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Finals > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Give examples of alarm features in an individual presenting with back pain.

A

Aged over 50, constant pain, nocturnal pain, worse when lying flat, loss of sensation, weight loss, night sweats, fever, active/previous cancer, weakness and immunosuppression.

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2
Q

What are the five most common causes of back pain in those aged 15-30 years?

A 
Mechanical back pain. 
Vertebral prolapse. 
Trauma. 
Ankylosing spondylitis. 
Pregnancy.
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3
Q

What are the three most common causes of back pain in those aged 30-50 years?

A

Degenerative disease.
Vertebral prolapse.
Malignancy.

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4
Q

What are the six most common causes of back pain in those aged over 50 years?

A 
Degenerative disease. 
Osteoporosis. 
Pagets. 
Malignancy. 
Myeloma. 
Spinal stenosis.
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5
Q

What is the general management of back pain?

A

NSAIDs, paracetamol, physiotherapy, movement techniques and low-dose amitriptyline.

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6
Q

What is the pathophysiology of simple lower back pain?

A

Muscle strain causes spasms and temporary paralysis of the spinal area which results in pain.

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7
Q

What is osteoarthritis?

A

A degenerative condition characterised by the loss of cartilage at the synovial joints.

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8
Q

What is the most common type of arthritis?

A

Osteoarthritis.

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9
Q

What are risk factors for the development of osteoarthritis?

A

Obesity, increasing age, occupation (e.g. manual intense labour), female and family history.

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10
Q

What joints are typically affected in osteoarthritis?

A 
Large, weight-bearing joints (hip, knee). 
Carpometacarpal joints (in the palm). 
Distal and proximal interphalangeal joints. 
Cervical spine.
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11
Q

What is the characteristic presentation of osteoarthritis?

A

Unilateral joint pain (ache) and stiffness without systemic upset.

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12
Q

Describe the stiffness associated with osteoarthritis.

A

Transient morning stiffness that lasts a few minutes.

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13
Q

What are the signs of osteoarthritis?

A

Joint line tenderness, limited range of movement, bony swelling, Heberden’s nodes and Bouchard’s nodes.

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14
Q

What radiological signs are found in patients with osteoarthritis?

A 
Loss of joint space (narrowing). 
Osteophytes. 
Subchondral sclerosis. 
Subchondral cysts. 
(Remember: LOSS)
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15
Q

How is osteoarthritis managed?

A

Encourage weight loss and muscle strengthening exercises. Give paracetamol and topical NSAIDs first-line. Consider oral NSAIDs second-line - give with proton-pump inhibitor.
Intrarticular steroid injections if symptoms aren’t well managed and arthroplasty.

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16
Q

How is joint pain in osteoarthritis associated with activity?

A

Pain is provoked by movement and relieved by rest.

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17
Q

What is rheumatoid arthritis?

A

A long-term autoimmune disorder that causes chronic inflammation of the synovial lining of the joints, tendon sheaths and bursa.

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18
Q

What is the characteristic presentation of rheumatoid arthritis?

A

Symmetrical distal polyarthropathy (painful, warm, swollen, stiff joints).

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19
Q

How is the joint pain of rheumatoid arthritis associated with rest/activity?

A

Pain is often worse after rest but improves with activity.

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20
Q

Describe the joint stiffness of rheumatoid arthritis.

A

Morning stiffness lasting at least thirty minutes.

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21
Q

What systemic features are associated with rheumatoid arthritis?

A

Fever and low energy.

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22
Q

What joints are most commonly affected in rheumatoid arthritis?

A

Proximal interphalangeal joints.

Metacarpophalangeal joints.

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23
Q

What signs of rheumatoid arthritis are found in the hands?

A

Z shaped deformity of the thumb.
Swan neck deformity.
Boutonnieres deformity.
Ulnar deviation of the fingers.

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24
Q

Give four examples of extra-articular manifestations of rheumatoid arthritis (excluding the eyes).

A

Pulmonary fibrosis.
Bronchiolitis obliterans.
Felty’s syndrome.
Secondary Sjogren’s syndrome.

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25
Q

Give three examples of ocular manifestations of rheumatoid arthritis.

A

Keratoconjunctivitis sicca (dry eyes).
Episcleritis (painless, red).
Scleritis (severe pain, photophobia).

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26
Q

The presence of which two antibodies are used in the diagnosis of rheumatoid arthritis?

A

Rheumatoid factor.

Anti-cyclic citrullinated peptide antibody.

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27
Q

Rheumatoid arthritis: what is the difference in utility of investigations of rheumatoid factor and anti-CCP antibody?

A

Anti-CCP antibody are more sensitive and specific than RF and can be detected up to ten years before the development of RA.

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28
Q

Other than rheumatoid arthritis, give examples of three conditions in which rheumatoid factor may be raised.

A

Sjogren’s syndrome.
SLE.
Infective endocarditis.

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29
Q

What is first-line treatment of rheumatoid arthritis?

A

DMARD monotherapy (methotrexate or sulfasalazine or hydroxychloroquine).

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30
Q

Rheumatoid arthritis: What monitoring is required for individuals taking DMARDs?

A

FBC and LFT monitoring due to risk of myelosuppression and liver cirrhosis.

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31
Q

What is second-line treatment of rheumatoid arthritis?

A

Two DMARDs.

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32
Q

What is the pharmacological management of rheumatoid arthritis following a failure to respond to two DMARDs?

A

Biologics - TNF-inhibitors such as etanercept, infliximab and adalimumab.

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33
Q

Describe the action of methotrexate.

A

Interferes with metabolism of folate and suppresses certain components of the immune system.

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34
Q

How often is methotrexate taken in the treatment of rheumatoid arthritis?

A

Once weekly.

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35
Q

What should be prescribed alongside methotrexate?

A

5mg folic acid taken on a different day to the methotrexate.

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36
Q

How should methotrexate use be managed during pregnancy?

A

Highly teratogenic - stop six months before conception in men and women.

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37
Q

What is psoriatic arthritis?

A

An inflammatory arthritis associated with psoriasis.

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38
Q

What % of patients with psoriasis develop psoriatic arthritis?

A

10-20%.

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39
Q

Give examples of patterns of psoriatic arthritis.

A

Symmetrical polyarthritis.
Asymmetrical pauciarthritis.
Spondylitic pattern.

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40
Q

What are the presenting features of psoriatic arthritis?

A

Psoriasis plaques on skin, pitting of the nails, onycholysis (separation of nail from nail bed), dactylics (inflammation of finger), enthesisitis.

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41
Q

What are extra-articular features of psoriatic arthritis?

A

Conjuncitivitis, anterior uveitis, aortitis, amyloidosis.

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42
Q

What does x-ray reveal in psoriatic arthritis?

A

Periostitis, ankylosis, osteolysis, dactylitis and pencil-in-cup appearance.

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43
Q

What is the management of psoriatic arthritis?

A

NSAIDs for pain.
DMARDs (methotrexate, sulfasalazine).
Anti-TNF (etanercept, infliximab).

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44
Q

What is reactive arthritis?

A

A condition of synovitis in the joints in reaction to a recent infection trigger.

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45
Q

Reactive arthritis: What is the typical pattern of disease?

A

Acute monoarthritis typically affecting the lower limb and most often the knee.

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46
Q

What clinical features are associated with reactive arthritis?

A

Warm, swollen, painful joint.

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47
Q

Give examples of possible triggers of reactive arthritis

A

Gastroenteritis.

Sexually transmitted infections (chlamydia, gonorrhoea).

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48
Q

Give examples of extra-articular features associated with reactive arthritis.

A

Conjunctivits, anterior uveitis, urethritis, circinate balantitis.

Remember: can’t see, can’t pee, can’t climb a tree.

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49
Q

Reactive arthritis: What is circinate balantitis?

A

Dermatitis of the head of the penis.

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50
Q

What important differential diagnosis for reactive arthritis must be excluded in the management of this condition?

A

Septic arthritis.

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51
Q

How is reactive arthritis managed while investigations are pending?

A

Antibiotics given to treat potential septic arthritis.

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52
Q

How is reactive arthritis investigated // septic arthritis excluded?

A

Joint aspirate followed by gram-staining, cultures and sensitivities. Crystal examination can also be performed for investigation of gout/pseudogout.

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53
Q

What is the management of reactive arthritis after septic arthritis has been excluded?

A

NSAIDs.
Intrarticular steroid injections.
Systemic steroids may be required.

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54
Q

Name three conditions within the seronegative group of spondyloarthropathies.

A

Ankylosing spondylitis.
Reactive arthritis.
Psoriatic arthritis.

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55
Q

The seronegative spondylorthropathy group of conditions are associated with what gene?

A

HLA B27.

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56
Q

What is ankylosing spondylitis?

A

Inflammatory condition affecting the spine.

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57
Q

What joints are most often affected in ankylosing spondylitis?

A

Sacroiliac joints.

Vertebral column joints.

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58
Q

Ankylosing spondylitis typically affects what group of people?

A

Young males.

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59
Q

What is the characteristic presentation of ankylosing spondylitis?

A

Pain and stiffness in the lower back and sacroiliac pain in the buttock. Pain is worse at night and can wake from sleep.

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60
Q

How does rest/activity affect the pain associated with ankylosing spondylitis?

A

Pain improves with movement and worsens with rest.

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61
Q

Describe the joint stiffness associated with ankylosing spondylitis.

A

Morning stiffness lasting at least 30 minutes.

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62
Q

Describe how joint inflammation can progress in ankylosing spondylitis.

A

Progresses to fusion of the vertebral and sacroiliac joints.

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63
Q

What is the characteristic finding on spinal x-ray of someone with later stage ankylosing spondylitis?

A

Bamboo spine.

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64
Q

What are the features of a bamboo spine on x-ray?

A 
Squaring of the vertebral bodies. 
Subchondral sclerosis. 
Subchondral erosions. 
Syndesmophytes. 
Ossification.
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65
Q

What investigations are performed in ankylosing spondylitis?

A

Inflammatory markers (CRP and ESR).
HLA B27 genetic testing.
Spinal and sacral x-ray.
Spinal MRI.

66
Q

What extra-articular features are associated with ankylosing spondylitis?

A 
Chest pain (costovertebral and costosternal joint inflammation). 
Plantart fasciitis (due to enthesitis). 
Dactylitis. 
Anaemia. 
Anterior uveitis. 
Aortitis. 
Heart block. 
Restrictive lung disease (restricted chest wall movement). 
Inflammatory bowel disease.
67
Q

What is the management of ankylosing spondylitis?

A

NSAIDs for pain, steroids to control flares, anti-TNF medication (etanercept) to suppress disease activity. Physiotherapy, exercise, smoking avoidance, bisphosphonates.

68
Q

What is systemic lupus erythematosus?

A

An inflammatory autoimmune connective tissue disease.

69
Q

What is the presentation of SLE?

A

Non-specific features: Fatigue, hair loss, arthralgia, myalgia, fever, weight loss, photosensitive malar rash, lymphadenopathy, splenomegaly, shortness of breath, pleuritic chest pain, mouth ulcers and Raynaud’s phenomenon.

70
Q

SLE: The disease is characterised by the presence of which autoantibody?

A

Anti-nuclear antibody.

71
Q

What % of people with SLE are positive for anti-nuclear antibody?

A

85%.

72
Q

How specific is anti-nuclear antibody for SLE?

A

Also present in healthy individuals and other autoimmune conditions (such as autoimmune hepatitis).

73
Q

Give an example of an autoantibody that is more specific for SLE than anti-nuclear antibody.

A

anti-dsDNA antibody.

74
Q

What is anti-dsDNA antibody?

A

Anti-double stranded DNA antibody is a subtype of anti-nuclear antibody that is specific for SLE. Levels vary with disease activity so can be used for monitoring.

75
Q

What syndrome of hypercoagulation is associated with SLE?

A

Antiphospholipid syndrome.

76
Q

Give examples of complications of SLE.

A

Cardiovascular disease, infection, anaemia of chronic disease, pericarditis, pleuritis lupus nephritis, neuropsychiatric SLE and recurrent miscarriage.

77
Q

What is first-line management for mild SLE?

A

NSAIDs, prednisolone, suncream/sunavoidance, hydroxychloroquine.

78
Q

What is management of moderate-severe SLE?

A

Immunosuppressants (methotrexate, mycophenolate mofetil, azathioprine).

79
Q

What is the management of SLE that fails to respond to immunosuppressants?

A

Biologics - rituximab, belimumab.

80
Q

What is systemic sclerosis?

A

An autoimmune inflammatory and fibrotic connective tissue disease that affects the skin (most notably) and internal organs.

81
Q

What are the two main patterns of systemic sclerosis?

A

Limited cutaneous systemic sclerosis (CREST syndrome).

Diffuse cutaneous systemic sclerosis.

82
Q

What autoantibody is positive in most patients with systemic sclerosis?

A

Anti-nuclear antibody.

83
Q

What are the features of limited cutaneous systemic sclerosis?

A 
Calcinosis. 
Raynaud's phenomenon. 
oEsophageal dysmotility. 
Sclerodactyly.
Telangiectasia.

Remember CREST.

84
Q

What autoantibody is most associated with limited cutaneous systemic sclerosis?

A

Anti-centromere antibody.

85
Q

What are the features of diffuse cutaneous systemic sclerosis?

A 
CREST features +
Cardiovascular disease (hypertension, coronary artery disease. 
Lung disease (pulmonary hypertension and pulmonary fibrosis). 
Renal disease (glomerulonephritis, scleroderma renal crisis).
86
Q

What autoantibody is most associated with diffused cutaneous systemic sclerosis?

A

Anti-Scl-70 antibody.

87
Q

Other than autoantibodies, what investigation can be performed in the diagnosis of systemic sclerosis?

A

Nailfold capillaroscopy (inspection of base of capillary to assess health of peripheral capillaries).

88
Q

What is the non-medical management of systemic sclerosis?

A

Stop smoking, gentle skin stretching, avoiding cold triggers, physiotherapy and occupational therapy.

89
Q

What is the medical management of systemic sclerosis?

A

Treat directly with steroids and immunosuppressants. Treat complications with emollients, nifedipine (Raynaud’s), omeprazole (gastro sx), analgesia (joint pain), antibiotics (skin infections) and antihypertensives.

90
Q

What is polymyalgia rheumatica?

A

Relatively common inflammatory condition.

91
Q

What group of people are classically affected by polymyalgia rheumatica?

A

White females > 50 years.

92
Q

What is the clinical presentation of polymyalgia rheumatica?

A

Two week history of bilateral shoulder pain and pelvic girdle pain (making rising from chair and overhead activities painful). Mild fever, weight loss, low mood and malaise.

93
Q

Polymyalgia rheumatica is associated with what vascular disease (and what are the features)?

A

Giant cell arteritis - unilateral headache, jaw claudication and visual disturbance.

94
Q

How is pain associated with rest/activity in polymyalgia rheumatica?

A

Worse with movement and interferes with sleep.

95
Q

Describe the stiffness associated with polymyalgia rheumatica.

A

Morning stiffness for at least 45 minutes.

96
Q

What investigations are performed in polymyalgia rheumatica?

A

ESR, CRP, TFTs, CK, rheumatoid factor and serum protein electrophoresis.

97
Q

What is the treatment of polymyalgia rheumatica?

A

High dose (15mg) prednisolone followed by steroid reducing regime.

98
Q

What should be given alongside steroids in management of polymyalgia rheumatica?

A

Bisphosphonates, calcium supplements, vitamin D supplements, proton pump inhibitor.

99
Q

What is temporal arteritis?

A

A vasculitis that affects the temporal artery.

100
Q

What is the clinical presentation of temporal arteritis?

A

Unilateral headache, jaw claudication, visual disturbances, tender + palpable temporal artery.

101
Q

Temporal arteritis is associated with which inflammatory condition?

A

Polymyalgia rheumatica (shoulder pain, pelvic girdle pain, morning stiffness).

102
Q

What investigations are performed in temporal arteritis (with results)?

A

ESR (raised).

Temporal artery biopsy (skip lesions of multinucleated giant cells).

103
Q

Why should temporal arteritis be treated urgently?

A

Visual loss is often irreversible.

104
Q

What is the management of temporal arteritis?

A

High-dose prednisolone followed by reducing-regime.

105
Q

What is Sjogren’s syndrome?

A

An autoimmune condition that affects the exocrine glands.

106
Q

What are the clinical features of Sjogren’s syndrome?

A

Dry mucous membranes (dry eyes, dry mouth, dry vagina).

107
Q

What is the difference between primary and secondary Sjogren’s syndrome?

A

Primary occurs in isolation.

Secondary is associated with SLE and rheumatoid arthritis.

108
Q

Sjogren’s syndrome is associated with which autoantibodies?

A

Anti-Ro.

Anti-La.

109
Q

What special test is performed in Sjogren’s syndrome?

A

Schirmer test.

110
Q

Sjogren’s: Describe the Schirmer test.

A

Filter paper placed under lower eyelid with strip hanging over eyelid for five minutes and tear travel distance is measured.

111
Q

What is the result of Schirmer test in a person with Sjogren’s?

A

< 10mm travel.

112
Q

What is the management of Sjogren’s?

A

Artificial tears, artificial saliva, vaginal lubricants.

Hydroxychloroquine given to halt disease progression.

113
Q

What are complications of Sjogren’s?

A 
Eye problems (conjunctivitis, corneal ulcers). 
Mouth problems (dental cavities, candida infections). 
Vaginal problems (sexual dysfunction, candidiasis).
114
Q

What is gout?

A

Crystal arthropathy (a form of inflammatory arthritis) associated with chronically high blood uric acid levels.

115
Q

What is the presentation of gout?

A

Hot, painful, swelling and erythema of joints.

116
Q

What is the most commonly affected joint in gout?

A

Metatarsophalangeal joint (base of the big toe).

117
Q

What is the pathophysiology of gout?

A

Deposition of monosodium rate crystals in the synovial as a result of chronic hyperuricaemia.

118
Q

What are three causes of decreased uric acid excretion?

A

Diuretics.
CKD.
Lead toxicity.

119
Q

What are three causes of increased production of uric acid?

A

Cytotoxic drugs.
Severe psoriasis.
Myeloprolifrative / lymphoproliferative disorders

120
Q

Gout: What are gouty tophi?

A

Subcutaneous deposits of uric acid in the small joints and connective tissues (of the hands, elbow and ears).

121
Q

What differential should be considered when diagnosing gout?

A

Septic arthritis.

122
Q

How is gout diagnosed?

A

Clinically.
Joint aspiration.
Imaging.

123
Q

What are the findings of joint aspiration in gout?

A

No bacterial growth.
Monosodium urate crystals.
Negatively birefringent of polarised light.
Needle shaped crystals.

124
Q

What are the findings on radiological imaging in gout?

A

Preservation of joint space.
Joint effusion.
Punched-out erosions.
Eccentric erosions.

125
Q

What is the acute management of gout?

A

1st line: Naproxen (NSAID) + lansoprazole.

2nd line: Colchicine.

126
Q

What can be given for gout prophylaxis?

A

Allopurinol.

127
Q

What lifestyle modifications can be made to reduce the risk of gout?

A

Reduce alcohol intake.
Weight loss.
Avoiding foods high in purines (liver, kidney, seafood, oily fish).

128
Q

What is pseudogout?

A

Crystal arthropathy the result of accumulation of calcium pyrophosphate dehydrate crystals within joint soft tissues.

129
Q

What is the presentation of pseudogout?

A

Hot, swollen, stiff, painful knee. Other affected joints include shoulders, wrists and hips.

130
Q

What investigations are performed in the diagnosis of pseudogout?

A

Joint aspiration.

X-ray.

131
Q

What are the findings on joint aspiration in pseudogout?

A

No bacterial growth.
Rhomboid shaped crystals.
Positive birefringent of polarised light.
Calcium pyrophosphate crystals.

132
Q

What is the pathognomic finding on X-ray in pseudogout?

A

Chondrocalcinosis.

133
Q

What is osteoporosis?

A

A condition of reduced mineral bone density that increases the risk of fractures.

134
Q

What are risk factors for the development of osteoporosis?

A

Increasing age, female sex, reduced mobility and activity, Low BMI, rheumatoid arthritis, smoking, alcohol and medications.

135
Q

Give examples of medications that increase the risk of developing osteoporosis?

A

Long-term corticosteroids, SSRIs, PPIs, anti-epileptics and anti-oestrogens.

136
Q

Which group of women are particularly at risk of osteoporosis (and why)?

A

Post-menopausal women as they have less oestrogen (unless on HRT).

137
Q

What tool is used to predict bone fracture risk?

A

FRAX.

138
Q

What does the FRAX tool specifically predict?

A

10-year-probability of major osteoporotic fracture or hip fracture.

139
Q

What investigation is used in the assessment of osteoporosis?

A

DEXA scan.

140
Q

What is a DEXA scan?

A

Dual-energy X-ray absorptiometry measures bone mineral density.

141
Q

The measurement of bone mineral density at which area of the body is used in the classification and management of osteoporosis?

A

Hip.

142
Q

DEXA scan: What is a T score?

A

The number of standard deviations below the mean bone mineral density of a healthy young adult.

143
Q

DEXA scan: A T score of more than -1 means what?

A

BMD normal.

144
Q

DEXA scan: A T score of -1 to -2.5 means what?

A

Osteopenia.

145
Q

DEXA scan: A T score of less than -2.5 means what?

A

Osteoporosis.

146
Q

DEXA scan: A T score of less than -2.5 plus a fracture means what?

A

Severe osteoporosis.

147
Q

What lifestyle changes are advised in the management of osteoporosis?

A

Activity and exercise, maintain healthy weight, vitamin D supplements, calcium supplements, smoking cessation, alcohol consumption reduction.

148
Q

What class of medications are used in the management of osteoporosis?

A

Bisphosphonates.

149
Q

What is the function of bisphosphonates in the management of osteoporosis?

A

Interfere with osteoclasts and reduce their activity… preventing reabsorption of bone.

150
Q

What instructions should be given to people taking bisphosphonates for the management of osteoporosis?

A

Take on an empty stomach, sit upright for at least 30 minutes.

151
Q

Osteoporosis management: What are the potential risks of bisphosphonate use?

A

Oesophageal erosions.
Atypical fractures.
Osteonecrosis of the jaw.
Osteonecrosis of the external auditory canal.

152
Q

What is osteomalacia?

A

A condition of defective bone mineralisation that leads to ‘soft’ bones.

153
Q

What causes osteomalacia?

A

Vitamin D deficiency.

154
Q

What is the presentation of osteomalacia?

A

Bone pain, muscle weakness/aches and fractures.

155
Q

Describe the physiology of how vitamin D is produced.

A

Vit. D is a hormone produced from cholesterol by the skin in response to ultraviolet radiation. The kidneys metabolise vitamin D to its active form.

156
Q

Give examples of two conditions that can result in vitamin D deficiency.

A

Malabsorption (inflammatory bowel disease).

Chronic kidney disease.

157
Q

Describe why vitamin D is essential in normal physiology.

A

Vitamin D is essential for calcium and phosphate absorption from the intestines and kidneys. Inadequate vitamin D = lack of calcium and phosphate. which are both required for the construction of bone.

158
Q

What endocrine disorder can result from low calcium as a result of vitamin D deficiency?

A

Secondary hyperparathyroidism.

159
Q

What main investigation is performed in osteomalacia?

A

Serum 25-hydroxyvitamin D (< 25 mol/L indicates deficiency).

160
Q

Other than serum vitamin D what investigations are performed in osteomalacia (with results).

A 
Serum calcium (low). 
Serum phosphate (low).
Parathyroid hormone (raised).
Xray (osteopenia). 
DEXA scan (low bone mineral density).

Finals (11 decks)

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