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DrFeelGood Stuffs > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

How should allopurinol be started for treatment of gout?

A
  • indicated for all patients after first attack of gout
  • delay until inflammation settled (once no longer in pain - no specific time frame)
  • initial dose 100mg OD then titrated every few weeks to aim for serum uric acid <360 micromol/L
  • colchicine or NSAID cover should be considered
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2
Q

What is the initial starting dose of allopurinol for gout?

A

100mg OD then titrate dose every few weeks to aim serum uric acid less than 360 micromol/L

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3
Q

Which patients should have a lower target uric acid level (<300 micromol/L)?

A
  • those with tophi
  • chronic gouty arthritis
  • ongoing frequent flares despite uric acid <360
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4
Q

How long does the BSR suggest colchicine may need to be continued for when given as cover once allopurinol started?

A

may be needed for 6 months

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5
Q

What may be a protective factor from osteoporosis?

A

obesity - can convert androgens into oestrogen, helps maintain bone density

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6
Q

What is second-line when allopurinol is not effective?

A

febuxostat (if refractory: uricase, pegloticase)

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7
Q

For how long should NSAIDs be used when treating acute gout?

A

until 1-2 days after symptoms have settled

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8
Q

What is the mechanism of action of colchicine?

A

inhibits microtubule polymerisation by binding to tubulin (interfering with mitosis); also inhibits neutrophil motility and activity

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9
Q

What is the pathophysiology of gout?

A

caused by deposition of monosodium urate monohydrate in the synovium

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10
Q

Which foods should be avoided for gout?

A

liver, kidneys, seafood, oily fish (mackerel, sardines), yeast products

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11
Q

What drugs can precipitate gout?

A

thiazide diuretics

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12
Q

Which antihypertensive may be useful lin gout?

A

losartan - has specific uricosuric action

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13
Q

What will the findings of creatinine kinase and EMG be in polymyalgia rheumatica?

A

normal

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14
Q

In addition to glucocorticoids what are 6 medications that may worsen osteoporosis?

A
  1. SSRIs
  2. antiepileptics
  3. PPIs
  4. glitazones
  5. long term heparin therapy
  6. aromatase inhibitors e.g. anastrozole
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15
Q

What investigations should be requested for patients with osteoporosis?

A

FBC, ESR/CRP, calcium, albumin, creatinine, phosphate, ALP, LFTs, TFTs
DEXA (bone densitometry)

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16
Q

What is pseudogout?

A

deposition of calcium pyrophosphate dihydrate (CPPD) in and around joints - especially articular and fibrocartilage

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17
Q

What are 5 X-ray changes seen in rheumatoid arthritis?

A
  1. Loss of joint space
  2. Juxta-articular osteoporosis
  3. Subluxation
  4. Periarticular erosions
  5. Soft tissue swelling
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18
Q

What will radiographic changes show in pseudogout?

A

chondocalcinosis, linear opacification of articular cartilage

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19
Q

How many pseudogout present?

A

may be asymptomatic, or acute pseudogout episode or chronic arthritis

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20
Q

Which 3 joints are most commonly affected in pseudogout?

A

knees, wrists, hips

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21
Q

How is a diagnosis of acute pseudogout made?

A

compensated polarised microscopy on joint aspirate - crystals are rhomboid-shaped and weakly positively birefringent

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22
Q

What is the treatment of pseudogout?

A
  • aspiration of joint to reduce pain
  • NSAIDs
  • intraarticular steroid
  • systemic steroid
  • colchicine if NSAIDs/steroids CI
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23
Q

What is one of the most common presenting features of patients with systemic amyloidosis?

A

renal dysfunction

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24
Q

How is a diagnosis of amyloidosis made?

A
  • Congo red-binding material (bright green fluorescence observed under polarised light after Congo red staining) demonstrated in a biopsy specimen
  • biopsies from any affected organ - capillaries in subcutaneous fat often involved + provide sufficient tissue
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25
Q

What is the treatment available for amyloidosis?

A

no specific treatment; therapy aims to suppress underlying plasma cell dyscrasia + supportive measures for organ function

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26
Q

What is the definition of reactive arthritis?

A

arthritis that develops following an infection where the organism cannot be recovered from the joint (urethritis + arthritis +- conjunctivitis)

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27
Q

How long after initial symptoms of infection does reactive arthritis tend to develop?

A

4 weeks

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28
Q

How long do symptoms tend to last for in reactive arthritis?

A

4-6 months

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29
Q

What pattern of arthritis is seen in reactive arthritis?

A

asymmetrical oligoarthritis of lower limbs (+- dactylitis)

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30
Q

Which 2 forms of eye disease may be seen in reactive arthritis?

A
  1. conjunctivitis
  2. anterior uveitis
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31
Q

What are 2 dermatological manifestations of reactive arthritis?

A
  1. circinate balanitis (painless vesicles on coronal margin of prepuce)
  2. keratoderma blenorrhagica (waxy yellow/brown papules on palms and soles)
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32
Q

When should allopurinol be started after an acute attack of gout?

A

once inflammation settled and patient no longer in pain (no specific time frame)

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33
Q

What is the underlying pathology in gout?

A

microcystal synovitis caused by deposition of monosodium urate monohydrate in synovium; caused by chronic hyperuricaemia

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34
Q

How long should NSAIDs/ colchicine be used for in an acute attack of gout?

A

until 1-2 days after symptoms have settled

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35
Q

What is the main side effect of colchicine?

A

diarrhoea

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36
Q

What treatment may be considered in an acute attack of gout if colchicine and NSAIDs are contra-indicated?

A

oral steroids e.g. pred 15mg / day

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37
Q

What is the mechanism of action of febuxostat?

A

xanthine oxidase inhibitor

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38
Q

Which joint is most commonly affected by gout + in what proportion of cases?

A

1st metatarsophalangeal (MTP) joint - 70%

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39
Q

What does synovial fluid analysis show in gout?

A

needle-shaped negatively birefringent monosodium urate crystals under polarised light

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40
Q

When should uric acid levels be checked in gout?

A

once acute episode has settled - usually 2 weeks later (may be high, normal or low during attack)

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41
Q

What are 6 findings on x-ray in gout?

A
  1. joint effusion (early)
  2. punched out erosions with sclerotic margins in juxt-articular distribution + overhanging edges
  3. preservation of joint space until late
  4. eccentric erosions
  5. no periarticular osteopenia (seen in RA)
  6. soft tissue tophi
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42
Q

What is Schober’s test in ankylosing spondylitis?

A

line drawn 10cm above and 5cm back dimples (dimples of Venus) - distance between should increase by >5cm on bending - if less test positive

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43
Q

What are 3 features on clinical examination of ankylosing spondylitis?

A
  • reduced lateral flexion
  • positive Schober’s test
  • reduced chest expansion
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44
Q

What are 8 additional features of ankylosing spondylitis?

A
  1. Achilles tendonitis
  2. Anterior uveitis
  3. Aortic regurgitation
  4. Apical fibrosis
  5. AV node block
  6. Amyloidosis
  7. Cauda equina syndrome
  8. Peripheral arthritis
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45
Q

What are 3 side-effects of methotrexate?

A
  1. mucositis
  2. myelosuppression
  3. liver cirrhosis
  4. pneumonitis
  5. pulmonary fibrosis
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46
Q

What are 4 side effects of sulfasalazine?

A
  1. rashes
  2. oligospermia
  3. Heinz body anaemia
  4. interstitial lung disease
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47
Q

What are 3 side-effects of leflunomide?

A
  1. liver impairment
  2. interstitial lung disease
  3. hypertension
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48
Q

What are 2 side effects of hydroxychloroquine?

A
  1. retinopathy
  2. corneal deposits
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49
Q

What is a key side effect of gold (to treat RA)?

A

proteinuria

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50
Q

What are 2 side effects of penicillamine?

A
  1. proteinuria
  2. exacerbation of myasthenia gravis
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51
Q

What are 2 side effects of etanercept?

A
  1. demyelination
  2. reactivation of tuberculosis
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52
Q

What is a side effect of infliximab?

A

reactivation of tubcerulosis

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53
Q

What is a side effect of adalimumab?

A

reactivation of tubcerulosis

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54
Q

What is a side effect of rituximab?

A

infusion reactions common

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55
Q

How useful is serum HLA-B27 for diagnosing ankylosing spondylitis?

A

not useful - positive in 90% of patients with AS but also 10% of normal patients

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56
Q

What is the most useful investigation to establish a diagnosis of ankylosing spondylitis?

A

plain x-ray of sacroiliac joints

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57
Q

What are 5 radiograph changes in ankylosing spondylitis?

A
  1. sacroiliitis - subchondral erosions, sclerosis
  2. squaring of lumbar vertebrae
  3. bamboo spine (late + uncommon)
  4. syndesmophytes - due to ossification fo outer fibres of annulus fibrosus
  5. CXR - apical fibrosis
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58
Q

What should be done if xray is negative for sacroiliac joints in suspected ankylosing spondylitis, but suspicion is still high?

A

MRI - can show signs of early inflammation involving sacroiliac joints (bone marrow oedema)

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59
Q

What may be seen in spirometry in ankylosing spondylitis and why?

A

restrictive defect - combination fo pulmonary fibrosis, kyphosis, ankylosis of costovertebral joints

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60
Q

What is the first line management of ankylosing spondylitis?

A

encourage regular exercise, physiotherapy, & NSAIDs

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61
Q

What is the only time disease-modifying drugs are useful in ankylosing spondylitis and what are examples?

A

if there is peripheral joint involvement - sulfasalazine

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62
Q

What drug is suggested to treat ankylosing spondylitis by EULAR guidelines if disease activity is high despite conventional treatment?

A

anti-TNF e.g. etanercept, adalimumab

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63
Q

What is the management of fragility fractures (e.g. fractured NOF, Colles) aged over 75 vs under 75?

A
  • > 75y: start bisphosphonate (e.g. alendronate) without waiting for DEXA
  • <75y: DEXA scan - input results into FRAX
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64
Q

What is the initial step for management of chronic stable RA?

A
  • DMARD monotherapy +- short course of bridging prednisolone: methotrexate most common (sulfasalazine/ leflunomide/ hydroxychloroquine)
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65
Q

What are 4 examples of DMARDs used for RA?

A
  1. methotrexate
  2. sulfasalazine
  3. leflunomide
  4. hydroxychloroquine
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66
Q

What monitoring is essential for patients on methotrexate and why?

A
  • FBC, U+E + LFT: risk of myelosuppression + liver cirrhosis
  • every week until therapy stabilised, then 2-3 monthly

other SE: pneumonitis

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67
Q

When is hydroxychloroquine considered for initial therapy in RA?

A

mild or palindromic disease

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68
Q

What is used to monitor response to treatment in RA?

A

CRP + disease activity (using composite score such as DAS28)

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69
Q

How is a flare of rheumatoid arthritis managed?

A

course of corticosteroids - oral or IM

70
Q

What is the indication for TNF-inhibitor use in RA?

A

inadequate response to at least 2 DMARDs including methotrexate

71
Q

What are 3 examples of TNF-inhibitors that can be used for RA?

A
  1. etanercept
  2. infliximab
  3. adalimumab
72
Q

How does etanercept work to treat RA?

A

recombinant human protein, acts as decoy receptor for TNF-alpha. given s/c

73
Q

How does infliximab work to treat RA?

A

monoclonal antibody, binds TNF-alpha and prevents it from binding with TNF receptors. IV administration

74
Q

How does adalimumab work to treat RA?

A

monoclonal ab, subcutaneous injection

75
Q

What are 3 types of biological therapies for RA?

A
  • TNF-inhibitors
  • rituximab (anti-CD20 monoclonal ab)
  • abatacept (influences T lymphocytes)
76
Q

How does rituximab work to treat RA?

A

anti-CD20, results in B-cell depletion. 2 x 1g IV infusion given 2 weeks apart

77
Q

How does abatacept work to treat RA?

A

fusion protein that modulates key signal required for activation of T lymphocytes. leads to decrease T-cell proliferation and cytokine production. given as infusion

78
Q

What is the inheritance pattern of Marfan’s syndrome?

A

autosomal dominant

79
Q

What genetic defect is responsible for Marfan’s?

A

defect in FBN1 gene on chromosome 15 - codes for protein fibrillin-1

80
Q

What is the typical arm span to height ratio in Marfan’s?

A

1.05

81
Q

What are 4 heart-related abnormalities seen in Marfan’s?

A
  1. Aortic aneurysm
  2. Aortic dissection
  3. Aortic regurgitation
  4. Mitral valve prolapse
82
Q

What are 3 ocular abnormalities seen in Marfan’s?

A
  1. Upwards lens dislocation (superotemporal ectopia lentis)
  2. Blue sclera
  3. Myopia
83
Q

What CNS abnormality may be seen in Marfan’s?

A

dural ectasia - ballooning of dural sac at the lumbosacral level

84
Q
A
85
Q

What is the mechanism of action of methotrexate?

A

Antimetabolite that inhibits dihydrofolate reductase, an enzyme responsible for synthesis of purines and pyramidines

86
Q

What is the most common pulmonary manifestation of methotrexate?

A

Pneumonitis

87
Q

What pattern of pneumonitis is seen with methotrexate use?

A

Similar to hypersensitivity pneumonitis secondary to inhaled organic antigens

88
Q

How quickly does pneumonitis secondary to methotrexate develop?

A

Within a year of starting treatment, either acutely or subacutely

89
Q

How does methotrexate induced pneumonitis tend to present?

A

Non-productive cough, dyspnoea, fever, malaise

90
Q

What is the guidance on avoiding pregnancy and methotrexate use?

A

Women need to avoid becoming pregnant during and for 6 months after treatment; men should use effective contraception for 6 months after treatment

91
Q

What should be co-prescribed in anyone taking methotrexate?

A

Folic acid 5mg once weekly (taken >24h after methotrexate dose)

92
Q

What is the starting dose of methotrexate?

A

7.5mg once weekly (only one strength of tablet e.g. 2.5mg should be prescribed)

93
Q

What are 2 important interactions of methotrexate?

A
  1. Trimethoprim or co-trimoxazole - increased risk of marrow aplasia
  2. High dose aspirin - increases risk of methotrexate toxicity (reduced renal excretion)
94
Q

What is the treatment of choice for methotrexate toxicity?

A

Folinic acid

95
Q

What are 2 tests that should be performed before starting biologics for RA e.g. adalimumab, etanercept?

A
  • CXR
  • tubculin skin test / IGRA

looking for TB - can cause reactivation

96
Q

Which patients should be assessed using FRAX / QFracture?

A
  • all women over 65, all men over 75
  • younger patients in the presence of risk factors (8):
    1. previous fragility fracture
    2. current use or frequent recent use of systemic glucocorticoid
    3. h/o falls
    4. FH hip fracture
    5. other causes of secondary osteoporosis
    6. low BMI <18.5
    7. smoking
    8. alcohol >14 units / week
97
Q

Which ages are the FRAX and QFracture tools validated for?

A
  • FRAX: 40-90 years
  • Qfracture: 30-99 years
98
Q

What investigation improves the accuracy of the results from FRAX?

A

bone mineral density

99
Q

When should DEXA scan be performed based on FRAX (without BMD)?

A

if FRAX shows an intermediate result

100
Q

Which of FRAX and QFracture includes a larger group of risk fractures?

A

QFracture

101
Q

What are 2 situations when NICE recommend using BMD rather than FRAX?

A
  1. before starting treatments that can rapidly affect bone density e.g. sex hormone deprivation for treatment for breast/prostate cancer
  2. <40 years with major risk factor e.g. multiple fragility fracture, major osteoporotic fracture, high-dose systemic steroids
102
Q

Waht is considered high-dose systemic glucocorticoid therapy?

A

more than 7.5 mg prednisolone or equivalent per day for 3 months or longer

103
Q

How is the result of FRAX assessment without bone mineral density interpreted?

A
  • low risk: reassure, lifestyle advice
  • intermediate: BMD test
  • high risk: offer bone protection
104
Q

How is the management determined by FRAX score with bone mineral density, based on the result?

A

automatically categorised into
* reassure
* consider treatment
* strongly recommend treatment

105
Q

How is the result from QFracture score interpreted?

A

not automatically categorised into low/intermediate/high risk - raw data given for 10 year risk, needs to be interpreted alongside local or national guidelines

106
Q

What are 2 situations when the FRAX/QFracture score should be re-calculated?

A
  1. if original risk was in region of intervention threshold for proposed treatment and only after minimum 2 years
  2. change in person’s risk factors
107
Q

What is usually the first-line antibody test for suspected RA?

A

Rheumatoid factor (RF)

108
Q

What are 2 tests for Rheumatoid factor?

A
  1. Rose-Waaler test - sheep red cell agglutination
  2. Latex agglutination test
109
Q

What are high levels of RF in rheumatoid arthritis associated with?

A

severe progressive disease (but not marker of disease activity)

110
Q

What are 10 conditions in addition to RA that RF is positive in?

A
  1. Felty’s syndrome (around 100%)
  2. Sjogren’s syndrome (around 50%)
  3. infective endocarditis (around 50%)
  4. SLE (= 20-30%)
  5. systemic sclerosis (= 30%)
  6. general population (= 5%)
  7. TB
  8. HBV
  9. EBV
  10. leprosy
111
Q

What is the most specific antibody test for RA?

A

anti-CCP

112
Q

When may anti-CCP be detectable in RA?

A

may be detectable up to 10 years before development of RA

113
Q

What is the sensitivity of RF and anti-CCP for RA?

A

both 70-75%

114
Q

What radiology do NICE recommend in all patients with suspected RA?

A

xray hands and feet

115
Q

What are 4 general features of SLE?

A
  1. fatigue
  2. fever
  3. mouth ulcers
  4. lymphadenopathy
116
Q

What are 6 dermatological manifestations of SLE?

A
  1. malar rash - spares nasolabial folds
  2. discoid rash - erythematous, well demarcated rash in sun-exposed areas
  3. photosensitivity
  4. raynaud’s phenomenon
  5. livedo reticularis
  6. non-scarring alopecia
117
Q

What may be the progression of the discoid rash seen in SLE?

A

can become pigmented and hyperkeratotic, then become atrophic

118
Q

What are 2 MSK features of SLE?

A
  1. arthralgia
  2. non-erosive arthritis
119
Q

What are 2 cardiovasular features of SLE?

A
  1. pericarditis
  2. myocarditis
120
Q

What are 2 respiratory features of SLE?

A
  1. pleurisy
  2. fibrosing alveolitis
121
Q

What are 2 renal features of SLE?

A
  1. proteinuria
  2. glomerulonephritis
122
Q

What is the commonest type of glomerulonephritis seen in SLE?

A

diffuse proliferative glomerulonephritis

123
Q

What are 3 neuropsychiatric features of SLE?

A
  1. anxiety and depression
  2. psychosis
  3. seizures
124
Q

What is the scale of low glucocorticoid activity/high mineralocorticoid activity to the other end of the scale in terms of specific steroids?

A
  • fludrocortisone
  • hydrocortisone
  • prednisolone
  • dexamethasone
  • betmethasone
125
Q

Does an asymmetrical presentation of joint inflammation (e.g. L knee and R MCP joint involvement) suggest rheumatoid arthritis or psoriatic arthritis?

A

psoriatic

126
Q

What proportion of patients with psoriatic skin lesions develop parthropathy?

A

10-20%

127
Q

What are 5 different patterns of psoriatic arthropathy?

A
  1. symmetric polyarthritis (30-40%)
  2. asymmetrical oligoarthritis (20-30%)
  3. sacroiliitis
  4. DIP joint disease (10%)
  5. arthritis mutilans (telescoping fingers)
128
Q

What are 3 examples of periarticular disease seen in psoriatic arthropathy?

A
  1. enthesitis (Achilles tendonitis, plantar fascitis)
  2. tenosynovitis
  3. dactylitis
129
Q

What are 3 xray findings in psoriatic arthropathy?

A
  1. erosive changes and new bone formation in coexistence
  2. periostitis
  3. pencil in cup appearance
130
Q

Who should manage psoriatic arthropathy?

A

rheumatologist

131
Q

What are 4 features of the management of psoriatic arthropathy that differ from/are similar to RA?

A
  1. mild peripheral arthritis/mild axial disease may be treated with ‘just’ an NSAID, rather than all patients being on disease-modifying therapy as with RA
  2. if more moderate/severe disease then methotrexate is typically used as in RA
  3. use of monoclonal antibodies such as ustekinumab (targets both IL-12 and IL-23) and secukinumab (targets IL-17)
  4. apremilast: phosphodiesterase type-4 (PDE4) inhibitor
132
Q

How does the prognosis of psoriatic arthropathy compare to RA?

A

better in psoriatic

133
Q

What malignancy is linked to Sjogren’s syndrome?

A

lymphoid malignancy

134
Q

What are 4 blood tests positive Sjogren’s syndrome and in what proportion?

A
  1. RF (50%)
  2. ANA positive (70%)
  3. Anti-Ro (70%)
  4. Anti-La (30%)
135
Q

What will histology show in Sjogren’s syndrome?

A

focal lymphocytic infiltration

136
Q

What are 2 aspects of the management of Sjogren’s syndrome?

A
  1. Artificial saliva + tear
  2. Pilocarpine may stimulate saliva production
137
Q

What are 3 conditions associated with Sjogren’s syndrome?

A
  1. Rheumatoid arthritis
  2. SLE
  3. connective tissue disorders
138
Q

What will bone tests show in Paget’s disease?

A
  • raised ALP
  • normal calcium, phosphate, PTH
139
Q

What is osteomalacia?

A

softening of bones secondary to low vitamin D levels, in turn leads to decreased bone mineral content

140
Q

What are 6 causes of osteomalacia?

A
  1. vitamin D deficiency - malabsorption, lack of sunlight, diet
  2. chronic kidney disease
  3. drug-induced e.g. anticonvulsants
  4. inherited - hypophosphataemic rickets
  5. liver disease e.g. cirrhosis
  6. coeliac disease
141
Q

What are the key features of osteomalacia?

A

bone pain, muscle tenderness, fractures (femoral neck), proximal myopathy

142
Q

What do bloods show in osteomalacia?

A
  • low vitamin D
  • low calcium
  • low phosphate
  • raised ALP
143
Q

What can be seen on xray in osteomalacia?

A

translucent bands (Looser’s zones or pseudofractures)

144
Q

What is the management of osteomalacia?

A

vitamin D supplementation (loading dose often used)
calcium supplementation if diet intake inadequate

145
Q

What are 2 groups NICE divide patients into for those at risk of corticosteroid-induced osteoporosis?

A
  1. Patients >65 years OR who previously had fragility fracture - offer bone protection
  2. < 65 y - offer bone density scan

If > 0: reassure
0 to -1.5: repeat bone desntity scan in 1-3 years
< - 1.5: bone protection

146
Q

What is the management in patients at risk of corticosteroid induced osteoporosis based on the bone density scan?

A

If > 0: reassure
0 to -1.5: repeat bone desntity scan in 1-3 years
< - 1.5: bone protection

147
Q

Which patients are deemed at risk of corticosteroid-induced osteoporosis

A

daily steroid equivalent to > 7.5 mg prednisolone / day for 3 months or more

148
Q

What are 4 adverse effects of azathioprine?

A
  1. bone marrow depression
  2. nausea / vomiting
  3. pancreatitis
  4. increased risk of non-melanoma skin cancer
149
Q

Which drug can azathioprine have a significant reaction with and what should be done?

A

allopurinol - use lower doses of azathioprine

150
Q

Is azathioprine safe to use in pregnancy?

A

yes

151
Q

What are 6 key adverse effects of bisphosphonates?

A
  1. oesophageal reactions - oesophagitis, ulcers
  2. osteonecrosis of the jaw
  3. atypical stress fractures of proximal femoral shaft
  4. acute phase response - fever, myalgia, arthralgia
  5. hypocalcaemia
152
Q

What is the guidance for how to take bisphosphonates?

A
  • swallowed whole with water, sitting or standing
  • take on empty stomach at least 30 minutes before breakfast or oral medication
  • stand or sit upright for at least 30 minutes after taking tablet’
153
Q

What should always be checked before giving bisphosphonates?

A

check for + correct hypocalcaemia + vitamin D deficiency

ca only prescribed if dietary intake inadequate - vit D normally given

154
Q

What is the duration of bisphosphonate therapy?

A

stop at 5 years if the following apply:
* patient is < 75-years-old
* femoral neck T-score of > -2.5
* low risk according to FRAX/NOGG

155
Q

What are 7 causes of raised ALP?

A
  1. liver: cholestasis, hepatitis, fatty liver, neoplasia
  2. Paget’s
  3. osteomalacia
  4. bone metastases
  5. hyperparathyroidism
  6. renal failure
  7. physiological: pregnancy, growing children, healing fractures
156
Q

What are 6 skin features of dermatomyositis?

A
  1. photosensitive
  2. macular rash over back and shoulder
  3. heliotrope rash in the periorbital region
  4. Gottron’s papules - roughened red papules over extensor surfaces of fingers
  5. ‘mechanic’s hands’: extremely dry and scaly hands with linear ‘cracks’ on the palmar and lateral aspects of the fingers
  6. nail fold capillary dilatation
157
Q

What are 4 blood test markers which may be present in dermatomyositis?

A
  1. ANA (80%)
    aminoacyl-tRNA synthetases (anti-synthetase) antibodies (30%):
  2. anti-Jo1
  3. anti-SRP
  4. anti-Mi-2
158
Q

What are 2 drugs recommended if patients cannot tolerate bisphosphonates?

A

strontium ranelate and raloxifene

159
Q

What type of drug is raloxifene?

A

selective oestrogen receptor modulator (SERM)

160
Q

What are 2 risks of raloxifene?

A
  1. may worsen menopausal symptoms
  2. increased risk of thromboembolic events
161
Q

What type of cancer may raloxifene decrease the risk of?

A

breast cancer

162
Q

What is the mechanism of action of strontium ranelate?

A

dual action bone agent: increases deposition of new bone by osteoblasts (promotes differentiation of pre-osteoblast to osteoblast) and reduced resoprtion of bone by inhibiting osteoclasts

163
Q

When should strontium ranelate be used for osteoporosis?

A

only when no other treatments that can be used due to concerns regarding safety profile

164
Q

What are 3 risks of strontium ranelate?

A
  1. increased risk of cardiovascular events
  2. increased risk of thromboembolic events
  3. serious skin reactions e.g. SJS
165
Q

What is the mechanism of denosumab?

A

human monoclonal antibody that inhibits RANK ligand - this inhibits maturation of osteoclasts

166
Q

Which antibodies are a good indicator of diffuse cutaneous systemic sclerosis?

A

Anti-Scl-70

167
Q

Which antibodies are a good indicator of limited cutaneous systemic sclerosis?

A

anti-centromere antibodies

168
Q

What is another name for CREST syndrome?

A

limited cutaneous systemic sclerosis

169
Q

What type of antibody is rheumatoid factor?

A

IgM

170
Q

What is the only type of antibody that can cross the placenta?

A

IgG

171
Q

What are 6 conditions that anticardiolipin antibodies are present in?

A
  1. antiphospholipid syndrome
  2. SLE
  3. ITP
  4. RA
  5. psoriatic arthritis
  6. Sjogrens syndrome
172
Q

What is Felty syndrome?

A

occurs in some cases of rheumatoid arthritis
SANTA mnemonic:
S: splenomegaly
A: anaemia
N: neutropenia
T: thrombocytopenia
A: arthritis (rheumatoid)

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