OA, RA Flashcards
Define osteoarthritis.
Degenerative disease (with inflammation) of bone and joint cartilage
What are the risk factors for osteoarthritis? (7 in total; first 3 are more impt)
1) Age (thinning of ECM, dec hydration, inc brittleness, wear-and-tear)
2) Obesity (inc load on weight-bearing joints, adipokine inflammation)
3) Joint injury (surgery, trauma etc)
4) Genetic predisposition
5) Gender
6) Occupation
7) Anatomical factors (bow-legged, knocked-knee)
Describe the pathophysiology of osteoarthritis and its 3 key features.
Compensatory responses of joint and surrounding tissues in “failed repair” to a variety of insults and ongoing joint destruction
1) Cartilage loss from degradation
- In response to cartilage damage over time, chondrocytes undergo phenotypic switch, leading to production of improperly mineralized collagen AND
- Degradation of collagen by vasoactive peptides and matrix metalloproteinases released by subchondral bone
2) Synovial inflammation
- Loose cartilage shards stimulate inflammatory response to remove debris –> pain (stimulate nociception)
- Inc joint fluid and damage to synovium –> distension of synovial capsule –> pain
3) Bone remodeling and osteophyte formation
- Thickening of subchondral bone, sclerosis and bone spur formation to increase stability of joint
- Causes widening of joints
OSMOSIS pathophysio expl:
1) Articular cartilage damage over time causes chrondrocytes to undergo phenotypic switch and produce improperly mineralised collagen. Over time, they also undergo apoptosis. Causing cartilage to continue to degrade over time
2) Cartilage breaks down, and flakes are detected by immune cells in the synovium leading to secretion of pro-inflammatory cytokines, causing synovitis
3) Cartilage breakdown causes bone to rub against each other, further weakening bone and decreases weight bearing ability, leading to bone remodelling and osteophyte growth to attempt to stabilise the joint causing widening of joints
Pain result from mechanical (bone rubbing) and chemical (inflammatory cytokines) activation of nociceptor fibres
- Inc joint fluid and damage to synovium –> distension of synovial capsule –> pain
Describe the clinical presentation of osteoarthritis (6).
1) Inflammation (Palpable warmth, swelling, pain)
2) Asymmetrical polyarthritis of weight-bearing joints (distal fingertips, hip, knees)
3) Limited joint motion and function (potential functional instability)
4) Pain with gradual onset, worse with joint use/motion, relieved by rest
5) Morning stiffness <30min
Other features:
- Crepitus on motion
Describe how osteoarthritis is diagnosed.
1) Asymmetrical polyarthritis of weight-bearing joints (distal fingertips, hip, knees) -> Activity related joint pain
2) Morning stiffness <30min
3) Typically in age 45 and above
WITHOUT imaging
What are some characteristics of osteoarthritic pain (5)?
- Affected by weather
- (knees) Worse going down the stairs
- Worse in late afternoon/early evening; sometimes night (in severe disease)
- Most severe over joint line
- Worse with motion, improve with rest
What are the goals of osteoarthritis treatment? (3)
- Relieve pain and inflammation (if any) [pharmaco]
- Improve/preserve joint range of motion and function [non-pharmaco]
- Improve QoL
Describe non-pharmacological management’s place in therapy for OA and the various options available (3).
Mainstay; 1st line for OA management
1) Exercise (LOW impact, strengthening exercises)
- Strengthen structures around joint to improve physical function and reduce pain
- Swimming, aquatic aerobics, walking (~6000 steps/d)
- Tai Chi, yoga for stability and to reduce fall risk
- ~30min, 3x/wk based on pt preference and profile
- Consider referral to physio for more supervised activity
2) Weight management (eat healthy diet)
- Reduce load on weight-bearing joints
- Reduce adipokine-related inflammation
- Aim for 10% body weight loss but any amount is still good
3) Information and support
- Engage and empower patient
- Recommended analgesics along with non-pharmacological management to encourage participation
What is the place in therapy of pharmacologics for OA management? State the general guide in the use of pharmacologics and list the classes used for OA
- Facilitate maximum function and engagement with non-pharmacological approaches
- Use lowest effective dose for shortest possible duration
1st line: TOP NSAIDs
2nd line: PO NSAIDs (+/- PPI)
Alternatives:
- PO paracetamol/tramadol
- IA glucocorticoids
- Duloxetine
Describe the place in therapy of PO Tramadol in OA management (including dosing frequency and max dose, what levels of pain, what it helps and d/n help, and other things to take note with its use).
- Alternative if CI/failed on NSAIDs
- For mod-to-severe pain
- 25-50mg TDS (max 400mg/d)
- Not suited for long-term use (addiction potential)
- Not v helpful for inflammation
- Risk of overdose
Describe the place in therapy of IA glucocorticoids in OA management incl Contraindications (5), frequency of dosing, as well as duration of effect.
Hint: For CI think when Steroid cannot use due to MOA and ADR
- Reserved for mod-to-severe pain and CI/failed NSAIDs
- 3-4 injections/year
- CI in periarticular infection/fracture, septic arthritis, juxtaarticular osteoporosis and joint instability
- Provides abt 4-6 wk of pain relief
Describe the place in therapy (incl pain severity) of duloxetine in OA management and list some of its ADRs.
- Mod-to-severe pain and CI/failed NSAIDs
- SEs (nausea, dry mouth, dizziness, sexual dysfunction, urinary hesitation)
List the ADRs of NSAID use in OA (7).
1) GI (N/V, bleeds, ulcers)
2) Renal (AKI, HTN)
3) Respi (bronchospasm in asthmatics)
4) CV (MI, stroke, vascular death)
5) Hypersensitivity (urticaria, angioedema, anaphylaxis)
6) Pseudo-allergy (urticaria, angioedema)
7) Teratogenicity (3rd trimester of pregnancy)
Describe NSAID selection and/or precautions taken for GI adverse effects (incl risk factors for GI ADR, what is high risk GI bleed).
Avoid non-selective NSAIDs in active GI bleed; use coxibs with caution OR add PPI if high risk (3 or more risk factors) of GI bleed
Risk Factors for GI ADRs:
- >65yo
- Hx of GI ulcers/bleeds
- Concomitant corticosteroids, antiplatelets, anticoagulants
- High dose/chronic NSAIDs
Describe NSAID selection and/or precautions taken for CV adverse effects (which CV conditions cannot use, which NSAIDs can be used and at what doses).
Avoid all NSAIDs in IHD, HF, PAD and uncontrolled HTN
Limit celecoxib dose to 200mg/d (< 400mg/d but tablets are 200mg) (more impt);
systemic diclofenac to max 100mg/d (if use for 4w or longer)
Describe NSAID selection and/or precautions taken (what to monitor/ when to avoid) for AKI (risk factor for AKI). (~8 points)
TOP NSAIDs > PO NSAIDs; Monitor SCr and electrolytes if necessary to use PO NSAID
CKD (risk factor for AKI as well):
- eGFR <60: Limit NSAID use to 5-7d
- eGFR <15: Avoid all NSAIDs
Avoid PO NSAIDs (use TOP except Nephrotic syndrome) in:
* Volume depletion (due to emesis, diarrhea, sepsis, hemorrhage)
* Effective arterial volume depletion (due to HF, nephrotic syndrome, cirrhosis)
* Severe hypercalcemia / renal artery stenosis
* Aminoglycosides, amphotericin B, radiocontrast material
* Diuretics & ACEI/ARB (also: hyperkalemia, hyponatremia)
Describe NSAID selection and/or precautions taken for hypersensitivity. (1st most impt)
Avoid ALL NSAIDs if anaphylaxis involved
Avoid non-selective NSAIDs (due to risk of cross-sensitivity)
Avoid coxibs if known allergy to coxibs and/or sulfonamides
Describe NSAID selection and/or precautions taken for pseudo-allergy.
Avoid non-selective NSAIDs (due to cross-sensitivity; pseudoallergy is related to COX-1 inhibition)
Use coxibs with caution
Describe NSAID selection and/or precautions taken for bronchospasm
Avoid non-selective NSAIDs
Use coxibs with caution
Describe the place in therapy of surgical treatment for OA management (indication, how long surgery benefits will last, CI to surgery, what needs to be done after)
Generally last-line, considered when
- QoL is substantially affected
- All other treatment options have been explored
Total joint arthroplasty lasts ~10-15 years, not recommended early on in course of OA
Post-operative rehab (physiotherapy) is essential
CI in active infection, or other conditions that do not allow for surgical procedure (e.g chronic lower extremity ischemia, skeletal immaturity)
