MSK Flashcards

1
Q

A patient presents with lower back pain. Give 5 differentials for each age:
15-30:
30-50:
>50:
Other:

A

15-30:
1) Postural/mechanical
2) Prolapsed disk
3) Trauma/fracture
4) Ankylosing spondylitis + Reactive arthritis
5) Spondylolisthesis
6) Pregnancy

30-50:
1) Postural
2) Prolapsed disc
3) Discitis
4) Spondyloarthropathies (Ankylosing spondylitis, psoriatic arthritis, Reactive arthritis)
5) Degenerative bone disease (OA, Spondylosis, Osteoporosis)

> 50:
1) Postural
2) Prolapsed disc
3) Malignancy
4) Myeloma
5) Degenerative joint disease (OA, spondylosis, osteoporosis)
6) Paget’s disease

Other:
1) Spinal stenosis
2) Spinal infection (Osteomyelitis, septic arthritis)
3) Cauda Equina
4) AAA

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2
Q

What is the difference between spinal stenosis and spinal compression

A

Spinal Stenosis is the narrowing of the spinal canal which can lead to nerve compression.

Spinal Compression involves direct pressure on the nerves or spinal cord, and can be a result of stenosis or other conditions like disc herniation or tumours.

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3
Q

What is encompassed within Spondyloarthropathies?

What do they all share?

A

Spondyloarthropathies are a group of HLA-B27 disorders that primarily affect the spine and are characterised by Enthesitis. They include:
Ankylosing spondylitis (15-30+30-50)
Psoriatic arthritis (30-50)
Reactive arthritis (15-30 + 30-50)

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4
Q

What organisms primarily cause reactive arthritis

A

Chlamydia
Food borne (Shigella campylobacter)

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5
Q

State 3 degenerative bone diseases

A

OsteoArthritis
Spondylosis (OA but for spine)
Osteoporosis (typically 50+)

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6
Q

What are the most common malignancies found on a bone scan

A

the vast majority of tumours found in bone scans are not primary but metastasis from another tumour (Prostate, breast, thyroid, kidney)

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7
Q

What is Paget’s disease of the bone?

What age group does it primarily affect?

A

Paget’s disease of the bone is a disease characterized by high turnover bone remodelling in a mosaic pattern leading to mis-shaped, fragile bones and bone pain

3 phases: (extra info)
1) Increased osteoclast activity => abnormal breakdown
2) Abnormal excessively increased osteoblast activity leading to disorganised, thickened bone
3) Cycle repeats leading to the high turnover bone remodelling

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8
Q

Go over the Dermatomes yourself (image in answer)
State the myotomes and the reflexes they are involved in if applicable

A

L2 - Hip flexion + adduction
L3 - Knee extension
L4 - Knee extension + Foot dorsiflexion
L5 - Knee flex + foot inversion + Big tow dorsiflexion
S1 - Knee flexion + Foor plantar flexion

Knee reflex (L3,L4)
Ankle reflex (S1,S2)

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9
Q

A joint that moves with ease suggests?

A

Inflammation as the cause (think RA for example which eases with movement)

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10
Q

How would you structure and hx and exam in MSK?

A

Hx
Pain (Socrates)
Deformity
Loss of function/Impact on QoL
Neurology

Exam
Look
Feel
Move
Special tests
+/- neuro

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11
Q

When conducting an examination in MSK, what routine neuro should you perform?

A

1) SLR (if backpain)
2) Sensory loss
3) Muscle weakness (power)

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12
Q

You are asked to conduct a focused examination of the spine. Go through what you will do and what you are looking for

A

Important to note that the lower limb must be examined along with the spine
Look: Deformity such as kyphosis (ank.spon), lumbar lordosis, scoliosis

Feel: Spine and paraspinal muscles for tenderness !stepdeformity, muscle spasm

Move: Flexion, extension, !!!lateral rotation and flexion.

Special tests: Straight leg raise (ipsilateral sciatica) + Schober test

Neuro:
Inspection: LL Muscle wasting
Palpation: LL Muscle wasting and LL sensory
Motor: Power + Reflexes!!

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13
Q

How is Schober test performed?

A

Mark at L5 and another 10cm above. Ask the patient to flex forward. If <+5 cm (total 15cm) => Ankylosing spondylitis

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14
Q

What are the red flags in MSK

A

!!!Saddle Anaesthesia
!!!Urinary incontinence
!!! Night time pain
Weight loss/past hx of cancer
Ages <20, >55
Non-mechanical pain/pain at rest
Pain that worsens when supine
Immunosuppression (Drugs, transplant, HIV, IVDU)
Systemically unwell

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15
Q

What screening tool is used in the evaluation of back pain? How would you explain what it involves?

How are the results interpreted?

A

The Keele STarT Back Screening Tool is a validated questionnaire used to classify patients with low back pain into categories of low, medium, or high risk for chronicity, based on their physical and psychosocial risk factors, to guide appropriate treatment strategies.

3 or less -> Avoid rest, advise on self-help and exercise
If 4+ -> we should look at questions 5-9
=> 3 or less => Physical therapy after 4 weeks
=> 4+ => Specialist referral

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16
Q

What is the general workup of a patient presenting with lower back pain in primary care including relevant general management

A

-> means If present then do
1) Triage with hx and exam
2) Rule out fracture -> Xray -> manage (cast, external/internal fixation)
3) Rule out Cauda Equina? -> Immediate admission
4) Rule out Red flags? -> Conduct bloods (ESR, Ca2+, PO4, Alk Phos, PSA, CA125) + Xray
5) Neurological signs? -> Referral if not resolving within 4 weeks
6) Keele STarT Back Pain Scoring Tool
Final management based on score
In all: NSAID + Omeprazole or Codeine + Paracetamol
3 or less -> Avoid rest, advise on self-help and exercise
If 4+ -> we should look at questions 5-9
=> 3 or less => Physical therapy after 4 weeks
=> 4+ => Specialist referral

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17
Q

What does physical therapy entail? Give 3 examples

A

Physiotherapy
Back exercises
Chiropractic
Osteopathy
Acupuncture

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18
Q

What is Cauda Equina?

How does it present?

How is it managed?

A

Compression below L2 e.g. disc protrusion at L4/L5
This is a lower motor neuron lesion (upper motor neuron lesion) =>
Perianal anaesthesia
Asymmetrical LL weakness (Dorsiflexion-L4, Plantar flexion-S1, Eversion-S1)
Hypoflexion
Bowel/Bladder incontinence (sphincter)
Loss of ankle reflex (S1)

Immediate admission to A&E and surgical intervention

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19
Q

A patient presents with a hx of thyroid cancer and new onset backpain worse on movement.
What is the most likely diagnosis?

Based on this what neurological symptoms may accompany this?

What imaging technique is best for this?

How is this managed?
If a patient is in the final stages of the disease, how is it managed?

A

Worse on backpain indicates that this isn’t due to inflammation
This is most likely spinal cord compression

Neurological signs:
In any case: LL weakness, urinary incontinence, constipation
Above L1 - UMN => increased tone and reflexes
Below L1 - LMN => reduced tone and reflexes

MRI (saggital view)

Management: Oral dexamethasone and referral for same-day assessment, surgery, and radiotherapy.
If final stage of disease, palliative care

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20
Q

What is Scoliosis?

Give 5 causes

Give 3 specific examination findings

How would you manage in primary care?

A

Scoliosis is the lateral curvature of the spine

Causes:
1) Congenital (butterfly vertebra)
2) TB of spine
3) Neoplasm
4) Trauma
5) Neuromuscular (Cerebral palsy, neurofibromatosis)
6) Metabolic (bone dysplasia)

Exam:
1) Asymmetrical shoulder height
2) lateral curvature of spine
3) !!Unequal space between the trunk and the upper limb

Management: Referral to ortho. If pain then urgent referral

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21
Q

What is postural scoliosis?

A

Scoliosis that disappears on bending.
It is not clinically significant

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22
Q

What joints are you feeling during a shoulder exam? what would you be looking for?

A

Sternoclavicular joint
Acromioclavicular joint
Glenohumeral joint
Looking for crepitus, numbness, paraesthesia, swelling, tenderness, muscle wasting, ridges

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23
Q

A patient presents with pain beginning at the shoulder and radiating down the arm anteriorly. Where is the pathology?

A

Shoulder joint

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24
Q

Sources of shoulder tip pain?

A

Acromioclavicular joint
Cervical spine disorder
Irritation of the phrenic nerve/diaphragm => Referred pain(MI or inflammation e.g. cholecystitis, ectopic pregnancy, splenic rupture peritonitis)

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25
Q

In a hx of shoulder problems, how would you assess for loss of function?

A

Inability to wear clothes, brushing hair, doing up bra

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26
Q

What is the drop arm test and what does it test for?

A

Abduct arm to 90 degrees and ask patient to slowly bring down to their sides. Tests for rotator cuff tear

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27
Q

What special tests should you perform in the shoulder test section. What does each test for

A

Empty can test (supraspinatus)
Drop arm test (Rotator cuff tear)
Lift off test (w/ resistance) (Subscapularis)
Scarf Test (AC joint pathologies such as arthritis)
Sulcus test (inferior instability)
Apprehension test (Shoulder/anterior stability)

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28
Q

A patient presents with painful limitation of movement in all directions. The pathology is likely to be caused by

A

Intraarticular disease

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29
Q

A patient presents with painful limitation of movement in one plane. The pathology is likely to be caused by

A

Tendonitis

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30
Q

A patient presents with painful weakness. The pathology is likely to be caused by

A

Tendon rupture or neurological signs

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31
Q

A patient presents with a stiff, painful shoulder joint. What are your differentials

A

Rotator cuff injury/Tendonitis
Shoulder osteoarthritis
Adhesive capsulitis
Prolonged immobilisation
Polymyalgia rheumatica

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32
Q

How does acute tendonitis present?

A

Holding shoulder immobile
Unable to lie on affected side

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33
Q

You suspect rotator cuff tear. What special test will you perform?

A

Drop arm test

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34
Q

You suspect subacromial impingement. On examination, what would help you reach a diagnosis?

A

Painful arc test
or internal rotation

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35
Q

What is the painful arc?

A

Abduction from 60-120 degrees as this is the range that the rotator cuffs are responsible for

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36
Q

How can a rotator cuff injury present (3)?

What is the pathophysiology behind them all?

What investigations will you perform?

How are these managed in primary care + escalations

A

Rotator Cuff injury can present as either to all 3 of the folllowing:
1) Acute tendonitis: Due to excessive use/trauma in <40yo. Patient would be holding shoulder immobile and cannot sleep on that side

2) Rotator cuff tear: From trauma, Drop arm test +ve

3) Subacromial impingement: Painful arc +ve or pain on internal rotation

Pathophysiology: Excessive use/trauma of the shoulder joint (controlled by the rotator cuff muscles) leads to acute tendonitis or tear which results in reduced space within the joint ending up with nerve impingement or subacromial impingement

Investigations: X-ray, Dynamic USS, MRI

Management: Rest->NSAIDs (+PPI) -> Physiotherapy -> Subacromial steroid injection -> Refer to Ortho

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37
Q

A 55 year old with no history of trauma presents holding his shoulder immobile. He complains of being unable to sleep on that side lately. What could be the likely cause of this presentation?

How is it treated?

A

With no history of trauma, it is more likely to be caused by inflammation around calcific deposits.
Tx = Steroid injection

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38
Q

What findings on X-ray would be consistent with rotator cuff injury?

What findings on Dynamic USS?

A

X-ray -> calcification (of Supraspinatous), Glenohumeral joint cysts

USS -> Impingement, tendonitis tears

Remember what X-ray can see and what USS can see better

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39
Q

Give 3 benefits and risks of steroid injections in joints

A

Benefits:
- Reduce inflammation
- Pain relief
- Joint function (mobility)

Risks:
- Site infection or even septic arthritis
- Cartilage damage and joint degradation
- Increased blood sugar levels
- Tendon weakening or rupture
- Bleeding/haemorrhage (US-guided may help)

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40
Q

What is the typical aetiology(ies) of shoulder osteoarthritis?

A

Trauma > chronic
Or Crystal-induced inflammation (Gout/Haemochromatosis)

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41
Q

What is the presentation of adhesive capsulitis?

What pathologies are associated with adhesive capsulitis?

Give the management escalations

A

Painfull stiff shoulder with global limitation of movement (intraarticular pathology that is !worse at night

DM, Intrathoracic pathologies (Lung disease, Ischaemic heart disease, cervical pathologies)

Management: Check HbA1c -> NSAIDs (+ppi) + Physiotherapy -> Local steroid injection -> Orthopaedic referral

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42
Q

What is the typical aetiology of anterior dislocation

What are complications of this?

What examination findings are associated with this?

How is this managed?

A

Fall on arm/shoulder in contact sports on an outstretched hand with !extended elbows (as opposed to Elbow dislocation)

Complications:
1) Labral tear-> Apprehension test, Sulcus test +ve
2) Axillary nerve damage -> reduced sensation over regimental patch

Management: Referral to A&E for Xray and reduction. Refer to ortho/physio if recurrent

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43
Q

What is the typical aetiology and presentation of rupture of the head of the biceps.

A

Lifting -> pop -> Swelling and discomforty -> bulge on elbow flexion (Popeye’s sign)

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44
Q

Acromioclavicular joint problems present as

A

Shoulder tip pain
Just a note, if you dont know how to treat something in ortho just say NSAIDs + PPI +/- steroid injection -> Refer to ortho

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45
Q

What is cleidocranial dystosis

A

AD condition characterised by missing part or all of clavicle, delayed ossification of the skull, a/w short stature.
No tx

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46
Q

You perform a clinical exam on a patient coming with elbow pain. You note nodules over the olecranon. What are your ddx

A

1) Psoriasis
2) RA nodule
3) Gouty Tophus
4) Olecranon bursa
5) Trauma

Note: When performing an elbow exam, dont forget to test for supination and pronation

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47
Q

Define Epicondylitis and then Go through epicondylitis you already know it

A

Extensor tendon inflammation at the epicondyles due to repeated strain

Tennis elbow = Lateral epicondylitis = pain on resisted wrist extension. Tenderness over lateral epicondyle

Golfer’s elbow = medial epicondyle = pain on resisted wrist pronation!!!. Tenderness over medial epicondyle

Management: Rest and stop triggering movements +/- NSAIDs (+ppi) +/- Steroid injections (speeds up recovery but increased risk of recurrence) + physiotherapy

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48
Q

What is the aetiology of olecranon bursa?
Management?

A

Traumatic bursitis due to repeated pressure on elbow => pain and swelling over olecranon which may become infected => abscess

Management:
Conservative: Rest + Ice + analgesia
Large/unresolving: Aspiration of fluid or steroid injection -> referral
Infected -> antibiotics

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49
Q

What is the most common distribution of numbness and paraesthesia in the upper limb?
What pathology in the elbow may lead to this?

A

Ulnar distribution

Ulnar Neuritis

50
Q

Ulnar neuritis typically begins with clumsiness -> weakness -> wasting of hand muscles -> reduced sensation over pinky + medial half of ring finger.
What is the aetiology of Ulnar neuritis?

How is it managed?

A

Narrowing of the ulnar groove from fracture or OA or RA leading to pressure on the ulnar nerve leading to ulnar neuropathy

Managed via ruling out metabolic or autoimmune causes of mononeuritis and then referring for ! Nerve conduction studies and surgical decompression

51
Q

What is the aetiology of elbow dislocation?

If you are looking at a person with elbow dislocation what would you see?

Management?

A

Fall on an outstretched hand with !flexed elbow (in contrast to shoulder dislocation)

Presentation: Swollen elbow with person holding it fixed in flexion! (in contrast to pulled elbow)

Send to ED for reduction

52
Q

What is the aetiology of a pulled elbow?

If you are looking at a child with a pulled elbow, what will you see?

Would you do an Xray?

How is this managed?

A

Children <5 due to traction injury causing subluxation of the radial head. Occurs when child is pulled up suddenly by the head.

Child not using arm, elbow held in !extension + pronation (in contrast to elbow dislocation)

X-ray is unhelpful. Reduce arm in clinic using

53
Q

What investigation is diagnostic for osteoporosis?

A

DEXA scan

54
Q

The DEXA scan can produce 2 score modalities. What are they? When should each be used?

A

T-score: Compares Bone Mineral Density of patient to the mean bone density of a 30 year old. For post-menopausal women and men >50.
Z-score: Compares Bone mineral density of patient to age-matched normal control. Not used to diagnose osteoporosis. Used for children, premenopausal women, and men <50

55
Q

Osteoporosis most commonly affects the hips and mostly females due to menopause. The DEXA scan best tests for this. How would you diagnose Osteoporosis?

A

Osteopenia = T-score b/w -1 -> -2.5
Osteoporosis = T-score <-2.5

56
Q

Give 5 RF for osteoporosis

A

Low BMI
Post-menopausal
Age
Steroid use
Immobility
Smoking
Alcohol

57
Q

What does the DEXA scan stand for?

A

Dual-energy X-ray Absorbtiometry

58
Q

What is required to request a DEXA scan testing for osteoporosis

A

Qfracture or FRAX

59
Q

Give 5 causes for osteoporosis

A

Primary Osteoporosis: Menopause and old age (even men)
Secondary Osteoporosis:
1) Endocrine: Hyperthyroidism, hyperparathyroidism, Hyperparathytoidism, hyperprolactinaemia, Cushing’s, Hypogonadism (anorexia, androgen blockade - GnRH, LHRH, Antiandrogens).
2) GI - Coeliac, IBD, Chronic liver diease, Chronic pancreatitis
3) Rheumatological - RA, Reactive arthritis, psoriatic arthritis
4) Other: CF, Multiple myeloma, Immobility, Steroid use

60
Q

The DEXA scoring such as the T score is measured in standard deviations from the mean. Each St. Dev = 2-3x risk of a fracture.
Define Fragility fracture

What are the most common sites of a fragility fracture?

A

Fracture when falling from a standing height or Vertebral collapse

Most common sites are Hip, wrist and vertebral

61
Q

A post-menopausal patient with low BMI presents with sudden onset severe lower back pain with no history of trauma. Their past history includes Rheumatoid arthritis for which she is taking long-term steroid for. What is your most likely diagnosis? How will you confirm it?

A

Osteoporosis, DEXA scan

62
Q

What lifestyle advice would you give to an osteopaenic/osteoporotic patient?

A

Lifestyle advice:
1) Nutrition: Maintain BMI >19 increased calcium in diet
2) Weight bearing exercises (+/- physiotherapy)
3) Smoking and alcohol cessation

63
Q

A post-menopausal patient with low BMI presents with sudden onset severe lower back pain with no history of trauma. Their past history includes Rheumatoid arthritis for which she is taking long-term steroid for. You conduct a DEXA scan and determine that the patient has a T-score of -1.5 consistent with osteopenia. How will you manage this patient?

A

Lifestyle advice:
1) Nutrition: Maintain BMI >19 increased calcium in diet
2) Weight bearing exercises (+/- physiotherapy)
3) Smoking and alcohol cessation

Medical: Vit. D and calcium supplements

Followup: Repeat DEXA in 2 years

64
Q

What do the Q-fracture and FRAX scores determine?

A

10-year probability of fracture (just like Qrisk)

65
Q

Give 2 examples of Bisphosphonates

How are they supposed to be taken?

What are the main side effects of bisphosphonates?

What are the Contraindications?

A

Alendronate/Ibandronate

Taken on an empty stomach in the morning >30 mins before eating. Sit upright for 30 minutes after taking

SE: Osteonecrosis of the jaw, atypical femoral fracture (subtrochanteric/mid-shaft fracture)

CI: Child-bearing age (teratogenic), CKD

66
Q

What is the medical management of osteoporosis along with its escalations

A

Women:
1) Bisphosphonates (Alendronate/Ibandronate)
2) Denosumab
3) Raloxifene (specific indication)
4) Teriparatide (technically 3rd line)

Men:
1) Bisphosphonates
2) Teriparatide

67
Q

When is Denosumab indicated?

How does it work?

A

Denosumab is indicated if bisphosphonates are CI (CKD, child-bearing) or not tolerated

Monoclonal antibody targeting osteoclast activity => reducing bone resorption

68
Q

What is Raloxifene?

When is it indicated for the tx of Osteoporosis?

A

It is a selective oestrogen receptor modulator

Indicated if previous fragility fracture or further fracture despite being on bisphosphonates

69
Q

Teriparatide is the 3rd line drug for post-menopausal women and second line for men with a past history of fragility fracture. It is given if other treatments are not tolerated and specifi T-score and clinical criteria are met (not in the book). This drug requires consultant initiation. How is it administered? What is the maximum duration?

A

Daily injection but maximum duration is 18 months

70
Q

When is HRT indicated for the treatment of osteoporosis?

A

!Only indicated for osteoporosis if premature menopause or everything else is contraindicated

71
Q

A post-menopausal patient with low BMI presents with sudden onset severe lower back pain with no history of trauma. Their past history includes Rheumatoid arthritis for which she is taking long-term steroid for. You conduct a DEXA scan and determine that the patient has a T-score of -2.6 consistent with osteoporosis. What is the full management plan for osteoporosis?

A

Lifestyle advice:
1) Nutrition: Maintain BMI >19 increased calcium in diet
2) Weight bearing exercises (+/- physiotherapy)
3) Smoking and alcohol cessation

Medical: Vit. D and calcium supplements +
Women:
1) Bisphosphonates (Alendronate/Ibandronate)
2) Denosumab
3) Raloxifene (specific indication)
4) Teriparatide (technically 3rd line)

Men:
1) Bisphosphonates
2) Teriparatide

Followup: Regular monitoring

72
Q

What is Osteoarthritis

A

Metabolically active joint degeneration involving all components including cartilage, bone, synovium, capsule, muscle).

73
Q

Give 5 risk factors for osteoarthritis

A

1) Age
2) Female
3) Genetic predisposition
4) Obesity
5) Surgical intervention e.g. Post-meniscectomy (knee)
6) Occupation e.g. farming, athlete

74
Q

What is the typically presentation of a patient with osteoarthritis?

A

!gradual onset over years!
Joint pain worse on movement
Joint stiffness in the morning, relieved in <30 mins
+/- exacerbations lasting weeks/months

75
Q

Where are Heberden nodes located?
Where are Bouchard nodes located?
What do these findings indicate

A

Heberden: Dorsal aspect, DIP
Bouchard: Dorsal aspect, PIP
They are bony growths indicating osteoarthritis

76
Q

You are asked to conduct a focused examination for osteoarthritis. Go over the findings you would be looking for

A

Note if this comes on exam, you should be looking for differentials as well and what findings are there => you would also be looking for things in RA for example

Look -> Heberden Nodes (DIP), Bouchard Nodes (PIP) swelling of DIPs, Deformity.
Feel -> Synovial thickening (=swelling), Effusions, Muscle wasting.
Move -> Crepitus, weakness

77
Q

What investigations would you conduct to confirm the diagnosis of osteoarthritis

A

Bloods: FBC, ESR (>30 indicates inflammatory arthritis

Imaging: X-ray

78
Q

You are investigating a patient with suspected osteoarthritis. You send bloods to the lab and the patient is getting their X-ray now. Blood results come back showing ESR >30. What would this mean?

A

This means that this is likely an inflammatory arthritis e.g. RA, psoriatic.

79
Q

What X-ray findings would indicate Osteoarthritis?

A

Joint space narrowing
Subchondral sclerosis
Subchondral cysts
Osteophytes (bony growths)

80
Q

A patient is suffering from a chronic bone disease. Explain the multidisciplinary management available (and should be mentioned in any ortho case) for every patient.

A

1) Physiotherapist: Exercise, strapping, splints
2) Chiropody/Podiatry: Foot care and insoles
3) Orthopaedic: Surgery if needed
4) Occupational Therapist: Aids (e.g. handles)
5) Social work: Disability benefits and housing
6) Counselling: Chronic bone diseases are a/w mental health deterioration

81
Q

What is the conservative management of Osteoarthritis?

A

1) Reduce load on joint via
a) Weight reduction
b) Using a walking stick (on opposite leg)
c) insoles via podiatry referral

2) Exercise: Swimming, cycling, Physiotherapy referral. Exercise is a/w reduced pain and disability

3) Complementary therapies (acupuncture, chiropractic). Not much evidence but only real evidence is chiropractic work with back pain.

+/- analgesia (Topical NSAIDs > Oral NSAIDs > Opioids)

82
Q

A patient with a history of OA presents to the clinic. They are having an acute exacerbation of OA. How would this present?

How is it managed?

A

Presents with increased intensity of pain and stiffness
+ swelling, warmth, tenderness
+ Further functional impairment
(lasts weeks to months)

Treated via joint aspiration (Steroid injections are not recommended according to NICE)

83
Q

Conservative management has proven to be unsuccessful for the treatment of OA in a patient. What management options are available?

A

Analgesia (if not already on it) Topical NSAIDs > Oral NSAIDs > Opioids.

Aspiration if acute exacerbation

Referral to rheumatology (if suspicion of co-existing inflammatory arthritis) or Orthopaedics (for hemi/total arthroplasty)

84
Q

What is the full management plan for Osteoarthritis

A

OA requires MDT management:
1) Physiotherapist: Exercise, strapping, splints
2) Chiropody/Podiatry: Foot care and insoles
3) Orthopaedic: Surgery if needed
4) Occupational Therapist: Aids (e.g. handles)
5) Social work: Disability benefits and housing
6) Counselling

Conservative management:
1) Reduce load on joint via
a) Weight reduction
b) Using a walking stick (on opposite leg)
c) insoles via podiatry referral

2) Exercise: Swimming, cycling, Physiotherapy referral. Exercise is a/w reduced pain and disability

3) Complementary therapies (acupuncture, chiropractic)

Medical management:
Analgesia (if not already on it) Topical NSAIDs > Oral NSAIDs > Opioids.

Surgical management/Referral:
Aspiration if acute exacerbation

Referral to rheumatology (if suspicion of co-existing inflammatory arthritis) or Orthopaedics (for hemi/total arthroplasty)

85
Q

RA is typically triggered by environmental factors in patients with genetic predisposition. What genetic mutation is a/w rheumatoid arthritis?

A

HLA DR4

86
Q

RA is characterised by its variable course of disease with periods of exacerbations and periods of remission. How would you assess disease activity in a patient with RA?

A

DAS 28 (disease activity score -28 joints). This considers number of swollen joints, number of tender joints, ESR/CRP levels, and patient’s global self-assessment

87
Q

What joints are typically affected in OA vs RA?

A

OA: Hip, knee, base of thumb => larger joints and typically asymmetrical

RA: Starts with smaller joints

88
Q

What is the typical presentation of RA? (not exam findings)

A

Typically presents within months of onset (more acute than OA)
Starts with symmetrical!! small joint involvement with pain + swelling
Early morning stiffness (>30 mins)
Pain on walking and doing daily activities => functional impairment (e.g. reduced grip strength => cannot hold kettle)

Note: Joint deformity and damage typically present later

89
Q

Where are rheumatoid nodules found?

A

Extensor surfaces of arms (typically elbow)

90
Q

What is Felty Syndrome?

A

Combination of RA, splenomegaly and Leucopenia

91
Q

Give 15 exam findings and other features associated with Rheumatoid arthritis

A

Hands:
1) Involvement (swelling + tenderness) of MCP and PIP and NOT DIP (OA)
2) Ulnar deviation of fingers
3) Z-deformity of the thumb
4) Boutonnier’s deformity (EM,FP)
5) Swan neck deformity (EP,FD)
6) Reduced grip strength
7) Bilateral carpal tunnel due to nerve entrapment
8) Palmer Erythema

Extra-articular:
1) Anemia (Microcytic)
2) Felty Syndrome (RA + Splenomegaly + Leucopenia)

Arms: Rheumatoid nodules (extensor surfaces)

Eyes: Scleritis + Episcleritis

Heart:
1) Pericarditis
2) Mitral regurgitation

Lungs: Pleural effusions

Shoulder: Adhesive capsulitis

Spine: (Risk of cord compression)
1) Cervical spine subluxation
2) Atlantoaxial instability

Legs and Feet:
1) Subluxation of metatarsal heads
2) Claw toes (pain walking => ask to walk for gait)
3) Baker’s cyst
4) Patellar tap => Swelling over joint

92
Q

How would a Baker cyst rupture in a patient with RA present?

A

Baker cyst rupture mimics DVT => sudden onset severe unilateral leg pain with swelling, heat and tenderness.

93
Q

What is Boutinniere’s deformity?

What is the Swan neck Deformity?

A

Deformities of the hand associated with RA whereby
Boutinniere’s: Extended MCP, Flexed PIP
Swan Neck deformity: Hyperextended PIP, flexed DIP

94
Q

A patient presents for the first time with signs and symptoms consistent with RA. You have conducted your Anti-CCP, RF, and ANA titre and all are positive. What is your next step?

A

Refer all suspected cases of RA to rheumatology as early detection significantly alters disease progression.

95
Q

A patient presets with joint pain in the hands. What are your differentials?

A

Rheumatoid arthritis
Osteoarthritis (usually large joints)
Psoriatic arthritis
SLE
Carpal tunnel syndrome
Polymyalgia rheumatica

96
Q

What relevant investigations would you conduct for RA? For each, state the findings you are looking for

A

FBC - looking for microcytic anemia and leucopenia (Felty)

Serology: Anti CCP, RF, ANA titre (+ve in RA)

Xray:
1) Periarticular soft tissue swelling
2) Joint space narrowing
3) Erosions (From infl. of socket +/- collapsed head)
4) Juxtaarticular osteopenia (black in bones = reduced density)

97
Q

Give 4 ways to differentiate between osteoarthritis and rheumatoid arthritis

A

1) Morning stiffness: OA <30 mins, RA >30 mins
2) OA usually affects less joints but bigger joints. RA affects more joints but smaller joints
3) OA is localised to joints and surrounding tissue whereas RA is systemic and has many extra-articular features
4) RA never affects the DIP, OA has heberden nodules on DIPs
5) OA is develops over years whereas RA is over weeks/months
6) OA is a degenerative disorder, RA is an autoimmune disorder

98
Q

How is an acute flareup of RA managed?

A

Intra-articular injections of steroids

99
Q

IA injection of steroids is used to acutely manage flareups of RA. If someone comes in with many acute flareups a year, can they still receive steroid injections?

A

The maximum safe amount is 3x/year in any particular joint
If someone is having more flareups, they probably need better medications to manage the symptoms.

100
Q

Give 3 examples of DMARDS used in the treatment of RA

A

Methotrexate (also used in psoriatic arthritis!)
Sulfalazine
Azathioprine
Intramuscular gold
Hydroxychloroquine
Leflunamide
Cyclophosphamide

101
Q

What is the medical management of RA including escalations? (Not acute)

A

a) NSAIDs + Paracetamol + PPi
b) DMARDs: Methotrexate, Sulfalazine
c) Biologics and JAK Inhibitors (Infliximab, Etanercept)

102
Q

Before starting DMARDs for RA, it is important to take baseline measurements within FBC (WCC, neutrophils, platelets), LFTs, and Urinalysis (haematuria, proteinuria) to be monitored throughout the course. Methotrexate is the first line drug in the tx of RA. What is the mechanism of action of methotrexate?

What is the regimen used in RA?

What are the side effects of methotrexate?

A

Methotrexate is a folic acid antagonist via inhibition of dihydrofolate reductase

Given with a once a week dose (PO or IM) + folic acid supplements to be taken 1-2/week but not on the day that methotrexate is administered

SE: Folic acid deficiency (mouth sores, GI upset), hepatotoxicity, BM suppression, B12/folate deficiency (megaloblastic anemia)

Note: Teratogenic => consider contraception or other Sulfalazine

103
Q

When is Sulfalazine indicated for the treatment of RA?

A

Pregnancy or child-bearing age
CI of methotrexate (liver failure, renal failure)

104
Q

When are biologics/JAK inhibitors indicated in the treatment of RA?

Give 2 examples

A

Indicated if 2 or more DMARDs already used

Infliximab
Etanercept

105
Q

A patient with RA presents with carpal tunnel.
Is it likely unilateral or bilateral?

How is this managed surgically?

A

Bilateral
Carpal tunnel release and Nerve decompression

106
Q

What are the options for surgical management of RA?

A

Orthopaedic referral for the following options
1) Joint fusion
2) Joint replacement (Arthroplasty)
3) Tendon transfer and repair
4) Carpal tunnel release + nerve decompression (carpal tunnel)

107
Q

What is the full management plan for a patient presenting with signs and symptoms consistent with rheumatoid arthritis?

A

First time? Refer to rheumatology directly
Acute? IA steroid injection

Conservative: MDT approach
1) Physiotherapist: Exercise, strapping, splints
2) Chiropody/Podiatry: Foot care and insoles
3) Orthopaedic: Surgery if needed
4) Occupational Therapist: Aids (e.g. handles)
5) Social work: Disability benefits and housing
6) Counselling

Medical:
a) NSAIDs + Paracetamol + PPi
b) DMARDs: Methotrexate, Sulfalazine
c) Biologics and JAK Inhibitors (Infliximab, Etanercept)

Surgical:
1) Joint fusion
2) Joint replacement (Arthroplasty)
3) Tendon transfer and repair
4) Carpal tunnel release + nerve decompression (carpal tunnel)

108
Q

Define Gout

What are the main causes of gout? Give 5

A

Crystal-induced arthritis due to hyperuricemia leading to the deposition of uric acid crystals causing inflammation
Caused by: (Urea is a waste product of cells)
1) Drugs: Thiazide diuretics, Cytotoxic drugs (chemo)
2) Increased cell turnover: Lymphoma, leukemia, haemolysis, psoriasis
3) Reduced elimination: CKD, Hyperparathyroidism
4) Disorders of purine synthesis: Leisch-Nyhan Syndrome

109
Q

Give 10 RF for Gout

A

1) Gout
2) Obesity
3) Excess alcohol
4) High purine diet (Fish, seafood, meat, beer)
5) Family hx
+ Causes of Gout
=> Cancer tx
=> Leukemia, lymphoma, psoriasis
=> CKD, Hyperparathyroidism
=> Leisch-Nyhan Syndrome

110
Q

What are the top 3 triggers of acute gout exacerbation

A

Surgery/trauma
Acute infection
Dehydration

111
Q

How does acute gout present?

A

Painful, swollen distal joints (big toe, feet, ankle) with an erythematous base +/- fever

112
Q

How does chronic gout present?

A

Recurrent acute attacks
tophi in pinna, tendons, and joints causing joint damage and deformity

113
Q

What is the top differential for acute gout that must be ruled out? How will you know?

How is it managed?

A

Septic arthritis
Patient would be systemically unwell. You can send synovial fluid for culture

Septic arthtitis requires emergency admission for IV antibiotics + surgical washout of joint.

Consider septic arthritis if the patient is young, ha a prosthetic, or recent surgery

114
Q

What investigations would you perform for a patient with gout (only include relevant) + what findings you expect.

A

Bloods: FBC (raised WCC), ESR (raised), Uric acid (raised)
Microscopy of synovial fluid showing sodium monourate crystals under polarised light
X-ray: Erosions if chronic (soft tissue swelling if acute but it is not typically performed)

Note: Uric acid is its own standalone test

115
Q

How is an acute gout attack managed?

A

1) Colchicine (500mcg BD/QDS)
2) NSAIDs + PPI
3) Corticosteroid injection (IM, IA)

116
Q

How would you manage lifestyle factors to reduce the risk of another gout attack?

A

Educate about gout
Physiotherapy referral for exercise
Dietician referral to manage weight and lower purine diet
Reduce alcohol intake to <14/week

117
Q

When is urate-lowering therapy indicated for gout?

What options are available?

A

Indicated after 1 attack of gout

1) Allopurinol
2) Febuxostat
3) Sulfinpyrazone

118
Q

You schedule a followup 4-6 weeks after an acute gout attack. What does this review include?

A

Assess lifestyle factors (exercise, weight, purine diet, alcohol intake)
Assess CVD RF and lipid profile
Check serum Uric acid + eGFR

!!Discuss Urate lowering therapy:
1) Allopurinol
2) Febuxostat
3) Sulfinpyrazone

Schedule review in 1 year

119
Q

Allopurinol is typically started low and increased every 4 weeks until the aim of urate-lowering therapy is reached.
What is the aim of urate lowering therapy?

A

Urate levels <300 micrimol/L
(Prophylactic colchicine may be given during titration to prevent an attack)

120
Q

What is the full management protocol for Gout starting from presentation with a painful swollen 1st metatarsal with confirmed sodium monourate crystals under polarised light.

A
121
Q

Attacks of pseudogout are less severe than gout and may be difficult to differentiate between other typies of arthritis (not gout). What is the medical word for pseudogout?

What is it associated with?

What joints are mostly affected?

What is the main finding on x-ray a/w pseudogout?

How is the diagnosis of pseudogout confirmed?

A

Calcium Pyrophosphate deposition disease a/w OA, Hyperparathyroidism, and haemochromatosis

Mostly affects knee, wrist and shoulder (ankle, toe and foot in normal gout).

Chondrocalcinosis on Xray

Rhomboidal/rod shaped crystals in synovial fluid under microscopy confirms diagnosis (gout is needle shaped)