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AAClinical school conditions > Musculoskeletal and rheumatological conditions > Flashcards

Musculoskeletal and rheumatological conditions Flashcards

1
Q

Osteoarthritis: epidemiology

A

Worldwide, uncommon in black population, twice as common in women, occurs in over 50s.

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2
Q

Osteoarthritis: age

A

Mostly over 60s.

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3
Q

Osteoarthritis: sex

A

Women over 55 more likely to have it than men of a similar age.

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4
Q

Osteoarthritis: clinical symptoms.

A

Joint pain - pain exacerbated by movement, relieved by rest. Gelling on rest.

functional limitation

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5
Q

Osteoarthritis: clinical signs

A

Crepitus
Restricted movement
Bony enlargement
Joint effusion and variable levels of inflammation.

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6
Q

Osteoarthritis: investigations.

A

Blood tests, X-rays, MRIs, aspiration of synovial fluid.

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7
Q

Osteoarthritis investigations: blood tests.

A

ESR normal, sometimes high-sensitivity CRP elevated. Rheumatoid factor and anti-nuclear antibodies are negative.

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8
Q

Osteoarthritis investigations: X-rays.

A

Abnormal only when advanced. Used pre-operatively.

Theoretically will show LOSS - loss of joint space, osteophytes, subarticular sclerosis, and subchondral cysts.

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9
Q

Osteoarthritis investigations: MRI

A

Used to look for for meniscal tears, early cartilage injury and subchondral bone marrow changes.

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10
Q

Osteoarthritis investigations: aspiration

A

Shows viscous fluid with few leukocytes.

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11
Q

Osteoarthritis treatments.

A

All aimed at relieving symptoms. Physical measures, paracetamol, NSAIDs, intra-articular steroids or surgery.
Hyaluronic acid injections, topical capsaicin.

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12
Q

Osteoarthritis pathology

A

Multifactorial process, mostly mechanical factors. Significant inflammation and also alteration of cartilage structure.

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13
Q

Red flag symptoms for back pain (divisions to help memory)

A

Divide into age, type of pain, associated symptoms, cancer, neuro and infectious to remember

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14
Q

Red flag symptoms for back pain (actual)

A

Age: under 20 or over 55.
Type of pain: If the pain is constant/progressive, nocturnal/worse when in a supine position, or if it is thoracic.
Associated symptoms: fever/night sweats/weight loss, morning stiffness or claudication in the leg.
Cancer: history of malignancy, abdo mass (also AAA).
Neuro: neurological disturbance (inc sciatica), leg pain (bilateral or alternating unilateral), sphincter disturbance.
Infection: current infection or immunosuppression.

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15
Q

Normal distribution of psoriasis

A

Forearm extensor surfaces.

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16
Q

Complications of chronic kidney failure

A

Hyperkalaemia, high levels of erythropoietin, hypocalcaemia.

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17
Q

Rheumatological conditions causing diffuse pain with no early morning stiffness

A

Chronic pain syndromes
Fibromyalgia
Malignancy

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18
Q

Rheumatological conditions causing diffuse pain with early morning stiffness

A

Polymyalgia rheumatica

Inflammatory myositis

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19
Q

Rheumatological conditions causing localised pain, with no early morning stiffness and no joint swelling

A

Osteoarthritis/arthropathy
Tendinopathy
Bursitis

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20
Q

Rheumatological conditions causing localised joint pain with early morning stiffness, in a single joint.

A

SEPTIC ARTHRITIS
Crystals (gout)
Reactive
Spondyloarthritis.

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21
Q

Rheumatological conditions causing localised joint swelling and pain with early morning stiffness, in multiple joints

A 
Rheumatoid 
Viral (if less than 6 weeks)
SLE
Sponyloarthritis
Crystals
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22
Q

Joints commonly affected by osteoarthritis

A

Distal interphalangeal joints, first CMC joint in hand, MTP joint of foot, and weight-bearing joints.

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23
Q

Heberden’s nodes

A

Bony swellings at DIPJ

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24
Q

Bouchard’s nodes

A

Bony swellings at PIPJ

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25
Q

Rheumatoid arthritis definition

A

A chronic symmetrical bony arthritis caused by a systemic autoimmune disorder with extra-articular involvement

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26
Q

Rheumatoid arthritis - epidemiology

A

Peak prevalence 30-50 years, pre-menopausal women affected more than men, familial association.

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27
Q

Rheumatoid arthritis - pathology

A

Activation of synovial T cells by unknown antigen leads to synovitis, synovial infiltration, angiogenesis and formation of a pannus. This leads to destruction of articular cartilage and subchondral bone. Rheumatoid nodules also form in the skin, pleura, pericardium and lung.

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28
Q

Rheumatoid arthritis - clinical features

A

Pain, early morning stiffness, and swelling of small joints. Joint effusions and wasting of surrounding muscles.
Periarticular features. Rheumatoid nodules at pressure points.
Progressive disease: joint instability, subluxation and deformity

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29
Q

Rheumatoid arthritis - investigations

A

Bloods: anaemia, raised inflammatory markers

Serum autoantibodies:RhF, antinuclear factor and anti-citrulline-contaiining peptide antibodies.

X-ray.
Aspiration: synovial fluid stirle with high neutrophil count.

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30
Q

Rheumatoid arthritis - treatment

A

Smoking cessation, NSAIDs, disease-modifying drugs (DMARDs). Anticytokine agents, coricosteroids, surgery.

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31
Q

Rheumatoid arthritis - joints affected

A

PIPJ, MCPs and wrist. Can involve elbows, shoulders, spine, knees, ankles and feet.

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32
Q

Ankylosing spondylitis - definition

A

An inflammatory disorder of the back

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33
Q

Ankylosing spondylitis - epidemiology

A

Typically young men

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34
Q

Ankylosing spondylitis - clinical features

A

Increasing pain and morning stiffness in lower back, alleviated by exercise not rest. Progressive loss of spinal movement.
Increased loss of lumbar lordosis and increased kyphosis. Limitation of lumbar mobility and chest expansion.

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35
Q

Ankylosing spondylitis - investigations

A

Bloods: raised inflammatory markers

X-ray may be normal or show erosion.

MR shows early changes suggestive of osteitis and oedema.

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36
Q

Ankylosing spondylitis - treatment

A

Exercises.
Slow release NSAIDs taken at night.
In severe AS if NSAIDs fail, use TNFa blockers such as adalimumab and golimumab.

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37
Q

What is a greenstick fracture?

A

A fracture in a child that involves partial cortical disruption.

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38
Q

Pars interarticularis position

A

A fracture of the area on a vertebra between the superior and inferior facet

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39
Q

Pars interarticularis result.

A

The fracture may lead to the vertebral body slipping anteriorly and leading to vertebral canal compression. Common in athletes at LIV and LV levels.

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40
Q

Which nerve weakness leads to inablility to raise the arm above the head and weakness in attempting to raise the shoulder?

A

CN XI

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41
Q

Which nerve damage leads to inability to do a pull up?

A

Thoracodorsal nerve

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42
Q

When do you see polyarticular gout?

A

Occasionally, but in chronic renal failure particularly

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43
Q

Which crystals cause gout?

A

Monosodium urate monophosphate

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44
Q

Which crystals cause pseudogout?

A

Calcium pyrophosphate dihydrate

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45
Q

Pattern of gout

A

Usually feet, esp first metatarsalphalangeal joint in men, and knee in women, but can affect any foot joint. Generally in men, affecting 1% of population.

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46
Q

Timescale of gout

A

Acute onset of swelling, pain and redness for a few days, before returning to normal. These intermittent attacks occur more frequently without treatment leading to chronic problems, as severity of flares decreases.

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47
Q

Examination findings in gout

A

Low grade pyrexia, redness, swelling and tenderness of joint. If chronic, tophi over pinna of ear, elbow and lateral hand.
DD is septic arthritis, gout and pseudogout.

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48
Q

Risk factors of gout.

A

What increases serum uric acid level?
Diet: animal purines, alcohol, seafood
Synthesis
Decreased renal excretion

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49
Q

Metabolic pathway key to pathogenesis of gout

A

Nucleic acids –> purines –> hypoxanthine –> xanthine –> URIC ACID (which we can’t metabolise and is not v water soluble, so is supersaturation level of serum)

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50
Q

Lesch-Nyhan syndrome

A

Paediatric condition due to mutation in uric acid pathway, leading to hyperuracemia in children.

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51
Q

What interferes with renal excretion of uric acid?

A

mutation in URAT1 channel in Mauris; drugs inc loop and thiazide diuretics, cyclosporin and low dose aspirin; lead toxicity; INSULIN RESISTANCE and high levels of insulin which interfere with excretion

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52
Q

What alters uric acid synthesis in the body?

A

Increased cellular turnover - lymphoproliferative disorders and malignancy;
Increased uric acid synthesis - fructose high diets.

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53
Q

How do uric acid crystals cause gout?

A

They are unstable, and can be released into the joint leading to recognition by innate immune system activating the inflammasome leading to neutrophil activation and symptoms of gout

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54
Q

What triggers gout attacks?

A

Intercurrent infection, acute increase or decrease in serum uric acid (commencing treatment, alcohol or dietary changes), possibly trauma.

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55
Q

Investigations when faced with suspected gout?

A

SYNOVIAL FLUID ANALYSIS (exclude septic arthritis)
Renal function (increased creatinine is a risk for gout)
Serum uric acid - a NEGATIVE marker as drops in an acute attack, so likely to be normal but can still be high.
Blood cultures

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56
Q

Synovial fluid appearance in septic arthritis and crystal synovitis

A

Runny, greenish, opaque. (crystal synovitis can be more yellowish)

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57
Q

Synovial fluid appearance in inflammatory arthritis and crystal synovitis

A

Cloudy, straw-coloured, low viscosity. (crystal synovitis can be more greenish).

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58
Q

Normal synovial fluid looks like…

A

Olive oil

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59
Q

What investigation is used to diagnose gout definitively?

A

Polarised light microscopy. Needle shaped crystals visible.

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60
Q

Treatment of gout - matches causing fire in joint. Fire extinguisher, dampen matches, reduce number of matches.

A

A fire extinguisher: NSAIDs very effective - carry with them, and take at start immediately. Steroidal anti-inflammatories also work if NSAIDs contraindicated.
Dampen matches: colchicine interferes with neutrophil microtubules. OD, BD or TD.
Reduce the number of matches: reduce uric acid levels in body. Decrease insulin - weight reduction. Check drugs. This risks flares.
Allopurinol inhibits xanthine oxidase.

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61
Q

What is pseudogout?

A

A crystal arthropathy that can be thought of as an aggressive form of nodal osteoarthritis.

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62
Q

What is likely to be a background history for patients with pseudogout?

A

Nodal osteoarthritis.

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63
Q

What is a ‘flare’ of osteoarthritis likely to be?

A

Pseudogout

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64
Q

Presentation of pseudogout

A

Episodes of pain, early morning stiffness, swelling and redness of affected joint, lasting weeks (not days).

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65
Q

Triggers for pseudogout

A

Intercurrent infection, dehydration, local trauma.

NOT diet.

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66
Q

Investigations for suspected pseudogout

A 
Joint aspiration - look for crystals, but can be difficult to see. Exclude septic arthritis
CRP/ESR raised
Blood cultures negative
Uric acid normal
X-ray as crystals are radioopaque
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67
Q

Management of pseudogout

A

Fire extinguisher: anti-inflammatories.
Dampening: colchicine BD/TD but no randomised trials.
Not possible to reduce crystals yet.

68
Q

What would you find on examination of a fibromyalgic patient?

A

Multiple tender points along spine and in her limbs.

69
Q

Secondary causes of fibromyalgia syndrome

A

Anaemia
Failures: liver and renal
Autoimmune conditions (e.g. RA, SLE, PMR)
Disseminated carcinoma
Disorders of bone metabolism (low Vitamin D, hyperparathyroidism)
Dysfunction: thyroid and pituitary.

Viral illnesses (e.g. influenza, parvovirus, rubella)

70
Q

What are some polymyalgia symptoms?

A

> 2 weeks of bilateral, shoulder and/or pelvic girdle myalgia, early morning stiffness >45 minutes, +/- evidence of an acute-phase response, in a patient over 50

71
Q

If someone has polymyalgia symptoms, and is over 50, what else should you consider?

A

GCA

72
Q

What are some systemic symptoms of giant cell arteritis?

A

fever, weight loss, decreased appetite, fatigue.

73
Q

What is a common presentation of GCA?

A

An abrupt onset unilateral headache in the temporal region (although it can be diffuse or bilateral). Often with scalp hyperalgesia.

74
Q

What is the most concerning symptom of GCA

A

Visual symptoms: amaurosis fugax, blurring and diplopia. Patients with GCA are at risk of permanent blindness.

75
Q

What are the red flags for GCA?

A

Visual loss and jaw claudication.

76
Q

What are digital infarcts with necrotic ulceration a sign of?

A

Vasculitis

77
Q

What is likely to be the cause of an inflammatory polyarthritis with a photosensitive rash and mouth ulcers?

A

SLE

78
Q 
What are the characteristic results in SLE for:
ESR
CRP
ANA
dsDNA
ENA
A

ESR is often raised with a normal CRP
ANA is positive in 95%
dsDNA is often positive, but a negative result does not rule out SLE
ENA is positive in severe disease.

79
Q

What therapy is used in an SLE flare-up?

A

Prednisolone.

80
Q

What therapy is used for an SLE associated vasculitis?

A

Cyclophosphamide

81
Q

Epidemiology of SLE

A

More women than men. More in African ethnicities.

82
Q

What are the major dangerous renal complication of SLE?

A

Glomerulonephritis leading to nephrotic syndrome.

83
Q

What are some blood changes associated with SLE

A

Anaemia
Leukopenia/lymphopenia
Thrombocytopenia.

84
Q

What are some cardiac issues associated with SLE?

A

Pericarditis, endocarditis and aortic valve lesions.

85
Q

What are some neurological issues associated with SLE?

A

Fits, hemiplegia, ataxia, polyneuropathy, cranial nerve lesions, psychosis or demyelinating syndrome.

86
Q

What eye and skin conditions can be associated with SLE?

A

Sjogren’s syndrome
Photosensitivity and butterfly rash
Vasculitis, purpura, urticaria.

87
Q

What respiratory conditions can be associated with SLE?

A

Pleurisy/effusion

88
Q

Are urate crystals negatively or positively birefringent?

A

Negatively

89
Q

Are calcium pyrophosphate crystals negatively or positively birefringent?

A

Positively

90
Q

What is diclofenac?

A

An NSAID used in MSK conditions

91
Q

Histological features of giant cell arteritis?

A

Intimal hypertrophy and inflammation of intima and sub-intima.
Breaking up of internal elastic lamina.

92
Q

Treatment for GCA?

A

Steroids

93
Q

What is the reactive arthritis triad?

A

Urethritis, arthritis and conjunctivitis.

94
Q

Ehlers-Danlos syndrome

A

Mitral valve prolapse, hyperelastic skin and aneurysms/GI bleeds. Joints loose and hypermobile, mutations exist e.g. in genes for procollagen.

95
Q

Ankylosing spondylitis - presentation

A

typically a young man who presents with lower back pain and stiffness of insidious onset
stiffness is usually worse in the morning and improves with exercise
the patient may experience pain at night which improves on getting up

96
Q

Ankylosing spondylitis - other features (the As)

A 
Apical fibrosis
Anterior uveitis
Aortic regurgitation
Achilles tendonitis
AV node block
Amyloidosis
and cauda equina syndrome
peripheral arthritis (25%, more common if female)
97
Q

What is Felty’s syndrome?

A

Splenomegaly and neutropenia in a patient with rheumatoid arthritis.

98
Q

Common cause of osteomyelitis

A

Staph aureus

99
Q

Causes of asymmetrical polyarthritis

A

Reactive arthritis

Psoriatic arthritis

100
Q

Causes of oligoarthritis (more than one joint, fewer than 5)

A

Crystal arthritis, psoriatic arthritis, reactive arthritis, ankylosing spondylitis, osteoarthritis.

101
Q

What is a likely cause of an arthritis with photosensitive rashes?

A

SLE

102
Q

What are the likely causes of an arthritis with Raynaud’s.

A

SLE, CREST, polymyositis and dermatomyositis.

103
Q

What is a likely cause of an arthritis with dry eyes and mouth?

A

Sjogren’s.

104
Q

What is a likely cause of an arthritis with red eyes, iritis.

A

Ankylosing spondylitis.

105
Q

What is the name of the syndrome of a reactive arthritis with diarrhoea/urethritis and conjunctivitis?

A

Reiter’s

106
Q

What are the likely causes of an arthritis with nodules or nodes?

A

Rheumatoid arthritis, TB, gout.

107
Q

What is a likely cause of an arthritis with mouth or genital ulcers?

A

Behcet’s disease.

108
Q

What are the likely causes of an arthritis with weight loss?

A

Malignancy or any systemic inflammatory disease.

109
Q

What abdominal condition is associated with ankylosing spondylitis?

A

Crohn’s disease and UC.

110
Q

What is a positive sacroiliac stretch test?

A

Pain on adduction of the hip when both hip and knee are flexed.

111
Q

What is a positive straight leg test?

A

When raising the extended leg causes pain below the knee.

112
Q

What is a positive femoral stretch test?

A

If the pt is lying on their front, extending their leg causes pain down the front of the thigh.

113
Q

What blood test do you do if you suspect Paget’s disease?

A

ALP

114
Q

What are you worried about with back pain, saddle anaesthesia, alternating or bilateral leg pain, and incontinence?

A

Cauda equina compression

115
Q

Risk factors for septic arthritis

A

Pre-existing joint disease, diabetes mellitus, immunosuppression, chronic renal failure, recent jint surgery, prosthetic joints, IV drug abuse.

116
Q

Antibiotics to treat suspected septic arthritis.

A

Flucloxacillin, vancomycin if MRSA or cefotaxime if gonococcal or gram -ive.

117
Q

Extra-articular features of rheumatoid arthritis

A

Nodules in the lungs, lymphadenopathy, vasculitis, fibrosing alveolitis, obliterative bronchiolitis, effusions, Raynaud’s, carpal tunnel syndrome, peripheral neuropathy, splenomegaly.

118
Q

How do you measure disease activity of rheumatoid arthritis?

A

DAS28 - the 28 joint disease activity score.

119
Q

What are the main DMARDs?

A

Methotrexate, sulfasalazine and hydroxychloroquine.

120
Q

What is the main side effect of using methotrexate?

A

Immunosuppression.

121
Q

Biological agents that affect rheumatoid arthritis.

A

TNFa inhibitors e.g. infliximab
B cell depletion e.g. rituximab
IL-1 and IL-6 inhibition e.g tocilizumab
Disruption of T cell function e.g. abatacept.

122
Q

Differentials for suspected gout.

A

Septic arthritis

haemarthrosis, CPPD and palindromic RA

123
Q

How to test for ankylosing spondylitis

A

MRI is most sensitive; the earliest X-ray feature is sacroiliitis.
Vertebral syndesmophytes are characteristic - they are bony proliferations between ligaments and vertebrae, which fuse to the vertebral body above leading to ankylosis.

124
Q

Associations of enteric arthropathy

A

IBD, GI bypass, coeliac and Whipple’s disease

125
Q

Treatment for enteric arthropathy

A

Beware NSAIDs as GI symptoms. Consider DMARDs for resistant cases.

126
Q

How many patients with psoriasis get psoriatic arthritis?

A

10-40%

127
Q

What is the patterns of psoriatic arthritis?

A

A symmetrical polyarthritis like RA
DIP joints
Asymmetric oligoarthritis
Spinal

128
Q

What extra articular features other than psoriasis are associated with psoriatic arthritis?

A

Nail changes, synovitis, acneiform rashes and palmoplantar pustulosis.

129
Q

Treatment for psoriatic arthritis

A

NSAIDs
Sulfasalazine, methotrexate
Cyclosporin
Anti-TNFa agents.

130
Q

What is reactive arthritis?

A

A sterile arthritis usually affecting the lower limb 1-4 weeks after urethritis or dysentery.

131
Q

Organisms associated with reactive arthritis

A

Urethritis: Chlamydia or Ureaplasma
Dysentery: Campylobacter, Salmonella, Shigella, or Yersinia.

132
Q

What is enthesitis and which arthitides is it associated with?

A

Inflammation of the site of insertion of a tendon or ligament into the bone - associated with spondyloarthropathies.

133
Q

What is the chance of someone with HLA B27 developing a spondyloarthitis or eye disease?

A

1 in 4.

134
Q

What are the autoimmune connective tissue disorders?

A

SLE, systemic sclerosis, primary Sjogren’s syndrome, idiopathic inflammatory myopathies, mixed connective tissue disease, relapsing polychondritis and Behcet’s disease.

135
Q

What are the key features of systemic sclerosis?

A

Scleroderma and vascular disease.

136
Q

What is the other name for CREST syndrome?

A

Limited cutaneous systemic sclerosis

137
Q

What are the features of CREST syndrome?

A 
Calcinosis of subcut tissues
Raynaud's 
Esophageal and gut dysmotility
Sclerodactyly
Telangiectasia.
138
Q

What life-threatening condition is associated with CREST?

A

Pulmonary hypertension

139
Q

What are the key features of diffuse cutaneous systemic sclerosis?

A

Diffuse skin involvement and early organ fibrosis (lung, cardiac, GI and renal)

140
Q

Management of systemic sclerosis

A

No cure.

Immunosuppressive regimens used for organ involvement and progressive skin disease.

141
Q

What is mixed connective tissue disease

A

A potentially separate disease combining features of systemic sclerosis, SLE and polymyositis.

142
Q

What is relapsing polychondritis?

A

An autoimmune connecti tissue disease attacking cartilage.

143
Q

What are polymyositis and dermatomyositis?

A

Rare conditions associated with insidious onset of progressive symmetrical proximal muscle weakness and autoimmune-mediated striated muscle inflammation associated with myalgia and arthralgia.

144
Q

Skin signs in dermatomyositis

A 
Macular rash (shawl sign)
Heliotrope rash on eyelids
Nailfold erythema
Gottron's papules
Subcut calcification
145
Q

What are Gottron’s papules?

A

Roughened red papules over the knuckles, elbows and knees.

146
Q

Tests for myositis

A

Blood: increase in muscle enzymes - ALT, AST, LDH, CK and aldolase.
EMG shows fibrillation potentials.
Muscle biopsy confirms diagnosis.
MRI shows muscle oedema in acute myositis.

147
Q

Management of myositis

A

Screen for malignancy.
Start low dose pred.
Immunosuppressives and cytotoxics can be used early in resistant cases.

148
Q

Which conditions almost always are positive for Rh factor?

A

Sjogren’s syndrome, Felty’s syndrome and RA.

149
Q

Which conditions are often Rh factor positive?

A

Infective endocarditis, hepatitis.
Mixed connective tissue disease
SLE
Systemic sclerosis.

150
Q

What blood test has 96% specificity for rheumatoid arthritis?

A

Anti-CCP Ab.

151
Q

SLE pathology

A

Autoantibodies are made againts variety of autoantigens, resulting in polyclonal B-cell secretion of pathogenic autoantibodies causing tissue damage via immune complex formation and deposition, complement activation and other effects.

152
Q

What is the course of SLE?

A

It is relapsing and remitting

153
Q

Maintenance therapy for joint and skin symptoms in SLE

A

NSAIDs and hydroxychloroquine.

Low dose steroids in chronic disease.

154
Q

How do you treat SLE lupus nephritis?

A

Steroids and cyclophosphamide.

155
Q

Antiphospholipid syndrome symptoms

A 
CLOT
Coagulation defects
Livedo reticularis
Obstetric (recurrent miscarriage)
Thrombocytopenia
156
Q

Large vasculitides

A

Giant cell arteritis, Takayasu’s arteritis

157
Q

Medium vessel vasculitides

A

Polyarteritis nodosa, Kawasaki disease

158
Q

Small ANCA +ive vasculitides

A

p-ANCA associated microscopic polyangiitis
glomerulonephritis
Churg-Strauss syndrome
c-ANCA Wegener’s granulomatosis

159
Q

Small ANCA -ive vasculitides

A

Henoch-Schonlein purpura, Goodpasture’s syndrome and cryoglobulinaemia.

160
Q

Treatment for GCA

A

Take ESR and start prednisolone immediately.

161
Q

Investigations for polymyalgia

A

Raised ESR, typically more than 40, raised CRP. ALP is sometimes raised.

162
Q

Key features of fibromyalgia

A

Widespread chronic pain esp at tender points

Fatigue.

163
Q

Fibromyalgia associations

A

CFS, IBS adn chronic headaches.

RA, SLE and AS.

164
Q

Tender points for fibromyalgia

A 
Suboccipital muscle insertion
Intertransverse spaces at C5-C7
Midpoint of trapezius
Origin of supraspinatus
Costochondral junction of 2nd rib
2cm distal of humeral epidcondyle
Upper outer luteal quadrant
Posterior to greater trochanter
Knee, at medial fat pad proximal to joint line.
165
Q

Investigations for fibromyalgia

A

All normal.

166
Q

Management of fibromyalgia

A

Eduationn
CBT
Graded exercise programmes
Pain control: consider amitriptyline and pregabalin

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