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ORTEM > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

How do you treat raynaud’s disease?

A
  • first-line: calcium channel blockers e.g. nifedipine, amlodipine
  • IV prostacyclin (epoprostenol) infusions: effects may last several weeks/months
  • sildenafil
  • SSRI (fluoxetine)
  • if v bad cut nerve fibres to hand
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2
Q

What are the factors that suggest an underlying connective tissue disease for raynauds?

A
  • onset after 40 years
  • unilateral symptoms
  • rashes
  • presence of autoantibodies
  • features which may suggest rheumatoid arthritis or SLE, for example arthritis or recurrent miscarriages
  • digital ulcers, calcinosis
  • very rarely: chilblains
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3
Q

How should you manage OA?

A
  • all patients should be offered help with weight loss, given advice about local muscle strengthening exercises and general aerobic fitness
  • paracetamol and topical NSAIDs are first-line analgesics. Topical NSAIDs are indicated only for OA of the knee or hand
  • second-line treatment is oral NSAIDs/COX-2 inhibitors, opioids, capsaicin cream and intra-articular corticosteroids. A proton pump inhibitor should be co-prescribed with NSAIDs and COX-2 inhibitors. These drugs should be avoided if the patient takes aspirin
  • non-pharmacological treatment options include supports and braces, TENS and shock absorbing insoles or shoes
  • if conservative methods fail then refer for consideration of joint replacement
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4
Q

What levels of uric acid would you expect in the blood for gout?

A

uric acid > 0.45 mmol/l

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5
Q

Who and how do you treat osteoporosis?

A
  • treatment is indicated following osteoporotic fragility fractures in postmenopausal women who are confirmed to have osteoporosis (a T-score of - 2.5 SD or below). In women aged 75 years or older, a DEXA scan may not be required ‘if the responsible clinician considers it to be clinically inappropriate or unfeasible’
  • vitamin D and calcium supplementation should be offered to all women unless the clinician is confident they have adequate calcium intake and are vitamin D replete
  • alendronate is first-line
  • around 25% of patients cannot tolerate alendronate, usually due to upper gastrointestinal problems. These patients should be offered risedronate or etidronate (see treatment criteria below)
  • strontium ranelate and raloxifene are recommended if patients cannot tolerate bisphosphonates (see treatment criteria below)
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6
Q

Give examples of bisphosphonates

A

Alendronate
Risedronate
Etidronate

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7
Q

Who gets ankylosing spondylitis?

What are the features?

A
  • 90% are HLA-B27 positive
  • males (sex ratio 3:1)
  • aged 20-30 years old
  • typically a young man who presents with lower back pain and stiffness of insidious onset (spares hands and feet)
  • stiffness is usually worse in the morning and improves with exercise
  • the patient may experience pain at night which improves on getting up
  • tendon disease
  • enthesitis
  • plantar fascitis
  • rash
  • bowels
  • eyes- anterior uveitis
  • lose lumbar lordosis
  • exaggerated kyphosis
  • knee flexion
    => question mark posture
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8
Q

What x-ray changes do you see for ankylosing spondylitis?

A
  • sacroilitis: subchondral erosions, sclerosis
  • squaring of lumbar vertebrae
  • ‘bamboo spine’ (late & uncommon) (a single central radiodense line related to ossification of supraspinous and interspinous ligaments which is called dagger sign)
  • syndesmophytes: due to ossification of outer fibers of annulus fibrosus
  • chest x-ray: apical fibrosis
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9
Q

How do you manage ankylosing spondylitis?

A
  • encourage regular exercise such as swimming
  • physiotherapy
  • NSAIDs are the first-line treatment
  • the disease-modifying drugs which are used to treat rheumatoid arthritis (such as sulphasalazine) are only really useful if there is peripheral joint involvement
  • the 2010 EULAR guidelines suggest: ‘Anti-TNF therapy should be given to patients with persistently high disease activity despite conventional treatments’ (if 2 x NSAIDS + BASDAI >4 then use biologics)
  1. anti TNF
  2. anti IL17 secukinumab
  3. anti IL12/23 Ustekinumab
  • research is ongoing to see whether anti-TNF therapies such as etanercept and adalimumab should be used earlier in the course of the disease
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10
Q

What conditions are associated with ankylosing spondylitis?

A 
Achiles disease
Aortic regurg (LVH)
AV node block so conduction abnormalities
Apical pulmonary fibrosis
Anterior uveitis
Amyloidosis
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11
Q

What are the features of drug induced lupus?

A
  • arthralgia
  • myalgia
  • skin (e.g. malar rash) and pulmonary involvement (e.g. pleurisy) are common
  • ANA positive in 100%, dsDNA negative
  • anti-histone antibodies are found in 80-90%
  • anti-Ro, anti-Smith positive in around 5%
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12
Q

What are the features of sjorgrens syndrome?

A
  • primary (PSS) or secondary to rheumatoid arthritis or other connective tissue disorders, where it usually develops around 10 years after the initial onset
  • females:males (ratio 9:1).
  • increased risk of lymphoid malignancy (40-60 fold).
  • dry eyes: keratoconjunctivitis sicca
  • dry mouth
  • vaginal dryness
  • arthralgia
  • Raynaud’s, myalgia
  • sensory polyneuropathy
  • recurrent episodes of parotitis
  • renal tubular acidosis (usually subclinical)
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13
Q

What investigations would you do for sjorgrens?

A
  • rheumatoid factor (RF) positive in nearly 100% of patients
  • ANA positive in 70%
  • anti-Ro (SSA) antibodies in 70% of patients with PSS
  • anti-La (SSB) antibodies in 30% of patients with PSS
  • Schirmer’s test: filter paper near conjunctival sac to measure tear formation
  • histology: focal lymphocytic infiltration
  • also: hypergammaglobulinaemia, low C4
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14
Q

How many different non-steroidal anti-inflammatory drugs must a patient with ankylosing spondylitis have failed to respond to before he can be started on anti-TNF alpha inhibitors, in someone with predominantly axial disease?

A

Anti-TNF alpha inhibitors should be used in axial ankylosing spondylitis that has failed on 2 different NSAIDS and meets criteria for active disease on 2 occasions 12 weeks apart

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15
Q

What auto-antibodies would you expect to be present in SLE?

A
  • 99% are ANA positive
  • 20% are rheumatoid factor positive
  • anti-dsDNA: highly specific (> 99%), but less sensitive (70%)
  • anti-Smith: most specific (> 99%), sensitivity (30%)
  • also: anti-U1 RNP (mixed connective tissue disease), SS-A (anti-Ro) and SS-B (anti-La)

If Ro positive you can get fetal heart block so monitor in pregnancy

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16
Q

What monitoring would you do for SLE?

A
  • ESR: during active disease the CRP is characteristically normal - a raised CRP may indicate underlying infection
  • complement levels (C3, C4) are low during active disease (formation of complexes leads to consumption of complement)
  • anti-dsDNA titres can be used for disease monitoring (but note not present in all patients)
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17
Q

What are the risk factors for pseudo gout?

A

WHALe MP

  • hyperparathyroidism
  • hypothyroidism
  • haemochromatosis
  • acromegaly
  • low magnesium, low phosphate
  • Wilson’s disease
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18
Q

What are the features of pseudo gout? And how do you manage it?

A

Features

  • knee, wrist and shoulders most commonly affected
  • joint aspiration: weakly-positively birefringent rhomboid shaped crystals
  • x-ray: chondrocalcinosis

Management

  • aspiration of joint fluid, to exclude septic arthritis
  • NSAIDs or intra-articular, intra-muscular or oral steroids as for gout
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19
Q

What are the features of reactive arthritis?

A
  • typically develops within 4 weeks of initial infection - symptoms generally last around 4-6 months
  • arthritis is typically an asymmetrical oligoarthritis of lower limbs
  • dactylitis
  • symptoms of urethritis
  • eye: conjunctivitis (seen in 10-30%), anterior uveitis
  • skin: circinate balanitis (painless vesicles on the coronal margin of the prepuce), keratoderma blenorrhagica (waxy yellow/brown papules on palms and soles)
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20
Q

What are the features of OA on x-ray?

A
  • decrease of joint space
  • subchondral sclerosis
  • subchondral cysts
  • osteophytes forming at joint margins
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21
Q

What’s the first line treatment for RA?

A

DMARD monotherapy +/- a short-course of bridging prednisolone

Monitoring of FBC & LFTs is essential due to the risk of myelosuppression and liver cirrhosis. Other important side-effects include pneumonitis

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22
Q

What are the features of antiphospholipid syndrome?

A
  • venous/arterial thrombosis
  • recurrent fetal loss
  • livedo reticularis
  • thrombocytopenia
  • prolonged APTT
  • other features: pre-eclampsia, pulmonary hypertension
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23
Q

What’s the diagnosis?

dactylitis and a first- degree relative with psoriasis, DIP affected, nail changes

A

Psoriatic arthritis

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24
Q

What can cause dactylitis?

A
  • spondyloarthritis: e.g. Psoriatic and reactive arthritis
  • sickle-cell disease
  • other rare causes include tuberculosis, sarcoidosis and syphilis
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25
Q

Which antibody is associated with limited cutaneous systemic sclerosis?

A

Anti-centromere

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26
Q

Which antibody is associated with diffuse systemic sclerosis?

A

Anti-Scl-70

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27
Q

What are the features of dermato/myositis?

A

Overview

  • symmetrical, proximal muscle weakness and characteristic skin lesions
  • polymyositis is a variant of the disease where skin manifestations are not prominent
  • may be idiopathic or associated with connective tissue disorders or underlying malignancy (typically ovarian, breast and lung cancer, found in 20-25% - more if patient older)

Skin features

  • photosensitive
  • macular rash over back and shoulder (shawl sign)
  • heliotrope rash in the periorbital region
  • mechanics’ hands
  • Gottron’s papules - roughened red papules over extensor surfaces of fingers, elbows, knees
  • nail fold capillary dilatation

Other features

  • myalgia of proximal muscles +/- arthralgia
  • dysphagia
  • dysphonia
  • resp muscle weakness
  • interstitial lung disease: e.g. Fibrosing alveolitis or organising pneumonia
  • myocarditis
  • arrhythmias
  • CK in 1000s!
  • Raynaud’s
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28
Q

What antibodies are seen in dermatomyositis?

A
  • most are ANA +ve
  • 25% are anti-Mi2 +ve
  • anti-Jo1 +ve
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29
Q

How do you treat Paget’s disease?

A

bisphosphonate (either oral risedronate or IV zoledronate)

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30
Q

What are the poor prognostic factors for RA?

A
  • rheumatoid factor positive
  • anti-CCP antibodies
  • insidious onset
  • systemic features
  • extra articular features e.g. nodules
  • poor functional status at presentation
  • HLA DR4
  • X-ray: early erosions (e.g. after < 2 years)
  • persistent disease > 12 months
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31
Q

What investigations and treatment would you give for polymyalgia rheumatica?

A

Investigations

  • ESR > 40 mm/hr
  • note CK and EMG normal
  • reduced CD8+ T cells

Treatment
- prednisolone e.g. 15mg/od - dramatic response

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32
Q

If an older patient presents with dermatomyositis what should you rule out?

A

ovarian, breast and lung tumours (paraneoplastic disease)

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33
Q

If bisphosphonates are given for a fragility fracture, when can you stop them?

A

At 5 years if:

  • patient is < 75-years-old
  • femoral neck T-score of > -2.5
  • low risk according to FRAX/NOGG
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34
Q

What are the complications of RA?

A

A wide variety of extra-articular complications occur in patients with rheumatoid arthritis (RA):
- respiratory: pulmonary fibrosis, pleural effusion, pulmonary nodules, bronchiolitis obliterans, methotrexate pneumonitis, pleurisy
- ocular: keratoconjunctivitis sicca (most common), episcleritis, scleritis, corneal ulceration, keratitis, steroid-induced cataracts, chloroquine retinopathy
osteoporosis
- ischaemic heart disease: RA carries a similar risk to type 2 diabetes mellitus
- increased risk of infections
- depression

Less common

  • Felty’s syndrome (RA + splenomegaly + low white cell count)
  • amyloidosis
35
Q

What are the types of osteomalacia?

A
  • vitamin D deficiency e.g. malabsorption, lack of sunlight, diet
  • renal failure
  • drug induced e.g. anticonvulsants
  • vitamin D resistant; inherited
  • liver disease, e.g. cirrhosis
36
Q

What are the investigations and treatment for osteomalacia/rickets?

A

Investigation

  • low 25(OH) vitamin D (in 100% of patients, by definition)
  • raised alkaline phosphatase (in 95-100% of patients)
  • low calcium, phosphate (in around 30%)
  • x-ray: children - cupped, ragged metaphyseal surfaces; adults - translucent bands (Looser’s zones or pseudofractures)

Treatment
- calcium with vitamin D tablets

37
Q

How do you manage gout acutely?

A
  • NSAIDs or colchicine are first-line
  • the maximum dose of NSAID should be prescribed until 1-2 days after the symptoms have settled. Gastroprotection (e.g. a proton pump inhibitor) may also be indicated
  • colchicine* has a slower onset of action. The main side-effect is diarrhoea
  • oral steroids may be considered if NSAIDs and colchicine are contraindicated. A dose of prednisolone 15mg/day is usually used
  • another option is intra-articular steroid injection
    if the patient is already taking allopurinol it should be continued

Urate-lowering therapy

  • allopurinol is first-line- titrate up
  • it has traditionally been taught that urate-lowering therapy should not be started until 2 weeks after an acute attack, as starting too early may precipitate a further attack. The evidence base to support this however looks weak
  • in 2017 the BSR updated their guidelines. They still support a delay in starting urate-lowering therapy because it is better for a patient to make long-term drug decisions whilst not in pain
  • initial dose of 100 mg od, with the dose titrated every few weeks to aim for a serum uric acid of < 300 µmol/l. Lower initial doses should be given if the patient has a reduced eGFR
  • colchicine cover should be considered when starting allopurinol. NSAIDs can be used if colchicine cannot be tolerated. The BSR guidelines suggest this may need to be continued for 6 months
  • the second-line agent when allopurinol is not tolerated or ineffective is febuxostat (also a xanthine oxidase inhibitor)
38
Q

What are the side effects of bisphosphonates?

A
  • oesophageal reactions: oesophagitis, oesophageal ulcers (especially alendronate)
  • osteonecrosis of the jaw
  • increased risk of atypical stress fractures of the proximal femoral shaft in patients taking alendronate
  • acute phase response: fever, myalgia and arthralgia may occur following administration
  • hypocalcaemia: due to reduced calcium efflux from bone. Usually clinically unimportant
39
Q

Myositis with +ve anti-Jo1 antibodies can predispose to which condition?

A

lung fibrosis

40
Q

Azathioprine and allopurinol have a severe interaction causing what?

A

bone marrow suppression

41
Q

How do you manage patients at risk of steroid induced osteoporosis?

A

Dexa scan (T score)

Greater than 0
Reassure

Between 0 and -1.5
Repeat bone density scan in 1-3 years

Less than -1.5
Offer bone protection

The first-line treatment is alendronate. Patients should also be calcium and vitamin D replete.

42
Q

What are the x-ray changes for RA?

A

Early x-ray findings

  • loss of joint space
  • juxta-articular osteoporosis
  • soft-tissue swelling

Late x-ray findings

  • periarticular erosions
  • subluxation
43
Q

When would you see dactylitis?

A

Psoriatic arthritis
Sarcoid
Sickle cell (most common cause)

44
Q

Which conditions are associated with enthesis?

A

Psoriatic arthritis

Ankylosing spondylitis

45
Q

What facts do you know about rheumatoid nodules?

A
  • definitively RF positive
  • more likely to be smokers
  • more likely to be resistant to biologics
  • methotrexate makes nodular disease worse
46
Q

What proportion of SLE patients have antiphospholipid syndrome?

A

1/3

47
Q

What does pericarditis look like on ECG?

A

Saddle shaped ST elevation in anterior leads

48
Q

What does mycophenolate do if a mother has it when pregnant?

A

Baby is born with small ears

49
Q

How do you investigate pulmonary hypertension for SLE?

A
  • Gold standard is catheterisation

- ECHO shows large R heart, tricuspid valve gets pulled apart, check ejection pressure

50
Q

How is the DAS28 score calculated?

A
  • 28 joints (swelling, tender)
  • ESR/CRP
  • visual analogue score

<2.6 remission
>5.1 severe

51
Q

Which conditions have overlapping features?

A 
IBD (Rash: erythema nodosa, pyoderma pyoderma gangrenosum, Bowels: GI, Eyes: iritis, anterior uveitis)
Reactive A (Rash: circinate balanitis, keratoderma blenorhagia, Bowels: yes/no, Eyes: anterior uveitis)
Psoriasis (Rash: yes, Bowels: x, Eyes: x)
Ankylosing spondylosis (Eyes: anterior uveitis)
52
Q

What are the features of anterior uveitis?

A
  • photophobic
  • injection
  • wonky pupil- sticks to iris
  • cillary muscle inflammation
  • hypopyon
53
Q

What’s used to help assess ankylosing spondylitis?

A

Bath ankylosing spondylitis metrology index (BASMI)

  • cervical rotation
  • wall to tragus
  • thoracic chest expansion
  • lumbar- Schober’s
  • lateral flexion
  • inter malleolar straddle

Schober’s index

Dimples of Venus on back (10 cm above, 5cm below), bend over and remeasure. Should be >20cm

A BASDAI (bath AS disease activity index) >4 is bad

54
Q

How do you treat giant cell arteritis/temporal arteritis?

A

All of these:

  • 1 mg/kg/day of oral prednisolone (but no higher)
  • PPI
  • bisphosphonate
  • calcium and vit D
  • 2 years of pred! weaning off takes 2 years
  • often add azothioprine/methylpred to help get off steroids
55
Q

How can you get short of breath with myositis?

A
  1. Diaphragm (SOB when lying down)
  2. Aspiration pneumonia
  3. ANA Jo1 interstitial lung disease
56
Q

Which sports are associated with spondylolysis?

A

Fencers and gymnasts- extend spines

57
Q

What investigations should you do for scoliosis?

A
  • most common in teens
  • adam’s test (bend over, look from behind)
  • measure Cobb angle (> 40 think about fixing it)
  • check for tethered cord
  • swim to strengthen core
58
Q

What’s the kocher criteria?

A

Helps to identify septic arthritis

  1. non-weight-bearing status
  2. fever>38.5°C
  3. white blood cell>12 K
  4. erythrocyte sedimentation rate>40 mm/h, CRP > 20 mg/l
59
Q

What are the differentials for septic arthritis?

A

gout
transient synoitis
reactive arthritis

60
Q

What imaging do you need to do for a child with a limp?

A

Frog leg lateral x-ray

61
Q

What is DDH? How do you identify it? How do you treat it?

A
  • 33% outside of acetabulum
  • US up to 4 months then x ray
  • Pavlik harness or surgery
62
Q

What are the features of still’s disease?

A
  • typically affects 16-35 year olds
  • arthralgia
  • elevated serum ferritin
  • rash: salmon-pink, maculopapular
  • pyrexia: typically rises in the late afternoon/early evening in a daily pattern and accompanies a worsening of joint symptoms and rash
  • lymphadenopathy
  • rheumatoid factor (RF) and anti-nuclear antibody (ANA) negative
63
Q

How do you treat still’s disease?

A

NSAIDs should be used to manage fever, joint pain and serositis in the first instance. They should be trialled for at least a week before steroids are added.

Steroids may control symptoms but won’t improve prognosis. If symptoms persist, the use of methotrexate, IL-1 or anti-TNF therapy can be considered

64
Q

Which drug should methotrexate not be prescribed with?

A

trimethoprim

65
Q

What are the risk factors for gout?

A

D- iuretics
A- lcohol
R- enal disease
T- rauma

66
Q

What would you see in a joint aspirate of OA?

A

calcium phosphate crystals associated with degeneration of cartilage, coffin-lid shaped with no birefringence

67
Q

What would you see in a joint aspirate of RA?

A

cholesterol crystals, these are rhombic/brick-shaped with a negative birefringence

68
Q

Which joints are affected by gout?

A
  • 70% of first presentations affect the 1st metatarsophalangeal (MTP) joint. Attacks of gout affecting this area were historically called podagra.
  • ankle
  • wrist
  • knee
69
Q

What are the radiological features of gout?

A
  • joint effusion is an early sign
  • well-defined ‘punched-out’ erosions with sclerotic margins in a juxta-articular distribution, often with overhanging edges
  • relative preservation of joint space until late disease
  • eccentric erosions
  • no periarticular osteopenia (in contrast to rheumatoid arthritis)
  • soft tissue tophi may be seen
70
Q

Pain worse on exercise

A

OA

71
Q

What are the features of polymyalgia rheumatica?

A

Features

  • typically patient > 60 years old
  • usually rapid onset (e.g. < 1 month)
  • aching, morning stiffness in proximal limb muscles (not weakness)
  • also mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats
  • There is no true weakness of limb girdles in polymyalgia rheumatica on examination. Any weakness of muscles is due to myalgia (pain inhibition)

Investigations

  • ESR > 40 mm/hr
  • note CK and EMG normal
  • reduced CD8+ T cells
72
Q

Which anti-body is associated with antiphospholipid syndrome?

A

anti-Cardiolipin

73
Q

What are the features of PAN?

A
  • fever, malaise, arthralgia
  • weight loss
  • hypertension
  • mononeuritis multiplex, sensorimotor polyneuropathy
  • testicular pain
  • livedo reticularis
  • haematuria, renal failure
  • perinuclear-antineutrophil cytoplasmic antibodies (ANCA) are found in around 20% of patients with ‘classic’ PAN
  • hepatitis B serology positive in 30% of patients
74
Q

What T scores indicate osteopaenia and osteoporosis?

A

> -1.0 = normal
-1.0 to -2.5 = osteopaenia
< -2.5 = osteoporosis

75
Q

How should bisphosphonates be taken?

A

‘Tablets should be swallowed whole with plenty of water while sitting or standing; to be given on an empty stomach at least 30 minutes before breakfast (or another oral medication); patient should stand or sit upright for at least 30 minutes after taking tablet’

76
Q

What’s the sensitivity and specificity for anti cyclic-citrullinated peptide antibody?

A

sensitivity similar to rheumatoid factor (around 70%) with a much higher specificity of 90-95%

77
Q

Which conditions are associated with pANCA?

A
  • microscopic polyangiitis, positive in 50-75%
  • Churg-Strauss syndrome, positive in 60%
  • primary sclerosing cholangitis, positive in 60-80%
  • granulomatosis with polyangiitis, positive in 25%
78
Q

A Schober’s test of what is indicative of AS?

A

An increase of < 5cm

79
Q

What is Felty’s syndrome?

A

Felty’s syndrome is a condition characterized by splenomegaly and neutropenia in a patient with rheumatoid arthritis. Hypersplenism results in destruction of blood cells which classically results in neutropenia but can also cause pancytopenia.

Although methotrexate use can certainly cause neutropaenia, we would not expect splenomegaly.

80
Q

Which immunoglobulin can be secreted in milk?

A

IgA

81
Q

Patients that are allergic to aspirin may also react to….

A

sulfasalazine

82
Q

Which scoring system is used to assess hypermobility?

A

Beighton score

83
Q

What are the ESR and CRP in temporal arteritis?

A

ESR > 40

CRP can be normal

ORTEM (4 decks)

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