Rheumatology Flashcards
What is Osteomyelitis?
Infection and inflammation of the bone.
Aetiology/Risk Factors for Osteomyelitis
Immunodeficiency (immunosuoppressants, HIV, etc)
DM - diabetic foot ulcers
Inflammatory arthritis e.g rheumatoid arthritis
Trauma
Sickle cell anaemia
Intravenous drug usage
Bacterial Aetiology of Osteomyelitsi
Staphylococcus aureus - most common
S.epidermidis - prosthetic joints
Salmonella - sickle cell disease
H.influenzae
P.aeruginosa - IVDU
What are the methods in which a bone can become infected?
Direct Inoculation - trauma, open wound
Contiguous Spread - infection of adjacent joint/tissue
Haematogenous Seeding - IVDU, catheter
Pathophysiology of Osteomyelitis
Inflammation due to infection causes inflammatory exudate in bone marow.
Results in increased intramedullary pressure - oedema.
Exudate can then go into the bone cortex and rupture periosteum.
Can interrupt perfusion and cause necrosis.
Leaves separated pieces of dead bone called sequestra.
New bone formation known as involucrum.
What is the most common site affected in children from haematogenous seeding osteomyelitis?
Metaphysis of long bones
Because blood flow is slower
Lack of endothelial basement membrane
Capillaries lack phagocytic lining cells.
What is the most common site affected in adutls from haematogenous seeding osteomyelitis?
Spinal vertebrae
Vertebrae get more vascular with age, allowing for increased likelihood of bacterial endplate seeding.
Acute pathophysiological changes seen in osteomyelitis
Oedema
Bone inflammation
Vascular congestion
Small vessel thrombi
Chronic pathophysiological changes seen in osteomyelitis
Necrotic bone ‘sequestra’
New bone formation - ‘involucrum
Lymphocytes and histiocytes
Exudate
Clinical Presentation of Acute Osteomyelitis
Onset over several days.
Dull pain at site which may be aggravated by movement.
Inflamed, swollen, tender at site of infection.
Clinical Presentation of Chronic Osteomyelitis
Deep / large ulcers that fail to heal despite several weeks treatment*
Non-healing fractures
Investigation of Osteomyelitis
FBC - leukocytosis
Raised CRP
First line: X-ray - can show osteopaenia - changes can be seen within 2 weeks of infection.
MRI scan - marrow oedema
GS: Blood cultures and bone biopsy
Differential Diagnoses of Osteomyelitis
Charcot joint - damage to sensory nerves due to diabetic neuropathy.
Cellulitis
Avascular necrosis of bone
Gout
Fracture
Medical Management of Osteomyelitis
Empirically vancomycin + ceftriaxone
Once organism is identified,
6 weeks IV antibiotics is considered minimum.
Stopping treatment is guided by CRP monitoring.
Surgical Management of Osteomyelitis
Debridement
Aetiolgy of Septic Arthritis in Adults
S.aureus
Streptococcus spp.
Neisseria gonorrhoeae
P.aeruginosa
Mycobacteria
Fungi
Aetiology of Septic Arthritis in children
S.aureus
H.influenzae
Kingella kingae
Risk Factors for Septic Arthritis
Immunosuppression (including steroids only)
Old age
Rheumatoid arthritis (or other immune-driven disease)
Diabetes mellitus
Prosthetic joint
Clinical Presentation of Septic Arthritis
Painful, red, swollen, hot joint
Mainly monoarthritis - single joint affected.
In children - may present as hesitation to use the joint.
Fever
Knee > hip > shoulder
Clincal Presentation of Gonococcal Septic Arthritis
Polyarthritis
Maculopapular – pustular rash
Investigation of Septic Arthritis
FBC: Leukocytosis
Raised CRP
Joint aspiration + culture - diagnostic
Infected joint fluid is turgid, viscous.
Blood cultures - mostly caused by bacteraemia seeding.
Management of Septic Arthritis
6 weeks minimum antibiotics
S.aureus - IV flucloxacillin
Gonococcal - IV ceftriaxone + azithromycin
Analgesia
Joint aspiration until no recurrent effusion.
What must be done for patients on corticosteroids with septic arthritis?
Temporary stoppage of short term immunosuppression.
If on long term steroids, prednisolone dose needs to be doubled in order to maintain glucocorticoid levels.
Investigation of Prosthetic Joint Infection
Serology: Alpha defensin positive - antimicrobial peptide found in synovial fluid.
Joint aspiration is diagnostic.
Mangement of Prosthetic Joint Infection
Antibiotic Suppression
Debridement and Implant Retention (DAIR) of Prosthesis - not for chronic infections.
Excision Arthroplasty
Exchange Arthroplasty
Amputation
Aetiology/RIsk Factors of Rheumatoid Arthritis
Female gender
HLA-DR4 presence
Smoking
Pathophysiology of Rheumatoid Arthritis
Overproduction of TNF-a leads to synovitis.
Further cytokine release causes synovium to grow past joint margins to form a pannus.
The pannus destroyed articular cartilage and subchondral bone resulting in erosions.
Mutation in process of arginine to citrulline conversion causes presence of anti-CCP (citric citrullinated peptide) antibodies.
Clinical Presentation of Rheumatoid Arthritis
Is a polyarthritis which affects joints symmetrically.
Swollen, painful and stiff joints.
Worse in the morning, improves throughout day.
Prolonged early morning stiffness (>60 mins)
Affects mainly small joints of hands such as MCP, PIP and feet like MTP.
DIP and spine sparing
Can affect elbows, shoulders, knees and ankles too.
Extra-Articular Manifestations of Rheumatoid Arthritis
Pericarditis (cardiovascular)
Episcleritis (ophthalmological)
Amyloidosis (renal)
Bronchiectasis (respiratory)
Peripheral neuropathy (neurological)
Subcutaneous nodules (dermatological)
Examination of Rheumatoid Arthritis
Decreased grip strength - cannot form fist.
Ulnar deviation of hand
Z-thumb
Boutonniere deformity - flexed PIP, extended DIP to form “^” shape at PIPJ.
Swan neck deformity - flexed DIP, extended PIP to form “^” shape at DIPJ.
Investigation of Rheumatoid Arthritis
FBC - may show normocytic normochromic anaemia
Raised CRP
Serology - Rheumatoid factor and Anti-CCP (cyclic citrullinated peptide) positive.
X-rays (may be normal at presentation but will get worse later)
Biopsy of nodules - cholesterol deposits.
What would be seen on an X-Ray for Rheumatoid Arthritis?
LESS
Loss of joint space
Erosion of bone
Soft tissue swelling
Soft bone (osteopaenia)
Management of Rheumatoid Arthritis
First line: DMARDs (Disease Modifying Anti-Rheumatic Drugs)
GS: Methotrexate 10-25mg per week
Sulphasalazine 2-3g daily
Leflunomide 10-30mg daily
Hydroxychloroquine 200mg
+ NSAIDs -Naproxen, Ibuprofen
Corticosteroids - Oral prednisolone or intra-articular injection
Biologics:
Anti TNF medications such as infliximab, adalimumab
Anti IL-6 such as tocilizumab.
Anti CD20 such as rituximab - last line.
Complication of Rheumatoid Arthritis
Felty Syndrome
Triad of RA + splenomegaly + granulocytopaenia.
More prone to infections since neutropaenia.
Pharmacodynamics of Methotrexate
Folate antagonists through inhibiting dihydrofolate reductase to reduce nucleic acid synthesis and cell replication.
Contraindications of Methotrexate
Contraindicated in pregnancy
Side effects of Methotrexate
Nausea, mouth ulcers, anaemia
Contraindications of adalimumab
Heart failure, ongoing infection.
Side effects of adalimumab
Agranulocytosis, anaemia, arrhythmias
What is the composition of gout crystals?
Monosodium urate
What is the composition of pseudogout crystals?
Calcium pyrophosphate
Epidemiology of crystal arthropathies
Gout - more common in males
Pseudogout - more common in females.
Physiology of purine metabolism
Xanthines are converted into uric acid by xanthine oxidase enzyme.
Humans lack uricase enzyme to further metabolise uric acid so it is excreted by kidneys.
Aetiology/Risk Factors of Gout
Hyperuricemia
Dietary - beer, red meats, high fructose diet.
CKD - limited excretion of purines
Drugs - Diuretics, aspirin
Pathophysiology of Gout
Caused by the deposition of sodium urate crystals within joint
The immunological reaction initiated to try and remove them, leads to acute pain and swelling
Soft drinks - fructose shares renal uric acid transporter which minimizes excretion of uric acid.
Clinical Presentation of Gout
Onset is usually at night.
Normally monoarticular, asymmetric arthritis.
Can be aggravated after high purine diet such as meats, seafood, alcohol.
Initial presentation of inflammation/pain of big toe - first MTP joint
Affect feet, ankles, knees, elbows, hands
Lower limbs are affected earlier on, upper limbs later.
If left to progress, can lead to tophi - erosion away from the articular margin.
Investigation of Gout
GS - Joint aspiration + microscopy
Negative birefringent needle-like crystals seen under polarized light.
FBC - leukocytosis due to inflammation
U + E - kidney status
Serum uric acid - often normal during attacks since the uric acid is not in the blood but in the form of joint crystals, but often raised in between attacks.
X-ray if recurrent episodes.
Lifestyle Management of Gout
Increased dairy intake
Reduced fructose intake
Reduced red meat and alcohol intake.
Management of Chronic Gout
Aim of management is to reduce uric acid below <300 micromols/L
Allopurinol – Xanthine Oxidase Inhibitor
Febuxostat – more potent Xanthine Oxidase Inhibitor
Complications of Gout
Renal calculi
Acute and chronic urate nephropathy
Clinical Presentation of Pseudogout
Polyarticular arthropathy.
Often affects the knee and wrist.
Investigation of Pseudogout
Joint aspiration + microscopy - rhomboid crystals, positive birefringence under polarized light.
X-ray: Chondrocalcinosis - cartilage calcification parallel to articular surface
Management of Acute Gout and Pseudogout
1st line: Oral NSAIDs (short course) unless renal failure, peptic ulcers
2nd line: Oral Colchicine 500ug 2-3 times daily
3rd line: Corticosteroids - Intra-articular injection or oral low dose (5-10mg short course) e.g prednisolone
Pharmacodynamics of Colchicine
Disrupts tubulin activity causing loss of microtubule based inflammatory chemotaxis.
Side effects of Colchicine
Abdo pain, nausea/vomiting, melena.
What is Osteoporosis?
A systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture
Epidemiology of Osteoporosis
50% of women and 33% of men will experience an osteoporotic fracture.
20% of people with hip fractures die within the first year.
Aetiology/Risk Factors of Osteoporosis
SHATTERED
Steroid use
Hypoparathyroidism & Hyperthyroidism
Alcohol and tobacco
Testosterone decrease - increased bone turnover
Early menopause - increased bone turnover
Renal failure
Erosive bone disease e.g RA
Dietary calcium decrease (malabosorption)
Previous and family history of fracture
Screening for Osteoporosis
FRAX Score
Gives risk of fractures over the next 10 years
Components of FRAX Score
Age
Smoking
Family history of hip fracture
Glucocorticoid use (eg, Prednisone)
Arthritis
Femoral neck bone mineral density
Pathophysiology of Osteoporosis
Osteoporosis results from increased bone breakdown by osteoclasts and decreased bone formation by osteoblasts, leading to loss of bone mass
Bone mass decreases with age, but will depend on the ‘peak’ mass attained in adult life and on the rate of loss in later life
What factors affect peak bone mass?
Genetic factors - most important
Dietary Vit.D intake
Levels of physical activity
Factors affecting bone strength
Bone density
Bone size
Bone quality (turnover, architecture, mineralization).
Age (increasing age increases fracture risk)
Changes in Trabecular Architecture with Ageing
Decrease in trabecular thickness
Decrease in horizontal inter-trabecular connections in order to preserve integrity of vertical trabecular connections.
Investigation of Osteoporosis
Bone Densitometry
DEXA scan (dual energy x-ray absorptiometry)
Measures the risk of having a fracture.
T-score
Standard deviation compared with gender matched young adult average.
What is the range and meaning of T-scores?
> -1 = normal
-1 to -2.5 = osteopaenia
< -2.5 = osteoporosis
< -2.5 + fracture = severe osteoporosis
Management of Osteoporosis
First line - bisphosphonates e.g IV zoledronate, oral alendronate
Denosumab - RANK ligand inhibitor
Teriparatide - PTH analogue
Pharmacokinetics of bisphosphonates
Inhibit farnesyl pyrophosphate synthase (FPP synthase) in the cholesterol synthesis pathway.
Reduces the ruffled border of osteoclasts, decreasing their activity and bone resorption.
Side effects of denosumab
Skin itching, back pain, cloudy urine.
Contraindications for bisphosphonates
Hypocalcaemia
Pharmacodynamics of denosumab
RANK receptor is expressed on osteoclast precursor.
RANK ligand expressed on osteoblasts.
Binding of ligand to receptor causes maturation into osteoblasts.
Is a monoclonal antibody to RANK ligand to does not allow osteoclast differentiation, reducing bone resorption.
Side effects of bisphosphonates
Increased risk of jaw osteonecrosis, oesophageal issues e.g oesophagitis, dysphagia.
Pharmacodynamics of teriparatide
PTH analogue that stimulates osteoblastic activity.
What are some inherited connective tissue disorders?
Marfan’s Syndrome
Ehler Dahnos Syndrome
What are some autoimmune connective tissue disorders?
Systemic Lupus Erythematosus
Sjorgen syndrome
Systemic Sclerosis
Dermatomyositis
Aetiology of Marfan’s Syndrome
Autosomal dominant FBN1 gene mutation on chromosome 15 affecting fibrillin-1 protein.
Pathophysiology of Marfan’s Syndrome
FIbrillin-1 is a glycoprotein that forms a sheath around elastin and sequesters TGF-β, a growth factor for connective tissue.
Lack of connective tissue structure and growth.
Clinical Presentation of Marfan’s Syndrome
Very tall, lanky people
Chest wall deformity - Pectus carinatum (pigeon chest), pectus excavatum (deep indentation at and around sternum)
Investigation of Marfan’s Syndrome
Diagnose through genetic testing for FBN-1 mutation.
Aetiology of Ehler-Danlos Syndrome
Mutation in Type V collagen gene causing defective collagen synthesis.
Clinical Presentation of Ehler-Danlos Syndrome
Joint hypermobility
Flexible skin
Easy bruising/bleeding.
Complications of Ehler-Danlos and Marfan’s Syndrome
Aortic aneurysms
Mitral regurgitation
Subarachnoid haemhorrage
Epidemiology of SLE
More common in women of childbearing age, Afro-Caribbean
Aetiology/Risk Factors for SLE
Drugs e.g isoniazid, sulfasalzine
UV light
EBV
Family history
Pathophysiology of SLE
T3 hypersensitivity reaction.
Recognition of self-antigens causes production of anti-nuclear autoantibodies. Results in immune complex deposition in tissues which results in cytokine release and systemic inflammation.
Clinical Presentation of SLE
FAME PEG
Fever
Arthritis (deforming, non-erosive arthritis)
Mouth ulcers
Episcleritis
Photosensitive malar rash
Erythema
Glomerulonephritis (haematuria)
Pericarditis, pleural effusion.
Reynaud’s = white fingers due to vasoconstriction and lack of blood flow.
Seizures (neuropsychiatric lupus)
P.E
Investigation of SLE
Raised ESR but not CRP
FBC: Normocytic anaemia , leukopenia.
Serology: Anti nuclear antibody positive, anti double stranded DNA.
Biopsy will show IgG and complement deposition.
Management of SLE
Reduce sunlight exposure
NSAIDs
Hydroxychloroquine - antimalarial.
Cyclophosphamide
Biologics - rituximab, belimumab.
What are the different types of systemic sclerosis (scleroderma)?
Limited cutaneous scleroderma (most common)
Diffuse cutaneous scleroderma
Pathophysiology of Systemic Sclerosis
Increased synthesis of T1 and T2 collagen causing connective tissue fibrosis and widespread vascular damage
Clinical Presentation of Systemic Sclerosis
CRESS
Calcinosis (subcutaneous calcium deposition)
Raynaud’s phenomenon
Esophageal dysmotility
Sclerodactyly - thickening and tightening of fingers and skin around fingers.
Spider veins
Investigation of Systemic Sclerosis
Serology: Anti-centromere antibodies in LCS, Anti-topoisomerase, anti-Scl-70 antibodies in DCS
Anti-nuclear antibodies in both.
Pathophysiology of Sjorgen Syndrome
Autoimmune exocrine gland destruction through lymphocytic infiltration.
Clinical Presentation of Sjogren Syndrome
Keratoconjunctivitis sicca (Dry eyes)
Joint pain
Xerostomia (decreased saliva production
Investigation of Sjogren Syndrome
Serology: RF positive, ANA positive, anti-Ro and anti La antibody positive.
Schirmer test where tears are put onto filter paper and travel <10mm when normally should be >20mm.
Management of Sjorgen Syndrome
Artificial tears and saliva administration
Hydroxychlroquine.
What is Polymyositis/Dermatomyositis
Inflammation + necrosis of skeletal muscle
If skin involved then dermatomyositis.
Clinical Presentation of Polymyositis
Symmetrical progressive muscle weakness.
Hard to stand from sitting
Clinical Presentation of Dermatomyositis
Gottron’s papules (scales on knuckles).
Heliotrope - purple eyelid.
Investigation of Polymyositis/Dermatomyositis
Muscle enzymes: Raised creatinine kinase, lactate dehydrogenase
GS: Muscle biopsy - shows necrosis and inflammationvo
Serology: ANA positive, anti-Jo-1 Ab positive
Management of Polymyositis/Dermatomyositis
IV corticosteroids like prednisolone.
What is Vasculitis
Inflammation and necrosis of blood vessel walls.
Can result in aneurysm and rupture.
Examples of large vessel vasculitis
Giant cell arteritis
Takayasu’s arteritis
Examples of medium vessel vasculitis
Classical polyarteritis nodosa
Kawasaki’s disease
Examples of small vessel vasculitis
ANCA associated:
p-ANCA: Microscopic polyangitis and eosiniphilic granulomatosis with polyangitis (Churg-Strauss)
c-ANCA: granulomatosis with polyangitis
Not ANCA associated:
Essential cryoglobulinaemia
General Investigations for Vasculitis
Raised ESR/CRP
FBC: Anaemia
Serology: Either negative or positive for p-ANCA or c-ANCA
General Management of Vasculitis
Steroids e.g prednisolone
Immunosuppression e.g cyclophosphamide.
Epidemiology of Giant Cell (Temporal) Arteritis & Polymyalgia Rheumatica
Normally affects women over 50
Pathophysiology of Giant Cell Arteritis
Can affect branches of the external carotid artery
E.g facial, ophthalmic, temporal artery.
Clinical Presentation of Giant Cell Arteritis
Unilateral headache on the temples.
Temporal artery tenderness
Jaw claudication
Can prevent with painless acute loss of sight.
Clinical Presentation of Polymyalgia Rheumatica
Pain occurs above and below torso (shoulders, thighs, neck, knees)
Can have systemic symptoms of fever, weight loss, night sweats.
Diagnostic Investigation of Giant Cell Arteritis & Polymyalgia Rheumatica
Temporal artery biopsy - can show inflammation and giant cells.
Managment of Temporal Arteritis
Oral prednisolone
If visual symptoms - IV methylprednisolone.
Can give oral aspirin prophylaxis.
Complications of Giant Cell Arteritis
Optic neuropathy causing sudden painless vision loss.
Aetiology/Risk Factors of Polyarteritis Nodosa
Associated with hepatitis B
More common in males
Clinical Presentation of Polyarteritis Nodosa
Weight loss
Melena
Numbness
Fever
Hypertension
Livedo reticularis - lace like purple rash.
Clinical Presentation of Microscopic Polyangitis
Dyspnoea
Renal failure
Investigation of Microscopic Polyangiitis
Serology: P-ANCA positive
Henoch-Schonlein Purpura
IgA Associated small vessel vasculitis
Associated with IgA nephropathy.
Investigation of Henoch-Schonlein Purpura
Immune complex deposition on tissue biopsy.
Investigation of Eosinophilic Granulomatosis with Polyangitis (Churg-Strauss)
Eosinophilia
Raised serum IgE
Serology: p-ANCA
Pathophysiology of Granulomatosis with Polyangitis
Necrotizing vasculitis
Necrotizing glomerulonephritis
Necrotizing granulomas in respiratory tract.
Investigation of Granulomatosis with Polyangitis (Wegener’s)
Serology: c-ANCA positive
CXR: Large nodular densities.
What is fibromyalgia?
A chronic pain syndrome
Clinical Presentation of Fibromyalgia
Chronic widespread pain despite exclusion of other disease.
Areas of tenderness
Arthralgia - stiffness
Sleeplessness
Cognitive disturbances.
Differential Diagnoses of Fibromyalgia
Polymyalgia rheumatica
Inflammatory arthritis
Management of Fibromyalgia
Physiotherapy
Regular exercise
Low does antidepressants e.g TCAs like amitryptiline
What are the serongative spondyloarthropathies?
Ankylosing spondylitis (axial spondyloarthritis)
Psoriatic arthritis
Acute anterior uveitis (acute iritis - synonymous with anterior uveitis)
Enteropathic arthritis (IBD)
Reactive arthritis
Undifferentiated spondyloarthritis
What immune molecule are all the seronegative spondyloarthropathies asssociated with?
HLA B27
Where is HLA B27 present?
On all cells except erythrocytes.
What are two theories for the pathophysiology of HLA-associated seronegative spondyloarthropathies?
Molecular Mimicry
HLA B27 misfolding
What is the HLA B27 molecular mimicry theory?
If antigen similar to HLA B27 is present on pathogens, there can be autoimmunity against existing HLA B27 containing cells.
What is the HLA B27 misfolding theory?
Misfolding of HLA-B27 heavy chains causes stress on endoplasmic reticulum causing an inflammatory and immune response.
IL 12/23 involvement.
Clinical Presentation of Sernoegative Spondyloarthritis
SPINEACHE
Sausage digit (dactylitis - swelling of whole finger or whole toe, synovitis + tenosynovitis)
Psoriasis - typically on extensor surfaces - back of elbows, front of knees
Inflammatory back pain
NSAID good response
Enthesitis (inflammation of tendon) - achilles tendon, heel.
Arthritis - normally asymmetric , large joint affecting.
Crohns/colitis/elevated CRP
HLA B27
Eye (uveitis)
What is ankylosing spondylitis?
Chronic inflammatory disorder of the spine, ribs, sacroiliac joints.
More common im men below age of 45.
Pathophysiology of Ankylosing Spondylitis
Repeated inflammation can result in fatty deposits and bone erosion.
Replacement by syndesmophyte formation occurs.
Causes bone fusion resulting in reduced mobility.
Affects areas like spine, ribs, sacroiliac joint, etc.
Clinical Presentation of Ankylosing Spondylitis
Back pain - can occur at night and gets better with exercise.
Kyphosis
Sacroiliac (buttock) pain.
Investigation of Ankylosing Spondylitis
Spinal X-ray: Bamboo spine appearance
MRI: periarticular bone marrow oedema
Management of Ankylosing Spondylitis
First line - NSAIDS e.g naproxen.
Second line - biologics
Anti TNF e.g infliximab, adalimumab
IL-17 blockers e.g secukinumab.
DMARDS are not very effective.
Clinical Presentation of Psoriatic Arthritis
Asymmetrical polyarthritis
DIP inflammation
Dactylitis – sausage digit / toe
Nail dystrophy
Enthesitis
Regions of psoriatic rash: Behind ears, scalp, under nails
Clinical presentation of Arthritis Mutilans
Complication of psoriatic arthritis.
Is where there is very destructive bone changes.
Causes floppy fingers and shortened fingers due to joint degeneration.
Investigation of Psoriatic Arthritis
X ray - pencil in cup sign in interphalangeal joints.
Management of Psoriatic Arthritis
First line: DMARDs - e.g methotrexate
Second line: Anti-TNF e.g adalimumab, infliximab.
Third line: Anti IL 12/23 e.g Ustekinumab
Reactive Arthritis
Sterile inflammation of synovial membrane, tendon and fascia triggered by an infection at a distal site.
Mostly post STI or enteric infection.
Aetiology/Risk Factors of Reactive Arthritis
Sexual activity
Gastrointestinal infection - shigella, salmonella, c.jejuni
STI - chlamydia, gonorrhoea
Clinical Presentation of Reactive Arthritis
Reiter’s Triad
Assymetrical, lower limb monoarthritis + enthesitis
Conjunctivitis
Urethritis
Keratoderma blennorrhagica - red-brown papules on plantar surface of feet
Genital inflammation
Management of Reactive Arthritis
First line: NSAIDs e.g as naproxen
If persisting: DMARDs e.g methotrexate.
Aetiology of Clinical Presentation of Enteropathic Arthritis
Associated with crohn’s disease and UC
Large joint, asymmetrical arthritis.
Examples of Primary Bone Tumours
Osteosarcoma
Chondroma
Ewing’s sarcoma
Clinical Presentation of Primary Bone Tumours
Localised pain, often worse at night (can wake up at night).
Can cause symptoms of hypercalcaemia.
Loss of mobility
Lumps
Features of Osteosarcoma
Associated with Paget’s disease
Can metastasize to lung
Has pleiomorphic osteoblasts.
Occurs in the metaphysis of long bones.
Most commonly knee and proximal humerus
Investigation of Osteosarcoma
X-Ray: Sunburst appearance
What is a Chondrosarcoma?
Cartilage cancer
Features of Ewing’s Sarcoma
Arises from mesenchymal stem cells
Most common in diaphysis of long bones.
Mostly affects children and young adults <15 years old.
Investigation of Ewing’s Sarcoma
X-ray - onion skin appearance.
Investigations of Bone Tumours
X-ray is first line.
Full length of bones imaging.
Can be evidence of bone destruction, periosteal/soft tissue swelling.
CT
Used to determine bone/tumour morphology
CT-CAP for primary tumour staging.
Biopsy
Diagnostic test
Fine needle aspiration cytology - carcinomas
Core biopsy for sarcomas
Staging of Musculoskeletal Tumours
Grade - low (G1) or high (G2)
Extent of Tumour (T) - intra (T1)/extracompartmental (T2)
Intra if not crossing the intramuscular septum
Metastasis
AJCC TNM
Size of the primary tumor (T)
Spread to nearby lymph nodes (N)
Metastasis to distant sites (M)
Surgical MSK Tumour Management
Bone:
Limb salvage - autograft, allograft, endoprosthetic replacement
Amputation
Soft Tissue:
Tumour excision
Angioembolization of feeding artery to tumour.
Medical MSK Tumour Management
Adjuvant or neo-adjuvant chemotherapy.
Radiotherapy - Definitive management of radiosensitive primary tumour.
What is Osteoarthritis?
Most common condition affecting synovial joints.
Age related, dynamic reaction pattern of a joint in
response to insult or injury.
Articular cartilage is most affected.
Risk Factors for Osteoarthritis
Age - cumulative effect of trauma on joints
Female gender - esp. Postmenopausal
Obesity
Occupation - jobs involving manual labour
Pathophysiology of Osteoarthritis
Mediated by cytokines (IL-1, TNF-a, NO)
Imbalance in degradation of cartilage and production by chondrocytes causing progressive destruction and loss of articular cartilage with an accompanying periarticular bone response
General Clinical Presentation of Osteoarthritis
Pain - improves with rest but gets worse throughout the day with weight bearing
Functional impairment - walking, gripping
Joint swelling - bony swelling
Short-lived morning stiffness
Clinical Presentation of Osteoarthritic Hand
Can involve DIP, PIP, CMC joints - especially 1st CMC (base of thumb)
Heberden’s nodes at DIP joints
Bouchard’s nodes at PIP
Investigation of Osteoarthritis
X-Ray - LOSS
Loss of joint space
Osteophyte formation
Subchondral sclerosis
Subchondral cysts
Abnormalities of bone contour.
Non-pharmacological management of Osteoarthritis
Physio/occupational therapy
Lifestyle changes - weight loss, increased exercise.
Walking aids e.g stick, walking frame
Pharmacological Management of Osteoarthritis
First line: Topical/oral NSAIDs or capsaicin
Second line: Add paracetamol
Intra-articular steroid injections
Surgical management of Osteoarthritis
Joint arthroscopy, arthrodesis, arthroplasty.
What is Osteomalacia?
Defect in bone mineralisation.
Occurs after fusion of epiphysis.
Rickets is defective bone mineralisation in children which occurs during bone growth.
Aetiology of Osteomalacia
Vitamin D deficiency
Hyperparathyroidism (causing hypophosphataemia)
CKD - no activation of vitamin D.
Drugs - anticonvulsants and rifampin.
Clinical Presentation of Osteomalacia
Muscle weakness - waddling gait, difficulty getting out of chair.
Bone pain
Pathological fractures - especially femoral neck.
Investigation of Osteomalacia
U + E
Low calcium, phosphate,
High ALP, High PTH
X-Ray - osteopaenia, looser’s zones
Diagnostic is bone biopsy - shows decreased mineralisation.
Management of Osteomalacia
Calcitriol supplementation
What is Paget’s Disease?
Focal disorder of bone remodelling.
Pathophysiology of Paget’s Disease
Uncoordinated excessive activity of osteoclasts and osteoblasts causes patchy areas of sclerosed and lytic new bone.
Increases the risk of pathological fractures.
Clinical Presentation of Paget’s Disease
Bone pain
Deformities such as bowed tibia
Deafness
Investigation of Paget’s Disease
Raised ALP
Normal calcium, phosphate
X ray
Areas of sclerosis and lytic regions
Cotton wool appearance of skull
Management of Paget’s Disease
Bisphosphonates e.g IV zoledronate, oral aledronate.
NSAIDs for pain
Aetiology of Antiphospholipid Syndrome
Can be primary or secondary to another autoimmune disorder e.g SLE.
More common in females.
Pathophysiology of Antiphospholipid Syndrome
Antiphospholipid antibodies (aPL) bind to
phospholipid on the surface of cells such as endothelial cells and platelets causing a state of hypercoagulability.
Cause CLOTS:
Coagulopathies
Livedo reticularis
Obstetric issues such as miscarriage
Thrombocytopaenia
Clinical Presentation of Antiphospholipid Syndrome
Livedo reticularis
Thrombosis
Ischaemic stroke
DVT
Investigation of Antiphospholipid Syndrome
Serology: Presence of antiphospholipid antibodies such as lupus anticoagulant, anticardiolipin antibodies, B2 glycoprotein antibodies.
Management of Antiphospholipid Syndrome
First line: Long term Warfarin
If pregnant: Heparin + aspirin
Aetiology of Mechanical Lower Back Pain
Scoliosis
Lumbar spondylosis - loss of intervertebral disc compliance
Facet joint syndrome
Sciatica
Vertebral disc degeneration - can cause prolapse
Osteoarthritis
Risk Factors of Mechanical Back Pain
Manual labour
Increasing age
Female gender
Smoking
Clinical Presentation of Mechanical Back Pain
Pain - often short lived & relieved by rest
Stiff back and scoliosis
Muscle spasms
Pathophysiology of Lumbar Spondylosis
Loss of compliance of intervertebral discs.
Most commonly in L4-S1.
Investigation of Mechanical Lower Back Pain
X-ray
Management of Mechanical Lower Back Pain
Analgesia - e.g NSAIDs, paracetamol,
Physiotherapy
