GC228 Knee Osteoarthritis: Part B
Knee osteoarthritis is a degenerative joint disease involving progressive cartilage loss, subchondral bone changes, and inflammation of the knee, with Part B focusing on its clinical management, rehabilitation, and surgical treatment options.
Knee Osteoarthritis – Part B
Big Idea: This lecture (Part B) by Professor Lewis PK Chan continues from Part A and focuses on the pharmacological management, intra-articular injections, and surgical interventions for knee osteoarthritis (KOA). The overarching message is that OA is a SERIOUS disease requiring a paradigm shift in Hong Kong's aging population — from passive reliance on painkillers toward evidence-based, multidisciplinary chronic disease management with the non-surgical triad (weight reduction + education + exercise) as first-line, and surgery reserved for appropriate indications [1].
Learning Objectives (from the slide deck):
- Epidemiology & clinical importance of KOA
- Pathophysiology & risk factors for developing KOA
- Clinical presentation & workup of KOA
- Non-pharmacological & pharmacological treatment options
- Surgical interventions for managing KOA
Part B primarily addresses objectives 4 and 5, building on the clinical foundation from Part A.
How it fits into exams: The Fourth Summative regularly tests OA management — particularly discriminating first-line treatment (non-pharmacological triad) from analgesics, the evidence against glucosamine and arthroscopy, indications for surgery, and drug choice in comorbid patients. The 2025 MCQ Q48 tested this directly [9].
"What is the first line management of Knee Osteoarthritis? Answer: Weight Reduction, Education & Exercise" — This is the lecture's concluding MCQ slide and is the single most important take-home message [1].
High Yield – First-Line is NOT Analgesics
A common exam trap is choosing "Paracetamol" or "Analgesic" as first-line management of OA knee. Per GC 228, the correct answer is Weight Reduction, Education & Exercise (the non-surgical triad). Analgesics are second-line adjuncts.
Why this triad?
- Weight reduction: Obesity is the strongest modifiable risk factor. Every 1 kg of body weight translates to ~4 kg of compressive force across the knee during walking. Reducing weight directly reduces mechanical load on already-damaged cartilage [1][2].
- Education: Patients must understand OA is a chronic disease requiring self-management — not a condition "cured" by a pill or injection. Education improves adherence to exercise and lifestyle changes.
- Exercise (especially quadriceps strengthening): The quadriceps acts as a shock absorber for the knee joint. Strengthening it reduces peak load transmitted to the articular cartilage, improves proprioception, and reduces pain. This has Grade A evidence from multiple systematic reviews.
2. Pharmacological Management of Knee OA
The lecture uses a patient-specific scenario: "M/60, IHD/AF on apixaban, Hx of gastritis" to illustrate how drug choice must be individualized [1].
The key options listed, with the lecture's ranking and reasoning:
| Drug | Lecture Position | Key Considerations |
|---|---|---|
| Paracetamol | Widely used but limited evidence | Network meta-analysis shows no demonstrable effect vs placebo at any dose; LFT abnormalities possible; impaired clearance in elderly [1] |
| NSAID / COX-2 | Effective but risky in this patient | Contraindicated/high-risk with IHD + AF on anticoagulant + gastritis history. GI bleed risk, CV risk, renal risk [1] |
| Topical NSAID | Good option for OA knee | Comparable efficacy to oral NSAIDs; lower GI adverse events; mild skin reactions; not available in HADF [1] |
| Opioid | Very limited role | Limited benefit for chronic OA pain; serious adverse effects (addiction, sedation, falls in elderly); pre-op opioid use predicts worse surgical outcomes [1] |
| Analgesic Balm | Adjunctive | Menthol 6%, Methyl Salicylate 14% — counter-irritant mechanism [1] |
"Network meta-analysis: paracetamol does not seem to confer any demonstrable effect or benefit in osteoarthritis, at any dose" [1]
Why paracetamol is still used despite poor evidence:
- It is used largely driven by a lack of effective or tolerated alternative treatments, and their relative safety (cf NSAID) [1]
- In other words, it's the "least harmful" option — not because it works well, but because NSAIDs are dangerous in many OA patients (elderly, cardiovascular disease, renal impairment, GI history)
Side effects to remember:
- Liver function abnormalities [1]
- Elderly people with impaired paracetamol clearance — higher risk of toxicity [1]
Exam Discriminator
If asked "Which is effective and evidence-supported treatment of knee OA?" — Paracetamol is NOT a strong answer. In the 2025 MCQ Q48, "Paracetamol" was a distractor and "Knee replacement" was the correct answer for a patient with established medial compartment OA [9].
Why they work: NSAIDs inhibit cyclooxygenase (COX), reducing prostaglandin synthesis. In OA, low-grade synovitis contributes to pain — prostaglandins mediate this inflammatory pain component. NSAIDs address this better than paracetamol.
Why they're dangerous in the case scenario (M/60, IHD/AF on apixaban, gastritis):
- GI risk: NSAIDs are pH-dependent in causing gastric mucosal damage. History of gastritis = major risk factor for GI bleed [3]
- Cardiovascular risk: NSAIDs (especially COX-2 selective) increase risk of MI and stroke — dangerous with IHD [3]
- Anticoagulant interaction: Patient on apixaban — adding NSAID dramatically increases bleeding risk
- Renal risk: NSAIDs reduce renal prostaglandin-mediated afferent arteriolar vasodilation → reduced GFR
If NSAIDs must be used:
- Use lowest effective dose for shortest duration
- Add PPI cover for GI protection
- COX-2 selective inhibitors have lower GI risk but similar/higher CV risk [3]
- Topical NSAID route avoids most systemic adverse effects
"Good pain relief in OA, not be instant. Comparable efficacy to oral NSAIDs for OA knee. Lower GI adverse events but may cause mild skin reactions. None available in HADF." [1]
Why topical works for the knee: The knee is a superficial joint — topical NSAIDs can achieve therapeutic concentrations in the synovial fluid through transdermal absorption. This is why topical NSAIDs are specifically recommended for knee OA (less so for hip, which is too deep).
Clinical pearl: Although effective and safer, topical NSAIDs are not available in HADF (Hospital Authority Drug Formulary) — meaning patients in the public healthcare system cannot routinely access them [1].
"Opioids offer only limited benefit for chronic OA — pain and function" [1]
Key points from the lecture:
| Issue | Detail |
|---|---|
| Efficacy | Only limited benefit for chronic OA pain and function [1] |
| Adverse effects | Drug abuse, addiction; sedation and dizziness predispose to falls and fractures in elderly [1] |
| Pre-operative impact | Pre-op opioid use independently predicts higher post-op opioid requirement, prolonged hospital stay, greater in-hospital complications, and early revision surgery [1] |
| Guideline stance | Updated Australian GP guideline: do NOT recommend opioids as a treatment option for OA [1] |
Why opioids fail in OA: OA pain is primarily nociceptive-mechanical (not central/visceral in nature early on). Opioids modulate central pain pathways — they don't address the biomechanical root cause. They create dependence, hyperalgesia with chronic use, and worsen surgical outcomes.
Clinical Pearl
If a patient is already on chronic opioids for OA and presents for TKA, expect worse outcomes. This is a teaching point that may appear in OSCE counselling stations — you should counsel patients to wean off opioids before surgery.
3. Glucosamine and Intra-Articular Injections
"Glucosamine and intra-articular injection: no strong evidence" [1]
What is glucosamine?
- Required for the synthesis of mucopolysaccharides [1]
- Found in tendons, ligaments, cartilage and synovial fluid [1]
- Biologically, it's a building block of glycosaminoglycans (GAGs) in cartilage matrix
Evidence:
- Glucosamine vs Placebo: No statistically significant difference in Pain Relief or Physical Function [1]
- Placebo effect accounts for any perceived benefit [1]
- Used as an alternative therapy — popular with patients but not evidence-supported
High Yield for MCQ
Glucosamine has NO proven benefit over placebo for OA knee. This is directly tested — in 2025 MCQ Q48, "Glucosamine" was a distractor [9].
| Injection Type | Evidence | Duration | Risks |
|---|---|---|---|
| Corticosteroids | Short benefit in pain — mean 2-4 weeks (Cochrane) | 2-4 weeks | Repeated injection may predispose to cartilage and joint damage, and increased risk of infection [1] |
| Viscosupplements (Hyaluronic Acid) | No clinically meaningful benefit over placebo (JAMA) | N/A | Risk of harm — painful effusion, infection [1] |
| Platelet Rich Plasma (PRP) | Initial clinical studies suggest benefit in pain relief | Unknown | Need higher quality studies; mechanism of action uncertain [1] |
Why corticosteroids give only short-term relief: Corticosteroids suppress the inflammatory component (synovitis) of OA. But OA is primarily a mechanical/degenerative disease — once the steroid wears off (2-4 weeks), the underlying cartilage loss and biomechanical malalignment remain. Repeated injections actually accelerate cartilage damage (JAMA 2017), creating a vicious cycle.
Why hyaluronic acid (viscosupplementation) doesn't work: The concept is to replenish synovial fluid viscosity. However, injected HA is rapidly cleared from the joint space (half-life < 24 hours). The molecular weight and rheological properties of injected HA differ from native synovial fluid. Clinical trials consistently show no meaningful benefit over saline placebo [1].
Link to 2024 MCQ Q31: A patient receiving "frequent injections for osteoarthritis of his knee for over 1 year" developed osteoporosis — the answer was iatrogenic due to exogenous steroid [8]. This demonstrates the real-world consequence of repeated intra-articular corticosteroid use.
4. Biology of OA Knee — New Drugs in the Pipeline
The lecture includes a complex biology diagram showing the interplay between cartilage, subchondral bone, and synovium [1]
Key pathological processes:
- Cartilage degradation: Chondrocytes produce excess ADAMTS (aggrecanases) and MMPs (matrix metalloproteinases) that degrade collagen II and proteoglycans
- Synovitis: Inflammatory cytokines (IL-1, IL-6, TNFα) from synoviocytes drive further cartilage degradation
- Subchondral bone changes: Increased loading and cytokines cause subchondral bone sclerosis and osteophyte formation
- Immune cell involvement: M1 macrophages, Th1/Th17 cells produce pro-inflammatory cytokines; M2 macrophages and Tregs attempt anti-inflammatory responses
- TGF-β paradox: TGF-β drives both fibrosis and some protective responses; also involved in osteophyte formation
- Wnt pathway: Important in disease progression — target of new drugs
"More Effective to prevent Disease Progression by intervention at early stages" [1]
The lecture presents a disease progression timeline:
| Stage | Detection Method | Changes |
|---|---|---|
| Molecular | Biomarkers | Initiation of disease process |
| Pre-Radiographic | MRI/Biomarkers | Changes in composition of bone, cartilage, soft tissues |
| Radiographic / Clinically Detectable OA | MRI/US, then X-ray | Structural changes visible |
| End-stage (Joint Death) | X-ray | Joint failure → Joint replacement needed |
Why this matters: Structural changes occur BEFORE symptoms. By the time a patient has pain and X-ray changes, significant cartilage loss has already occurred. This is why prevention (weight management, avoiding injury) is far more effective than treatment.
All were in Phase 3 trials as of 2019 OARSI Meeting [1]
| Drug | Mechanism | Notes |
|---|---|---|
| Lorecivivint | Intra-articular Wnt pathway inhibitor | Targets key OA signalling pathway |
| CNTX-4975 | Trans-capsaicin targeting TRPV1 receptor | Deactivates pain fibers |
| Invossa (TG-C) | Allogenic chondrocytes expressing TGF-β1 | Cell-based therapy |
| Ampion | Cyclic dipeptide targeting NMDA receptor, Serotonin receptor | Novel mechanism |
| AXS-02 | Zoledronic acid (osteoclast inhibitor) | Targets subchondral bone remodelling |
| Fasinumab, Tanezumab | Anti-NGF monoclonal antibodies | Block nerve growth factor → pain modulation |
Why anti-NGF drugs are notable: NGF (nerve growth factor) is upregulated in OA joints and sensitizes nociceptors. Blocking it provides potent analgesia. However, there are safety concerns — rapidly progressive OA and osteonecrosis have been reported, likely because pain suppression allows continued damaging joint loading.
Current status: As of now, no DMOAD has reached widespread clinical use. This remains an area of active research.
5. Surgical Management of Knee OA
"Limited role of Knee Arthroscopy in OA Knee" [1]
Evidence:
- Average effect size in pain: 0.14 (from BMJ meta-analysis) — this is clinically insignificant [1]
- Multiple RCTs (including sham surgery controls) show arthroscopic debridement/lavage provides no meaningful benefit over placebo
Limited indications:
- Frequent Locking Symptoms caused by meniscal tears and loose bodies [1]
- Short term relief of locking symptoms only [1]
Potential complications:
- DVT (0.4%), PE (0.1%), death (0.03%) [1]
- Increases rate of progression of osteoarthritis [1]
- Shortens time to joint replacement [1]
Why arthroscopy fails in OA: Arthroscopy can remove loose bodies and trim torn menisci, but it cannot restore articular cartilage. The underlying disease process continues. Worse, removing meniscal tissue reduces the load-distributing function of the meniscus, accelerating cartilage wear in the affected compartment.
5.2 Recommended Surgical Options
Three recommended surgical options: High Tibial Osteotomy (HTO), Partial Knee Replacement (UKA), Total Knee Replacement (TKR) [1]
"HTO improves pain, function, delays OA progression in young active patients" [1]
Principle: Shift mechanical axis [1]
Why it works: In a varus (bow-legged) knee, the mechanical axis passes medial to the knee center, overloading the medial compartment. HTO creates a controlled fracture of the proximal tibia and realigns it to shift load from the diseased medial compartment to the relatively preserved lateral compartment.
Ideal patient: Young ( < 60), active, isolated medial compartment OA with varus deformity, good ROM, intact lateral compartment and ligaments.
Advantages: Preserves native joint; delays need for arthroplasty; allows return to high-demand activities.
Disadvantages: Technically demanding; long recovery; eventual conversion to TKA may be needed years later.
| Feature | HTO | UKA | TKR |
|---|---|---|---|
| Age | Young, active | Middle-aged | Older, end-stage |
| Compartment | Isolated medial | Isolated one compartment | Multi-compartment |
| Bone preservation | Maximal | Good | Least |
| Recovery speed | Slow | Fast | Moderate (now faster with ERAS) |
| Long-term | May need eventual TKA | May need conversion to TKA | Definitive |
Advantages of UKA: Quicker rehabilitation, Less Periop Complication, Retained normal knee kinematics and proprioception, Preserved bone stock, In the case of failure — easier surgery (Conversion to TKA) [1]
Why UKA over TKA (when appropriate):
The lecture explicitly addresses "Why UKA NOT TKA?" [1]:
- UKA is safer surgery: Medicare data showed rates of wound complication, myocardial infarction, periprosthetic joint infection, pulmonary embolism, and stiffness were significantly higher among TKA recipients compared to UKA [1]
- Rapid Recovery: The lecture shows UKA can be done as outpatient surgery (Prof Chan's first outpatient UKA was in 2016) [1]
- Retained kinematics: UKA preserves the cruciate ligaments and the uninvolved compartment, maintaining more natural knee movement and proprioception
- Preserved bone stock: Less bone is removed, making future revision surgery (conversion to TKA) technically easier
Indications for UKA: Isolated single-compartment OA (usually medial), intact ACL, correctable deformity, adequate ROM.
- Definitive treatment for end-stage OA with multi-compartment involvement
- Both Part A and Part B emphasize that TKR is the final surgical option when conservative measures fail
- Provides marked pain relief and functional improvement [4]
"Not Very Painful, Rapid Recovery — Enhanced Recovery After Surgery (ERAS): Discharge D1 after TKA, Exercise 4 hr after TKA" [1]
ERAS principles in joint replacement:
- Multimodal analgesia (regional nerve blocks, local infiltration analgesia, paracetamol, NSAIDs — avoiding opioids)
- Early mobilization (exercise 4 hours post-surgery)
- Discharge Day 1 (previously patients stayed 5-7 days)
- Optimized pre-operative medical condition
"Robotic-assisted Surgery: Accurate Surgical Execution" [1]
Why robotic surgery matters: Robotic-assisted TKA and UKA allow CT-planned, patient-specific bone cuts with sub-millimeter accuracy. This improves implant alignment and soft tissue balance, which theoretically improves longevity and function of the prosthesis.
"XR: Deformity, Debris, Destruction, Density, Dead bone (the 5 D's)" [1]
This is the case study (Case 5) from the lecture — a patient with knee instability on walking.
Causes (from lecture): Diabetes mellitus, leprosy, syphilis, poliomyelitis, chronic alcoholism, syringomyelia [1]
Why it happens: Loss of protective pain sensation → repeated unrecognized microtrauma → progressive joint destruction. The neuropathic joint undergoes a cycle of:
- Inflammation and effusion (acute Charcot)
- Bony fragmentation and dislocation
- Coalescence and attempted healing with deformity
Key management points from the lecture:
- System disease — not only knee joint? Consider foot and ankle hygiene (especially in diabetics) [1]
- Optimize underlying disease — especially DM control [1]
- Options of Mx: Arthrodesis/Arthroplasty [1]
- Phase of disease: Eichenholtz stages — pass bony destruction before surgical intervention [1]
Eichenholtz Classification:
| Stage | Name | Features |
|---|---|---|
| I | Development/Fragmentation | Acute inflammation, bony fragmentation |
| II | Coalescence | Absorption of debris, new bone formation |
| III | Reconstruction/Consolidation | Bone remodelling, residual deformity |
Surgical timing: Surgery should ideally wait until past bony destruction (Stage II-III) when the inflammatory process has subsided, to reduce risk of hardware failure and non-union.
"Osteoarthritis is a SERIOUS disease. A paradigm shift urgently needed in aging population in HK. Evidence-based Management. Multi-disciplinary Chronic disease management. Non-surgical Mx in OA (Triad)." [1]
The lecture concludes with the OA Management Triad pyramid (from Stefan Lohmander, Ewa Roos):
- Base (for ALL patients): Weight reduction, Education, Exercise
- Middle (if needed): Pharmacological therapy (topical NSAIDs preferred; paracetamol despite weak evidence; avoid opioids)
- Apex (for end-stage): Surgery (HTO → UKA → TKR depending on patient factors)
Clinical Approach Summary
- Pain characteristics: mechanical (worse with activity, better with rest), morning stiffness < 30 minutes
- Functional limitations: stairs, rising from chair, walking distance
- Locking/giving way (may indicate meniscal tear → consider arthroscopy for locking only)
- Previous trauma, obesity, occupational/recreational overuse
- Comorbidities: CV disease, GI history, renal function, anticoagulation — all affect drug choice
- Current medications including OTC supplements (glucosamine)
- Gait, alignment (varus/valgus)
- Quadriceps wasting
- Effusion (patellar tap, bulge sign)
- Range of motion, crepitus
- Ligament stability (important to exclude in planning UKA — need intact ACL)
- Compartment tenderness (medial vs lateral vs patellofemoral)
- Weight-bearing AP X-ray (must be standing — lying down underestimates joint space loss) [5]
- X-ray features: LOSS mnemonic — Loss of joint space, Osteophytes, Subchondral sclerosis, Subchondral cysts [4]
- MRI: for pre-radiographic OA, meniscal pathology, or if considering UKA (to assess all compartments)
- Bloods: generally normal in OA (ESR/CRP not elevated — helps distinguish from inflammatory arthritis)
- All patients: Non-pharmacological triad
- Add pharmacology: Topical NSAID (preferred for knee) → Paracetamol → Oral NSAID/COX-2 (with PPI, shortest duration) → Avoid opioids
- Consider injection: IA corticosteroid for acute flares only (expect 2-4 weeks benefit max)
- Surgery when conservative Mx fails: HTO (young, active, unicompartmental) → UKA (single compartment, intact ACL) → TKR (end-stage, multi-compartment)
Exam Intelligence
| Distractor | Why It's Wrong |
|---|---|
| Paracetamol as first-line | Evidence shows no demonstrable benefit over placebo at any dose |
| Glucosamine | No statistically significant benefit vs placebo — placebo effect only |
| Arthroscopic debridement | Clinically insignificant effect size (0.14); increases OA progression; shortens time to TKR |
| Viscosupplementation (HA) | No clinically meaningful benefit over placebo; risk of effusion and infection |
| Opioids | Limited benefit; addiction risk; worsens surgical outcomes |
- "First-line management" → Always answer Weight Reduction + Education + Exercise, not any drug
- "Evidence-supported treatment" → Knee replacement YES; arthroscopic debridement/glucosamine/paracetamol NO
- Repeated IA steroid injections → Can cause iatrogenic osteoporosis (2024 MCQ Q31), cartilage damage, infection
- Topical NSAID → Effective and safer but not in HADF — may come up as a practical limitation
- Anterior uveitis association → OA is NOT associated with anterior uveitis (2020 MCQ Q12 tested this)
Past Paper Questions
Stem: "A 68-year-old lady suffered from left knee mechanical pain for 3 years. X-ray of the left knee showed reduced joint space in the medial compartment with marginal osteophyte formation. Which of the following is an effective and evidence-supported treatment of knee osteoarthritis? A. Arthroscopic debridement, B. Glucosamine, C. Knee replacement, D. Paracetamol" [9]
Answer: C. Knee replacement
- Arthroscopic debridement: effect size 0.14, increases OA progression — NOT evidence-supported
- Glucosamine: no benefit over placebo
- Paracetamol: network meta-analysis shows no demonstrable effect
- Knee replacement: definitive treatment with proven pain relief and functional improvement for established OA
Stem: "A 50-year-old business man presented to AED with severe low back pain... X-ray showed osteopenia and wedge fracture of L3. Further questioning revealed he had been receiving frequent injections for osteoarthritis of his knee for over 1 year. Which of the following is the MOST LIKELY cause of his osteoporosis? A. Hyperparathyroidism, B. Hypogonadism, C. Hypothyroidism, D. Iatrogenic due to exogenous steroid" [8]
Answer: D. Iatrogenic due to exogenous steroid
- "Frequent injections for OA" = repeated IA corticosteroid injections
- Systemic absorption of corticosteroids → osteoporosis → vertebral compression fracture
- Links to lecture point: repeated injection may predispose to cartilage and joint damage
Stem: "Which of the following is NOT associated with anterior uveitis? A. Juvenile idiopathic arthritis, B. Osteoarthritis, C. Psoriatic arthritis, D. Behcet disease" [7]
Answer: B. Osteoarthritis
- OA is a non-inflammatory/degenerative arthropathy — no autoimmune association
- Anterior uveitis is associated with HLA-B27 spondyloarthropathies, JIA, Behcet's, and sarcoidosis
Stem: "A 50-year-old lady complains of deformities of her fingers in the DIP and PIP joints. There are Heberden's nodes in the DIP joints." [6]
Answer: E. Osteoarthritis
- Heberden's nodes (DIP) and Bouchard's nodes (PIP) are pathognomonic for nodal OA
- Discriminator: RA spares DIP joints; OA affects DIP/PIP/1st CMC
While Q9 (Reiter's syndrome) and Q10 (Adult onset Still's disease) test other conditions, OA (option D) appears in the stem list, testing whether students can discriminate OA from inflammatory arthritides [10].
High Yield Summary
First-line management of OA knee = Weight Reduction + Education + Exercise (NOT analgesics)
Pharmacology hierarchy: Topical NSAID (best for knee) > Paracetamol (weak evidence but safer than oral NSAIDs) > Oral NSAID/COX-2 (shortest duration, PPI cover) > NEVER chronic opioids
NO evidence for: Glucosamine (placebo effect only), Viscosupplementation/HA (no benefit over placebo), Arthroscopic debridement (increases OA progression)
IA corticosteroid: Short benefit (2-4 weeks only); repeated injections → cartilage damage, infection, iatrogenic osteoporosis
Surgical options: HTO (young, active, shift mechanical axis) → UKA (single compartment, faster recovery, safer than TKA) → TKR (definitive for end-stage)
UKA advantages: Quicker rehab, less periop complications, preserved kinematics/proprioception, preserved bone stock, easier revision
Charcot Joint (5 D's on X-ray): Deformity, Debris, Destruction, Density change, Dead bone — causes include DM, syphilis, syringomyelia
OA is a SERIOUS disease requiring a paradigm shift toward evidence-based, multidisciplinary chronic disease management
Active Recall - Knee OA Part B
[1] Lecture slides: GC 228. Knee Osteoarthritis_Part B.pdf [2] Lecture slides: GC 228. Knee Osteoarthritis_Part A.pdf [3] Senior notes: Block A - Upper abdominal pain_ peptic ulcer; pancreatitis and gallstone.pdf (NSAID GI risk section) [4] Senior notes: Maksim Surgery Notes.pdf (p.269 – OA section) [5] Lecture slides: LL exam Clinical Skill Practice Session 2023.pdf (Apley's OA section, p.78) [6] Past papers: 2018 Fourth Summative MCQ.pdf (Q22) [7] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q12) [8] Past papers: 2024 Fourth Summative MCQ.pdf (Q31) [9] Past papers: 2025 Fourth Summative MCQ.pdf (Q48) [10] Past papers: 2019 Fourth Summative MCQ.pdf (Arthritis EMQ section)
GC228 Knee Osteoarthritis: Part A
Knee osteoarthritis is a degenerative joint disease characterized by progressive loss of articular cartilage, subchondral bone changes, and osteophyte formation, leading to pain, stiffness, and impaired mobility.
GC229 Hip Arthritis
Degenerative or inflammatory disease of the hip joint characterized by cartilage loss, pain, stiffness, and progressive limitation of mobility.