Musculoskeletal Flashcards

1
Q

What are the pain pathways?

A

Pain perception is mediated by free nerve endings: nociceptors
A-delta fibres give rise to perception of sharp, immediate pain
C-fibres give rise to slower onset, prolonged pain
Sensory impulses enter the cord via the dorsal root and then ascend in the dorsal posterior column of the spinothalamic tract

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2
Q

What can pain lead to?

A

Multiple psychological effects
Leads to catecholamine release, with the resultant vasoconstriction leading to increased cardiac work and delayed healing

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3
Q

What is an overusuage/strain injuries presentation?

A

Exact time/mechanism of injury can be identified
Pain is non-progressive and produced by one/few moments
On examination there is localised tenderness and pain produced on resisted active movement/stress testing

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4
Q

What is osteoarthritis?

A

Most common type of osteoarthritis
Results from a disparity between the stress applied to articular cartilage and the ability of the cartilage to withstand that stress
Commonly affects the hip, knee, DIP, PIP, thumb CMJ and hallux MTP joints
Classically spares the MCPJs

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5
Q

What are the clinical features of OA?

A

Progressive pain: initial activity related to pain, then finally a constant rest pain
Stiffness: characteristically worse after periods of rest (gelling), but lasts <30 mins
Symptoms classically follow a waxing and waning course (good/bad days)
Later features are muscle wasting, loss of mobility, deformity and joint instability

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6
Q

What is seen on examination in OA?

A

Look: bony swelling, muscle wasting
Feel: joint line tenderness, possible effusion, crepitus
Move: limited range of movement

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7
Q

What are the risk factors for OA?

A
Age
Obesity
Family history: genetic predisposition 
Gender: polyarticular OA more common in women, particularly after menopause 
Hypermobility 
Previous trauma 
Occupation (miners, farmers) 
Protective factors: osteoporosis
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8
Q

What can secondary OA develop due to?

A

Pre-existing joint damage: inflammatory/septic/crystal arthritis, AVN, trauma
Metabolic disease: acromegaly, chonedrocalcinosis, haemochromatosis
Systemic disease: haemophilia (leading to haemarthroses)

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9
Q

What is hip OA?

A

More common in males, unilateral at presentation
Generally does poorly and requires arthroplasty
On examination: painful and decreased internal and external rotation of the hip
Positive Trendelenburg’s test (sound side sags)

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10
Q

What is knee OA?

A

Strong relationship with obesity, oath other risk factors being previous trauma or knee soft tissue injuries
Often bilateral and most commonly leads to genuflects various deformities due to medial disease
Classically on examination there will be a moderate effusion, decreased range of movement, crepitus and quadriceps wasting

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11
Q

What is nodal generalised OA?

A

Joints of the hands are affected one by one over many years, first presenting with painful swelling and impairment of function
Classically presents in menopausal women
Familial tendency, thought to have an autoimmune aetiology

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12
Q

What is affected in nodal generalised OA?

A

DIPs affected much more than PIPs and the inflammatory phase settles after months/years to have painless bony swellings posterolaterally
Herberdens (DIP) and Bouchard’s (PIPs) nodes
Function is generally still good
CMC and MCP joints of the thumb, bony swellings and fixed adduction leading to the classical ‘squared hand’ in OA
MCPJs are generally spared
Generally large joint involvement

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13
Q

What is erosive OA?

A

Rare with characteristic cysts seen on XR and a poor prognosis

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14
Q

What is crystal associated OA?

A

Calcium pyrophosphate deposition in the cartilage leads to chonedrocalcinosis (pseudo gout)
This can be asymptomatic or lead to the signs/symptoms of OA
Knees and wrists are most commonly affected

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15
Q

Who does rheumatoid arthritis affect?

A

Affects around 3% of women and 1% of men over their lifetimes
Pre-menopausal women affected more than men
No gender differences post-menopause
The disease is familial, yet inheritance is sporadic

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16
Q

What is the presentation of RA classically in 30-50 year old women?

A

Red, warm, painful and swollen peripheral joints, typically of the hands/feet
Then progresses to affect larger joints (still symmetrical)
This is worse in the morning, evolving over weeks/months

17
Q

What occurs in 15% of people who present with OA?

A

There is a rapid onset of symptoms over days/overnight (better prognosis)
General malaise, weight loss and disturbed sleep is common
Extra-articular features may be present

18
Q

What are rare presentations of RA?

A

Palindromic RA (recurring mono/poly arthritis), persistent mono-arthritis or systemic illness with extra-articular symptoms

19
Q

What is the differential diagnosis of RA?

A

Includes reactive arthritis, seronegative spondyloarthropathies, polymyalgia rheumatica or acute nodal osteoarthritis

20
Q

What are characteristic deformities in the hand in RA?

A

Ulnar deviation at the MCJPs
Radial deviation at the wrist
Boutonniere deformity: hyper flexed PIPJs, hyperextended DIPJs
Swan-neck deformity: hyper flexed DIPjs, hyperextended PIPJs
Z deformity in the thumb: flexed MCPJs, extension at IPJ
Subluxation is a late deformity: volar subluxation at the MCPJs/wrist

21
Q

What can RA lead to in the hands?

A

Ankylosis (fusion) across the joint
Rupture of the little/ring finger extensor tendons can occur due to swelling and subluxation and this requires urgent surgical repair
Carpel tunnel syndrome is also very common due to inflamed tendon sheaths

22
Q

What occurs in the feet in RA?

A

MPTJ swelling is one of the earliest manifestations
The foot becomes broader and a hammer-toe deformity develops
Ulcers/callouses can occur due to exposure of the metatarsal heads to pressure due to migration of the protective fat pad

23
Q

What is large joint involvement in RA?

A

The knee is most commonly affected then the shoulder/hip
In the knee a genu valgus deformity and secondary OA can develop
Once severely affected, large joints require total replacement to restore function

24
Q

How is RA diagnosed via blood tests?

A

FBC: leucocytosis and thrombocytosis in acute inflammatory phase, normocytic anaemia and chronic disease
CRP/ESR: elevated in active disease
Rheumatoid factor (RF): elevation in 70% but non-specific
Anti-CCP: more specific, rises predate clinical disease by several years
ANA: if suspecting connective tissue disease, however raised in 30%
Anti-nuclear antibody

25
Q

How is RA diagnosed via X-ray?

A

Early findings: soft tissue swellings around the PIPjs and MCPJs (DIPJs usually spared (c.f OA)
Uniform joint space narrowing
Juxta-articular osteopenia: can become more diffuse as disease progresses
Periarticular erosions: form at extremities of the joint where the hyaline cartilage ends, as it is invaded by the pannus
Subluxation/dislocation may also be seen

26
Q

What is the pathogenesis of RA?

A

In the rheumatoid synovitis there is swollen synovial showing a villous pattern and neutrophil infiltration
Leads to exudative effusion in the joint (boggy, swollen)
Vascular granulation tissue (pannus: formed by osteoclasts and macrophages) grows from the peripheries inwards, destroying articular cartilage
Th inflammatory pannus causes focal destruction of bone, causing erosions
Clinically this can lead to joint deformities

27
Q

What occurs in long standing disease of RA?

A

Whole cartilage may be destroyed and replaced by fibrous pannus, leading to secondary osteoarthritic changes

28
Q

What is morning stiffness due to in RA?

A

Cortisol trough or the build up of inflammatory mediators during non-activity

29
Q

What is osteoporosis?

A

Disease characterised by reduced bone mineral density and microarchitectual deterioration of bone tissue, leading to increased bone fragility and an increased risk of fracture

30
Q

What is the WHO definition of osteoporosis?

A

Boen mineral density >2.5 SDs below that of a young adult male with values between 1 and 2.5 described as osteopenia
Fractures related to osteoporosis are a major public health problem in developed countries affecting up to 30% of women and 12% of men

31
Q

What is the pathogenesis of osteoporosis?

A

In normal individuals, bone mass increases during childhood to reach a peak between 20-30, when there is a period of consolidation before it falls thereafter
Women have an accelerated phase of bone loss after the menopause as a result of oestrogen deficiency

32
Q

What are the risk factors for osteoporosis?

A

Age
Female sex
Genetics: 80% of peak bone mass determined by genetics, also rate of bone turnover
Low peak bone mass: limited early exercise, limited early calcium intake and low body habitus in childhood make up the environmental component
Disuse- following a fracture, ‘disuse atrophy’
Smoking

33
Q

What are the secondary causes of osteoporosis identified in around 50% of male cases?

A

Primary hyperparathyroidism: high PTH leads to increase bone turnover, which aggravates imbalances in resorption/formation
Thyrotoxicosis: increases bone turnover
Steroid-induced: risk is directly directed to dose/duration of therapy
Cushing’s disease: as for steroids
Anorexia nervosa: calcium deficiency and secondary hyper PTH
Chronic inflammatory disease/neoplastic disease: inflammatory cytokines increase bone resorption and suppress bone formation

34
Q

How do steroid cause osteoporosis?

A

Cause decreased interstitial calcium absorption and increased renal calcium excretion, leading to secondary hyperparathyroidism
This is combined with a direct inhibition of osteoblast activity and stimulation of osteoblast apoptosis

35
Q

What are the first symptoms of osteoporosis?

A

Fragility fractures
Back pain
Height loss
Kyphosis

36
Q

What are the common sites for osteoporotic fractures?

A

Wrist (colles)
Neck of femur or spine (vertebral crush/wedge fracture)
If one of these is detected patient should be referred on for bone densitometry

37
Q

How os osteoporosis diagnosed?

A

BMD measurements using a dual energy x-ray absorptiometry (DXA) measured at the lumbar spine and iliac crest

38
Q

What is the T and Z score?

A

T score: measures how many standard deviations the BMD deviates from a young adult male
Diagnostic if score falls below -2.5 whereas scores from -1 to -2.5 are in the osteopenic range
Z score: measures how many SDs BMD deviates from an age-matched control

39
Q

Once osteoporosis is confirmed what further tests need to be carried out?

A

Serum calcium and phosphate, TFTs and ESR are important routine tests
Sex hormone panel in men and amenorrheic women below 50
Vitamin D/PTH is suspecting vitamin D deficiency or hyperparathyroidism