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MSK Flashcards

1
Q

Difference between strain and sprain

A

Sprain = injury to ligament

Strain = injury to tendon

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2
Q

Feature of 3rd degree strain

A

muscle tears all the way through

‘pop’ sensation – muscle rips into 2 or shears away from tendon

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3
Q

Symptoms of ankle sprain/strain

A
  • Swelling
  • bruising
  • pain after injury
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4
Q

Most common ankle sprain

A

inversion ankle sprain = where excessive plantar flexion and supination cause the anterior talofibular ligament (ATF) to be affected.

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5
Q

What imaging is used to identify fractures/dislocation?

A

x-ray

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6
Q

Management of ankle fracture/dislocation

A

open = surgical fixation

closed = reduce and splint

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7
Q

When is x-ray indicated in ankle fractures?

A

Clinical exam with Ottawa rules:

X-rays are only necessary if there is pain in the malleolar zone and:
1. Inability to weight bear for 4 steps
2. Tenderness over the distal tibia
3. Bone tenderness over the distal fibula

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8
Q

What is fibromyalgia?

A

Widespread pain throughout the body with tender points at specific anatomical sites.

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9
Q

Features of fibromyalgia

A
  1. Chronic, long term, widespread pain >3months
    –> Pain in back and neck, or “all over”
    –> Worsened in cold weather, stress, activity, and associated morning stiffness
  2. Additional symptoms: fatigue, trouble sleeping, memory difficulties, mood difficulties
  3. O/E: diffuse tenderness, with 11/18 tender trigger points (used less and less in practice)

Diagnosis is clinical

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10
Q

Management of fibromyalgia

A
  1. Non-Pharm: Education, exercise, CBT
  2. Pharm 1st line : amitriptyline
    –> Pregabalin, duloxetine
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11
Q

Define polymyalgia rheumatica

A

Inflammatory condition causing pain in the hip and shoulder girdles.
Pain NOT weakness
–> in older people characterised by muscle stiffness and raised inflammatory markers.

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12
Q

Features of polymyalgia rheumatica

A
  1. usually rapid onset (e.g. < 1
  2. aching, morning stiffness in proximal limb muscles
  3. also mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats
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13
Q

Investigations for polymyalgia rheumatica

A

Raised inflammatory markers : ESR > 40 mm/hr, elevated CRP

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14
Q

What symptom is not associated with polymyalgia rheumatica?

A

weakness

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15
Q

Management of polymyalgia rheumatica

A

Prednisolone – 15mg/OD
–> Usually dramatically resolves

  • Associated Giant Cell Arteritis/Temporal Cell (Rheum Emergency : Vision loss. Must be treated with steroids!)
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16
Q

What is gout?

A
  1. Form of inflammatory arthritis
  2. Uric acid crystal deposition in joint causing episodic acute swelling/pain in joint(s).
  3. monosodium urate monohydrate in the synovium
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17
Q

Features of gout

A
  1. Painful swollen joint - can mimic septic arthritis
  2. Acute
    - Sudden onset of pain lasting 1-2wks
    - Spontaneous but may have trigger
    - Big toe, ankle joint, finger joints, elbow
    - Skin is red and shiny, swollen and hot, tender
    - VERY PAINFUL – SHEET CANNOT TOUCH TOE
    - May have associated skin findings, Tophi (stone)
    - Intermittent attacks of acute joint pain, very tender, red
  3. Typically first presentation is the 1st MTP - PODAGRA
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18
Q

Gold standard for gout

A

Joint aspiration and crystal analysis.
Negatively birefringent crystals

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19
Q

Other investigations for gout

A
  1. Serum uric acid levels- may be raised
  2. ***PEARL: Patients may have chronic raised uric acid but during an acute attack, uric concentrations may fall and uric acid during a flare is not a good diagnostic test
  3. Leucocytosis, raised ESR and CRP during acute attack
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20
Q

What are the radiological features for gout?

A
  1. joint effusion is an early sign
  2. well-defined ‘punched-out’ erosions with sclerotic margins in a juxta-articular distribution, often with overhanging edges
  3. relative preservation of joint space until late disease
  4. eccentric erosions
  5. no periarticular osteopenia (in contrast to rheumatoid arthritis)
  6. soft tissue tophi may be seen
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21
Q

Acute treatment of gout

A
  1. Resolves <2wk
  2. Exclude infection
  3. Rest, elevate, ice packs
  4. NSAIDS
  5. Colchicine 500mcg bd
  6. Prednisolone
  7. Steroid joint injection- caution need to be certain of diagnosis (cannot give if infection)
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22
Q

Prophylactic treatment of gout

A
  1. Allopurinol – given as a daily medication to prevent frequent attacks
  2. If attacks occur frequently/ needing regular doses of steroids/NSAIDs/pain medications
  3. PEARL Never give allopurinol during an acute attack. Will make the acute attack worse
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23
Q

What is pseudogout?

A

Form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium

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24
Q

Features of pseudogout

A
  1. knee, wrist and shoulders most commonly affected
  2. joint aspiration: weakly-positively birefringent rhomboid-shaped crystals
  3. Red, hot swollen, episodic attacks.
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25
Q

Investigation for pseudogout

A
  1. x-ray: chondrocalcinosis
    –> in the knee this can be seen as linear calcifications of the meniscus and articular cartilage
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26
Q

Management of pseudogout

A
  1. aspiration of joint fluid, to
    exclude septic arthritis
  2. NSAIDs or intra-articular, intra-muscular or oral steroids as for gout
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27
Q

What is rheumatoid arthritis?

A

Systemic, Inflammatory Joint disorder

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28
Q

What is osteoarthritis?

A

AKA “degenerative joint disorder” as it is a degenerative form of arthritis that gets worse with age and is associated with overuse.

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29
Q

Clinical features of osteoarthritis

A
  1. All joints can be affected: mostly knees, hip, hands, lumbar and cervical spine
  2. Worse with more activity and use
    - Joint pain and disability
    - Affects one or more weight bearing joints
  3. Decreased ROM + function, joint crepitus, deformity, effusion, muscle weakness, wasting
  4. Joint pain without or without stiffness. Pain&raquo_space;>Stiffness
  5. Symptoms increase with activity; diminish with rest
  6. Usually little or no swelling or redness of adjacent tissues
  7. Heberden’s nodes (DIP) - (osteophytes on distal interphalangeal joints)
  8. Bouchard’s nodes (PIP) - (osteophytes on proximal Interphalangeal joints)
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30
Q

Joints affected by Osteoarthritis vs Rheumatoid arthritis

A

Osteoarthritis = Large weight-bearing joints (hip, knee)
Carpometacarpal joint
DIP, PIP joints

Rheumatoid arthritis = MCP, PIP joints

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31
Q

How is osteoarthritis diagnosed?

A

1st line = x-ray:

  1. Loss of joint space/joint space narrowing (because of cartilage loss)
  2. subchondral sclerosis (cysts)
  3. osteophytes (new bony formation)
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32
Q

Clinical features of Rheumatoid arthritis

A
  1. Predominantly peripheral joints (hands,feet)
    - Ulnar deviation
    - Swan neck deformity (hyper extended PIP, flexed DIP)
    - Boutonniere (hyper extended of DIP, flexed PIP)
    - Z thumb deformity (hyperextension of interphalangeal joint)
  2. Polyarthritis (multiple joints)
  3. Symmetrical joint pain, effusions, soft tissue swelling
  4. Functional loss (especially in the hands)
  5. Progresses to joint destruction and deformity
  6. Tendons may rupture; bone alignment affected
  7. Systemic signs of inflammation (fever, malaise, anorexia)
  8. Early morning stiffness that doesn’t get better/worse with activity/time
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33
Q

What test would you carry out in rheumatoid arthritis?

A

Positive squeeze test
- discomfort on squeezing across the metacarpal or metatarsal joints

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34
Q

How do you diagnose rheumatoid arthritis?

A

Anti cyclic citrullinated peptide antibody (anti CCP) is the most SPECIFIC test for rheumatoid arthritis.
- If you have CCP+, you likely have RA

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35
Q

Investigations for rheumatoid arthritis

A
  1. Rheumatoid factor – positive in many patients, but not as specific.
  2. anti CCP = positive in RA
  3. ESR and/or CRP increased (inflammatory joint disease)
  4. ANA titre positive in some patients
  5. Xray findings: Erosions of bone
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36
Q

Treatment for rheumatoid arthritis

A
  1. Usually initiated in secondary care
  2. DMARDs (Disease modifying anti-rheumatic drugs)
    - Methotrexate or sulfasalazine are most common
    - Methotrexate: High toxicity profile. Hepatotoxic. Absolutely contraindicated in pregnancy.
  3. Short-term bridging treatment with steroids
    - often used when starting a new DMARD to improve symptoms while waiting for the DMARD to take effect (which can take 2–3 months).
    - Taken once weekly with folic acid
  4. Flares: corticosteroids (oral or IM)
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37
Q

Management of osteoarthritis

A
  1. Educate patient
  2. Weight reduction
  3. Exercises and improving muscle strength
  4. Pain control
    1st line = paracetamol + topical NSAIDs
    2nd line = oral NSAIDs, intra-articular corticosteroids
    - Aspiration of joint effusions and joint injections
  5. Minimize progression + optimize function
    - Physiotherapist, OT-, chiropodist-, social worker-, orthopaedic surgeon
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38
Q

Define osteoporosis

A
  1. Thinning/weakening of the bones putting patients at risk for fractures.
  2. Mild thinning is called Osteopenia. Severe thinning is called osteoporosis.

Symptoms:
• ASYMPTOMATIC UNTIL A FRACTURE APPEARS. Osteoporosis

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39
Q

Risk Factors for osteoporosis

A
  • post-menopausal women
  • increasing age
  • smoking
  • steroid use
  • low BMI
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40
Q

Symptoms of osteoporosis

A

ASYMPTOMATIC UNTIL A FRACTURE APPEARS.

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41
Q

Diagnosis of osteoporosis

A

Diagnostic: DEXA scan
- Look at the T score on a DEXA scan.

T score = 0, normal bone density. Your bones are as strong as people your sex/age
- T score >0, good bone density. Your bones are stronger than people your age/sex
- T score between -2.5 and 0, osteopenia
- T score

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42
Q

Treatment of osteoporosis

A

1st line = Bisphosphonates - alendronate
- Bisphosphonates – side effects rare but serious, osteonecrosis of the jaw
- Must be given a ”drug holiday” (time off of the medication) after taking bisphosphonates for 3-5 years

  1. Calcium + vitamin D must be given to all patients
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43
Q

Define Pagets disease

A

Disease of increased but uncontrolled bone turnover.
- It is thought to be primarily a disorder of osteoclasts, with excessive osteoclastic resorption followed by increased osteoblastic activity.

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44
Q

clinical features of paget’s disease

A

Symptoms: only 5% are symptomatic
1. older male with bone pain and an isolated raised ALP

  1. bone pain (e.g. pelvis, lumbar spine, femur)
  2. classical, untreated features: bowing of tibia, bossing of skull
  3. raised alkaline phosphatase (ALP) - calcium* and phosphate are typically normal
  4. other markers of bone turnover include: procollagen type I N-terminal propeptide (PINP), serum C-telopeptide (CTx), urinary N-telopeptide (NTx), and urinary hydroxyproline
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45
Q

Investigation for Paget’s disease

A
  1. Bloods:
    -raised alkaline phosphatase (ALP)
    - calcium* and phosphate are typically normal
  2. other markers of bone turnover include:
    - procollagen type I N-terminal propeptide (PINP)
    - serum C-telopeptide (CTx)
    - urinary N-telopeptide (NTx)
    - urinary hydroxyproline
  3. skull x-ray
    - thickened vault, osteoporosis circumscripta
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46
Q

Treatment for Paget’s disease

A

Indication for Tx include bone pain, skull or long bone deformity, fracture:
- Bisphosphonate
- Calcitonin

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47
Q

Renal bone disease: basic problems in CKD

A
  1. Low vitamin D (1-alpha hydroxylation normally occurs in the kidneys)
  2. high phosphate
  3. low calcium: due to lack of vitamin D, high phosphate
  4. secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D
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48
Q

Clinical manifestations of renal bone disease

A
  1. Osteitis fibrosa cystica
    aka hyperparathyroid bone disease
  2. Adynamic
    - reduction in cellular activity (both osteoblasts and osteoclasts) in bone
    - may be due to over treatment with vitamin D
  3. Osteomalacia
    - due to low vitamin D
  4. Osteosclerosis
  5. Osteoporosis
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49
Q

Management of renal bone disease

A
  1. 1st line = reduced dietary intake of phosphate
  2. phosphate binders
  3. vitamin D: alfacalcidol, calcitriol
  4. parathyroidectomy may be needed in some cases
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50
Q

Complication of vitamin D deficiency

A

Osteomalacia – softening of the bones secondary to low vitamin D levels
- In turn leads to decreased bone mineral content

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51
Q

Symptoms of vitamin D deficiency

A
  • Bone pain
  • Bone/muscle tenderness
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52
Q

Investigations for vitamin D deficiency

A

Diagnostics:
1. Bloods – low vitamin D, calcium, phosphate
- Raised ALP

  1. X-Ray – translucent bands
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53
Q

Treatment for vitamin D deficiency

A
  1. Vitamin D supplementation
    - A loading dose is needed initially
  2. Calcium supplementation
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54
Q

What is metabolic bone disease?

A

Disorders of bone strength usually caused by abnormalities of minerals (such as calcium or phosphorus), vitamin D, bone mass or bone structure

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55
Q

What is Reiter’s syndrome also known as? 2B

A

reactive arthritis

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56
Q

Define reactive arthritis 2B

A

an arthritis that develops following an infection where the organism cannot be recovered from the joint.

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57
Q

Classic presentation of reactive arthritis 2B

A

‘Can’t see, pee or climb a tree’

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58
Q

Features of reactive arthritis 2B

A
  1. Time course
    - typically develops within 4 weeks of initial infection - symptoms generally last around 4-6 months
  2. arthritis is typically an asymmetrical oligoarthritis of lower limbs
  3. dactylitis
  4. symptoms of urethritis
  5. eye
    - conjunctivitis
    - anterior uveitis
  6. skin
    - circinate balanitis (painless vesicles on the coronal margin of the prepuce)
    - keratoderma blenorrhagica (waxy yellow/brown papules on palms and soles)
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59
Q

Management of reactive arthritis 2B

A
  1. symptomatic: analgesia, NSAIDS, intra-articular steroids
  2. sulfasalazine and methotrexate are sometimes used for persistent disease
  3. symptoms rarely last more than 12 months
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60
Q

What is Polyarteritis nodosa (PAN)? 2B

A

vasculitis affecting medium-sized arteries with necrotizing inflammation leading to aneurysm formation.

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61
Q

Features of Polyarteritis nodosa (PAN) 2B

A
  1. fever, malaise, arthralgia
  2. weight loss
  3. hypertension
  4. mononeuritis multiplex, sensorimotor polyneuropathy
  5. testicular pain
  6. haematuria, renal failure
  7. perinuclear-antineutrophil cytoplasmic antibodies (ANCA)
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62
Q

What is polymyositis? 2B

A
  1. inflammatory disorder causing symmetrical, proximal muscle weakness
  2. thought to be a T-cell mediated cytotoxic process directed against muscle fibres
  3. associated with malignancy
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63
Q

Features of polymyositis (2B)

A
  1. proximal muscle weakness
  2. +/- tenderness
  3. Raynaud’s
  4. respiratory muscle weakness
  5. interstitial lung disease: e.g. fibrosing alveolitis or organising pneumonia
  6. dysphagia, dysphonia
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64
Q

Investigations for polymyositis (2B)

A
  1. elevated creatine kinase
  2. other muscle enzymes (lactate dehydrogenase (LDH), aldolase, AST and ALT)
  3. EMG
  4. muscle biopsy
  5. anti-synthetase antibodies
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65
Q

What is scleroderma? (2B)

A

uncommon condition that results in hard, thickened areas of skin
- sometimes problems with internal organs and blood vessels.

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66
Q

Features of scleroderma (2B)

A

tightening and fibrosis of skin
may be manifest as plaques (morphoea) or linea

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67
Q

What is Sjogren’s syndrome?
(2B)

A

autoimmune disorder affecting exocrine glands resulting in dry mucosal surfaces.

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68
Q

Features of Sjogren’s syndrome
(2B)

A
  1. dry eyes: keratoconjunctivitis sicca
  2. dry mouth
  3. vaginal dryness
  4. arthralgia
  5. Raynaud’s, myalgia
  6. sensory polyneuropathy
  7. recurrent episodes of parotitis
  8. renal tubular acidosis
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69
Q

Investigation for Sjogren’s syndrome
(2B)

A
  1. rheumatoid factor (RF) positive in nearly 50% of patients
  2. ANA positive in 70%
  3. anti-Ro (SSA) antibodies in 70% of patients with PSS
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70
Q

Management of Sjogren’s syndrome
(2B)

A
  1. artificial saliva and tears
  2. pilocarpine may stimulate saliva production
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71
Q

What is Juvenile idiopathic arthritis? (2B)

A

arthritis occurring in someone who is less than 16 years old that lasts for more than 6 weeks
- Systemic onset JIA is a type of JIA

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72
Q

Features of systemic onset JIA
(2B)

A
  • pyrexia
  • salmon-pink rash
  • lymphadenopathy
  • arthritis
  • uveitis
  • anorexia and weight loss
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73
Q

Investigations for Juvenile idiopathic arthritis (2B)

A
  1. ANA may be positive,
  2. rheumatoid factor is usually negative
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74
Q

What is Systemic lupus erythematosus (SLE)? (2B)

A

A chronic multi-system autoimmune disorder
- most commonly affects women during their reproductive years
- can affect any body system

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75
Q

Features of SLE (2B)

A

General
1. fatigue
2. fever
3. mouth ulcers
4. lymphadenopathy

Skin:
1. malar (butterfly) rash: spares nasolabial folds
2. discoid rash: scaly, erythematous, well demarcated rash in sun-exposed areas.
3. photosensitivity
4. Raynaud’s phenomenon
5. non-scarring alopecia

MSK:
1. arthralgia
2. non-erosive arthritis

Cardiovascular
1. pericarditis: the most common cardiac manifestation
2. myocarditis

Respiratory
1. pleurisy
2. fibrosing alveolitis

Renal
1. proteinuria
2. glomerulonephritis

Neuropsychiatric
1. anxiety and depression
2. psychosis
3. seizures

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76
Q

Investigations for SLE (2B)

A

Antibodies:
1. ANA positive
—>This means if you someone has a negative ANA, they do not likely have lupus. If someone has a positive ANA, use clinical judgement. IS NOT DIAGNOSED FOR SLE

  1. dsDNA+
    - Less sensitive but more specific for SLE than ANA
    - Rarely found in healthy patients
    - Generally diagnostic for SLE
  2. Complements (C3 and C4)
    - used to track disease activity. Low complements (low C3 and C4) suggest higher disease activity
  3. Anti-Sm (Anti smith) – very specific for SLE
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77
Q

Management of SLE (2B)

A

1st line = anti malarias: hydroxychloroquine

  • NSAIDs
  • Steroids
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78
Q

What is Slipped Upper Femoral Epiphysis?

A

Displacement of the femoral head epiphysis postero-inferiorly
- Displacement of the upper femoral epiphysis. Slippage occurs through the growth plate (epiphysis between the head and neck of the bone).
- The femoral epiphysis remains in the acetabulum (hip socket), while the metaphysis (end of the femur) move in an anterior direction.

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79
Q

Risk Factors for Slipped Upper Femoral Epiphysis

A
  1. typically age group is 10-17 years
  2. More common in obese children and boys
  3. Males > Females
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80
Q

Features of Slipped Upper Femoral Epiphysis

A
  1. hip, groin, medial thigh or knee pain
  2. Limp with leg externally rotated,
    - loss of internal rotation of the leg in flexion
    - restricted range of motion (ROM) on exam
81
Q

Investigations for Slipped Upper Femoral Epiphysis

A
  1. AP and lateral (typically frog-leg) views are diagnostic
  2. AP xrays of bilateral hips and frog-leg lateral
82
Q

Management of Slipped Upper Femoral Epiphysis

A
  • surgical fixation (usually with 1-2 screws in the centre of the epiphysis)
    –> sometimes the bilateral side is done prophylactically
83
Q

Femoral neck fracture

A

Classically: Elderly woman with osteoporosis, minimal injury.

84
Q

Symptoms of Femoral neck fracture

A
  • Pain in groin and unable to bear weight
  • leg may be shortened, externally rotated, and abducted.
85
Q

Hip Dislocation

A
  • 90% are posterior; Example: Dashboard injury
  • Compared to femoral neck fracture, MAJOR injury/high impact/trauma, any age
86
Q

Symptoms of Hip Dislocation

A
  • Pain, inability to bear weight
  • deformity (hip and leg in slight flexion, adduction, and internal rotation)
  • leg shorter
87
Q

Investigation for Hip Dislocation

A

Diagnostic: X-Ray

88
Q

What is septic arthritis?

A

Spread of bacteraemia, periarticular osteomyelitis, infection due to diagnostic or therapeutic procedure or from infection elsewhere

  • Involves single joint
  • Commonly knee, hip, shoulder, ankle, wrist
89
Q

Features of septic arthritis

A
  1. Joint is hot, acute swelling, tender, restricted ROM
  2. Effusion, tenderness to palpation, increased pain, minimal ROM
  3. fever
90
Q

Investigation for septic arthritis

A

Diagnostics – Aspirate native joint for culture and gram stain before starting antibiotics

–> *Pearl: Never aspirate a prosthetic joint. Refer to ortho specialist!

91
Q

Treatment for septic arthritis

A

1.. IV antibiotics
–> Flucloxacillin or clindamycin

  1. needle aspiration should be used to decompress the joint
92
Q

What is acute osteomyelitis?

A

inflammatory condition of bone caused by an infecting organism
- It usually involves a single bone

93
Q

Most common cause of osteomyelitis

A

Staphylococcus aureus.

94
Q

Symptoms of osteomyelitis

A
  • Non-specific pain
  • fever
  • malaise/fatigue
  • inflammation
  • swelling
95
Q

Investigations for osteomyelitis

A
  • WBC (inc), CRP&ESR (inc), - xray – osteopenia & bone destruction
  • MRI – imaging of choice
96
Q

Treatment of osteomyelitis

A

High dose antibiotics
- Flucloxacillin (6 weeks) or Clindamycin

97
Q

Complication of chronic osteomyelitis

A

sequestra- dead bone after few weeks

98
Q

Osteosarcoma

A

most common primary malignant bone tumour
- seen mainly in children and adolescents

99
Q

X-ray finding of osteosarcoma

A
  • Codman triangle (from periosteal elevation) and ‘sunburst’ pattern
100
Q

Specific test for Rheumatoid arthritis

A

RF - positive
CCP - Most specific

ANA - low positive
ESR/CRP - often elevated

101
Q

Specific test for SLE

A

dsDNA & anti Sm - positive, very specific

RF - often positive
CCP - negative

ANA - low positive
ESR/CRP - often elevated
C3/C4 - often low

102
Q

Specific test for Sjogren’s

A

SSA/SSB - positive, very specific

RF - often positive
CCP - negative

ESR/CRP - often elevated

103
Q

Specific test for Myositis

A

CK - increased
Anti Jo-1 - positive

ANA - often positive
ESR/CRP - often elevated

104
Q

Specific test for Scleroderma (limited)

A

ANA - positive
Anti-centromere - positive

Anti-Scl 70 - negative

ESR/CRP - often elevated

105
Q

Specific test for Scleroderma (diffuse)

A

ANA - positive
Anti-centromere - negative

Anti-Scl 70 - positive

ESR/CRP - often elevated

106
Q

Specific test results in normal patients

A

RF - possibly positive
CCP - negative

dsDNA & anti Sm - negative

ANA - possibly positive
ESR/CRP - typically normal

107
Q

What is adhesive capsulitis commonly known as

A

frozen shoulder

108
Q

epidemiology of adhesive capsulitis

A

middle-aged females

109
Q

medical condition associated with adhesive capsulitis

A

diabetes mellitus

110
Q

onset of adhesive capsulitis

A

develops over days

111
Q

examination sign of adhesive capsulitis

A

external rotation affected more than internal rotation or abduction

112
Q

how long do episodes of adhesive capsulitis last

A

6 months to 2 years

113
Q

how is diagnosis of adhesive capsulitis made

A

clinical though imaging may be use if sx persist

114
Q

management of adhesive capsulitis

A

NSAIDs
physio
oral/intra-articular corticosteroids

115
Q

Name the rotator cuff muscles

A

SIts

Supraspinatus
Infraspinatus
Teres minor
Subscapularis

116
Q

Which rotator cuff muscle is most commonly injured

A

supraspinatus

117
Q

Sx of rotator cuff injury

A

shoulder pain worse on abduction

118
Q

Clinical sign of rotator cuff injury

A

positive painful arc

60-120 degrees - subacromial impingement
<60 degrees - rotator cuff tear

119
Q

What is a subluxation

A

partial dislocation

120
Q

Which investigation is required in subluxation?

A

xray to confirm

121
Q

Treatment of subluxation

A

analgesia

reduction and stabilisation

122
Q

What should be checked before and after reducing a dislocation?

A

neurovascular status

123
Q

Examination findings of rotator cuff injuries

A

Supraspinatus - empty can test & pain on resisted abduction

Infraspinatus (pain on resisted lateral rotation)

Subscapularis (pain on resisted medial rotation).

124
Q

Are shoulder dislocations usually anterior or posterior

A

98% anterior - classically after FOOSH

125
Q

Management of shoulder sprain

A
  • sling
  • analgesia
  • RICE
126
Q

Lateral epicondylitis cause

A

tennis elbow - overuse of epicondyle in activities like playing tennis/house painting

127
Q

sign and sx of Lateral epicondylitis

A
  • localised pain and tenderness
  • pain worse on resisted wrist extension with elbow extended
128
Q

tx of epicondylitis

A

RICE
NSAIDs
steroid injections
physio

129
Q

Medial Epicondylitis

A

golfers elbow - overuse of flexor/pronators

130
Q

sx of Medial Epicondylitis

A

pain from the elbow to the wrist on the inside (medial side) of the elbow

point tenderness

131
Q

Which type of fall typically leads of a Colles fracture

A

FOOSH

132
Q

What is a colles fracture

A

Distal radius fracture with dorsal displacement of fragments

133
Q

characteristic sign of colles fracture

A

dinner fork deformity

134
Q

tx of colles fracture

A

straighten deformity, immbolise in cast for ~6 weeks

135
Q

Colles fracture mnemonic!

A

Dorsally Displaced Distal radius → Dinner fork Deformity

136
Q

Who is particularly at risk of colles fracture?

A

elderly and osteoporotic

137
Q

epidemiology of pulled elbow

A

children <5yo commonly after swinging them by hands

138
Q

s/s of pulled elbow

A

-not using arm
-elbow in extension & forearm in pronation
-pain with supination of forearm

139
Q

tx of pulled elbow

A

reduction and mobilisation

140
Q

Smiths vs Colles

A

Smiths - ventral displacement (reverse colles)
Colles - dorsal displacement

141
Q

Sx of scaphoid fracture

A

pain at base of thumb / radial aspect of wrist

loss of grip/pinch strength

142
Q

What is the danger of missing a scaphoid fracture?

A

avascular necrosis caused by interrupted blood supply

143
Q

Pain in anatomical snuffbox and normal xray -> next step?

A

IMMOBILISE IF ANY DOUBT

144
Q

Definitive investigation to confirm or exclude diagnosis of scaphoid fracture

A

MRI (check)

145
Q

What is carpal tunnel syndrome

A

compression of median nerve in carpal tunnel

146
Q

sx of carpal tunnel syndrome

A
  • pain and pins and needles in thumb, index, middle finger
  • relieved by shaking hand / hanging hand off bed
  • worse at night
147
Q

clinical examination findings of carpal tunnel syndrome

A
  • weakness of thumb abduction
  • thenar eminence wasting
  • positive Tinels and Phalens
148
Q

Diagnostic investigation of carpal tunnel syndrome

A

Nerve conduction studies

149
Q

Tx of carpal tunnel syndrome

A
  • corticosteroid injection
  • wrist splints at night
  • surgical decompression
150
Q

What is de Quervain’s tenosynovitis?

A

the sheath
of the tendons on the thumb side of the
wrist becomes inflamed or swollen,
restricting the tendons’ movement

151
Q

s/s of de Quervain’s tenosynovitis

A

pain with turning wrist

+ finkelsteins

152
Q

tx of de Quervain’s tenosynovitis

A
  • analgesia
  • steroid injection
  • immobilisation with thumb splint
  • surgical treatment if needed
153
Q

Boxer’s fracture

A

Fracture of 5th Metatarsal

usually after punching something

154
Q

Back pain red flags!

A
  • suspected spinal infection
  • saddle anaesthesia
  • loss of anal sphincter tone
  • bowel/bladder incontinence or urinary retentions
  • motor/sensory deficit
155
Q

Back pain investigation

A

none needed if no red flags

MRI

156
Q

What should be avoided if possible in the conservative management of back pain

A

avoid bed rest

157
Q

Management of back pain

A

NSAIDs - first line

PPI co-prescribed if over 45yo

Most cases are self limiting and resolve

158
Q

How to differentiate mechanical vs inflammatory back pain

A

MECHANICAL
- worse on movement
- cause is injury
- fluctuating sx

INFLAMMATORY
- morning stiffness >1hr
- better with movement
- insidious onset
- progressive
- younger pt

159
Q

Kyphosis

A

> 45 degree curvature of the spine that causes the top of the back to appear more rounded than normal

160
Q

Scoliosis

A

twisting and curving of the spine

161
Q

Hernated nucleus pulposus

A

pain in leg due to compression of spinal nerve

162
Q

sx of Hernated nucleus pulposus

A
  • Unilateral
  • leg pain worse than low back pain
  • pain worse when sitting
  • pain radiates to foot or toes
  • numbness and paraesthesia
163
Q

diagnostic investigation of Hernated nucleus pulposus

A

MRI

164
Q

Which nerve roots are affected if pain radiates from back to hip and/or anterior thigh

A

L1-L3

165
Q

Which nerve roots are affected if pain radiates from back to below the knee

A

L4-S1

166
Q

spinal stenosis

A

Narrowing of spinal canal

167
Q

complications of spinal stenosis

A

root compression and ischaemia

168
Q

sx of spinal stenosis

A
  • insidious back pain
  • paraesthesia with movement, relievd by lying supine
  • bilateral leg pain, relieved by leaning forward
  • numbness in lower extremity
169
Q

Which nerves are compressed in cauda equina

A

L5-S1

170
Q

Sx of CES

A
  • Saddle (perianal/perineal) anaesthesia
  • bladder dysfunction
  • faecal incontinence
  • neurological deficit
171
Q

Management of CES

A

MRI AND IMMEDIATE DECOMPRESSION

172
Q

Ankylosing Spondylitis

A

Chronic inflammatory joint disease of spine
Affecting spine and sacroilliac joints

173
Q

epidemiology of ankylosing Spondylitis

A

caucasian males - mean onset 26yo

174
Q

classic vignette of ankylosing spondylitis

A

insidious onset, morning stiffness, young man, with a
family history and pain relieved by exercise

175
Q

clinical examination findings of ankylosing Spondylitis

A
  • reduced lateral flexion
  • reduced forward flexion
  • reduced chest expansion
176
Q

which genetic component is associated with Ankylosing Spondylitis

A

HLA-B27

177
Q

Classic xray finding of Ankylosing Spondylitis

A

bamboo spine

178
Q

Osgood schlatter epidemiology

A

teenagers 10-14yo

179
Q

What is osgood schlatter a type of

A

osetochondritis - joint condition in which bone underneath the cartilage of a joint dies due to lack of blood flow

180
Q

cause of Osgood schlatter

A

excessive muscle pull on growing bone (growing pains)

181
Q

epidemiology of Osgood schlatter

A

active young people,
commonly footballers

182
Q

s/s Osgood schlatter

A

Pain and swelling directly over the tibial tubercle

Point tenderness

Pain is aggravated by loaded knee extension activity

183
Q

tx of Osgood schlatter

A

physio, modify trigger excercises, NSAIDs

184
Q

Bursitis

A

inflammation of a bursa

185
Q

s/s bursitis

A
  • localized swelling and erythema overlying the patella
  • difficulty kneeling/walking
186
Q

investigations for bursitis

A
  • aspiration
  • xray
  • bloods
187
Q

What is bursal aspiration used to rule out?

A

septic bursitis or crystal-induced bursitis

188
Q

Tx of bursitis

A

if sure non-septic:

  • RICE
  • Analgesia (paracetemol and NSAIDs)
189
Q

Investigation for meniscal injury

A

MRI

190
Q

special tests - meniscal injury

A

McMurray and Apley

191
Q

Cause of meniscal injury

A

twisting injury while weight bearing

192
Q

sx of meniscal injury

A
  • catching/locking of knee joint
  • pain in knee joint
  • swelling
193
Q

What causes the knee pain in meniscal injury

A

if a meniscus is torn the torn fragment can
be trapped in the joint and cause
transient locking/catching, which often
causes severe pain knee

194
Q

Chondromalacia patella

A

loss of cartilage underneath the patella

195
Q

What aggravates knee pain in Chondromalacia patella

A

deep bending

196
Q

clinical signs of Chondromalacia patella

A

hypermobile patella with significant crepitus

197
Q

What is seen on an xray in Chondromalacia patella

A

skyline view show ”bone on bone” patella and femur

198
Q

management of chondromalacia patella

A
  • paracetemol and NSAIDs
  • physio
  • surgery not usually needed

FCM Matrix (17 decks)

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