MSK Flashcards
Don't you wanna come with me? Don't you wanna feel my boneson your bones? It's only natural
What are the X-ray changes in OA?
LOSS
Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts
What are some hand signs of OA?
Heberden’s nodes (DIP)
Bouchard’s nodes (PIP)
Squaring at the base of the thumb (CMC)
Weak grip
Reduced range of motion
How can OA be diagnosed clinically according to NICE guidelines?
The NICE guidelines (2022) suggest that a diagnosis can be made without any investigations if the patient is over 45, has typical pain associated with activity and has no morning stiffness (or stiffness lasting under 30 minutes).
Management for OA
- Non-pharm: exercise, weight loss, OT
- Pharm: topical NSAIDs, then oral NSAIDs
:::::::::::::weak opiates and paracetamol only for short-term, strong opiates not recommended:::::::::::::: - Intra-articular steroid injections may temporarily improve symptoms
- Joint replacement
What is the most common associated gene with RA?
HLA DR4
What antibodies are associated with RA? What are the sensitivities?
RF and anti-CCP (anti-cyclic citrullinated peptide)
RF present in 70% of RA pts
anti-CCP present in 80% of RA pts, more sensitive and specific
What are the hand signs in RA?
Z-shaped deformity to the thumb
Swan neck deformity (hyperextended PIP and flexed DIP)
Boutonniere deformity (hyperextended DIP and flexed PIP)
Ulnar deviation of the fingers at the MCP joints
How can RA affect the cervical spine?
Atlantoaxial subluxation => SCC (emergency)
risk of this during GA and intubation
What are some extra-articular manifestations of RA?
Pulmonary fibrosis
Felty’s syndrome (a triad of rheumatoid arthritis, neutropenia and splenomegaly)
Sjögren’s syndrome (with dry eyes and dry mouth)
Anaemia of chronic disease
Cardiovascular disease
Eye manifestations:
:::::::::Dry eye syndrome (keratoconjunctivitis sicca)
Episcleritis
Scleritis
Keratitis
Cataracts (secondary to steroids)
Retinopathy (secondary to hydroxychloroquine):::::::::::::::
Rheumatoid nodules (firm, painless lumps under the skin, typically on the elbows and fingers)
Lymphadenopathy
Carpel tunnel syndrome
Amyloidosis
Bronchiolitis obliterans (small airway destruction and airflow obstruction in the lungs)
Caplan syndrome (pulmonary nodules in patients with rheumatoid arthritis exposed to coal, silica or asbestos dust)
How is RA diagnosed?
urgent rheum referral (within 3w) for persistent synovitis
Bloods:
- RF
- anti-CCP Ab’s
- inflam markers: CRP, ESR
- X-rays of hands and feet
- USS/MRI to detect synovitis
What are the X-ray findings in RA?
LESS
Loss of joint space
Erosions
Soft tissue swellings
Soft bones (periarticular osteopenia)
What are some scoring systems for RA?
Health Assessment Questionnaire (HAQ) - functional ability
Disease Activity Score 28 Joints (DAS28) - monitor disease activity and response to treatment
What is the management of RA and how do you monitor response to treatment?
Short-term steroids while initiating treatment and during flares
conventional disease-modifying anti-rheumatic drugs (cDMARDs) and biologic DMARDs e.g.
1. monotherapy: methotrexate, leflunomide or sulfasalazine
2. combination treatment with multiple cDMARDs
3. biologic therapies alongside methotrexate
hydroxychloroquine - in mild disease, mildest DMARD, safe in pregnancy
cDMARDs - azathioprine, ciclosporin, cyclophosphamide, mycophenolate
What DMARDs are safe in pregnancy?
Hydroxychloroquine - mildest DMARD
Sulfasalazine - needs extra folic acid
Methotrexate and leflunomides are VERY BAD AND TERATOGENIC!!!
What are some different biologic therapies for RA?
Tumour necrosis factor (TNF) inhibitors (e.g., adalimumab, infliximab, etanercept, golimumab and certolizumab)
Anti-CD20 on B cells (e.g., rituximab)
Anti-interleukin-6 inhibitors (e.g., sarilumab and tocilizumab)
JAK inhibitors (e.g., upadacitinib, tofacitinib and baricitinib)
T-cell co-stimulation inhibitors (e.g., abatacept)
Which autoantibody is most associated with SLE? How do they function?
anti-nuclear antibodies (ANA) - positive in 85% of pts
autoantibodies against protein within cell nucleus
generate chronic inflammatory response
Name some associated symptoms/signs of SLE
Photosensitive malar rash “butterfly” shape
Arthralgia (joint pain), Non-erosive arthritis
Myalgia (muscle pain)
Fatigue, Weight loss, Fever
Shortness of breath, Pleuritic chest pain
Lymphadenopathy, Splenomegaly
Mouth ulcers
Hair loss
Raynaud’s phenomenon
Oedema (due to nephritis)
What lab findings are seen in SLE?
Autoantibodies - ANA in 85% of pts
anti-dsDNA (anti-double stranded DNA) - highly specific to SLE
anti-Sm, anti-centromere, anti-Ro, anti-La, anti-Scl-70, anti-Jo-1
FBC:
::::::::: anaemia of chronic disease, low WCC, low plt
Chem: CRP and ESR may be raised
C3 and C4 (reminder: compliment cascade in immune response, low levels indicate autoimmune disease)
Urinalysis: urine Pr:Cr shows proteinuria and lupus nephritis
Renal biopsy: lupus nephritis
What autoantibodies can be present in SLE?
⭐⭐anti-nuclear antibodies (ANA) - positive in 85% of pts
⭐Anti-double stranded DNA (anti-dsDNA) antibodies - highly specific, can be used to monitor disease activity
- Anti-Sm (highly specific to SLE but not very sensitive)
- Anti-centromere antibodies (most associated with limited cutaneous systemic sclerosis)
- Anti-Ro and anti-La (most associated with Sjögren’s syndrome)
- Anti-Scl-70 (most associated with systemic sclerosis)
- Anti-Jo-1 (most associated with dermatomyositis)
What can be used as diagnostic criteria for SLE?
European League Against Rheumatism (EULAR) / American College of Rheumatology (ACR) criteria (2019)
What are some complications of SLE?
- Cardiovascular disease - leading cause of death
- Infection
- Anaemia - anaemia of chronic disease, autoimmune haemolytic anaemia, bone marrow suppression by medications or kidney disease
- Pericarditis
- Pleuritis
- Interstitial lung disease => pulmonary fibrosis
- Lupus nephritis
- Neuropsychiatric SLE - optic neuritis, transverse myelitis, psychosis
- Recurrent miscarriage, IUGR, pre-eclampsia, pre-term labour
- VTE (assoc w antiphospholipid syndrome)
What is the management of SLE?
1st line:
::::::::: hydroxychloroquine ⭐
NSAIDS
steroids e.g. pred
2nd line:
::::::::::::DMARDs e.g. methotrexate, mycophenolate mofetil, cyclophosphamide
:::::::::::::Biologics - rituximab (targets CD20 protein on the surface of B cells), belimumab (targets B-cell activating factor)
What biologics can be used in SLE and what do they target?
rituximab (targets CD20 protein on the surface of B cells)
belimumab (targets B-cell activating factor)
Which genetic factors are most associated with SLE?
major histocompatibility complex (MHC) region, notably HLA-DR2 and HLA-DR