Rheumatology Flashcards
What is rheumatology?
The medical management of musculoskeletal disease.
Give two rough categories that joint pain can be divided into.
- Inflammatory
- Non-inflammatory
Give three examples of inflammatory joint problems.
- Autoimmune
- Crystal arthritis
- Infection
Give three examples of autoimmune rheumatological diseases.
- Rheumatoid arthritis
- Spondyloarthropathy
- Connective tissue disease
Give an example of a degenerative rheumatoid condition.
Osteoarthritis
Give an example of a non-degenerative, non-inflammatory rheumatoid condition.
Fibromyalgia
Compare the pain in inflammatory and degenerative rheumatological conditions.
INFLAMMATORY = eases with use DEGENERATIVE = increases with use, clicks/clunks
Compare the stiffness in inflammatory and degenerative rheumatological conditions.
INFLAMMATORY = Significant (>60mins), early morning, at rest (evening) DEGENERATIVE = Not prolonged (<30mins), morning/evening
Compare the swelling in inflammatory and degenerative rheumatological conditions.
INFLAMMATORY = Synovial +/- bony DEGENERATIVE = No synovial, bony
Compare the inflammation in inflammatory and degenerative rheumatological conditions.
INFLAMMATORY = may be hot and red DEGENERATIVE = Not clinically inflamed
Compare the patient demographics in inflammatory and degenerative rheumatological conditions.
INFLAMMATORY = young, psoriasis, family history DEGENERATIVE = older, prior occupation, sport
Compare the joint distribution in inflammatory and degenerative rheumatological conditions.
INFLAMMATORY = hands and feet DEGENERATIVE = 1st CMCJ, DIPJ, knees
Compare the NSAID response in inflammatory and degenerative rheumatological conditions.
INFLAMMATORY = good response DEGENERATIVE = Less convincing
Describe the pattern of pain in bone pain.
Pain at rest and at night.
Give three things that can cause bone pain.
- Tumour
- Infection
- Fracture
Describe the pattern of pain in inflammatory joint pain.
Pain and stiffness in joints in the morning, at rest, and with use.
Give two things that can cause inflammatory joint pain.
- Inflammatory
- Infective
Describe the pattern of pain in osteoarthritis.
Pain on use and at the end of the day.
Describe the pattern of pain in neuralgic pain.
Pain and paraesthesia in dermatomal distribution worsened by specific activity.
What causes neuralgic pain?
Root or peripheral nerve compression
Describe the pattern of pain in referred pain.
Pain unaffected by local movement.
If the distal interphalangeal joint is involved in a rheumatological disorder, what are the two potential diagnoses?
- Psoriatic arthritis
- Osteoarthritis
How quickly does ESR rise and fall?
Slowly (days to weeks)
How quickly does CRP rise and fall?
Rapidly
Define spondyloarthritis.
Spondyloarthritis is an umbrella term encompassing several forms of arthritis.
Give seven forms of spondyloarthritis.
- Ankylosing spondylitis
- Psoriatic arthritis
- Reactive arthritis
- Enteropathic arthritis
- Acute anterior uveiits (iritis)
- Enthesis related juvenile idiopathic arthritis
- Undifferentiated spondyloarthritis
Give a genetic factor which all of the spondyloarthropathies are related to.
HLA B27
Give three theories as to how HLA B27 causes disease.
- Molecular mimicry (previous infectious agent has peptides similar to HLA)
- Mis-folding of HLA B27 stimulates cytokines
- Heavy chain homodimer activates T cells
What are the clinical features of spondyloarthritis?
SPINEACHE
- Sausage digits (dactylitis)
- Psoriasis
- Inflammatory back pain
- NSAIDs (good response)
- Enthesitis (heel)
- Arthritis (may be asymmetrical oligoarthritis)
- Crohn’s/Colitis/CRP elevated
- HLA B27
- Eye (uveitis)
What is ankylosing spondylitis?
Inflammatory arthritis of the spine and rib cage.
Describe what happens to the vertebra in ankylosing spondylitis.
Patients lay down new bone in spine due to inflammation and this forms sheets of calcified ligaments.
In what age group does ankylosing spondylitis usually present?
Late teenage years/20s
What are the six characteristics of inflammatory back pain associated with ankylosing spondylitis?
- Onset below 40yrs
- Insidious onset
- Lasting >3months
- Morning stiffness
- Improvement with exercise
- Pain at night
Give two signs of ankylosing spondylitis which can be seen on an XRay.
- Syndesmophytes
- Sacroiliitis
What are syndesmophytes?
New bone formation and vertical growth from anterior vertebral corners.
What is sacroiliitis?
Sclerosis, erosions, loss of joint space, and fusion of the sacroiliac joint.
How can ankylosing spondylitis be diagnosed earlier than just using XR?
Inflammation and bone marrow oedema in the sacroiliac joints show up earlier on MRI.
Give three treatment options for ankylosing spondylitis.
- Exercise
- NSAIDs
- Anti-TNF and Anti-IL17 drugs
Give a complication of ankylosing spondylitis.
Fusing of the spine (severe kyphosis of thoracic and vertebral spine).
Give the five patterns of psoriatic arthritis.
- DIPJ only
- RA like (symmetrical small joint)
- Large joint oligoarthritis
- Axial
- Arthritis mutilans
Give two radiological changes that occur in psoriatic arthritis.
- Erosive changes
- ‘Pencil in cup’ deformity in severe cases
Give three treatment options of psoriatic arthritis.
- DMARDs (salfasalazine)
- Anti TNF drugs (infliximab)
- IL12/IL23/IL17 blockers
What is reactive arthritis?
Sterile inflammation of the synovial membrane, tendons, and fascia, triggered by an infection at a distant site (usually gastrointestinal or genital).
Give four gut infections that are associated with reactive arthritis.
- Salmonella
- Shigella
- Yersinia
- Campylobacter
Give two sexually acquired infections which are associated with reactive arthritis.
- Chlamydia
- Ureaplasma urealyticum
Give the three classical features of reactive arthritis (also known as Reiter’s syndrome).
- Arthritis (typically 2 days to 2 weeks post infection)
- Conjunctivitis
- (Sterile) urethritis
Give two signs/features associated with reactive arthritis.
- Keratoderma blenorrhagica (brown raised plaques on palms and soles)
- Circinate balanitis (painless penile ulceration, secondary to chlamydia)
Give three investigations that should be carried out in reactive arthritis.
- Raised ESR/CRP
- Aspirate joint to exclude infection/crystals
- Urethral swab/stool culture
Give two differential diagnoses that must be excluded in reactive arthritis.
- Septic arthritis
- Gout
What is enteropathic arthritis?
Episodic peripheral synovitis which occurs in up to 20% of patients with IBD.
What is the most common pattern of enteropathic arthritis?
Asymmetric lower limb arthritis
How is enteropathic arthritis related to the inflammatory bowel disease?
Arthritis usually reflects disease activity, and remission is generally related to suppression of the bowel disease.
Which gender is rheumatoid arthritis more common in?
Women
What is the most common age to develop rheumatoid arthritis?
40-60years
What percentage of the population does rheumatoid arthritis affect?
1%
Describe the pathology behind rheumatoid arthritis.
- Tissue inflamed due to infiltration of lymphocytes, macrophages, and plasma cells
- Synovium proliferates to form pannus, which grows over the articular cartilage
- Pannus invades and erodes the bone
How do autoantibodies contribute to the development of rheumatoid arthritis?
Autoantibodies form immune complexes, which results in immunoglobulins and cytokines present in synovial fluid.
Give three methods of bone loss in rheumatoid arthritis.
- Focal erosion
- Periarticular osteoporosis
- Generalised osteoporosis in skeleton may result from RA
Give two things that contribute to cartilage loss in rheumatoid arthritis.
- Neutrophils release enzymes
- Pannus releases pro-inflammatory cytokines
What enzymes do neutrophils release which contribute to cartilage destruction in rheumatoid arthritis?
Matrix metalloproteinases
Describe the classical presenting joint pattern in rheumatoid arthritis.
Symmetrical, deforming, polyarthropathy
In >80% of cases, which parts of the body does rheumatoid arthritis affect?
Hands and feet
Describe the rate of onset in rheumatoid arthritis.
Usually insidious onset
Describe the articular symptoms in rheumatoid arthritis.
Early morning stiffness and pain, which may improve with activity but lasts several hours.
Loss of function, especially fine motor movements.
Give two systemic symptoms of rheumatoid arthritis.
- Fatigue
- Malaise
Give five consequences of lung involvement in RA.
- Pleural effusion
- Fibrosing alveolitis
- Rheumatoid nodules
- Caplan’s syndrome
- Small airways disease
Give three consequences of cardiac involvement in RA.
- Pericardial rub
- Pericarditis
- Pericardial effusion
Give four consequences of skin involvement in RA.
- Vasculitis
- Small digital infarcts along nail beds
- Ischaemic mononeuropathy
- Raynaud’s phenomenon
Give four consequences of eye involvement in RA.
- Sicca (dry eyes)
- Seconday Sjogren’s
- Episcleritis
- Scleritis
Give two consequences of renal involvement in RA.
- Amyloidosis
- Analgesic neuropathy
Give three consequences of nervous system involvement in RA.
- Sensory peripheral neuropathy
- Entrapment neuropathies
- Cervical instability
Give four consequences of soft tissue involvement in RA.
- Nodules
- Bursitis
- Tenosynovitis
- Muscle wasting
Give three consequences of haematological involvement in RA.
- Palpable lymph nodes
- Enlarged spleen
- Anaemia
What are the three aspects of Felty’s Syndrome?
- Seropositive rheumatoid arthritis
- Splenomegaly
- Neutropenia
What would blood tests show in RA?
- Anaemia
- High ESR/CRP
Give three antibodies that may appear in the serum of people with RA.
- Rheumatoid factor
- Anti-cyclic citrullinated peptide antibody
- Anti-nuclear antibody
What percentage of people with RA test positive for RF?
70%
What percentage of people with RA test positive for anti-cyclic citrullinated peptide antibody?
80%
What percentage of people with RA test positive for ANA?
<50%
What percentage of people with RA are sero-negative?
20%
Which antibody is specific for RA?
Anti-cyclic citrullinated peptide antibody
What does rheumatoid factor bind to?
The Fc portion of IgG
Give the four factors that are taken into account when making a diagnosis of RA.
- Joint involvement
- Serology
- Acute phase reactants
- Duration of symptoms
Give three DMARDs that can be used to treat rheumatoid arthritis.
- Methotrexate
- Sulfasalazine
- Hydroxychloroquine
Give two TNF-a inhibitors that can be used to treat RA.
- Infliximab
- Enteracept
Give a biological agent which is used to deplete B cells in RA.
Rituximab
Give a biological agent which inhibits IL-1/IL-6 in RA.
Tocilizumab
Gives a biological agent which disrupts T cell function in RA.
Abatacept
What can be used in acute inflammation in RA?
Steroids (prednisolone)
What drugs can relieve symptoms in RA?
NSAIDs
Give two non-pharmacological management techniques for RA.
- Physiotherapy
- Occupational therapy
Define osteoarthritis.
An age-related, dynamic reaction pattern of a joint in response to insult or injury.
Which tissue/s of the joint are involved in osteoarthritis?
All tissues are involved, but articular cartilage is the most affected.
Briefly describe the pathogenesis of osteoarthritis.
Metabolically active and dynamic process mediated by cytokines, and driven by mechanical forces.
Give three cytokines which are involved in osteoarthritis.
- IL-1
- TNF-a
- NO
Give the two main pathological features of osteoarthritis.
- Loss of cartilage
- Disordered bone repair
Name eight risk factors for osteoarthritis.
- Age
- Gender
- Genetic predisposition
- Obesity
- Occupation
- Local trauma
- Inflammatory arthritis
- Abnormal biomechanics
Why is age a risk factor for osteoarthritis?
Due to cumulative effect of traumatic insult and decline in neuromuscular function.
Describe the age distribution of osteoarthritis.
- Uncommon under 45yrs
- Common over 65yrs
Describe how gender is a risk factor for osteoarthritis.
- Affects more females, with increased prevalence after menopause
Give two ethnic groups that have a lower prevalence of OA hip.
- Afro-Caribbean
- Asian
Give two ethnic groups which have a lower prevalence of OA hand.
- Black African
- Malaysian
Describe why obesity is a risk factor for osteoarthritis.
Obesity is a low grade inflammatory state (release of IL-1, TNF, adipokines).
*Not thought to be due to mechanical factors
Give three examples of how occupation acts as a risk factor for osteoarthritis.
- Manual labour associated with OA of small hand joints
- Farming associated with OA of hips
- Football associated with OA of knees
Give three examples of abnormal mechanics which can cause osteoarthritis.
- Joint hypermobility
- Congenital hip dysplasia
- Neuropathic conditions
Describe the symptoms of OA.
- Pain worse with use and at end of day
- Morning stiffness <30mins
- Functional impairment (walking, activities of daily living)
Give some signs of OA.
- Alteration in gait
- Joint swelling (bony enlargement, effusion, very occasionally synovitis)
- Crepitus
- Limited range of movement
- Tenderness
- Deformities
Give the five radiological features of osteoarthritis.
- Joint space narrowing
- Osteophyte formation
- Subchondral sclerosis
- Subchondral cysts
- Abnormalities of bone contour
Describe the inflammatory phase in OA of hands.
Occurs early, as nodes are forming.
Which joints are involved in OA of the hands?
- DIP
- PIP
- CMC
What causes reduced hand function in OA hand?
Bony swelling and cyst formation.
Which form of hand OA has a strong genetic component (especially in women)?
Nodal form
Describe the nodes in hand OA.
- Heberden’s Nodes at DIP joints
- Bouchard’s Nodes at PIP joints
What are the three patterns of knee OA?
(Which is the commonest)?
- Medial (commonest)
- Lateral
- Patellofemoral
Describe the evolution of OA of the knee (without significant trauma).
Evolution may be slow.
What is meant by ‘loose bodies’ in the knee?
Bone or cartilage fragment present in the joint.
What is the main symptom of loose bodies in the knee?
Locking of the knee
What is the main presentation of OA hip?
Groin pain
What is erosive/inflammatory OA, and how is it treated differently to OA?
- A subset of OA with a strong inflammatory component
- DMARD therapy used in addition to standard management
Give some non-medical management methods for OA.
- Patient education
- Activity/exercise
- Weight loss
- Physiotherapy
- Occupational therapy
- Footwear
- Walking aids
What is the role of intra-articular steroid injections in OA?
The role remains unclear.
Give some forms of pain relief used in OA.
- NSAIDs
- Capsaicin (topical)
- Paracetamol
- Opioids
- Buprenorphine
- Lignocaine
Give four surgical treatments for OA.
- Arthroscopy
- Osteotomy (cutting bone)
- Arthroplasty
- Fusion
When is arthroscopy used in OA?
ONLY for loose bodies
When is osteotomy used in OA?
Mostly in young people with knee OA.
When is arthroplasty used in OA?
For uncontrolled pain (particularly at night) and significant limitation of function.
On which joint would fusion usually be used in OA, and what is the down side of this treatment?
- Usually used in ankle and foot
- However results in a limited range of movement
Define vasculitis.
Inflammation and necrosis of blood vessel walls with subsequent impaired blood flow.
Give two consequences of vessel wall destruction in vasculitis.
- Perforation
- Haemorrhage into tissues
Give two consequences of endothelial injury in vasculitis.
- Thrombosis
- Ischaemia/infarction of dependent tissues
Give three histological features of vasculitis.
- Vessel wall infiltration by neutrophils, mononuclear cells, +/- giant cells
- Fibrinoid necrosis inside vessel wall
- Leukocytoclasis (dissolution of leukocytes)
Give four ways of classifying vasculitis.
- Size of vessel
- Target organ
- Anti-neutrophil cytoplasmic antibodies (ANCA) involvement
- Primary vs secondary
In which types of vasculitis can anti-neutrophil cytoplasmic antibodies be present?
Small/medium vessel vasculitis.
What are anti-neutrophil cytoplasmic antibodies?
Specific antibodies for antigens in cytoplasmic granules of neutrophils and monocyte lysosomes.
How are ANCAs detected?
Using indirect immunofluorescence microscopy.
Give the two different types of ANCA.
- cytoplasmic ANCA
- peri-nuclear ANCA
What are the two potential targets for ANCA?
- Proteinase 3
- Myeloperoxidase
How do ANCA contribute to the disease process in vasculitis?
They contribute to blood vessel damage.
Why is vasculitis so hard to diagnose?
There is no single typical presentation, as vasculitis can affect any vessel or organ.
Give some general signs/symptoms of vasculitis.
- Systemically unwell
- Fever
- Arthralgia/arthritis
- Rash
- Weight loss
- Headache
- Footdrop
- Major event (stroke, bowel infarction)
Give two differential diagnoses of vasculitis.
- Sepsis
- Malignancy
Give a type of large vessel vasculitis.
Giant cell (temporal arteritis)
What is giant cell (temporal) arteritis?
Granulomatous arteritis of the aorta and larger extracranial branches of carotid arteries.
What age range does giant cell (temporal) arteritis affect?
> 50yrs (incidence increases with age)
Give two groups of patients in which giant cell (temporal) arteritis is more common.
- Women
- Caucasians
What does giant cell (temporal) arteritis increase the risk of?
Stroke
Describe the symptoms of giant cell (temporal) arteritis.
- Headache
- Scalp tenderness
- Jaw claudication
- Acute blindness (medical emergency)
- Non-specific malaise
- Associated symptoms of polymyalgia rheumatica
- Anterior ischaemic optic neuropathy
Give three signs of giant cell (temporal) arteritis.
Temporal arteries palpable, tender, and reduced pulsation.
Describe anterior ischaemic optic neuropathy.
What disease is it a feature of?
Sudden, painless, monocular and severe visual loss, may be preceded by transient visual loss (curtains coming over eyes).
It is a feature of giant cell (temporal) arteritis.
What is the gold standard investigation for giant cell (temporal) arteritis?
Temporal artery biopsy
To diagnose giant cell (temporal) arteritis, three or more of the following 5 criteria must be present:
- Age >50
- New headache
- Temporal artery tenderness or decreased pulsation
- ESR>50
- Abnormal artery biopsies
What is the treatment for giant cell (temporal) arteritis?
Prompt corticosteroids (prednisolone)
How quick is the usual response to treatment in giant cell (temporal) arteritis?
48hrs
In giant cell (temporal) arteritis, how long does treatment usually last?
50% are off steroids at two years.
What other type of drug can be used in giant cell (temporal) arteritis?
Steroid sparing agents (azathioprine/methotrexate/biologics)
What prophylaxis treatment must be given in giant cell (temporal) arteritis?
Prophylaxis of osteoporosis from the steroids.
Give an example of small vessel vasculitis.
Granulomatosis with polyangiitis (Wegener’s Granulomatosis, GPA)
Describe the pathology in GPA.
- Necrotizing, granulomatous vasculitis of arterioles, capillaries, and post capillary venules
- Associated with anti-neutrophil cytoplasmic antibodies (c-ANCA)
What age does GPA usually affect?
25-60yrs (but can affect any age)
What is the classic triad of affected organs in GPA?
- Upper respiratory tract
- Lungs
- Kidney
How is GPA described if there is no renal involvement?
It is limited
What are the consequences of GPA affecting the upper respiratory tract?
- Sinusitis
- Otitis
- Nasal crusting
- Bleeding
What are the consequences of GPA affecting the lungs?
- Pulmonary nodules
- Haemorrhage
What are the consequences of GPA affecting the kindey?
Glomerulonephritis
What are the consequences of GPA affecting the skin?
- Purpura
- Ulcers
What are the consequences of GPA affecting the nervous system?
- Mononeuritis multiplex
- CNS vasculitis
What are the consequences of GPA affecting the eyes?
- Proptosis
- Scleritis
- Episcleritis
- Uveitis
- Swelling of muscles behind the eye
What are the consequences of GPA affecting the nose, how common is it?
Saddle nose deformity.
Rare now due to better treatments.
Give four ‘miscellaneous’ consequences of GPA.
- Synovitis
- Pericarditis
- GI
- GU
What is the treatment for severe (organ-threatening) GPA?
High does steroids/cyclophosphamide/biologics
What is the treatment for non-end organ threatening GPA?
Moderate dose steroids + methotrexate/mycophenolate/azathioprine
What is the commonest autoimmune connective tissue disease?
Systemic lupus erythematosus
Give an ethnic group in which SLE is more common?
Afro-Caribbeans
Is SLE more common in men or women?
90% patients are women
What is the typical age range for development of SLE?
14-64yrs
Describe the pathogenesis of SLE.
Inflammation and immune reactions against self antigens lead to immune complex mediated tissue damage.
What causes increased risk of thrombosis in SLE?
Phospholipid antibodies.
Give some clinical features of SLE.
- Fatigue
- Arthritis
- Skin rashes
- Mucosal ulceration
- Alopecia
- Pleurisy
- Pericarditis
- Raynaud’s phenomenon
- Glomerulonephritis
- Venous/arterial thrombosis
- Recurrent abortion
- Vasculitis
- Depression
- Psychosis
- Lymphadenopathy
- Neuro-psychiatric features
- Anaemia
- Throbocytopenia
- Neutropenia
- Lymphopenia
Describe the arthritis in SLE.
- Symmetrical
- Less proliferative than RA
- Can be deforming
- Non-erosive
Give four types of rash that can occur in SLE.
- Discoid rash
- Photosensitive rash
- Subacute lupus rash
- Butterfly rash
Give the three features of glomerulonephritis in SLE.
- Hypertension
- Proteinuria
- Renal failure
Describe the anaemia in SLE.
Coombs positive haemolytic anaemia
Give the three main antibodies in SLE.
- Anti-nuclear antibody
- Double stranded DNA antibody
- Anti-phospholipid antibody
Which antibody is specific for lupus?
Double stranded DNA antibody
How does anti-nuclear antibody help to diagnose lupus?
It is sensitive (95%) but not specific.
Give six other antibodies that may be detected in lupus.
- Rheumatoid factor
- Cardiolipin antibodies
- Anti Ro/La/Sm/RNP
A diagnosis of SLE is made if 4 out of this 11 criteria are met…
- Malar rash (Butterfly rash)
- Discoid rash
- Photosensitivity
- Oral ulcers
- Non-erosive arthritis
- Serositis (pleuritis, pericarditis)
- Renal disorder (persistent proteinuria, cellular casts)
- CNS disorder (seizures, psychosis)
- Haematological disorder (haemolytic anaemia, leukopaenia, lymphopaenia, thrombocytopaenia)
- Immunological disorder (presence of specific antibodies)
- Antinuclear antibodies
Describe the non-pharmacological management for SLE.
- Patient education and support
- UV protection
- Assessment of lupus activity (clinical/immunological)
- Screening for major organ involvement
- Assessment of damage
Give some methods of drug treatment for SLE.
- No treatment
- Topical (sunscreens, steroids, cytotoxic)
- NSAIDs
- Antimalarial (hydroxychloroquine)
- Steroids
- Cytotoxic
- Anticoagulants
- Biological
- Plasmapheresis
- Stem cell transplant
Give five cytotoxic treatments that can be used in SLE.
- Azathioprine
- Mycophenolate
- Ciclosporin
- Methotrexate
- Cyclophosphamide
Describe the ESR and CRP in lupus.
ESR tends to be high but CRP tends to be normal.
Is primary or secondary Raynaud’s phenomenon more common?
Primary
Give three things that can cause secondary Raynaud’s phenomenon.
- Connective tissue disease
- Drugs
- Vascular damage
Give three connective tissue diseases that can cause Raynaud’s phenomenon.
- Systemic sclerosis
- Mixed connective tissue disease
- SLE
Give three factors which can cause vascular damage, which can result in Raynaud’s phenomenon.
- Atherosclerosis
- Frost bite
- Vibrating tools
Describe the colour changes in Raynaud’s phenomenon.
White in cold
Then blue (lack of oxygen)
Red on warmth (vasodilation)
What is dermatomyositis/polymyositis?
Inflammation of muscle and skin, causing rash and muscle weakness.
What is the consequence of lung involvement in dermatomyositis/polymyositis?
Interstitial lung disease
As well as a ‘primary’ disease, how else can dermatomyositis/polymyositis present?
As a paraneoplastic syndrome.
What are the clinical features of dermatomyositis/polymyositis?
- Myalgia
- Arthralgia
- Rash
- Dysphagia
- Dysphonia
- Respiratory weakness
What investigations should be carried out in dermatomyositis/polymyositis?
- Muscle enzymes
- EMG
- Muscle/skin biopsy
- Screen for malignancy
- Antibody screen
- Chest XR, PFTs, high resolution CT lungs
What will the muscle enzymes show in dermatomyositis/polymyositis?
High creatine kinase
What is the management of dermatomyositis/polymyositis?
- Steroids
- Immunosuppressive drugs
Give four clinical subsets of systemic sclerosis.
- Limited cutaneous
- Diffuse cutaneous
- Sine (without) scleroderma
- Overlap syndromes/mixed connective tissue disease
Is systemic sclerosis more common in men or women?
Women
What is the most common age for systemic sclerosis to present?
30-40yrs
Give three elements of the pathogenesis of systemic sclerosis.
- Vasculopathy
- Inflammation and excessive collagen deposition by fibroblasts
- Auto-antibody production
Give three antibodies that may appear in systemic sclerosis.
- Anti-nuclear antibodies
- Anti-centromere antibodies
- Anti-topoisomerase antibodies
What percentage of patients with systemic sclerosis test positive for ANA?
65%
In which type of systemic sclerosis might anti-centromere antibodies appear, and in what percentage of patients?
70-80% of patients with limited SSc
In which type of systemic sclerosis might anti-topoisomerase antibodies appear, and in what percentage of patients?
40% of patients with diffuse SSc
What are five features of limited cutaneous SSc?
CREST
- Calcinosis (subcutaneous tissue)
- Raynaud’s (long history)
- Esophageal and gut dysmotility
- Sclerodactyly (hard fingers)
- Telangiectasia (spider veins)
Describe the skin involvement in limited cutaneous SSc.
Limited to face, hands, and feet.
What is a late feature of limited cutaneous SSc?
Pulmonary hypertension
Give five clinical features of diffuse cutaneous SSc.
- Proximal scleroderma and trunk involvement (diffuse skin involvement)
- Short history of Raynaud’s
- Increased risk of renal crisis
- Increased risk of cardiac involvement
- Increased risk of interstitial lung disease
What is the treatment for systemic sclerosis?
- Treat Raynaud’s (physical protection, vasodilators)
- PPIs for life (for GORD)
- ACEi to inhibit renal crisis
- Early detection of pulmonary arterial hypertension
- Treatment of skin oedema (cytotoxic drugs, autologous stem cell transplant)
- Treatment of pulmonary fibrosis (cyclophosphamide)
Give five things that may cause secondary Sjogren’s syndrome.
- SLE
- Rheumatoid arthritis
- Scleroderma
- Primary biliary cirrhosis
- Other auto-immune diseases
Briefly describe the pathology of Sjogren’s syndrome.
Lymphocytic infiltration and fibrosis of exocrine glands.
What are the clinical features of sjogren’s syndrome?
- Dry eyes
- Dry mouth
- Arthritis
- Rash
- Neurological features
- Vasculitis
- Interstitial lung disease
- Renal tubular acidosis
Give a condition which is strongly associated with Sjogren’s syndrome.
Gluten sensitivity
Sjogren’s syndrome increases the risk of which condition?
Lymphoma
Give the laboratory features of Sjogren’s syndrome.
- Positive ANA
- Positive RF
- Positive Ro and La
- Negative DS DNA
- Raised immunoglobulins
- Abnormal salivary glands on ultrasound
- Sialadenitis on lip biopsy (infection of salivary glands)
What is the treatment for Sjogren’s syndrome?
- Tear and saliva replacement
- Immune-suppression for systemic complications
Give two features of both crystal arthritis and infection.
- Rapid onset
- Very red and hot joints
How can crystal disease and infection be differentiated?
- Clinical history
- Joint aspirate
Give five differential diagnoses of systemic diseases.
- Infection
- Auto-immune diseases
- Malignancy
- Endocrine diseases
- Metabolic diseases
Give two inherited connective tissue diseases.
- Marfan’s Syndrome
- Ehler Danlos Syndrome
Give the pattern of inheritance for Marfan’s syndrome.
Autosomal dominant
Give five features of Marfan’s syndrome.
- Tall/long arms
- Lens dislocation
- Aortic valve incompetence/dilated aortic root
- High arched palate
- Sunken chest
Give two features of Ehler Danlos syndrome.
- Stretchy skin
- Joint hypermobility
What is the prevalence of fibromyalgia?
0.5-4%
Is fibromyalgia more common in men or women?
Women
Give five risk factors for fibromyalgia.
- Female sex
- Middle age
- Low household income
- Divorced
- Low educational status
Give three other conditions that are associated with fibromyalgia.
- Chronic fatigue syndrome
- Irritable bowel syndrome
- Chronic headaches syndrome
Describe the clinical features of fibromyalgia.
- Chronic pain (>3months)
- Pain is widespread
- Absence of inflammation
- Presence of pain on palpation of at lease 11/18 specified ‘tender points’
- Morning stiffness
- Fatigue
- Poor concentration
- Low mood
- Sleep disturbance
What do the investigations show in fibromyalgia?
All are normal
Describe the principles of management of fibromyalgia.
- Education of patient and family
- Explanation and reassurance
- Cognitive behavioural therapy
- Antidepressants may help to relieve pain
What is another name for Paget’s disease?
Osteitis deformans
What age group is Paget’s disease more common in?
Over 40s
Briefly describe the pathology of Paget’s disease.
- Increased numbers of osteoblasts and osteoclasts
- Increased bone turnover and remodelling
- Resulting in bone enlargement, deformity and weakness
Describe the clinical features of Paget’s disease.
- Asymptomatic in about 70%
- Deep, boring pain
- Bony deformity and enlargement
Give five sites where Paget’s disease commonly manifests.
- Pelvis
- Lumbar spine
- Skull
- Femur
- Tibia
Give six complications of Paget’s disease.
- Pathological fractures
- Osteoarthritis
- Hypercalcaemia
- Nerve compression due to bone overgrowth
- High output congestive heart failure
- Osteosarcoma
Give two consequences of nerve compression in Paget’s disease.
- Deafness
- Root compression
Give two radiological features of Paget’s disease.
- Localised enlargement of bone
- Patchy cortical thickening with sclerosis, osteolysis, and deformity
Describe the calcium, phosphate, and alkaline phosphate levels in Paget’s disease.
- Calcium normal
- Phosphate normal
- Alkaline phosphate raised
Describe the treatment for Paget’s disease.
- Analgesia
- Alendronate (to reduce pain/deformity if analgesia fails)
What is ‘osteomalacia’ called if it occurs during the period of bone growth?
Rickets
Briefly describe the pathophysiology of osteomalacia.
- Normal bone amount but low mineral content
- Excess uncalcified osteoid and cartilage
Give six causes of osteomalacia.
- Vitamin D deficiency
- Renal osteodystrophy (renal failure)
- Drug-induced
- Vitamin D resistance
- Liver disease
- Tumour-induced osteomalacia
What are the signs/symptoms of rickets?
- Growth retardation
- Hypotonia
- Apathy in infants
- Knock-kneed
- Bow-legged
- Deformities of metaphyseal-epiphyseal junction
- Features of hypocalcaemia (usually mild)
Give the signs/symptoms of osteomalacia.
- Bone pain and tenderness
- Fractures (especially femoral neck)
- Proximal myopathy
- Low phosphate and vitamin D
What would plasma investigations show in osteomalacia?
- Mild hypocalcaemia (but may be severe)
- Low phosphate
- High alkaline phosphatase
- High PTH
- Low vitamin D (except in Vitamin D resistance)
What would the bone biopsy show in osteomalacia?
Incomplete mineralisation
What would the muscle biopsy show in osteomalacia?
Normal
Give two radiological features of osteomalacia.
- Loss of cortical bone
- Apparent partial fractures without displacement
Give a radiological feature of Rickets.
Cupped, ragged metaphyseal surfaces
What would the treatment be for osteomalacia caused by vitamin D deficiency?
Vitamin D
What treatment would be given in vitamin D resistant osteomalacia or renal disease?
- Alfacalcidiol
- Calcitriol
What is type I vitamin D resistance rickets?
Low renal 1a-hydroxylase activity
What is type II vitamin D resistance rickets?
End-organ resistance to 1,25-dihydroxycholecalciferol
How are both type I and type II vitamin D resistance rickets treated?
Large doses of calcitriol
Describe the inheritance pattern of X-linked hypophosphataemic rickets.
Dominant X linked
Briefly describe the pathology in X-linked hypophosphataemic rickets.
Defect in renal phosphate handling
How is X-linked hypophosphataemic rickets treated?
High doses of oral phosphate and calcitriol
Give eight things associated with developing carpel tunnel syndrome.
- Obesity
- Short stature
- Pregnancy
- Oral contraceptive pill
- Diabetes
- Hypothyroidism
- Rheumatoid arthritis
- Acromegaly
Give two work-related causes of carpel tunnel syndrome.
- Forceful and repetitive work (painters, meat processors)
- Hand-transmitted vibration
Give two special tests that can be used to diagnose carpal tunnel syndrome.
- Tinel’s test
- Phalen’s test
Describe Tinel’s test.
Tap lightly over the median nerve and see if patient feels paresthesia distally.
Describe Phalen’s test.
Patient fully flexes elbows and wrists (upside down prayer position) and if symptoms occur the test is positive.
What causes hand-arm vibration syndrome?
Excessive exposure to hand-transmitted vibration (chain saws, angle grinders, jack hammers, drills)
Describe the presentation of hand-arm vibration syndrome.
- Vascular (blanching)
- Neural (tingling, numbness, loss of dexterity)
Hand-arm vibration syndrome is a secondary cause of what condition?
Raynaud’s phenomenon
Briefly describe hypothenar hammer syndrome.
Occlusion of ulnar artery and superficial palmar arch.
What is the most common cause of tenosynovitis?
Inflammation of abductor pollicis longus and extensor pollicis brevis tendon sheath.
Give an occupational risk of developing tenosynovitis.
Job requires forceful and repetitive hand movements.
Give a special test used to diagnose tenosynovitis.
Finkelstein’s test
Describe Finkelstein’s test.
The examiner pulls the thumb of the patient in ulnar deviation and if there is pain in the radial styloid process the test is positive.
Give four methods of treatment for tenosynovitis.
- NSAIDs
- Steroid injection
- Rest
- Change job
What is another name for lateral epicondylitis.
Tennis elbow
What is another name for medial epicondylitis?
Golfer’s elbow
What causes epicondylitis?
Forceful flexion-extension of the wrist or forceful pronation-supination.
Give a special test used to diagnose lateral epicondylitis.
Cozen’s test
Describe Cozen’s test.
Patient’s elbow in 90degree flexion, hand in radial deviation, forearm pronation.
Patient extends wrist against resistance.
Pain = positive.
Give five methods of treatment for epicondylitis.
- NSAIDs
- Steroid injection
- Clasp
- Rest
- Surgery
What is repetitive strain disorder?
Non-specific pain in the hand
Give four treatment methods for repetitive strain disorder.
- Rest breaks
- Job rotation
- Reduced force
- Ergonomically neutral working postures
Describe briefly what causes writers cramp.
A focal dystonia (neurological condition affecting the nerves).
Briefly describe usual rotator cuff problems.
Tendonitis or a tear, usually affecting the supraspinatus tendon.
Give two occupational associations with rotator cuff problems.
- Shoulder impingement
- OA of acromioclavicular joint
Describe the presentation of rotator cuff problems.
Painful arc
Give a special sign used to diagnose rotator cuff problems.
Hawkin’s sign
Describe Hawkin’s sign.
Shoulder flexed to 90degrees.
Elbow flexed to 90degrees.
Quickly rotate arm internally.
Pain below acromioclavicular joint is positive.
Give three high risk activities that can increase likelihood of developing rotator cuff problems.
- Heavy manual lifting
- Lifting above shoulder height
- Throwing
Describe thoracic outlet syndrome.
Pain or tingling down arm or blanching of fingers related to posture of arm.
Describe what causes thoracic outlet syndrome.
Compression of brachial plexus trunks or subclavian artery in neck under clavicle.
May be due to anatomical abnormalities in the neck.
Give two occupational associations with thoracic outlet syndrome.
- Poor posture
- Loading of shoulders
Give three things (including a special test) that can be used to diagnose thoracic outlet syndrome.
- Roos sign
- X-ray neck
- MRI
Describe Roos sign.
Patient has both arms in 90degree abduction-external rotation position.
Patients opens and closes hands slowly over 3 minute period.
Normal if only forearm muscles fatigue, other signs are positive.
What is the treatment for thoracic outlet syndrome?
Surgery
Describe Dupytren’s contracture.
Thickening of palm fascia caused by vibrating tools, resulting in flexion of one or more fingers.
What is Seamstress’ finger?
Heberden’s nodes at distal interphalangeal joints.
Give a classical feature of rheumatoid arthritis on X ray.
Peri-articular erosions
As well as in the back, where else might pain be felt in inflammatory back pain?
Across the costochondral joints.
What antibody is usually positive in all autoimmune connective tissue disorders?
Anti-nuclear antibody
What type of arthritis (deforming or erosive) is associated with systemic lupus erythematosus?
Deforming
Give a rheumatological condition in which thrombocytosis may be a feature.
Rheumatoid arthritis
What is osteomyelitis?
An infection localised to bone.
Why is there increasing incidence of chronic osteomyelitis?
There is increasing risk of pre-disposing conditions.
Give two age groups in which osteomyelitis is more common?
Children and elderly
Give seven risk factors for osteomyelitis.
- Non-native joint
- Diabetes mellitus
- Inflammatory arthritis
- Immune deficiency
- Peripheral vascular disease
- Sickle cell disease
- (Behavioural) risk of trauma
Briefly describe the pathology of osteomyelitis.
- Inflammatory cells, oedema, vascular congestion, and small vessel thrombosis increase intramedullary pressure
- This causes periosteum to rupture and periosteal blood supply is interrupted, causing necrosis
- Necrotic bone is left behind (sequestra)
- New bone formation occurs (involucrum)
What is sequestra in osteomyelitis?
Necrotic bone which is left behind
What is involucrum in osteomyelitis?
New bone formation
Give three methods of infection in osteomyelitis.
- Direct inoculation
- Contiguous spread
- Haematogenous seeding
In osteomyelitis, is direct inoculation usually monomicrobial or polymicrobial?
Can be either
In osteomyelitis, is contiguous spread monomicrobial or polymicrobial?
Can be either
In osteomyelitis, is haematogenous seeding usually monomicrobial or polymicrobial?
Monomicrobial
Give two ways that bones can be infected by direct inoculation.
- Trauma
- Surgery
Describe contiguous spread in osteomyelitis.
Spread of infection from adjacent tissue.
Give four ‘conditions’ that increase likelihood of contiguous spread in osteomyelitis.
- Diabetes mellitus
- Chronic ulcers
- Vascular disease
- Arthroplasties
In which bone/s is osteomyelitis more likely to occur by haematogenous seeding in adults and why?
Vertebra.
Because vertebrae become more vascular with age.
In which bone/s is osteomyelitis more likely to occur by haematogenous seeding in children and why?
Long bones.
Because in metaphyses blood flow is easier, basement membrane is absent, capillaries lack phagocytic lining, and there is high blood flow to developing bones.
Give two risk factors for contracting osteomyelitis via haematogenous seeding.
- IV drug users
- People with risk factor for bacteraemia
What is the most common causative organism in osteomyelitis?
Staphylococcus aureus
Why is Staph.aureus good at infecting bones?
It binds host proteins and can survive in macrophages.
Give the three usual organisms which can cause osteomyelitis.
- Staphylococcus aureus
- Coagulase -ve staph
- Aerobic gram -ve bacilli
Give five less common organisms which can cause osteomyelitis.
- Streptococci
- Enterococci
- Anaerobes
- Fungi
- Mycobacteria
Which organism commonly causes osteomyelitis in sickle cell disease?
Salmonella
Give two organisms which cause osteomyelitis in IV drug users.
- Pseudomonas aeruginosa
- Serratia marcescens
Describe the symptoms of osteomyelitis.
Dull pain at site of infection, may be aggravated by movement.
Describe the rate of onset of osteomyelitis symptoms.
Onset over several days
Give four systemic signs of osteomyelitis.
- Fever
- Rigors
- Sweats
- Malaise
Give four local acute signs of osteomyelitis.
- Tenderness
- Warmth
- Swelling
- Erythema
Give seven local chronic signs of osteomyelitis.
- Tenderness
- Warmth
- Swelling
- Erythema
- Draining sinus tract
- Deep/large ulcers that fail to heal
- Non-healing fractures
Give three findings on a blood test in oesteomyelitis.
- High WCC (chronic can have normal)
- Raised CRP
- Raised ESR
What type of imaging can be carried out to diagnose acute osteomyelitis.
MRI (or CT/nuclear bone scan)
Why aren’t X-rays that sensitive to acute osteomyelitis?
They take about 2 weeks for changes to appear
Give two investigations to identify the causative organism in osteomyelitis.
- Bone biopsy (sample to microbiology and histology)
- Blood cultures
Give six signs of chronic osteomyelitis on X-ray.
- Cortical erosion
- Periosteal reaction
- Mixed lucency
- Sclerosis
- Sequestra
- Soft tissue swelling
Give two features of osteomyelitis on MRI.
- Marrow oedema
- Delineation on cortical, bone marrow, and soft tissue inflammation
Give seven differential diagnoses of osteomyelitis.
- Soft tissue infection (cellulitis, erysipelas)
- Charcot joint
- Avascular necrosis of bone
- Gout
- Fracture
- Bursitis
- Malignancy
Give the two steps in the management of osteomyelitis.
- Surgery
- Antimicrobial therapy
What does surgery for osteomyelitis involve?
Debridement and hardware replacement/removal
Give two things that choice of antimicrobial therapy in osteomyelitis depends on.
- Infective organism
- Bone penetration of drug
How long should antibiotics be given for in osteomyelitis?
6 weeks minimum, treatment length guided by ESR/CRP
How does the presentation of mycobacterial osteomyelitis differ from other forms of osteomyelitis?
- Slower onset
- More systemic symptoms
What investigation is essential to diagnose mycobacterial osteomyelitis?
Biopsy
How long is the typical treatment for mycobacterial osteomyelitis?
12 months
Is septic arthritis more common in males or females?
They are equal
What percentage of septic arthritis cases occur in patients over 65yrs?
45%
Give nine risk factors for septic arthritis.
- Prosthetic joint
- Rheumatoid arthritis
- Immunosuppression
- Elderly
- Diabetes
- Any cause for bacteraemia
- Trauma
- Local skin breaks/ulcers
- Damages joints
What is the main causative organism in septic arthritis (native joints)?
Staphylococcus aureus
Give six less common causative organisms of septic arthritis.
- Streptococci
- Neisseria gonorrhoea
- Gram -ve bacilli
- Anaerobes
- Mycobacterium
- Fungi
What used to be a major cause of septic arthritis in children, but now isn’t due to immunisation?
Haemophilus influenzae
Give four features of gonococcal septic arthritis.
- Fever
- Arthritis (polyarticular)
- Tenosynovitis
- Rash
Give three presenting features of septic arthritis.
- Painful, red, swollen, hot joint
- Disuse (especially in children)
- Fever
Is septic arthritis usually monoarthritis or polyarthritis?
90% monoarthritis, but polyarthritis can occur (eg. In gonorrhoea)
Give the relative frequencies of septic arthritis the hip, knee, and shoulder.
Knee>hip>shoulder
Give two investigations to carry out in suspected septic arthritis.
- Joint aspirate
- Blood cultures
Give three features of joint aspirate that would suggest septic arthritis.
- Turgid fluid
- High leukocyte content
- Gram stain (+ve cocci)
What additional investigation may be required if mycobacterial septic arthritis is suspected?
Synovial biopsy
Give seven management strategies for septic arthritis.
- Aspiration
- Stop DMARDs and biologics
- High dose/long course antibiotics (6 weeks minimum)
- Double dose steroids
- Analgesia
- Splinting/rest
- Joint aspiration and washout
What should be done first: blood cultures or antibiotics?
And why?
Blood cultures, because antibiotics may eradicate the bacteria in the sample to give a false negative.
How is a prosthetic joint infection caught after surgery?
Haematogenous spread
What is the most common causative organism of prosthetic joint infections?
Coagulase -ve staphylococci
Give three causative organisms of prosthetic joint infections.
- Coagulase -ve staphylococci
- Staphylococcus aureus
- Enterobacteria
Give four preventative techniques that orthopaedic surgeons can use to prevent infections in prosthetic joints.
- Double glove
- Air filters
- Separation between surgeons and anaesthetists in theatre
- Prophylactic antibiotics
Give three X ray features that may suggest an infection in a prosthetic joint.
- Prosthetic loosening
- Periosteal thickening
- Ectopic bone formation
Give a highly sensitive/specific inflammatory marker that can be used to diagnose prosthetic joint infections.
Alpha defensin
When would antibiotic suppression be used to treat prosthetic joint infection?
If the patient is unfit for surgery
When would debridement and retention of prosthesis be used to treat prosthetic joint infection?
If it is an early postoperative infection or in an acute haematogenous infection.
When would excision arthroplasty be used to treat prosthetic joint infection?
If at higher risk.
What is the consequence of an excision arthroplasty being used to treat prosthetic joint infection?
Poor functional outcome
What does a one stage exchange arthroplasty to treat prosthetic joint infections involve?
Debridement of all infected/dead tissues, soft tissue cover/reconstruction, and new prosthesis (all in one).
What does two stage exchange arthroplasty to treat prosthetic joint infection involve?
Debridement, then wait before inserting new prosthesis.
Describe the presentation of bone tumours.
- Vague symptoms
- Pain
- Swelling
- Erythema
- Limp or disuse
- Failure to thrive/meet milestones (children)
- Unremitting pain
- Night pain
- Pain on mobilising
- Altered neurology
- Symptoms from primary tumour (if metastatic)
What lab tests can be carried out in a suspected bone tumour?
- PSA
- Serum/urine electrophoresis
- ESR
- CRP
- Calcium
- Alkaline phosphatase
What imaging can be carried out to assess bone tumours?
- Plain X ray
- Potentially CT/MRI/Bone scan
Give three things that can be determined from imaging of a bone tumour.
- Location of tumour
- Tumour-bone/Bone-tumour interaction
- Look at matrix (medullary cavity)
Describe how biopsies are carried out in bone tumours.
Performed by the surgeon who will be operation, as tract must be excised along with tumour as it will contain tumour cells.
Give three features that can be looked at to determine if a bone tumour is benign or malignant.
- Zone of transition
- Periosteal reaction
- Cortical destruction
What does a narrow zone of transition suggest about the malignancy of a bone tumour?
It is likely to be benign
What does a wide zone of transition suggest about the malignancy of a bone tumour?
It is likely to be a more aggressive disease
What does a solid periosteal reaction suggest about the malignancy of a bone tumour?
The tumour is less malignant
What does a lamellated periosteal reaction suggest about the malignancy of a bone tumour?
It is more malignant than a solid periosteal reaction but still not too aggressive.
What does a sunburst periosteal reaction suggest about the malignancy of a bone tumour?
The tumour is malignant, but not the most malignant it can be.
What does a Codman’s triangle periosteal reaction suggest about the malignancy of a bone tumour?
It is a very malignant tumour
How useful is cortical destruction in determining whether a bone tumour is benign or malignant?
Not very useful, as some benign lesions can cause destruction.
What does complete cortical destruction suggest about the malignancy of a bone tumour?
It is an aggressive disease
Give four radiographic features of a benign bone tumour.
- Well defined, sclerotic border
- Lack of soft tissue mass
- Solid periosteal reaction
- Geographic bone destruction
Give four radiographic features of a malignant bone tumour.
- Interrupted periosteal reaction
- Moth-eaten or permeative bone destruction
- Soft tissue mass
- Wide zone of transition
What is a major complicating factor in bone tumours?
Fracture
What is Mirel’s scoring system in bone tumours?
A score given to determine a patient’s risk of fractures.
What four factors are considered when calculating Mirel’s score in bone tumours?
- Site
- Pain
- Lesion type (blastic/mixed/lytic)
- Lesion size
Is it more common for a bone tumour to be primary or secondary?
Secondary
How do patients with primary bone tumours commonly present?
Constant, non-mechanical pain.
Give an example of a primary bone tumour that typically occurs in patients aged between 10 and 19 years.
Osteosarcoma
Give an example of a primary bone tumour which typically occurs in patients <18yrs of age.
Ewing’s sarcoma
Give an example of a primary bone tumour which is usually found in people >40yrs, and with Paget’s disease.
Chondrosarcoma
Describe the bone lesions in metastatic bone tumours.
They are lytic
Describe developmental dysplasia of the hip.
Hip socket too shallow and femoral head not held tightly in place.
Give two treatment options for developmental dysplasia of the hip.
- Harness
- Surgery
Describe slipped capital femoral epiphysis.
The epiphyseal growth plate slips and the femur moves superiorly compared to the epiphysis.
How does sepsis in a joint lead to arthritis?
It causes chondrolysis
What three aspects of an orthopaedic history are ‘most important’/
- SOCRATES
- Occupation
- Handedness (left/right)
Briefly describe the blood supply to the femoral head.
The profunda femoris artery gives rise to the lateral and medial circumflex arteries.
Which type of hip fracture can cut off the blood supply to the femoral head?
Intracapsular fracture
Describe a type 1 intracapsular hip fracture.
Incomplete, doesn’t affect blood supply to head
Describe a type 2 intracapsular hip fracture.
Complete, not displaced, doesn’t cut off blood supply to head
Describe a type 3 and type 4 hip fracture.
Displaced, interrupted blood supply to femoral head
How are type 1 and type 2 hip fractures fixed?
Using screws
How are type 3 and type 4 hip fractures fixed?
Hemiarthroplasty or full arthroplasty
Describe an extracapsular hip fracture in terms of blood supply.
The blood supply to the femoral head is maintained.
How are extracapsular hip fractures fixed?
Screws
Give the three principles of management of orthopaedic trauma.
- Reduce (put back in line)
- Stabilise (nails)
- Rehabilitate (walk)
Give the four stages of fracture healing.
- Haematoma formation
- Fibrocartilagenous callus formation
- Bony callous formation
- Bone remodelling
Give six cytokines/molecules requires for haematoma formation after a fracture.
- IL-1
- IL-6
- IL-12
- TNF-a
- PDGF
- COX2 (required for osteoblasts)
What is cauda equina syndrome?
Compression or damage of the cauda equina below the spinal cord.
Describe and explain the typical urinary symptoms experienced in cauda quina syndrome.
- Pudendal nerve compression
- Can’t relax external sphincter
- Overflow incontinence
Give five signs/symptoms of cauda equina syndrome.
- Uni/bilateral leg pain
- Perineal numbness
- Back pain
- Urinary symptoms
- May have faecal problems
What is the treatment for cauda equina syndrome?
Decompression
What is contained within hyaline cartilage which attracts water to it?
Proteoglycans (hyaluronic acid)
What is crystal arthritis?
Arthritis caused by crystal deposition in the joint lining.
What is a crystal?
A homogenous solid formed of ions bonded closely in ordered, repeating, symmetric arrangement.
Give two reasons why crystals are necessary in animals.
- To strengthen exoskeleton and endoskeleton
- Remove excess ions by surface binding
What does crystal deposition in the body lead to?
Local inflammatory response and tissue damage.
What is the condition called when crystals are deposited in the gallbladder or kidney.
Nephrolithiasis
Give four types of crystal that can be deposited in joints to cause crystal arthritis.
- Monosodium urate
- Calcium pyrophosphate
- Calcium hydroxyapatite
- Cholesterol
What is the medical condition which results from monosodium urate crystal deposition in the joints?
Gout
Is gout more common in men or women?
Men
When does the incidence of gout rise in women?
Postmenopause (often related to identifiable trigger)
What is the commonest arthritis in men >40yrs?
Gout
Give some causes of under-excretion of urate.
- Alcohol
- Renal impairment
- Hypertension
- Inherited metabolic
- Hypothyroidism
- Hyperparathyroidism
- Obesity
- Diabetes
- Low dose aspirin
- Diuretics
- Cyclosporine/tacrolimus
- Ethambutol/pyrazinamide
Give some causes for over-production of urate.
- Diet
- Metabolic syndrome (hyperlipidaemia)
- Proliferative (myeloproliferative, cytotoxic drugs)
- Psoriasis
- Lesch-Nyhan syndrome
Give nine dietary factors which may increase urate levels in the body.
- Red meat
- Fizzy drinks
- Sugar
- Alcohol
- Shellfish
- Offal
- Gravy
- Yeast
- Fructose
Give a dietary factor that may be protective against gout.
Dairy products
Give nine factors that may cause a sudden alteration in uric acid concentration, leading to acute attacks of gout.
- Aggressive hypouricaemic therapy
- Alcohol/shellfish binge
- Sepsis
- MI
- Acute severe illness
- Sudden cessation of hypouricaemic therapy
- Trauma
- Surgery
- Dehydration
How is uric acid produced in the body?
Purine metabolism by xanthine oxidase.
What is the concentration of uric acid at which the serum is saturated?
0.3mmol/L
At what serum level of uric acid is a patient at risk of crystal deposition?
> 0.36mmol/L
At what serum level of uric acid does supersaturation occur, making crystal deposition very likely?
> 0.42mmol/L
Give the steps in purine metabolism leading to uric acid.
Purine -> hypoxanthine -> xanthine -> uric acid
Describe the acute presentation of gout.
- Hot, swollen, painful joint
- Often affects first metatarso-phalangeal joint
- Systemically unwell
How does chronic gout usually present?
Longer term joint damage and tophi under the skin.
What are tophi?
Onion-like aggregates of urate crystals with inflammatory cells.
How long does it take to control attacks of tophaceous gout?
6-9months
How long can it take for tophi to resolve?
Up to 2 years
Give three investigations that should be carried out in gout.
- Joint aspiration
- Blood tests
- X rays
What would you expect the serum urate level to be in gout?
May be high, but may be normal or low in acute attacks.
Give two features of gout that may be seen on an xray.
- Punched out bone lesions
- Narrow joint space
How would the crystals appear under a microscope in gout?
Negatively birefringent needles
How would the crystals appear under the microscope in pseudogout?
Weakly positive birefringent rhomboids
Give four things that can be used to treat acute attacks of gout.
- Anti-inflammatories
- NSAIDs
- Colchicine
- Steroids
Describe the longer term treatment for prevention of gout.
- Xanthine oxidase inhibitors (allopurinol or febuxostat)
- Cover with colchicine or NSAID at start (otherwise gouty flare may be induced)
What is the disease called when calcium pyrophosphate crystals are deposited on a joint surface?
Pseudogout
Give two groups of patients in whom pseudogout is more common.
- Elderly
- Females
What other rheumatological condition often occurs with pseudogout?
Osteoarthritis
Give four places that pseudogout typically affects.
- Knees
- Wrists
- Shoulders
- Hips
Give some triggers of acute pseudogout attacks.
- Direct trauma
- Intercurrent illness
- Surgery (parathyroidectomy)
- Blood transfusion
- IV fluid
- T4 replacement
- Joint lavage
- Most are spontaneous
Describe the presentation of pseudogout.
- Acute synovitis
- Acute monoarthritis in elderly
- Severe pain, stiffness, swelling
- Fever
Give a classical joint distribution which suggests pseudogout instead of osteoarthritis.
2nd and 3rd metacarpo-phalangeal joint swelling
What would the X ray show in pseudogout?
Chondrocalcinosis
Describe the treatment for pseudogout.
Usually resolves in 1-3 weeks.
Drugs not very effective.
What can be used to treat the symptoms of pseudogout?
- NSAIDs
- Analgesia
- Aspiration
- Injection
- Physiotherapy
What treatment may be tried if there are continued inflammatory changes in pseudogout?
- Anti-rheumatic treatment
- Synovectomy
- Surgery
Give the typical patient demographic for calcium hydroxyapatite crystal arthropathy.
Elderly females
Describe the damage that occurs in calcium hydroxyapatite crystal arthropathy.
Destructive attacks on the shoulders
Give eight metabolic diseases which are associated with gout.
- Haemochromatosis
- Hyperparathyroidism
- Hypophosphatasia
- Hypomagnesaemia
- Hypothyroidism
- Acromegaly
- Familial hypocalciuric hypercalcaemia
- X-linked hypophosphataemic rickets
Give four indications to screen for a metabolic disease when someone presents with gout.
- Early onset (<55)
- Polyarticular
- Frequent recurrent attack
- Additional clinical or radiographic clues
Define osteoporosis.
A metabolic bone disease characterised by a generalised reduction in bone mass, increased bone fragility, and predisposition to fracture.
What is the likely consequence if trabecular bone is affected by osteoporosis?
Crush fractures of the vertebrae
What is the likely consequence if cortical bone is affected by osteoporosis?
Long bone fractures
What is the prevalence of osteoporosis in men over 50 years?
6%
What is the prevalence of osteoporosis in women over 50 years?
18%
What are the risk factors for developing osteoporosis?
SHATTERED FeMur
- Steroid use
- Hyperthyroidism, hyperparathyroidism, hypercalciuria
- Alcohol and tobacco use
- Thin (BMI<22)
- Testosterone low
- Early menopause (or low oestrogen)
- Renal or liver failure
- Erosive/inflammatory bone or bowel disease (myeloma/RA)
- Dietary (low calcium, malabsorption, Type 1 DM)
- Family history
- Mobility low
Briefly describe the pathology of osteoporosis.
- Peak bone mass and rate of bone loss affect bone mineral density
- Bone turnover and architecture affect bone quality
- Bone quality and density affect strength, and reduced strength leads to fractures
Describe what causes post-menopausal osteoporosis, and its features.
- Loss of restraining effects of oestrogen on bone turnover
- Characterised by high bone turnover, predominantly cancellous bone affected, and microarchitectural disruption
Give three ways that osteoporosis develops with age.
- Decrease in trabecular thickness
- Decrease in connections between horizontal trabeculae
- Decrease in trabecular strength and increased susceptibility to fracture
Why aren’t Xrays usually used to diagnose osteoporosis?
They have low sensitivity and specificity
What would blood tests usually show in osteoporosis?
Normal calcium, phosphate, and alkaline phosphatase
What test is used to diagnose osteoporosis?
DEXA
What does DEXA stand for?
Dual energy X-ray absorptiometry
Which bones are used for a DEXA scan?
- lumbar spine
- proximal femur
- distal radius
What does DEXA measure?
Bone mineral density (g/cm2) compared to a young healthy adult
What is meant by the DEXA T-score?
The number of standard deviations away from the bone mineral density of a young adult.
What does a DEXA T-score >0 mean?
BMD better than the reference
What does a DEXA T-score 0 to -1 mean?
BMD in the top 84%, no evidence of osteoporosis
What does a DEXA T-score of -1 to -2.5 mean?
Osteopenia
What action should be taken for a DEXA T-score of -1 to -2.5?
Give lifestyle advice
What does a DEXA T-score of -2.5 or worse mean?
Osteoporosis
What action should be taken for a DEXA T-score worse than 2.5?
Lifestyle advice and treatment
What risk assessment tool can estimate the 10yr risk of an osteoporotic fracture?
FRAX
Give six lifestyle advice treatments for osteoporosis.
- Quit smoking
- Reduce alcohol consumption
- Weight-bearing exercise may increase BMD
- Balance exercise reduces risk of falls
- Calcium and vitamin D rich diet
- Home-based fall prevention programme
How do anti-resorptive pharmacological treatments for osteoporosis work in general?
Decrease osteoclast activity and bone turnover.
Give three anti-resorptive pharmacological treatments for osteoporosis.
- Bisphoshonates
- Hormone replacement therapy
- Denosumab
Name a bisphosphonate used to treat osteoporosis.
Alendronate
How do bisphosphonates work to treat osteoporosis?
Inhibit an enzyme in the cholesterol synthesis pathway (farnesyl pyrophosphate synthase) to cause apoptosis of osteoclasts.
How does denosumab work to treat osteoporosis?
Monoclonal antibody to RANK-L
How do anabolic pharmacological treatments for osteoporosis work in general?
Increase osteoblast activity and bone formation.
Give an anabolic pharmacological treatment for osteoporosis.
Teriparatide (recombinant PTH)
How is strontium ranelate used to treat osteoporosis?
It reduces fracture rates and can be an alternative to bisphosphonates.
How does raloxifine work to treat osteoporosis?
It is a selective oestrogen receptor modulator
How is calcitonin beneficial in osteoporosis?
It may reduce pain after a vertebral fracture
What is implied by the term ‘mechanical’, when applied to lower back pain?
The pathology lies within the spinal joints, discs, vertebrae, or soft tissues.
Give six associations with mechanical lower back pain.
- Heavy manual handling
- Stooping and twisting whilst lifting
- Exposure to whole body vibration
- Psychosocial distress
- Smoking
- Dissatisfaction with work
Where might the pathology lie if the patient experiences pain on bending forwards?
Intervertebral discs
Where might the pathology lie if the patient experiences pain on bending backwards?
Facet joints
Give two normal findings on an MRI scan in mechanical lower back pain.
- Disc degeneration
- Bulging discs
Give five management points for mechanical lower back pain.
- Avoid prolonged inactivity
- Maintain normal activities within limits of back pain
- Simple analgesics or NSAIDs
- Spinal manipulative therapy
- Spinal exercises, behavioural therapy, and workplace adaptations (to return patient to work)
How early do vertebral discs undergo degeneration compared to other connective tissues in the body?
They are the earliest connective tissue to undergo degeneration.
Give three strong associations with vertebral disc degeneration.
- Back pain
- Sciatica
- Disc herniation or prolapse
What is a Schmorl’s node?
Formed when the nucleus pulposus of a vertebral disc herniates vertically into an adjacent vertebral body.
Give three pathological steps in vertebral disc degeneration.
- Disc becomes more disorganised
- Nerves and blood vessels increasingly found
- Cell death by necrosis
What percentage of women will have a fracture due to osteoporosis in their lifetime?
50%
Why do cortisol and steroids cause osteoporosis?
Cortisol increases bone resorption and induces osteoblast apoptosis.
Why does ageing cause degeneration of the horizontal bone trabeculae before vertical trabeculae?
Vertebral trabeculae are preserved because most skeletal strain is vertical.
Give three deformities that may be seen in the hand in Rheumatoid Arthritis.
- Ulnar deviation
- Boutonniere deformity
- Swan neck deformity
Describe Boutonniere deformity.
Proximal interphalangeal joint flexion and distal interphalangeal joint extension.
Describe swan neck deformity.
Proximal interphalangeal joint extension and distal interphalangeal joint flexion.
Give another name for the popliteal cyst which may appear in Rheumatoid arthritis.
Baker’s cyst
Describe what causes a Baker’s cyst in Rheumatoid Arthritis.
The synovial sack of the knee joint bulges posteriorly.
Give an antibody found in the antiphospholipid syndrome.
Anti-cardiolipin
Give three features of antiphospholipid syndrome.
- Arterial thrombosis
- Venous thrombosis
- Recurrent abortion
