MSK Flashcards
What is the peak age of incidence for Acute Lymphoblastic Leukaemia (ALL), and which gender is more commonly affected?
The peak incidence of ALL is around 2-5 years of age, with boys being affected slightly more commonly than girls.
What are the features of Acute Lymphoblastic Leukaemia (ALL) associated with bone marrow failure?
Features associated with bone marrow failure include:
- Anaemia: Lethargy and pallor
- Neutropenia: Frequent or severe infections
- Thrombocytopenia: Easy bruising, petechiae
What are other clinical features of Acute Lymphoblastic Leukaemia (ALL)?
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
What are the types of Acute Lymphoblastic Leukaemia (ALL)?
The types of ALL are:
- Common ALL: 75%, CD10 present, pre-B phenotype
- T-cell ALL: 20%
- B-cell ALL: 5%
What are the poor prognostic factors for Acute Lymphoblastic Leukaemia (ALL)?
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
What are ankle fractures commonly associated with?
Admission to casualty.
What rules help guide the use of x-rays in ankle injuries?
The Ottawa ankle rules.
According to the Ottawa ankle rules, when are x-rays necessary?
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.
What are some classification systems used to describe ankle fractures?
Potts, Weber, and AO systems.
How is the Weber classification system related to ankle fractures?
It is related to the level of the fibular fracture.
What defines a Weber Type A fracture?
A fracture below the syndesmosis.
What defines a Weber Type B fracture?
A fracture that starts at the level of the tibial plafond and may extend proximally to involve the syndesmosis.
What defines a Weber Type C fracture?
A fracture above the syndesmosis, which may itself be damaged.
What is a Maisonneuve fracture?
A subtype of ankle fracture involving a spiral fibular fracture with syndesmosis disruption and widening of the ankle joint, requiring surgery.
What factors determine the management of ankle fractures?
Stability of the ankle joint and patient co-morbidities.
Why should all ankle fractures be promptly reduced?
To remove pressure on the overlying skin and prevent necrosis.
What is the typical management for young patients with unstable or high-velocity ankle injuries?
Surgical repair, often using a compression plate.
Why are elderly patients with unstable ankle injuries often managed conservatively?
Because their thin bone does not hold metalwork well, and they fare better with conservative management.
What is ankylosing spondylitis associated with genetically?
HLA-B27.
What is the typical demographic for ankylosing spondylitis?
Males aged 20-30 years old, with a sex ratio of 3:1.
What are the typical presenting symptoms of ankylosing spondylitis?
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.
What does clinical examination of ankylosing spondylitis reveal?
Reduced lateral flexion, reduced forward flexion (assessed with Schober’s test), and reduced chest expansion.
How is Schober’s test performed?
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.
What are the ‘A’s associated with ankylosing spondylitis?
Apical fibrosis, Anterior uveitis, Aortic regurgitation, Achilles tendonitis, AV node block, Amyloidosis, Cauda equina syndrome.
What percentage of patients with ankylosing spondylitis experience peripheral arthritis, and in which gender is it more common?
25%, more common in females.
What is another name for anterior uveitis?
Iritis.
What part of the eye is affected in anterior uveitis?
The anterior portion of the uvea, including the iris and ciliary body.
What genetic marker is anterior uveitis associated with?
HLA-B27.
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.
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).
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.
What is cervical spondylosis?
A degenerative condition affecting the cervical spine, essentially osteoarthritis of the cervical vertebral bodies.
What causes neurological dysfunction in cervical spondylitic myelopathy?
Narrowing of the spinal canal, which presses on the spinal cord.
What percentage of patients with cervical spondylosis are thought to develop myelopathy?
5-10%.
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.
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.’
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.
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.
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.
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).
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.
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.
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.
What is the initial symptom of chickenpox?
Fever.
What is the progression of the rash in chickenpox?
Starts as macular, then papular, and finally vesicular.
Where does the chickenpox rash typically start?
On the head and trunk before spreading.
How severe is the systemic upset in chickenpox?
It is usually mild.
What are the prodromal symptoms of measles?
Irritability, conjunctivitis, and fever.
What are Koplik spots?
White spots (‘grain of salt’) on the buccal mucosa, seen in measles.
Where does the measles rash start and spread?
Starts behind the ears and spreads to the whole body, becoming blotchy and confluent.
What are the initial symptoms of mumps?
Fever, malaise, and muscular pain.
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.
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.
Which lymph nodes are commonly involved in rubella?
Suboccipital and postauricular lymphadenopathy.
What is another name for erythema infectiosum?
Fifth disease or ‘slapped-cheek syndrome.’
What virus causes erythema infectiosum?
Parvovirus B19.
What are the symptoms of erythema infectiosum?
Lethargy, fever, headache, and a ‘slapped-cheek’ rash that spreads to the proximal arms and extensor surfaces.
What causes scarlet fever?
Erythrogenic toxins produced by Group A haemolytic streptococci.
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).
What virus causes hand, foot, and mouth disease?
The coxsackie A16 virus.
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.
How common are cleft lip and palate?
They affect around 1 in every 1,000 babies.
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%).
What is the inheritance pattern of cleft lip and palate?
Polygenic inheritance.
How does maternal antiepileptic use affect cleft lip and palate risk?
It increases the risk.
What causes cleft lip developmentally?
Failure of the fronto-nasal and maxillary processes to fuse.
What causes cleft palate developmentally?
Failure of the palatine processes and nasal septum to fuse.
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.
At what age is cleft lip typically repaired?
Practices vary, but repair usually occurs from the first week of life to three months.
At what age is cleft palate typically repaired?
Between 6-12 months of age.
What is developmental dysplasia of the hip (DDH)?
A condition replacing the term ‘congenital dislocation of the hip,’ affecting around 1-3% of newborns.
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.
Which hip is more commonly affected by DDH?
The left hip.
What percentage of DDH cases are bilateral?
Around 20%.
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.
What are the tests used to screen for DDH in newborns and at the six-week check?
The Barlow and Ortolani tests.
What does the Barlow test assess?
It attempts to dislocate an articulated femoral head.
What does the Ortolani test assess?
It attempts to relocate a dislocated femoral head.
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.
What imaging modality is used to confirm a diagnosis of DDH in infants under 4.5 months?
Ultrasound.
What imaging modality is used if the infant is older than 4.5 months?
X-ray.
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.
What device is used to manage DDH in children younger than 4-5 months?
A Pavlik harness (dynamic flexion-abduction orthosis).
What is the management for older children with DDH?
Surgery may be required.
What is discitis?
An infection in the intervertebral disc space that can lead to complications such as sepsis or an epidural abscess.
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).
What is the most common bacterial cause of discitis?
Staphylococcus aureus.
What are the possible causes of discitis?
Bacterial (most commonly Staphylococcus aureus), Viral, TB, Aseptic.
What imaging modality has the highest sensitivity for diagnosing discitis?
MRI.
When might a CT-guided biopsy be needed in discitis?
To guide antimicrobial treatment.
What is the standard treatment for discitis?
Six to eight weeks of intravenous antibiotic therapy.
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).
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.
What tests are used to assess for endocarditis in patients with discitis?
Transthoracic echo or transesophageal echo.
What are the complications of discitis?
Sepsis
Epidural abscess
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.
How quickly do acute gout episodes reach maximal intensity?
Within 12 hours.
What are the main symptoms of a gout flare?
Significant pain
Swelling
Erythema
What percentage of first presentations of gout affect the 1st metatarsophalangeal (MTP) joint?
Around 70%.
What is the term for gout affecting the 1st MTP joint?
Podagra.
What other joints are commonly affected by gout?
Ankle
Wrist
Knee
What can happen if gout is left untreated?
Repeated acute episodes can lead to chronic joint damage.
What is the role of uric acid measurement in gout diagnosis?
A uric acid level ≥ 360 µmol/L supports a diagnosis of gout.
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.
What is the hallmark finding in synovial fluid analysis for gout?
Needle-shaped negatively birefringent monosodium urate crystals under polarised light.
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
What is haemophilia?
An X-linked recessive disorder of coagulation caused by a deficiency of clotting factors.
What clotting factor is deficient in haemophilia A?
Factor VIII.
What clotting factor is deficient in haemophilia B (Christmas disease)?
Factor IX.
What percentage of haemophilia cases have no family history?
Up to 30%.
What are the main clinical features of haemophilia?
Haemoarthroses
Haematomas
Prolonged bleeding after surgery or trauma
What are the typical blood test findings in haemophilia?
Prolonged APTT
Normal bleeding time, thrombin time, and prothrombin time
What complication can develop in 10-15% of patients with haemophilia A?
Development of antibodies to factor VIII treatment.
What are the typical features of influenza?
Fever > 38ºC
Myalgia
Lethargy
Headache
Rhinitis
Sore throat
Cough
Diarrhoea and vomiting
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.
What is the first-line antiviral treatment for influenza?
Oseltamivir.
What is the second-line antiviral treatment for influenza?
Zanamivir.
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.
How does septic arthritis or osteomyelitis present in children?
With an unwell child and a high fever.
How does juvenile idiopathic arthritis typically present in a limping child?
The limp may be painless.
What feature of the history often points to trauma as the cause of a limp in a child?
A clear history of injury.
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.
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.
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.
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)
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
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
How is spinal stenosis diagnosed?
It requires MRI to confirm the diagnosis.
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)
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
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.
What is the median age at presentation for multiple myeloma?
70 years old.
What mnemonic is used to remember the key features of myeloma?
CRABBI: Calcium, Renal, Anaemia, Bleeding, Bones, Infection.
What causes hypercalcaemia in multiple myeloma?
Increased osteoclastic bone resorption caused by cytokines (e.g., IL-1, tumour necrosis factor) released by myeloma cells.
What are the symptoms of hypercalcaemia in myeloma?
Constipation, nausea, anorexia, and confusion.
What causes renal impairment in multiple myeloma?
Monoclonal immunoglobulin light chain deposition in renal tubules, amyloidosis, nephrocalcinosis, or nephrolithiasis.
What are the symptoms of renal impairment in myeloma?
Dehydration and increased thirst.
What causes anaemia in multiple myeloma?
Bone marrow crowding suppresses erythropoiesis.
What are the symptoms of anaemia in myeloma?
Fatigue and pallor.
What causes bleeding in multiple myeloma?
Thrombocytopenia due to bone marrow crowding.
What bone-related symptoms are seen in multiple myeloma?
Pain, lytic bone lesions, and an increased risk of pathological fractures.
Why are infections common in myeloma?
Due to reduced production of normal immunoglobulins.
What other features may occur in multiple myeloma?
Amyloidosis, carpal tunnel syndrome, neuropathy, and hyperviscosity.
What are the key blood investigation findings in myeloma?
Anaemia, rouleaux formation on blood film, renal failure, and hypercalcaemia.
What is found on protein electrophoresis in multiple myeloma?
Monoclonal IgA/IgG proteins in serum and Bence Jones proteins in urine.
How is the diagnosis of myeloma confirmed?
Bone marrow aspiration showing significantly raised plasma cells.
What imaging findings are associated with myeloma?
‘Rain-drop skull’ on X-ray or lytic bone lesions on whole-body MRI.
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.
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.
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.
What cancers are commonly associated with spinal cord compression?
Lung, breast, and prostate cancer.
What is the earliest and most common symptom of spinal cord compression?
Back pain.
How does back pain in spinal cord compression typically present?
It may worsen when lying down or coughing.
What neurological features may occur in spinal cord compression?
Lower limb weakness, sensory loss, and numbness.
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.
How are tendon reflexes affected in spinal cord compression?
Reflexes are increased below the lesion level and absent at the lesion level.
What is the key imaging investigation for spinal cord compression?
Urgent whole-spine MRI within 24 hours of presentation.
What is the first-line medical management for spinal cord compression?
High-dose oral dexamethasone.
What specialist intervention should be urgently considered in spinal cord compression?
Oncological assessment for radiotherapy or surgery.
What is osteoarthritis (OA) of the hand also referred to as?
Nodal arthritis.
What causes osteoarthritis of the hand?
Loss of cartilage at synovial joints, often accompanied by degeneration of underlying bone.
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.
At what age does hand osteoarthritis typically present?
Rarely before 55 years of age.
Which joints are most commonly affected by hand osteoarthritis?
Carpometacarpal joints (CMC), distal interphalangeal joints (DIPJs), and less commonly the proximal interphalangeal joints (PIPJs).
What are Heberden’s nodes?
Painless bony swellings at the distal interphalangeal joints (DIPJs).
What are Bouchard’s nodes?
Painless bony swellings at the proximal interphalangeal joints (PIPJs).
What deformity is referred to as ‘squaring of the thumbs’ in OA?
Fixed adduction of the thumb due to deformity of the carpometacarpal joint.
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.
What risk factors increase the likelihood of hand osteoarthritis?
Previous joint trauma, obesity, hypermobility, and certain occupations such as cotton workers and farmers.
Which condition reduces the risk of developing osteoarthritis?
Osteoporosis.
What radiological features are seen in hand osteoarthritis?
Osteophytes and joint space narrowing.
When can radiological signs of OA be visible relative to symptoms?
Signs may be visible on X-ray before symptoms develop.
What is osteomalacia?
Softening of the bones secondary to low vitamin D levels, leading to decreased bone mineral content.
What term is used for osteomalacia in growing children?
Rickets.
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.
What are the key features of osteomalacia?
Bone pain, bone/muscle tenderness, fractures (especially femoral neck), and proximal myopathy leading to a waddling gait.
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).
What radiological feature is characteristic of osteomalacia?
Translucent bands (Looser’s zones or pseudofractures) on X-ray.
What is the treatment for osteomalacia?
Vitamin D supplementation (with an initial loading dose) and calcium supplementation if dietary calcium is inadequate.
What is osteomyelitis?
Infection of the bone, subclassified into haematogenous and non-haematogenous osteomyelitis.
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.
What are the risk factors for haematogenous osteomyelitis?
Sickle cell anaemia, intravenous drug use, immunosuppression (medication or HIV), and infective endocarditis.
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.
What are the risk factors for non-haematogenous osteomyelitis?
Diabetic foot ulcers, pressure sores, diabetes mellitus, and peripheral arterial disease.
What is the most common cause of osteomyelitis?
Staphylococcus aureus, except in patients with sickle-cell anaemia, where Salmonella species predominate.
What is the imaging modality of choice for osteomyelitis?
MRI, with a sensitivity of 90-100%.
What is the standard management for osteomyelitis?
Flucloxacillin for 6 weeks or clindamycin if penicillin-allergic.
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.
What are the most commonly affected sites in Paget’s disease?
The skull, spine/pelvis, and long bones of the lower extremities.
What are the predisposing factors for Paget’s disease?
Increasing age, male sex, northern latitude, and family history.
How often is Paget’s disease symptomatic?
Only 5% of patients are symptomatic.
What is the stereotypical presentation of Paget’s disease?
An older male with bone pain and an isolated raised alkaline phosphatase (ALP).
What are the clinical features of untreated Paget’s disease?
Bone pain, bowing of the tibia, and bossing of the skull.
What are the key findings in blood investigations for Paget’s disease?
Raised alkaline phosphatase (ALP) with typically normal calcium and phosphate levels.
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.
What imaging is used to assess sites of active bone lesions in Paget’s disease?
Bone scintigraphy, showing increased uptake at active bone lesions.
What are the indications for treatment of Paget’s disease?
Bone pain, skull or long bone deformity, fracture, or periarticular Paget’s.
What is the main treatment for Paget’s disease?
Bisphosphonates (oral risedronate or IV zoledronate).
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.
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.
What causes Perthes’ disease?
Impaired blood supply to the femoral head, leading to bone infarction.
How common is Perthes’ disease in boys compared to girls?
It is 5 times more common in boys.
What percentage of Perthes’ disease cases are bilateral?
Around 10% of cases.
What are the features of Perthes’ disease?
Hip pain developing progressively over a few weeks, limp, stiffness, and reduced range of hip movement.
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.
How is Perthes’ disease diagnosed?
Plain x-ray, with technetium bone scan or MRI if the x-ray is normal and symptoms persist.
What are the complications of Perthes’ disease?
Osteoarthritis and premature fusion of the growth plates.
What is Catterall Stage 1 of Perthes’ disease?
Clinical and histological features only.
What is Catterall Stage 2 of Perthes’ disease?
Sclerosis with or without cystic changes and preservation of the articular surface.
What is Catterall Stage 3 of Perthes’ disease?
Loss of structural integrity of the femoral head.
What is Catterall Stage 4 of Perthes’ disease?
Loss of acetabular integrity.
What is the management goal for Perthes’ disease?
To keep the femoral head within the acetabulum using casts or braces.
How is Perthes’ disease managed in children under 6 years?
Observation.
How is Perthes’ disease managed in older children or severe deformities?
Surgical management.
What is the prognosis for Perthes’ disease?
Most cases resolve with conservative management, and early diagnosis improves outcomes.
What is polyarthritis?
Inflammation of five or more joints simultaneously within the first six weeks of symptom onset.
What are the typical features of polyarthritis?
Pain, swelling, and stiffness in multiple joints, which may have a symmetrical or asymmetrical pattern.
What systemic symptoms may accompany polyarthritis?
Fever, weight loss, and fatigue, reflecting the underlying systemic inflammatory process.
What are some inflammatory arthritis conditions associated with polyarthritis?
Rheumatoid arthritis, psoriatic arthritis, SLE, and seronegative spondyloarthropathies.
What viral infections can cause polyarthritis?
EBV, HIV, hepatitis, mumps, and rubella.
What infective causes other than viral can lead to polyarthritis?
Tuberculosis and disseminated gonococcal infection.
What are some symptoms reflecting the underlying systemic inflammatory process?
Fever, weight loss, and fatigue.
What are some non-infectious differential diagnoses for polyarthritis?
Pseudogout, Henoch-Schönlein purpura, and sarcoidosis.
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.
What age group is typically affected by PMR?
Patients older than 60 years.
What is the usual onset pattern of PMR?
Rapid onset, typically within less than one month.
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.
Is weakness a symptom of PMR?
No, weakness is not considered a symptom of PMR.
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.
What is the treatment for PMR?
Prednisolone, typically 15 mg/day, with patients usually responding dramatically to steroids.
What should be considered if a patient does not respond to steroids in PMR?
An alternative diagnosis should be considered.
What causes pseudogout?
Pseudogout is caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium.
What is the more accurate term for pseudogout?
Acute calcium pyrophosphate crystal deposition disease.
What is pseudogout strongly associated with?
Increasing age.
What underlying risk factors are associated with pseudogout in patients under 60?
Haemochromatosis, hyperparathyroidism, low magnesium, low phosphate, acromegaly, and Wilson’s disease.
Which joints are most commonly affected by pseudogout?
The knee, wrist, and shoulders.
What are the findings in joint aspiration for pseudogout?
Weakly positively birefringent rhomboid-shaped crystals.
What are the x-ray findings in pseudogout?
Chondrocalcinosis, seen as linear calcifications of the meniscus and articular cartilage.
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.
What is psoriatic arthropathy?
Psoriatic arthropathy is an inflammatory arthritis associated with psoriasis, classified as one of the seronegative spondyloarthropathies.
How does psoriatic arthropathy correlate with cutaneous psoriasis?
It correlates poorly with cutaneous psoriasis and may precede the development of skin lesions.
What percentage of patients with skin lesions develop psoriatic arthropathy?
Around 10-20%.
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.
What is arthritis mutilans?
A severe deformity of the fingers or hands, leading to ‘telescoping fingers.’
What are some other signs of psoriatic arthropathy?
Psoriatic skin lesions, enthesitis, tenosynovitis, dactylitis, and nail changes (e.g., pitting, onycholysis).
What are the characteristic x-ray findings in psoriatic arthropathy?
Erosive changes with new bone formation, periostitis, and a ‘pencil-in-cup’ appearance.
How is mild psoriatic arthropathy managed?
Mild peripheral arthritis or mild axial disease may be treated with NSAIDs.
What treatments are used for moderate to severe psoriatic arthropathy?
Methotrexate, monoclonal antibodies (e.g., ustekinumab, secukinumab), and apremilast.
How does the prognosis of psoriatic arthropathy compare to rheumatoid arthritis?
Psoriatic arthropathy has a better prognosis than rheumatoid arthritis.
What is reactive arthritis?
Reactive arthritis is an arthritis that develops after an infection where the organism cannot be recovered from the joint.
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.
What is the classic triad of reactive arthritis?
Urethritis, conjunctivitis, and arthritis.
What is the mnemonic associated with reactive arthritis?
“Can’t see, pee, or climb a tree.”
What are the two forms of reactive arthritis?
Post-dysenteric form and post-STI form (sexually acquired reactive arthritis or SARA).
Which organisms are commonly associated with the post-dysenteric form?
Shigella flexneri, Salmonella typhimurium, Salmonella enteritidis, Yersinia enterocolitica, and Campylobacter.
Which organism is commonly associated with the post-STI form?
Chlamydia trachomatis.
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.
How is reactive arthritis managed?
Symptomatic treatment includes analgesia, NSAIDs, and intra-articular steroids. Sulfasalazine and methotrexate are sometimes used for persistent disease.
How long do symptoms of reactive arthritis typically last?
Symptoms rarely last more than 12 months.
What is scleritis?
Scleritis is a full-thickness inflammation of the sclera, typically causing a red, painful eye.
What are the risk factors for scleritis?
Rheumatoid arthritis (most commonly associated), systemic lupus erythematosus, sarcoidosis, and granulomatosis with polyangiitis.
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.
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.
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.
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.
What is the most common cause of septic arthritis?
Hematogenous spread, often from distant bacterial infections such as abscesses.
Which joint is most commonly affected in adults with septic arthritis?
The knee.
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.
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.
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.
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.
Which joints are most commonly affected in children with septic arthritis?
The hip, knee, and ankle.
What are the typical symptoms of septic arthritis in children?
Joint pain, limp, fever, and systemic unwellness such as lethargy.
What are the signs of septic arthritis in children?
A swollen, red joint with only minimal movement possible.
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.
What is the Kocher criteria for diagnosing septic arthritis in children?
Fever >38.5°C, non-weight bearing, raised ESR, raised WCC.
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.
