:
* Strengthening
* Neuromuscular training
* Low impact aerobic eg. walking (min 6000 steps/d)/aquatic aerobics
* Mind-body eg. Tai Chi (improves blanace & reduce fall risk)
* Consider referral to physiotherapist for supervised exercise

Question 20

State 2 main pharmacological treatment options for OA

Answer 20

1. Topical NSAIDs
2. PO NSAIDs/Coxibs

paracetamol/tramadol, IA glucocorticoid inj for short term relief

Question 21

State 2 alternative pharmacological treatments options for OA

Answer 21

1) PO paracetamol/tramadol
* Tramadol, mod-severe pain: 25-50mg TDS (max 400mg/d)

2) Intraarticular (IA) glucocorticoid injections for short term sx relief
3) Duloxetine

Question 22

Topical NSAIDs are less effective for which areas of the body?

Answer 22

1. Hands - freq handwashing
2. Hip - depth of joints beneath skin surface

Question 23

When should PO NSAIDs be given when treating OA?

Answer 23

If topicals are not effective or suitable (eg. hip,hand OA)

Question 24

List 3 considerations when starting PO NSAIDs/coxibs

Answer 24

1. Consider potential GI, CVS, renal toxicity & CI
2. Use lowest effective dose & only when needed
3. Add PPI prophylaxis with NSAID use

Question 25

When is PO paracetamol or PO tramadol used to treat OA?

Answer 25

Contraindicated to NSAIDs or Coxibs - Both no anti-inflammatory activity but may help pain relief

Question 26

List the side effects of NSAIDs

Answer 26

* **Common:** Nausea, dyspepsia, abdominal pain, anorexia * **GI Toxicity:** GI bleed, ulceration, perforation * **Cardiovascular events:** MI, stroke, vascular death * **Renal toxicity**: AKI * **Allergic & Pseudoallergic reactions** * **Hypertension** * **Skin reactions** * **Hematologic effects** * **CNS complaints** - drowsiness, dizziness, headache, tinnitus | In general, NOT drowsy

Question 27

List the risk factors for NSAID-induced GI ulcer/bleeds

Answer 27

* > 65 yo * Hx of ulcer (complicated or uncomplicated) * Use of high dose/chronic NSAID * Concurrent glucocorticoids / antiplatelets / anticoagulants

Question 28

When is a high risk for NSAID-induced GI ulcer/bleed considered?

Answer 28

1. >/= 3 risk factors, OR 2. Hx of complicated ulcer

Question 29

When should NSAID-induced GI complications be referred?

Answer 29

1. Fatigue symptoms 2. Severe dyspepsia 3. Signs of GI bleeding (melena) 4. Unexplained blood loss anemia 5. Iron deficiency

Question 30

List 2 strategies to mange high risk NSAID-induced GI ulcers/bleeds

Answer 30

1. Use Coxib 2. Add PPI ## Footnote -avoid coxib in active PUD due to cox-1 inhibition -PPI over H2RA

Question 31

The risk of peptic ulcers is increased after using NSAIDs for x days?

Answer 31

> 5 days

Question 32

List 2 examples of NSAIs with cardiovascular risks

Answer 32

1. Coxibs 2. Diclofenac

Question 33

The use of diclofenac at doses (dose) mg for more than (duration) is contraindicated with established CV disease

Answer 33

dose = 150mg/d duration = >3-4 weeks

Question 34

State the **max daily dose** of **diclofenac** to be given in patients with established CV disease, uncontrolled HTN, or significant CV risk factors (HTN, hyperlipidemia, sf CV risk factors)

Answer 34

≤100mg/d if treatment > 4 weeks

Question 35

State the max dose of celecoxib

Answer 35

400mg/d

Question 36

When can NSAIDs be prescribed in CKD?

Answer 36

eGFR< 60 for < 5-7 days

Question 38

In CKD, NSAIDs & Coxibs should be avoided when eGFR is less than...

Answer 38

eGFR < 15

Question 39

List the risk factors for NSAID-induced AKI & state the management

Answer 39

1. CKD 2. Vol depletion (emesis, diarrhea, sepsis, hemorrhage) 3. Effective arterial volume depletion (due to HF, nephrotic syndrome, cirrhosis) 4. Severe hypercalcemia/renal artery stenosis 5. Aminoglycosides, amphotericin B, radiocontrast material 6. Diuretics & ACEi/ARB (also hyperkalemia, hyponatremia) 7. >65 yo For 2-6: Give topical NSAID over PO NSAID

Question 40

Can NSAIDs &/or Coxibs be given in IgE mediated allergic reactions? ## Footnote Possible rxns: Urticaria, angioedema, anaphylaxis

Answer 40

No. To avoid all NSAIDs and Coxibs in anaphylaxis | IF REALLY NEEDED, can give coxibs, but caution cox-1 inhibition

Question 41

Can NSAIDs &/or Coxibs be given in **pseudoallergic reactions?** | nonimmunologic, related to cox-1 inhibition

Answer 41

Avoid nonselective NSAID, but can use Coxibs with caution (still have some cox-1 inhibition)

Question 42

Tramadol is indicated for what pain severity?

Answer 42

Moderate-severe

Question 43

State the dose of tramadol for mod-severe pain

Answer 43

25-50mg TDS (max 400mg/d)

Question 44

IA glucocorticoid injections provide short term relief for how long?

Answer 44

4-6 weeks

Question 45

When are IA-glucocorticoid injections used?

Answer 45

1. Moderate-severepain 2. Contraindicated/failure with NSAIDs | NOT FOR LONG TERM USE

Question 46

List at least 2 contraindications for IA glucocorticoids

Answer 46

1. Periarticular infection 2. Septic arthritis 3. Periarticular # 4. Joint instability 5. Juxtaarticular osteoporosis

Question 47

State the place in therapy for duloxetine

Answer 47

* Alternative option * Moderate-severe sx with CI/inadequate response to NSAIDs * Has SNRI effects

Question 48

State a surgical procedure for OA

Answer 48

Total joint arthroplasty (replacement)

Question 49

When should joint replacement be considered for OA?

Answer 49

1. QoL substantially affected 2. Nonsurgical tx is ineffective/unsuitable 3. Able to perform postoperative rehabilitation, which is essential for successful tx outocme