MSK week 4 Flashcards

1
Q

What is mechanical back pain?

A

Recurrent relapsing and remitting back pain with no neurological symptoms.
Back pain that is relieved by rest and worsened by activity.

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2
Q

What are the causes of mechanical back pain?

A

Obesity, lack of physical activity, spondylosis, OA, poor posture, poor lifting technique.

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3
Q

What is spondylosis?

A

As you age, the water content in your intervertebral discs decreasing meaning they lose some of their cushioning properties. This puts an increased pressure on the facet joints.

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4
Q

Treatment for mechanical back pain

A

NSAIDs and simple analgesia, physiotherapy

NO BED REST.

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5
Q

When would spinal stabilisation surgery be appropriate in mechanical back pain?

A

If two adjacent vertebrae are affected- spinal fusion of the two may benefit them. Tends to be a minority of patients since most of the time they have multilevel disease.
Conservative management has to have failed first.

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6
Q

When does an acute disc tear occur?

A

Classicly after lifting a heavy object.

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7
Q

Why do you feel pain in an acute disc tear?

What makes the pain worse?

A

The outer annulus fibrosis is richly innervated so you feel pain.
Coughing makes the pain worse because it increases the pressure on the disc.

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8
Q

Treatment of an acute disc tear?

A

Usually resolves itself in 2-3 months however in the meantime physiotherapy and analgesia.

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9
Q

What is sciatic/lumbar radiculopathy?

A

Disc material can impinge on exiting nerve roots causing altered sensation in a dermatomal distribution and weakness in a myotomal distribution

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10
Q

Where does radiculopathy most commonly occur?

A

In the lumbar spine- L4, L5 and S1 nerve roots which contribute to the sciatic nerve.

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11
Q

What does radiculopathy feel like?

A

Neuralgic burning or severe tingling pain- which radiates down the thigh to below the knee.

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12
Q

If a L3/L4 disc prolapse occured- which nerve root would be entrapped and what consequences would this have?

A

L4 nerve root would be entrapped. It would cause pain down to the medial ankle, loss of quadriceps power and a reduced knee jerk.

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13
Q

If a L4/L5 disc prolapse occurred- which nerve root would be entrapped and what consequences would this have?

A

L5 nerve root would be entrapped. It would cause pain down to the dorsum of the foot, reduced power in extensor hallicus longs and tibias anterior.

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14
Q

If a L5/S1 disc prolapse occured- which nerve root would be entrapped and what consequences would this have?

A

S1 would be entrapped. It would cause pain to the sole of the foot and reduced power plantarflexion and reduced ankle jerk.

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15
Q

Describe the anatomy of the transversing nerve root and the exiting nerve root. Which is more likely to be affected by a discogenic tear and why?

A

At each level (e.g. lumbar 4) there is an exiting nerve root that exits at that same level and a transversing nerve root that passes to the level below. The transversing nerve root is more likely to become trapped by a discogenic tear however a very lateral tear may affect the exiting nerve root.

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16
Q

What is bony nerve root entrapment? What is the treatment for it?

A

OA on the facet joints creates osteophytes that can impinge on the exiting nerve root. Treatment involves trimming of osteophytes.

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17
Q

What is spinal stenosis?

A

In conditions such as bulging discs, the disc can compress the spinal cord (or cauda equina).
It characteristically presents as claudication.

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18
Q

How can you tell between vascular claudication and neurogenic claudication?

A

Neurogenic claudication distance is inconsistent. The pain is burning rather than a cramping sensation. Pain is less walking uphill (spinal flexion offers more space) and pedal pulses are preserved.

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19
Q

Management of spinal stenosis

A

Conservative management - physio and weight loss.

Surgical management- if there is MRI evidence of stenosis- decompression surgery may be performed.

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20
Q

What is cauda equina syndrome?

A

When a disc prolapse (or other cause) compresses all the nerve roots of the cauda equina.
Affected nerve roots include S4 and S5 which control defecation and urination.

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21
Q

Symptoms of cauda equina syndrome?

A

Parathesia or numbness around the sitting area.
Bilateral leg pain
Urinary retention (sometimes incontinence)
Faecal incontinence and/or constipation.

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22
Q

What are the consequences of prolonged compression in cauda equina syndrome?

A

Prolonged compression can potentially cause permanent nerve damage. Even with quick intervention- patients may still have bladder and bowel dysfunction.

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23
Q

What are the red flag symptoms in spinal presentations?

A

New back pain in young people (<20)- young people are more susceptible to infection, as well as some malignant and benign tumours.
New back pain in older people (>60)- Neoplasia
Nature of the pain is constant, severe pain and worse at night. This indicates pain from tumour.
Systemic upset- fever, night sweats, fatigue may indicate presence of infection or tumour.

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24
Q

What are osteoporotic crush fractures?

A

In severe osteoporosis- spontaneous fractures can occur leading to acute pain and kyphosis.

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25
Q

What is the treatment of osteoporotic crush fractures?

A

generally conservative-
Patients with chronic pain- vertebroplasty (inserting a balloon into the vertebral body and filling it with cement)- has had some good results.

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26
Q

What is cervical spondylosis?

A

Loss of water from the intervertebral discs leads to accelerated OA.

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27
Q

How will patients present with cervical spondylosis?

A

They will have slow onset of stiffness and pain in the neck that can radiate locally to the shoulder and occiput.

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28
Q

Treatment of cervical spondylosis? What are complications of untreated CS?

A

Physiotherapy and analgesics are the mainstay.

Osteophytes that may form may start to impinge on exiting nerve roots causing radiculopathy.

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29
Q

Presentation of a cervical disc prolapse?

A

Shooting neuralgic pain down a dermatomal distribution with weakness and loss of reflexes.

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30
Q

Investigation and treatment of cervical disc prolapses?

A

Investigations include MRI to find the affected level. Treatment is conservative however persistent cases may have surgery considered.

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31
Q

What diseases may be related to spinal instability?

A

Can occur in Downs syndrome and rheumatoid arthritis.

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32
Q

What are children with Downs syndrome at risk of developing (in terms of the spine)? How would you prevent this from happening?

A

Atlanta-axial instability potentially causing subluxation and spinal cord compression.
Screening with flexion-extension X-rays will show abnormal motion. Children with minor degrees of injury- no contact sports. Severe instability may require surgery.

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33
Q

What are patients with RA spinal instability at risk of?

How is this prevented?

A

Atlanto-axial subluxation can occur due to destruction of the synovial joint between the atlas and the dens.
Subluxation can result in cord compression
Mild cases- wear a collar to prevent flexion. More severe cases will need surgical fusion.

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34
Q

What is the treatment of sciatic/lumbar radiculopathy?

A

Analgesia, maintaining mobility and physiotherapy.
Occasionally drugs for neuropathic pain can be used (gabapentin).
Very occasionally- discectomy is indicated when physio isn’t helping, localising signs suggesting a specific nerve root and positive MRI present.

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35
Q

What is impingement syndrome?

A

Syndrome where the tendons of the rotator cuff (predominantly supraspinatous) are compressed into the tight subacromial space during movement which produces pain.

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36
Q

Presentation of the patient with impingement syndrome?

A

Painful arc from 60-120 degrees
Pain characteristically radiates to the deltoid and upper arm.
Tenderness may be felt below the lateral edge of the acromion.

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37
Q

Causes of impingement syndrome

A

Tendonitis
Subacromial bursitis
Acromioclavicular OA with inferior osteophytes
A hooked acromion rotator cuff tear.

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38
Q

Treatment of impingement syndrome?

A

Conservative- majority of cases will heal with NSAIDs, analgesics, physio and subacromial steroid injection
If these don’t work- subacromial decompression surgery which creates more space for the tendon to pass through.

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39
Q

What is a rotator cuff tear? How does it occur?

A

A tear in the tendon of one of the rotator cuff muscles (usually supraspinatous). Can be due to degenerative changes to the tendon meaning little or no trauma causes the tear.

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40
Q

Typical history of a rotator cuff tear

A

A sudden jerk in a patient that is older than 40 with subsequent pain and weakness.

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41
Q

If there is a tear in the supraspinatous tendon, what will the patient not be able to do

A

Weakness in initiation of abduction.

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42
Q

If there is a tear in the infraspinatous tendon, what will the patient not be able to do

A

Weakness externally rotating.

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43
Q

If there is a tear in the subscapularis tendon, what will the patient not be able to do

A

Weakness internally rotating

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44
Q

If there is a tear in the teres minor tendon, what will the patient not be able to do

A

Weakness externally rotating also.

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45
Q

How would you confirm a rotator cuff tear?

A

Ultrasound or MRI.

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46
Q

Treatment of rotator cuff tears?

A

Surgical- rotator cuff repair (open or arthroscopic) with subacromial decompression can be performed in an attempt to improve/maintain strength. However failure occurs in a third of patients and very large tears may be irreparable.
Non-operative- physio to strengthen remaining muscles and subacromial injection to reduce symptoms.

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47
Q

What is adhesive capsulitis?

A

Frozen shoulder- disorder characterised by progressive pain and stiffness of the shoulder in patients between 40 and 60, resolving after 18-24 months.

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48
Q

Presentation of adhesive capsulitis

A

Patients usually complain of pain for the first 2-9 months. This then subsides and stiffness ensues for about 4-12 months. The stiffness gradually ‘thaws’ out over time- usually with good recovery of shoulder motion.

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49
Q

What is the principle clinical sign of adhesive capsulitis?

A

Loss of external rotation.

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50
Q

Causes of adhesive capsulitis?

A

The capsule and glenohumeral ligaments become inflamed and then contract. This is sometimes after shoulder surgery. Diabetics are particularly prone to it. It is associated with hypercholestronaemia and Dupuytrens contracture.

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51
Q

Treatment of adhesive capsulitis

A

Non-operative- aim to prevent pain and further stiffening while the condition resolves naturally. Physio and analgesics help. Intra-articular (not subacromial) injections can help
Operative- Once the pain has subsided but the patient cannot tolerate loss of function-manipulation under anaesthetic can occur (involves tearing the capsule) to increase ROM.

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52
Q

What is acute calcific tendonitis?

A

Calcium deposits in the supraspinatous tendon causing acute onset of severe shoulder pain.

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53
Q

Where can the calcium deposits be seen on Xray

A

Just proximal to the greater tuberosity of the humerus.

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54
Q

Treatment of acute calcific tendonitis

A

Subacromial steroid injection offers great relief. Along with subacromial anaesthetic.
Condition is self limiting as the calcium will eventually be reabsorbed.

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55
Q

What is instability of the shoulder?

A

Recurrent dislocations or subluxation or painful abnormal translation movements of the shoulder joint.

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56
Q

Two types of instability

A

Traumatic- after a previous anterior dislocation-the shoulder does not stabilise and recurrent dislocations with minimal force occur.
Atraumatic- ligamentous laxity

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57
Q

Treatment of traumatic instability

A

Bankurt repair can stabilise the shoulder by reattaching the labrum and capsule to the anterior glenoid.

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58
Q

Treatment of atraumatic instability

A

Treatment difficult as soft tissue procedures don’t work.

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59
Q

What is carpal tunnel syndrome?

A

Pressure increase between the flexor retinaculum and the the carpal bones (the carpal tunnel) compressing the median nerve.

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60
Q

What runs through the carpal tunnel?

A

The median nerve

9 flexor tendons and their synovial coverings.

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61
Q

What occurs to produce pain in carpal tunnel syndrome?

A

The compression of the nerve causes pain to be felt- tendons are not as sensitive to pressure whereas nerves are extremely sensitive.

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62
Q

What are the causes of carpal tunnel syndrome?

A
Most idiopathic 
Pregnancy
Secondary to RA
Conditions resulting in fluid retention e.g. diabetes, renal failure, hypothyroidism
Consequence of fractures.
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63
Q

Presentation of carpal tunnel syndrome

A

Parathesia in the median nerve innervated digits (thumb and radial 2 and a half digits.
Worse at night
Loss of sensation and weakness in the thumb.

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64
Q

On examination of carpal tunnel syndrome- what would you expect to see (and what tests would you perform)?

A

Demonstateable loss of sensation and/or muscle wasting in the thenar eminence.
Symptoms reproduced by Tinels test (percussing over the median nerve) or Phalens test (holding the wrist hyper flexed to decrease space in the carpal tunnel).

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65
Q

Treatment of carpal tunnel syndrome?

A

Non-operative- use of wrist splints at night to prevent flexion. Injection of corticosteroid.
Surgical- carpal tunnel decompression- involves division of the flexor retinaculum. Highly successful op (small risk of damage to the median nerve).

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66
Q

What aids your diagnosis of carpal tunnel syndrome?

A

Nerve conduction studies with slowing of conduction across the wrist.

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67
Q

What is cubital tunnel syndrome?

A

Compression of the ulnar nerve at the elbow behind the medial epicondyle.

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68
Q

What would the patient complain of with cubital tunnel syndrome?

A

Parathesia in the ulnar 1 and a half fingers. Tinels test over the cubital tunnel is positive.
Weakness of the ulnar innervated muscles may be present- including 1st dorsal interosseous (abduct index finger) and the adductor pollicus.
Tested with froments test.

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69
Q

Causes of cubital tunnel syndrome?

A

Tight band of fascia forming the roof of the cubital tunnel (Osbornes fascia).
Tightness at the inter muscular septum as the nerve passes through.

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70
Q

How would you confirm the diagnosis of cubital tunnel syndrome? Treatment?

A

Nerve conduction studies confirm the diagnosis. Surgical release may be needed.

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71
Q

What is tennis elbow also known as?

A

Lateral epicondylitis. T in laTeral and T for tennis.

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72
Q

What causes tennis elbow?

A

Repetitive strain injury in tennis players who regularly perform who regularly perform resisted extension of the wrist.
It can also be due to degenerative enthesopathy (inflammation of the origin or insertion of a tendon or ligament onto a bone)

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73
Q

Pathology of tennis elbow?

A

Micro-tears in the common extensor origin.

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74
Q

Clinical features of tennis elbow?

A

Painful and tender lateral epicondyle.

Pain on resisted middle finger and wrist extension.

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75
Q

Treatment of tennis elbow?

A

Self limiting condition. Improves with rest from activities that exacerbate the pain. Physio, NSAIDs, steroid injections, use of brace.

Rarely cases may be offered surgery which involves division and/or excision of the common extensor origin.

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76
Q

What is golfers elbow also known as?

A

Medial epicondylitis

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77
Q

What causes golfers elbow?

A

Repeated strain or degeneration at the common flexor origin. Less common that lateral.

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78
Q

Treatment of golfers elbow?

A

Self limiting
Physio, NSAIDs
Not injection- carries risk of damage to the ulnar nerve.

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79
Q

What type of arthritis is the elbow likely to get?

A

Most commonly RA.

OA isn’t doesn’t normally occur here- only after trauma.

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80
Q

How can arthritis at the radio-capetellar joint be treated?

A

If conservative management has failed-can be treated with surgical excision of the radial head which affords good pain relief with minimal functional limitation.

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81
Q

How can arthritis at the humero-ulnar joint be treated?

A

If conservative management has failed- can be treated with total elbow replacement.
Only downside is that after the replacement you are only allowed to lift 2.5kg.

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82
Q

What is dupuytrens contracture?

A

Proliferative connective tissue disorder where the specialised palmar fascia undergoes hyperplasia with normal fascial bands forming nodules and cords progressing to contractures at the MCP and PIP joints.

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83
Q

Pathology of dupuytrens contracture?

A

Proliferation of myofibroblast cells and the production of abnormal collagen (type 3 rather than type 1)

84
Q

Presentation of dupuytrens contracture?

A

Skin on the hand may adhere to the fascia and become puckered out.
Palpable nodules may be present
Most commonly affects the ring and little finger.
Half of the cases have bilateral involvement.

85
Q

Causes of dupuytrens contracture?

A

Can be familial (autosomal dominant)- high prevelance in northern Europe.
Feature of alcoholic cirrhosis
Common in diabetics
Side effect of phenytoin therapy
Can occur with other fibromatoses including Peyronie’s disease (affecting the penis) and plantar fibrzomatosis (ledderhose disease- affecting the feet)

86
Q

Who gets dupuytrens contracture?

A

More common in males.

Patients with fibromatoses are likely to have more aggressive forms of the disease.

87
Q

Treatment of dupuytrens contracture?

A

Mild contractures may be tolerated.
Surgery can be offered if contractures are interfering with function.
Fasciotomy- division of cords
Fasciectomy- removal of diseased fascia

88
Q

What joints in the hand and wrist is OA likely to affect?

A

DIP and PIP

89
Q

Post menopausal women get OA in which joint?

A

DIP usually.

90
Q

What are Herberdens nodes?

A

Stiffness and bony thickening due to OA at the DIP.

91
Q

What are dorsal ganglion cysts?

A

Mucous cysts adjacent to a tendon or synovial joint. Common at the DIP and wrist. May be associated with OA.

92
Q

How would you treat DIP OA?

A

Mild to moderate- removal of osteophytes and excision of any mucous cysts.
Severe pain- arthrodesis.

93
Q

Swelling of the PIP’s due to OA?

A

Bouchards nodes.

94
Q

When would you offer arthrodesis for PIP OA?

A

If it is in the index finger to preserve pincher grip.

95
Q

When does OA affect MCPs?

A

Rarely happens but if it does usually due to a specific cause e.g. gout, infection, previous injury.

96
Q

Treatment of OA in the MCPs?

A

MCP joint replacements are available however complications are common.

97
Q

What is a swan neck deformity?

A

Hyperextension PIP

Flexion DIP

98
Q

What is boutonnieres deformity?

A

Flexion at PIP

Hyperextension at DIP.

99
Q

How would you treat swan neck, boutonnieres and Z shaped thumb deformities?

A

Tenosynovectomy (excision of the synovial sheath) may prevent tendon rupture. However once this happens there is not treatment.

100
Q

What are ganglion cysts?

A

Common mucous filled cysts found adjacent to a tendon or synovial joint. (Bakers cyst in the knee)

101
Q

What do ganglion cysts cause?

A

Localised pain or irritation

Many patients want them removed for cosmetic reasons.

102
Q

Describe ganglion cysts (gross appearance)?

A

Firm, smooth and rubbery. Should transilluminate.

103
Q

What is trigger finger?

A

Tendonitis of a flexor tendon to a digit can result in nodular enlargement of the affected tendon. Usually distal to the fascial pulley.
Movement of the finger produces a clicking sensation as the nodule catches and then passes under the pulley. It can be painful and the finger may lock in a flexed position.

104
Q

How would you treat trigger finger?

A

Steroid injection relieves symptoms. If not- surgical excision of the A1 pulley.

105
Q

Where does hip pathology typically produce pain?

A

Typically in the groin which may radiate to the knee.

106
Q

What is the difference between total hip arthroplasty and total hip replacement?

A

Total hip arthroplasty- generally given to people with lower physical needs. Includes procedures like hip resurfacing which, as they don’t require replacement of the femoral head, aren’t strictly hip replacement.
Total hip replacement- uses cemented metal/polyethylene.

107
Q

How can you gauge the level of pain a patient is in?

A

Analgesic use, sleep disturbance and rest pain.

108
Q

How can disability be determined?

A

Walking distance, activities of daily living and the impact of the hip on hobbies.

109
Q

Early local complications of hip replacement?

A

Infection, dislocations, nerve injuries.

110
Q

General complications of surgery?

A

DVT/PE, MI, blood loss.

111
Q

What do you do if a hip replacement fails?

A

It can be re-done (revision hip replacement) however it is a bigger and more complex surgery- functional outcome is poorer.

112
Q

Why wouldn’t you perform total hip replacement in young patients?

A

They are likely to need another hip replacement later on in life.

113
Q

What is the most common site to get AVN?

A

The hip

114
Q

Secondary causes of AVN at the hip?

A

Alcohol abuse
Steroids
Hyperlipidaemia
Thrombophillia

115
Q

How would a patient with AVN of the hip present?

A

Groin pain

116
Q

What will investigations into AVN show?

A

Early changes will only be viewed on MRI
Later changes show patchy sclerosis of the weight bearing area
Lytic zone underneath formed by granulation tissue in an attempted repair.
The femoral head may have collapsed with irregularity of the articular surfaces and subsequent secondary OA

117
Q

How is avascular necrosis of the hip treated?

A

If its detected early enough (pre collapse)- drill holes can be made in the femoral neck and into the abnormal bone to relieve pressure and promote healing
If past collapse- THR.

118
Q

What is trochanteric bursitis also known as?

A

Gluteal cuff syndrome

119
Q

Why is the trochanter of the femur so susceptible to this?

A

The insertion of the abductor muscles is under considerable strain and subject to tendonitis and degeneration leading to tendon tears. The trochanteric bursa can also become inflamed.

120
Q

How do patients with trochanteric bursitis present?

A

Pain and tenderness in the region of the greater trochanter with pain on resisted abduction

121
Q

Treatment of trochanteric bursitis?

A

Analgesics, anti-inflammatories, physio and steroid injection.

122
Q

What is the role of the ACL?

A

Prevents abnormal internal rotation of the tibia.

123
Q

What is the role of the PCL?

A

Prevents hyperextension and anterior translation of the femur.

124
Q

Role of the medial collateral ligament?

A

Resists valgising forces

125
Q

Role of the lateral collateral ligament?

A

Resists varus force and abnormal external rotation of the tibia.

126
Q

Where does the PCL connect?

A

Connects the posterior intercondylar area of the tibia with the medial condyle of the femur.

127
Q

Where does the ACL connect?

A

Originates from the medial and anterior aspect of the tibial plateu to the lateral femoral condyle.

128
Q

What predisposes you to OA of the knee?

A

Previous meniscal tears, ligament injuries and malalignment (genu varum- medial epicondylitis, genu valgum- lateral epicondylitis)

129
Q

What does patella femoral dysfunction predispose too?

A

Patellofemoral OA

130
Q

Younger patient with medial epicondyle OA treatment?

A

Especially if varus alignment- osteotomy of the proximal tibia can be offered to shift the load to the lateral compartment. This is particularly helpful to manual workers as a knee replacement would fail quickly.

131
Q

When would a knee replacement for OA be considereD?

A

When substantial pain, disability and conservative management has failed.

132
Q

When would you use unicompartmental knee replacement?

A

Treatment for patients with isolated OA.
Less invasive
Good for younger people
However failure is higher than TKR.

133
Q

Risks of unicompartmental knee replacement?

A

Similar to that with TKR-
unexplained pain
Younger patients more likely to need revision surgery.

134
Q

Typical history of meniscal tear?

A

Twisting force of a loaded knee e.g. turning in football
Patient will be able to localise pain to the medial or lateral joint line.
An effusion will develop the following day
Patient will complain of pain and mechanical symptoms- either catching sensation or locking where they have difficulty stretching the knee to full extension.

135
Q

Presentation and examination findings of a meniscal tear?

A

Younger patients- usually a sporting injury
25% also have ACL ruptures.

Exam- effusion
Joint line tenderness
Positive Steinmanns test- tibial rotation
Bucket handle meniscal tears will show 15 degrees block to full extension.

136
Q

What is more common, medial or lateral meniscal tears?

A

Medial meniscal tears are much more common- due to the medial meniscus being more fixed and less mobile.

137
Q

What is a bucket handle meniscal tear?

A

Usually results from large longitudinal tears where large meniscal fragment is able to flip out of its normal position and displace anteriorly. Means the knee is unable to fully extend.

138
Q

What are degenerative meniscal tears?

A

Can occur as the meniscus weakens with age. It can tear spontaneously or with minimal force. Can also be the first stage in OA.

139
Q

Treatment of meniscal tears?

A

The menisci only have blood supply to their outer third and therefore limited healing potential. Healing potential also decreases with age.

ONLY- reasonably new longitudinal tears in the outer 1/3rd of the meniscus in a younger patient is to be considered for a meniscal repair.

140
Q

Typical history of an ACL rupture?

A

Usually occur with a higher rotational force- turning the upper body laterally on a planted foot- often in high impact sports e.g. football, rugby.
Pop usually heard
Haemarthrosis (effusion due to bleeding in the joint) occurs almost immediately.
Deep pain in the knee- patient may complain of rotatory instability (knee giving way on a planted foot)

141
Q

Clinical examination of an ACL rupture?

A

Knee swelling

Excessive anterior translation of the tibia.

142
Q

Treatment of ACL rupture?

A

1/3rd of patients will compensate well and still do whatever they please (inc sport)
1/3rd will manage by avoiding certain movements and high impact sports.
ACL reconstruction- in athletes and people who’s knees give way on sedentary activity.

143
Q

Describe the process of ACL reconstruction?

A

Involves a tendon graft (usually patella or semitendonosis) being passes through tibial and femoral tunnels to the usual location of the ACL.

144
Q

Typical history of a PCL rupture?

A

Uncommon injury.

Direct blow to the anterior tibia or hyperextension on its own.

145
Q

Who (In PCL ruptures) is considered for surgery?

A

Frequent hyperextension

Unstable descending stairs

146
Q

How would you tear you MCL?

A

Valgus injuries.

147
Q

Typical history of an MCL tear?

A

Rugby tackle from the side. High forces can also potentially damage the ACL.

148
Q

How is MCL treated?

A

It has a good blood supply therefore healing occurs in the majority of cases.
Acute tears- hinged knee brace
Chronic MCL tears-tightening or reconstructing with tendon graft.

149
Q

Typical history of an LCL tear?

A

A varus stress may rupture the lateral collateral with/without damage to the PCL.

150
Q

Treatment of LCL tears?

A

Usually surgical with early repair or later reconstruction with a tendon graft.
Patients usually have marked instability on rotational movements.

151
Q

What may be affected by LCL tears?

A

Common perineal nerve

Popliteal artery.

152
Q

What is a complete knee dislocation?

A

Rupture of all 4 of the ligaments. High incidence of neurovascular injury.

153
Q

Management of complete knee dislocation?

A

Reduced as an emergency and may require external fixation. Regular checks of circulation needed.

154
Q

What are osteochondral/chondral injuries?

A

Bit of cartilage or cartilage attached to bone comes off due to direct blow or impact.
Assessment is performed by MRI, Xray and arthroscopy.

155
Q

If there is a large fragment of bone due to osteochondral injury- management?

A

Pin the bone back into place.

156
Q

If there is little bone or it is a non-weight bearing area- management of osteochondral injury?

A

Remove arthroscopically.

157
Q

What are extensor mechanism ruptures?

A

Extensor mechanism- made up of the tibial tuberosity, the patella tendon, the patella and the quadriceps muscle.

158
Q

What extensor mechanism ruptures may occur?

A

The quadriceps/patella tendon may rupture with rapid contractile force (e.g. lifting a heavy weight)
Patella ruptures tend to be in younger age group whereas quadriceps tends to be in the older age group >40

159
Q

Predisposing factors to extensor mechanism ruptures?

A
History of tendonitis
Chronic steroid use
Diabetes
RA
Chronic renal failure
Quinolone antibiotics.
160
Q

What tests the extensor mechanism?

A

Straight leg raise.

161
Q

Treatment of extensor mechanism rupture?

A

Surgical repair with tendon to tender repair or reattachment of the tendon to the patella.

162
Q

What is patellofemoral dysfunction?

A

Describes disorders of the patellofemoral articulation resulting in anterior knee pain
Encompasses chondromalacia patellae (damage to the cartilage at the back of the kneecap), adolescent anterior knee pain and lateral patella compression.

163
Q

What do patients complain of with patellofemoral dysfunction?

A

Anterior knee pain
Worse downhill
Stiffness after prolonged sitting causing psuedolocking.

164
Q

How is patellofemoral dysfunction treated?

A

Physio aimed at rebalancing quadriceps muscle.

165
Q

How do you get patella instability?

A

Can occur with a direct blow or sudden twist to the knee.

166
Q

Which way does the patella dislocate?

A

Always dislocates laterally and may spontaneously reduce when the knee is straightened.

167
Q

What ligament tears when the patella is dislocated? What does this cause?

A

medial patellofemoral ligament and osteochondral fracture may occur.

168
Q

What predisposes you to patella instability?

A

Ligamentous laxity, female gender, shallow trochlear groove, genu valgum, femoral neck ante version.

169
Q

What is pes cavus?

A

Abnormally high arch in the foot.

170
Q

What causes pes cavus?

A

Can be idiopathic

Can also relate to neuromuscular disorders including cerebral palsy, polio and spinal cord tethering.

171
Q

What often accompanies pes cavus?

A

Claw toes.

172
Q

How would you treat pes cavus?

A

Pain can be treated with soft tissue release and tendon transfer if supple or calcaneal.
Osteotomy if rigid.

173
Q

What is hallux valgus?

A

Bunions. Deformity of the great toe. Medial deviation of the 1st metatarsal and lateral deviation of the toe itself.

174
Q

who gets hallux valgus?

A

Condition is commoner in females
Often familial.
Incidence increases with age.
Incidence higher in populations who don’t wear footwear.
More common in association with other inflammatory arthropathies and RA.

175
Q

What symptoms will a patient with hallux valgus get?

A

Could be painful due to joint incongruence and a widened forefoot may also cause rubbing of shoes resulting in an inflamed bursa of the medial 1st metatarsal head.

176
Q

Treatment of hallux valgus?

A

Conservative treatment- wider and deeper shoes to accomadate space. Use of spacer in first webspace to stop rubbing between the great and second toes.

Surgical treatment- caution should be applied when offering it for cosmetic reasons.
Osteotomies- realign bones and soft tissue procedures to tighten slack tissues and release tight tissues.

177
Q

What is hallux rigidus?

A

1st MTP OA

Can be primary (degenerative) or secondary (osteochondral injury)

178
Q

Treatment of hallux rigidus?

A

Conservative- wearing stiff soled shoes to limit the motion of the MTP.
Removal of osteophytes may help.

Gold standard surgical treatment- arthrodesis- fusion should alleviate pain and sacrifice little movement however women would not be allowed to wear heels.

179
Q

What is Mortons neuroma?

A

Plantar interdigital nerves (which arise from the medial and lateral plantar nerves) are subject to repeated trauma. Irritated nerves can become inflamed and swollen (forming a neuroma)

180
Q

Presentation of Mortons neuroma?

A

Burning pain and tingling radiating into the affected toes.

Women are 4 x more likely to get this than men.

181
Q

Which nerve is most commonly affected by Mortons neuroma?

A

The 3rd interspace nerve (between the 3rd and 4th toe).

182
Q

Clinical exam of Mortons neuroma?

A

May reveal loss of sensation on the affected web spaces.
Mediolateral compression of the metatarsal heads (squeezing the forefoot) may reproduce symptoms or produce a characteristic click- mulders click test.

183
Q

Tests for Mortons neuroma?

A

Ultrasound may be useful- demonstrates swollen nerve

184
Q

Treatment of Mortons neuroma?

A

Conservative- use of metatarsal pad offloading in sole
Steroid and local anaesthetic injections may relieve symptoms
A neuroma can be excised however some patients continue to feel pain and there is a small risk of recurrence

185
Q

Where do metatarsal stress fractures most commonly occur?

A

2nd and then the 3rd.

186
Q

Who usually gets metatarsal stress fractures?

A

Runners, soldiers on prolonged marches, dancers or people doing distance walking when they are not used to it.

187
Q

When will an Xray demonstrate a fracture for metatarsal stress fractures?

A

Around 3 weeks until reabsorption at the fracture end occurs or a callus forms.

188
Q

What tests might you do to look into metatarsal stress fractures?

A

Bone scan may be useful.

189
Q

Treatment of metatarsal stress fractures?

A

Prolonged rest for 6-12 weeks in a rigid souled boot.

190
Q

What causes achilles tendonitis and rupture?

A

Can occur due to repetitive strain (from sports) which leads to peritendonitis
Or due to degenerative process with intrasubstance micro tears.

191
Q

What predisposes you to achilles tendonitis?

A

Quinolone antibiotics (ciprofloxacin), RA, gout and other inflammatory arthropathies.

192
Q

Where would you feel pain in achilles tendonitis?

A

Pain would be in the main substance of the achilles tendon or in the insertion to the calcaneous.

193
Q

Treatment of achilles tendonitis?

A

Rest, physio boot or splint.
Resistant cases may benefit from tendon decompression and resection of paratendon however scars in this area can be problematic and the condition is usually self limiting.

194
Q

Tendonitis predisposes to achilles tendon rupture. True or false. What is the significance?

A

True- if you give steroid injection you run the risk of rupture.

195
Q

Who does achilles tendon rupture usually affect?

A

The middle aged or older groups. Usually due to degenerative processes or recent tendonitis.

196
Q

What motion may have caused achilles tendon rupture? What symptoms will they have?

A

Sudden declaration with resisted calf muscle contraction leads to sudden pain (like being kicked in the back of the leg) and difficulty weight bearing.

197
Q

Treatment of achilles tendon rupture?

A

Suture repair. Protected by around 8 weeks of casts. Wound problems may occur after surgery.

Many surgeons recommend non-op management. Series of casts in equinous position- the ankle plantar flexed and the toes pointing down- gives good functional outcome.

198
Q

What is plantar fasciitis?

A

Another self-limiting repetitive stress/overload degenerative condition of the foot.

199
Q

Symptoms of plantar fasciitis?

A

Pain is felt on walking with localised tenderness on palpation of the site.

200
Q

Risk factors for plantar fasciitis?

A

Diabetes, obesity, frequent walking on hard surfaces with no cushioning.

201
Q

Treatment of plantar fasciitis?

A

Rest. Achilles and plantar fascia stretching exercises. Gel filled heel pads.
Corticosteroid injection may alleviate symptoms. Surgery is not really valued and you may damage plantar nerves.

202
Q

What is tibialis posterior tendon dysfunction?

A

The tendon is under repeated stress and especially with degeneration may develop tendonitis, elongation and eventually rupture.

203
Q

How would you treat tibialis posterior tendon dysfunction?

A

Splint with medial arch support.

If this fails- surgical decompression and tenosynovectomy may prevent rupture.

204
Q

What does rupture of the tibialis posterior tendon cause?

A

Loss of medial arch with resulting valgus of the heel and flattening of the medial arch of the foot.
If no OA develops- tendon transfer may work. if OA develops- arthrodesis.

205
Q

Why do you get claw and hammer toes?

A

Due to imbalance between the flexor and extensor mechanisms

206
Q

What is claw toe?

A

Hyperextension at the MTPJ

Hyperflexion at the DIP and PIP

207
Q

What is hammer toe?

A

Hyperextension at the MTPJ and hyperflexion at the PIPI. Hyperextension at the DIP.