Rheumatology Flashcards
1
Q
What is rheumatology?
A
The medical management of musculoskeletal disease.
2
Q
Give two rough categories that joint pain can be divided into.
A
- Inflammatory
- Non-inflammatory
3
Q
Give three examples of inflammatory joint problems.
A
- Autoimmune
- Crystal arthritis
- Infection
4
Q
Give three examples of autoimmune rheumatological diseases.
A
- Rheumatoid arthritis
- Spondyloarthropathy
- Connective tissue disease
5
Q
Give an example of a degenerative rheumatoid condition.
A
Osteoarthritis
6
Q
Give an example of a non-degenerative, non-inflammatory rheumatoid condition.
A
Fibromyalgia
7
Q
Compare the pain in inflammatory and degenerative rheumatological conditions.
A
INFLAMMATORY = eases with use DEGENERATIVE = increases with use, clicks/clunks
8
Q
Compare the stiffness in inflammatory and degenerative rheumatological conditions.
A
INFLAMMATORY = Significant (>60mins), early morning, at rest (evening) DEGENERATIVE = Not prolonged (<30mins), morning/evening
9
Q
Compare the swelling in inflammatory and degenerative rheumatological conditions.
A
INFLAMMATORY = Synovial +/- bony DEGENERATIVE = No synovial, bony
10
Q
Compare the inflammation in inflammatory and degenerative rheumatological conditions.
A
INFLAMMATORY = may be hot and red DEGENERATIVE = Not clinically inflamed
11
Q
Compare the patient demographics in inflammatory and degenerative rheumatological conditions.
A
INFLAMMATORY = young, psoriasis, family history DEGENERATIVE = older, prior occupation, sport
12
Q
Compare the joint distribution in inflammatory and degenerative rheumatological conditions.
A
INFLAMMATORY = hands and feet DEGENERATIVE = 1st CMCJ, DIPJ, knees
13
Q
Compare the NSAID response in inflammatory and degenerative rheumatological conditions.
A
INFLAMMATORY = good response DEGENERATIVE = Less convincing
14
Q
Describe the pattern of pain in bone pain.
A
Pain at rest and at night.
15
Q
Give three things that can cause bone pain.
A
- Tumour
- Infection
- Fracture
16
Q
Describe the pattern of pain in inflammatory joint pain.
A
Pain and stiffness in joints in the morning, at rest, and with use.
17
Q
Give two things that can cause inflammatory joint pain.
A
- Inflammatory
- Infective
18
Q
Describe the pattern of pain in osteoarthritis.
A
Pain on use and at the end of the day.
19
Q
Describe the pattern of pain in neuralgic pain.
A
Pain and paraesthesia in dermatomal distribution worsened by specific activity.
20
Q
What causes neuralgic pain?
A
Root or peripheral nerve compression
21
Q
Describe the pattern of pain in referred pain.
A
Pain unaffected by local movement.
22
Q
If the distal interphalangeal joint is involved in a rheumatological disorder, what are the two potential diagnoses?
A
- Psoriatic arthritis
- Osteoarthritis
23
Q
How quickly does ESR rise and fall?
A
Slowly (days to weeks)
24
Q
How quickly does CRP rise and fall?
A
Rapidly
25
Define spondyloarthritis.
Spondyloarthritis is an umbrella term encompassing several forms of arthritis.
26
Give seven forms of spondyloarthritis.
- Ankylosing spondylitis
- Psoriatic arthritis
- Reactive arthritis
- Enteropathic arthritis
- Acute anterior uveiits (iritis)
- Enthesis related juvenile idiopathic arthritis
- Undifferentiated spondyloarthritis
27
Give a genetic factor which all of the spondyloarthropathies are related to.
HLA B27
28
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
29
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)
30
What is ankylosing spondylitis?
Inflammatory arthritis of the spine and rib cage.
31
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.
32
In what age group does ankylosing spondylitis usually present?
Late teenage years/20s
33
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
34
Give two signs of ankylosing spondylitis which can be seen on an XRay.
- Syndesmophytes
| - Sacroiliitis
35
What are syndesmophytes?
New bone formation and vertical growth from anterior vertebral corners.
36
What is sacroiliitis?
Sclerosis, erosions, loss of joint space, and fusion of the sacroiliac joint.
37
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.
38
Give three treatment options for ankylosing spondylitis.
- Exercise
- NSAIDs
- Anti-TNF and Anti-IL17 drugs
39
Give a complication of ankylosing spondylitis.
Fusing of the spine (severe kyphosis of thoracic and vertebral spine).
40
Give the five patterns of psoriatic arthritis.
- DIPJ only
- RA like (symmetrical small joint)
- Large joint oligoarthritis
- Axial
- Arthritis mutilans
41
Give two radiological changes that occur in psoriatic arthritis.
- Erosive changes
| - ‘Pencil in cup’ deformity in severe cases
42
Give three treatment options of psoriatic arthritis.
- DMARDs (salfasalazine)
- Anti TNF drugs (infliximab)
- IL12/IL23/IL17 blockers
43
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).
44
Give four gut infections that are associated with reactive arthritis.
- Salmonella
- Shigella
- Yersinia
- Campylobacter
45
Give two sexually acquired infections which are associated with reactive arthritis.
- Chlamydia
| - Ureaplasma urealyticum
46
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
47
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)
48
Give three investigations that should be carried out in reactive arthritis.
- Raised ESR/CRP
- Aspirate joint to exclude infection/crystals
- Urethral swab/stool culture
49
Give two differential diagnoses that must be excluded in reactive arthritis.
- Septic arthritis
| - Gout
50
What is enteropathic arthritis?
Episodic peripheral synovitis which occurs in up to 20% of patients with IBD.
51
What is the most common pattern of enteropathic arthritis?
Asymmetric lower limb arthritis
52
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.
53
Which gender is rheumatoid arthritis more common in?
Women
54
What is the most common age to develop rheumatoid arthritis?
40-60years
55
What percentage of the population does rheumatoid arthritis affect?
1%
56
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
57
How do autoantibodies contribute to the development of rheumatoid arthritis?
Autoantibodies form immune complexes, which results in immunoglobulins and cytokines present in synovial fluid.
58
Give three methods of bone loss in rheumatoid arthritis.
- Focal erosion
- Periarticular osteoporosis
- Generalised osteoporosis in skeleton may result from RA
59
Give two things that contribute to cartilage loss in rheumatoid arthritis.
- Neutrophils release enzymes
| - Pannus releases pro-inflammatory cytokines
60
What enzymes do neutrophils release which contribute to cartilage destruction in rheumatoid arthritis?
Matrix metalloproteinases
61
Describe the classical presenting joint pattern in rheumatoid arthritis.
Symmetrical, deforming, polyarthropathy
62
In >80% of cases, which parts of the body does rheumatoid arthritis affect?
Hands and feet
63
Describe the rate of onset in rheumatoid arthritis.
Usually insidious onset
64
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.
65
Give two systemic symptoms of rheumatoid arthritis.
- Fatigue
| - Malaise
66
Give five consequences of lung involvement in RA.
- Pleural effusion
- Fibrosing alveolitis
- Rheumatoid nodules
- Caplan’s syndrome
- Small airways disease
67
Give three consequences of cardiac involvement in RA.
- Pericardial rub
- Pericarditis
- Pericardial effusion
68
Give four consequences of skin involvement in RA.
- Vasculitis
- Small digital infarcts along nail beds
- Ischaemic mononeuropathy
- Raynaud’s phenomenon
69
Give four consequences of eye involvement in RA.
- Sicca (dry eyes)
- Seconday Sjogren’s
- Episcleritis
- Scleritis
70
Give two consequences of renal involvement in RA.
- Amyloidosis
| - Analgesic neuropathy
71
Give three consequences of nervous system involvement in RA.
- Sensory peripheral neuropathy
- Entrapment neuropathies
- Cervical instability
72
Give four consequences of soft tissue involvement in RA.
- Nodules
- Bursitis
- Tenosynovitis
- Muscle wasting
73
Give three consequences of haematological involvement in RA.
- Palpable lymph nodes
- Enlarged spleen
- Anaemia
74
What are the three aspects of Felty’s Syndrome?
- Seropositive rheumatoid arthritis
- Splenomegaly
- Neutropenia
75
What would blood tests show in RA?
- Anaemia
| - High ESR/CRP
76
Give three antibodies that may appear in the serum of people with RA.
- Rheumatoid factor
- Anti-cyclic citrullinated peptide antibody
- Anti-nuclear antibody
77
What percentage of people with RA test positive for RF?
70%
78
What percentage of people with RA test positive for anti-cyclic citrullinated peptide antibody?
80%
79
What percentage of people with RA test positive for ANA?
<50%
80
What percentage of people with RA are sero-negative?
20%
81
Which antibody is specific for RA?
Anti-cyclic citrullinated peptide antibody
82
What does rheumatoid factor bind to?
The Fc portion of IgG
83
Give the four factors that are taken into account when making a diagnosis of RA.
- Joint involvement
- Serology
- Acute phase reactants
- Duration of symptoms
84
Give three DMARDs that can be used to treat rheumatoid arthritis.
- Methotrexate
- Sulfasalazine
- Hydroxychloroquine
85
Give two TNF-a inhibitors that can be used to treat RA.
- Infliximab
| - Enteracept
86
Give a biological agent which is used to deplete B cells in RA.
Rituximab
87
Give a biological agent which inhibits IL-1/IL-6 in RA.
Tocilizumab
88
Gives a biological agent which disrupts T cell function in RA.
Abatacept
89
What can be used in acute inflammation in RA?
Steroids (prednisolone)
90
What drugs can relieve symptoms in RA?
NSAIDs
91
Give two non-pharmacological management techniques for RA.
- Physiotherapy
| - Occupational therapy
92
Define osteoarthritis.
An age-related, dynamic reaction pattern of a joint in response to insult or injury.
93
Which tissue/s of the joint are involved in osteoarthritis?
All tissues are involved, but articular cartilage is the most affected.
94
Briefly describe the pathogenesis of osteoarthritis.
Metabolically active and dynamic process mediated by cytokines, and driven by mechanical forces.
95
Give three cytokines which are involved in osteoarthritis.
- IL-1
- TNF-a
- NO
96
Give the two main pathological features of osteoarthritis.
- Loss of cartilage
| - Disordered bone repair
97
Name eight risk factors for osteoarthritis.
- Age
- Gender
- Genetic predisposition
- Obesity
- Occupation
- Local trauma
- Inflammatory arthritis
- Abnormal biomechanics
98
Why is age a risk factor for osteoarthritis?
Due to cumulative effect of traumatic insult and decline in neuromuscular function.
99
Describe the age distribution of osteoarthritis.
- Uncommon under 45yrs
| - Common over 65yrs
100
Describe how gender is a risk factor for osteoarthritis.
- Affects more females, with increased prevalence after menopause
101
Give two ethnic groups that have a lower prevalence of OA hip.
- Afro-Caribbean
| - Asian
102
Give two ethnic groups which have a lower prevalence of OA hand.
- Black African
| - Malaysian
103
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
104
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
105
Give three examples of abnormal mechanics which can cause osteoarthritis.
- Joint hypermobility
- Congenital hip dysplasia
- Neuropathic conditions
106
Describe the symptoms of OA.
- Pain worse with use and at end of day
- Morning stiffness <30mins
- Functional impairment (walking, activities of daily living)
107
Give some signs of OA.
- Alteration in gait
- Joint swelling (bony enlargement, effusion, very occasionally synovitis)
- Crepitus
- Limited range of movement
- Tenderness
- Deformities
108
Give the five radiological features of osteoarthritis.
- Joint space narrowing
- Osteophyte formation
- Subchondral sclerosis
- Subchondral cysts
- Abnormalities of bone contour
109
Describe the inflammatory phase in OA of hands.
Occurs early, as nodes are forming.
110
Which joints are involved in OA of the hands?
- DIP
- PIP
- CMC
111
What causes reduced hand function in OA hand?
Bony swelling and cyst formation.
112
Which form of hand OA has a strong genetic component (especially in women)?
Nodal form
113
Describe the nodes in hand OA.
- Heberden’s Nodes at DIP joints
| - Bouchard’s Nodes at PIP joints
114
What are the three patterns of knee OA?
| (Which is the commonest)?
- Medial (commonest)
- Lateral
- Patellofemoral
115
Describe the evolution of OA of the knee (without significant trauma).
Evolution may be slow.
116
What is meant by ‘loose bodies’ in the knee?
Bone or cartilage fragment present in the joint.
117
What is the main symptom of loose bodies in the knee?
Locking of the knee
118
What is the main presentation of OA hip?
Groin pain
119
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
120
Give some non-medical management methods for OA.
- Patient education
- Activity/exercise
- Weight loss
- Physiotherapy
- Occupational therapy
- Footwear
- Walking aids
121
What is the role of intra-articular steroid injections in OA?
The role remains unclear.
122
Give some forms of pain relief used in OA.
- NSAIDs
- Capsaicin (topical)
- Paracetamol
- Opioids
- Buprenorphine
- Lignocaine
123
Give four surgical treatments for OA.
- Arthroscopy
- Osteotomy (cutting bone)
- Arthroplasty
- Fusion
124
When is arthroscopy used in OA?
ONLY for loose bodies
125
When is osteotomy used in OA?
Mostly in young people with knee OA.
126
When is arthroplasty used in OA?
For uncontrolled pain (particularly at night) and significant limitation of function.
127
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
128
Define vasculitis.
Inflammation and necrosis of blood vessel walls with subsequent impaired blood flow.
129
Give two consequences of vessel wall destruction in vasculitis.
- Perforation
| - Haemorrhage into tissues
130
Give two consequences of endothelial injury in vasculitis.
- Thrombosis
| - Ischaemia/infarction of dependent tissues
131
Give three histological features of vasculitis.
- Vessel wall infiltration by neutrophils, mononuclear cells, +/- giant cells
- Fibrinoid necrosis inside vessel wall
- Leukocytoclasis (dissolution of leukocytes)
132
Give four ways of classifying vasculitis.
- Size of vessel
- Target organ
- Anti-neutrophil cytoplasmic antibodies (ANCA) involvement
- Primary vs secondary
133
In which types of vasculitis can anti-neutrophil cytoplasmic antibodies be present?
Small/medium vessel vasculitis.
134
What are anti-neutrophil cytoplasmic antibodies?
Specific antibodies for antigens in cytoplasmic granules of neutrophils and monocyte lysosomes.
135
How are ANCAs detected?
Using indirect immunofluorescence microscopy.
136
Give the two different types of ANCA.
- cytoplasmic ANCA
| - peri-nuclear ANCA
137
What are the two potential targets for ANCA?
- Proteinase 3
| - Myeloperoxidase
138
How do ANCA contribute to the disease process in vasculitis?
They contribute to blood vessel damage.
139
Why is vasculitis so hard to diagnose?
There is no single typical presentation, as vasculitis can affect any vessel or organ.
140
Give some general signs/symptoms of vasculitis.
- Systemically unwell
- Fever
- Arthralgia/arthritis
- Rash
- Weight loss
- Headache
- Footdrop
- Major event (stroke, bowel infarction)
141
Give two differential diagnoses of vasculitis.
- Sepsis
| - Malignancy
142
Give a type of large vessel vasculitis.
Giant cell (temporal arteritis)
143
What is giant cell (temporal) arteritis?
Granulomatous arteritis of the aorta and larger extracranial branches of carotid arteries.
144
What age range does giant cell (temporal) arteritis affect?
>50yrs (incidence increases with age)
145
Give two groups of patients in which giant cell (temporal) arteritis is more common.
- Women
| - Caucasians
146
What does giant cell (temporal) arteritis increase the risk of?
Stroke
147
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
148
Give three signs of giant cell (temporal) arteritis.
Temporal arteries palpable, tender, and reduced pulsation.
149
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.
150
What is the gold standard investigation for giant cell (temporal) arteritis?
Temporal artery biopsy
151
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
152
What is the treatment for giant cell (temporal) arteritis?
Prompt corticosteroids (prednisolone)
153
How quick is the usual response to treatment in giant cell (temporal) arteritis?
48hrs
154
In giant cell (temporal) arteritis, how long does treatment usually last?
50% are off steroids at two years.
155
What other type of drug can be used in giant cell (temporal) arteritis?
Steroid sparing agents (azathioprine/methotrexate/biologics)
156
What prophylaxis treatment must be given in giant cell (temporal) arteritis?
Prophylaxis of osteoporosis from the steroids.
157
Give an example of small vessel vasculitis.
Granulomatosis with polyangiitis (Wegener’s Granulomatosis, GPA)
158
Describe the pathology in GPA.
- Necrotizing, granulomatous vasculitis of arterioles, capillaries, and post capillary venules
- Associated with anti-neutrophil cytoplasmic antibodies (c-ANCA)
159
What age does GPA usually affect?
25-60yrs (but can affect any age)
160
What is the classic triad of affected organs in GPA?
- Upper respiratory tract
- Lungs
- Kidney
161
How is GPA described if there is no renal involvement?
It is limited
162
What are the consequences of GPA affecting the upper respiratory tract?
- Sinusitis
- Otitis
- Nasal crusting
- Bleeding
163
What are the consequences of GPA affecting the lungs?
- Pulmonary nodules
| - Haemorrhage
164
What are the consequences of GPA affecting the kindey?
Glomerulonephritis
165
What are the consequences of GPA affecting the skin?
- Purpura
| - Ulcers
166
What are the consequences of GPA affecting the nervous system?
- Mononeuritis multiplex
| - CNS vasculitis
167
What are the consequences of GPA affecting the eyes?
- Proptosis
- Scleritis
- Episcleritis
- Uveitis
- Swelling of muscles behind the eye
168
What are the consequences of GPA affecting the nose, how common is it?
Saddle nose deformity.
| Rare now due to better treatments.
169
Give four ‘miscellaneous’ consequences of GPA.
- Synovitis
- Pericarditis
- GI
- GU
170
What is the treatment for severe (organ-threatening) GPA?
High does steroids/cyclophosphamide/biologics
171
What is the treatment for non-end organ threatening GPA?
Moderate dose steroids + methotrexate/mycophenolate/azathioprine
172
What is the commonest autoimmune connective tissue disease?
Systemic lupus erythematosus
173
Give an ethnic group in which SLE is more common?
Afro-Caribbeans
174
Is SLE more common in men or women?
90% patients are women
175
What is the typical age range for development of SLE?
14-64yrs
176
Describe the pathogenesis of SLE.
Inflammation and immune reactions against self antigens lead to immune complex mediated tissue damage.
177
What causes increased risk of thrombosis in SLE?
Phospholipid antibodies.
178
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
179
Describe the arthritis in SLE.
- Symmetrical
- Less proliferative than RA
- Can be deforming
- Non-erosive
180
Give four types of rash that can occur in SLE.
- Discoid rash
- Photosensitive rash
- Subacute lupus rash
- Butterfly rash
181
Give the three features of glomerulonephritis in SLE.
- Hypertension
- Proteinuria
- Renal failure
182
Describe the anaemia in SLE.
Coombs positive haemolytic anaemia
183
Give the three main antibodies in SLE.
- Anti-nuclear antibody
- Double stranded DNA antibody
- Anti-phospholipid antibody
184
Which antibody is specific for lupus?
Double stranded DNA antibody
185
How does anti-nuclear antibody help to diagnose lupus?
It is sensitive (95%) but not specific.
186
Give six other antibodies that may be detected in lupus.
- Rheumatoid factor
- Cardiolipin antibodies
- Anti Ro/La/Sm/RNP
187
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
188
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
189
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
190
Give five cytotoxic treatments that can be used in SLE.
- Azathioprine
- Mycophenolate
- Ciclosporin
- Methotrexate
- Cyclophosphamide
191
Describe the ESR and CRP in lupus.
ESR tends to be high but CRP tends to be normal.
192
Is primary or secondary Raynaud’s phenomenon more common?
Primary
193
Give three things that can cause secondary Raynaud’s phenomenon.
- Connective tissue disease
- Drugs
- Vascular damage
194
Give three connective tissue diseases that can cause Raynaud’s phenomenon.
- Systemic sclerosis
- Mixed connective tissue disease
- SLE
195
Give three factors which can cause vascular damage, which can result in Raynaud’s phenomenon.
- Atherosclerosis
- Frost bite
- Vibrating tools
196
Describe the colour changes in Raynaud’s phenomenon.
White in cold
Then blue (lack of oxygen)
Red on warmth (vasodilation)
197
What is dermatomyositis/polymyositis?
Inflammation of muscle and skin, causing rash and muscle weakness.
198
What is the consequence of lung involvement in dermatomyositis/polymyositis?
Interstitial lung disease
199
As well as a ‘primary’ disease, how else can dermatomyositis/polymyositis present?
As a paraneoplastic syndrome.
200
What are the clinical features of dermatomyositis/polymyositis?
- Myalgia
- Arthralgia
- Rash
- Dysphagia
- Dysphonia
- Respiratory weakness
201
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
202
What will the muscle enzymes show in dermatomyositis/polymyositis?
High creatine kinase
203
What is the management of dermatomyositis/polymyositis?
- Steroids
| - Immunosuppressive drugs
204
Give four clinical subsets of systemic sclerosis.
- Limited cutaneous
- Diffuse cutaneous
- Sine (without) scleroderma
- Overlap syndromes/mixed connective tissue disease
205
Is systemic sclerosis more common in men or women?
Women
206
What is the most common age for systemic sclerosis to present?
30-40yrs
207
Give three elements of the pathogenesis of systemic sclerosis.
- Vasculopathy
- Inflammation and excessive collagen deposition by fibroblasts
- Auto-antibody production
208
Give three antibodies that may appear in systemic sclerosis.
- Anti-nuclear antibodies
- Anti-centromere antibodies
- Anti-topoisomerase antibodies
209
What percentage of patients with systemic sclerosis test positive for ANA?
65%
210
In which type of systemic sclerosis might anti-centromere antibodies appear, and in what percentage of patients?
70-80% of patients with limited SSc
211
In which type of systemic sclerosis might anti-topoisomerase antibodies appear, and in what percentage of patients?
40% of patients with diffuse SSc
212
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)
213
Describe the skin involvement in limited cutaneous SSc.
Limited to face, hands, and feet.
214
What is a late feature of limited cutaneous SSc?
Pulmonary hypertension
215
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
216
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)
217
Give five things that may cause secondary Sjogren’s syndrome.
- SLE
- Rheumatoid arthritis
- Scleroderma
- Primary biliary cirrhosis
- Other auto-immune diseases
218
Briefly describe the pathology of Sjogren’s syndrome.
Lymphocytic infiltration and fibrosis of exocrine glands.
219
What are the clinical features of sjogren’s syndrome?
- Dry eyes
- Dry mouth
- Arthritis
- Rash
- Neurological features
- Vasculitis
- Interstitial lung disease
- Renal tubular acidosis
220
Give a condition which is strongly associated with Sjogren’s syndrome.
Gluten sensitivity
221
Sjogren’s syndrome increases the risk of which condition?
Lymphoma
222
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)
223
What is the treatment for Sjogren’s syndrome?
- Tear and saliva replacement
| - Immune-suppression for systemic complications
224
Give two features of both crystal arthritis and infection.
- Rapid onset
| - Very red and hot joints
225
How can crystal disease and infection be differentiated?
- Clinical history
| - Joint aspirate
226
Give five differential diagnoses of systemic diseases.
- Infection
- Auto-immune diseases
- Malignancy
- Endocrine diseases
- Metabolic diseases
227
Give two inherited connective tissue diseases.
- Marfan’s Syndrome
| - Ehler Danlos Syndrome
228
Give the pattern of inheritance for Marfan’s syndrome.
Autosomal dominant
229
Give five features of Marfan’s syndrome.
- Tall/long arms
- Lens dislocation
- Aortic valve incompetence/dilated aortic root
- High arched palate
- Sunken chest
230
Give two features of Ehler Danlos syndrome.
- Stretchy skin
| - Joint hypermobility
231
What is the prevalence of fibromyalgia?
0.5-4%
232
Is fibromyalgia more common in men or women?
Women
233
Give five risk factors for fibromyalgia.
- Female sex
- Middle age
- Low household income
- Divorced
- Low educational status
234
Give three other conditions that are associated with fibromyalgia.
- Chronic fatigue syndrome
- Irritable bowel syndrome
- Chronic headaches syndrome
235
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
236
What do the investigations show in fibromyalgia?
All are normal
237
Describe the principles of management of fibromyalgia.
- Education of patient and family
- Explanation and reassurance
- Cognitive behavioural therapy
- Antidepressants may help to relieve pain
238
What is another name for Paget’s disease?
Osteitis deformans
239
What age group is Paget’s disease more common in?
Over 40s
240
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
241
Describe the clinical features of Paget’s disease.
- Asymptomatic in about 70%
- Deep, boring pain
- Bony deformity and enlargement
242
Give five sites where Paget’s disease commonly manifests.
- Pelvis
- Lumbar spine
- Skull
- Femur
- Tibia
243
Give six complications of Paget’s disease.
- Pathological fractures
- Osteoarthritis
- Hypercalcaemia
- Nerve compression due to bone overgrowth
- High output congestive heart failure
- Osteosarcoma
244
Give two consequences of nerve compression in Paget’s disease.
- Deafness
| - Root compression
245
Give two radiological features of Paget’s disease.
- Localised enlargement of bone
| - Patchy cortical thickening with sclerosis, osteolysis, and deformity
246
Describe the calcium, phosphate, and alkaline phosphate levels in Paget’s disease.
- Calcium normal
- Phosphate normal
- Alkaline phosphate raised
247
Describe the treatment for Paget’s disease.
- Analgesia
| - Alendronate (to reduce pain/deformity if analgesia fails)
248
What is ‘osteomalacia’ called if it occurs during the period of bone growth?
Rickets
249
Briefly describe the pathophysiology of osteomalacia.
- Normal bone amount but low mineral content
| - Excess uncalcified osteoid and cartilage
250
Give six causes of osteomalacia.
- Vitamin D deficiency
- Renal osteodystrophy (renal failure)
- Drug-induced
- Vitamin D resistance
- Liver disease
- Tumour-induced osteomalacia
251
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)
252
Give the signs/symptoms of osteomalacia.
- Bone pain and tenderness
- Fractures (especially femoral neck)
- Proximal myopathy
- Low phosphate and vitamin D
253
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)
254
What would the bone biopsy show in osteomalacia?
Incomplete mineralisation
255
What would the muscle biopsy show in osteomalacia?
Normal
256
Give two radiological features of osteomalacia.
- Loss of cortical bone
| - Apparent partial fractures without displacement
257
Give a radiological feature of Rickets.
Cupped, ragged metaphyseal surfaces
258
What would the treatment be for osteomalacia caused by vitamin D deficiency?
Vitamin D
259
What treatment would be given in vitamin D resistant osteomalacia or renal disease?
- Alfacalcidiol
| - Calcitriol
260
What is type I vitamin D resistance rickets?
Low renal 1a-hydroxylase activity
261
What is type II vitamin D resistance rickets?
End-organ resistance to 1,25-dihydroxycholecalciferol
262
How are both type I and type II vitamin D resistance rickets treated?
Large doses of calcitriol
263
Describe the inheritance pattern of X-linked hypophosphataemic rickets.
Dominant X linked
264
Briefly describe the pathology in X-linked hypophosphataemic rickets.
Defect in renal phosphate handling
265
How is X-linked hypophosphataemic rickets treated?
High doses of oral phosphate and calcitriol
266
Give eight things associated with developing carpel tunnel syndrome.
- Obesity
- Short stature
- Pregnancy
- Oral contraceptive pill
- Diabetes
- Hypothyroidism
- Rheumatoid arthritis
- Acromegaly
267
Give two work-related causes of carpel tunnel syndrome.
- Forceful and repetitive work (painters, meat processors)
| - Hand-transmitted vibration
268
Give two special tests that can be used to diagnose carpal tunnel syndrome.
- Tinel’s test
| - Phalen’s test
269
Describe Tinel’s test.
Tap lightly over the median nerve and see if patient feels paresthesia distally.
270
Describe Phalen’s test.
Patient fully flexes elbows and wrists (upside down prayer position) and if symptoms occur the test is positive.
271
What causes hand-arm vibration syndrome?
Excessive exposure to hand-transmitted vibration (chain saws, angle grinders, jack hammers, drills)
272
Describe the presentation of hand-arm vibration syndrome.
- Vascular (blanching)
| - Neural (tingling, numbness, loss of dexterity)
273
Hand-arm vibration syndrome is a secondary cause of what condition?
Raynaud’s phenomenon
274
Briefly describe hypothenar hammer syndrome.
Occlusion of ulnar artery and superficial palmar arch.
275
What is the most common cause of tenosynovitis?
Inflammation of abductor pollicis longus and extensor pollicis brevis tendon sheath.
276
Give an occupational risk of developing tenosynovitis.
Job requires forceful and repetitive hand movements.
277
Give a special test used to diagnose tenosynovitis.
Finkelstein’s test
278
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.
279
Give four methods of treatment for tenosynovitis.
- NSAIDs
- Steroid injection
- Rest
- Change job
280
What is another name for lateral epicondylitis.
Tennis elbow
281
What is another name for medial epicondylitis?
Golfer’s elbow
282
What causes epicondylitis?
Forceful flexion-extension of the wrist or forceful pronation-supination.
283
Give a special test used to diagnose lateral epicondylitis.
Cozen’s test
284
Describe Cozen’s test.
Patient’s elbow in 90degree flexion, hand in radial deviation, forearm pronation.
Patient extends wrist against resistance.
Pain = positive.
285
Give five methods of treatment for epicondylitis.
- NSAIDs
- Steroid injection
- Clasp
- Rest
- Surgery
286
What is repetitive strain disorder?
Non-specific pain in the hand
287
Give four treatment methods for repetitive strain disorder.
- Rest breaks
- Job rotation
- Reduced force
- Ergonomically neutral working postures
288
Describe briefly what causes writers cramp.
A focal dystonia (neurological condition affecting the nerves).
289
Briefly describe usual rotator cuff problems.
Tendonitis or a tear, usually affecting the supraspinatus tendon.
290
Give two occupational associations with rotator cuff problems.
- Shoulder impingement
| - OA of acromioclavicular joint
291
Describe the presentation of rotator cuff problems.
Painful arc
292
Give a special sign used to diagnose rotator cuff problems.
Hawkin’s sign
293
Describe Hawkin’s sign.
Shoulder flexed to 90degrees.
Elbow flexed to 90degrees.
Quickly rotate arm internally.
Pain below acromioclavicular joint is positive.
294
Give three high risk activities that can increase likelihood of developing rotator cuff problems.
- Heavy manual lifting
- Lifting above shoulder height
- Throwing
295
Describe thoracic outlet syndrome.
Pain or tingling down arm or blanching of fingers related to posture of arm.
296
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.
297
Give two occupational associations with thoracic outlet syndrome.
- Poor posture
| - Loading of shoulders
298
Give three things (including a special test) that can be used to diagnose thoracic outlet syndrome.
- Roos sign
- X-ray neck
- MRI
299
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.
300
What is the treatment for thoracic outlet syndrome?
Surgery
301
Describe Dupytren’s contracture.
Thickening of palm fascia caused by vibrating tools, resulting in flexion of one or more fingers.
302
What is Seamstress’ finger?
Heberden’s nodes at distal interphalangeal joints.
303
Give a classical feature of rheumatoid arthritis on X ray.
Peri-articular erosions
304
As well as in the back, where else might pain be felt in inflammatory back pain?
Across the costochondral joints.
305
What antibody is usually positive in all autoimmune connective tissue disorders?
Anti-nuclear antibody
306
What type of arthritis (deforming or erosive) is associated with systemic lupus erythematosus?
Deforming
307
Give a rheumatological condition in which thrombocytosis may be a feature.
Rheumatoid arthritis
308
What is osteomyelitis?
An infection localised to bone.
309
Why is there increasing incidence of chronic osteomyelitis?
There is increasing risk of pre-disposing conditions.
310
Give two age groups in which osteomyelitis is more common?
Children and elderly
311
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
312
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)
313
What is sequestra in osteomyelitis?
Necrotic bone which is left behind
314
What is involucrum in osteomyelitis?
New bone formation
315
Give three methods of infection in osteomyelitis.
- Direct inoculation
- Contiguous spread
- Haematogenous seeding
316
In osteomyelitis, is direct inoculation usually monomicrobial or polymicrobial?
Can be either
317
In osteomyelitis, is contiguous spread monomicrobial or polymicrobial?
Can be either
318
In osteomyelitis, is haematogenous seeding usually monomicrobial or polymicrobial?
Monomicrobial
319
Give two ways that bones can be infected by direct inoculation.
- Trauma
| - Surgery
320
Describe contiguous spread in osteomyelitis.
Spread of infection from adjacent tissue.
321
Give four ‘conditions’ that increase likelihood of contiguous spread in osteomyelitis.
- Diabetes mellitus
- Chronic ulcers
- Vascular disease
- Arthroplasties
322
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.
323
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.
324
Give two risk factors for contracting osteomyelitis via haematogenous seeding.
- IV drug users
| - People with risk factor for bacteraemia
325
What is the most common causative organism in osteomyelitis?
Staphylococcus aureus
326
Why is Staph.aureus good at infecting bones?
It binds host proteins and can survive in macrophages.
327
Give the three usual organisms which can cause osteomyelitis.
- Staphylococcus aureus
- Coagulase -ve staph
- Aerobic gram -ve bacilli
328
Give five less common organisms which can cause osteomyelitis.
- Streptococci
- Enterococci
- Anaerobes
- Fungi
- Mycobacteria
329
Which organism commonly causes osteomyelitis in sickle cell disease?
Salmonella
330
Give two organisms which cause osteomyelitis in IV drug users.
- Pseudomonas aeruginosa
| - Serratia marcescens
331
Describe the symptoms of osteomyelitis.
Dull pain at site of infection, may be aggravated by movement.
332
Describe the rate of onset of osteomyelitis symptoms.
Onset over several days
333
Give four systemic signs of osteomyelitis.
- Fever
- Rigors
- Sweats
- Malaise
334
Give four local acute signs of osteomyelitis.
- Tenderness
- Warmth
- Swelling
- Erythema
335
Give seven local chronic signs of osteomyelitis.
- Tenderness
- Warmth
- Swelling
- Erythema
- Draining sinus tract
- Deep/large ulcers that fail to heal
- Non-healing fractures
336
Give three findings on a blood test in oesteomyelitis.
- High WCC (chronic can have normal)
- Raised CRP
- Raised ESR
337
What type of imaging can be carried out to diagnose acute osteomyelitis.
MRI (or CT/nuclear bone scan)
338
Why aren’t X-rays that sensitive to acute osteomyelitis?
They take about 2 weeks for changes to appear
339
Give two investigations to identify the causative organism in osteomyelitis.
- Bone biopsy (sample to microbiology and histology)
| - Blood cultures
340
Give six signs of chronic osteomyelitis on X-ray.
- Cortical erosion
- Periosteal reaction
- Mixed lucency
- Sclerosis
- Sequestra
- Soft tissue swelling
341
Give two features of osteomyelitis on MRI.
- Marrow oedema
| - Delineation on cortical, bone marrow, and soft tissue inflammation
342
Give seven differential diagnoses of osteomyelitis.
- Soft tissue infection (cellulitis, erysipelas)
- Charcot joint
- Avascular necrosis of bone
- Gout
- Fracture
- Bursitis
- Malignancy
343
Give the two steps in the management of osteomyelitis.
- Surgery
| - Antimicrobial therapy
344
What does surgery for osteomyelitis involve?
Debridement and hardware replacement/removal
345
Give two things that choice of antimicrobial therapy in osteomyelitis depends on.
- Infective organism
| - Bone penetration of drug
346
How long should antibiotics be given for in osteomyelitis?
6 weeks minimum, treatment length guided by ESR/CRP
347
How does the presentation of mycobacterial osteomyelitis differ from other forms of osteomyelitis?
- Slower onset
| - More systemic symptoms
348
What investigation is essential to diagnose mycobacterial osteomyelitis?
Biopsy
349
How long is the typical treatment for mycobacterial osteomyelitis?
12 months
350
Is septic arthritis more common in males or females?
They are equal
351
What percentage of septic arthritis cases occur in patients over 65yrs?
45%
352
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
353
What is the main causative organism in septic arthritis (native joints)?
Staphylococcus aureus
354
Give six less common causative organisms of septic arthritis.
- Streptococci
- Neisseria gonorrhoea
- Gram -ve bacilli
- Anaerobes
- Mycobacterium
- Fungi
355
What used to be a major cause of septic arthritis in children, but now isn’t due to immunisation?
Haemophilus influenzae
356
Give four features of gonococcal septic arthritis.
- Fever
- Arthritis (polyarticular)
- Tenosynovitis
- Rash
357
Give three presenting features of septic arthritis.
- Painful, red, swollen, hot joint
- Disuse (especially in children)
- Fever
358
Is septic arthritis usually monoarthritis or polyarthritis?
90% monoarthritis, but polyarthritis can occur (eg. In gonorrhoea)
359
Give the relative frequencies of septic arthritis the hip, knee, and shoulder.
Knee>hip>shoulder
360
Give two investigations to carry out in suspected septic arthritis.
- Joint aspirate
| - Blood cultures
361
Give three features of joint aspirate that would suggest septic arthritis.
- Turgid fluid
- High leukocyte content
- Gram stain (+ve cocci)
362
What additional investigation may be required if mycobacterial septic arthritis is suspected?
Synovial biopsy
363
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
364
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.
365
How is a prosthetic joint infection caught after surgery?
Haematogenous spread
366
What is the most common causative organism of prosthetic joint infections?
Coagulase -ve staphylococci
367
Give three causative organisms of prosthetic joint infections.
- Coagulase -ve staphylococci
- Staphylococcus aureus
- Enterobacteria
368
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
369
Give three X ray features that may suggest an infection in a prosthetic joint.
- Prosthetic loosening
- Periosteal thickening
- Ectopic bone formation
370
Give a highly sensitive/specific inflammatory marker that can be used to diagnose prosthetic joint infections.
Alpha defensin
371
When would antibiotic suppression be used to treat prosthetic joint infection?
If the patient is unfit for surgery
372
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.
373
When would excision arthroplasty be used to treat prosthetic joint infection?
If at higher risk.
374
What is the consequence of an excision arthroplasty being used to treat prosthetic joint infection?
Poor functional outcome
375
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).
376
What does two stage exchange arthroplasty to treat prosthetic joint infection involve?
Debridement, then wait before inserting new prosthesis.
377
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)
378
What lab tests can be carried out in a suspected bone tumour?
- PSA
- Serum/urine electrophoresis
- ESR
- CRP
- Calcium
- Alkaline phosphatase
379
What imaging can be carried out to assess bone tumours?
- Plain X ray
| - Potentially CT/MRI/Bone scan
380
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)
381
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.
382
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
383
What does a narrow zone of transition suggest about the malignancy of a bone tumour?
It is likely to be benign
384
What does a wide zone of transition suggest about the malignancy of a bone tumour?
It is likely to be a more aggressive disease
385
What does a solid periosteal reaction suggest about the malignancy of a bone tumour?
The tumour is less malignant
386
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.
387
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.
388
What does a Codman’s triangle periosteal reaction suggest about the malignancy of a bone tumour?
It is a very malignant tumour
389
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.
390
What does complete cortical destruction suggest about the malignancy of a bone tumour?
It is an aggressive disease
391
Give four radiographic features of a benign bone tumour.
- Well defined, sclerotic border
- Lack of soft tissue mass
- Solid periosteal reaction
- Geographic bone destruction
392
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
393
What is a major complicating factor in bone tumours?
Fracture
394
What is Mirel’s scoring system in bone tumours?
A score given to determine a patient’s risk of fractures.
395
What four factors are considered when calculating Mirel’s score in bone tumours?
- Site
- Pain
- Lesion type (blastic/mixed/lytic)
- Lesion size
396
Is it more common for a bone tumour to be primary or secondary?
Secondary
397
How do patients with primary bone tumours commonly present?
Constant, non-mechanical pain.
398
Give an example of a primary bone tumour that typically occurs in patients aged between 10 and 19 years.
Osteosarcoma
399
Give an example of a primary bone tumour which typically occurs in patients <18yrs of age.
Ewing’s sarcoma
400
Give an example of a primary bone tumour which is usually found in people >40yrs, and with Paget’s disease.
Chondrosarcoma
401
Describe the bone lesions in metastatic bone tumours.
They are lytic
402
Describe developmental dysplasia of the hip.
Hip socket too shallow and femoral head not held tightly in place.
403
Give two treatment options for developmental dysplasia of the hip.
- Harness
| - Surgery
404
Describe slipped capital femoral epiphysis.
The epiphyseal growth plate slips and the femur moves superiorly compared to the epiphysis.
405
How does sepsis in a joint lead to arthritis?
It causes chondrolysis
406
What three aspects of an orthopaedic history are ‘most important’/
- SOCRATES
- Occupation
- Handedness (left/right)
407
Briefly describe the blood supply to the femoral head.
The profunda femoris artery gives rise to the lateral and medial circumflex arteries.
408
Which type of hip fracture can cut off the blood supply to the femoral head?
Intracapsular fracture
409
Describe a type 1 intracapsular hip fracture.
Incomplete, doesn’t affect blood supply to head
410
Describe a type 2 intracapsular hip fracture.
Complete, not displaced, doesn’t cut off blood supply to head
411
Describe a type 3 and type 4 hip fracture.
Displaced, interrupted blood supply to femoral head
412
How are type 1 and type 2 hip fractures fixed?
Using screws
413
How are type 3 and type 4 hip fractures fixed?
Hemiarthroplasty or full arthroplasty
414
Describe an extracapsular hip fracture in terms of blood supply.
The blood supply to the femoral head is maintained.
415
How are extracapsular hip fractures fixed?
Screws
416
Give the three principles of management of orthopaedic trauma.
- Reduce (put back in line)
- Stabilise (nails)
- Rehabilitate (walk)
417
Give the four stages of fracture healing.
1. Haematoma formation
2. Fibrocartilagenous callus formation
3. Bony callous formation
4. Bone remodelling
418
Give six cytokines/molecules requires for haematoma formation after a fracture.
- IL-1
- IL-6
- IL-12
- TNF-a
- PDGF
- COX2 (required for osteoblasts)
419
What is cauda equina syndrome?
Compression or damage of the cauda equina below the spinal cord.
420
Describe and explain the typical urinary symptoms experienced in cauda quina syndrome.
- Pudendal nerve compression
- Can’t relax external sphincter
- Overflow incontinence
421
Give five signs/symptoms of cauda equina syndrome.
- Uni/bilateral leg pain
- Perineal numbness
- Back pain
- Urinary symptoms
- May have faecal problems
422
What is the treatment for cauda equina syndrome?
Decompression
423
What is contained within hyaline cartilage which attracts water to it?
Proteoglycans (hyaluronic acid)
424
What is crystal arthritis?
Arthritis caused by crystal deposition in the joint lining.
425
What is a crystal?
A homogenous solid formed of ions bonded closely in ordered, repeating, symmetric arrangement.
426
Give two reasons why crystals are necessary in animals.
- To strengthen exoskeleton and endoskeleton
| - Remove excess ions by surface binding
427
What does crystal deposition in the body lead to?
Local inflammatory response and tissue damage.
428
What is the condition called when crystals are deposited in the gallbladder or kidney.
Nephrolithiasis
429
Give four types of crystal that can be deposited in joints to cause crystal arthritis.
- Monosodium urate
- Calcium pyrophosphate
- Calcium hydroxyapatite
- Cholesterol
430
What is the medical condition which results from monosodium urate crystal deposition in the joints?
Gout
431
Is gout more common in men or women?
Men
432
When does the incidence of gout rise in women?
Postmenopause (often related to identifiable trigger)
433
What is the commonest arthritis in men >40yrs?
Gout
434
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
435
Give some causes for over-production of urate.
- Diet
- Metabolic syndrome (hyperlipidaemia)
- Proliferative (myeloproliferative, cytotoxic drugs)
- Psoriasis
- Lesch-Nyhan syndrome
436
Give nine dietary factors which may increase urate levels in the body.
- Red meat
- Fizzy drinks
- Sugar
- Alcohol
- Shellfish
- Offal
- Gravy
- Yeast
- Fructose
437
Give a dietary factor that may be protective against gout.
Dairy products
438
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
439
How is uric acid produced in the body?
Purine metabolism by xanthine oxidase.
440
What is the concentration of uric acid at which the serum is saturated?
0.3mmol/L
441
At what serum level of uric acid is a patient at risk of crystal deposition?
>0.36mmol/L
442
At what serum level of uric acid does supersaturation occur, making crystal deposition very likely?
>0.42mmol/L
443
Give the steps in purine metabolism leading to uric acid.
Purine -> hypoxanthine -> xanthine -> uric acid
444
Describe the acute presentation of gout.
- Hot, swollen, painful joint
- Often affects first metatarso-phalangeal joint
- Systemically unwell
445
How does chronic gout usually present?
Longer term joint damage and tophi under the skin.
446
What are tophi?
Onion-like aggregates of urate crystals with inflammatory cells.
447
How long does it take to control attacks of tophaceous gout?
6-9months
448
How long can it take for tophi to resolve?
Up to 2 years
449
Give three investigations that should be carried out in gout.
- Joint aspiration
- Blood tests
- X rays
450
What would you expect the serum urate level to be in gout?
May be high, but may be normal or low in acute attacks.
451
Give two features of gout that may be seen on an xray.
- Punched out bone lesions
| - Narrow joint space
452
How would the crystals appear under a microscope in gout?
Negatively birefringent needles
453
How would the crystals appear under the microscope in pseudogout?
Weakly positive birefringent rhomboids
454
Give four things that can be used to treat acute attacks of gout.
- Anti-inflammatories
- NSAIDs
- Colchicine
- Steroids
455
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)
456
What is the disease called when calcium pyrophosphate crystals are deposited on a joint surface?
Pseudogout
457
Give two groups of patients in whom pseudogout is more common.
- Elderly
| - Females
458
What other rheumatological condition often occurs with pseudogout?
Osteoarthritis
459
Give four places that pseudogout typically affects.
- Knees
- Wrists
- Shoulders
- Hips
460
Give some triggers of acute pseudogout attacks.
- Direct trauma
- Intercurrent illness
- Surgery (parathyroidectomy)
- Blood transfusion
- IV fluid
- T4 replacement
- Joint lavage
- Most are spontaneous
461
Describe the presentation of pseudogout.
- Acute synovitis
- Acute monoarthritis in elderly
- Severe pain, stiffness, swelling
- Fever
462
Give a classical joint distribution which suggests pseudogout instead of osteoarthritis.
2nd and 3rd metacarpo-phalangeal joint swelling
463
What would the X ray show in pseudogout?
Chondrocalcinosis
464
Describe the treatment for pseudogout.
Usually resolves in 1-3 weeks.
| Drugs not very effective.
465
What can be used to treat the symptoms of pseudogout?
- NSAIDs
- Analgesia
- Aspiration
- Injection
- Physiotherapy
466
What treatment may be tried if there are continued inflammatory changes in pseudogout?
- Anti-rheumatic treatment
- Synovectomy
- Surgery
467
Give the typical patient demographic for calcium hydroxyapatite crystal arthropathy.
Elderly females
468
Describe the damage that occurs in calcium hydroxyapatite crystal arthropathy.
Destructive attacks on the shoulders
469
Give eight metabolic diseases which are associated with gout.
- Haemochromatosis
- Hyperparathyroidism
- Hypophosphatasia
- Hypomagnesaemia
- Hypothyroidism
- Acromegaly
- Familial hypocalciuric hypercalcaemia
- X-linked hypophosphataemic rickets
470
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
471
Define osteoporosis.
A metabolic bone disease characterised by a generalised reduction in bone mass, increased bone fragility, and predisposition to fracture.
472
What is the likely consequence if trabecular bone is affected by osteoporosis?
Crush fractures of the vertebrae
473
What is the likely consequence if cortical bone is affected by osteoporosis?
Long bone fractures
474
What is the prevalence of osteoporosis in men over 50 years?
6%
475
What is the prevalence of osteoporosis in women over 50 years?
18%
476
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
477
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
478
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
479
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
480
Why aren’t Xrays usually used to diagnose osteoporosis?
They have low sensitivity and specificity
481
What would blood tests usually show in osteoporosis?
Normal calcium, phosphate, and alkaline phosphatase
482
What test is used to diagnose osteoporosis?
DEXA
483
What does DEXA stand for?
Dual energy X-ray absorptiometry
484
Which bones are used for a DEXA scan?
- lumbar spine
- proximal femur
- distal radius
485
What does DEXA measure?
Bone mineral density (g/cm2) compared to a young healthy adult
486
What is meant by the DEXA T-score?
The number of standard deviations away from the bone mineral density of a young adult.
487
What does a DEXA T-score >0 mean?
BMD better than the reference
488
What does a DEXA T-score 0 to -1 mean?
BMD in the top 84%, no evidence of osteoporosis
489
What does a DEXA T-score of -1 to -2.5 mean?
Osteopenia
490
What action should be taken for a DEXA T-score of -1 to -2.5?
Give lifestyle advice
491
What does a DEXA T-score of -2.5 or worse mean?
Osteoporosis
492
What action should be taken for a DEXA T-score worse than 2.5?
Lifestyle advice and treatment
493
What risk assessment tool can estimate the 10yr risk of an osteoporotic fracture?
FRAX
494
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
495
How do anti-resorptive pharmacological treatments for osteoporosis work in general?
Decrease osteoclast activity and bone turnover.
496
Give three anti-resorptive pharmacological treatments for osteoporosis.
- Bisphoshonates
- Hormone replacement therapy
- Denosumab
497
Name a bisphosphonate used to treat osteoporosis.
Alendronate
498
How do bisphosphonates work to treat osteoporosis?
Inhibit an enzyme in the cholesterol synthesis pathway (farnesyl pyrophosphate synthase) to cause apoptosis of osteoclasts.
499
How does denosumab work to treat osteoporosis?
Monoclonal antibody to RANK-L
500
How do anabolic pharmacological treatments for osteoporosis work in general?
Increase osteoblast activity and bone formation.
501
Give an anabolic pharmacological treatment for osteoporosis.
Teriparatide (recombinant PTH)
502
How is strontium ranelate used to treat osteoporosis?
It reduces fracture rates and can be an alternative to bisphosphonates.
503
How does raloxifine work to treat osteoporosis?
It is a selective oestrogen receptor modulator
504
How is calcitonin beneficial in osteoporosis?
It may reduce pain after a vertebral fracture
505
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.
506
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
507
Where might the pathology lie if the patient experiences pain on bending forwards?
Intervertebral discs
508
Where might the pathology lie if the patient experiences pain on bending backwards?
Facet joints
509
Give two normal findings on an MRI scan in mechanical lower back pain.
- Disc degeneration
| - Bulging discs
510
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)
511
How early do vertebral discs undergo degeneration compared to other connective tissues in the body?
They are the earliest connective tissue to undergo degeneration.
512
Give three strong associations with vertebral disc degeneration.
- Back pain
- Sciatica
- Disc herniation or prolapse
513
What is a Schmorl’s node?
Formed when the nucleus pulposus of a vertebral disc herniates vertically into an adjacent vertebral body.
514
Give three pathological steps in vertebral disc degeneration.
- Disc becomes more disorganised
- Nerves and blood vessels increasingly found
- Cell death by necrosis
515
What percentage of women will have a fracture due to osteoporosis in their lifetime?
50%
516
Why do cortisol and steroids cause osteoporosis?
Cortisol increases bone resorption and induces osteoblast apoptosis.
517
Why does ageing cause degeneration of the horizontal bone trabeculae before vertical trabeculae?
Vertebral trabeculae are preserved because most skeletal strain is vertical.
518
Give three deformities that may be seen in the hand in Rheumatoid Arthritis.
- Ulnar deviation
- Boutonniere deformity
- Swan neck deformity
519
Describe Boutonniere deformity.
Proximal interphalangeal joint flexion and distal interphalangeal joint extension.
520
Describe swan neck deformity.
Proximal interphalangeal joint extension and distal interphalangeal joint flexion.
521
Give another name for the popliteal cyst which may appear in Rheumatoid arthritis.
Baker’s cyst
522
Describe what causes a Baker’s cyst in Rheumatoid Arthritis.
The synovial sack of the knee joint bulges posteriorly.
523
Give an antibody found in the antiphospholipid syndrome.
Anti-cardiolipin
524
Give three features of antiphospholipid syndrome.
- Arterial thrombosis
- Venous thrombosis
- Recurrent abortion
