Rheumatology Flashcards
1
Q
What is Rheumatology?
A
The medical management of musculoskeletal disease.
Made up of inflammatory (caused by autoimmune, crystal arthritis, infection) and non-inflammatory (can be degenerative or non-degenerative).
2
Q
What is inflammation?
A
Reaction of microcirculation Movement of fluid and white blood cells into extra-vascular tissues Releases pro-inflammatory cytokines - Red, painful, hot, swollen - Stiffness - Poor mobility/function - Deformity
3
Q
How can you differentiate between inflammatory and degenerative causes of musculoskeletal pain?
A
- Pain: will ease with use (I) or increases with use (D)
- Stiffness: significant >60mins (I) or not prolonged 30mins (D)
- Swelling: synovial +/- bony (I) or none (D)
- Inflammation: hot and red (I) or none (D)
- Demographics: Pt is young with family history (I) or Pt is older with prior occupation
- Joint distribution: hands and feet (I) or 1st CMCJ, DIPJ, knees (D)
- NSAIDs: responds (I) or doesn’t respond (D)
4
Q
How can the patterns of pain indicate conditions?
A
Bone pain at rest and night - tumour, infection, fracture
Pain and stiffness in joints in the morning, at rest and with use - inflammatory joint pain
Pain on use, at end of day - osteoarthritis
Pain and paraesthesia in dermatomal distribution, worsened by specific activity - Root or peripheral nerve compression
Pain unaffected by local movement - referred pain
5
Q
What is ESR and what can it tell us?
A
Erythrocyte sedimentation rate
The rate that red blood cells settle to the bottom of a test tube after centrifugation. Fibrinogen is an “acute phase protein” ie a protein made in excess level in the body in response to inflammation or infection. So a high ESR means the red cells settle to the bottom of the tube quicker, because of high levels of fibrinogen in the face of inflammation/ infection.
Can have false positives due to age, female, obesity, racial difference, hypercholesterolaemia, high immunoglobulins (inc. myeloma), anaemia.
6
Q
What is CRP can what can it tell us?
A
C-reactive protein Acute phase protein – pentameric peptide Released in inflammation/ infection Produced by liver in response to IL-6, binds to damaged cells and activates complement - phagocytosis Rises and falls rapidly High @ 6 hrs; peak 48 hrs
7
Q
What factors can be markers of rheumatoid arthritis and SLE?
A
Rheumatoid Arthritis - RF (Rheumatoid Factor) or CCP (cyclic citrullinated peptide)
SLE - ANA (anti nuclear antibody), binds to Antigens within cell nucleus or dsDNA (double stranded DNA)
8
Q
What is Spondyloarthropathy/spondyloarthritis?
A
Group of over-lapping conditions which are all variously associated with the tissue type HLA B27
Includes:
Each condition variably associated = AS (up to 95%; less now with MRI diagnosis), Uveitis (50%), PsA (50-60%), ReA (60-80%)
Patients often display features of more than one individual disease from this group
9
Q
What are the main conditions of Spondyloarthropathy?
A
Ankylosing spondylitis Enteropathic Arthritis (Crohns/ UC) Reactive Arthritis Psoriatic Arthritis Acute anterior uveitis (iritis) Undifferentiated Spondyloarthritis Juvenile Idiopathic Arthritis (enthesitis related)
10
Q
What is HLA B27?
A
Human Leucocyte Antigen (HLA) B27
Class I surface antigen (all cells, except red blood cells)
Encoded by Major Histocompatibility Complex (MHC) on chromosome 6
Antigen presenting cell
You can either positive or negative for it
11
Q
How is HLA B27 linked with Spondyloarthritis?
A
3 THEORIES
- Molecular mimicry: Infection → immune response → infectious agent has peptides very similar to HLA B27 molecule → auto-immune response triggered against HLA B27
- Mis-folding theory: Unfolded HLA-B27 proteins accumulate in the endoplasmic reticulum. A proinflammatory stress response called the endoplasmic reticulum unfolded protein response (ERUPR) ensues. As a result, interleukin 23 (IL-23) is released, activating a proinflammatory response via interleukin-17+ T lymphocytes.
- HLA B27 heavy chain homodimer hypothesis: B27 heavy chains can form stable dimers, which tend to dimerize and accumulate in the ER. In turn, this initiates the proinflammatory ERUPR. In addition, these heavy chains and dimers can bind to other regulatory immune receptors such as the natural killer receptors. This causes the expression and survival of more proinflammatory leukocytes and subsequent production of proinflammatory mediators.
12
Q
What are the clinical features of Spondyloarthritis?
A
Inflammatory arthritis of the “axial skeleton” which results in new bone formation and “fusion” of the vertebrae
Enthesitis (inflammation of junction between ligament/ tendon and bone)
Acute anterior uveitis (irits) - inflammation of the anterior chamber of the eye
Peripheral arthritis
Skin psoriasis
May also have (sub-clinical) inflammatory bowel disease.
13
Q
What are the major features of Spondyloarthritis?
A
Sausage digit (dactylitis) Psoriasis Inflammatory back pain NSAID good reponse Enthesitis (heel) Arthritis Crohn’s/ Colitis/ elevated CRP* HLA B27 Eye (uveitis)
14
Q
What is Ankylosing Spondylitis or “Axial Spondyloarthritis”?
A
Inflammatory arthritis of the spine and rib cage – eventually leading to new bone formation and fusion of the joints
Typically starts in late teenage years/20s & was always thought to be more common in men, but with MRI diagnosis, incidence in women is increasingly recognised (although may be different phenotype – less new bone formation, more B27 (-))
Worst prognosis is male, smokers, B27 (+), syndesmophytes at presentation and high CRP
15
Q
What are Syndesmophytes?
A
New bone formation and vertical growth from anterior vertebral corners (Romanus lesions)
16
Q
What is Sacroiliitis?
A
One or both of the sacroiliac joints become inflamed.
May occur in Ankylosing Spondylitis
17
Q
How does structural damage occur in Ankylosing Spondylitis?
A
“Delayed damage theory” ie once inflammation has occurred – new bone formation is inevitable, therefore once treatment started, new bone continues to form for some time after
Sets in motion a chain reaction that is difficult to stop
18
Q
How is Axial Spondyloarthritis diagnosed?
A
Sacroilitis on imaging and one or more clinical features (inflammatory back pain, arthritis, enthesitis, uveitis, dactylitis, psoriasis, Crohn’s/UC, good response to NSAIDs, family history, HLA-B27, elevated CRP)
OR
HLA-B27 plus 2 or more features
19
Q
What are the treatments available for Ankylosing Spondylitis?
A
Physiotherapy
Long term and high dose NSAIDs (risks of gastric ulcer, vascular disease, renal damage)
TNFi remain the only NICE approved drug: Improves symptoms almost instantly in vast majority
New group of drugs – JAK inhibitors (biologic tablets)
20
Q
What are the 5 types of Psoriatic Arthritis?
A
Symmetrical (both sides of the body) Asymmetric and few joints Spondylitis Distal interphalangeal joints Arthritis mutilans - resorption of bones and the consequent collapse of soft tissue
21
Q
How is Psoriatic Arthritis managed?
A
Similar to RA
Early intervention with DMARDs - MTX, leflunomide, ciclosporin, sulfasalazine
DMARDs often help skin disease
Anti TNF drugs - Etanercept, adalimumab, golimumab, certolizumab, infliximab
IL12/23 blockers - ustekinumab
22
Q
What is Reactive Arthritis?
A
Sterile inflammation of the synovial membrane, tendons and fascia triggered by an infection at a distant site, usually gastro-intestinal or genital.
Gut associated infections: Salmonella, Shigella, Yersinia
Sexually acquired infection (NSU): Chlamydia, Ureaplasma urealyticum
23
Q
What are the features of Reactive Arthritis?
A
CLASSIC TRIAD
Arthritis – large joint oligo/ monoarthritis, enthesitis/ dactylitis/ sacroiliitis
Conjunctivitis
Sterile urethritis
Psoriatic like skin lesions – keratoderma/ circinate balanitis
24
Q
How would you investigate/diagnose Reactive Arthritis?
A
Exclude Septic arthritis and Gout Hot swollen joint Raised ESR/CRP Aspirate joint to exclude infection/crystals Urethral swab, stool culture Contact tracing if necessary
25
What is Enteropathic Arthritis?
Episodic peripheral synovitis occurs in up to 20% of patients with IBD
Asymmetric lower limb arthritis
Usually reflects the disease activity
Remission generally related to suppression of bowel disease.
AS occurs in 7% of patients with IBD.
Activity unrelated to other disease activity
50% of patients with IBD and HLA-B27 +ve develop sacroiliitis
Management similar to reactive arthritis.
26
What is osteoporosis?
A systemic skeletal disease characterised by low bone mass and micro-architectural deterioration of bone tissue with a consequent increase in bone fragility and perfectibility to fracture.
27
Who is at risk of osteoporosis?
Tend to be those who are older, with comorbidities.
20% of those with a hip fracture will die within a year.
30% will have permanent disability.
28
What is the pathophysiology contributing to a fracture?
Trauma (due to increased propensity to fall)
Bone strength:
- Bone size
- Bone mineral density (peak bone mass and rate of bone loss)
- Bone quality (dependent on bone turnover, architecture and mineralisation)
29
How does bone growth change through your lifetime?
Bones grow quickly in childhood - mostly your limbs
| Bones grow even more quickly in adolescent - mostly your spine
30
What is the most important risk factor for fractures?
Age is the most important risk factor for fracture risk
More likely to break hip in old age because protective reactions (hands to the floor) are less effective, so more likely to break hip instead of wrist.
31
What is the bone remodelling cycle in osteoporosis?
Microcrack in the bone - resorption - formation - returned to normal
But in osteoporosis, this mechanism cannot be performed so there is a net loss of bone.
32
What is postmenopausal osteoporosis?
Loss of restraining effects of oestrogen on bone turnover
Preventable by oestrogen replacement
Characterised by high bone turnover, predominantly cancellous bone loss and microarchitectural disruption.
33
How does trabecular architecture change with ageing?
Decrease in trabecular thickness, more pronounced for non-load bearing horizontal trabeculae
Decrease in connections between horizontal trabeculae
Decrease in trabecular strength and increased susceptibility to fracture
34
What is bone densitometry used for?
For risk assessment and for diagnosis, the characteristic of major importance is the ability of a technique to predict fractures.
35
What does dual energy X ray absorptiometry do?
Measuring the sites which are most prone to fracture - good predictor of risk.
Very low radiation dose.
36
What is the T score?
Standard deviation score
Compared with a gender-matched young adult average
Asks how much bone have you lost since you were a young adult?
37
How can endocrine disease increase the risk of osteoporosis?
Thyroid hormone and parathyroid hormone increase bone turnover so hyperthyroidism and hyperparathyroidism can increase this even more.
Cortisol increases bone resorption and induces osteoblast apoptosis so cushing's syndrome can increase even more.
Oestrogen/testosterone control bone turnover which can increase in patients with early menopause, male hypergonadism or anorexia/athletes.
38
How does reduced skeletal loading affect the bones?
Increases resorption in the bone
If your body weight is very low, it has a big impact on the skeletal system - it is less needed, so there is increased resorption. This occurs if you are immobile or in space travel.
39
What are the risk factors for osteoporosis?
```
Age
Previous fracture
Family history of osteoporosis or fracture
Alcohol
Smoking
```
40
What medication can cause osteoporosis?
```
Glucocorticoids
Depo-provera
Aromatase inhibitors
GnRH analogues
Androgen deprivation
```
41
How to treat osteoporosis?
Anti-resorptive - decrease osteoclast acitivity and bone activity: biphosphonates, HRT, denosumab
Anabolic - increase osteoblast activity and bone formation: teriparatide
42
What are the benefits and risks of HRT?
```
Benefits:
- Reduces risk of fractures by 50%
- Stop bone loss, bone density may increase by 10%
- Prevents hot flushes and other menopausal symptoms
- Reduces risk of colon cancer
Risks:
- Breast cancer
- Stroke
- Cardiovascular disease
- Venous thrombo-embolic disease
- Vaginal bleeding
```
43
What are biphosphonates?
Biphosphonates inhibit an enzyme in the cholesterol synthesis pathway
First line treatment for osteoporosis
Cheap, effective, many years of experience
44
What is Denosumab?
Monoclonal antibody to RANK ligand
| Used in osteoporosis treatment
45
What is Teriparatide?
Reduces the risk of fractures by more than 50%
Increases bone density, improves trabecular structure
Bone density may increase up to 70%
46
What is vasculitis?
```
Rare multi-system diseases
Inflammation of blood vessels
Classified by vessel size and common features
Heterogeneous
Challenging to recognize and diagnose
```
47
How is vasculitis classified?
By vessel size
| Consensus classification
48
What is Giant Cell Arteritis?
Commonest large vessel vasculitis
Medical emergency if present with…
Strokes
Blindness (a stroke affecting the retina and optic nerve)
Two distinct clinical patterns of disease with considerable overlap
- Cranial GCA
- Large vessel GCA (LV-GCA)
49
What is the pathogenesis of Giant cell arteritis?
Activation of dendritic cells in the adventitia
Recruitment and activation of T Cells
Recruitment of CD8+ cells and monocytes
Vascular damage and remodelling
50
What are the clinical features of giant cell arteritis?
CRANIAL
New headache (abrupt, unilateral, temporal)
Scalp tenderness (pain when brushing hair)
Jaw claudication
Visual symptoms (vision loss, diplopia)
LV-GCA
Constitutional symptoms (fever, malaise)
Polymyalgia
Limb claudication
51
What are the physical signs of giant cell arteritis?
Physical signs include:
Scalp tenderness
Temporal artery tenderness
Reduced/absent pulsation
52
What are the complications of giant cell arteritis?
Prompt treatment preventative:
Highest risk of visual loss within 4 weeks of starting steroid
Visual loss <20% (higher in ophthalmology cohorts and pre corticosteroid use)
Strokes 1.5 -7.5%
53
How would you investigate giant cell arteritis?
Temporal artery biopsy
Ultrasound 54% sensitivity vs. 39% Temporal artery biopsy
PET-CT scan - Helpful to identify LV-GCA
54
How would you treat giant cell arteritis?
Glucocorticoids (promptly!)
If failure to wean glucocorticoids:
DMARD e.g. Methotrexate, Lefunomide
Tocilizumab
Mitigating effects of treatment:
Osteoporosis prevention
Diabetes mellitus monitoring
55
What is ANCA-associated vasculitis?
Rare, life threatening, multisystem disease causing damage to predominantly small arteries
Anti-neutrophil cytoplasmic antibodies (ANCA) are implicated in the pathogenesis and can be measured
Two patterns of disease are observed: PR3-ANCA and MPO-ANCA.
Types:
Granulomatosis with polyangiitis (GPA)
Eosinophilic granulomatosis with poly angiitis
Microscopic polyangiitis
56
When to test for ANCA-associated vasculitis?
Glomerulonephritis
Pulmonary haemorrhage
Cutaneous vasculitis with systemic features
Multiple lung nodules
Chronic destructive disease of the upper airways
57
What are the clinical features of Granulomatosis with polyangiitis?
Variable presentation from ‘limited’ to ‘generalised’ multi-system disease
Epistaxis, crusts, stiffiness, hearing loss, hoarseness, stridor
Iritis, diplopia
Cough, dyspnoea, haemoptysis
Rash (‘vasculitic rash’)
Numbness, tingling, foot/wrist drop
Joint pain, swelling
58
How would you investigate Granulomatosis with polyangiitis?
1. Confirm the diagnosis - history, examination, ANCA testing, tissue biopsy
2. Assessment of organ involvement - CT thorax, urine protein/creatinine ratio, CT head/sinuses/neurophysiology
3. Assessment of disease activity - vasculitis damage index
59
How would you treat Granulomatosis with polyangiitis?
Induction of remission
Cyclophosphamide or Rituximab* +
Glucocorticoids
Plasma exchange for specific complications (pulmonary haemorrhage, severe renal creatinine >500)
Maintenance of remission (3-6 months onwards)
DMARD e.g. azathioprine, mycophenolate mofetil
Rituximab (if rituximab induction)
Glucocorticoid taper
60
What is osteoarthritis?
Osteoarthritis is an age-related, dynamic reaction pattern of a joint in response to insult or injury
All tissues of the joint are involved
Articular cartilage is the most affected
Changes in underlying bone at the joint margins
61
What is the pathogenesis of osteoarthritis?
Originally considered to be an inevitable consequence of ageing and trauma, traditionally viewed as ‘degenerative’ and ‘non-inflammatory’.
No longer thought to be the case - metabolically active and dynamic process mediated by cytokines IL-1, TNF-α, Nitric oxide
Main pathological features:
Loss of cartilage
Disordered bone repair
62
What are the risk factors for osteoarthritis?
- Age: due to cumulative effect of low grade traumatic insult and decline in neuromuscular function
- Gender: increase prevalence in females
- Genetic predisposition: Most relevant in polyarticular disease
- Obesity: Linear relationship between BMI and risk of hip and knee OA. Thought to be due to the fact that obesity is a low grade inflammatory state. Release of IL-1
TNF, Adipokines.
- Occupation: Manual labour
- Other factors: local trauma, inflammatory arthritis, abnormal bio-mechanics - joint hypermobility, congenital hip dysplasia, neuropathic conditions
63
What are the symptoms of osteoarthritis?
Pain
Often reason patient seeks medical advice
May not be present despite significant changes on x-ray
Functional impairment of walking and activities of daily living
64
What are the clinical signs of osteoarthritis?
Alteration in gait
Joint swelling: bony enlargement, effusion, synovitis (if inflammatory component)
Other joint abnormalities: limited range of movement, crepitus – cracking sound when moving the joint, tenderness, deformities
65
What are the radiological features of osteoarthritis?
```
Joint space narrowing (not specific to osteoarthritis)
Osteophyte formation
Subchondral sclerosis
Subchondral cysts
Abnormalities of bone contour
```
66
What are the features of osteoarthritis in the hands?
DIP, PIP, CMC joints
Relapsing, remitting course over a few years
‘Nodal’ form has a strong genetic component – often down the female blood line
Each involved joint often has an early ‘inflammatory’ phase
Bony swelling and cyst formation
Reduced hand function
- Heberden’s nodes at DIP joints
- Bouchard’s nodes at PIP joints
67
What are the features of osteoarthritis in the knee?
3 compartments
- Medial (commonest)
- Lateral
- Patellofemoral
Any may be affected in isolation or in combination
Without significant trauma, evolution very slow
Once established, often remains stable for years
68
What is erosive/inflammatory osteoarthritis?
Subset of OA
Strong inflammatory component
In addition to standard management, DMARD therapy (usually milder agents) often used
Very mixed results
69
What are loose bodies in the knee?
Associated with ‘locking’ of knee
Bone or cartilage fragment broken off and left floating around
The only indication for arthroscopy in osteoarthritis
70
How can osteoarthritis be treated non-medically?
```
Patient education
Activity and exercise
Weight loss – to reduce inflammation
Physiotherapy – to aid with day to day tasks
Occupational therapy
Footwear
Orthoses
Walking aids: stick or frame
```
71
How can osteoarthritis be treated pharamcologically?
Topical – fairly safe, don’t always work for patients
NSAIDs and Capsaicin
Oral
Paracetamol
NSAIDs (with caution especially in old people)
Opioids
Transdermal patches – local effect
Buprenorphine
Lignocaine
Intra-articular steroid injections
Role remains unclear
DMARDs have a role in inflammatory OA
72
What are the alternative therapies for osteoarthritis?
```
Glucosamine - delay in progression of cartilage loss
Chondroitin
Nettle extract
Turmeric
Chinese herbal medicine
```
73
How can osteoarthritis be treated surgically?
Arthroscopy - only for loose bodies
Osteotomy – cut bone away
Arthroplasty
Fusion – stopping the bones grinding together to relieve pain. Usually ankle and foot, difficult to operate on.
74
What are the indications for arthroplasty?
```
Uncontrolled pain (particularly at night)
Significant limitation of function
```
75
How can connective tissue disorders be classified?
Inherited
| Auto-immune (inflammatory)
76
Give examples of inherited connective tissue disorders?
Marfan's Syndrome - Arm span greater than their height
Long fingers, Risk of aortic dilatation and aneurysms
Ehler Danlos Syndrome - can be vascular or skeletal, skin hyperplasticity
77
What are the features of auto-immune connective tissue disorders?
Pathology: Inflammation leading to scarring (damage) in organs affected
Can lead to organ failure: potentially high morbidity and mortality
Early systemic involvement may not give rise to any symptoms
Any system can be affected: commonly skin, joints, kidney, lungs, blood cells and nervous system
Inflammation can be treated with immunosuppressive drugs, damage is irreversible
78
What are the major connective tissue disorders?
Systemic Lupus Erythematosus (SLE)
Systemic Sclerosis
Primary Sjögren’s Syndrome
Dematomyositis/ Polymyositis
79
What is the epidemiology of SLE?
Incidence: 4/100 000/year
90% women (14-64 years)
Genetic Association: HLA: DR2, DR3, C4 A Null Allele
80
What is the pathophysiology of SLE?
Inflammation: Immune complex mediated tissue damage
Thrombosis: Phospholipid antibodies
81
How can SLE present dermatologically?
```
Acute
Malar “butterfly” rash
Generalised erythema
Bullous LE
Subacute
Annular
Psoriasiform
Chronic
Discoid
scarring alopecia
Lupus profundus
```
82
How can SLE present?
```
Rashes
Inflammatory arthritis - symmetrical, can be deforming, non-erosive
Nephritis/Nephrosis
Renal failure
Pericarditis/myocarditis
Acute MI
Pleural effusion
Pulmonary embolism
Psychosis
Oral ulceration
Recurrent abortions
Pregnancy complications
Cytopenias
Abnormal clotting
```
83
How can SLE present haematologically?
Anaemia (Haemolytic, Coombs positive)
Thrombocytopenia
Neutropenia
Lymphopenia
84
What are the auto-antibodies present in SLE?
Anti-nuclear antibody: Not specific for lupus (screening test for all connective tissue diseases) Frequently positive in healthy people.
Double stranded DNA antibody: Specific to SLE
Other antibodies: Rheumatoid factor, Cardiolipin antibodies, Anti Ro, La, Sm, RNP
85
How to manage SLE?
Patient education and support
UV protection – high factor sun cream
Assessment of lupus activity clinical and immunological
Screening for major organ involvement
Assessment of damage
Identify patients with phospholipid antibodies
Management of lupus in pregnancy
Good liaison with other specialists
Assessment and management of atherosclerosis risk factors
86
What drugs can be used in SLE?
No Treatment
Topical - Sunscreens, Steroids, Cytotoxic
NSAIDs
Antimalarial
Steroids
Cytotoxic
Anticoagulants
Biological target B cells which make the antibodies
Stem cell transplant – using the patient’s own stem cells (rare)
87
What are the types of Raynaud’s disease?
- Primary (very common 15%)
- Secondary
Connective tissue diseases - Systemic sclerosis, Mixed connective tissue disease, SLE
Drugs particularly vasoconstricting drugs
Vascular damage: Atherosclerosis, Frost bite, Vibrating tools
88
What are the major features of Systemic Sclerosis?
Vasculopathy
Excessive collagen deposition
Inflammation
Auto-antibody production
89
What are the subtypes of Systemic Sclerosis?
Limited Cutaneous
Diffuse Cutaneous
Sine (without) scleroderma
Overlap syndromes/Mixed connective tissue disease
90
What are the features of limited cutaneous systemic sclerosis?
Sclerodactyly
Long history of Raynaud’s phenomenon
Late-stage complications
Pulmonary arterial hypertension
91
What are the features of diffuse cutaneous systemic sclerosis?
```
Proximal scleroderma and trunk involvement
Short History of Raynaud’s
Increased risk of renal crisis
Increased risk of cardiac involvement
Increased risk of ILD
```
92
How would you manage systemic sclerosis?
- Raynaud’s: Physical protection, Vasodilators
(Nifedipine, Iloprost, Sildenafil, Bosentan), Fluoxetin,
Sympathectomy
- Gastro-oesophageal reflux: Proton pump inhibitors for life
- Prevention of renal crisis: ACE inhibitors
- Early detection of pulmonary arterial hypertension
- Treatment of skin oedema: No treatment, Cytotoxic drugs, Autologus stem cell transplant
- Treatment of pulmonary fibrosis: Cyclophosphamide
93
What are the different types of Sjögren’s Syndrome?
- Primary (a disease in its own right)
- Secondary
SLE
Rheumatoid arthritis
Scleroderma
Primary billiary cirrhosis
Other auto-immune diseases
94
What are the clinical features of Sjögren’s Syndrome?
```
Dry eyes
Dry mouth
Arthritis
Rash
Neurological features
Vasculitis
ILD
Renal tubular acidosis
Strong association with gluten sensitivity
Increased risk of lymphoma
```
95
What are the lab features of Sjögren’s Syndrome?
```
Positive ANA
Positive RF
Positive Ro and La
Negative DS DNA
Raised Immunoglobulins
Abnormal salivary glands on ultrasound
Sialadenitis on lip biopsy
```
96
How would you treat Sjögren’s Syndrome?
Tear and saliva replacement
HCQ for fatigue, myalgia, arthralgia, rashes
Corticosteroids/immunosuppressants for organ-threatening extra-glandular disease
Biological therapies
97
What is Dermatomyositis/Polymyositis?
Muscle and skin mainly affected: rash and muscle weakness
Lungs can be affected (Interstitial lung disease)
Can present as a para-neoplastic syndrome
98
What are the investigations for Dermatomyositis/Polymyositis?
```
Muscle enzymes
Antibody screen
EMG
Muscle/skin biopsy
Screen for malignancy (PET)
Chest X ray, PFTs, High resolution CT lungs
```
99
How would you manage Dermatomyositis/Polymyositis?
Steroids
| Immunosuppressive drugs
100
What is good musculoskeletal health?
Healthy/disease-free muscles, joints, bones
| Ability to carry out a wide range of physical activities/functions both effectively and symptom free
101
What are Musculoskeletal conditions?
Injuries, inflammatory conditions (eg arthritis), multifactorial conditions causing pain (eg chronic lower back pain).
They may be acute or chronic (including relapsing) conditions.
102
What are the different types of prevention for musculoskeletal conditions?
Primary prevention = reduce prevalence of risk factors, maximise MSK health
Secondary prevention = screening for asymptomatic conditions (manage them early)
Tertiary prevention = management of conditions to reduce impact
103
What is strategies can be used for effective and cost-effective MSK risk management?
Vitamin D/ calcium – adequate dietary intake +/- supplements
Weight management – calorie intake and calorie expenditure
Physical activity – balance + strength + mobility (+/- fitness)
Injury prevention – home; workplace; recreational; travel related
104
How can MSK risk be managed over the course of a patient's lifetime?
Maternal health – smoking, diet, vitamin D (related to infant bone density)
Child health – physical activity, diet (bone density and healthy body weight)
Adult health – injury prevention, workplace health, healthy weight/weight loss
Healthy ageing – dietary protein, calcium, vitamin D, strength and balance exercises for older patients
105
What are the criteria for a condition for it to have a screening programme put in place?
The condition should be an important health problem as judged by its frequency and/or severity. The epidemiology, incidence, prevalence and natural history of the condition should be understood, including development from latent to declared disease and/or there should be robust evidence about the association between the risk or disease marker and serious or treatable disease.
106
What are the criteria for a screening test?
There should be a simple, safe, precise and validated screening test.
The distribution of test values in the target population should be known and a suitable cut-off level defined and agreed.
The test, from sample collection to delivery of results, should be acceptable to the target population.
There should be an agreed policy on the further diagnostic investigation of individuals with a positive test result and on the choices available to those individuals.
107
What are the criteria for screening in terms of intervention?
There should be an effective intervention for patients identified through screening, with evidence that intervention at a pre-symptomatic phase leads to better outcomes for the screened individual compared with usual care.
There should be agreed evidence based policies covering which individuals should be offered interventions and the appropriate intervention to be offered.
108
What are the criteria for screening in terms of the screening programme itself?
Effective in reducing mortality or morbidity
Benefit gained by individuals from the screening programme should outweigh any harms
Opportunity cost of the screening programme should be economically balanced in relation to expenditure
109
Do we offer screening for Developmental Dysplasia of the Hip?
Screening for congenital dislocated hip (CDH) and developmental dysplasia of the hip (DDH) is part of the physical examination of newborn and 6-8 week old babies.
Early detection, confirmation of diagnosis and conservative management can reduce need for surgery and have better outcome than late diagnosis.
Ultrasound screening should not be offered to all babies. Could otherwise lead to over diagnosis and treatment of cases that would resolve without treatment.
110
Do we offer screening for osteoporosis?
UK NSC cannot recommend population screening for osteoporosis in postmenopausal women.
Due to concerns about:
- Accuracy of the test
- Effect of treatment and changes in lifestyle
- Screening all women does not reduce fractures from osteoporosis compared to usual care.
111
Do we offer screening for vitamin D deficiency?
No unless:
- they have symptoms of deficiency
- they are considered to be at particularly high risk of deficiency (for example, very low exposure to sunlight)
- there is a clinical reason to do so for example, they have osteomalacia (marked softening of your bones) or a fall
112
Should we screen for physical inactivity?
A known risk factor
Can be identified by direct questions in a clinical setting
“Brief intervention” (just 5-10 mins during clinical consultation) can be an effective and cost-effective intervention
113
How is physical activity involved in primary prevention of MSK injury?
Maintaining good musculoskeletal health
Population and individual level interventions to ensure optimum levels of activity to maintain strength, balance, cardiorespiratory fitness
Whose responsibility? – local authorities, transport planners
114
How is physical activity involved in tertiary prevention of MSK injury?
Managing chronic conditions for which symptoms and/or prognosis is improved by activity, including:
- MSK, cardiac, respiratory, diabetes, depression, cancer etc
115
How is physical activity linked to health and wellbeing?
Evidence from cross-sectional studies that a wide range of chronic conditions associated with reduced levels of PA
Evidence from cohort studies that reduced PA is early symptom of dementia
BUT
Pain, fatigue, anxiety related to chronic conditions will make it more difficult to be active
Condition-specific barriers include joint pain and stiffness, depression symptoms, risk/fear of falling, stress incontinence
116
How are Musculoskeletal health and mental health linked?
Chronic musculoskeletal conditions, like many chronic conditions, are associated with a high prevalence of anxiety and depression
Effective management of chronic back pain and other musculoskeletal conditions where pain is a significant symptom may include psychological management (“biopsychosocial” interventions)
Physical activity is an element in prevention and management of chronic conditions that has benefits for mental (and social) as well as physical health
117
What is osteomyelitis?
An infection of the bone, a rare but serious condition. Bones can become infected in a number of ways: Infection in one part of the body may spread through the bloodstream into the bone, or an open fracture or surgery may expose the bone to infection.
Can become chronic - long-term and present of dead bone
118
How does infection occur in osteomyelitis?
Direct inoculation is most common in adults - infection into the bone marrow
Predominantly polymicrobial
Contiguous spread - soft tissue swelling (ulcers) which spreads to the deep bone
Often start as monomicrobial and then becomes polymicrobial
Rarely fungi and TB
119
Where does haematogenous seeding most often occur in osteomyelitis?
Haematogenous - spread to infection to the bone via the blood
Haematogenous seeding can also affect adults (vertebrae) as well as children (long bones)
Most commonly children
120
How would you investigate osteomyelitis?
Non-specific blood tests - can’t give an accurate diagnosis
Good imaging and sensitivities in culture
Plain radiograph used to look for any other causes
121
What biochemistry results would you expect from a joint infection?
High total white cell count (WCC)
Predominantly neutrophilia
CRP is high (Over 100 – think about infection rather than inflammation)
CRP goes up quickly withing hours or days of inflammation
ESR takes longer to increase
122
How would you make a diagnosis of a joint infection?
Blood cultures – joint is usually seeded by bacteraemia
Joint aspiration - Clear straw-coloured fluid suggests a non-infective/inflammatory cause. Turbid fluid suggests inflammation or infection.
123
How would you manage a joint infection?
```
Aspiration - ALWAYS
Antibiotics guided by this
Long course antibiotics
6 weeks minimum
Joint washout/ repeated aspiration until no recurrent effusion (to remove pus)
Rest/ splint/physio
Analgesia
Stop any immuno-suppression temporarily if you can
```
124
What's the epidemiology for septic arthritis?
2-8 cases: 100 000 population/ PA
45% > 65 years old
M=F
Prosthetic joint infection > native (see later)
Becoming more of an issue because there are more people with prosthetic limbs
125
What are the common microorganisms causing naive joint infections in adults?
```
Staph Aureus (RA, diabetics)
Streptococci
-Gp A (β haemolytic) Strep
-Gp B Strep
-Strep pneumoniae
Neisseria gonorrhoea (young, sexually active)
Gram (-) bacilli (very young, very old, systemically unwell)
-E.Coli
-Pseudomonas Aeruginosa
Anaerobes (diabetics)
-Clostridium
-Bacteroides
Mycobacterium (immunocompromised)
Fungi (immunocompromised)
```
126
What are the common microorganisms causing naive joint infections in children?
```
< 2 years
Staph Aureus
GpA Streptococci
Kingella Kingae (Gram (-) bacilli)
> 2 years
Staph Aureus
Streptococci
Gram - bacilli
```
127
How would a septic joint typically present?
```
Painful, red, swollen, hot joint
Remember children may just not use it
Fever
90% monoarthritis
So don’t rule out in polyarticular presentations
Knee > hip > shoulder
```
128
What are the risk factors for a septic joint?
Any cause for bacteraemia
Direct/ penetrating trauma
Local skin breaks/ ulcers
Damaged joints
Immunosuppression (including steroids only)
Elderly
Rheumatoid arthritis (or other immune-driven disease)
Diabetes
129
What is Gonococcal Arthritis?
Occurs with disseminated gonococcal infection
Typically polyarthritis
Synovial fluid is often negative
Accompanied by fever, arthritis, tenosynovitis
- Multiple joints, small & large: “polyarticular”
Maculopapular – pustular rash
- Common in peripheries eg palms, soles
- Painful before visible
- Usually > 5 lesions
130
How to prevent a prosthetic infection?
Use a clean environment as much as possible
Use cement with permanent antibiotics in them
Give patients systemic antibiotics during surgery too.
131
How might a prosthetic infection present?
Red, hot, swollen and painful - high index of suspicion
Maybe more subtle, most just have an irritable joint.
Should ask about any recent infections or whether the prosthetic operation has been performed recently.
132
How to investigate a prosthetic infection?
History, examination, x-rays, FBC, ESR, CRP, microbiology culture from aspiration
CRP 12-20 consistent with a prosthetic joint infection
```
No test has a diagnostic accuracy of 100%
Single CRP (>10) and ESR (>30)
If increased, 50% chance of infection
If normal, 90% chance not infected
```
Multiple CRPT and ESR
If increased, 80% chance of infection
If normal, 95% chance not infected
Alpha defensin - expensive but more accurate
133
What are the treatment options for prosthetic infection?
Antibiotic suppression - reserved for patients who aren’t fit for surgery, multiple prosthetic joint infections, poor distal skin/soft tissues, low virulence infecting organisms, available oral antibiotics, patient tolerates antibiotics, prosthesis not loose.
Debridement and Implant retention (DAIR) - early postoperative infections or acute haematogenous infections, not for chronic infections (best results within the first week), prosthesis is not loose.
Excision Arthroplasty - high risk (frail, multiple comorbidities), low functional demand, uncontrolled with antibiotic suppression, high risk re-infection (poor skin or soft tissue), good infection control
134
What are the steps involved with Excision Arthroplasty?
Know the organism and their sensitivities
Debridement of all infected and dead tissues
Confirmatory intraoperative micro samples
Appropriate and sufficient antibiotic cover
Sufficient soft tissue cover/reconstruction
Sufficient, stable, joint reconstruction
135
What are the two types of Excision Arthroplasty?
One-stage exchange
Radical debridement
Dirty-clean approach
Implantation of new prosthesis - cemented with antibiotics in it
Two-stage exchange
Radial debridement
Local antibiotic space and systemic antibiotics
Interval stage
Implantation of new prosthesis as per aseptic reconstruction
136
What are the microorganisms that commonly cause prosthetic joint infection?
Staph Aureus
CNS infection
Enterococcus
MRSA
137
Why are propionibacteria much more of a significant problem in upper limbs?
They are colonisers of humans from the above the waist
Can even be shed by blinking the eyes
Therefore may represent more of a threat in upper limb prostheses and spines
Suspect they are a very significant pathogen of upper limb surgery
However also common contaminants of microbiology cultures
138
Why are Propionibacteria such a problem in prosthetic joint infection?
Because they are slow growing, even contaminants take 7 days to grow
Longer when causing clinical infection (Upper limb and spines)
- They rarely turn a broth cloudy
- Frequently don’t trigger blood culture detection systems
- You rely on finding them by Terminal subculture of prolonged broths
They are also very indolent organisms
- Seldom cause acute infections
- May not significantly raise inflammatory markers
139
How does Propionibacteria cause infection?
Mechanism likely to be due to Prop’ colonisation of skin and introduced at time of previous surgery
140
How can the lab help in the fight against prosthetic joint infection?
Minimise Contamination
Increase confidence that what grows is real
Use of Laminar flow
Accurate Identification to species level and beyond
Maximise Yield of hard to grow bugs
Prolonged enrichment broths
Terminal Subculture
141
Why is Malidi-tof useful?
Can now rapidly identify bacteria in minutes, very cheaply, right down to the sub-species.
142
What are the red flags for MSK malignancy?
```
Suspected infection
Systemically unwell
Unremitting night pain
PMH cancer
Constant/progressive non-mechanical pain
Rapid deterioration - inability to weight bear
Structural deformity
Loss of function
```
143
How to assess a MSK tumour?
Is the lesion neoplastic or infective?
Is it benign or malignant?
Is it primary or secondary? (image whole bone, CT chest/abdomen with contrast)
How extensive is it?
144
What aspects of a MSK tumour need to be determined?
Sclerotic or lytic
Zone of transition
Age of patient
```
Also:
Periosteal reaction
Cortical destruction
Location
Matrix
Polyostotic?
```
145
How to differentiate between sclerotic or lytic MSK tumour?
Most primary bone tumour are osteolytic
Sclerotic lesions in patients >20 years are often healed Benign lytic lesions in younger years
In older patient consider metastases (prostate/breast)
Always consider granulation and infection
146
How to identify the zone of transition in a MSK tumour?
The area between normal and abnormal bone
WIDE
Ill-defined border
Cardinal sign of malignancy
Can be mimicked by infection and eosinophilic granuloma
NARROW
Well-defined border
In young, almost certainly benign
In >40 consider plasmacytoma/myeloma
147
What impact does age have on a MSK tumour?
If >30 then thick metastasis or myeloma, if <40 then primary bone tumour most likely.
148
What are the different types of Periosteal reaction in a MSK tumour?
Reaction caused by any irritation to periosteum, trauma, infection, tumour etc
Appearance = speed of growth
Slow - chance for consolidation and bone formation e.g. callus
Fast - interrupts process and either causes layering (moderately aggressive) or continually bursts through periosteum (very aggressive)
- Sunburst spicules
- Onion skinning
- Codman's triangle - the edge of the periosteum is lifted off by the tumour
149
How might location effect the type of MSK tumour?
In body - can be a clue, humerus and either side of knee are most common and almost all tumours can be found here
In bone - epiphysis, metaphysis, diaphysis? Centric, eccentric, corical, juxtacortical?
Common links between location of tumour and diagnosis of certain types of cancer, but nothing is diagnostic.
150
How do the changes in the matrix give indication to the type of MSK tumour?
The appearance of the lesion itself is caused by mineralisation within it.
Chondroid - cartilaginous tumours e.g. chondrosarcoma, enchondroma ‘popcorn stippling’
Osteoid - bone forming tumours e.g. osteoid ‘fluffy’ ‘cloud-like’ ‘trabecular
151
Why should you consider whether a MSK tumour is polyostotic?
```
Most bone tumours exist in isolation
Multiple lesions - must consider other potential diagnoses
Metastases
Multifocal osteomyelitis
Myeloma
Hyperparathyroidism
```
152
What are the common types of bone tumour?
- Osteosarcoma: most common. The cancerous cells produce bone. Most often in children and young adults, in the bones of the leg or arm. In rare circumstances, osteosarcomas can arise outside of bones (extraskeletal osteosarcomas).
- Chondrosarcoma: Second most common form of bone cancer. The cancerous cells produce cartilage. Usually occurs in the pelvis, legs or arms in middle-aged and older adults.
- Ewing sarcoma: Most commonly arise in the pelvis, legs or arms of children and young adults.
153
What is inflammation?
Inflammation is a reaction of microcirculation
Movement of fluid and white blood cells into extra-vascular tissues
Involvement of pro-inflammatory cytokines
154
How does Crystal Disease & Infection present?
```
Rapid onset of symptoms
Very red & hot joints
Relevant clinical history
GOUT
- Medications e.g. diuretics
- Obesity
- Hypertension
- Alcohol
INFECTION – bacteraemia, age, immunosuppressed
- Joint aspiration helpful
```
155
What are the features of a normal synovial joint?
2 articulating bone surfaces covered with hyaline cartilage
Fibrous capsule lined with synovium
Joint space filled with synovial fluid
Inflammation of these structures=arthritis
156
Where does rheumatoid arthritis occur?
Primary site of pathology is the synovium of the joints
Tissues become inflamed and proliferate forming pannus which invades bone cartilage and ligaments leading to damage and deformities
157
What is the pathology of rheumatoid arthritis?
2 pathological characteristics of the synovium
- Inflammation
Chronic inflammatory reaction
Infiltration of lymphocytes, macrophages, plasma cells
- Proliferation
Tumour like mass “pannus”
Grows over articular cartilage
158
What is rheumatoid arthritis?
~1% population
2-3 x more common in women
Chronic, severe inflammatory, autoimmune disorder
Symmetrical, deforming, polyarthropathy
Hands & feet > 80% cases
Early morning stiffness
Can be subacute (20%) or insidious (70%) onset, acute in 10%
Progressive inflammation of joint
Pain, loss of function, deformity and damage
159
How can RA affect the body other than the joints?
```
Extra-articular involvement (15-25%)
Lungs
Heart
Gastrointestinal tract
Skin
Eyes
Kidneys
```
160
What are the symptoms of RA?
```
Joint pain often worse in morning
(may improve with activity)
Morning stiffness-several hours
Loss of function
General-fatigue, malaise
Extra-articular involvement
```
161
What is the aeitology of RA?
Aetiology unknown
Possibly multifactorial
genetic and environmental factors
Immunological basis
- Auto-antibodies present e.g. Rheumatoid Factor, anti cyclic citrullinated peptide
- Immune complexes
- Immunoglobulins and cytokines present in synovial fluid
- Defective cell-mediated immunity
- Association with other organ-specific autoimmune conditions
162
What are the features of a Rheumatoid nodule?
Palisading ring of macrophages and fibroblasts
Central fibrinoid necrosis
Cuff of connective tissue containing clusters of lymphocytes and plasma cells
163
How does RA affect the eyes? (extra-articular)
Sicca (dry eyes)
Secondary Sjogren’s syndrome
Episcleritis
Scleritis (corneal ulceration)
164
How does RA affect the neurological system?
- Mild primarily sensory peripheral neuropathy (Legs>arms)
- Entrapment neuropathies
- Cervical instability (Myelopathy and Atlanto-axial subluxation)
165
Where does RA cause entrapment neuropathies?
Soft tissue swelling due to inflammation at site where rigid structures contain nerves
- Carpal tunnel (median nerve)
- Elbow (ulnar)
- Popliteal space and fibular head (anterior tibial nerve)
- Tarsal tunnel (posterior tibial nerve)
166
How does RA cause cervical instability?
```
Instability of cervical spine
Advanced RA
Erosive process
C1-C2 region (subluxation)
Nerve root compression
Severe neck, occipital pain
Spinal cord compression
Neurological symptoms
- Sensory loss
- Weakness
- Disturbed bladder function
```
167
How does RA affect the haematological system?
Felty’s syndrome
Rare
Triad of seropositive RA + splenomegaly + neutropenia
```
Anaemia
Normochromic normocytic
Fe-deficiency
Peptic ulcers (NSAIDs, prednisolone use)
Haemolytic
rare, anti-body mediated or drugs
Part of pancytopenia- drugs, Felty’s
```
168
How does RA affect the lungs?
```
Pleural effusion
Interstitial lung disease
Rheumatoid nodules
Caplan’s syndrome
Small airways disease
```
169
What problems can RA cause in the heart?
Pericardial rub
Pericarditis
Pericardial effusion
170
What problems can RA cause in the kidneys?
Amyloidosis
- Advanced RA
- Deposits of amyloid protein
- 5-60% at post-mortem
- Proteinuria
Analgesic nephropathy
171
How does RA affect the skin?
Vasculitis
Small digital infarcts along nailbeds (most common)
Abrupt onset of ischaemic mononeuropathy (MMx) or progressive scleritis typical of rheumatoid vasculitis
Seropositive usually, persistently active disease
can occur when joints inactive
172
What are the investigations for RA?
```
Anaemia
High ESR/CRP
Positive RF 70%
Anti-Cyclic Citrullinated Peptide (Anti-CCP) antibody 70%
Anti-nuclear antibody (ANA) < 50%
Negative for all 30%
```
173
What is the Rheumatoid Factor?
Antibody against the Fc portion of IgG molecule as their antigen
Fc: region within heavy chain, role in modulating immune response
Occurs in many other diseases
174
What is the Anti-Cyclic Citrullinated Peptide Antibody?
Highly specific for RA (98%)
Can be present for years before disease manifestations
Marker of disease activity but not pathogenic itself
Citrullination
conversion αα arginine → αα citrulline
Protein shape change (positive to neutral charge)
Can occur in inflammation (activated macrophages)
175
What is a fracture?
A soft tissue injury with a loss of continuity of bone
176
How do you manage a fracture?
Reduction - pain relief, and push it back into alignment, reduces pain and pressure on the structures around
Immobilisation - put in a cast,
Rehabilitation - getting moving as quickly as possible to avoid stiffness and weakness
177
What are the stages of fracture healing?
1) Hematoma formation - neutrophils, macrophages, platelets
2) Fibrocartilaginous callus formation
3) Bony callus formation by osteocytes
4) Bone remodelling
178
What are the different types of fracture?
```
Transverse
Linear
Oblique, nondisplaced
Oblique, displaced
Spiral
Greenstick
Comminuted
```
179
What are the early local complications of fractures?
- Damage to surrounding structures - vascular (may need to repair the blood supply to the limb first), nerves, soft tissue, organs
- Contamination - infection
- Compartment syndrome - usually in your arm or leg, damage to blood supply there, if you don’t act quickly, you can lose the limb
180
What are the early systemic complications of fractures?
- Fat embolism - dyspnea, brown rash
- Shock
- Crush syndrome - crush on the muscle causes the muscle to die, release myoglobin which can cause renal failure
Usually occur when a patient hasn’t been able to move for a long time due to their injury:
- Pulmonary embolism
- Pneumonia
181
What are the late complications of fractures?
Delayed union, non-union, mal union (deformity due to medical error)
Avascular necrosis e.g. hip and scaphoid fractures - cut off the blood supply and bone begins to die, can lead to arthritis
Stiffness
Arthritis
Osteomyelitis - usually with open fractures
182
How does a fracture of the neck of the femur present?
```
Fall
Groin pain
Inability to weight bear
Externally rotated and short
Pain on axial loading
```
183
How is a fracture of the neck of the femur managed?
Analgesia - morphine and a regional nerve block (local anesthetic) - before AND after surgery
Replace hip joint - hemi (quicker but doesn’t last long) or total hip replacement
DHS or cannulated hip screws (when everything is still in line - not displaced)
184
How are ankle fractures classified according to the Weber classification?
Type A: Fracture of the lateral malleolus distal to the syndesmosis
Type B: Fracture of the fibula at the level of the syndesmosis.
Type C: Fracture of the fibula proximal to the syndesmosis.
185
What are the Ottawa Ankle Rules?
Bone tenderness at the posterior edge or tip of the lateral malleolus (A)
Bone tenderness at the posterior edge or tip of the medial malleolus (B)
OR.
An inability to bear weight both immediately and in the emergency department for four steps.
186
How is an ankle sprain managed?
Analgesia
Ice
Elevation
Early mobilisation
187
How is an open fracture treated?
Think about the infection risk - given antibiotics, tetanus injection
Splint the joint, wash/clean, take photos, document neurovascular pulse
188
What is a compartment syndrome?
```
Can occur in arm or leg
Increased in intracompartmental pressure
Puts pressure on nerves and arteries
Features:
Pain disproportionate to injury - worse on passive stretching
Paresthesia
Tense compartment
```
5 Ps: pain, pallor, perishingly cold, paralysis, pulselessness
189
How is compartment syndrome treated?
Fasciotomy - big incisions into the compartment, leave them for 24 hours to assess whether the muscle is viable, remove all the dead tissue, can be covered with a skin graft from the thigh.
190
What happens in an ACL injury?
Important stabiliser of the knee joint - limits anterior translation of the tibia and also contributes to knee rotational stability.
Presentation: swelling, pain, knee giving way
Investigations: positive lachman’s, anterior draw test, MRI
Management: RICE, conservative - physiotherapy, surgery - tendon repair, artificial graft
191
What are the red flags for cauda equina syndrome?
Bilateral sciatica
Severe or progressive bilateral neurological deficit of the legs, such as major motor weakness with knee extension, ankle eversion of foot dorsiflexion
Difficulty initiating micturition or impaired sensation of urinary flow, if untreated this may lead to irreversible - urinary retention with overflow urinary incontinence
Loss of sensation of rectal fullness, if untreated this may lead to irreversible - faecal incontinence
Perianal, perineal or genital sensory loss (saddle anaesthesia or paraesthesia)
Laxity of the anal sphincter
192
How would you manage cauda equina syndrome?
Management - urgent decompression and discectomy
| Take out the edge of the bone, check that the nerve root is untrapped.
193
How does shoulder dislocation present itself?
Usually when they happen once to someone, they continue to happen.
Most commonly an anterior dislocation.
- Pain
- Struggling to lift arm up
- Flattened deltoid
Check the neurovascular supply - remember the axillary nerve (test the sensation before and after putting the shoulder back in)
Given sedation and then push shoulder back in
In a sling for about 2 weeks.
Recurrent dislocation - may be due to an anatomical abnormality
Labrum makes the cup deeper - may have a tear in the labrum (this can be repaired)
194
How can rotator cuff injuries be classified?
Rotator cuff tears are classified as either acute (lasting <3 months) or chronic (lasting >3 months) tears. They can be either partial thickness or full thickness tears.
195
What is the management for rotator cuff injuries?
```
- Conservative
Analgesia
Physiotherapy
Activity modification
Corticosteroid injections
- Surgical
Arthroscopic
Other
```
196
What is a crystal?
Homogenous solid: ions bonded closely in ordered, repeating, symmetric arrangement
Stable, hard, high density
All animals need crystals
- strengthen endo & exo-skeleton
- remove excess ions through surface binding
197
When are crystals pathological?
```
Form in abnormal sites
Deposition of crystals results in local inflammatory response and tissue damage, over time it will cause joint damage too.
Joints
- Crystal arthropathies
- Urate (gout), calcium pyrophosphate (pseudo-gout), hydroxyapatite
Kidney
- nephrolithiasis (stones)
Gallbladder
- nephrolithiasis (stones)
```
198
What is crystal arthropathy?
Arthritis caused by crystal deposition in joint lining
Urate = gout
Pyrophosphate = pseudogout
Usually present with
- acutely with hot, swollen joints
- chronically with longer term damage (can try and prevent any more damage occurring)
Diagnosis is based on history, pattern, aspiration of joint to look for crystals and blood tests/XRs
199
How do gout and pseudo gout crystals differ?
Gout - Negatively birefringent needles
Pseduogout - Positively birefringent rhomboids
Thicker shape to them
200
What are the different types of gout?
Acute inflammation ‘gouty arthritis’ or ‘gout attack’
| Long term deposition ‘tophaceous gout’
201
What is the epidemiology of gout?
```
Commonest arthritis in men >40yrs
Uncommon men<30yrs
Rises in post-menopausal women
M:F – 2-7:1
Chinese, Polynesian, Filipino – uncommon in native country, but increased if westernized diet [racial underexcretion urate]
```
202
Where does gout most commonly occur?
```
Big toe
Ankle/foot
Knee
Finger
Elbow
```
203
What is uric acid?
Uric acid: produced from nucleic acids/ purine metabolism
Key enzyme in pathway is xanthine oxidase
Serum saturation = 0.3mmol/l - Urate in solution
Serum levels > 0.36mnol/l - Risk of crystal deposition
Plasma concentration >0.42mmol/l - Supersaturation; crystal deposition very likely
204
How do purines become monosodium urate?
Purines become HypoXanthine and then Xanthine via Xanthine oxidase.
It becomes uric acid then monosodium urate.
205
What are the stages of gout pathogenesis?
```
Renal, diet, drugs
Excessive urate
Urate crystals
Phagocyte activation
Inflammation
```
206
What affects the amount of crystals?
Levels of cartilage damage affected by OA or trauma
| Levels of crystal deposition affected by age, heredity and metabolic damage.
207
What is Hyperuricaemia?
```
Affects up to 10% population
Usually due to underexcretion
Major risk factor for gout
- Gout can occur with normal serum uric acid
- Acute gout can lower serum uric acid
```
208
What are the causes of under-excretion of uric acid?
```
Alcohol
Renal impairment/low urinary volume
Hypertension
Inherited?
Metabolic
Hypothyroid, Hyperparathyroidism
Obesity
Diabetes (insulin resistance)
Low dose aspirin (↓renal excretion)
Diuretics (esp thiazides)
Cyclosporin/ Tacrolimus
Ethambutol/ Pyrazinamide
[Lead poisoning]
```
209
What are the causes of over-excretion of uric acid?
```
Metabolic Syndrome - Hyperlipidaemia
Proliferative - Myeloproliferative disease, Cytotoxic drugs
Psoriasis
Lesch-Nyhan Syndrome
Alcohol
Excess meat, shellfish, offal
Gravy, meat extract
Yeast extract
Fructose sweetened drinks
```
210
What are the common precipitants of an gout attack?
Anything that causes sudden alteration in uric acid concentration
- Aggressive introduction of hypouricaemic therapy
- Alcohol or shellfish binges
- Sepsis, MI, acute severe illness
- Sudden cessation of hypouricaemic therapy
- Trauma (including minor), surgery, dehydration
Treatment
- Antiinflammatories; NSAID, colchicine, steroids
211
What are Tophi?
Onion like aggregates of urate crystals with inflammatory cells
6 - 9 months to control attacks
Up to 2 years for tophi to resolve
212
What is the longer term treatment of gout?
Xanthine oxidase inhibitors
Allopurinol (or febuxostat)
To reduce excessive urate
Side effects: 2% rash, headache, myalgia (very rare hypersensitivity syndrome)
100 mg/day to start
Increase by 100mg/fortnight
Watch renal function
Cover with Colchicine 500 μg od or bd for 6 months, or, NSAID for 6 weeks otherwise you may induce a gouty flare
(inhibits phagocyte activation and inflammation)
213
What is pseudogout?
AKA Pyrophosphate arthropathy
Deposition of Calcium Pyrophosphate crystals on joint surface
Crystals elicit acute inflammatory response
Typical distribution – (MCPs), wrists, knees, (ankles)
214
What is the epidemiology of pseudogout?
Predominantly disease of the elderly, tends to occur alongside degenerative disease
F:M 2:7.1
Chronic arthropathy overlap with osteoarthritis
Typically affects knees, wrists, shoulders and hips
215
What are the clinical features of pseudogout?
```
Acute monoarthritis in the elderly
Knee > wrist > shoulder > ankle > elbow
Polyarticular attacks rare
Severe pain, stiffness, swelling
Marked synovitis, difficult to distinguish from gout
Fever
Resolution in 1-3 weeks
```
216
What are the triggers of an acute attack of pseudogout?
Direct trauma to the joint
Intercurrent illness
Surgery – especially parathyroidectomy
Blood transfusion, IV fluid – affect the calcium homeostasis
T4 replacement
Joint lavage (wash out any loose tissue or debris)
Most are spontaneous, don’t always find a reason
217
How is pseudogout managed?
```
ACUTE
NSAIDs, analgesia
Aspiration, injection
Physiotherapy exercise – not a quick fix
LONG TERM
If continued inflammatory changes – trial of anti-rheumatic treatment e.g. methotrexate, hydroxychloroquine
Synovectomy in troublesome disease – synovium of the joint are stripped away
Surgery
```
