MSK Flashcards
1
Q
What is the peak age of incidence for Acute Lymphoblastic Leukaemia (ALL), and which gender is more commonly affected?
A
The peak incidence of ALL is around 2-5 years of age, with boys being affected slightly more commonly than girls.
2
Q
What are the features of Acute Lymphoblastic Leukaemia (ALL) associated with bone marrow failure?
A
Features associated with bone marrow failure include:
- Anaemia: Lethargy and pallor
- Neutropenia: Frequent or severe infections
- Thrombocytopenia: Easy bruising, petechiae
3
Q
What are other clinical features of Acute Lymphoblastic Leukaemia (ALL)?
A
Other features include:
- Bone pain (secondary to bone marrow infiltration)
- Splenomegaly
- Hepatomegaly
- Fever (present in up to 50% of new cases, representing infection or constitutional symptoms)
- Testicular swelling
4
Q
What are the types of Acute Lymphoblastic Leukaemia (ALL)?
A
The types of ALL are:
- Common ALL: 75%, CD10 present, pre-B phenotype
- T-cell ALL: 20%
- B-cell ALL: 5%
5
Q
What are the poor prognostic factors for Acute Lymphoblastic Leukaemia (ALL)?
A
Poor prognostic factors include:
- Age < 2 years or > 10 years
- WBC > 20 * 10^9/L at diagnosis
- T or B cell surface markers
- Non-Caucasian ethnicity
- Male sex
6
Q
What are ankle fractures commonly associated with?
A
Admission to casualty.
7
Q
What rules help guide the use of x-rays in ankle injuries?
A
The Ottawa ankle rules.
8
Q
According to the Ottawa ankle rules, when are x-rays necessary?
A
X-rays are necessary if there is pain in the malleolar zone and:
- Inability to weight bear for 4 steps.
- Tenderness over the distal tibia.
- Bone tenderness over the distal fibula.
9
Q
What are some classification systems used to describe ankle fractures?
A
Potts, Weber, and AO systems.
10
Q
How is the Weber classification system related to ankle fractures?
A
It is related to the level of the fibular fracture.
11
Q
What defines a Weber Type A fracture?
A
A fracture below the syndesmosis.
12
Q
What defines a Weber Type B fracture?
A
A fracture that starts at the level of the tibial plafond and may extend proximally to involve the syndesmosis.
13
Q
What defines a Weber Type C fracture?
A
A fracture above the syndesmosis, which may itself be damaged.
14
Q
What is a Maisonneuve fracture?
A
A subtype of ankle fracture involving a spiral fibular fracture with syndesmosis disruption and widening of the ankle joint, requiring surgery.
15
Q
What factors determine the management of ankle fractures?
A
Stability of the ankle joint and patient co-morbidities.
16
Q
Why should all ankle fractures be promptly reduced?
A
To remove pressure on the overlying skin and prevent necrosis.
17
Q
What is the typical management for young patients with unstable or high-velocity ankle injuries?
A
Surgical repair, often using a compression plate.
18
Q
Why are elderly patients with unstable ankle injuries often managed conservatively?
A
Because their thin bone does not hold metalwork well, and they fare better with conservative management.
19
Q
What is ankylosing spondylitis associated with genetically?
A
HLA-B27.
20
Q
What is the typical demographic for ankylosing spondylitis?
A
Males aged 20-30 years old, with a sex ratio of 3:1.
21
Q
What are the typical presenting symptoms of ankylosing spondylitis?
A
Lower back pain and stiffness of insidious onset, worse in the morning and improving with exercise, and pain at night that improves on getting up.
22
Q
What does clinical examination of ankylosing spondylitis reveal?
A
Reduced lateral flexion, reduced forward flexion (assessed with Schober’s test), and reduced chest expansion.
23
Q
How is Schober’s test performed?
A
A line is drawn 10 cm above and 5 cm below the back dimples. The distance between the two lines should increase by more than 5 cm when the patient bends forward.
24
Q
What are the ‘A’s associated with ankylosing spondylitis?
A
Apical fibrosis, Anterior uveitis, Aortic regurgitation, Achilles tendonitis, AV node block, Amyloidosis, Cauda equina syndrome.
25
What percentage of patients with ankylosing spondylitis experience peripheral arthritis, and in which gender is it more common?
25%, more common in females.
26
What is another name for anterior uveitis?
Iritis.
27
What part of the eye is affected in anterior uveitis?
The anterior portion of the uvea, including the iris and ciliary body.
28
What genetic marker is anterior uveitis associated with?
HLA-B27.
29
What are the features of anterior uveitis?
Acute onset, Ocular discomfort and pain (may increase with use), Small and/or irregular pupil, Photophobia (often intense), Blurred vision, Red eye, Lacrimation, Ciliary flush (ring of red spreading outwards), Hypopyon (pus and inflammatory cells in the anterior chamber), Visual acuity initially normal, later impaired.
30
What conditions are associated with anterior uveitis?
Ankylosing spondylitis, Reactive arthritis, Ulcerative colitis, Crohn's disease, Behcet's disease, Sarcoidosis (may present with bilateral disease).
31
How is anterior uveitis managed?
Urgent review by ophthalmology, Cycloplegics (e.g., atropine, cyclopentolate) to dilate the pupil and relieve pain/photophobia, Steroid eye drops.
32
What is cervical spondylosis?
A degenerative condition affecting the cervical spine, essentially osteoarthritis of the cervical vertebral bodies.
33
What causes neurological dysfunction in cervical spondylitic myelopathy?
Narrowing of the spinal canal, which presses on the spinal cord.
34
What percentage of patients with cervical spondylosis are thought to develop myelopathy?
5-10%.
35
What are the features of cervical spondylitic myelopathy?
Motor weakness, sensory loss, and bladder/bowel dysfunction, Neck pain, Wide-based, ataxic, or spastic gait, Upper motor neuron weakness in the lower legs (increased reflexes, increased tone, and upgoing plantars), Bladder dysfunction, such as urgency or retention.
36
What is cervical spondylosis?
A degenerative condition affecting the cervical spine, including the intervertebral discs, vertebral bodies, and facet joints, often referred to as 'cervical osteoarthritis.'
37
What is the prevalence of cervical spondylosis in individuals over 60?
More than 85% of individuals over the age of 60 show radiographic evidence of cervical spondylosis, though many are asymptomatic.
38
What are the main steps in the pathogenesis of cervical spondylosis?
Intervertebral disc degeneration: Dehydration and shrinkage of the nucleus pulposus lead to reduced disc height and elasticity. Osteophyte formation: Bone spurs develop to stabilise the spine, potentially encroaching on the spinal canal and intervertebral foramina. Facet joint arthropathy: Degenerative changes in facet joints cause instability, inflammation, and nerve root or spinal cord compression. Ligamentous hypertrophy: Thickening of ligaments like the ligamentum flavum contributes to spinal canal stenosis.
39
What are the common clinical features of cervical spondylosis?
Chronic neck pain with stiffness and limited range of motion. Radiculopathy: Radicular pain, paraesthesia, and weakness in the upper limbs following a dermatomal pattern. Myelopathy: Symptoms include clumsiness in the hands, gait disturbance, limb weakness, and bowel/bladder dysfunction in advanced cases. Occipital headaches from irritation of cervical nerve roots or upper cervical muscles.
40
What findings may be observed on clinical examination of cervical spondylosis?
Reduced neck range of motion, tenderness over the cervical spine, and signs of radiculopathy (e.g., Spurling's test) or myelopathy (e.g., hyperreflexia, gait instability).
41
What imaging modalities are used for diagnosing cervical spondylosis?
X-rays: Show disc space narrowing, osteophytes, and facet joint arthropathy. MRI: Gold standard for detailed soft tissue imaging of the spinal cord, nerve roots, and discs. Electrophysiological studies: Nerve conduction studies and electromyography help differentiate cervical radiculopathy from other conditions.
42
What are the conservative management options for cervical spondylosis?
Analgesia: NSAIDs as first-line pain management. Physiotherapy: Exercises for neck strength, flexibility, and postural training. Cervical collar: Temporary use for acute symptom relief, avoiding long-term use to prevent muscle weakness.
43
What interventional procedures are available for cervical spondylosis?
Cervical epidural steroid injections: For temporary relief of radicular symptoms by reducing inflammation. Facet joint injections or radiofrequency ablation: For patients with chronic facet-mediated pain.
44
What is the initial symptom of chickenpox?
Fever.
45
What is the progression of the rash in chickenpox?
Starts as macular, then papular, and finally vesicular.
46
Where does the chickenpox rash typically start?
On the head and trunk before spreading.
47
How severe is the systemic upset in chickenpox?
It is usually mild.
48
What are the prodromal symptoms of measles?
Irritability, conjunctivitis, and fever.
49
What are Koplik spots?
White spots ('grain of salt') on the buccal mucosa, seen in measles.
50
Where does the measles rash start and spread?
Starts behind the ears and spreads to the whole body, becoming blotchy and confluent.
51
What are the initial symptoms of mumps?
Fever, malaise, and muscular pain.
52
What is parotitis and how does it progress in mumps?
Parotitis is pain in the parotid glands, starting unilaterally and becoming bilateral in 70% of cases.
53
What is the rash like in rubella?
A pink maculopapular rash that starts on the face and spreads to the whole body, usually fading by days 3-5.
54
Which lymph nodes are commonly involved in rubella?
Suboccipital and postauricular lymphadenopathy.
55
What is another name for erythema infectiosum?
Fifth disease or 'slapped-cheek syndrome.'
56
What virus causes erythema infectiosum?
Parvovirus B19.
57
What are the symptoms of erythema infectiosum?
Lethargy, fever, headache, and a 'slapped-cheek' rash that spreads to the proximal arms and extensor surfaces.
58
What causes scarlet fever?
Erythrogenic toxins produced by Group A haemolytic streptococci.
59
What are the symptoms of scarlet fever?
Fever, malaise, tonsillitis, 'strawberry' tongue, and a rash with fine punctate erythema sparing the area around the mouth (circumoral pallor).
60
What virus causes hand, foot, and mouth disease?
The coxsackie A16 virus.
61
What are the symptoms of hand, foot, and mouth disease?
Mild systemic upset, sore throat, fever, and vesicles in the mouth and on the palms and soles of the feet.
62
How common are cleft lip and palate?
They affect around 1 in every 1,000 babies.
63
What are the most common variants of cleft lip and palate?
Isolated cleft lip (15%), Isolated cleft palate (40%), Combined cleft lip and palate (45%).
64
What is the inheritance pattern of cleft lip and palate?
Polygenic inheritance.
65
How does maternal antiepileptic use affect cleft lip and palate risk?
It increases the risk.
66
What causes cleft lip developmentally?
Failure of the fronto-nasal and maxillary processes to fuse.
67
What causes cleft palate developmentally?
Failure of the palatine processes and nasal septum to fuse.
68
What are the problems associated with cleft lip and palate?
Feeding difficulties, which may benefit from orthodontic devices. Speech problems; 75% of children develop normal speech with therapy. Increased risk of otitis media, particularly in cleft palate babies.
69
At what age is cleft lip typically repaired?
Practices vary, but repair usually occurs from the first week of life to three months.
70
At what age is cleft palate typically repaired?
Between 6-12 months of age.
71
What is developmental dysplasia of the hip (DDH)?
A condition replacing the term 'congenital dislocation of the hip,' affecting around 1-3% of newborns.
72
What are the risk factors for DDH?
Female sex: 6 times greater risk, Breech presentation, Positive family history, Firstborn children, Oligohydramnios, Birth weight > 5 kg, Congenital calcaneovalgus foot deformity.
73
Which hip is more commonly affected by DDH?
The left hip.
74
What percentage of DDH cases are bilateral?
Around 20%.
75
Which infants require routine ultrasound screening for DDH?
Those with a first-degree family history of hip problems in early life, Breech presentation at or after 36 weeks gestation, Multiple pregnancy.
76
What are the tests used to screen for DDH in newborns and at the six-week check?
The Barlow and Ortolani tests.
77
What does the Barlow test assess?
It attempts to dislocate an articulated femoral head.
78
What does the Ortolani test assess?
It attempts to relocate a dislocated femoral head.
79
What are other clinical signs of DDH?
Symmetry of leg length, Level of knees when hips and knees are bilaterally flexed, Restricted abduction of the hip in flexion.
80
What imaging modality is used to confirm a diagnosis of DDH in infants under 4.5 months?
Ultrasound.
81
What imaging modality is used if the infant is older than 4.5 months?
X-ray.
82
What is the management for unstable hips in infants under 3-6 weeks?
Most unstable hips will spontaneously stabilise by 3-6 weeks of age.
83
What device is used to manage DDH in children younger than 4-5 months?
A Pavlik harness (dynamic flexion-abduction orthosis).
84
What is the management for older children with DDH?
Surgery may be required.
85
What is discitis?
An infection in the intervertebral disc space that can lead to complications such as sepsis or an epidural abscess.
86
What are the main features of discitis?
Back pain, General features: pyrexia, rigors, sepsis, Neurological features: changing lower limb neurology (if an epidural abscess develops).
87
What is the most common bacterial cause of discitis?
Staphylococcus aureus.
88
What are the possible causes of discitis?
Bacterial (most commonly Staphylococcus aureus), Viral, TB, Aseptic.
89
What imaging modality has the highest sensitivity for diagnosing discitis?
MRI.
90
When might a CT-guided biopsy be needed in discitis?
To guide antimicrobial treatment.
91
What is the standard treatment for discitis?
Six to eight weeks of intravenous antibiotic therapy.
92
What is the key factor in choosing antibiotics for discitis treatment?
Identifying the organism with a positive culture (e.g., blood culture or CT-guided biopsy).
93
Why should patients with discitis be assessed for endocarditis?
Discitis is usually due to haematogenous seeding of the vertebrae, implying prior bacteraemia, which may also have seeded other areas like the heart.
94
What tests are used to assess for endocarditis in patients with discitis?
Transthoracic echo or transesophageal echo.
95
What are the complications of discitis?
Sepsis
Epidural abscess
96
What is gout?
A form of inflammatory arthritis characterized by acute episodes of joint pain, swelling, and erythema, often with symptom-free periods between flares.
97
How quickly do acute gout episodes reach maximal intensity?
Within 12 hours.
98
What are the main symptoms of a gout flare?
Significant pain
Swelling
Erythema
99
What percentage of first presentations of gout affect the 1st metatarsophalangeal (MTP) joint?
Around 70%.
100
What is the term for gout affecting the 1st MTP joint?
Podagra.
101
What other joints are commonly affected by gout?
Ankle
Wrist
Knee
102
What can happen if gout is left untreated?
Repeated acute episodes can lead to chronic joint damage.
103
What is the role of uric acid measurement in gout diagnosis?
A uric acid level ≥ 360 µmol/L supports a diagnosis of gout.
## Footnote
If uric acid level is < 360 µmol/L during a flare and gout is strongly suspected, repeat measurement at least 2 weeks after the flare has settled.
104
What is the hallmark finding in synovial fluid analysis for gout?
Needle-shaped negatively birefringent monosodium urate crystals under polarised light.
105
What are the radiological features of gout?
Joint effusion (early sign)
Well-defined 'punched-out' erosions with sclerotic margins in a juxta-articular distribution, often with overhanging edges
Relative preservation of joint space until late disease
Eccentric erosions
No periarticular osteopenia (in contrast to rheumatoid arthritis)
Soft tissue tophi may be seen
106
What is haemophilia?
An X-linked recessive disorder of coagulation caused by a deficiency of clotting factors.
107
What clotting factor is deficient in haemophilia A?
Factor VIII.
108
What clotting factor is deficient in haemophilia B (Christmas disease)?
Factor IX.
109
What percentage of haemophilia cases have no family history?
Up to 30%.
110
What are the main clinical features of haemophilia?
Haemoarthroses
Haematomas
Prolonged bleeding after surgery or trauma
111
What are the typical blood test findings in haemophilia?
Prolonged APTT
Normal bleeding time, thrombin time, and prothrombin time
112
What complication can develop in 10-15% of patients with haemophilia A?
Development of antibodies to factor VIII treatment.
113
What are the typical features of influenza?
Fever > 38ºC
Myalgia
Lethargy
Headache
Rhinitis
Sore throat
Cough
Diarrhoea and vomiting
114
When should antiviral treatment for influenza be considered?
If all the following criteria are met:
The patient is in an at-risk group or at risk of serious complications:
65 years old
Pregnant
Chronic disease (respiratory, cardiac, renal, hepatic, neurological)
Diabetes
Immunosuppressed
Morbidly obese
Circulating influenza nationally (typically during winter).
Treatment can start within 48 hours of symptom onset.
115
What is the first-line antiviral treatment for influenza?
Oseltamivir.
116
What is the second-line antiviral treatment for influenza?
Zanamivir.
117
What is the typical presentation of transient synovitis in children?
Acute onset limp, usually following a viral infection, with a well or mildly febrile child. It is more common in boys aged 2-12 years.
118
How does septic arthritis or osteomyelitis present in children?
With an unwell child and a high fever.
119
How does juvenile idiopathic arthritis typically present in a limping child?
The limp may be painless.
120
What feature of the history often points to trauma as the cause of a limp in a child?
A clear history of injury.
121
How is developmental dysplasia of the hip usually detected, and who is more at risk?
It is typically detected in neonates and is 6 times more common in girls.
122
What age group is most commonly affected by Perthes disease, and what is the underlying cause?
Children aged 4-8 years, caused by avascular necrosis of the femoral head.
123
What is slipped upper femoral epiphysis, and in what age group does it typically occur?
A condition involving postero-inferior displacement of the femoral head epiphysis, most common in children aged 10-15 years.
124
What are some red flags for lower back pain?
Age < 20 years or > 50 years, History of previous malignancy, Night pain, History of trauma, Systemically unwell (e.g., weight loss, fever)
125
What are the clinical features of facet joint-related lower back pain?
May be acute or chronic, Pain worse in the morning and on standing, Pain over the facets on examination, Pain worse on extension of the back
126
What are the typical symptoms of spinal stenosis?
Gradual onset, Unilateral or bilateral leg pain, numbness, and weakness (with or without back pain), Pain worse on walking and relieved by sitting down, leaning forward, or crouching, Clinical examination often normal
127
How is spinal stenosis diagnosed?
It requires MRI to confirm the diagnosis.
128
What are the typical features of ankylosing spondylitis-related lower back pain?
Typically occurs in young men, Presents with lower back pain and stiffness, Stiffness is worse in the morning and improves with activity, Peripheral arthritis occurs in 25% of cases (more common in females)
129
What are the key features of lower back pain caused by peripheral arterial disease?
Pain on walking, relieved by rest, Absent or weak foot pulses, Signs of limb ischemia, Past history may include smoking and other vascular diseases
130
What is multiple myeloma (MM)?
A haematological malignancy characterised by plasma cell proliferation due to genetic mutations occurring as B-lymphocytes differentiate into mature plasma cells.
131
What is the median age at presentation for multiple myeloma?
70 years old.
132
What mnemonic is used to remember the key features of myeloma?
CRABBI: Calcium, Renal, Anaemia, Bleeding, Bones, Infection.
133
What causes hypercalcaemia in multiple myeloma?
Increased osteoclastic bone resorption caused by cytokines (e.g., IL-1, tumour necrosis factor) released by myeloma cells.
134
What are the symptoms of hypercalcaemia in myeloma?
Constipation, nausea, anorexia, and confusion.
135
What causes renal impairment in multiple myeloma?
Monoclonal immunoglobulin light chain deposition in renal tubules, amyloidosis, nephrocalcinosis, or nephrolithiasis.
136
What are the symptoms of renal impairment in myeloma?
Dehydration and increased thirst.
137
What causes anaemia in multiple myeloma?
Bone marrow crowding suppresses erythropoiesis.
138
What are the symptoms of anaemia in myeloma?
Fatigue and pallor.
139
What causes bleeding in multiple myeloma?
Thrombocytopenia due to bone marrow crowding.
140
What bone-related symptoms are seen in multiple myeloma?
Pain, lytic bone lesions, and an increased risk of pathological fractures.
141
Why are infections common in myeloma?
Due to reduced production of normal immunoglobulins.
142
What other features may occur in multiple myeloma?
Amyloidosis, carpal tunnel syndrome, neuropathy, and hyperviscosity.
143
What are the key blood investigation findings in myeloma?
Anaemia, rouleaux formation on blood film, renal failure, and hypercalcaemia.
144
What is found on protein electrophoresis in multiple myeloma?
Monoclonal IgA/IgG proteins in serum and Bence Jones proteins in urine.
145
How is the diagnosis of myeloma confirmed?
Bone marrow aspiration showing significantly raised plasma cells.
146
What imaging findings are associated with myeloma?
'Rain-drop skull' on X-ray or lytic bone lesions on whole-body MRI.
147
What are the major diagnostic criteria for multiple myeloma?
Plasmacytoma, ≥30% plasma cells in bone marrow, and elevated M protein levels in blood or urine.
148
What are the minor diagnostic criteria for multiple myeloma?
10-30% plasma cells in bone marrow, minor M protein elevation, osteolytic lesions, and low levels of non-myeloma antibodies.
149
What is neoplastic spinal cord compression?
An oncological emergency caused by compression of the spinal cord, often due to vertebral body metastases, affecting up to 5% of cancer patients.
150
What cancers are commonly associated with spinal cord compression?
Lung, breast, and prostate cancer.
151
What is the earliest and most common symptom of spinal cord compression?
Back pain.
152
How does back pain in spinal cord compression typically present?
It may worsen when lying down or coughing.
153
What neurological features may occur in spinal cord compression?
Lower limb weakness, sensory loss, and numbness.
154
How do neurological signs differ based on the level of the lesion in spinal cord compression?
Lesions above L1 cause upper motor neuron signs and a sensory level; lesions below L1 cause lower motor neuron signs and perianal numbness.
155
How are tendon reflexes affected in spinal cord compression?
Reflexes are increased below the lesion level and absent at the lesion level.
156
What is the key imaging investigation for spinal cord compression?
Urgent whole-spine MRI within 24 hours of presentation.
157
What is the first-line medical management for spinal cord compression?
High-dose oral dexamethasone.
158
What specialist intervention should be urgently considered in spinal cord compression?
Oncological assessment for radiotherapy or surgery.
159
What is osteoarthritis (OA) of the hand also referred to as?
Nodal arthritis.
160
What causes osteoarthritis of the hand?
Loss of cartilage at synovial joints, often accompanied by degeneration of underlying bone.
161
What is the gender ratio for osteoarthritis of the hand?
It is more common in women with a male-to-female ratio of 1:3.
162
At what age does hand osteoarthritis typically present?
Rarely before 55 years of age.
163
Which joints are most commonly affected by hand osteoarthritis?
Carpometacarpal joints (CMC), distal interphalangeal joints (DIPJs), and less commonly the proximal interphalangeal joints (PIPJs).
164
What are Heberden's nodes?
Painless bony swellings at the distal interphalangeal joints (DIPJs).
165
What are Bouchard's nodes?
Painless bony swellings at the proximal interphalangeal joints (PIPJs).
166
What deformity is referred to as 'squaring of the thumbs' in OA?
Fixed adduction of the thumb due to deformity of the carpometacarpal joint.
167
What distinguishes stiffness in hand OA from rheumatoid arthritis?
Stiffness in hand OA lasts only a few minutes, whereas in rheumatoid arthritis it is prolonged.
168
What risk factors increase the likelihood of hand osteoarthritis?
Previous joint trauma, obesity, hypermobility, and certain occupations such as cotton workers and farmers.
169
Which condition reduces the risk of developing osteoarthritis?
Osteoporosis.
170
What radiological features are seen in hand osteoarthritis?
Osteophytes and joint space narrowing.
171
When can radiological signs of OA be visible relative to symptoms?
Signs may be visible on X-ray before symptoms develop.
172
What is osteomalacia?
Softening of the bones secondary to low vitamin D levels, leading to decreased bone mineral content.
173
What term is used for osteomalacia in growing children?
Rickets.
174
What are the main causes of osteomalacia?
Vitamin D deficiency, malabsorption, lack of sunlight, diet, chronic kidney disease, drug-induced (e.g. anticonvulsants), inherited (e.g. hypophosphatemic rickets), liver disease (e.g. cirrhosis), and coeliac disease.
175
What are the key features of osteomalacia?
Bone pain, bone/muscle tenderness, fractures (especially femoral neck), and proximal myopathy leading to a waddling gait.
176
What blood test abnormalities are associated with osteomalacia?
Low vitamin D levels, low calcium and phosphate (in ~30%), and raised alkaline phosphatase (in 95-100% of patients).
177
What radiological feature is characteristic of osteomalacia?
Translucent bands (Looser's zones or pseudofractures) on X-ray.
178
What is the treatment for osteomalacia?
Vitamin D supplementation (with an initial loading dose) and calcium supplementation if dietary calcium is inadequate.
179
What is osteomyelitis?
Infection of the bone, subclassified into haematogenous and non-haematogenous osteomyelitis.
180
What are the characteristics of haematogenous osteomyelitis?
Results from bacteraemia, usually monomicrobial, most common in children, and vertebral osteomyelitis is the most common form in adults.
181
What are the risk factors for haematogenous osteomyelitis?
Sickle cell anaemia, intravenous drug use, immunosuppression (medication or HIV), and infective endocarditis.
182
What are the characteristics of non-haematogenous osteomyelitis?
Results from contiguous spread of infection from adjacent soft tissues or direct injury to bone, often polymicrobial, and most common in adults.
183
What are the risk factors for non-haematogenous osteomyelitis?
Diabetic foot ulcers, pressure sores, diabetes mellitus, and peripheral arterial disease.
184
What is the most common cause of osteomyelitis?
Staphylococcus aureus, except in patients with sickle-cell anaemia, where Salmonella species predominate.
185
What is the imaging modality of choice for osteomyelitis?
MRI, with a sensitivity of 90-100%.
186
What is the standard management for osteomyelitis?
Flucloxacillin for 6 weeks or clindamycin if penicillin-allergic.
187
What is Paget's disease of the bone?
A disease of increased but uncontrolled bone turnover, primarily a disorder of osteoclasts with excessive osteoclastic resorption followed by increased osteoblastic activity.
188
What are the most commonly affected sites in Paget's disease?
The skull, spine/pelvis, and long bones of the lower extremities.
189
What are the predisposing factors for Paget's disease?
Increasing age, male sex, northern latitude, and family history.
190
How often is Paget's disease symptomatic?
Only 5% of patients are symptomatic.
191
What is the stereotypical presentation of Paget's disease?
An older male with bone pain and an isolated raised alkaline phosphatase (ALP).
192
What are the clinical features of untreated Paget's disease?
Bone pain, bowing of the tibia, and bossing of the skull.
193
What are the key findings in blood investigations for Paget's disease?
Raised alkaline phosphatase (ALP) with typically normal calcium and phosphate levels.
194
What are the typical x-ray findings in Paget's disease?
Osteolysis in early disease, mixed lytic/sclerotic lesions later, and thickened skull vault or osteoporosis circumscripta on skull x-ray.
195
What imaging is used to assess sites of active bone lesions in Paget's disease?
Bone scintigraphy, showing increased uptake at active bone lesions.
196
What are the indications for treatment of Paget's disease?
Bone pain, skull or long bone deformity, fracture, or periarticular Paget's.
197
What is the main treatment for Paget's disease?
Bisphosphonates (oral risedronate or IV zoledronate).
198
What are the complications of Paget's disease?
Deafness (cranial nerve entrapment), bone sarcoma (1% if affected for > 10 years), fractures, skull thickening, and high-output cardiac failure.
199
What is Perthes' disease?
A degenerative condition affecting the hip joints of children, typically between the ages of 4-8 years, due to avascular necrosis of the femoral head.
200
What causes Perthes' disease?
Impaired blood supply to the femoral head, leading to bone infarction.
201
How common is Perthes' disease in boys compared to girls?
It is 5 times more common in boys.
202
What percentage of Perthes' disease cases are bilateral?
Around 10% of cases.
203
What are the features of Perthes' disease?
Hip pain developing progressively over a few weeks, limp, stiffness, and reduced range of hip movement.
204
What are the early and late x-ray findings in Perthes' disease?
Early changes include widening of the joint space; later changes include decreased femoral head size/flattening.
205
How is Perthes' disease diagnosed?
Plain x-ray, with technetium bone scan or MRI if the x-ray is normal and symptoms persist.
206
What are the complications of Perthes' disease?
Osteoarthritis and premature fusion of the growth plates.
207
What is Catterall Stage 1 of Perthes' disease?
Clinical and histological features only.
208
What is Catterall Stage 2 of Perthes' disease?
Sclerosis with or without cystic changes and preservation of the articular surface.
209
What is Catterall Stage 3 of Perthes' disease?
Loss of structural integrity of the femoral head.
210
What is Catterall Stage 4 of Perthes' disease?
Loss of acetabular integrity.
211
What is the management goal for Perthes' disease?
To keep the femoral head within the acetabulum using casts or braces.
212
How is Perthes' disease managed in children under 6 years?
Observation.
213
How is Perthes' disease managed in older children or severe deformities?
Surgical management.
214
What is the prognosis for Perthes' disease?
Most cases resolve with conservative management, and early diagnosis improves outcomes.
215
What is polyarthritis?
Inflammation of five or more joints simultaneously within the first six weeks of symptom onset.
216
What are the typical features of polyarthritis?
Pain, swelling, and stiffness in multiple joints, which may have a symmetrical or asymmetrical pattern.
217
What systemic symptoms may accompany polyarthritis?
Fever, weight loss, and fatigue, reflecting the underlying systemic inflammatory process.
218
What are some inflammatory arthritis conditions associated with polyarthritis?
Rheumatoid arthritis, psoriatic arthritis, SLE, and seronegative spondyloarthropathies.
219
What viral infections can cause polyarthritis?
EBV, HIV, hepatitis, mumps, and rubella.
220
What infective causes other than viral can lead to polyarthritis?
Tuberculosis and disseminated gonococcal infection.
221
What are some symptoms reflecting the underlying systemic inflammatory process?
Fever, weight loss, and fatigue.
222
What are some non-infectious differential diagnoses for polyarthritis?
Pseudogout, Henoch-Schönlein purpura, and sarcoidosis.
223
What is polymyalgia rheumatica (PMR)?
PMR is a condition in older people characterized by muscle stiffness and raised inflammatory markers, often associated with temporal arteritis.
224
What age group is typically affected by PMR?
Patients older than 60 years.
225
What is the usual onset pattern of PMR?
Rapid onset, typically within less than one month.
226
What are the key features of PMR?
Aching and morning stiffness in proximal limb muscles, mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, and night sweats.
227
Is weakness a symptom of PMR?
No, weakness is not considered a symptom of PMR.
228
What investigations are used for PMR, and what are the findings?
Raised inflammatory markers such as ESR > 40 mm/hr, with normal creatine kinase and EMG results.
229
What is the treatment for PMR?
Prednisolone, typically 15 mg/day, with patients usually responding dramatically to steroids.
230
What should be considered if a patient does not respond to steroids in PMR?
An alternative diagnosis should be considered.
231
What causes pseudogout?
Pseudogout is caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium.
232
What is the more accurate term for pseudogout?
Acute calcium pyrophosphate crystal deposition disease.
233
What is pseudogout strongly associated with?
Increasing age.
234
What underlying risk factors are associated with pseudogout in patients under 60?
Haemochromatosis, hyperparathyroidism, low magnesium, low phosphate, acromegaly, and Wilson's disease.
235
Which joints are most commonly affected by pseudogout?
The knee, wrist, and shoulders.
236
What are the findings in joint aspiration for pseudogout?
Weakly positively birefringent rhomboid-shaped crystals.
237
What are the x-ray findings in pseudogout?
Chondrocalcinosis, seen as linear calcifications of the meniscus and articular cartilage.
238
How is pseudogout managed?
Aspiration of joint fluid to exclude septic arthritis, followed by NSAIDs or intra-articular, intra-muscular, or oral steroids as for gout.
239
What is psoriatic arthropathy?
Psoriatic arthropathy is an inflammatory arthritis associated with psoriasis, classified as one of the seronegative spondyloarthropathies.
240
How does psoriatic arthropathy correlate with cutaneous psoriasis?
It correlates poorly with cutaneous psoriasis and may precede the development of skin lesions.
241
What percentage of patients with skin lesions develop psoriatic arthropathy?
Around 10-20%.
242
What are the patterns of psoriatic arthropathy?
Symmetric polyarthritis (30-40%, most common), asymmetrical oligoarthritis (20-30%), sacroiliitis, DIP joint disease (10%), and arthritis mutilans.
243
What is arthritis mutilans?
A severe deformity of the fingers or hands, leading to 'telescoping fingers.'
244
What are some other signs of psoriatic arthropathy?
Psoriatic skin lesions, enthesitis, tenosynovitis, dactylitis, and nail changes (e.g., pitting, onycholysis).
245
What are the characteristic x-ray findings in psoriatic arthropathy?
Erosive changes with new bone formation, periostitis, and a 'pencil-in-cup' appearance.
246
How is mild psoriatic arthropathy managed?
Mild peripheral arthritis or mild axial disease may be treated with NSAIDs.
247
What treatments are used for moderate to severe psoriatic arthropathy?
Methotrexate, monoclonal antibodies (e.g., ustekinumab, secukinumab), and apremilast.
248
How does the prognosis of psoriatic arthropathy compare to rheumatoid arthritis?
Psoriatic arthropathy has a better prognosis than rheumatoid arthritis.
249
What is reactive arthritis?
Reactive arthritis is an arthritis that develops after an infection where the organism cannot be recovered from the joint.
250
What was the former name for reactive arthritis and why is it no longer used?
It was formerly called Reiter's syndrome, but the term is no longer used due to Reiter's association with the Nazi party.
251
What is the classic triad of reactive arthritis?
Urethritis, conjunctivitis, and arthritis.
252
What is the mnemonic associated with reactive arthritis?
"Can't see, pee, or climb a tree."
253
What are the two forms of reactive arthritis?
Post-dysenteric form and post-STI form (sexually acquired reactive arthritis or SARA).
254
Which organisms are commonly associated with the post-dysenteric form?
Shigella flexneri, Salmonella typhimurium, Salmonella enteritidis, Yersinia enterocolitica, and Campylobacter.
255
Which organism is commonly associated with the post-STI form?
Chlamydia trachomatis.
256
What is the gender prevalence for each form of reactive arthritis?
The post-STI form is much more common in men (10:1), while the post-dysenteric form has an equal sex incidence.
257
How is reactive arthritis managed?
Symptomatic treatment includes analgesia, NSAIDs, and intra-articular steroids. Sulfasalazine and methotrexate are sometimes used for persistent disease.
258
How long do symptoms of reactive arthritis typically last?
Symptoms rarely last more than 12 months.
259
What is scleritis?
Scleritis is a full-thickness inflammation of the sclera, typically causing a red, painful eye.
260
What are the risk factors for scleritis?
Rheumatoid arthritis (most commonly associated), systemic lupus erythematosus, sarcoidosis, and granulomatosis with polyangiitis.
261
How does scleritis typically present?
A red eye, often with significant pain (in contrast to episcleritis), watering, photophobia, and sometimes a gradual decrease in vision.
262
What is the main difference between scleritis and episcleritis?
Scleritis is typically more painful and involves full-thickness inflammation, while episcleritis is usually less painful and superficial.
263
How is scleritis managed?
Same-day assessment by an ophthalmologist, oral NSAIDs first-line, oral glucocorticoids for severe cases, and immunosuppressive drugs for resistant cases or associated systemic diseases.
264
What is the most common organism causing septic arthritis in adults?
Staphylococcus aureus is the most common organism overall, while Neisseria gonorrhoeae is most common in sexually active young adults.
265
What is the most common cause of septic arthritis?
Hematogenous spread, often from distant bacterial infections such as abscesses.
266
Which joint is most commonly affected in adults with septic arthritis?
The knee.
267
What are the typical features of septic arthritis?
Acute, swollen joint, restricted movement in 80% of cases, warm/fluctuant joint on examination, and fever in the majority of patients.
268
How is septic arthritis investigated?
Synovial fluid sampling is essential and should be performed before antibiotics if possible. The fluid typically shows leucocytosis with neutrophil predominance. Blood cultures and joint imaging may also be performed.
269
How is septic arthritis managed?
Intravenous antibiotics (e.g., flucloxacillin or clindamycin for penicillin-allergic patients) for 4-6 weeks, with a switch to oral antibiotics after 2 weeks. Needle aspiration to decompress the joint. Arthroscopic lavage if required.
270
What is the incidence and gender predominance of septic arthritis in children?
The incidence is around 4-5 per 100,000 children, and it is more common in boys, with an M:F ratio of 2:1.
271
Which joints are most commonly affected in children with septic arthritis?
The hip, knee, and ankle.
272
What are the typical symptoms of septic arthritis in children?
Joint pain, limp, fever, and systemic unwellness such as lethargy.
273
What are the signs of septic arthritis in children?
A swollen, red joint with only minimal movement possible.
274
What investigations are essential for diagnosing septic arthritis in children?
Joint aspiration for culture (shows raised WBC), raised inflammatory markers (e.g., ESR), blood cultures.
275
What is the Kocher criteria for diagnosing septic arthritis in children?
Fever >38.5°C, non-weight bearing, raised ESR, raised WCC.
276
What is transient synovitis, and what age group is most commonly affected?
Transient synovitis, also known as irritable hip, is the commonest cause of hip pain in children, typically affecting those aged 3-8 years.
277
What are the typical features of transient synovitis?
Limp or refusal to weight bear, groin or hip pain, and occasionally a low-grade fever.
278
What should raise suspicion of a more serious condition like septic arthritis?
A high fever is a red flag and warrants urgent specialist assessment.
279
What criteria allow for monitoring a child in primary care with a presumptive diagnosis of transient synovitis?
The child should be aged 3-9 years, well, afebrile, and mobile but limping, symptomatic for less than 72 hours.
280
What is the management for transient synovitis?
It is self-limiting and requires rest and analgesia.
281
What are Achilles tendon disorders, and how can they present?
Achilles tendon disorders include tendinopathy, partial tear, and complete rupture, presenting as posterior heel pain, morning stiffness, or sudden pain and inability to walk following a rupture.
282
What are the risk factors for Achilles tendon disorders?
Risk factors include quinolone use (e.g., ciprofloxacin) and hypercholesterolemia (predisposing to tendon xanthomata).
283
What are the features of Achilles tendinopathy (tendinitis)?
Gradual onset of posterior heel pain, worse after activity, with common morning pain and stiffness.
284
How is Achilles tendinopathy managed?
Management involves simple analgesia, reducing aggravating activities, and calf muscle eccentric exercises, either self-directed or under physiotherapy.
285
How does an Achilles tendon rupture typically present?
Sudden onset of significant pain during sports or running, an audible 'pop' in the ankle, and inability to walk or continue activity.
286
What is Simmond's triad, and how is it used to diagnose Achilles tendon rupture?
Simmond's triad includes increased dorsiflexion in the injured foot, a palpable gap in the tendon, and no plantarflexion during a calf squeeze test, indicating a rupture.
287
What is the initial imaging modality of choice for suspected Achilles tendon rupture?
Ultrasound is the initial imaging modality of choice.
288
How should a suspected Achilles tendon rupture be managed?
An acute referral to an orthopaedic specialist is required, with treatment options including surgical repair or conservative management with immobilization.
289
What are the Ottawa Rules for determining the need for an ankle x-ray?
An ankle x-ray is required if there is pain in the malleolar zone and one of the following: bony tenderness at the lateral malleolar zone, bony tenderness at the medial malleolar zone, or inability to walk four weight-bearing steps immediately after the injury and in the emergency department.
290
What is the sensitivity of the Ottawa Rules for ankle x-rays?
The Ottawa Rules for ankle x-rays have a sensitivity approaching 100%.
291
Are there Ottawa Rules available for injuries other than the ankle?
Yes, Ottawa Rules are also available for both foot and knee injuries.
292
What are the bony components of the ankle joint and how are they secured?
The bony components of the ankle joint include the distal tibia, distal fibula, and the superior aspect of the talus, forming a mortise. These are secured by the syndesmosis (AITFL, PITFL, IOL, interosseous membrane), lateral collateral ligaments (ATFL, PTFL, calcaneofibular ligament), and the deltoid ligament.
293
What are the two main types of ankle sprains?
High ankle sprains, involving the syndesmosis, and low ankle sprains, involving the lateral collateral ligaments.
294
What is the most common type of ankle sprain and its presentation?
Low ankle sprains (>90%) are the most common, often caused by an inversion injury, with the ATFL being the most frequently injured ligament. Symptoms include pain, swelling, tenderness, and sometimes bruising.
295
How are low ankle sprains classified?
Grade I (mild): Stretch or micro-tear; minimal bruising/swelling; normal weight-bearing. Grade II (moderate): Partial tear; moderate bruising/swelling; minimal pain on weight-bearing. Grade III (severe): Complete tear; severe bruising/swelling; severe pain on weight-bearing.
296
What investigations are recommended for low ankle sprains?
Radiographs based on the Ottawa ankle rules, as 15% of sprains are associated with fractures. MRI may be used for persistent pain or to evaluate peroneal tendons.
297
What is the treatment for low ankle sprains?
Non-operative management with the RICE protocol (rest, ice, compression, elevation). Orthosis, casts, or crutches may be used for short-term relief. Severe or persistent cases may require MRI and possible surgical intervention.
298
How do high ankle sprains typically occur and present?
High ankle sprains are rare (0.5%) and severe, caused by external rotation of the foot pushing the fibula laterally. Symptoms include painful weight-bearing and pain when squeezing the tibia and fibula together (Hopkin's squeeze test).
299
What investigations are used for high ankle sprains?
Radiographs to detect widening of the tibiofibular joint or ankle mortise. MRI is used if syndesmotic injury is suspected but plain films are normal.
300
What is the treatment for high ankle sprains?
Non-weight-bearing orthosis or cast if no diastasis is present. Operative fixation is warranted for diastasis or failed non-operative management.
301
What should be considered if there is an isolated injury to the deltoid ligament?
Isolated deltoid ligament injuries are rare and often associated with fractures. Look for a Maisonneuve fracture of the proximal fibula. Treatment is similar to low ankle sprains if the ankle mortise is anatomically reduced; otherwise, reduction and fixation may be required.
302
What is Ankylosing Spondylitis and who is most commonly affected?
Ankylosing spondylitis is an HLA-B27 associated spondyloarthropathy that typically presents in males aged 20-30 years with a sex ratio of 3:1.
303
What are the typical findings in inflammatory markers for Ankylosing Spondylitis?
Inflammatory markers such as ESR and CRP are typically raised, but normal levels do not exclude ankylosing spondylitis.
304
How useful is HLA-B27 testing in diagnosing Ankylosing Spondylitis?
HLA-B27 testing has limited diagnostic utility as it is positive in 90% of patients with ankylosing spondylitis and 10% of normal individuals.
305
What is the most useful investigation for diagnosing Ankylosing Spondylitis?
A plain x-ray of the sacroiliac joints is the most useful investigation for diagnosis, though radiographs may be normal early in the disease.
306
What are the late x-ray findings in Ankylosing Spondylitis?
Sacroiliitis: subchondral erosions, sclerosis; squaring of lumbar vertebrae; bamboo spine (uncommon and late finding); syndesmophytes due to annulus fibrosus ossification; apical fibrosis on chest x-ray.
307
What is the next step if sacroiliac joint involvement is not visible on an x-ray but suspicion remains high?
An MRI should be performed to identify early inflammation, such as bone marrow oedema in the sacroiliac joints, to confirm the diagnosis.
308
What spirometry findings may be seen in Ankylosing Spondylitis?
Spirometry may show a restrictive defect due to pulmonary fibrosis, kyphosis, and ankylosis of costovertebral joints.
309
What are the first-line treatments for Ankylosing Spondylitis?
Regular exercise, such as swimming; NSAIDs; physiotherapy.
310
When are disease-modifying drugs like sulphasalazine useful in Ankylosing Spondylitis?
These drugs are only useful if there is peripheral joint involvement.
311
When should anti-TNF therapy be considered for Ankylosing Spondylitis?
Anti-TNF therapy, such as etanercept and adalimumab, is recommended for patients with persistently high disease activity despite conventional treatments.
312
What are the most common tumors causing bone metastases in descending order?
Prostate, breast, and lung.
313
What are the most common sites for bone metastases in descending order?
Spine, pelvis, ribs, skull, and long bones.
314
What features, other than bone pain, may indicate bone metastases?
Pathological fractures, hypercalcaemia, and raised alkaline phosphatase (ALP).
315
What is compartment syndrome characterized by?
Raised pressure within a closed anatomical space, leading to compromised tissue perfusion and potential necrosis.
316
What are the two main fractures associated with compartment syndrome?
Supracondylar fractures and tibial shaft injuries.
317
What are the key features of compartment syndrome?
Pain (especially on movement), excessive use of breakthrough analgesia, paresthesiae, pallor, and possible paralysis of the muscle group.
318
Does the presence of a pulse rule out compartment syndrome?
No, the presence of a pulse does not rule out compartment syndrome.
319
How is compartment syndrome diagnosed?
By measuring intracompartmental pressure; pressures >20 mmHg are abnormal, and >40 mmHg is diagnostic.
320
What is the treatment for compartment syndrome?
Prompt and extensive fasciotomies, aggressive IV fluids to manage myoglobinuria, and possible debridement or amputation for necrotic muscle groups.
321
How quickly can muscle necrosis occur in compartment syndrome?
Within 4-6 hours.
322
What is gout caused by?
Deposition of monosodium urate monohydrate in the synovium due to chronic hyperuricaemia (uric acid > 0.45 mmol/l).
323
What are the drug causes of gout?
Diuretics (thiazides, furosemide), ciclosporin, alcohol, cytotoxic agents, pyrazinamide, and aspirin (both high-dose and low-dose).
324
Does low-dose aspirin increase the risk of gout attacks?
Yes, low-dose aspirin increases the risk of gout attacks, but this must be balanced against its cardiovascular benefits.
325
How can the risk of gout attacks from low-dose aspirin be mitigated?
Coprescribing allopurinol can mitigate the increased risk of gout attacks associated with low-dose aspirin.
326
What causes gout?
Gout is caused by the deposition of monosodium urate monohydrate in the synovium due to chronic hyperuricaemia (> 450 µmol/l).
327
What are first-line treatments for acute gout?
NSAIDs or colchicine.
328
When should NSAIDs be stopped in acute gout treatment?
NSAIDs should be continued until 1-2 days after symptoms have settled.
329
What are the key characteristics and side effects of colchicine?
Colchicine inhibits microtubule polymerization, interferes with mitosis, and inhibits neutrophil activity. Its main side effect is diarrhoea.
330
When are oral steroids or intra-articular steroid injections used in gout?
When NSAIDs and colchicine are contraindicated.
331
Should allopurinol be stopped during an acute gout attack?
No, allopurinol should be continued during an acute attack.
332
When is urate-lowering therapy (ULT) recommended?
ULT is offered to all patients after their first attack and is particularly recommended for those with ≥2 attacks in 12 months, tophi, renal disease, uric acid stones, or those on cytotoxic or diuretic prophylaxis.
333
What is the first-line urate-lowering therapy?
Allopurinol, starting at 100 mg daily and titrated to maintain serum uric acid < 360 µmol/l (or < 300 µmol/l in cases of tophi or frequent flares).
334
What is the second-line treatment if allopurinol is not tolerated?
Febuxostat, another xanthine oxidase inhibitor.
335
What lifestyle modifications are recommended for gout management?
Reduce alcohol intake, lose weight if obese, avoid high-purine foods, and consider increased vitamin C intake.
336
Which drugs should be considered for discontinuation in gout management?
Precipitating drugs such as thiazides.
337
What antihypertensive drug may benefit patients with gout?
Losartan, due to its uricosuric action.
338
What is another name for greater trochanteric pain syndrome?
Trochanteric bursitis.
339
What causes greater trochanteric pain syndrome?
Repeated movement of the fibroelastic iliotibial band.
340
What is the typical demographic affected by greater trochanteric pain syndrome?
Women aged 50-70 years.
341
What are the features of greater trochanteric pain syndrome?
Pain over the lateral side of the hip/thigh and tenderness on palpation of the greater trochanter.
342
What is a common demographic affected by hip fractures?
Osteoporotic, elderly females.
343
Why is avascular necrosis a risk in displaced hip fractures?
The blood supply to the femoral head runs up the neck and can be disrupted in displaced fractures.
344
What are the classic signs of a hip fracture?
A shortened and externally rotated leg.
345
What classification system is commonly used for hip fractures?
The Garden classification system.
346
What are the types of fractures in the Garden classification?
Type I: Stable fracture with impaction in valgus. Type II: Complete fracture but undisplaced. Type III: Displaced fracture, usually rotated and angulated, but still has boney contact. Type IV: Complete boney disruption.
347
What are the types of fractures in the Garden classification?
Type I: Stable fracture with impaction in valgus.
Type II: Complete fracture but undisplaced.
Type III: Displaced fracture, usually rotated and angulated, but still has boney contact.
Type IV: Complete boney disruption.
348
What type of hip fractures are at the highest risk of blood supply disruption?
Garden Type III and Type IV fractures.
349
How are undisplaced intracapsular hip fractures managed?
Internal fixation, or hemiarthroplasty if the patient is unfit.
350
What is the recommended management for displaced intracapsular hip fractures according to NICE?
Replacement arthroplasty (total hip replacement or hemiarthroplasty).
351
When is total hip replacement preferred over hemiarthroplasty for displaced intracapsular fractures?
If the patient can walk independently outdoors with no more than a stick.
If the patient is not cognitively impaired.
If the patient is medically fit for anaesthesia and the procedure.
352
How are stable intertrochanteric extracapsular hip fractures managed?
With a dynamic hip screw.
353
What is the management for reverse oblique, transverse, or subtrochanteric extracapsular hip fractures?
Intramedullary device.
354
What conditions can cause increased uric acid synthesis in hyperuricaemia?
Lesch-Nyhan disease, myeloproliferative disorders, diet rich in purines, exercise, psoriasis, and cytotoxics.
355
What factors lead to decreased uric acid excretion in hyperuricaemia?
Low-dose aspirin, diuretics, pyrazinamide, pre-eclampsia, alcohol, renal failure, and lead.
356
Which metabolic conditions are associated with hyperuricaemia?
Hyperlipidaemia, hypertension, and metabolic syndrome.
357
Can hyperuricaemia occur in asymptomatic patients?
Yes, hyperuricaemia may be found in asymptomatic patients who have not experienced attacks of gout.
358
What is a common cause of lateral knee pain in runners?
Iliotibial band syndrome.
359
Where is tenderness typically located in iliotibial band syndrome?
Tenderness is 2-3 cm above the lateral joint line.
360
What is the initial management for iliotibial band syndrome?
Activity modification and iliotibial band stretches.
361
What is the next step if symptoms of iliotibial band syndrome do not improve?
Referral to physiotherapy.
362
What is juvenile idiopathic arthritis (JIA)?
JIA is arthritis occurring in someone less than 16 years old that lasts for more than 6 weeks.
363
What are the three types of juvenile idiopathic arthritis?
Systemic onset (Still's disease), polyarticular (more than 4 joints), and pauciarticular (4 or fewer joints).
364
What is pauciarticular juvenile idiopathic arthritis (JIA)?
Pauciarticular JIA refers to cases of JIA where 4 or fewer joints are affected, accounting for around 60% of cases.
365
What are the features of pauciarticular JIA?
Joint pain and swelling (usually in medium-sized joints such as knees, ankles, and elbows), limp, and positive ANA, which is associated with anterior uveitis.
366
What is systemic onset juvenile idiopathic arthritis (JIA)?
Systemic onset JIA, also known as Still's disease, is a type of JIA characterized by systemic symptoms along with arthritis in children under 16 years lasting more than 6 weeks.
367
What are the features of systemic onset JIA?
Pyrexia, salmon-pink rash, lymphadenopathy, arthritis, uveitis, anorexia, and weight loss.
368
What are the investigation findings in systemic onset JIA?
ANA may be positive, especially in oligoarticular JIA, while rheumatoid factor is usually negative.
369
What is the most commonly injured knee ligament?
The anterior cruciate ligament (ACL).
370
What are common mechanisms of ACL injury?
Non-contact injuries like sudden twisting or awkward landing are most common. Other mechanisms include lateral blows to the knee and skiing.
371
What are the features of an ACL injury?
A sudden 'popping' sound, knee swelling, instability (feeling the knee will give way), and positive findings on anterior draw and Lachman's tests.
372
How is the anterior draw test performed?
The patient lies supine with the knee at 90 degrees. The examiner pulls the tibia forward while stabilizing the femur to assess anterior tibial movement.
373
How is Lachman's test different from the anterior draw test?
Lachman's test is performed with the knee at 20-30 degrees and is more reliable than the anterior draw test in assessing anterior tibial translation.
374
What is the typical cause of a meniscal tear?
Twisting injuries.
375
What are the features of a meniscal tear?
Pain worse on straightening the knee, knee giving way, knee locking due to displaced meniscal tears, and tenderness along the joint line.
376
What is Thessaly's test?
A test performed with the patient weight-bearing at 20 degrees of knee flexion, supported by the doctor. It is positive if there is pain on twisting the knee.
377
What is the most commonly fractured metatarsal?
The proximal 5th metatarsal.
378
What is the least commonly fractured metatarsal?
The 1st metatarsal.
379
What is a proximal avulsion fracture of the 5th metatarsal also known as?
Pseudo-Jones fracture.
380
What is a Jones fracture?
A transverse fracture at the metaphyseal-diaphyseal junction of the 5th metatarsal.
381
What is the most common site of metatarsal stress fractures?
The 2nd metatarsal shaft.
382
What symptoms are associated with metatarsal fractures?
Pain, bony tenderness, swelling, and an antalgic gait.
383
What imaging modality is used if stress fractures are not visible on X-rays?
Isotope bone scan or MRI.
384
When might periosteal reactions appear on X-rays in stress fractures?
2–3 weeks after the injury.
385
What causes Lyme disease?
Lyme disease is caused by the spirochaete Borrelia burgdorferi and is spread by ticks.
386
What is the characteristic early sign of Lyme disease?
Erythema migrans, a 'bulls-eye' rash.
387
When does erythema migrans typically develop?
1–4 weeks after the tick bite.
388
What systemic features may be present in early Lyme disease?
Headache, lethargy, fever, and arthralgia.
389
What cardiovascular complications can occur in late Lyme disease?
Heart block and peri/myocarditis.
390
What neurological complications are associated with late Lyme disease?
Facial nerve palsy, radicular pain, and meningitis.
391
How is Lyme disease diagnosed if erythema migrans is present?
Clinically, without further tests.
392
What is the first-line investigation for Lyme disease if erythema migrans is absent?
ELISA antibodies to Borrelia burgdorferi.
393
What should be done if the initial ELISA test is negative but Lyme disease is still suspected?
Repeat the ELISA 4–6 weeks after the first test.
394
What is the treatment for early Lyme disease?
Doxycycline or amoxicillin if doxycycline is contraindicated.
395
What is the treatment for disseminated Lyme disease?
Ceftriaxone.
396
What reaction may occur after initiating antibiotics for Lyme disease?
Jarisch-Herxheimer reaction, characterized by fever, rash, and tachycardia.
397
Should antibiotics be routinely given for asymptomatic tick bites?
No, according to NICE guidelines.
398
How should ticks be removed?
Using fine-tipped tweezers, grasping the tick close to the skin, and pulling upwards firmly.
399
What is chondromalacia patellae?
Softening of the cartilage of the patella, commonly seen in teenage girls.
400
What are the key features of chondromalacia patellae?
Anterior knee pain on walking up and down stairs and rising from prolonged sitting, usually responds to physiotherapy.
401
What is Osgood-Schlatter disease?
A condition seen in sporty teenagers causing pain, tenderness, and swelling over the tibial tubercle.
402
What are the key features of osteochondritis dissecans?
Pain after exercise, intermittent swelling, and locking of the knee.
403
What is patellar subluxation?
Lateral subluxation of the patella causing medial knee pain and a sensation that the knee may give way.
404
What are the key features of patellar tendonitis?
Chronic anterior knee pain that worsens after running and tenderness below the patella on examination, more common in athletic teenage boys.
405
What condition can cause referred knee pain in children?
Hip problems such as slipped upper femoral epiphysis.
406
What is osteoarthritis of the hip?
It is the second most common presentation of osteoarthritis after the knee, associated with significant morbidity and often requiring total hip replacement.
407
What are the risk factors for hip osteoarthritis?
Increasing age, female gender, obesity, and developmental dysplasia of the hip.
408
What are the features of hip osteoarthritis?
Chronic groin ache following exercise and relieved by rest; red flag features include rest pain, night pain, and morning stiffness lasting > 2 hours.
409
How is the severity of hip osteoarthritis assessed?
Using the Oxford Hip Score.
410
What is the first-line investigation for suspected hip osteoarthritis if clinical diagnosis is uncertain?
Plain x-rays.
411
What are the management options for hip osteoarthritis?
Oral analgesia, intra-articular injections for short-term relief, and total hip replacement as the definitive treatment.
412
What are the perioperative complications of total hip replacement?
Venous thromboembolism, intraoperative fracture, nerve injury, and surgical site infection.
413
What are the postoperative complications of total hip replacement?
Leg length discrepancy, posterior dislocation (presents with a 'clunk', pain, inability to weight bear, internal rotation, and shortening), aseptic loosening (most common reason for revision), and prosthetic joint infection.
414
What are the first steps in managing osteoarthritis according to the 2022 NICE guidelines?
Offer help with weight loss, advice on local muscle strengthening exercises, and general aerobic fitness.
415
What is the first-line analgesic treatment for osteoarthritis?
Topical NSAIDs, particularly beneficial for OA of the knee or hand.
416
What is the second-line treatment for osteoarthritis?
Oral NSAIDs, co-prescribed with a proton pump inhibitor.
417
When should paracetamol or weak opioids be considered for osteoarthritis?
Only infrequently for short-term pain relief if all other pharmacological treatments are contraindicated, not tolerated, or ineffective.
418
What treatments are not recommended for osteoarthritis by NICE?
Glucosamine and strong opioids.
419
What non-pharmacological options are available for osteoarthritis?
Walking aids for knee and hip OA, and intra-articular steroid injections for short-term relief (2-10 weeks).
420
When should patients with osteoarthritis be referred for joint replacement?
If conservative methods fail.
421
What is the management approach for patients aged 75 years or older following a fragility fracture?
They are presumed to have underlying osteoporosis and should be started on first-line therapy (oral bisphosphonate) without the need for a DEXA scan.
422
What do the 2014 NOGG guidelines recommend for women over the age of 50 who've had a fragility fracture?
Treatment should be started, though BMD measurement may sometimes be appropriate, particularly in younger postmenopausal women.
423
What is the management approach for patients aged 75 years or older following a fragility fracture?
They are presumed to have underlying osteoporosis and should be started on first-line therapy (oral bisphosphonate) without the need for a DEXA scan.
424
What do the 2014 NOGG guidelines recommend for women over the age of 50 who've had a fragility fracture?
Treatment should be started, though BMD measurement may sometimes be appropriate, particularly in younger postmenopausal women.
425
What is the management approach for patients under 75 years of age following a fragility fracture?
A DEXA scan should be arranged, and the results used with a FRAX assessment to determine ongoing fracture risk.
426
How is a 79-year-old woman with a Colles' fracture managed?
She is presumed to have osteoporosis and started on oral alendronate 70 mg once weekly without arranging a DEXA scan.
427
At what ages should all women and men be assessed for osteoporosis risk?
Women aged ≥ 65 years and men aged ≥ 75 years should be assessed.
428
When should younger patients be assessed for osteoporosis risk?
When risk factors such as previous fragility fractures, glucocorticoid use, history of falls, family history of hip fracture, secondary osteoporosis, low BMI, smoking, or excessive alcohol intake are present.
429
What should be excluded as a first step in assessing osteoporosis risk?
Secondary causes of osteoporosis and non-osteoporotic causes of fragility fractures (e.g., bone metastases, myeloma, Paget's disease).
430
When should a DEXA scan be offered without calculating a fragility risk score?
Patients > 50 years of age with a history of fragility fracture.
Patients < 40 years of age with a major risk factor for fragility fracture.
Before starting treatments that may rapidly affect bone density (e.g., hormone deprivation therapy for cancer).
431
Which tools are recommended by NICE for assessing a 10-year risk of fracture?
Clinical prediction tools such as FRAX or QFracture.
432
What should be done for patients with a 10-year fracture risk ≥ 10% using QFracture?
A DEXA scan should be arranged.
433
How are FRAX results interpreted?
Green zone: Low risk, no further action.
Orange zone: DEXA scan recommended to refine risk.
Red zone: DEXA scan recommended for baseline and to guide treatment.
434
When should osteoporosis risk be reassessed according to NICE?
If the original risk was near the intervention threshold and only after a minimum of 2 years.
When there has been a change in the person's risk factors.
435
What are the significant demographic risk factors for osteoporosis?
Advancing age and female sex.
436
What are the six 'important' risk factors for osteoporosis included in major tools like FRAX?
History of glucocorticoid use
Rheumatoid arthritis
Alcohol excess
History of parental hip fracture
Low body mass index
Current smoking
437
What are other general risk factors for osteoporosis?
Sedentary lifestyle, premature menopause, Caucasian or Asian ethnicity, and various medical conditions like endocrine disorders, gastrointestinal disorders, multiple myeloma, and chronic kidney disease.
438
Name medications, other than glucocorticoids, that may worsen osteoporosis.
SSRIs, antiepileptics, proton pump inhibitors, glitazones, long-term heparin therapy, aromatase inhibitors (e.g., anastrozole).
439
Why does NOGG recommend investigations in patients with osteoporosis or fragility fractures?
To exclude diseases mimicking osteoporosis, identify contributory factors, assess fracture risk, and select appropriate treatment.
440
What are the baseline investigations recommended for all osteoporosis patients?
Full blood count
Urea and electrolytes
Liver function tests
Bone profile
C-reactive protein (CRP)
Thyroid function tests
441
What additional tests may be performed if indicated?
Lateral spine radiographs or DXA-based vertebral imaging
Protein immunoelectrophoresis and urinary Bence-Jones proteins
25OHD, PTH
Hormonal tests: serum testosterone, SHBG, FSH, LH (in men), serum prolactin
Tests for coeliac disease: endomysial/tissue transglutaminase antibodies
24-hour urinary cortisol/dexamethasone suppression test
Bone turnover markers
Urinary calcium excretion
442
What is the T score in a DEXA scan based on?
The bone mass of a young reference population.
443
What does a T score of -1.0 indicate?
Bone mass is one standard deviation below that of the young reference population.
444
What is a Z score in a DEXA scan adjusted for?
Age, gender, and ethnic factors.
445
What T score range is considered normal?
Greater than -1.0.
446
What T score range indicates osteopenia?
Between -1.0 and -2.5.
447
What T score defines osteoporosis?
Less than -2.5.
448
When does the risk of glucocorticoid-induced osteoporosis significantly rise?
When a patient takes the equivalent of prednisolone 7.5 mg/day for 3 or more months.
449
How should patients likely to take steroids for over 3 months be managed?
Bone protection should be started immediately in an anticipatory manner.
450
What are the two groups in the RCP guidelines for managing corticosteroid-induced osteoporosis?
1. Patients over 65 years or those with a previous fragility fracture.
2. Patients under 65 years.
451
What is the management for patients over 65 years or with a fragility fracture?
Offer bone protection.
452
What should be done for patients under 65 years regarding glucocorticoid-induced osteoporosis?
Offer a bone density scan, with further management based on T score.
453
How is a T score greater than 0 managed in glucocorticoid-induced osteoporosis?
Reassure the patient.
454
What is the management for a T score between 0 and -1.5 in glucocorticoid-induced osteoporosis?
Repeat the bone density scan in 1-3 years.
455
What is the management for a T score less than -1.5 in glucocorticoid-induced osteoporosis?
Offer bone protection.
456
What is the first-line treatment for glucocorticoid-induced osteoporosis?
Alendronate.
457
What additional supplementation should patients receiving bone protection also have?
Calcium and vitamin D.
458
What is the patella?
A sesamoid bone within the quadriceps tendon that enhances the efficiency of the knee's extensor mechanism and protects the knee from trauma.
459
What are the two parts of the quadriceps tendon divided by the patella?
The quadriceps tendon superiorly and the patellar ligament inferiorly.
460
What is the role of the patella in the extensor mechanism of the knee?
It increases the distance of the quadriceps tendon from the knee joint's center of rotation, improving efficiency.
461
What are the surfaces of the patella?
The anterior surface is flat, and the posterior surface has medial and lateral facets that articulate with the femur.
462
What are the two main mechanisms of patella fractures?
Direct injury and indirect injury.
463
What causes a direct patella injury?
A direct blow or trauma to the knee, such as a fall or dashboard injury, leading to an undisplaced crack or comminuted fracture with an intact extensor mechanism.
464
What causes an indirect patella injury?
Forceful contraction of the quadriceps against resistance, resulting in a transverse fracture and potential extensor mechanism disruption.
465
What are the clinical features of a patella fracture?
Swelling, bruising, localized pain and tenderness, possible palpable gap, and impaired ability to straight leg raise if the extensor mechanism is disrupted.
466
What imaging is used to diagnose a patella fracture?
Plain X-rays with AP and lateral views; skyline view may be used if diagnosis is uncertain.
467
How are undisplaced patella fractures managed?
With a hinged knee brace for 6 weeks, allowing full weight-bearing.
468
What are the indications for operative management of a patella fracture?
Displaced fractures or loss of the extensor mechanism.
469
What surgical techniques are used for patella fracture management?
Tension band wiring, inter-fragmentary screws, or cerclage wires.
470
What is the postoperative care for operative patella fracture management?
Use of a hinged knee brace for 4–6 weeks with full weight-bearing allowed.
471
What are the general management points for osteoporosis?
Lifestyle changes, adequate dietary calcium and vitamin D intake, weight-bearing and muscle-strengthening exercises, consideration of secondary causes, and bisphosphonates as first-line drug treatment.
472
What are the first-line drug treatments for osteoporosis?
Oral bisphosphonates such as alendronate and risedronate.
473
When is IV zoledronate recommended in osteoporosis management?
Following a hip fracture, as per NOGG guidelines.
474
What are the second-line drug treatments for osteoporosis?
Denosumab, with other options including strontium ranelate, raloxifene, teriparatide, and romosozumab.
475
What should be done for a patient at high risk of fragility fractures based on QFracture or FRAX scores?
Perform a DEXA scan to assess bone mineral density (BMD) and manage osteoporosis as indicated.
476
What is the BMD threshold for defining osteoporosis?
A T-score of -2.5 SD or below.
477
What is the management for patients starting oral glucocorticoids at ≥7.5 mg/day of prednisolone for at least 3 months?
Start bone protective treatment immediately with oral bisphosphonates, without waiting for a DEXA scan.
478
How should a symptomatic osteoporotic vertebral fracture in postmenopausal women or men ≥50 be managed?
Begin treatment straight away with oral bisphosphonates.
479
Is a DEXA scan necessary for women ≥75 with a hip fracture?
No, a DEXA scan is not required to diagnose osteoporosis; bisphosphonates should be commenced based on clinical presentation.
480
What is the follow-up plan for osteoporosis treatment with bisphosphonates?
Prescribe oral bisphosphonates for at least 5 years or IV bisphosphonates for at least 3 years, then reassess fracture risk.
481
What is the most common cause of heel pain in adults?
Plantar fasciitis.
482
Where is the pain typically worst in plantar fasciitis?
Around the medial calcaneal tuberosity.
483
What are the management steps for plantar fasciitis?
Rest the feet, wear shoes with good arch support and cushioned heels, and use insoles or heel pads.
484
How many men are diagnosed with prostate cancer each year in the UK?
Up to 30,000 men.
485
What are the common symptoms of early prostate cancer?
Early prostate cancers have few symptoms.
486
What symptoms might indicate metastatic prostate cancer?
Bone pain.
487
What are the diagnostic methods for prostate cancer?
Prostate-specific antigen (PSA) measurement, digital rectal examination (DRE), transrectal ultrasound (TRUS) with or without biopsy, MRI/CT, and bone scan for staging.
488
What is the normal upper limit for PSA?
4 ng/ml.
489
What PSA value suggests cancer, based on free: total PSA percentage?
Values of <20% are suggestive of cancer, and biopsy is advised.
490
What percentage of prostate cancers are adenocarcinomas?
95%.
491
What is the grading system used for prostate cancer?
The Gleason grading system.
492
How is the Gleason score calculated?
By adding the two most dominant grades (on a scale of 1–5), resulting in a score between 2 (best prognosis) and 10 (worst prognosis).
493
What are the main treatment options for prostate cancer?
Watch and wait, radiotherapy, surgery (radical prostatectomy), and hormonal therapy.
494
What is the preferred management option for low-risk men according to NICE?
Active surveillance.
495
What are the criteria for active surveillance in prostate cancer?
Clinical stage T1c, Gleason score 3+3, PSA density < 0.15 ng/ml/ml, cancer in less than 50% of biopsy cores, and < 10 mm of any core involved.
496
What should candidates for active surveillance undergo?
At least 10 biopsy cores and at least one re-biopsy.
497
What should be offered if men on active surveillance show evidence of disease progression?
Radical treatment.
498
What is the most common cancer in adult males in the UK?
Prostate cancer.
499
What is the second most common cause of cancer-related death in men after lung cancer?
Prostate cancer.
500
What are the risk factors for prostate cancer?
Increasing age, obesity, Afro-Caribbean ethnicity, and family history (5–10% of cases).
501
Why is localised prostate cancer often asymptomatic?
Because cancers tend to develop in the periphery of the prostate and don't cause obstructive symptoms early on.
502
What are possible features of prostate cancer?
Bladder outlet obstruction: hesitancy, urinary retention
Haematuria, haematospermia
Pain: back, perineal, or testicular
Digital rectal examination: asymmetrical, hard, nodular enlargement with loss of median sulcus.
503
What is a boxer fracture?
A minimally displaced fracture of the fifth metacarpal.
504
What is the typical cause of a boxer fracture?
Punching a hard surface, such as a wall.
505
What is a Colles' fracture?
A distal radius fracture with dorsal displacement of fragments, typically caused by a fall onto an outstretched hand (FOOSH).
506
What is the classic deformity seen in Colles' fractures?
A dinner fork deformity.
507
What are the classical features of a Colles' fracture?
Transverse fracture of the radius.
1 inch proximal to the radio-carpal joint.
Dorsal displacement and angulation.
508
What mnemonic helps remember Colles' fracture characteristics?
Colles' - Dorsally Displaced Distal radius → Dinner fork Deformity.
509
What are the early complications of a Colles' fracture?
Median nerve injury (acute carpal tunnel syndrome).
Compartment syndrome.
Vascular compromise.
Malunion.
Rupture of the extensor pollicis longus tendon.
510
What are the late complications of a Colles' fracture?
Osteoarthritis.
Complex regional pain syndrome.
511
What are the key features of lateral epicondylitis (tennis elbow)?
Pain and tenderness localized to the lateral epicondyle.
Pain worsens on resisted wrist extension with the elbow extended or supination of the forearm with the elbow extended.
Episodes last 6 months to 2 years, with acute pain for 6-12 weeks.
512
What are the key features of medial epicondylitis (golfer's elbow)?
Pain and tenderness localized to the medial epicondyle.
Pain aggravated by wrist flexion and pronation.
Symptoms may include numbness/tingling in the 4th and 5th fingers due to ulnar nerve involvement.
513
What is radial tunnel syndrome, and how does it present?
Most commonly due to compression of the posterior interosseous branch of the radial nerve from overuse.
Symptoms resemble lateral epicondylitis but occur around 4-5 cm distal to the lateral epicondyle.
Pain worsens with elbow extension and forearm pronation.
514
What are the features of cubital tunnel syndrome?
Initially intermittent tingling in the 4th and 5th fingers.
Symptoms worsen with elbow resting on a firm surface or prolonged flexion.
Later numbness in the 4th and 5th fingers with associated weakness.
515
How does olecranon bursitis typically present?
Swelling over the posterior aspect of the elbow, often with pain, warmth, and erythema.
Most commonly affects middle-aged male patients.
516
What is a Colles' fracture, and how does it present?
A transverse fracture of the radius, 1 inch proximal to the radiocarpal joint, with dorsal displacement and angulation.
Caused by a fall onto an extended outstretched hand.
Associated with a 'dinner fork deformity.'
517
What is a Smith's fracture, and how does it differ from a Colles' fracture?
A distal radius fracture with volar angulation of the distal fragment, described as a 'garden spade deformity.'
Caused by falling backwards onto the palm of an outstretched hand or falling with wrists flexed.
It is also referred to as a reverse Colles' fracture.
518
What is a Bennett's fracture?
An intra-articular fracture of the first carpometacarpal joint.
Caused by an impact on a flexed metacarpal, such as during fist fights.
X-ray shows a triangular fragment at the ulnar base of the first metacarpal.
519
What is a Monteggia's fracture, and how does it occur?
Dislocation of the proximal radioulnar joint associated with an ulna fracture.
Caused by a fall on an outstretched hand with forced pronation.
Requires prompt diagnosis to prevent disability.
520
What is a Galeazzi fracture?
A radial shaft fracture with dislocation of the distal radioulnar joint.
Typically caused by a direct blow.
521
What is a Pott's fracture, and how does it occur?
A bimalleolar ankle fracture.
Caused by forced foot eversion.
522
What is a Barton's fracture?
A distal radius fracture (similar to Colles' or Smith's) with associated radiocarpal dislocation.
Caused by a fall onto an extended and pronated wrist.
523
How are humeral fractures classified?
Proximal humeral fractures: Typically seen in the elderly.
Humeral shaft fractures.
Distal humeral fractures: Common in children, includes supracondylar fractures.
524
What are supracondylar fractures, and in which population are they common?
Fractures of the distal humerus just above the elbow joint.
Typically seen in children and are the most common type of elbow fracture in this demographic.
525
What are the features of a supracondylar fracture?
Usually result from a fall onto an outstretched hand.
Pain and swelling over the elbow immediately after the injury.
The elbow is typically held in a semi-flexed position.
Complications may involve neurovascular structures such as the median nerve, radial nerve, brachial artery, or ulnar nerve.
526
How are supracondylar fractures managed?
Non-displaced fractures: Managed with a collar and cuff.
Displaced fractures: Require manipulation under anesthesia with fixation.
527
What is lateral epicondylitis and what activities commonly cause it?
Lateral epicondylitis, or tennis elbow, typically follows unaccustomed activity such as house painting or playing tennis. It is most common in people aged 45-55 years and usually affects the dominant arm.
528
What are the features of lateral epicondylitis?
Pain and tenderness localized to the lateral epicondyle.
Pain worsened by wrist extension against resistance with the elbow extended or supination of the forearm with the elbow extended.
Episodes typically last between 6 months and 2 years, with acute pain lasting 6-12 weeks.
529
What are the management options for lateral epicondylitis?
Advice on avoiding muscle overload.
Simple analgesia.
Steroid injections.
Physiotherapy.
530
What is a common clinical presentation of a prolapsed lumbar disc?
A prolapsed lumbar disc usually produces clear dermatomal leg pain associated with neurological deficits. Leg pain is often worse than back pain and is aggravated by sitting.
531
What are the features of L3 nerve root compression?
Sensory loss over the anterior thigh.
Weakness in hip flexion, knee extension, and hip adduction.
Reduced knee reflex.
Positive femoral stretch test.
532
What are the features of L4 nerve root compression?
Sensory loss over the anterior knee and medial malleolus.
Weakness in knee extension and hip adduction.
Reduced knee reflex.
Positive femoral stretch test.
533
What are the features of L5 nerve root compression?
Sensory loss over the dorsum of the foot.
Weakness in foot and big toe dorsiflexion.
Reflexes intact.
Positive sciatic nerve stretch test.
534
What are the features of S1 nerve root compression?
Sensory loss over the posterolateral leg and lateral aspect of the foot.
Weakness in foot plantar flexion.
Reduced ankle reflex.
Positive sciatic nerve stretch test.
535
How is a prolapsed disc managed initially?
Similar to other musculoskeletal lower back pain: analgesia, physiotherapy, and exercises.
NICE recommends NSAIDs +/- proton pump inhibitors as first-line treatment, rather than neuropathic analgesia.
536
When should referral for MRI be considered in a prolapsed disc?
If symptoms persist after 4-6 weeks, referral for consideration of MRI is appropriate.
537
What is the mechanism of action of methotrexate?
Methotrexate is an antimetabolite that inhibits dihydrofolate reductase, an enzyme essential for the synthesis of purines and pyrimidines.
538
What are the main indications for methotrexate?
Inflammatory arthritis, especially rheumatoid arthritis.
Psoriasis.
Some chemotherapy regimens, such as for acute lymphoblastic leukaemia.
539
What are the adverse effects of methotrexate?
Mucositis.
Myelosuppression.
Pneumonitis: the most common pulmonary manifestation, presenting with non-productive cough, dyspnoea, malaise, and fever.
Pulmonary fibrosis.
Liver fibrosis.
540
What are the guidelines regarding methotrexate and pregnancy?
Women should avoid pregnancy for at least 6 months after stopping methotrexate.
Men should use effective contraception for at least 6 months after stopping methotrexate.
541
How is methotrexate prescribed and monitored?
Methotrexate is taken weekly, not daily.
Regular monitoring of FBC, U&E, and LFTs is required: weekly until therapy stabilizes, then every 2-3 months.
Folic acid 5 mg once weekly should be co-prescribed, taken more than 24 hours after the methotrexate dose.
The starting dose is 7.5 mg weekly.
Only one strength of methotrexate tablet (usually 2.5 mg) should be prescribed.
542
What drugs should be avoided when prescribing methotrexate?
Trimethoprim or co-trimoxazole: increases the risk of marrow aplasia.
High-dose aspirin: increases the risk of methotrexate toxicity due to reduced excretion.
543
What is the treatment of choice for methotrexate toxicity?
Folinic acid.
544
What is a complete fracture in children?
A complete fracture is when both sides of the bone cortex are breached.
545
What is a toddler's fracture?
A toddler's fracture is an oblique tibial fracture commonly seen in infants and toddlers.
546
What is a plastic deformity in pediatric fractures?
A plastic deformity is stress on the bone causing deformation without cortical disruption.
547
What is a greenstick fracture?
A greenstick fracture involves a unilateral cortical breach, meaning only one side of the bone cortex is broken.
548
What is a buckle (torus) fracture?
A buckle fracture is an incomplete cortical disruption that results in a periosteal hematoma only.
549
What is a Salter-Harris Type I fracture?
A Salter-Harris Type I fracture involves the physis only and often appears normal on X-ray.
550
What is a Salter-Harris Type II fracture?
A Salter-Harris Type II fracture involves the physis and the metaphysis.
551
What is a Salter-Harris Type III fracture?
A Salter-Harris Type III fracture involves the physis and epiphysis, extending into the joint.
552
What is a Salter-Harris Type IV fracture?
A Salter-Harris Type IV fracture involves the physis, metaphysis, and epiphysis.
553
What is a Salter-Harris Type V fracture?
A Salter-Harris Type V fracture is a crush injury involving the physis, which may appear normal on X-ray but disrupts growth.
554
What are common signs of non-accidental injury (NAI)?
Delayed presentation, multiple injuries, injuries at uncommon sites, and lack of concordance between the injury and the stated mechanism.
555
What is osteogenesis imperfecta?
Osteogenesis imperfecta is a congenital condition characterized by defective collagen formation, leading to fragile bones and frequent fractures.
556
What are wormian bones?
Wormian bones are irregular ossification patches in the skull, often seen in osteogenesis imperfecta.
557
What is osteopetrosis?
Osteopetrosis is a condition where bones become overly dense and hard, often appearing as 'marble bone' on X-ray.
558
What is the significance of a Salter-Harris Type V fracture?
Type V fractures are associated with disrupted growth and may resemble Type I on X-ray.
559
What is the most common type of elbow fracture in children?
Supracondylar fractures are the most common type of elbow fractures in children.
560
What complications are associated with supracondylar fractures?
Complications include neurovascular involvement affecting the median, radial, or ulnar nerves and the brachial artery.
561
What is the initial management for a non-displaced supracondylar fracture?
A collar and cuff should be used for immobilization.
562
How are displaced supracondylar fractures treated?
Displaced supracondylar fractures require manipulation under anesthesia with fixation.
563
What is osteoporosis?
Osteoporosis is a condition where bones gradually decrease in bone mineral density, increasing the likelihood of fragility fractures.
564
What are fragility fractures?
Fragility fractures are fractures caused by mechanical forces that would not usually lead to a fracture.
565
What is one of the most common sites of osteoporotic fractures?
The spine (vertebra).
566
What is the male-to-female ratio for osteoporosis prevalence?
The male-to-female ratio is 1:6.
567
By what age will 25% of women have developed osteoporosis?
By the age of 80.
568
Why is the prevalence of vertebral osteoporotic fractures difficult to determine?
Many patients do not present to a clinician, and fractures may not always be identifiable on X-ray.
569
What are major risk factors for osteoporotic fractures?
Advancing age, previous fragility fractures, glucocorticoid use, falls, family history of hip fractures, low BMI, tobacco smoking, and high alcohol intake.
570
What population should be assessed for fracture risk?
Women ≥ 65 years old and men ≥ 75 years old.
571
How does menopause contribute to osteoporosis?
Post-menopausal women have reduced estrogen levels, which is a risk factor for osteoporosis.
572
What are typical presentations of osteoporotic vertebral fractures?
Asymptomatic, acute back pain, breathing difficulties, gastrointestinal problems, and rarely a history of fall/trauma.
573
What are common signs of osteoporotic vertebral fractures?
Loss of height, kyphosis, and localized tenderness on palpation of spinous processes.
574
What is the first investigation ordered for suspected vertebral fractures?
X-ray.
575
What is the first investigation ordered for suspected vertebral fractures?
X-ray of the spine.
576
What can an X-ray show in osteoporotic vertebral fractures?
Wedging of the vertebra due to compression and old fractures with a sclerotic appearance.
577
What additional imaging can provide more detail on vertebral fractures?
CT spine and MRI spine.
578
What is the purpose of a DEXA scan in osteoporosis?
To assess bone mineral density and estimate the risk of future fractures.
579
What tools can estimate the 10-year fracture risk?
The FRAX tool and QFracture tool.
580
What was the traditional investigation for suspected prostate cancer?
Transrectal ultrasound-guided (TRUS) biopsy.
581
What is the first-line investigation for suspected clinically localised prostate cancer according to recent NICE guidelines?
Multiparametric MRI.
582
What is the reported complication rate of sepsis from TRUS biopsy?
1% of cases.
583
What percentage of patients experience pain lasting ≥ 2 weeks after a TRUS biopsy?
15%, with 7% experiencing severe pain.
584
What are other complications of TRUS biopsy besides sepsis and pain?
Fever (5%), haematuria, and rectal bleeding.
585
What scale is used to report the results of a multiparametric MRI?
The 5-point Likert scale.
586
What action is recommended if the Likert scale score is ≥ 3?
A multiparametric MRI-influenced prostate biopsy is offered.
587
What should be discussed with patients if the Likert scale score is 1-2?
The pros and cons of having a biopsy.
588
What are the management options for localised prostate cancer (T1/T2)?
Conservative (active monitoring & watchful waiting), radical prostatectomy, and radiotherapy (external beam and brachytherapy).
589
What are the management options for localised advanced prostate cancer (T3/T4)?
Hormonal therapy, radical prostatectomy, radiotherapy (external beam and brachytherapy).
590
What is a common complication of radical prostatectomy?
Erectile dysfunction.
591
What are potential risks associated with radiotherapy for prostate cancer?
Proctitis and increased risk of bladder, colon, and rectal cancer.
592
What is a key aim of treating metastatic prostate cancer?
Reducing androgen levels.
593
What are examples of GnRH agonists used in anti-androgen therapy?
Goserelin (Zoladex).
594
What phenomenon occurs during the initial phase of GnRH agonist therapy?
Tumour flare due to a temporary rise in testosterone levels.
595
What is used to prevent tumour flare in GnRH agonist therapy?
An anti-androgen.
596
What advantage do GnRH antagonists like degarelix have over agonists?
They suppress testosterone without causing the flare phenomenon.
597
What is bicalutamide, and how does it work?
A non-steroidal anti-androgen that blocks the androgen receptor.
598
What is cyproterone acetate, and why is it less commonly used?
A steroidal anti-androgen that prevents DHT binding; it is used less commonly since the introduction of non-steroidal anti-androgens.
599
What is abiraterone, and when is it used?
An androgen synthesis inhibitor used for hormone-relapsed metastatic prostate cancer with no or mild symptoms after androgen deprivation therapy has failed.
600
What surgical option is used to rapidly reduce testosterone levels in metastatic prostate cancer?
Bilateral orchidectomy.
601
What chemotherapy drug is used in prostate cancer management?
Docetaxel.
602
What is PSA, and why is it significant?
PSA (prostate-specific antigen) is a serine protease enzyme produced by normal and malignant prostate epithelial cells, used as a tumour marker for prostate cancer.
603
When should PSA testing be considered?
In men with suspected prostate cancer or men older than 50 who request a PSA test.
604
What is the PSA threshold for a 40–49-year-old to warrant referral on the suspected cancer pathway?
PSA > 2.5 ng/ml.
605
What is the PSA threshold for a 50–59-year-old?
PSA > 3.5 ng/ml.
606
What is the PSA threshold for a 60–69-year-old?
PSA > 4.5 ng/ml.
607
What is the PSA threshold for a 70–79-year-old?
PSA > 6.5 ng/ml.
608
What should be done for men under 40 or over 79 with possible symptoms of prostate cancer?
Use clinical judgment.
609
Name conditions or factors that can raise PSA levels.
Benign prostatic hyperplasia (BPH), prostatitis, urinary tract infection, ejaculation (within the last 48 hours), vigorous exercise (within the last 48 hours), urinary retention, and instrumentation of the urinary tract.
610
How long should PSA testing be postponed after prostatitis or urinary tract infection treatment?
At least 6 weeks.
611
What percentage of men with a PSA of 4-10 ng/ml are found to have prostate cancer?
Around 33%.
612
What percentage of men with a PSA of 10-20 ng/ml are found to have prostate cancer?
Around 60%.
613
What percentage of men with prostate cancer have a normal PSA?
Around 15%.
614
What methods are used to add meaning to a PSA level?
Age-adjusted upper limits, PSA velocity, and PSA doubling time.
615
Name some respiratory complications of rheumatoid arthritis (RA).
Pulmonary fibrosis, pleural effusion, pulmonary nodules, bronchiolitis obliterans, methotrexate pneumonitis, and pleurisy.
616
What is the most common ocular complication of RA?
Keratoconjunctivitis sicca.
617
List other ocular complications of RA.
Episcleritis, scleritis, corneal ulceration, keratitis, steroid-induced cataracts, and chloroquine retinopathy.
618
What cardiovascular risk does RA share with type 2 diabetes mellitus?
Increased risk of ischemic heart disease.
619
What bone-related complication is common in RA?
Osteoporosis.
620
What psychological complication is associated with RA?
Depression.
621
Name a rare syndrome associated with RA that includes splenomegaly and low white cell count.
Felty's syndrome.
622
What protein-related systemic complication can occur in RA?
Amyloidosis.
623
Q: What is rituximab and its mechanism of action in RA treatment?
A: Rituximab is an anti-CD20 monoclonal antibody that results in B-cell depletion.
624
Q: What are common risks associated with TNF-inhibitors like infliximab and etanercept?
A: Reactivation of tuberculosis and demyelination (etanercept).
625
Q: How is abatacept used in RA management?
A: It is a fusion protein that modulates T-cell activation but is not currently recommended by NICE.
626
Q: What percentage of rheumatoid arthritis (RA) patients experience ocular manifestations?
A: 25%.
627
Q: What is the most common ocular manifestation of rheumatoid arthritis?
A: Keratoconjunctivitis sicca.
628
Q: Name two inflammatory ocular conditions associated with RA that involve erythema.
A: Episcleritis and scleritis.
629
Q: Which ocular manifestation of RA is associated with both erythema and pain?
A: Scleritis.
630
Q: Name two serious corneal complications of RA.
A: Corneal ulceration and keratitis.
631
Q: What are two iatrogenic ocular complications in RA patients?
A: Steroid-induced cataracts and chloroquine retinopathy.
632
Q: When should women with early or poorly controlled rheumatoid arthritis (RA) defer conception?
A: Until their disease is more stable.
633
Q: How does RA typically behave during pregnancy?
A: RA symptoms tend to improve during pregnancy but only resolve in a small minority; patients tend to have a flare following delivery.
634
Q: Which DMARDs are not safe for use in pregnancy?
A: Methotrexate and leflunomide.
635
Q: How long before conception should methotrexate be stopped?
A: At least 6 months.
636
Q: Which DMARDs are considered safe in pregnancy?
A: Sulfasalazine and hydroxychloroquine.
637
Q: What have studies on TNF-α blockers and pregnancy outcomes shown?
A: No significant increase in adverse outcomes, although many patients stopped TNF-α blockers once they found out they were pregnant.
638
Q: What medication can be used at low doses during pregnancy to control RA symptoms?
A: Corticosteroids.
639
Q: Until what gestational week can NSAIDs be used in pregnancy?
A: Until 32 weeks.
640
Q: Why should NSAIDs be withdrawn after 32 weeks of pregnancy?
A: Due to the risk of early closure of the ductus arteriosus.
641
Q: Why should RA patients be referred to an obstetric anesthetist during pregnancy?
A: Due to the risk of atlanto-axial subluxation
642
Q: What are the early x-ray findings of rheumatoid arthritis?
A: Loss of joint space, juxta-articular osteoporosis, soft-tissue swelling, periarticular erosions, and subluxation.
643
Q: What is the typical mechanism of injury for a scaphoid fracture?
A: Falling onto an outstretched hand (FOOSH) or during contact sports such as football or rugby.
644
A: Due to its unusual blood supply, a scaphoid fracture can lead to avascular necrosis, especially in proximal injuries.
A: Due to its unusual blood supply, a scaphoid fracture can lead to avascular necrosis, especially in proximal injuries.
645
Q: What are the main symptoms of a scaphoid fracture?
A: Pain along the radial aspect of the wrist, at the base of the thumb, and loss of grip/pinch strength.
646
Q: What is a key physical exam finding for a scaphoid fracture?
A: Point of maximal tenderness over the anatomical snuffbox.
647
Q: What other clinical signs support the diagnosis of a scaphoid fracture?
A: Wrist joint effusion, pain on telescoping of the thumb, tenderness of the scaphoid tubercle, and pain on ulnar deviation of the wrist.
648
Q: What imaging is first-line for a suspected scaphoid fracture?
A: Plain film radiographs with anterior-posterior and lateral views, including scaphoid views.
649
Q: What imaging modality is considered definitive for scaphoid fractures?
A: MRI, which is superior in confirming or excluding the diagnosis.
650
Q: How is an undisplaced scaphoid waist fracture managed?
A: Immobilization in a cast for 6-8 weeks, with union achieved in >95% of cases.
651
Q: What is the management for a displaced scaphoid waist fracture?
A: Surgical fixation.
652
Q: What are the complications of a scaphoid fracture?
A: Non-union, leading to pain and early osteoarthritis, and avascular necrosis.
653
Q: What are the general features of systemic lupus erythematosus (SLE)?
A: Fatigue, fever, mouth ulcers, lymphadenopathy.
654
Q: What are the key skin manifestations of systemic lupus erythematosus (SLE)?
A: Malar rash, discoid rash, photosensitivity, Raynaud's phenomenon, livedo reticularis, non-scarring alopecia.
655
Q: What are the musculoskeletal features of systemic lupus erythematosus (SLE)?
A: Arthralgia and non-erosive arthritis.
656
Q: What are the cardiovascular manifestations of systemic lupus erythematosus (SLE)?
A: Pericarditis and myocarditis.
657
Q: What are the respiratory complications of systemic lupus erythematosus (SLE)?
A: Pleurisy and fibrosing alveolitis.
658
Q: What are the renal manifestations of systemic lupus erythematosus (SLE)?
A: Proteinuria and glomerulonephritis, with diffuse proliferative glomerulonephritis being the most common type.
659
Q: What are the neuropsychiatric features of systemic lupus erythematosus (SLE)?
A: Anxiety, depression, psychosis, and seizures.
660
A: 9:1, much more common in females.
A: 9:1, much more common in females.
661
Q: Which ethnic groups are more commonly affected by systemic lupus erythematosus (SLE)?
A: Afro-Caribbeans and Asian communities.
662
Q: At what age does systemic lupus erythematosus (SLE) typically onset?
A: Usually between 20-40 years of age.
663
Q: What type of hypersensitivity reaction is systemic lupus erythematosus (SLE)?
A: A type 3 hypersensitivity reaction.
664
Q: Which HLA types are associated with systemic lupus erythematosus (SLE)?
A: HLA B8, DR2, and DR3.
665
Q: What causes systemic lupus erythematosus (SLE)?
A: Immune system dysregulation leading to immune complex formation, with deposition affecting various organs including skin, joints, kidneys, and brain.
666
Q: What percentage of systemic lupus erythematosus (SLE) patients are ANA positive?
A: 99%.
667
Q: Why is ANA a useful rule-out test for systemic lupus erythematosus (SLE)?
A: Because it has a high sensitivity, although it has low specificity.
668
Q: Which antibody is highly specific for systemic lupus erythematosus (SLE) but has a sensitivity of 70%?
A: Anti-dsDNA.
669
Q: Which antibody is highly specific for systemic lupus erythematosus (SLE) with a sensitivity of 30%?
A: Anti-Smith.
670
Q: What other antibodies may be found in systemic lupus erythematosus (SLE)?
A: Anti-U1 RNP, SS-A (anti-Ro), and SS-B (anti-La).
671
Q: What inflammatory marker is generally used to monitor systemic lupus erythematosus (SLE)?
A: ESR.
672
Q: What does a normal CRP level during active systemic lupus erythematosus (SLE) indicate?
A: That a raised CRP may suggest an underlying infection rather than active SLE.
673
Q: What happens to complement levels (C3, C4) during active systemic lupus erythematosus (SLE)?
A: They are low due to consumption from immune complex formation.
674
Q: Which antibody titre can be used for disease monitoring in systemic lupus erythematosus (SLE)?
A: Anti-dsDNA titres.
675
Q: What are the basic management options for systemic lupus erythematosus (SLE)?
A: NSAIDs and sun-block.
676
Q: What is the treatment of choice for systemic lupus erythematosus (SLE)?
A: Hydroxychloroquine.
677
Q: What treatments should be considered for systemic lupus erythematosus (SLE) with internal organ involvement?
A: Prednisolone and cyclophosphamide.
678
Q: What is a severe renal complication of systemic lupus erythematosus (SLE)?
A: Lupus nephritis.
679
Q: How should SLE patients be monitored for renal complications?
A: By performing regular urinalysis to rule out proteinuria.
680
Q: What is Class IV lupus nephritis in the WHO classification?
A: Diffuse proliferative glomerulonephritis.
681
Q: What are characteristic findings of Class IV lupus nephritis on renal biopsy?
A: Endothelial and mesangial proliferation, 'wire-loop' appearance, subendothelial immune complex deposits on electron microscopy, and granular appearance on immunofluorescence.
682
Q: What is the initial therapy for focal (class III) or diffuse (class IV) lupus nephritis?
A: Glucocorticoids with either mycophenolate or cyclophosphamide.
683
Q: What is a Colles' fracture?
A: A transverse fracture of the radius, 1 inch proximal to the radiocarpal joint, with dorsal displacement and angulation, caused by a fall onto an extended outstretched hand (dinner fork deformity).
684
Q: What is a Smith's fracture (reverse Colles')?
A: A fracture with volar angulation of the distal radius fragment (garden spade deformity), caused by falling backwards onto the palm of an outstretched hand or falling with wrists flexed.
685
Q: What is a Bennett's fracture?
A: An intra-articular fracture at the base of the thumb metacarpal, often caused by impact on a flexed metacarpal (e.g., fist fights), with a triangular fragment visible on X-ray.
686
Q: What is a Monteggia's fracture?
A: A fracture involving dislocation of the proximal radioulnar joint and an associated ulna fracture, caused by a fall on an outstretched hand with forced pronation.
687
Q: What is a Galeazzi fracture?
A: A radial shaft fracture with associated dislocation of the distal radioulnar joint, caused by a fall on the hand with rotational force superimposed.
688
Q: What is a Barton's fracture?
A: A distal radius fracture (similar to Colles' or Smith's) with associated radiocarpal dislocation, caused by a fall onto an extended and pronated wrist.
689
Q: What are scaphoid fractures?
A: The most common carpal fractures, typically involving the waist, tubercle, or proximal third of the scaphoid, caused by a fall onto an outstretched hand. They present with swelling and tenderness in the anatomical snuffbox and risk of avascular necrosis.
690
Q: What is a radial head fracture?
A: A common fracture in young adults caused by a fall on an outstretched hand, presenting with local tenderness, impaired elbow movements, and sharp pain at the lateral elbow during pronation and supination extremes.
