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MSK - CLINICAL CONDITIONS Flashcards

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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
what investigations should you do for psoriatic arthritis?
- ESR + CRP: raised - HLA-B27 associated - FBC: shows anaemia of chronic disease - rheumatoid factor negative - X-RAY: erosions, pencil-in-cup deformities
26
what is the line of management for psoriatic arthritis?
- 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)
27
what are the causes / risk factors for reactive arthritis? (also most common bacteria)
- 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
28
what are the clinical features of reactive arthritis?
- 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
29
what investigations should you do for reactive arthritis?
- 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
30
what is the line of management for reactive arthritis?
- 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)
31
what is reactive arthritis?
- reactive arthritis is an aseptic arthritis that occurs after an infection
32
what is enteropathic arthritis?
- enteropathic arthritis is an arthritis occurring with inflammatory bowel disease (IBD)
33
what are the causes / risk factors for enteropathic arthritis?
- occurs in 10-20% of patients with Crohn disease or ulcerative colitis
34
what are the clinical features of enteropathic arthritis?
- 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
35
what investigations should you do for enteropathic arthritis?
- X-RAY + MRI: shows inflammation | - if IBD suspected then refer to gastroenterologist
36
what is the line of management for enteropathic arthritis?
- 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)
37
what is gout?
- gout is the consequence of high lvls of hyperuricemia and uric acid crystal formation
38
what are some of the risk factors for gout?
- male - alcohol - high protein diet - obesity - diuretic use - psoriasis
39
what are the clinical features of gout?
- 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
40
what investigations should be done for gout and what are the findings?
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
41
what is the line of management for gout?
(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
42
what is pseudogout?
- pseudogout is also known as calcium pyrophosphate dihyrdate (CPPD) disease - it is an arthropathy associated with the deposition of CPPD crystals
43
what are some risk factors / causes for pseudogout?
- 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)
44
what are the clinical features of pseudogout?
- 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)
45
what investigations should be done for pseudogout and what are your findings?
- 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
46
what is the line of management for pseudogout?
- (usually self-limiting) - ANALGESIA: paracetamol, aspirin, codeine, hydrocodone - NSAIDs - colchicine - corticosteroid injections - LIFESTYLE: lose weight, physio
47
how can infection of the bone be caused? (2 ways)
- 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)
48
what is the most common infecting organism in osteomyelitis?
- Stapholococcus aureus | - (bone and joint infection are common among IV drug users)
49
what are some of the common pathogens in osteomyelitis? (newborn, children, adults, immunocompromised)
- 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
50
what is the line of management for osteomyelitis?
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)
51
what is septic arthritis?
- an infection within a synovial joint
52
what are the causes of septic arthritis?
- Staphylococcus aureus is most common causative pathogen - in children: Haemophilus influenzae - in sexually active adults: Neisseria gonorrhae - (infection can spread from bone to joint)
53
what are the clinical features of septic arthritis?
- acutely hot swollen joint - systemically unwell and fever - severe pain, patient cannot weight bear or move joint
54
what investigations should be done for suspected septic arthritis?
- 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
55
what is the line of management for septic arthritis?
- aspiration should be done ASAP, before antibiotics are given - analgesia and splint - treatment is either repeated aspiration or surgical with arthroscopy / arthrotomy
56
what is tuberculosis caused by and how does MSK TB occur?
- Mycobacterium tuberculosis infection | - MSK TB results when primary TB (lung) becomes widespread
57
how does MSK TB present?
- 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
58
what investigations should be done for MSK TB?
- 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
59
what is the line of management for MSK TB?
- drugs commonly used: rifampicin, isoniazid, ethambutol | - joint replacement if repeated TB infections
60
what is vasculitis?
- vasculitis is inflammation of blood vessels | - vasculitis is a feature of many illnesses and can be primary or secondary
61
what investigations should be done for vasculitis?
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
62
what are the two large vessel vasculitides?
- GIANT CELL (OR TEMPORAL) ARTERITIS | - TAKAYASU ARTERITIS
63
what are the common features seen in giant cell (or temporal) arteritis?
- 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
64
what is the line of management for giant cell (or temporal) arteritis?
- 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
65
what are the clinical features for Takayasu arteritis and line of management?
- affects younger women - claudication, visual changes, dizziness, stroke - CT / MRI for diagnosis, steroids prescribed
66
what are the two medium vessel vasculitides?
- Polyarteritis Nodosa | - Kawasaki Disease
67
what are the main features of polyarteritis nodosa and line of management?
- typically seen secondary to hepatitis B - SYMPTOMS: skin ulcerations and rashes (livedo reticularis), peripheral neuropathy, renal disease - MANAGEMENT: nerve biopsies, corticosteroids prescribed
68
what are the main features of Kawasaki disease and what is the line of management?
- 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
69
what are the 5 small vessel vasculitides?
- Granulomatosis with polyangiitis (GPA) - Eosinophilic granulomatosis with polyangiitis (Churg Strauss syndrome) - Microscopic polyarteritis - Henoch-Schonlein purpura (IgA vasculitis) - Bechet disease
70
what are the main features of granulomatosis with polyangiitis (GPA) and what is the line of management?
- 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
what are the main features of eosinophilic granulomatosis with polyangiitis (Churg Strauss syndrome) and what is the line of management?
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
what are the main features of microscopic polyarteritis?
- SHARES MANY FEATURES WITH GRANULOMATOSIS WITH POLYANGIITIS | - SYMPTOMS: rash, glomerulonephritis
73
what are main features of Henoch-Schonlein purpura and line of management?
- 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
what are main features of Bechet disease?
- SYMPTOMS: oral and genital ulceration, uveitis, cutaneous lesions, GI features
75
what does T-score tell you?
- 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
what are some risk factors for osteoporosis?
- older age, female, early menopause, family hsitory | - poor calcium and vitamin D intake, lack of exercise, smoking, alcohol excess
77
what medications can cause osteoporosis?
- corticosteroids - anti-convulsants - heparin
78
what is a typical presentation of osteoporosis?
- 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
what investigations should you do for osteoporosis?
- Dual-energy x-ray absorptiometry (DEXA scan): measures BMD
80
what is the line of management for osteoporosis?
- 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
what is Paget disease?
- 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
what are the risk factors for Paget disease?
- very rare in Asians - over 40 yrs old - strong genetic contribution
83
how might Paget disease present clinically?
- 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
what investigations should be done for Paget disease?
- 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
what is the line of management for Paget disease?
- 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
what is Rickets and what is osteomalacia?
- 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
what is the most common cause for Rickets and osteomalacia?
VITAMIN D DEFICIENCY is the most common cause: - low dietary intake and low sunlight exposure - intestinal malabsorption (coeliac disease, liver disease, renal disease)
88
what are the clinical features of Rickets?
- growth is impaired - bone pain - muscle weakness - bowing of long bones (varus / valgus deformity of the knee)
89
what are the clinical features of osteomalacia?
- vague bone pain - proximal myopathy (proximal muscle disease) - fatigue
90
what investigations should you do for Rickets and osteomalacia?
- calcium: low - phopshate: low - vitamin D: low - alklaline phosphatase: raised - PTH lvls: raised
91
what is the management for Rickets and osteomalacia?
- vitamin D supplements / replacement | - underlying cause of the vitamin D deficiency should be addressed
92
what is carpal tunnel syndrome?
- results from compression of the median nerve
93
what are some causes / risk factors for carpal tunnel syndrome?
- very common and usually idiopathic | - but can be associated with local trauma/wrist fractures, diabetes mellitus, hypothyroidism, RA, preganancy)
94
how does carpal tunnel syndrome present?
- 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
what investigations should you do for carpal tunnel syndrome?
- 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
what is the line of management for carpal tunnel syndrome?
- wrist splint - corticosteroid injection to relieve pain - surgical decompression of the carpal tunnel - behaviour modification
97
what is ulnar nerve entrapment?
- ulnar nerve can become compressed as it passes nehind the medial epicondyle or through Guyon canal in the wrist
98
what are the causes / risk factors for ulnar nerve entrapment?
- 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
what are the clinical features of ulnar nerve entrapment?
- 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
what is the management for ulnar nerve entrapment?
- surgical decompression | - ulnar nerve compressoin due to elbow synovitis may respond to corticosteroid injections of the elbow
101
how do radial nerve injuries typically present?
- 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
what is the line of management for radial nerve injuries/palsy?
- wrist should be splinted immediately | - fracture/dislocation reduction can help with nerve entrapement relief
103
where is the common peroneal nerve located?
- 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
how do common peroneal nerve injuries present?
- 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
what is the line of management for common peroneal nerve injuries?
- pressure on the nerve should be relieved and a splint applied - nerve conduction studies
106
how does SLE present?
- 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
which autoantibody is associated with SLE?
- anti-double stranded DNA
108
which autoantibody is associated with drug induced lupus?
- histone
109
which autoantibody is associated with Sjorgen syndrome and SLE?
- anti-Ro | - anti-La (only in 15% of SLE patients)
110
which autoantibody is associated with limited cutaneous systemic sclerosis?
- anti-centromere
111
which autoantibody is associated with diffuse systemic sclerosis?
- anti-Scl-70 (topoisomerase)
112
which autoantibody is associated with mixed connective tissue disease?
- anti-RNP
113
which autoantibody is associated with polymyositis and dermatomyositis?
- anti-Jo-1 (polymyositis) | - anti-Mi-2 (dermatomyositis)
114
what investigations should be done for SLE?
- 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
what is the line of management for SLE?
- 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
what are the causes / risk factors for antiphospholipid syndrome?
- partial association with SLE | - antiphospholipid antibodies (lupus anticoagulant, anticardiolipin)
117
what are the clinical features of antiphospholipid syndrome?
- venous thrombosis - arterial thrombosis: cerebral ischaemia, peripheral ischaemia - recurrent miscarriages and premature births - thrombocytopenia (low platelets) - livedo reticularis - epilepsy / migraine
118
what investigations should be done for antiphospholipid syndrome?
- antiphospholipid antibodies: lupus anticoagulant and anticardiolipin - FBC: thrombocytopenia (low platelets)
119
what is the line of management for antiphospholipid syndrome?
- avoidance of oral contarceptive pill - avoidance of smoking - low dose aspirin - warfarin (anti-coagulant) (NOTE: if woman is pregnant then stop warfarin)
120
what is Sjorgen syndrome associated with?
- RA, SLE, systemic sclerosis, polymyositis
121
how does Sjorgen syndrome present?
- 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
what investigations should be done for Sjorgen syndrome?
- anti-Ro and anti-La: may be present - ANA: usually positive - Schirmer test: measure conjunctival dryness - ESR: raised
123
what is the line of management for Sjorgen syndrome?
- eye drops - NSAIDs and hydroxychloroquine to treat arthralgia - corticosteroids for severe cases
124
what are the risk factors for polymyositis and dermatomyositis?
- female | - 40-60 yrs old
125
how does polymyositis and dermatomyositis typically present?
- 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
what investigations should be done for polymyositis and dermatomyositis?
- 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
what is the line of management for polymyositis and dermatomyositis?
- corticosteroids - methotrexate and azathioprine - cyclophosphamide (only if severe interstitial lung disease)
128
what is sclerosis?
- 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
how does sclerosis typically present? (include both limited and diffuse)
- 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
what is the line of management for sclerosis?
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
what are the 9 main paediatric MSK conditions?
- 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
what is developmental dysplasia of the hip (DDH), clinical features, investigations, and management?
- 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
what is Perthes disease, clinical features, investigations, management?
- 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
what is Osgood-Schlatter disease, clinical features, and investigation?
- 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
what are the risk factors for a slipped upper femoral epiphysis (SUFE), clinical features, investigations, management?
- 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
what is osteochondritis dissecans, clinical features, investigations, management?
- 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
what is congenital talipes equinovarus (clubfoot), risk factors, clinical features, investigations, management?
- 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
what is cerebral palsy, clinical features, management?
- 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
what is osteogenesis imperfecta, clinical features, investigations, management?
- 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
what are the clinical features of juvenile idiopathic arthritis (JIA)?
- 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
what are the 6 types of JIA?
- 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
how is JIA diagnosed?
- diagnosis is clinical
143
what is the line of management for juvenile idiopathic arthritis (JIA)?
- physio - NSAIDs and corticosteroids - Anti-TNFs - eye-screening
144
give 3 examples of benign primary bone tumours.
- enchondroma - osteochondroma - osteoid osteoma
145
give 3 examples of malignant primary bone tumours.
- osteosarcoma - chondrosarcoma - Ewing sarcoma
146
what is leukaemia?
- malignancy of WBCs - most common malignancy of childhood - can present with bone pain similar to septic arthritis
147
how are undisplaced intracapsular fractures of the neck of femur managed?
- 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
how are displaced intracapsular fractures of the neck of femur managed?
- Displaced intracapsular fractures: have a high chance of disruption to blood supply and are treated with hemiarthroplasty (ie. The femoral head is removed)
149
how are extra-capsular fractures of the neck of femur managed?
- Extracapsular fractures: treated with internal fixation with either a dynamic hip screw (trochanteric) or an intramedullary nail (subtrochanteric)
150
what is the Salter-Harris classification for fractures in children?
- 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
what is compartment syndrome and what are the complications?
- 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
what is the treatment for compartment syndrome?
- 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
as well as compartment syndrome, what is another serious complication that can result from a fracture?
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
what is a Colles fracture and Smith fracture?
- Colles: wrist is fractured and in extension (outward) - Smith: wrist is fractured and in flexion (inward) (treatment is immobilisation with a cast)
155
what is the risk of an intra-capsular fracture of the neck of femur?
- 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
what is a prolapsed intervertebral disc?
- A disc prolapse occurs when part of the nucleus pulposus herniates through the annulus fibrosus and presses on a spinal nerve root
157
what are the risk factors and clinical features of an intervertebral prolapsed disc?
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
what is a serious complication of an intervertebral prolapsed disc?
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
what is spondylolisthesis and clinical features?
- 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
what x-ray findings would you see for spondylolithesis?
- classic 'collar' on dog appearance (break in bone)
161
what is spinal stenosis and clinical features?
- 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
what is discitis and vertebral osteomyelitis?
- Discitis is infection of the disc space | - Vertebral osteomyelitis is infection of a vertebral body
163
what are the risk factors for discitis/vertebral osteomyelitis?
- 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
what is the line of management for discitis/vertebral osteomyelitis?
- IV antibiotics for 6 weeks, follow-up MRI after 6 weeks too - any abscess drained, if spine has deformity then stabilise
165
what is a Galeazzi fracture and what is a Monteggia fracture?
- 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
describe how a short head of biceps rupture would present?
- 'pop eye' sign - anterior 'bulge' or swelling - bicep tendon injury from excess load on flexion
167
what is the most common type of carpal bone fracture?
- scaphoid fracture
168
what is th emost common type of psoriatic arthritis?
- asymmetrical oligoarthritis
169
what main side effect does prednisolone have on your appearance?
- 'moon face'
170
what gene is associated with Bechet's disease?
- HLA-B51 associated

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

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