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((archived year 1 med)) > MSK - CLINICAL CONDITIONS > Flashcards

MSK - CLINICAL CONDITIONS Flashcards

1
Q

what are causes / risk factors for RA?

A
  • linked with HLA-DR1 gene
  • family history
  • smoking
  • female
  • 30-60 yrs old
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2
Q

what are the articular features of RA?

A
  • polyarthritis: swollen, painful joints (symmetrical and hand involvement)
  • early morning stiffness (lasting more than 1hr), eases with movement
  • MCP, and PIP joints (DIP joints often NOT involved), MTP also commonly involved
  • ulnar deviation, boutonniere and swan-neck deformities of fingers
  • subluxation of hand joints
  • if RA affects C1-C2 joint then can threaten spinal cord (patient will have neck pain)
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3
Q

what are the extra-articular features of RA?

A
  • rheumatoid nodules (fingers, elbows, Achilles tendon, lung nodules rare)
  • olecranon and subacromial bursitis/tenosynovitis common
  • carpal tunnel syndrome (synovitis can entrap median nerve)
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4
Q

what are the systemic features of RA?

A
  • can be systemically unwell (fever, weight loss, fatigue)
  • anaemia of chronic disease
  • Felty syndrome (patient has triad of RA, splenomegaly, and leukopenia)
  • rheumatoid lung disease (pulmonary fibrosis)
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5
Q

what drug makes rheumatoid nodules worse?

A
  • methotrexate
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6
Q

what investigations should you do for RA?

A

AUTOANTIBODIES:

  • Rheumatoid factor: found in 70-90% of patients
  • Anti-CCP: highly specific (98%)

ESR + CRP: raised

FBC: shows anaemia of chronic disease

Bilateral plain X-RAY: soft tissue swelling, periarticular osteoporosis, erosions, joint space narrowing

(HLA-DR1 associated)

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7
Q

what is the line of management for RA? (start with first-line)

A

SHORT-TERM:

  • NSAIDs (use PPI if long-term use: omeprazole)
  • Corticosteroids (prednisolone)

LONGER TERM:

  • DMARDs (methotrexate, leflunomide, hydroxychloroquine, sulfasalazine)
  • Anti-TNF biologics (infliximab, entanercept, adalimumab)
  • NOTE: when anti-TNF biologics do not work then use other biologic RITUXIMAB (monoclonal antibody against B cells)
  • (use multidisciplinary team: rheumatologist, physio, OT)
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8
Q

what measuring score is used to measure disease activity in RA?

A
  • DAS-28 score

- aim to reduce score to <3

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9
Q

which DMARD can pregnant women not have?

A
  • methotrexate
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10
Q

what type of joints does OA affect?

A
  • synovial joints
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11
Q

what are the risk factors / causes of OA?

A
  • older age
  • female
  • occupation
  • obesity
  • muscle weakness
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12
Q

what are the clinical features of OA?

A
  • aching/burning pain, swelling, deformity, stiffness (DIP involvement)
  • gradual onset
  • worse with activity and after
  • night pain
  • usually asymmetrical
  • Heberden nodes and Bouchard nodes on hands
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13
Q

what are the radiographical features seen in OA?

A
  • joint space narrowing
  • sclerosis
  • subchondral cysts and osteophytes
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14
Q

what investigations should you do for OA?

A
  • EXAMINATION: tenderness, movement painful, crepitus, loss of range of movement
  • X:RAY: joint space narrowing, sclerosis, subchondral cysts and osteophytes
  • (only role of blood tests is to rule out other causes)
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15
Q

what is the line of management for OA?

A
  • (no cure for OA, treatment is to reduce pain and maintain function)

CONSERVATIVE:

  • lifestyle changes (exercise, lose weight)
  • physio
  • NSAIDs early, then paracetamol and codeine, then corticosteroid injections if needed

SURGICAL (last resort):

  • Arthroplasty: commonly knee or hip, effective and lasts for 10yrs
  • Arthrodesis (fusion): commonly ankle and foot, helps pain but movement is lost
  • Osteotomy (realignment): correction of deformity)
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16
Q

what are the 4 seronegative arthritis’?

A
  • ankylosing spondylitis
  • psoriatic arthritis
  • reactive arthritis
  • enteropathic arthritis
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17
Q

what does ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and enteropathic arthritis have in common?

A
  • all positive for HLA-B27
  • all negative for rheumatoid factor
  • all have extra-skeletal features
  • all typically involve inflammatory back pain with morning stiffness
  • all typically involve axial arthritis (sacroiliitis and spondylitis)
  • all typically involve enthesitis and dactylitis
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18
Q

what are the causes / risk factors for ankylosing spondylitis?

A
  • male
  • peak onset is mid 20’s
  • association with osteoporosis
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19
Q

what are the SKELETAL features of ankylosing spondylitis?

A
  • pain and stiffness in low back, buttocks, and/or hips
  • reduced mobility of lumbar spine (Schober’s test)
  • early morning stiffness or after sitting still for a while, improves with movement/exercise
  • sacroiliac joints tender
  • involvement of thoracic spine and enthesitis of costovertebral joints can cause chest pain and breathlessness
  • as disease progresses: posture deteriorates, normal lumbar lordosis lost, thoracic and cervical spine become more kyphotic (? posture)
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20
Q

what are the EXTRA-SKELETAL features of ankylosing spondylitis?

A
  • Acute anterior uveitis (eye becomes red and painful, blurred vision)
  • Aortitis
  • Atypical lung fibrosis
  • Amyloidosis (build up of amyloid proteins, affects organ and tissue function)
  • (can also get Achilles tendonitis)
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21
Q

what investigations should be done for ankylosing spondylitis?

A
  • X-RAY + MRI: to see the inflammation (sacroiliitis), syndesmophytes (bamboo spine), and small erosions at corners of vertebral bodies (squaring)
  • EXAMINATION: Schober’s test (mark at L5, mark 5cm below, mark 10cm above, gap should increase by at least 5cm when lumbar spine flexed)
  • ESR + CRP: raised
  • HLA-B27 associated
  • FBC: shows anaemia of chronic disease
  • rheumatoid factor: negative
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22
Q

what is the line of management for ankylosing spondylitis?

A
  • physio
  • NSAIDs (use PPI if long-term: omeprazole)
  • corticosteroid injections if needed
  • Anti-TNF biologics (infliximab, entanercept, adalimumab)
  • Anti-IL17A biologics (secukinumab)
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23
Q

what are the causes / risk factors for psoriatic arthritis?

A
  • psoriasis occurs in 1-3% of population, and roughly 10% of those are affected by psoriatic arthritis
  • more common in patients with psoriatic nail involvement
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24
Q

what are the clinical features of psoriatic arthritis?

A
  • psoriasis usually presents first then arthritis follows
  • can present as asymmetrical oligoarthritis, affecting <3 joints
  • can present as symmetrical arthritis of hands and feet (similar to RA)
  • can present as spondylitis (stiffness of neck and spine)
  • can present as DIP presentation of fingers and toes
    (- can present as psoriatic arthritis mutilans (very rare))
  • psoriatic nail dystrophy (oncholysis, pitting, hyperkeratosis)
  • dactylitis
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25
Q

what investigations should you do for psoriatic arthritis?

A
  • ESR + CRP: raised
  • HLA-B27 associated
  • FBC: shows anaemia of chronic disease
  • rheumatoid factor negative
  • X-RAY: erosions, pencil-in-cup deformities
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26
Q

what is the line of management for psoriatic arthritis?

A
  • NSAIDs (use PPI if long-term: omeprazole)
  • corticosteroid injections if needed
  • DMARDs (methotrexate, leflunomide, sulfasalazine, hydroxychloroquine)
  • Anti-TNF biologics (infliximab, entanercept, adalimumab)
  • Anti-IL17A biologics (secukinumab)
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27
Q

what are the causes / risk factors for reactive arthritis? (also most common bacteria)

A
  • patient has had a recent infection (few days/weeks prior to joint pain)
  • most common bacteria for reactive arthritis is Chlamydia trachomatis (causes urethritis)
  • enteric bacteria are also common (salmonella, shigella, yersinia, campylobacter, clostridium difficile), these cause gastroenteritis and colitis
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28
Q

what are the clinical features of reactive arthritis?

A
  • asymmetrical arthritis of large-weight bearing joints (knees/sacroiliac joints), can also affect fingers and toes
  • dactylitis
  • conjunctivitis (sterile)
  • urethritis (sterile), often causes dysuria
  • enthesitis
  • Reiter syndrome: triad of arthritis, conjunctivitis, and uveitis
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29
Q

what investigations should you do for reactive arthritis?

A
  • always joint aspirate: gram stain + culture to rule out septic arthritis
  • cultures on urine (and swabs from urethra, cervix, throat): Chlamydia trachomatis
  • cultures on stool samples: Enteric bacteria
  • ESR + CRP: raised
  • HLA-B27 associated
  • FBC: shows anaemia of chronic disease
  • rheumatoid factor negative
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30
Q

what is the line of management for reactive arthritis?

A
  • treat any underlying infection with antibiotics
  • NSAIDs (use PPI if long-term: omeprazole)
  • corticosteroid injections if needed
  • Anti-TNF biologics (infliximab, entanercept, adalimumab)
  • Anti-IL17A biologics (secukinumab)
  • (DMARDs rarely used)
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31
Q

what is reactive arthritis?

A
  • reactive arthritis is an aseptic arthritis that occurs after an infection
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32
Q

what is enteropathic arthritis?

A
  • enteropathic arthritis is an arthritis occurring with inflammatory bowel disease (IBD)
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33
Q

what are the causes / risk factors for enteropathic arthritis?

A
  • occurs in 10-20% of patients with Crohn disease or ulcerative colitis
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34
Q

what are the clinical features of enteropathic arthritis?

A
  • commonly peripheral arthritis
  • worsens with flaring of the bowel disease, and improves if the affected bowel is surgically removed
  • spondylitis and sacroiliitis also common (not related to activity of the IBD)
  • enthesitis
  • dactylitis
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35
Q

what investigations should you do for enteropathic arthritis?

A
  • X-RAY + MRI: shows inflammation

- if IBD suspected then refer to gastroenterologist

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36
Q

what is the line of management for enteropathic arthritis?

A
  • treatment of the IBD is priority and will help with the peripheral arthritis
  • DMARDs (methotrexate, leflunomide, sulfasalaine, hydroxychloroquine)
  • corticosteroid injections if needed
  • Anti-TNF biologics (infliximab, entanercept, adalimumab)
    (helps with IBD too)

(NOTE: avoid NSAIDs as will make GI symptoms worse)

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37
Q

what is gout?

A
  • gout is the consequence of high lvls of hyperuricemia and uric acid crystal formation
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38
Q

what are some of the risk factors for gout?

A
  • male
  • alcohol
  • high protein diet
  • obesity
  • diuretic use
  • psoriasis
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39
Q

what are the clinical features of gout?

A
  • severe pain
  • usually affects first MTP joint (great toe), also common cause of olecranon bursitis
  • red and shiny skin, joint inflammation
  • uric acid renal stones
  • renal disease
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40
Q

what investigations should be done for gout and what are the findings?

A

SYNOVIAL FLUID ANALYSIS: shows negatively birefringent needle-shaped monosodium urate crystals
(also perform gram stain to rule out infection)

URIC ACID lvls: raised

ESR + CRP + WCC: raised

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41
Q

what is the line of management for gout?

A

(usually self-limiting)

ACUTE:

  • NSAIDs
  • colchicine

CHRONIC:
- allopurinol, febuxostat (lowers lvls of uric acid)

  • corticosteroid injections
  • LIFESTYLE: lose weight, reduce alcohol, reduce high protein foods
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42
Q

what is pseudogout?

A
  • pseudogout is also known as calcium pyrophosphate dihyrdate (CPPD) disease
  • it is an arthropathy associated with the deposition of CPPD crystals
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43
Q

what are some risk factors / causes for pseudogout?

A
  • less common than gout, but more common in elderly
  • rare in patients <50 yrs old
  • associated with OA and some metabolic diseases (hypothyroidism, hyperparathyroidism, haemocchromatosis)
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44
Q

what are the clinical features of pseudogout?

A
  • acute synovitis (pseudogout): most common cause of acute monoarthritis in elderly (wrists and knees most commonly affected)
  • chronic pyrophosphate arthropathy: similar to OA with a gradual onset (wrists and knees most commonly affected)
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45
Q

what investigations should be done for pseudogout and what are your findings?

A
  • SYNOVIAL FLUID ANALYSIS: weakly positive birefringent rhomboid-shaped crystals
    (also perform gram stain to rule out infection)
  • radiography: similar changes as seen in OA, chondrocalcinosis (soft tissue calcium deposition)
  • calcium lvls: raised
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46
Q

what is the line of management for pseudogout?

A
  • (usually self-limiting)
  • ANALGESIA: paracetamol, aspirin, codeine, hydrocodone
  • NSAIDs
  • colchicine
  • corticosteroid injections
  • LIFESTYLE: lose weight, physio
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47
Q

how can infection of the bone be caused? (2 ways)

A
  • infection of the bone can be caused by direct inoculation (exogenous) or blood-borne bacteria (haematogenous)
  • in children, osteomyelitis usually caused by haematogenous spread of bacteria
  • in adults, the source of infection is likely to be exogenous, most commonly due to infection after surgery or after a penetrating injury (eg. open fracture)
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48
Q

what is the most common infecting organism in osteomyelitis?

A
  • Stapholococcus aureus

- (bone and joint infection are common among IV drug users)

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49
Q

what are some of the common pathogens in osteomyelitis? (newborn, children, adults, immunocompromised)

A
  • NEWBORN: Staph. A, Strept. A and Strept B, Enterobacter
  • CHILDREN: Staph. A, Haemophilus influenzae, Streptococcus, Enterobacter
  • ADULTS: Staph. A, Streptococcus, Enterobacter
  • IMMUNOCOMPROMISED: pseudomonas, mycobacterium tuberculosis, fungal infection
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50
Q

what is the line of management for osteomyelitis?

A

CONSERVATIVE:

  • analgesia, splintage, antibiotics
  • (flucloxacillin is common first-line antibiotic as acts against Staph. A)
  • (antibiotics usually given IV for 6 weeks)
  • (antibiotic-resistant strains such as MRSA are more common now and if suspected then vancomycin or teicoplanin should be used instead)

SURGICAL:

  • if there is an abscess then drain it
  • debridement if there’s dead bone
  • (if infection spreads to joint then risk of septic arthritis)
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51
Q

what is septic arthritis?

A
  • an infection within a synovial joint
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52
Q

what are the causes of septic arthritis?

A
  • Staphylococcus aureus is most common causative pathogen
  • in children: Haemophilus influenzae
  • in sexually active adults: Neisseria gonorrhae
  • (infection can spread from bone to joint)
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53
Q

what are the clinical features of septic arthritis?

A
  • acutely hot swollen joint
  • systemically unwell and fever
  • severe pain, patient cannot weight bear or move joint
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54
Q

what investigations should be done for suspected septic arthritis?

A
  • JOINT ASPIRATION: synovial fluid sent for urgent gram stain, culture, and examination for crystals
  • ESR + CRP + WCC: raised
  • X-RAY: normal initially then joint destruction later
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55
Q

what is the line of management for septic arthritis?

A
  • aspiration should be done ASAP, before antibiotics are given
  • analgesia and splint
  • treatment is either repeated aspiration or surgical with arthroscopy / arthrotomy
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56
Q

what is tuberculosis caused by and how does MSK TB occur?

A
  • Mycobacterium tuberculosis infection

- MSK TB results when primary TB (lung) becomes widespread

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57
Q

how does MSK TB present?

A
  • systemically unwell: malaise, weight loss, cough, loss of appetite
  • unlike osteomyelitis and septic arthritis, MSK TB presents with gradual symptoms of pain and is initially confused as OA or inflammatory arthritis
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58
Q

what investigations should be done for MSK TB?

A
  • bone / synovial fluid samples: sent for culture, if mycobacterium infection suspected then Ziehl-Neelsen stain should be asked for to look for acid-fast bacilli
  • Mantoux and Heaf tests: skin hypersensitivity tests
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59
Q

what is the line of management for MSK TB?

A
  • drugs commonly used: rifampicin, isoniazid, ethambutol

- joint replacement if repeated TB infections

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60
Q

what is vasculitis?

A
  • vasculitis is inflammation of blood vessels

- vasculitis is a feature of many illnesses and can be primary or secondary

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61
Q

what investigations should be done for vasculitis?

A

Antineutrophil cytoplasmic antibodies (ANCA): associated with vasculitis

  • c-ANCA (or anti-PR3): associated with granulomatosis with polyangiitis
  • p-ANCA (or anti-MPO): associated with polyarteritis nodosa, eosinophilic granulomatosis with polyangiitis, and microscopic polyangiitis
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62
Q

what are the two large vessel vasculitides?

A
  • GIANT CELL (OR TEMPORAL) ARTERITIS

- TAKAYASU ARTERITIS

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63
Q

what are the common features seen in giant cell (or temporal) arteritis?

A
  • often co-exists with polymyalgia rheumatica
  • unilateral headache (around temples) and scalp tenderness
  • jaw claudication (pain on chewing food)
  • visual changes (due to optic artery ischaemia)
  • polymyalgia rheumatica: symmetrical pain and stiffness in shoulders and pelvic girdle
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64
Q

what is the line of management for giant cell (or temporal) arteritis?

A
  • IMMEDIATE: IV corticosteroids to reduce risk of blindness
  • temporal artery biopsy
  • as well as prednisolone 15-20mg a day, also prescribe bisphosphonates, calcium, and vitamin D to avoid osteoporosis
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65
Q

what are the clinical features for Takayasu arteritis and line of management?

A
  • affects younger women
  • claudication, visual changes, dizziness, stroke
  • CT / MRI for diagnosis, steroids prescribed
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66
Q

what are the two medium vessel vasculitides?

A
  • Polyarteritis Nodosa

- Kawasaki Disease

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67
Q

what are the main features of polyarteritis nodosa and line of management?

A
  • typically seen secondary to hepatitis B
  • SYMPTOMS: skin ulcerations and rashes (livedo reticularis), peripheral neuropathy, renal disease
  • MANAGEMENT: nerve biopsies, corticosteroids prescribed
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68
Q

what are the main features of Kawasaki disease and what is the line of management?

A
  • mainly affects children under 5 yrs old
  • SYMPTOMS: desquamation (peeling) of skin of the hands and feet, conjunctival congestion, strawberry tongue
  • MANAGEMENT: IV immunoglobulin and low dose aspirin
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69
Q

what are the 5 small vessel vasculitides?

A
  • Granulomatosis with polyangiitis (GPA)
  • Eosinophilic granulomatosis with polyangiitis (Churg Strauss syndrome)
  • Microscopic polyarteritis
  • Henoch-Schonlein purpura (IgA vasculitis)
  • Bechet disease
70
Q

what are the main features of granulomatosis with polyangiitis (GPA) and what is the line of management?

A
  • peak onset is 30-40 yrs old
  • SYMPTOMS: rhinorrhoea (runny nose), cough, pleuritic pain, arthritis/arthralgia, upper airways disease, ‘saddle-nose’ deformity, skin rashes
  • MANAGEMENT: cyclophosphamide with corticosteroids, Rituximab also effective (if not life-threatening then methotrexate, azathioprine given)
71
Q

what are the main features of eosinophilic granulomatosis with polyangiitis (Churg Strauss syndrome) and what is the line of management?

A

SYMPTOMS (3 phases):

  • phase 1: rhinitis (runny nose), adult-onset asthma
  • phase 2: high eosinophil lvls in blood causes night sweats, cough, diarrhoea, and wheeze
  • phase 3: rashes, neuritis, renal failure, abdominal pains
  • MANAGEMENT: cyclophosphamide with corticosteroids, Rituximab also effective (if not life-threatening then methotrexate and azathioprine can be given)
72
Q

what are the main features of microscopic polyarteritis?

A
  • SHARES MANY FEATURES WITH GRANULOMATOSIS WITH POLYANGIITIS

- SYMPTOMS: rash, glomerulonephritis

73
Q

what are main features of Henoch-Schonlein purpura and line of management?

A
  • more common in children and adolescents
  • SYMPTOMS: rash on legs and buttocks, GI involvement causes abdominal pains, asymmetrical arthritis, 40% of patients develop glomerulonephritis
  • MANAGEMENT: usually self-limiting, in severe cases immunossuppressants given
74
Q

what are main features of Bechet disease?

A
  • SYMPTOMS: oral and genital ulceration, uveitis, cutaneous lesions, GI features
75
Q

what does T-score tell you?

A
  • measure of bone mineral density (BMD)
  • T-score of less than -2.5 is osteoporosis
  • T-score of between -1 and -2.5 is osteopenia
76
Q

what are some risk factors for osteoporosis?

A
  • older age, female, early menopause, family hsitory

- poor calcium and vitamin D intake, lack of exercise, smoking, alcohol excess

77
Q

what medications can cause osteoporosis?

A
  • corticosteroids
  • anti-convulsants
  • heparin
78
Q

what is a typical presentation of osteoporosis?

A
  • patient comes in with fragility fracture from a low impact trauma / fall
  • typical fractures of osteoporosis include Colles fracture of the wrist, fractured neck of femur, vertebral body fracture (vertebral compression or wedge fractures)
79
Q

what investigations should you do for osteoporosis?

A
  • Dual-energy x-ray absorptiometry (DEXA scan): measures BMD
80
Q

what is the line of management for osteoporosis?

A
  • calcium and vitamin D supplements
  • Bisphosphonates (inhibit osteoclast activity): alendronic acid, zoledronic acid
  • Denosumab (monoclonal antibody directed against RANK ligand): use if patient is intolerant to bisphosphonates
  • Teriparatide: PTH drug, increases osteoblast activation, BMD increases (very expensive but useful if patient cannot tolerate other medications)
  • Calcitonin: inhibits osteoclast activity
  • reduce risk of falls: OT, physio, social workers
81
Q

what is Paget disease?

A
  • a disorder of bone metabolism characterised by focal increases in bone remodelling, resulting in abnormal bone production
  • leads to mechanical weakness of the bone
82
Q

what are the risk factors for Paget disease?

A
  • very rare in Asians
  • over 40 yrs old
  • strong genetic contribution
83
Q

how might Paget disease present clinically?

A
  • often low-energy femoral shaft fractures
  • many patients are not symptomatic and are diagnosed due to abnormal blood tests (raised alkaline phophatase) and x-ray findings
84
Q

what investigations should be done for Paget disease?

A
  • Alkaline phosphatase: raised and correlates to the amount of skletal involvement
  • plain radiographs: shows areas of disorgansied bone with areas of lysis and sclerosis
  • isotope bone scans: often show multiple areas of focal increased uptake and are the most sensitive test for detecting Pagetic lesions
85
Q

what is the line of management for Paget disease?

A
  • Bisphosphonates: alendronic acid, zoledronic acid
  • Calcitonin: sometimes used, but less tolerated
  • surgery: only if complications (surgical stabilisation for fractures)
    (NOTE: Pagetic bone is highly vascualr and bleeds a lot in surgery, ensure patients are cross-matched for blood in advance)
86
Q

what is Rickets and what is osteomalacia?

A
  • Rickets affects the growing skelton in children and is a disorder of effective mineralisation of cartilage in the epiphyseal growth plates of children
  • Osteomalacia occurs in adults, it is weakening of the bone due to problems with bone formation or the bone-building process
  • (osteomalacia is different from osteoporosis as osteoporosis is a weakening of living bone that is already formed and being remodelled)
87
Q

what is the most common cause for Rickets and osteomalacia?

A

VITAMIN D DEFICIENCY is the most common cause:

  • low dietary intake and low sunlight exposure
  • intestinal malabsorption (coeliac disease, liver disease, renal disease)
88
Q

what are the clinical features of Rickets?

A
  • growth is impaired
  • bone pain
  • muscle weakness
  • bowing of long bones (varus / valgus deformity of the knee)
89
Q

what are the clinical features of osteomalacia?

A
  • vague bone pain
  • proximal myopathy (proximal muscle disease)
  • fatigue
90
Q

what investigations should you do for Rickets and osteomalacia?

A
  • calcium: low
  • phopshate: low
  • vitamin D: low
  • alklaline phosphatase: raised
  • PTH lvls: raised
91
Q

what is the management for Rickets and osteomalacia?

A
  • vitamin D supplements / replacement

- underlying cause of the vitamin D deficiency should be addressed

92
Q

what is carpal tunnel syndrome?

A
  • results from compression of the median nerve
93
Q

what are some causes / risk factors for carpal tunnel syndrome?

A
  • very common and usually idiopathic

- but can be associated with local trauma/wrist fractures, diabetes mellitus, hypothyroidism, RA, preganancy)

94
Q

how does carpal tunnel syndrome present?

A
  • pain and/or paraesthesia in the median nerve distribution, ache, pins and needles, muscle weakness

(palm side of hand, thumb, first finger, second finger, and half of ring finger)

95
Q

what investigations should you do for carpal tunnel syndrome?

A
  • Phalen test (flex wrists and hold for 60 secs, numbness is positive)
  • Tinel test (tap anterior aspect of wrist and will reproduce pain/pins and needles)
  • nerve conduction studies
96
Q

what is the line of management for carpal tunnel syndrome?

A
  • wrist splint
  • corticosteroid injection to relieve pain
  • surgical decompression of the carpal tunnel
  • behaviour modification
97
Q

what is ulnar nerve entrapment?

A
  • ulnar nerve can become compressed as it passes nehind the medial epicondyle or through Guyon canal in the wrist
98
Q

what are the causes / risk factors for ulnar nerve entrapment?

A
  • common, can be idiopathic or due to an underlying condition
  • underlying conditions are local trauma / fractures of the elbow, prolongerd leaning on the elbow, elbow synovitis)
99
Q

what are the clinical features of ulnar nerve entrapment?

A
  • pain and/or paraesthesisa on median side of elbow, which radiates to median side of forearm and the ulnar nerve distribution of the hand
  • pain is often exacerbated by elbow flexion
  • ulnar clawing of the hand can occur in severe cases
100
Q

what is the management for ulnar nerve entrapment?

A
  • surgical decompression

- ulnar nerve compressoin due to elbow synovitis may respond to corticosteroid injections of the elbow

101
Q

how do radial nerve injuries typically present?

A
  • typically seen when a person falls asleep with their arm over the back of a chair
  • fractures of the humeral shaft can also cause radial nerve palsy
  • wrist extensors are paralysed, resulting in wrist drop
  • grip strength is reduced
  • nerve injury in the axilla also leads to paralysis of the triceps
102
Q

what is the line of management for radial nerve injuries/palsy?

A
  • wrist should be splinted immediately

- fracture/dislocation reduction can help with nerve entrapement relief

103
Q

where is the common peroneal nerve located?

A
  • the common peroneal nerve wraps around the fibula and is in a vulnerable position
  • it may be damaged by neck of fibula fractures or pressure from a tight bandage
104
Q

how do common peroneal nerve injuries present?

A
  • paralysis of ankle and foot extensors
  • foot may appear plantar flexed and inverted (foot drop)
  • patients may adopt a high stepping gait due to foot drop
  • loss of sensitivity over anterior and lateral sides of the leg and dorsum of the foot and toes
105
Q

what is the line of management for common peroneal nerve injuries?

A
  • pressure on the nerve should be relieved and a splint applied
  • nerve conduction studies
106
Q

how does SLE present?

A
  • SYSTEMIC FEATURES: fatigue, malaise, weight loss, headaches
  • MSK: non-erosive arthritis, myalgia and myositis (inflamed muscle), 1/3 suffer from Raynaud phenomenon
  • DERMATOLOGICAL: malar rash (over nose and cheeks) or butterfly rash, lesions, hair loss, oral ulcers, cutaneous vasculitis (livedo reticularis)
107
Q

which autoantibody is associated with SLE?

A
  • anti-double stranded DNA
108
Q

which autoantibody is associated with drug induced lupus?

109
Q

which autoantibody is associated with Sjorgen syndrome and SLE?

A
  • anti-Ro

- anti-La (only in 15% of SLE patients)

110
Q

which autoantibody is associated with limited cutaneous systemic sclerosis?

A
  • anti-centromere
111
Q

which autoantibody is associated with diffuse systemic sclerosis?

A
  • anti-Scl-70 (topoisomerase)
112
Q

which autoantibody is associated with mixed connective tissue disease?

113
Q

which autoantibody is associated with polymyositis and dermatomyositis?

A
  • anti-Jo-1 (polymyositis)

- anti-Mi-2 (dermatomyositis)

114
Q

what investigations should be done for SLE?

A
  • anti-double stranded DNA: associated with SLE
  • Complement: low C3 and C4 lvls
  • FBC: anaemia, leukopenia, and thrombocytopenia
  • ESR: raised during a flare
  • urine dipstick: look for blood and protein (nephritis)
115
Q

what is the line of management for SLE?

A
  • EDUCATION: avoid risk factors (overexposure to sunlight/UV light B, osetrogen-containing contraceptive therapy, stress, infection)
  • NSAIDs: ibuprofen, diclofenac, naproxen, celecoxib
  • Hydroxychloroquine
  • corticosteroids
  • azathioprine and methotrexate
  • FOR SEVERE SLE: cyclophosphamide, rituximab, belimumab
116
Q

what are the causes / risk factors for antiphospholipid syndrome?

A
  • partial association with SLE

- antiphospholipid antibodies (lupus anticoagulant, anticardiolipin)

117
Q

what are the clinical features of antiphospholipid syndrome?

A
  • venous thrombosis
  • arterial thrombosis: cerebral ischaemia, peripheral ischaemia
  • recurrent miscarriages and premature births
  • thrombocytopenia (low platelets)
  • livedo reticularis
  • epilepsy / migraine
118
Q

what investigations should be done for antiphospholipid syndrome?

A
  • antiphospholipid antibodies: lupus anticoagulant and anticardiolipin
  • FBC: thrombocytopenia (low platelets)
119
Q

what is the line of management for antiphospholipid syndrome?

A
  • avoidance of oral contarceptive pill
  • avoidance of smoking
  • low dose aspirin
  • warfarin (anti-coagulant)
    (NOTE: if woman is pregnant then stop warfarin)
120
Q

what is Sjorgen syndrome associated with?

A
  • RA, SLE, systemic sclerosis, polymyositis
121
Q

how does Sjorgen syndrome present?

A
  • dry and red eyes (bacterial conjunctivitis is common)
  • dry mouth: dysphagia (difficulty swallowing), dry cough
  • fatigue, malaise, weight loss
  • non-erosive arthritis
  • Raynaud phenomenon (affects 50%)
  • vasculitis
122
Q

what investigations should be done for Sjorgen syndrome?

A
  • anti-Ro and anti-La: may be present
  • ANA: usually positive
  • Schirmer test: measure conjunctival dryness
  • ESR: raised
123
Q

what is the line of management for Sjorgen syndrome?

A
  • eye drops
  • NSAIDs and hydroxychloroquine to treat arthralgia
  • corticosteroids for severe cases
124
Q

what are the risk factors for polymyositis and dermatomyositis?

A
  • female

- 40-60 yrs old

125
Q

how does polymyositis and dermatomyositis typically present?

A
  • symmetrical and progressive proximal muscle weakness
  • (patients describe difficulty in getting out of a chair or walking up the stairs)
  • (patients find it difficult to reach things above head height)
  • respiratory problems and dysphagia (difficulty swallowing)
  • systemic: fever, malaise, weight loss
  • Raynaud phenomenon
  • interstitial lung disease
  • vasculitis

CUTANEOUS (only dermatomyostitis):

  • Gottron papules (erythematous, scaley (hands and elbows)
  • Heliotrope rash (over eyelids)
  • erythematous rash on face, neck, chest, shoulders, and hands
126
Q

what investigations should be done for polymyositis and dermatomyositis?

A
  • screen for malignancy (10-15% of adults with inflammatory muscle disease have an underlying malignancy)
  • creatine kinase: raised due to myositis
  • Anti-Jo-1: associated with polymyositis
  • Anti-Mi-2: associated with dermatomyositis
  • muscle biopsy
  • MRI
  • electromyography and nerve conduction studies
127
Q

what is the line of management for polymyositis and dermatomyositis?

A
  • corticosteroids
  • methotrexate and azathioprine
  • cyclophosphamide (only if severe interstitial lung disease)
128
Q

what is sclerosis?

A
  • hardening of the skin
  • cutaneous means it is confined to the skin
  • systemic means it involves organs (2 types: limited systemic sclerosis and diffuse systemic sclerosis)
129
Q

how does sclerosis typically present? (include both limited and diffuse)

A
  • skin fibrosis is limited to the face, hands, and neck

LIMITED systemic sclerosis (CRESTM):

  • Calcinosis
  • Raynaud phenomenon
  • oEseophageal disease
  • Sclerodactyl (sclerosis affecting the fingers)
  • Telangiectasia (spider veins)
  • (Microstomia: tightness around the mouth)

DIFFUSE systemic sclerosis: organ fibrosis (lung, cardiac, and renal disease)

130
Q

what is the line of management for sclerosis?

A

no cure, treat organ diseases individually…

  • Raynaud phenomenon: hand warmers, vasodilators
  • Pulmonary fibrosis: prednisolone, with cyclophosphamide
  • Pulmonary hypertension: warfarin and heparin
  • GI problems: omeprazole (PPI)
  • Renal crisis: RED FLAG, urgent treatment required (antihypertensives)
131
Q

what are the 9 main paediatric MSK conditions?

A
  • developmental dysplasia of the hip (DDH)
  • Perthes disease
  • Osgood-Schlatter disease
  • Slipped upper femoral epiphysis (SUFE)
  • osteochondritis dissecans
  • congenital talipes equinovarus (clubfoot)
  • cerebral palsy
  • osteogenesis imperfecta
  • juvenile idiopathic arthritis (JIA)
132
Q

what is developmental dysplasia of the hip (DDH), clinical features, investigations, and management?

A
  • DDH occurs due to the failure of normal development of the acetabulum resulting in abnormal hip anatomy

CLINICAL FEATURES:
- most cases picked up on routine baby checks
- loss of abduction, leg length discrepancy
- late-presenting DDH can occur as the child begins to walk, the child with have a limp and shortness of one leg (if unilateral)
INVESTIGATIONS:
- Barlow test: attempt to dislocate a reduced hip
- Ortolani test: attempt to reduce a dislocated hip
- ultrasound / x-ray
MANAGEMENT:
- abduction splint
- reduce hip if needed

133
Q

what is Perthes disease, clinical features, investigations, management?

A
  • Perthes disease is a rare disease in which blood supply to femoral head is interrupted, causing avascular necrosis and collapse of the femoral head
CLINICAL FEATURES:
- gradual history of hip or knee pain
- loss of hip motion
INVESTIGATIONS:
- plain x-ray and MRI
- ESR and CRP: to rule out septic arthritis
MANAGEMENT:
- 75% of children require no treatment
- older children and female patients (closer to skeletal maturity) may require containment of femoral head (eg. pelvic/femoral osteotomy)
134
Q

what is Osgood-Schlatter disease, clinical features, and investigation?

A
  • very common in adolescent boys
  • tender and swollen tibial tuberosity
  • management: simple analgesia, patient can choose to continue activity (won’t make condition worse)
135
Q

what are the risk factors for a slipped upper femoral epiphysis (SUFE), clinical features, investigations, management?

A
  • SUFE is when there is a structural failure through the growth plate of an immature hip

RISK FACTORS:
- 11-14yrs old boys, athletic, obesity
CLINICAL FEATURES:
- child presents with groin or knee pain and a limp
- externally rotated leg with limited range of movement
INVESTIGATIONS:
- x-ray
MANAGEMENT:
- epiphysis is pinned in situ to prevent further displacement

136
Q

what is osteochondritis dissecans, clinical features, investigations, management?

A
  • osteochondritis dissecans is a small area of avascular bone on an articular surface, usually in the knee

CLINICAL FEATURES:
- due to repeated trauma
- intermittent ache, swelling, and catching in the knee
- patient may complain of the knee giving way with acute sharp episodes of pain
INVESTIGATIONS:
- x-ray: shows lesion on medial femoral condyle
MANAGEMENT:
- activity modification
- surgery only if lesion becomes detached

137
Q

what is congenital talipes equinovarus (clubfoot), risk factors, clinical features, investigations, management?

A
  • clubfoot is a deformity of the lower limb with calf wasting and the classic inwardly pointing foot
    RISK FACTORS:
  • more common in boys
  • half of cases are bilateral
  • family history is important
    CLINICAL FEATURES:
  • inward pointing foot, underdeveloped calf muscle compared to normal leg
    INVESTIGATIONS:
  • baby should be examined for associated conditions (such as spina bifida)
  • diagnosis based on clinical findings
    MANAGEMENT:
  • manipulation and casting over 3 months (90% success rate)
138
Q

what is cerebral palsy, clinical features, management?

A
  • cerebral palsy is a non-progressive upper motor neurone condition that results from injury to an immature brain
CLINICAL FEATURES:
- muscle weakness and spasticity
- characteristic joint deformities
MANAGEMENT:
- physio, OT, speech and language therapy
- surgery only if deformities
139
Q

what is osteogenesis imperfecta, clinical features, investigations, management?

A
  • osteogenesis imperfecta is also known as brittle bone disease, it is a type I collagen disorder predisposed to multiple fractures

CLINICAL FEATURES:
- often presents with a low-energy fracture (can be confused as NAI)
- children are usually small and have joint deformities
INVESTIGATIONS:
- x-ray: multiple fractures, thin-looking cortex, deformities
MANAGEMENT:
- IV bisphosphonates to strengthen bone
- intramedullary telescoping rods to prevent deformities and further fracture, osteotomy for current deformity

140
Q

what are the clinical features of juvenile idiopathic arthritis (JIA)?

A
  • joint disease: pain, stiffness, swelling
  • eye disease: some forms of JIA are associated with acute anterior uveitis (pain and redness of eye)
  • systemic: fatigue, malaise
141
Q

what are the 6 types of JIA?

A
  • oligoarticular disease (highest risk of developing anterior uveitis)
  • extended oligoarticular disease
  • polyarticular disease (RF +ve and RF -ve)
  • systemic-onset disease (characterised by infection/malignancy)
  • enthesitis-related arthritis (Achilles tendonitis is common, often HLA-B27 positive)
  • psoriatic arthritis
142
Q

how is JIA diagnosed?

A
  • diagnosis is clinical
143
Q

what is the line of management for juvenile idiopathic arthritis (JIA)?

A
  • physio
  • NSAIDs and corticosteroids
  • Anti-TNFs
  • eye-screening
144
Q

give 3 examples of benign primary bone tumours.

A
  • enchondroma
  • osteochondroma
  • osteoid osteoma
145
Q

give 3 examples of malignant primary bone tumours.

A
  • osteosarcoma
  • chondrosarcoma
  • Ewing sarcoma
146
Q

what is leukaemia?

A
  • malignancy of WBCs
  • most common malignancy of childhood
  • can present with bone pain similar to septic arthritis
147
Q

how are undisplaced intracapsular fractures of the neck of femur managed?

A
  • Undisplaced intracapsular fractures: have a low chance of disruption to blood supply and can be treated with internal fixation (however avascular necrosis and non-union are still a risk)
148
Q

how are displaced intracapsular fractures of the neck of femur managed?

A
  • Displaced intracapsular fractures: have a high chance of disruption to blood supply and are treated with hemiarthroplasty (ie. The femoral head is removed)
149
Q

how are extra-capsular fractures of the neck of femur managed?

A
  • Extracapsular fractures: treated with internal fixation with either a dynamic hip screw (trochanteric) or an intramedullary nail (subtrochanteric)
150
Q

what is the Salter-Harris classification for fractures in children?

A
  • Type I: fracture through physis only
  • Type II (most common): fracture through physis and part of metaphysis is involved
  • Type III: epiphyseal segment separated (intra-articular fracture)
  • Type IV: fracture involves metaphysis and epiphysis and crosses through the physis
  • Type V: crush injury
151
Q

what is compartment syndrome and what are the complications?

A
  • EMERGENCY
  • viscous cycle of increased compartmental pressure, tissue hypoxia, oedema, and cellular death (necrosis)
  • complication is rhabdomyolysis (muscles break down)
  • proteins such as creatine kinase and myoglobin leak into the bloodstream
  • myoglobin is toxic for kidneys and can cause acute renal failure
152
Q

what is the treatment for compartment syndrome?

A
  • if cast on leg then remove ASAP
  • fasciotomy must be done
  • fasciotomy relieves pressure and re-establishes blood flow (fascia can be left open for days)
153
Q

as well as compartment syndrome, what is another serious complication that can result from a fracture?

A

FAT EMBOLUS:

  • may occur after long bone fractures (particularly femur)
  • occurs due to fat entering bloodstream and embolising to the lungs
    (condition occurs as medullary canal of long bones contains fat)
  • treatment is oxygen and fluids, transfer to HDU
154
Q

what is a Colles fracture and Smith fracture?

A
  • Colles: wrist is fractured and in extension (outward)
  • Smith: wrist is fractured and in flexion (inward)

(treatment is immobilisation with a cast)

155
Q

what is the risk of an intra-capsular fracture of the neck of femur?

A
  • fracture line is between the blood supply and the femoral head
  • so risk of losing blood supply to femoral head, therefore risk of avascular necrosis and non-union
156
Q

what is a prolapsed intervertebral disc?

A
  • A disc prolapse occurs when part of the nucleus pulposus herniates through the annulus fibrosus and presses on a spinal nerve root
157
Q

what are the risk factors and clinical features of an intervertebral prolapsed disc?

A

RISK FACTORS:

  • heavy lifting
  • regular automobile use

CLINICAL FEATURES:

  • uncomfortable to sit
  • sciatica
  • abnormal posture: stooped to one side and knee flexed to relieve pressure
158
Q

what is a serious complication of an intervertebral prolapsed disc?

A

CAUDA EQUINA SYNDROME:

  • altered bladder/anal function (urinary continence or constipation)
  • perineal paraesthesia (due to compression of nerves within the cauda equine)
  • bilateral leg pain
  • perineal pain
    (urgent MRI needed)
159
Q

what is spondylolisthesis and clinical features?

A
  • Spondylolisthesis is where one vertebral body slips over another

CLINICAL FEATURES:

  • Common, gymnastics and fast bowlers in cricket more common
  • Most common cause of persistent back pain in children
  • back pain and sometimes sciatica
  • spinal tenderness and hyperextension is painful
160
Q

what x-ray findings would you see for spondylolithesis?

A
  • classic ‘collar’ on dog appearance (break in bone)
161
Q

what is spinal stenosis and clinical features?

A
  • Spinal stenosis is caused by degenerative changes narrowing the spinal canal and causing compression of the nerve roots

CLINICAL FEATURES:

  • Discomfort when walking, with pain referred to buttock, calves, and feet
  • Often worse with exercise and relieved with rest
  • ‘shopping cart sign’: able to walk greater distances when they have a flexed spine (leaning on their shopping trolley)
  • Pain is worse with extension of spine and relieved with rest and flexion of spine
162
Q

what is discitis and vertebral osteomyelitis?

A
  • Discitis is infection of the disc space

- Vertebral osteomyelitis is infection of a vertebral body

163
Q

what are the risk factors for discitis/vertebral osteomyelitis?

A
  • IV drug users, immunocompromised, and patients with diabetes are predisposed to spinal infection
  • Common infective organisms in adults: staphylococci and streptococci
  • Common infective organisms in children: staphylococci and Haemophilus
164
Q

what is the line of management for discitis/vertebral osteomyelitis?

A
  • IV antibiotics for 6 weeks, follow-up MRI after 6 weeks too
  • any abscess drained, if spine has deformity then stabilise
165
Q

what is a Galeazzi fracture and what is a Monteggia fracture?

A
  • GALEAZZI: fracture of distal third of radial shaft with dislocation of radio-ulnar joint
  • MONTEGGIA: fracture of proximal third of ulnar shaft with anterior dislocation of radial head
166
Q

describe how a short head of biceps rupture would present?

A
  • ‘pop eye’ sign
  • anterior ‘bulge’ or swelling
  • bicep tendon injury from excess load on flexion
167
Q

what is the most common type of carpal bone fracture?

A
  • scaphoid fracture
168
Q

what is th emost common type of psoriatic arthritis?

A
  • asymmetrical oligoarthritis
169
Q

what main side effect does prednisolone have on your appearance?

A
  • ‘moon face’
170
Q

what gene is associated with Bechet’s disease?

A
  • HLA-B51 associated

((archived year 1 med)) (15 decks)

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