Orthopaedics and Rheumatology Flashcards

1
Q

What are the most commonly used treatments for osteoporosis?

A

Bisphosphonates, HRT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is osteoporosis?

A

A systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What condition can result from progressive vertebral fractures not being treated?

A

Kyphosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When does a person reach peak bone mass?

A

Around 30-40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the biggest risk factor for fracture?

A

Age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why does the risk of developing osteoporosis increase significantly following menopause?

A

The restraining effects of oestrogen on bone turnover are lost, which can result in bone resorption > formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does osteoporotic bone compared with non-osteoporotic bone on HR-pQCT imaging?

A

The trabeculae are larger and more numerous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is osteoporosis diagnosed?

A

DEXA scan used to calculate bone density. T-score of 2.5 or lower is diagnostic of osteoporosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is classified as severe osteoporosis?

A

A T-score of -2.5 or lower + a fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why do inflammatory diseases such as rheumatoid arthritis and inflammatory bowel disease increase the risk of osteoporosis?

A

Due to an increase in inflammatory cytokines, which increase bone resorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why does Cushing’s disease increase the risk of osteoporosis?

A

Cushing’s disease results in increased cortisol, which increases bone resorption and induces osteoblast apoptosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why do hyperthyroidism and primary hyperparathyroidism increase the risk of osteoporosis?

A

Thyroid hormone and PTH increase bone turnover.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why do low body weight and immobility increase the risk of osteoporosis?

A

Reduced skeletal loading increases resorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which medications increase the risk of osteoporosis?

A
Glucocorticoids
Depo-provera
Aromatase inhibitors
GnRH analogues
Androgen deprivation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name 4 risk factors for osteoporosis aside from medications/other conditions.

A
  1. Smoking
  2. Alcohol
  3. Family history of osteoporosis or fracture
  4. Previous fracture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the two types of osteoporosis treatment?

A
  1. Anti-resorptive, i.e. decreasing osteoclast activity and bone turnover
  2. Anabolic, i.e. increasing osteoblast activity and bone formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Bisphosphonates are the first line of treatment for osteoporosis. Name some.

A

Alendronate, risedronate, ibandronate, etidronate (oral)
Ibandronate can also be given intravenously
Zoledronate - once yearly intravenous infusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do bisphosphonates work?

A

They block the cholesterol synthesis pathway by inhibiting FPP synthase enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Denosumab is a monoclonal antibody that can be used to treat osteoporosis. What is its mechanism of action?

A

It is a monoclonal antibody to RANKL, acts as a decoy receptor and therefore disrupts the RANK pathway by preventing osteoclast activation, thereby reducing bone resoprtion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the main problem with denosumab?

A

There is a rebound increase in bone turnover when the drug is stopped.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which drug is used as a second line treatment for osteoporosis?

A

Teriparatide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does teriparatide work?

A

It is a PTH analogue, which increases bone density and improves trabecular structure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does inflammatory arthritis present?

A

Sudden onset of soft and squishy joint swelling, which is often red and warm to touch with stiffness in the morning and following periods of inactivity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Name 4 types of inflammatory arthritis

A
  1. Rheumatoid arthritis
  2. Seronegative spondyloarthritis
  3. Crystal arthritis
  4. Septic arthritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are the main risk factors for rheumatoid arthritis?
Family history | Smoking
26
Which joints tend to be affected by rheumatoid arthritis?
Symmetrical small joints of the hands, wrists and feet with sparing of the DIP joints Large joints may be involved later on in the disease process. No spinal involvement.
27
Which joints tend to be affected by seronegative arthritis?
Asymmetrical large joints | Spinal involvement
28
What non-joint symptoms are associated with seronegative arthritis?
Inflammatory bowel, GI infection, eye inflammation and psoriasis.
29
What are the main clinical features of psoriatic arthritis?
Pitting of the nails, nails lifting off, sausage toe (whole digit swells up as opposed to just the joint).
30
What may be different about a blood result for psoriatic arthritis when compared to other forms of inflammatory arthritis?
CRP may not be significantly raised
31
What are the main differences between inflammatory arthritis and osteoarthritis?
Osteoarthritis comes on much more gradually, typically in weight bearing joints (e.g. DIPJs, PIPJs, base of thumb, big toes), no early morning stiffness, normal CRP. Inflammatory arthritis usually symmetrical pattern and can be accompanied by fatigue, fever and night sweats.
32
What is crystal arthritis?
Gout/pseudogout. Acute intermittent episodes of joint inflammation due to crystal deposits (uric acid in the case of gout, calcium pyrophosphate in the case of pseudogout)
33
What are the main risk factors for gout?
Beer, renal impairment, diuretics, aspirin, family history
34
What blood tests would you carry out for suspected rheumatoid arthritis?
Rheumatoid factor (RF) CCP+ CRP +/- ESR
35
What blood test would you carry out for gout and when?
Uric acid to be checked between attacks of gout as the level drops during an actual attack.
36
Why should inflammatory arthritis be treated as soon as possible?
Inflammation is reversible but damage is not, therefore inflammation should be treated before damage occurs.
37
How does rheumatoid arthritis present?
Pain and swelling of joints (typically small joints of hands, wrists and forefeet) Early morning stiffness Sudden change in function Decreased grip strength/fist formation DIPJs are spared Usually symmetrical No deformity (unless presenting at advanced stage)
38
What changes may be seen on x-ray in rheumatoid arthritis?
Soft tissue swelling Periarticular osteopenia Joint space narrowing Bone erosion
39
What cheap and effective drugs are often used to treat rheumatoid arthritis?
Methotrexate Sulphasalazine Leflunomide Hydroxychloroquine
40
What biological treatments can be used to treat rheumatoid arthritis?
Anti-TNF medications (e.g. infliximab, etanercept, adalimumab) Rituximab (anti CD20) Abatacept (anti T cell) Tocilizumab (anti IL-6)
41
What inflammatory conditions does the term 'spondyloarthritis' cover?
Ankylosing spondylitis Enteropathic arthritis Reactive arthritis Psoriatic arthritis
42
What antigen, which is more prevalent in Scandinavians and some native American tribes, is linked with spondyloarthritis?
HLA B27 - human leukocyte antigen, class I surface antigen present on all cells except RBCs and encoded by MHC on chromosome 6.
43
What are the clinical features of spondyloarthritis?
Inflammation of the spine with possible fusion of vertebrae leading to kyphosis and stiff neck Swelling of Achilles tendon Patella tendon swelling Medial/lateral epicondyl swelling Acute anterior uveitis (photophobic, blurred vision) Skin psoriasis
44
What are the features of spondyloarthritis denoted by the SPINEACHE acronym?
``` Sausage digit Psoriasis Inflammatory back pain NSAID good response Enthesitis Arthritis Crohn's/Colitis/CRP elevation HLA-27 Eye (uveitis) ```
45
What features can be seen on x-ray of a person with ankylosing spondylitis?
'Bamboo spine' due to continuous line of calcification, which results in fusion of the vertebrae - Before this stage is reached, syndesmophytes can be seen in between the vertebrae, growing vertically along the anterior longitudinal ligament - Joint fusion of the sacroiliac joints
46
Why is ankylosing spondylitis sometimes misdiagnosed as sciatica?
Because as the sacroiliac joints are fusing, this causes a constant ache at the top of the buttock going into the buttock, which can sometimes go right down to the knee.
47
Which investigation is considered the 'gold standard' for diagnosis of ankylosing spondylitis?
MRI, which can be used to visualise acute sacroilitis
48
What are the features of inflammatory back pain?
Patients often under the age of 40 | Stiffness in the morning and evening, which often builds up over years and usually gets better with movement
49
What is a symptom of sacroilitis?
Alternating buttock pain
50
How is psoriatic arthritis treated?
Early intervention with DMARDs Possible introduction of anti-TNF drugs (etanercept, infliximab etc) IL-12/23 blockers (ustekinumab) IL-17 blockers (secukinumab)
51
What are DMARDs?
Disease-Modifying Anti-rheumatic drugs
52
Give four examples of DMARDs
1. Methotrexate 2. Leflunomide 3. Ciclosporin 4. Sulfasalazine
53
How does methotrexate reduce inflammation?
Methotrexate inhibits several enzymes that are required for nucleotide synthesis, which reduces inflammation and also cell division (methotrexate is also used in cancer treatment).
54
What is reactive arthritis?
Inflammation of the synovial membrane, tendons and fascia triggered by an infection at a distant site.
55
What kinds of infections are usually responsible for reactive arthritis?
GI infections such as salmonella, shigella and yersinia, STIs such as chlamydia and ureaplasma urealyticum
56
What other features may occur in reactive arthritis?
Mucopurulent discharge around the eye, keratoderma blenorrhagica, circinate balanitis.
57
What is enteropathic arthritis?
An episodic asymmetric lower limb arthritis associated with inflammatory bowel disease.
58
Which 5 things should make you think about spondyloarthritis?
1. Inflammatory back pain 2. Asymmetrical (large joint) arthritis 3. Skin psoriasis 4. Inflammatory bowel disease 5. Inflammatory eye disease
59
Name 2 inherited connective tissue diseases
Marfan's syndrome | Elher Danlos syndrome
60
Marfan's syndrome results in faulty collagen. What are the features of Marfan's syndrome?
Pectus excavatum Arachnodactyly Dilation of the aorta
61
What are the features of Ehler Danlos syndrome?
Hypermobile joints Stretchy skin Some types also cause vascular problems, which can lead to aneurysms
62
Name 4 autoimmune connective tissue diseases
1. Systemic lupus erythematosus 2. Systemic sclerosis 3. Primary Sjogren's syndrome 4. Dermatomyositis/polymositis
63
SLE sufferers can present with various rashes, but what type of rash is particularly common with this condition?
A 'butterfly' rash over the cheeks and nose
64
How does systemic lupus erythematosus present?
Symptoms can present in many systems, so the patient can show up in any department! Skin rashes, mucosa ulcers, alopecia, arthritis, neuro-psychiatric features (aseptic meningitis, strokes, headaches, seizures, anxiety), lupus nephritis, anaemia, thrombocytopenia, neutropenia
65
How is SLE diagnosed?
Antibody testing ANA (antinuclear antibody) should be positive, but not specific for lupus Specific test: double-stranded DNA antibody
66
How is SLE treated?
Can't be cured, but symptoms can be managed: Topical treatments: sunscreen, steroids Short term NSAIDs Hydroxychloroquine - safe option for arthritis and rashes Cytotoxic drugs e.g. azathioprine, mycophenolate, ciclosporin, methotrexate, cyclophosphamide
67
Raynaud's phenomenon is often seen in patients with connective tissue disorders. How is it diagnosed?
From skin colour change on exposure to cold. From white, to blue, to red.
68
What are the main features of systemic sclerosis?
Vasculopathy Excessive collagen deposition Auto-antibody production Inflammation
69
What are the 3 clinical subsets of systemic sclerosis?
1. Limited cutaneous 2. Diffuse cutaneous 3. SS without scleroderma (involves organs but not skin)
70
What are the features of limited cutaneous systemic sclerosis?
- Sclerodactyly - Long history of Raynaud's phenomenon - Late-stage complications - Pulmonary arterial hypertension
71
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 interstitial lung disease (fibrosis due to excessive collagen) - Ulcers (esp. digital) - Calcinosis - Telangiectasia - GI symptoms 'watermelon stomach' with chronic anaemia due to bleeding
72
How is Raynaud's phenomenon managed?
Gloves | Vasodilators e.g. nifedipine, iloprost, sildenafil, bosentan
73
How is renal crisis prevented in patients with systemic sclerosis?
ACE inhibitors
74
How is the risk of pulmonary arterial hypertension managed in systemic sclerosis?
Early detection with annual echo and pulmonary function tests
75
What are the options for treating skin oedema in systemic sclerosis?
No treatment Mycophenolate Autologous stem cell transplant
76
How is pulmonary fibrosis treated in systemic sclerosis?
Cyclophosphamide, nintedanib
77
What are the two types of Sjogren's syndrome?
Primary | Secondary - from other autoimmune diseases e.g. SLE, rheumatoid arthritis, scleroderma, primary biliary cirrhosis
78
What are the clinical features of primary Sjogren's syndrome?
``` Dry eyes and mouth Arthritis Rash Neurological features Vasculitis Interstitial lung disease Renal tubular acidosis ```
79
Patients with primary Sjogren's syndrome are more likely to be sensitive to what?
Gluten
80
Patients with primary Sjogren's syndrome have an increased risk of developing which type of cancer?
Lymphoma
81
What would you expect to see on lab tests for primary Sjogren's syndrome?
``` Positive ANA Positive RF Positive Ro and La antibodies Negative double-stranded DNA Raised immunoglobulins Abnormal salivary gland biopsy ```
82
How is primary Sjogren's syndrome treated?
Tear and saliva replacement Hydroxychloroquine for fatigue/myalgia/arthralgia/rash Corticosteroids/immunosuppressants for organ-threatening extra-glandular disease
83
What is the difference between dermatomyositis and polymyositis?
Polymyositis affects tendons and ligaments, dermatomyositis also affects the skin
84
How do dermatomyositis and polymyositis present?
Muscle weakness Dermatomyositis also presents with rash Can also affect lungs (interstitial lung disease)
85
What investigations are required for dermatomyositis and polymyositis?
Muscle enzymes, antibody screen, EMG, muscle/skin biopsy, PET-CT to check for malignancy (can also present as paraneoplastic syndrome), chest x-ray, pulmonary function tests, high resolution CT lungs.
86
What types of drugs are used to manage dermatomyositis and polymyositis?
Steroids | Immunosuppressive drugs
87
What is osteomyelitis?
Infection localised to the bone - literally means "bone marrow inflammation"
88
Which age groups are most at risk of osteomyelitis?
Bimodal age distribution - younger patients and older patients?
89
What possible cause of osteomyelitis is mostly seen in children and why?
Haematogenous seeding due to high blood flow in developing bones
90
What normally causes osteomyelitis in adolescents and adults?
Contiguous spread from direct trauma
91
What are the three routes via which a pathogen can find its way into the bone?
1. Direct inoculation of infection into the bone 'smashed window' e.g. trauma, surgery 2. Contiguous spread from soft tissues and joints 3. Haematogenous seeding
92
What three conditions affecting vasculature increase the risk of developing osteomyelitis?
1. Arterial disease 2. Sickle cell disease 3. Diabetes mellitus
93
What two conditions affecting the bones/joints increase the risk of developing osteomyelitis?
1. Inflammatory arthritis | 2. Prosthetic material
94
Where is osteomyelitis more likely to develop in children?
In the long bones
95
Where is osteomyelitis more likely to develop in adults over 50 years and why?
Vertebrae as vasculature increases with age, making bacterial seeding of the vertebral endplate more likely
96
Where is osteomyelitis more likely to develop in IV drug users?
Clavicle and pelvis
97
Which 3 pathogens are the usual causes of osteomyelitis?
Staph aureus Coagulase-negative staph Aerobic gram-negative bacilli
98
What are the symptoms of osteomyelitis?
Onset over several days | Dull pain at the site of OM, which may be aggravated by movement
99
What are the signs of osteomyelitis?
Systemic signs e.g. fever, rigors, sweats, malaise Local: tenderness, warmth, erythema, swelling In chronic OM may have non-healing ulcers and fractures
100
What might blood tests for osteomyelitis show?
WCC will be raised in acute OM but may be normal in chronic OM CRP may be normal or raised
101
What might a plain x-ray show in cases of chronic osteomyelitis?
``` Cortical erosion Periosteal reaction Mixed lucency Sclerosis Sequestra Soft tissue swelling ```
102
Why would an MRI scan be preferable to a plain x-ray for detecting early osteomyelitis?
It takes 1-2 weeks before any bone changes are seen on plain x-ray Marrow oedema can be seen from 3-5 days on MRI and can distinguish cortical, bone marrow and soft tissue inflammation.
103
What investigation would be used to make a definitive diagnosis of osteomyelitis?
Bone biopsy with culture and 16s RNA PCR
104
What are the differential diagnoses for osteomyelitis?
``` Soft tissue infection (e.g. cellulitis) Charcot joint Avascular necrosis of bone Gout Fracture Bursitis Malignancy ```
105
How is osteomyelitis treated?
Surgery with debridement/hardware replacement or removal Antimicrobial therapy with initial empirical treatment with broad spectrum antibiotics, then tailor to culture and sensitivity findings, administer for prolonged duration (weeks).
106
Which type of osteomyelitis requires treatment for at least six months?
TB osteomyelitis
107
What is the usual method of infection of joints?
Haematogenous spread
108
What investigations would be carried out for suspected joint infection?
Blood cultures | Aspiration of joint
109
What joint aspirate appearances would suggest infection?
Thick, opaque, sticky, turgid fluid
110
What would you expect to see on blood tests for a patient with joint infection?
Possibly raised WCC Raised CRP ESR rises and falls more slowly - depends on history
111
How is joint infection managed?
- Aspiration (always) - Antibiotics depending on aspiration - long course (minimum 6 weeks) - Joint washout/repeated aspiration until no recurrent effusion - Rest/splint/physio for rehab - Analgesia - Stop immunosuppression temporarily if possible
112
What is the next step if you suspect infection in a joint and the joint aspirate doesn't tell you?
Synovial biopsy (usually done by interventional radiologists)
113
How does gonococcal arthritis present?
Occurs alongside gonococcal infection | Fever, arthritis, tenosynovitis, maculopapular - pustular rash
114
What investigation should you carry out if you suspect gonococcal arthritis?
Mucous membrane swabs
115
What are the three most common organisms that infect prosthetic joints?
1. Coagulase negative staphylococcus 2. Staph aureus 3. Enterococcus
116
What is the most common route of infection in prosthetic joints?
Infection introduced when the joint is fitted (not haematogenous spread)
117
What precautions can be taken in theatre to help prevent infection of prostheses?
Sterility Prophylactic antibiotics Use of laminar flow
118
How do prosthetic joint infections present?
Sometimes with evidence of acute infection (hot, red, swollen, pus etc) but sometimes only low grade symptoms, e.g. patient has not been quite right since it was put in.
119
How should suspected prosthetic joint infection be investigated?
X-rays, FBC, ESR, CRP, aspirate and culture (preferably over extended period i.e. 14 days - patient must be off antibiotics)
120
What would you expect to see on blood tests for prosthetic joint infection?
WCC may or may not be raised | CRP may only be slightly raised
121
What are the treatment options for infected prosthesis?
- Antibiotic suppression (not preferred) - Debridement and retention of prosthesis - Excision arthroplasty - One or two-stage exchange arthroplasty - Amputation
122
What are the indications for antibiotic suppression?
- Patient unfit for surgery - Multiple prosthetic joint infections - Poor distal skin/soft tissues - Low virulence infecting organisms - Available oral antibiotics - Patient tolerates antibiotics - Prosthesis not loose - If not possible to eradicate infection through surgery
123
When would debridement and implant retention be used to treat prosthesis infection?
- Early post-op infections - Acute haematogenous infections i.e. not chronic infections
124
When might excision arthroplasty be indicated?
- High risk, frail patients with multiple comorbidities - Low functional demand - Uncontrolled with antibiotic suppression - High risk of re-infection (i.e. poor skin/soft tissues)
125
What antibiotics should be given to empirically treat a prosthetic joint infection?
Trick question - prosthetic joint infections should not be treated empirically with antibiotics. Always aspirate first!
126
What are the 4 Rs for treating fractures?
1. Resuscitate - you can't fix the fracture if the patient is dead 2. Reduce - realign the fracture, restore anatomy (vessels, muscles, nerves etc need to be in the right place) 3. Retain - keep in position e.g. fixation, plaster cast, skin traction 4. Rehabilitation
127
What 6 things need to be considered when looking at an x-ray of a fracture?
1. Which bone is it? 2. Is it intra- or extra-articular? 3. Position 4. Pattern 5. Condition 6. Displacement
128
What are the different patterns of fractures?
Transverse Oblique Spiral
129
What are the different 'conditions' of fractures?
1. Comminuted (lots of bits) 2. Segmental (two fractures with a segment in the middle with poor blood supply) 3. Impacted (hasn't moved far, blood supply likely intact)
130
What things need to be considered regarding displacement?
Length Alignment Rotation
131
What are the two forms of bone healing?
1. Bone remodelling cycle - direct, primary bone healing | 2. Callous formation - inflammatory reaction, indirect, secondary bone healing
132
What are the 4 stages of the bone remodelling cycle?
1. Resting 2. Resorption 3. Formation 4. Mineralisation
133
What conditions have to be met for primary healing of a fracture?
Absolute stability Gap of <1mm Compression
134
What are the 4 stages of callous formation?
1. Bleeding 2. Soft callous 3. Bony callous 4. Remodelling
135
What conditions have to be met for secondary healing of a fracture?
Relative but not absolute stability - if there is no movement at all, the cells are not stimulated and the callous doesn't form.
136
What can a patient do to improve bone healing?
Stop smoking Stop NSAIDs Improve nutrition
137
What is the most common condition affecting synovial joints?
Osteoarthritis
138
What mediates the pathogenesis of osteoarthritis?
Cytokines IL-1, TNF-a, NO
139
What are the main pathological features of osteoarthritis?
Loss of cartilage | Disordered bone repair
140
What causes synovial hypertrophy in osteoarthritis?
Wear and tear (as opposed to inflammatory response)
141
What are the five main risk factors for osteoarthritis?
1. Age 2. Gender (female preponderance) 3. Genetic predisposition 4. Obesity 5. Occupation
142
What are the main symptoms of osteoarthritis?
Pain | Functional impairment
143
What are the main signs of osteoarthritis?
Alteration in gait Joint swelling Other joint abnormalities (limited ROM, crepitus, tenderness, deformities)
144
What radiological features are often seen in osteoarthritis?
1. Loss of joint space 2. Osteophytes 3. Subchondral sclerosis 4. Subchondral cysts 5. Abnormalities of bone contour
145
Involvement of which joint is commonly seen osteoarthritis, but not in rheumatoid arthritis?
Distal interphalangeal joint (DIPJ)
146
Osteoarthritis can affect which joints in the hands?
DIP, PIP and CMC joints
147
Which nodes are seen at which joints of the hands in osteoarthritis?
Heberden's nodes seen at the DIP joints | Bouchard's nodes seen at the PIP joints
148
Which compartment of the knee is most likely to be affected by osteoarthritis?
Medial
149
What is used to treat erosive/inflammatory osteoarthritis in addition to standard management?
DMARDs - usually milder agents e.g. hydroxychloroquine as opposed to methotrexate
150
What is associated with 'locking' of the knee in osteoarthritis?
Loose body in the knee, i.e. a bone/cartilage fragment
151
What topical treatments can be used in the management of osteoarthritis?
NSAIDs | Capsaicin
152
What oral medications can be used in the management of osteoarthritis?
Paracetamol NSAIDs (with caution) Opioids
153
What transdermal patches can be used in the management of osteoarthritis?
Buprenorphine, lignocaine
154
What surgical procedures can be performed to help manage osteoarthritis?
Arthroscopy (for loose bodies) Osteotomy Arthroplasty Fusion (usually ankle and foot)
155
What type of crystals are formed in gout?
Urate crystals
156
What type of crystals are formed in pseudogout?
Pyrophosphate crystals
157
How does gout normally present?
Sudden onset of a hot, swollen joint with excruciating pain that normally resolves in a few weeks
158
Which joint is affected in 70% of gout cases?
1st MTPJ (big toe)
159
What is the target for gout treatment?
Xanthine, which is the precursor to uric acid formed from purines
160
At what level of urate in plasma does the risk of crystal deposition start to increase?
>0.36mmol/l
161
What things in a person's diet can increase the risk of gout?
Alcohol (especially beer) Fructose sweetened drinks Excess meat/shellfish/offal Yeast extract
162
What diseases can increase the risk of gout?
``` Myeloproliferative disease Psoriasis Tumour lysis syndrome Lesch-Nyhan syndrome Renal impairment ```
163
What medications can increase the risk of gout?
``` Thiazide diuretics Low dose aspirin Tacrolimus Ciclosporin Ethambutol Pyrazinamide ```
164
Most attacks of gout are spontaneous, but what things can possibly trigger an attack?
``` Direct trauma to the joint Intercurrent illness Alcohol/shellfish binge Surgery Dehydration ```
165
What investigations can be performed for gout?
- Fluid aspiration from the joints (needle-shaped crystals may be seen on sediment) - Routine bloods to exclude other diagnoses - Inflammatory markers (CRP often >100) - Uric acid (may not necessarily be raised but needed to inform treatment dose) - X-ray
166
What drugs are used to treat acute attacks of gout?
NSAIDs (use with caution as renal impairment is a risk factor for gout) Colchicine 500mg bd Prednisolone (oral or inject into joint)
167
What drug can be prescribed for chronic gout, but should not be started during an attack?
Allopurinol (or Febuxostat) - xanthine oxidase inhibitors
168
How does pseudogout present?
Sudden onset of hot, swollen joint similar to gout. However, affects different joints. Knees > wrist > shoulder > ankle > elbow
169
What conditions increase the risk of developing pseudogout?
``` Haemochromatosis Hyperparathyroidism Hypophosphatasia Hypomagnesaemia Diabetes Hyper/hypothyroidism ```
170
What investigations should be performed for pseudogout?
Routine bloods (including iron, PTH, PO4, Mg and TSH) Inflammatory markers Uric acid (should be normal) Joint aspiration (rhomboid-shaped crystals) X-ray
171
How are acute attacks of pseudogout treated?
NSAIDs if safe Colchicine Prednisolone (oral/injection)
172
How is chronic pseudogout treated?
Long term low dose prednisolone (if frequent attacks) - monitoring required Long term low dose colchicine Trial of hydroxychloroquine/methotrexate (~6 months only)
173
What is vasculitis?
Inflammation and necrosis of blood vessels with subsequent impaired blood flow
174
What are the local consequences of vasculitis?
Vessel wall destruction | Endothelial injury
175
What is seen on histology of vasculitis?
Vessel wall infiltration with the presence of neutrophils, mononuclear cells +/- giant cells Fibrinoid necrosis Leukocytoclasis (dissolution of leukocytes)
176
How is vasculitis classified?
With some difficulty is there is a lot of overlap. Generally classified by: 1. Size of vessel affected (small/medium/large) 2. Target organs 3. Presence or absence of anti-neutrophil cytoplasmic antibodies (ANCA)
177
Name 3 primary vasculitis disorders of large arteries
1. Giant cell arteritis 2. Takayasu's arteritis 3. Isolated CNS angiitis
178
What disorders can cause secondary vasculitis in large arteries?
Aortitis | Infection e.g. syphilis
179
Name 2 primary vasculitis disorders of medium arteries
1. Classical polyarteritis nodosa | 2. Kawasaki disease
180
What disorders can cause secondary vasculitis in medium arteries?
Infection e.g. hep B | Hairy cell leukaemia
181
Name 3 types of primary vasculitis that affect medium/small arteries
1. Wegener's granulomatosis 2. Churg-Strauss syndrome 3. Microscopic polyangiitis
182
What disorders can cause secondary vasculitis in medium/small arteries?
Autoimmune diseases Malignancy Drugs Infection e.g. HIV
183
Name 3 types of primary vasculitis affecting small vessels
1. Henoch Schonlein purpura 2. Essential mixed cytoglobulinaemia 3. Cutaneous leukocytoclastic angiitis
184
What disorders can cause secondary vasculitis in small vessels?
Drugs Malignancy Infection e.g. hep B/C
185
How does vasculitis present?
No single typical presentation, can be easily confused with other diseases Systemic illness, fever, arthralgia/arthritis, rash, weight loss, headache, foot drop, major event (e.g. stroke/bowel infarction)
186
Which type of vasculitis is ANCA positive?
Small/medium vessel vasculitis
187
What is giant cell arteritis?
Granulomatous arteritis affecting the aorta and larger vessels + extracranial branches of the carotid arteries
188
Which demographics are more at risk of developing giant cell arteritis?
Over 50s, twice as common in females
189
How does giant cell arteritis present?
``` Headache Scalp tenderness Jaw claudication Acute blindness (medical emergency) Non-specific malaise Associated symptoms of polymyalgia rheumatica ```
190
What are the diagnostic criteria for giant cell arteritis?
``` 3 or more of: Age > 50 New headache Temporal artery tenderness/decreased pulsation ESR > 50 Abnormal temporal artery biopsy ```
191
What is AION?
Arteritic anterior ischaemic optic neuropathy - causes sudden, painless monocular visual loss. The optic disc becomes pale and swollen, often with flame-shaped haemorrhages at the margin.
192
What investigations should be performed if giant cell arteritis is suspected?
- Suspect in >50 developing new type of headache with jaw claudication and unexplained fever - Check ESR/CRP - Temporal artery biopsy
193
How is giant cell arteritis treated?
Prednisolone (prompt treatment) - 30-40mg per day if no visual disturbance, 80mg/day if visual disturbance Should respond within 48 hours Also: - Steroid sparing agents e.g. azathioprine, methotrexate, biologics Prophylaxis of osteoporosis (lifestyle advice, calcium/vitamin D, bisphosphonate)
194
What is Wegener's granulomatosis also known as?
Granulomatosis with polyangiitis
195
What antibodies are associated with Wegener's/GPA?
cANCA
196
What are the symptoms of Wegener's/GPA?
``` Depends on system affected e.g. URT - sinusitis/otitis/nasal crusting Lungs - pulmonary nodules, haemorrhage Kidneys - glomerulonephritis Skin - purpura, ulcers Nervous system - mononeuritis, multiplex/CNS, vasculitis Eye - proptosis, scleritis, episcleritis, uveitis etc. etc. ```
197
What nasal deformity might be seen in Wegener's/GPA?
Saddle nose deformity
198
How is Wegener's/GPA treated?
Steroids (dose depending on severity) Cyclophosphamide Biologics Methotrexate, mycophenolate, azathioprine