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MSK Flashcards

1
Q

Mechanical causes of joint pain

A

Trauma - # and sprains
OA
Hypermobility disorders
Contractures

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2
Q

Inflammatory causes of joint pain

A 
Gout/Pseudogout
Septic Arthritis
RA
Spondyloarthropathies
Autoimmune connective tissue disorders (SLE, systemic sclerosis)
Osteomyelitis
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3
Q

Mechanical and inflammatory causes of joint pain

A

Bursitis
Polio
Carpal Tunnel Syndrome (CTS)
Tendonitis

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4
Q

What are the Spondyloarthropathies?

A

Psoriatic arthritis
Ankylosing spondylitis
Reactive arthritis
Enteropathic arthritis

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5
Q

What is important to remember in a back pain Hx?

A

Important to remember – RISK:

Referred Pain
Ischaemia
Sepsis
Kids

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6
Q

Back pain Hx - HPC:

A

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.

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7
Q

Back pain Hx - PMHx:

A 
Previous joint disease
Hx of recent illness
Surgeries
Trauma – fractures, open fractures, sprains
Thyroid disease
Periods of immobility
Sickle cell disease
Malignancy
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8
Q

Back pain Hx - DHx:

A

Allergies

OTC
Hormone therapy
Chemotherapy
Polypharmacy – falls risk

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9
Q

Back pain Hx - SHx:

A 
Smoking, alcohol, drug use.
Occupation
Exercise/leisure
ADLs
Dependence or caring responsibilities
Accommodation – stairs, etc.
Diet and fluids.
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10
Q

Back pain Hx - FHx:

A

FHx of Any MSK/inflammatory conditions

May also impact the patients understanding/pre-conceptions.

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11
Q

Osteoarthritis

A

= 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.

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12
Q

Risk factors for OA

A

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.
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13
Q

Prevalence of OA

A

Women > Men.
Uncommon before 50

In adults aged >50 – knee most common, followed by hip and hand

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14
Q

Changes occurring in OA

A

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

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15
Q

OA - radiological findings

A

L – loss of joint space
O – osteophytes
S – subchondral sclerosis
S – subchondral cysts

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16
Q

Most common joints affected in OA

A

Cervical/Lumbar spine
Tibiofemoral joint
Acetabulofemoral joint

PIPs and DIPs
Carpometacarpal joint
Metacarpophalangeal joint
1st Metatarsophalangeal joint

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17
Q

Symptoms of OA

A

Continuous pain
Worsens on movement, improves on rest
No significant morning stiffness (<30 mins)

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18
Q

Signs of OA

A

Bony enlargement of the affected joint

Reduced Range of Movement

Joint Crepitus

Deformity - Varus/valgus

Effusion

Antalgic gait

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19
Q

Name for the bony expansion of DIP joints

A

= Heberden’s nodes

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20
Q

Name for the bony expansion of PIP joints

A

= Bouchard’s nodes

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21
Q

Varus deformity

A

= deformity in which an anatomical part is turned inwards towards the midline

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22
Q

Valgus deformity

A

= deformity in which an anatomical part is turned outward away from the midline

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23
Q

Rheumatoid Arthritis

A

= 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

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24
Q

Prevalence of RA

A

~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.

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25
Q

Pathophysiology of RA

A
  1. 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.
  2. Synovial membrane becomes vascularised and there is villous hypertrophy leading to pannus (vascularised granulation tissue) formation.
  3. Joint deformity due to subluxation results as articular surfaces are destroyed.
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26
Q

the systemic nature of RA

A

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.
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27
Q

Which joints are most commonly affected by RA?

A 
MCPs
PIPs
Wrist
Elbow
Glenohumeral joint
Cervical spine
Hip
Knee
Ankle,
Tarsal
MTPs
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28
Q

RA - clinical presentation

A

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

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29
Q

Good questions to look for extra-articular manifestations of RA:

A
  • 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?
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30
Q

RA-associated disease - skin

A

rheumatoid nodules,
fragility,
vasculitis (rare),
Pyoderma gangrenosum

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31
Q

RA-associated disease - lungs

A 
pleural effusions
interstitial lung disease
bronchiolitis
rheumatoid nodules of the lung
vasculitis
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32
Q

RA-associated disease - heart

A

pericarditis
premature atherosclerosis
vasculitis
valvular disease

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33
Q

RA-associated disease - eye

A

Keratoconjunctivitis Sicca (dry eyes)
episcleritis
peripheral ulcerative keratopathy
thinning of the sclera

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34
Q

RA-associated disease - neurological

A

carpal tunnel syndrome
peripheral neuropathy
mononeuritis multiplex

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35
Q

RA-associated disease - haematopoeitic

A

anaemia,
thrombocytosis
lymphadenopathy
felty syndrome

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36
Q

RA-associated disease - bone

A

osteopaenia

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37
Q

Rheumatoid nodules

A

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).

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38
Q

RA - on examination of early disease

A

Erythema
Palpable inflammation
Warm to touch
Tenderness on MCP/forefoot squeeze

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39
Q

RA - on examination of advanced disease

A

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

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40
Q

Boutonniere deformities

A

Fixed flexion at the PIP joint and extension at DIP joint

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41
Q

Swan-neck deformities

A

Extension at the PIP and fixed flexion at the DIP.

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42
Q

Investigations for RA

A
  • 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
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43
Q

Radiological findings in RA

A

Loss of joint space
Erosion
Soft tissue swelling
Soft bones (osteopenia)

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44
Q

What are some variants of RA?

A
  • Juvenile variant
  • Felty’s syndrome (RA associated with Splenomegaly and Neutropenia)
  • RA associated with UC and Sjogren’s syndrome
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45
Q

What is a bursa?

A

= a sac with a potential space that reduces friction

160 in the body - commonly around joints, muscles and bones

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46
Q

what is bursitis?

A

= inflammation of a bursa

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47
Q

what is an enthesis?

what is enthesitis?

A

= the connective tissue at the junction of a bone and tendon

enthesitis = inflammation of an enthesis

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48
Q

What does a tendon do?

A

Dense and compact collagenous tissue, which connects muscle to bone

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49
Q

What is tendinitis and what is tendinosis?

A

tendinitis = acute or chronic inflammation of a tendon

tendinosis = non-inflammatory intra-tendinous atrophy, often associated with chronic tendinitis

50
Q

What is a ligament?

A

= collagenous tissue which connects bone to bone

51
Q

Sprain vs strain

A 
sprain = tearing of a ligament
strain = tearing of muscle fibres
52
Q

what is a Regional periarticular pain disorder?

A

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

53
Q

What are some periarticular syndromes of the elbow?

A

Lateral epicondylitis
Medial epicondylitis
Olecranon bursitis

54
Q

what does the subacromial bursa do?

A

provides a cushion between the acromion and supraspinatus muscles it also cushions between the deltoid tendon and the greater tubercle of the humerus

55
Q

Symptoms of subacromial bursitis and findings OE

A

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.
56
Q

Complications of subacromial bursitis

A

May lead to a tear of the rotator cuff, if the supraspinatus tendon degenerates

57
Q

What inserts into the lateral epicondyle?

A

The insertion point of the common extensor tendon

Extensor carpi radialis brevis also inserts superior to common extensor tendon

58
Q

what is lateral epicondylitis?

A

“tennis elbow”

= a tendinitis (inflammation) or tendinopathy (degeneration) of the extensor tendon, due to repetitive use of the extensor muscles.

59
Q

Symptoms of lateral epicondylitis and findings OE

A
  • 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.

60
Q

Plantar aponeurosis

A

= a band of connective tissue supporting the arch of the foot.

It runs from the calcaneal tuberosity to the base of the toes

61
Q

Plantar fasciitis

A

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

62
Q

Plantar fasciitis - symptoms and OE

A
  • 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.

63
Q

Ganglion Cyst

A

= 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).

64
Q

What are the autoimmune connective tissue disorders?

A

Rheumatoid arthritis

Scleroderma

Systemic lupus erythematosus (SLE)

Polymyositis

65
Q

types of scleroderma

A

Can have either:

  1. Limited cutaneous scleroderma (1/3) – only affects the skin
  2. Systemic scleroderma (2/3) – there is cutaneous sclerosis with visceral involvement.
66
Q

What are the clinical features of scleroderma in the skin?

A

Sclerodactyly
Raynaud’s phenomenon
abnormalities of nail bed (e.g. splinter haemorrhages)

puffy/swollen hands, tightness of fingers

67
Q

What are the clinical features of scleroderma in the MSK system?

A

arthralgias - joint pain

myalgias - muscle pain

68
Q

What are the clinical features of scleroderma in the GI system?

A

oesophageal dysphagia

dyspepsia

69
Q

What are the clinical features of scleroderma in the lungs?

A

pulmonary artery hypertension

interstitial lung disease

70
Q

What are the clinical features of scleroderma in the CV system?

A

pericardial/myocardial disease

71
Q

what is SLE?

A

= a chronic multisystem inflammatory disease of autoimmune nature

fairly uncommon, gradual onset

72
Q

pathophysiology of SLE

A

Deposition of immune complexes (DNA and antibodies) cause inflammatory lesions in kidney, brain, heart, spleen, lung, GI tract, skin, peritoneum

73
Q

what are the skin signs of SLE?

A

often the first signs

  • facial rash, redness
  • rash on body
  • sensitive to sun
  • hair loss/nail changes
74
Q

where are the primary sagittal curvatures ?

A 
the thoracic (kyphosis) 
sacrococcygeal regions.
75
Q

where are the secondary sagittal curvatures?

A

cervical (lordosis) region

lumbar (lordosis) region

76
Q

What are the joints of the spine?

A

Facet joints are synovial joints between the superior and inferior articular processes.

Vertebral Discs are fibro-cartilaginous joints

77
Q

What movements do the facet joints allow in the throacic/lumbar spine?

A

Lumbar spine: allow flexion/extension and no rotation or lateral flexion.

Thoracic spine: allow more rotation and lateral flexion.

78
Q

Ligaments of the Spine

A

Posterior longitudinal ligament
Anterior longitudinal ligament

Supraspinous ligament
Interspinous ligament

Ligamentum flavum

79
Q

Posterior longitudinal ligament

A

C2 to sacrum

attached to posterior aspect of vertebral bodies and intervertebral discs

maintains stability.

80
Q

Anterior longitudinal ligament

A

C1 to sacrum

attached to anterior surface of vertebral bodies and intervertebral discs

maintains stability

81
Q

Supraspinous ligament

A

cross tips of spinous processes from C7 to sacrum.

82
Q

Intraspinous ligament

A

link adjacent spinous processes

83
Q

Ligamentum flavum

A

unite adjacent laminae, limits flexion of vertebral bodies.

Preserves curvature of spine.

84
Q

How many spinal nerve roots are there?

A
  • Eight cervical (seven vertebrae)
  • Twelve thoracic
  • Five lumbar
  • Five sacral and one coccygeal.
85
Q

Where does the adult spinal cord terminate?

A

L1

86
Q

What is a radiculopathy?

A

= irritation or damage to a nerve root, causing pain along a dermatome

can also be called a pinched spinal nerve

87
Q

what makes up the vertebral disc?

A 
Anulus fibrosus (outer, fibrous component)
Nucleus pulposus (inner, gel-like component)
88
Q

Disc prolapse

A

when the Anulus fibrosus ruptures and the Nucleus pulposus is forced out, exerting pressure on local nerves or the spinal cord.

89
Q

What are the types of back pain?

A

Non-specific - no obvious cause

Mechanical: caused by joint, bones or soft tissues around the spine

90
Q

What is a form of mechanical back pain which is an emergency?

A

cauda equina syndrome

91
Q

Lumbar sprain/strain

A

Intense pain followed by spasm
very common

due to stretching/tearing of muscle or ligament fibres

surrounding muscle fibres spasm to protect the injury

92
Q

Degenerative disc/facet joints

A

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

93
Q

what is spinal stenosis?

A

anatomical narrowing of the spinal canal, secondary to osteophytes and facet joint hypertrophy

94
Q

what is important to find out in a back pain history?

A
  1. If your patient had trauma of a fall.
  2. Differentiate between mechanical and non-mechanical back pain.
    => Is there pain at night or at rest? (usually non-mechanical cause)
  3. Location of the pain
    - Lumbar back pain is usually mechanical.
    - Thoracic back pain is more likely to be serious.
  4. any Red flag symptoms
95
Q

Red flag back pain symptoms

A
  • 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
96
Q

Red flag symptoms for cauda equine syndrome

A
  • Change in sensation (saddle anaesthesia)
  • Change in bladder or bowel function
  • Weakness or loss of sensation in the lower limbs
97
Q

What are the non-mechanical causes of back pain?

A

Infection - osteomyelitis, disctitis, epidural abscess
Malignancy
Inflammatory - spondyloarthropathies, RA
Autoimmune

98
Q

Bone malignancy

A

Metastases - 25x more common than primary bone tumours
=> commonly from breast, thyroid, kidney, lung, prostate

Primary bone tumours - Osteosarcoma, chondrosarcoma, Ewing’s sarcoma

99
Q

what is osteoporosis?

A

= 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

100
Q

what is the long-term outcome of osteoporosis

A

loss of bone strength - bones become fragile and break more easily (= fragility fractures).

101
Q

Why is osteoporosis referred to as the “silent thief”

A

The process of Osteoporosis is completely asymptomatic

102
Q

Diagnosis of osteoporosis

A

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

103
Q

what is the FRAX tool used for?

A

to calculate the 10-year probability of developing Osteoporosis.

104
Q

Risk factors for osteoporosis

A

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

105
Q

Management of osteoporosis

A

Diet - Calcium and vitamin D supplementation
Exercise - weight bearing exercises

Smoking cessation, alcohol reduction

Review medications

MDT interventions

Medication - symptom control, Anti-resorptives, etc.

106
Q

what is gout?

A

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

107
Q

where can excess uric acid deposit?

A

in the joints => gout

in the urinary tract => kidney stones

108
Q

what can cause excess uric acid in the body?

A
  1. Uric acid production increases

2. The kidneys are not excreting uric acid efficiently enough

109
Q

Gout - presentation

A

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

110
Q

Diet risk factors for gout

A

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

111
Q

Non-diet risk factors for gout

A 
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
112
Q

Diagnosis of gout

A

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

113
Q

Potential problems with serum rate levels in diagnosis of gout

A

can be useful, but sometimes misleading (especially during an acute attack) as this can appear normal or even low.

114
Q

What is septic arthritis?

What causes it?

A

= 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.

115
Q

what joint(s) are normally affected in septic arthritis?

A

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.

116
Q

why is prompt treatment of septic arthritis required?

A

The infection can quickly and severely damage the cartilage and bone within the joint

117
Q

Risk Factors for septic arthritis

A

Existing joint problems – e.g. RA, OA, gout, previous joint injury/surgery

Artificial joint

Immunosuppression

Skin fragility

Joint trauma

118
Q

Septic arthritis - clinical presentation

A

Redness, heat and pain of joint(s)
Restricted joint movement
Fever

119
Q

Septic arthritis - investigations

A
  • Routine bloods
  • X ray of joint
  • USS of the joint
  • Synovial fluid aspiration, arthrocentesis for crystals and organisms
  • Blood culture
120
Q

Tuberculosis infective arthritis

A
  • 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
121
Q

Arthritis associated with Lyme Disease

A
  • 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.

CP1 (12 decks)

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