MSK Flashcards
Mechanical causes of joint pain
Trauma - # and sprains
OA
Hypermobility disorders
Contractures
Inflammatory causes of joint pain
Gout/Pseudogout Septic Arthritis RA Spondyloarthropathies Autoimmune connective tissue disorders (SLE, systemic sclerosis) Osteomyelitis
Mechanical and inflammatory causes of joint pain
Bursitis
Polio
Carpal Tunnel Syndrome (CTS)
Tendonitis
What are the Spondyloarthropathies?
Psoriatic arthritis
Ankylosing spondylitis
Reactive arthritis
Enteropathic arthritis
What is important to remember in a back pain Hx?
Important to remember – RISK:
Referred Pain
Ischaemia
Sepsis
Kids
Back pain Hx - HPC:
S - Which joints are involved? (patterns?)
O - Sudden or insidious onset?
C - Describe the pain
R - Does it radiate anywhere?
A - Systemic symptoms? Changes in Sensation?
T - Continuous? On and Off? Progressive?
E - Improves or worsens on movement? Any morning stiffness?
S - Pain score 1-10 & Quantify loss of function
SR:
Extra-articular manifestations – eyes, skin, bowels
Night sweats, fevers, weight loss.
Back pain Hx - PMHx:
Previous joint disease Hx of recent illness Surgeries Trauma – fractures, open fractures, sprains Thyroid disease Periods of immobility Sickle cell disease Malignancy
Back pain Hx - DHx:
Allergies
OTC
Hormone therapy
Chemotherapy
Polypharmacy – falls risk
Back pain Hx - SHx:
Smoking, alcohol, drug use. Occupation Exercise/leisure ADLs Dependence or caring responsibilities Accommodation – stairs, etc. Diet and fluids.
Back pain Hx - FHx:
FHx of Any MSK/inflammatory conditions
May also impact the patients understanding/pre-conceptions.
Osteoarthritis
= a dynamic but slow process of remodelling and proliferation of new bone, cartilage and connective tissues, as well as focal degeneration of articular cartilage.
Any synovial joint can be affected but most commons sites are knees, hips and small joints of the hands.
Risk factors for OA
Any factor that increases stress on a joint or affects physiological response to joint damage is a risk factor.
- Genetic factors
- Patient factors – ageing, females, obesity, high bone density
- Biomechanical factors – history of joint injury, occupational or recreational use of the joint, reduced muscle strength, joint laxity, joint malalignment.
Prevalence of OA
Women > Men.
Uncommon before 50
In adults aged >50 – knee most common, followed by hip and hand
Changes occurring in OA
Loss of articular cartilage
Subchondral bone is affected:
- Osteophytes
- Sclerosis – thickening of the bone
- Cysts – lytic loss of bone density
Influx of immune cells to the joint
OA - radiological findings
L – loss of joint space
O – osteophytes
S – subchondral sclerosis
S – subchondral cysts
Most common joints affected in OA
Cervical/Lumbar spine
Tibiofemoral joint
Acetabulofemoral joint
PIPs and DIPs
Carpometacarpal joint
Metacarpophalangeal joint
1st Metatarsophalangeal joint
Symptoms of OA
Continuous pain
Worsens on movement, improves on rest
No significant morning stiffness (<30 mins)
Signs of OA
Bony enlargement of the affected joint
Reduced Range of Movement
Joint Crepitus
Deformity - Varus/valgus
Effusion
Antalgic gait
Name for the bony expansion of DIP joints
= Heberden’s nodes
Name for the bony expansion of PIP joints
= Bouchard’s nodes
Varus deformity
= deformity in which an anatomical part is turned inwards towards the midline
Valgus deformity
= deformity in which an anatomical part is turned outward away from the midline
Rheumatoid Arthritis
= an inflammatory arthritis (severe form of chronic synovitis), leading to destruction and ankylosis of the joints
The condition is of autoimmune aetiology, believed to be initiated by a microbial agent.
RA is polyarticular, symmetrical and systemic
Prevalence of RA
~1% of UK population.
F:M - 3:1
Onset peaks in people aged 30-50
Approx. 1/3 of people stop work within 2 years of onset.
Pathophysiology of RA
- Inflammatory cells infiltrate into synovial joint:
- T cells, B cells, macrophages and plasma cells release cytokines
- Causes the synovium to release proteolytic enzymes, which destroy bone and cartilage in the joint. - Synovial membrane becomes vascularised and there is villous hypertrophy leading to pannus (vascularised granulation tissue) formation.
- Joint deformity due to subluxation results as articular surfaces are destroyed.
the systemic nature of RA
The inflammatory process is systemic, and synovitis occurs in multiple joints.
This leads to a characteristic pattern of disease – symmetrical and polyarticular
Classic history: pain, swelling and erythema of the small joints of the hands (and/or feet) bilaterally due to synovitis.
Systemic symptoms:
- Fever and fatigue are very common.
- Depression
- Associated with complications in numerous body systems.
Which joints are most commonly affected by RA?
MCPs PIPs Wrist Elbow Glenohumeral joint Cervical spine Hip Knee Ankle, Tarsal MTPs
RA - clinical presentation
On and off pain, which improves on movement and worsens on rest.
Deformities of hands/feet
Morning stiffness (>30-60 mins)
Erythema and swelling.
Fatigue and Fever
Good questions to look for extra-articular manifestations of RA:
- Any skin changes or lumps or bumps?
- Any unusual bruising?
- Any shortness of breath or difficulty breathing?
- Any soreness or redness of the eyes?
- Any change in sensation of the hands/feet?
RA-associated disease - skin
rheumatoid nodules,
fragility,
vasculitis (rare),
Pyoderma gangrenosum
RA-associated disease - lungs
pleural effusions interstitial lung disease bronchiolitis rheumatoid nodules of the lung vasculitis
RA-associated disease - heart
pericarditis
premature atherosclerosis
vasculitis
valvular disease
RA-associated disease - eye
Keratoconjunctivitis Sicca (dry eyes)
episcleritis
peripheral ulcerative keratopathy
thinning of the sclera
RA-associated disease - neurological
carpal tunnel syndrome
peripheral neuropathy
mononeuritis multiplex
RA-associated disease - haematopoeitic
anaemia,
thrombocytosis
lymphadenopathy
felty syndrome
RA-associated disease - bone
osteopaenia
Rheumatoid nodules
seen in ~20% of patients with RA,
seen almost exclusively in patients who have Rheumatoid factor or anti-CCP antibodies (blood tests).
Nodules can occur anywhere but are often on extensor surfaces (e.g. olecranon and ulnar border).
RA - on examination of early disease
Erythema
Palpable inflammation
Warm to touch
Tenderness on MCP/forefoot squeeze
RA - on examination of advanced disease
Ulnar deviation of the fingers at the MCP joints.
Boutonniere deformities
Swan-neck deformities
Toe deformities: Hammer toes, claw toes, mallet toes
Deformity/displacement of wrist.
Rheumatoid nodules
Boutonniere deformities
Fixed flexion at the PIP joint and extension at DIP joint
Swan-neck deformities
Extension at the PIP and fixed flexion at the DIP.
Investigations for RA
- FBC, U&E, LFTs, CRP/ESR
- Serum Rheumatoid factor (found in ~60-70% of people with RA)
- Serum Anti CCP (found in ~80% of people with RA)
- X ray of joints
- USS/MRI of joints
Radiological findings in RA
Loss of joint space
Erosion
Soft tissue swelling
Soft bones (osteopenia)
What are some variants of RA?
- Juvenile variant
- Felty’s syndrome (RA associated with Splenomegaly and Neutropenia)
- RA associated with UC and Sjogren’s syndrome
What is a bursa?
= a sac with a potential space that reduces friction
160 in the body - commonly around joints, muscles and bones
what is bursitis?
= inflammation of a bursa
what is an enthesis?
what is enthesitis?
= the connective tissue at the junction of a bone and tendon
enthesitis = inflammation of an enthesis
What does a tendon do?
Dense and compact collagenous tissue, which connects muscle to bone
What is tendinitis and what is tendinosis?
tendinitis = acute or chronic inflammation of a tendon
tendinosis = non-inflammatory intra-tendinous atrophy, often associated with chronic tendinitis
What is a ligament?
= collagenous tissue which connects bone to bone
Sprain vs strain
sprain = tearing of a ligament strain = tearing of muscle fibres
what is a Regional periarticular pain disorder?
Painful, sometimes disabling musculoskeletal syndromes.
Not articular in origin but arising from tendons and bursae.
Also known as “overuse” or “repetitive use” syndromes.
These may be ignored/misdiagnosed as arthritis/blamed on ageing
What are some periarticular syndromes of the elbow?
Lateral epicondylitis
Medial epicondylitis
Olecranon bursitis
what does the subacromial bursa do?
provides a cushion between the acromion and supraspinatus muscles it also cushions between the deltoid tendon and the greater tubercle of the humerus
Symptoms of subacromial bursitis and findings OE
pain at the front and side of the shoulder,
pain on movement of arm (sport and activities of daily living),
difficulty sleeping,
stiffness.
OE: • pain on shoulder abduction; • pain on palpation of anterior shoulder, • mild swelling anteriorly, • reduced function.
Complications of subacromial bursitis
May lead to a tear of the rotator cuff, if the supraspinatus tendon degenerates
What inserts into the lateral epicondyle?
The insertion point of the common extensor tendon
Extensor carpi radialis brevis also inserts superior to common extensor tendon
what is lateral epicondylitis?
“tennis elbow”
= a tendinitis (inflammation) or tendinopathy (degeneration) of the extensor tendon, due to repetitive use of the extensor muscles.
Symptoms of lateral epicondylitis and findings OE
- pain at the outer elbow or upper forearm,
- pain on gripping objects (pen, cup, tennis racquet),
- pain on twisting arm (such as opening a door),
- occupational pain (e.g. painter/decorator)
OE:
• tenderness on palpation of lateral epicondyle and extensor muscles,
• pain (possibly weakness) of resisted extension of wrist and fingers.
Plantar aponeurosis
= a band of connective tissue supporting the arch of the foot.
It runs from the calcaneal tuberosity to the base of the toes
Plantar fasciitis
Degeneration of the plantar aponeurosis
often due to overuse through running and standing or increased body weight
The collagen fibres of the aponeurosis become disorganised and weaken
Plantar fasciitis - symptoms and OE
- Plantar heel pain – particularly on initiation of weight bearing (worse in the morning after sleep or period of immobilisation).
- Pain is bad initially but improves with activity.
OE:
• Tenderness on palpation of the plantar aponeurosis/ calcaneus,
• Pain worse on dorsiflexion of the foot.
• Achilles tendon may feel tight.
Ganglion Cyst
= fluid filled cystic extension of the joint capsules and tendon sheaths.
Insidious onset, usually painless, soft lump.
Often occurs on back of wrist
Often affects the young (<30).
What are the autoimmune connective tissue disorders?
Rheumatoid arthritis
Scleroderma
Systemic lupus erythematosus (SLE)
Polymyositis
types of scleroderma
Can have either:
- Limited cutaneous scleroderma (1/3) – only affects the skin
- Systemic scleroderma (2/3) – there is cutaneous sclerosis with visceral involvement.
What are the clinical features of scleroderma in the skin?
Sclerodactyly
Raynaud’s phenomenon
abnormalities of nail bed (e.g. splinter haemorrhages)
puffy/swollen hands, tightness of fingers
What are the clinical features of scleroderma in the MSK system?
arthralgias - joint pain
myalgias - muscle pain
What are the clinical features of scleroderma in the GI system?
oesophageal dysphagia
dyspepsia
What are the clinical features of scleroderma in the lungs?
pulmonary artery hypertension
interstitial lung disease
What are the clinical features of scleroderma in the CV system?
pericardial/myocardial disease
what is SLE?
= a chronic multisystem inflammatory disease of autoimmune nature
fairly uncommon, gradual onset
pathophysiology of SLE
Deposition of immune complexes (DNA and antibodies) cause inflammatory lesions in kidney, brain, heart, spleen, lung, GI tract, skin, peritoneum
what are the skin signs of SLE?
often the first signs
- facial rash, redness
- rash on body
- sensitive to sun
- hair loss/nail changes
where are the primary sagittal curvatures ?
the thoracic (kyphosis) sacrococcygeal regions.
where are the secondary sagittal curvatures?
cervical (lordosis) region
lumbar (lordosis) region
What are the joints of the spine?
Facet joints are synovial joints between the superior and inferior articular processes.
Vertebral Discs are fibro-cartilaginous joints
What movements do the facet joints allow in the throacic/lumbar spine?
Lumbar spine: allow flexion/extension and no rotation or lateral flexion.
Thoracic spine: allow more rotation and lateral flexion.
Ligaments of the Spine
Posterior longitudinal ligament
Anterior longitudinal ligament
Supraspinous ligament
Interspinous ligament
Ligamentum flavum
Posterior longitudinal ligament
C2 to sacrum
attached to posterior aspect of vertebral bodies and intervertebral discs
maintains stability.
Anterior longitudinal ligament
C1 to sacrum
attached to anterior surface of vertebral bodies and intervertebral discs
maintains stability
Supraspinous ligament
cross tips of spinous processes from C7 to sacrum.
Intraspinous ligament
link adjacent spinous processes
Ligamentum flavum
unite adjacent laminae, limits flexion of vertebral bodies.
Preserves curvature of spine.
How many spinal nerve roots are there?
- Eight cervical (seven vertebrae)
- Twelve thoracic
- Five lumbar
- Five sacral and one coccygeal.
Where does the adult spinal cord terminate?
L1
What is a radiculopathy?
= irritation or damage to a nerve root, causing pain along a dermatome
can also be called a pinched spinal nerve
what makes up the vertebral disc?
Anulus fibrosus (outer, fibrous component) Nucleus pulposus (inner, gel-like component)
Disc prolapse
when the Anulus fibrosus ruptures and the Nucleus pulposus is forced out, exerting pressure on local nerves or the spinal cord.
What are the types of back pain?
Non-specific - no obvious cause
Mechanical: caused by joint, bones or soft tissues around the spine
What is a form of mechanical back pain which is an emergency?
cauda equina syndrome
Lumbar sprain/strain
Intense pain followed by spasm
very common
due to stretching/tearing of muscle or ligament fibres
surrounding muscle fibres spasm to protect the injury
Degenerative disc/facet joints
usually older patient
Gradual onset of pain
Due to osteoarthritic changes to vertebrae
If worse on extension - facet joint
if worse on flexion - disc joint
what is spinal stenosis?
anatomical narrowing of the spinal canal, secondary to osteophytes and facet joint hypertrophy
what is important to find out in a back pain history?
- If your patient had trauma of a fall.
- Differentiate between mechanical and non-mechanical back pain.
=> Is there pain at night or at rest? (usually non-mechanical cause) - Location of the pain
- Lumbar back pain is usually mechanical.
- Thoracic back pain is more likely to be serious. - any Red flag symptoms
Red flag back pain symptoms
- Profound neurological deficit
- Systemic features – weight loss, night sweats, fever, fatigue
- Medication – prolonged steroid use
- Patient age and frailty
- History of cancer
- History of injecting drug use
Red flag symptoms for cauda equine syndrome
- Change in sensation (saddle anaesthesia)
- Change in bladder or bowel function
- Weakness or loss of sensation in the lower limbs
What are the non-mechanical causes of back pain?
Infection - osteomyelitis, disctitis, epidural abscess
Malignancy
Inflammatory - spondyloarthropathies, RA
Autoimmune
Bone malignancy
Metastases - 25x more common than primary bone tumours
=> commonly from breast, thyroid, kidney, lung, prostate
Primary bone tumours - Osteosarcoma, chondrosarcoma, Ewing’s sarcoma
what is osteoporosis?
= the loss of trabecular bone
occurs when bones lose an excessive amount of their protein and mineral content, particularly calcium
Over time, bone mass and bone strength are decreased
what is the long-term outcome of osteoporosis
loss of bone strength - bones become fragile and break more easily (= fragility fractures).
Why is osteoporosis referred to as the “silent thief”
The process of Osteoporosis is completely asymptomatic
Diagnosis of osteoporosis
DEXA scan to measure the average mineral content of the bone
T-Score is calculated from the bone mineral density (BMD) measurement by working out how much it deviates from that of a young adult
A T-score of less than -2.5 indicates osteoporosis.
A T-score of -1 and -2.5 indicates osteopenia
what is the FRAX tool used for?
to calculate the 10-year probability of developing Osteoporosis.
Risk factors for osteoporosis
Asian/Caucasian
Female
Early menopause (46 years) Late menarche
Slender build (BMI < 18)
Smoking
> 4 units alcohol per day
Chronic liver/kidney disease Crohn’s Disease Coeliac Disease RA FHx of osteoporosis COPD Overactive thyroid
Steroids
Management of osteoporosis
Diet - Calcium and vitamin D supplementation
Exercise - weight bearing exercises
Smoking cessation, alcohol reduction
Review medications
MDT interventions
Medication - symptom control, Anti-resorptives, etc.
what is gout?
a crystal arthropathy
occurs when excess uric acid (a normal waste product) collects in the body, and needle‐like urate crystals deposit in the joints
where can excess uric acid deposit?
in the joints => gout
in the urinary tract => kidney stones
what can cause excess uric acid in the body?
- Uric acid production increases
2. The kidneys are not excreting uric acid efficiently enough
Gout - presentation
intense episodes of painful swelling in single joints
most often in the feet, especially the big toe.
the swollen site may be red and warm
Diet risk factors for gout
Foods high in purines – Shellfish, cod, salmon, gravies, red meat, soups and organ meats such as liver.
Sugary drinks and foods that are high in fructose
Alcohol in excess
Non-diet risk factors for gout
Obesity Hypertension Hyperlipidaemia Diabetes Kidney Disease
Stress/infections/illness/hospitalisations
Some medications, such as:
- low-dose aspirin
- certain diuretics such as hydrochlorothiazide and spironoloactone
- immunosuppressants used in organ transplants such as cyclosporine and tacrolimus
Diagnosis of gout
Pattern of joint involvement, characteristic symptoms and time course,
Synovial fluid aspiration and microscopy
Blood tests - routine and serum urate
X ray – may show joint damage in gout of long duration
USS/CT – can show early features of gouty joint involvement
Potential problems with serum rate levels in diagnosis of gout
can be useful, but sometimes misleading (especially during an acute attack) as this can appear normal or even low.
What is septic arthritis?
What causes it?
= an infection of a joint
most commonly caused by bacteria from the bloodstream or direct inoculation from a penetrating injury to the joint.
It can also be caused by a virus or skin infection.
what joint(s) are normally affected in septic arthritis?
Any joint in the body can be affected, but most commonly the knee.
It can affect more than one joint (= polyarticular septic arthritis) but this is rare.
why is prompt treatment of septic arthritis required?
The infection can quickly and severely damage the cartilage and bone within the joint
Risk Factors for septic arthritis
Existing joint problems – e.g. RA, OA, gout, previous joint injury/surgery
Artificial joint
Immunosuppression
Skin fragility
Joint trauma
Septic arthritis - clinical presentation
Redness, heat and pain of joint(s)
Restricted joint movement
Fever
Septic arthritis - investigations
- Routine bloods
- X ray of joint
- USS of the joint
- Synovial fluid aspiration, arthrocentesis for crystals and organisms
- Blood culture
Tuberculosis infective arthritis
- Haematogenous spread or from a focus of nearby osteomyelitis
- Most common site is the spine – Pott disease.
- Has a more destructive process than suppurative arthritis
Arthritis associated with Lyme Disease
- Joint gets affected several days or week/s after the initial skin infection
- Remitting and migratory type of arthritis
• Involves large joints
- Clears spontaneously or with treatment
- In 10% of the cases, permanent damage ensues.
