Yr4 MSK - Lectures Flashcards
(119 cards)
What is OA?
- Which joints are typically affected?
- OA is a group of overlapping genetic and mechanically driven disorders with similar morphologic features and clinical outcomes: end result is joint failure.
- Causation is unclear but genetic factors (heritability estimated at 40 – 70 %), and environmental factors such as occupation and joint injury are likely to be the major aetiologic contributors (e.g. farm workers have a 5 fold increased risk for hip OA).
Role of Ageing in OA?
Role of BMI in OA?
BMI (weight) and OA
* Obesity increases the risk of OA in females.
* Framingham data shows that a Wt. loss of 5 kg reduced the risk of Knee OA by a half and that weight loss (averaging 4kg) reduced knee pain.
* Decreased body mass improves mobility.
List 3 differences between OA and RA?
What is Erosive OA?
- What pattern on radiographs?
Erosive OA
* Probably a separate or unique disease (phenotype), however still a matter of conjecture
* Note the marked cartilage and central bone erosion
List 6 Signs & Symptoms of OA?
2 Classic clinical features?
Symptoms and Signs of OA
1. Joint pain – worse with use or activity
2. Transient post-resting joint stiffness
3. Loss of movement or pain on movement with restricted range
4. Tenderness – articular and peri-articular
5. Bony and soft tissue swelling
6. Crepitus
Why do some patients with OA experience pain and others don’t?
- Pain may arise from stretching of the capsule and/or “inflammation” in the synovium (MRI studies show that change in synovial thickening correlates with change in pain severity (r = 0.3, P <0.005)
- Pain may arise from the bone – there is a correlation between pain and bone marrow oedema lesions on MRI (longitudinal studies show that when pain gets worse, BMLs get larger)
List 5 Current Drug Therapy in OA.
- Proposed Therapy Pyramid in OA?
- Effect size of OA therapies?
- Advantages & Limitations?
Current Drug Therapy in OA
1. Analgesics
2. NSAIDs – topical and oral (parenteral rarely used in chronic disease)
3. Coxibs
4. IA Glucocorticoids
5. IA Hyaluronan
List 5 Possible future therapies for OA?
Possible future therapies for OA
1. CINODs (cyclo-oxygenase inhibiting nitric oxide donors, e.g. Naproxcinod)
2. Topical NSAIDs with improved drug delivery.
3. IL-1 antagonists (Orthokine, Anakinra, Canakinumab for selected disease)
4. Regenerative strategies - autologous chondrocytes (ACI) & autologous stem cells
5. Improved surgical techniques
List the Radiological features of OA (6) vs. RA (4)?
Diagnosis of OA?
- When to consider additional testing?
Diagnosis of OA
Clinical diagnosis - can be made confidently on clinical grounds alone if the following are present:
- persistent activity related pain in one or several joints
- age ≥45 years
- morning stiffness ≤30 minutes
When to consider additional testing
- younger individuals with joint symptoms/signs of OA
- presence of atypical symptoms and signs
- presence of weight loss or constitutional symptoms
Rheumatoid Arthritis - Epidemiology
- Prevalence?
- Median age at diagnosis?
- Gender?
Rheumatoid Arthritis - Epidemiology
- 1% population
- median age at dx = 50yr
- females x 3
What causes RA?
Describe the pathophysiology?
RA - Cause… (unknown)
Multifactorial
- genes + environment
- associated with HLA-DR4
Immune-mediated attack on joints
- Activated T-cells, macrophages, fibroblasts = Produce inflammatory cytokines…
Inflammation of synovium
- Proliferation, fluid secretion
- Invasion of cartilage and bone, joint destruction
- ?over-simplification
Rheumatoid Arthritis
- Presentation?
- Diagnosis?
- Early recognition?
RA - Presenting complaint
- Joint pains = “Inflammatory”
- Improved with activity & NSAIDs
- Worsened by rest
- Morning stiffness >1hr (fluid resorbed)
- Joint swelling
- Polymyalgic symptoms
- Systemic symptoms = fatigue, vasculitis, fever…
JOINT PAIN – Don’t just use SOCRATES!
Rheumatoid Arthritis
- Describe the joint involvement?
- 2 typical features on clinical examination?
- Which 2 conditions are associated & their treatments?
**RA - Joint involvement **
- Symmetrical
- Polyarticular (May be oligoarticular at onset)
- Small and large joints
- MCPs, wrists, MTPs = RA until proven otherwise
- PIPs NOT DIPs
- Knee, shoulder, hip, ankle (most peripheral joints)
- Cervical spine, TMJ - Will not involve the lower back!
- PMR – up to 30% will have - Tx = steroids (15mg) 12months
- Consider GCA - gold standard diagnosis = temporal artery biopsy (can also ultrasound) - Tx = steroids (50mg)
What is the most common cause of joint pain?
= viral
List the investigations you would order for suspected RA? (8)
- What Abs and what %?
List 7 Extra-articular manifestations of RA?
RA – Extra-articular manifestations
1. Nodules (RF+)
2. Ocular – Sicca (dry mucous membranes/eyes), epi/scleritis
3. Pulmonary - Nodules, serositis, alveolitis, fibrosis
4. Neuropathy - Entrapment, mononeuritis, peripheral neuropathy, cervical myelopathy
5. Vasculitis
6. Splenomegaly + Neutropaenia = Felty’s syndrome (extraordinarily rare)
7. Cardiac - Pericarditis, valvular/ conduction abnormalities
- Pay attention to cardiac risk factors
Outline the treatment for RA? (4)
RA - Treatment
1) Disease-modifying medication
- Methotrexate
- Leflunomide, Hydroxychloroquine, Sulfasalazine
2) Anti-inflammatories
- Prednisolone
- NSAIDs
3) Biological agents
4) Monitoring/ treatment of related conditions = Heart disease, osteoporosis
Main tx for RA: Low-dose Methotrexate
- MOA?
- Dosing?
- What must you also prescribe?
- 6 symptoms of methotrexate toxicity?
Other than methotrexate, list 4 other DMARDs you may use in the management of RA?
- MOA?
- Dosing?
- Toxicity/SEs?
What is Tumour Necrosis Factor (TNF)?
- List 6 anti-TNF bDMARDs?
Tumour Necrosis Factor (TNF)
- Key pro-inflammatory cytokine
- Secreted by macrophages, lymphocytes
- Stimulates cell activation, adhesion molecules, enzyme induction, other pro-inflammatory CKs
- Elevated levels in RA serum, synovium
- TNF transgenic mice - erosive arthritis
Discuss the Biological Agents used in RA
- Side effects?
- Monitoring - which 3 blood tests? Treatment efficacy?
Biological Agents in RA
- Well-tolerated
- Increased infection risk
- TB = Need to screen for TB as will cause dissemination of ghon complex
- Upper respiratory tract, soft tissue infections
- ? Increased malignancy risk Skin cancers
- Similar efficacy across the group
List the non-pharmacological treatments of RA?
RA – Other treatment aspects
- Physiotherapy = Improve strength, function (incl. Hydrotherapy)
- Occupational therapy - Wrist splints, Functional aids
- Support groups
- Surgery - Wrist fusion, MCP prosthetics = Becoming less common