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Y3 Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What are the key presenting features in RA (new diagnosis)?

A

bilateral swollen, painful joints in hands and feet (PIP and MCP)
stiffness worse in the morning, improves with use
gradually gets worse with larger joints becoming involved
presentation usually develops over a few months
positive ‘squeeze test’ - discomfort on squeezing across the metacarpal or metatarsal joints

OR less common presentations:
acute onset with marked systemic disturbance
relapsing/remitting monoarthritis of different large joints (palindromic rheumatism)

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2
Q

What are late features of RA?

A

Swan neck and boutonnière deformities

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3
Q

How is RA diagnosed?

A

Clinical diagnosis is the most important thing

2010 American College of Rheumatology criteria
- used for patients with at least 1 joint with definite clinical synovitis that is not better explained by another disease
- need a score of 6/10 for diagnosis

Categories:
joint involvement, serology, acute phase reactants, duration of symptoms

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4
Q

How is RA investigated?

A

Antibodies:

Rheumatoid Factor: RF is a circulating antibody (usually IgM) that reacts with the Fc portion of the patients IgG. It is the first-line antibody test for patients with suspected RA.

Rose-Waaler test for RF: sheep red cell agglutination
Latex agglutination test for RF(less specific)

Anti-CCP Antibodies : allows early detection of patients suitable for aggressive anti-TNF therapy (present before symptoms)

X-Rays of hands and feet

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5
Q

What are the X-ray findings in RA?

A

Early x-ray findings:
loss of joint space
juxta-articular osteoporosis
soft-tissue swelling

Late x-ray findings:
periarticular erosions
subluxation

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6
Q

What is the first line tx for RA?

A

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

Example DMARDs:

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

sulfasalazine
leflunomide
hydroxychloroquine

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7
Q

How is response to tx monitored in RA? When flares are picked up how are they managed?

A

using a combination of CRP and disease activity (using a composite score such as DAS28)

flares of RA are often managed with corticosteroids - oral or intramuscular

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8
Q

Give some extra-articular complications of RA (think in a head to toe manner to remember)

A

neuro: depression

ocular: keratoconjunctivitis sicca (most common), scleritis, corneal ulceration, keratitis, steroid-induced cataracts, chloroquine retinopathy

cardio: ischaemic heart disease (RA carries a similar risk to type 2 diabetes mellitus)

respiratory: pulmonary fibrosis, pleural effusion, pulmonary nodules, bronchiolitis obliterans, methotrexate pneumonitis, pleurisy

MSK: osteoporosis

Also increased risk of infections

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9
Q

What is Felty’s syndrome?

A

RA + splenomegaly + low white cell count

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10
Q

Give some poor prognostic features in RA

A

rheumatoid factor positive
anti-CCP antibodies
poor functional status at presentation
X-ray: early erosions (e.g. after < 2 years)
extra articular features e.g. nodules
HLA DR4
insidious onset

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11
Q

What is SLE?

A

a multisystem, autoimmune disorder

type 3 hypersensitivity reaction - caused by immune complex deposition

It typically presents in early adulthood and is more common in women and people of Afro-Caribbean origin.

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12
Q

Give some general presenting features of SLE

A

fatigue
fever
mouth ulcers
lymphadenopathy

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13
Q

Presentation of SLE in the skin?

A

malar (butterfly) rash: spares nasolabial folds
discoid rash: scaly, erythematous, well demarcated rash in sun-exposed areas. Lesions may progress to become pigmented and hyperkeratotic before becoming atrophic
photosensitivity
Raynaud’s phenomenon
livedo reticularis
non-scarring alopecia

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14
Q

MSK manifestations of SLE?

A

arthralgia
non-erosive arthritis

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15
Q

Cardiac manifestations of SLE?

A

pericarditis: the most common cardiac manifestation
myocarditis

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16
Q

Respiratory manifestations of SLE?

A

pleurisy
fibrosing alveolitis

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17
Q

Renal manifestations of SLE?

A

proteinuria
glomerulonephritis (diffuse proliferative glomerulonephritis is the most common type)

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18
Q

How is SLE investigated?

A

Antibodies:
99% are ANA positive
(this high sensitivity makes it a useful rule out test, but it has low specificity)
20% are rheumatoid factor positive
anti-dsDNA: highly specific (> 99%), but less sensitive
anti-Smith

also: anti-U1 RNP, SS-A (anti-Ro) and SS-B (anti-La)

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19
Q

How is SLE disease progression monitored?

A

Inflammatory markers:

ESR is generally used

during active disease the CRP may be 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)

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20
Q

How is SLE managed?

A

Hydroxychloroquine first line

NSAIDs and suncream important

If internal organ involvement e.g. renal, neuro, eye then consider prednisolone, cyclophosphamide

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21
Q

Lupus nephritis is a severe manifestation of SLE that can result in end-stage renal disease. Patients should be monitored by performing urinalysis at regular check-up appointments to rule out proteinuria.

How is lupus nephritis managed?

A

treat hypertension

initial therapy for focal (class III) or diffuse (class IV) lupus nephritis: glucocorticoids with either mycophenolate or cyclophosphamide

subsequent therapy : mycophenolate is generally preferred to azathioprine to decrease the risk of developing end-stage renal disease

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22
Q

Ankylosing spondylitis is a HLA-B27 associated spondyloarthropathy. It typically presents in males (sex ratio 3:1) aged 20-30 years old.

What are its key presenting features?

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

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23
Q

What are the As of ankylosing spondylitis?

A

Anterior uveitis
Apical fibrosis
Aortic regurgitation
AV node block
Achilles tendonitis
Amyloidosis
and cauda equina syndrome
peripheral arthritis

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24
Q

What will be seen on examination in ankylosing spondylitis?

A

reduced lateral flexion

reduced forward flexion - Schober’s test - a line is drawn 10 cm above and 5 cm below the back dimples (dimples of Venus). The distance between the two lines should increase by more than 5 cm when the patient bends as far forward as possible

reduced chest expansion

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25
Q

How should ankylosing spondylitis be investigated?

A

Plain x-ray of the sacroiliac joints is the most useful investigation

If the x-ray is negative for sacroiliac joint involvement in ankylosing spondylitis but suspicion for AS remains high, the next step in the evaluation should be obtaining an MRI

Radiographs may be normal early in disease, later changes include:
sacroiliitis: subchondral erosions, sclerosis
squaring of lumbar vertebrae
‘bamboo spine’ (late & uncommon)
syndesmophytes: due to ossification of outer fibers of annulus fibrosus
chest x-ray: apical fibrosis

26
Q

How is ankylosing spondylitis managed?

A

NSAIDs are the first-line treatment
physiotherapy
encourage regular exercise such as swimming

DMARDs which are used to treat RA (such as sulphasalazine) are only really useful if there is peripheral joint involvement

27
Q

Gout is a form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium. It is caused by chronic hyperuricaemia.

What predisposes to it?

A

Decreased excretion of uric acid
drugs: diuretics
chronic kidney disease
lead toxicity

Increased production of uric acid
myeloproliferative/lymphoproliferative disorder
cytotoxic drugs
severe psoriasis

28
Q

How does gout present?

A

Inflammatory arthritis

episodes last several days when their gout flares and patients are often symptom-free between episodes

Significant pain, swelling and erythema

1st metatarsophalangeal (MTP) joint is most commonly affected

29
Q

How is gout investigated?

A

Synovial fluid analysis
- needle shaped negatively birefringent monosodium urate crystals under polarised light

Uric acid
- should be checked once the acute episode has settled down (typically 2 weeks later) as may be high, normal or low during the acute attack

Xray:
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

30
Q

How is gout managed?

A

NSAIDs or colchicine are first-line

Urate lowering therapy

Lifestyle: reduce alcohol, lose weight, increase Vit C intake

31
Q

Fibromyalgia is a syndrome characterised by widespread pain throughout the body with tender points at specific anatomical sites. Most common in women aged 30-50.

How does it present?

A

chronic pain: at multiple site, sometimes ‘pain all over’
lethargy
cognitive impairment: ‘fibro fog’
sleep disturbance, headaches, dizziness are common

the American College of Rheumatology criteria lists 9 pairs of tender points on the body. If a patient is tender in at least 11 of these 18 points it makes a diagnosis of fibromyalgia more likely

32
Q

How is fibromyalgia managed?

A

explanation
aerobic exercise: has the strongest evidence base
cognitive behavioural therapy
medication: pregabalin, duloxetine, amitriptyline

33
Q

Osteomalacia describes softening of the bones secondary to low vitamin D levels. What causes it?

A

vitamin D deficiency
(malabsorption ,lack of sunlight, diet)
CKD
drug induced e.g. anticonvulsants
inherited: hypophosphatemic rickets (previously called vitamin D-resistant rickets)
liver disease: e.g. cirrhosis

34
Q

How does osteomalacia present?

A

bone pain
bone/muscle tenderness
fractures: especially femoral neck
proximal myopathy: may lead to a waddling gait

35
Q

How is osteomalacia investigated?

A

bloods:
low vitamin D levels
low calcium, phosphate (in around 30%)
raised alkaline phosphatase (in 95-100% of patients)

x-ray:
translucent bands (Looser’s zones or pseudofractures)

36
Q

Osteoporosis is a disorder affecting the skeletal system characterised by loss of bone mass that significantly increase risk of fragility fractures.

What are the risk factors to developing it?

A

Older female
corticosteroid use
smoking and alcohol
low BMI
family history

37
Q

How should you assess the 10-year risk of a patient developing a fragility fracture?

A

screening tool such as FRAX or QFracture

38
Q

How should osteoporosis be investigated?

A

History and physical examination

Blood cell count, sedimentation rate or CRP, serum calcium, albumin, creatinine, phosphate, alkaline phosphatase and liver transaminases

Thyroid function tests

To assess the actual bone mineral density a dual-energy X-ray absorptiometry (DEXA) scan is used. The DEXA scan looks at the hip and lumbar spine. If either have a T score of < -2.5 then treatment is recommended.

39
Q

What is the first line tx for osteoporosis?

A

Bisphosphonates: 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

40
Q

What are the x-ray changes seen in osteoarthritis?

A

LOSS

Loss of joint space
Osteophytes forming at joint margins
Subchondral sclerosis
Subchondral cysts

41
Q

How does OA of the hands present?

A

Usually one joint at a time is affected over a period of several years. The carpometacarpal joints (CMCs), distal interphalangeal joints (DIPJs) are affected more than the proximal interphalangeal joints (PIPJs)

Episodic joint pain: intermittent ache. Provoked by movement and relieved by rest
Stiffness: worse after long periods of inactivity e.g. waking up in the morning (only lasts a few minutes compared to the morning joint stiffness seen in rheumatoid arthritis)

Painless nodes (bony swellings):
Heberden’s nodes at the DIP joints
Bouchard’s Nodes at the PIP joints
- these nodes are the result of osteophyte formation.

42
Q

How does OA of the hip present?

A

chronic history of groin ache following exercise and relieved by rest
red flag features suggesting an alternative cause include rest pain, night pain and morning stiffness > 2 hours
the Oxford Hip Score is widely used to assess severity

43
Q

How is OA of the hip managed?

A

oral analgesia
intra-articular injections: provide short-term benefit
total hip replacement remains the definitive treatment

44
Q

First line tx for OA?

A

paracetamol and topical NSAIDs are first-line analgesics. Topical NSAIDs are indicated only for OA of the knee or hand

45
Q

Polymyalgia rheumatica (PMR) is a relatively common condition seen in older people characterised by muscle stiffness and raised inflammatory markers.

How does it present?

A

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

46
Q

How is PMR treated?

A

prednisolone e.g. 15mg/od
patients typically respond dramatically to steroids, failure to do so should prompt consideration of an alternative diagnosis

47
Q

What causes visual impairment in GCA?

A

Anterior ischemic optic neuropathy - fundoscopy typically shows a swollen pale disc and blurred margins

48
Q

Give 3 key x-ray findings for ankylosing spondylitis

A

subchondral erosions, sclerosis
and squaring of lumbar vertebrae

49
Q

cANCA =
pANCA =

A

cANCA = granulomatosis with polyangiitis

pANCA = eosinophilic granulomatosis with polyangiitis + others

50
Q

What should you check before initiating azathioprine tx?

A

thiopurine methyltransferase deficiency (TPMT)

51
Q

Dermatomyositis is an inflammatory disorder causing symmetrical, proximal muscle weakness and characteristic skin lesions.

What is an important investigation to do in people with this diagnosis?

A

malignancy screening - often paraneoplastic

52
Q

Risk of hydroxychloroquine?

A

bull’s eye retinopathy - may result in severe and permanent visual loss

monitor visual acuity

53
Q

What should you always check in a man w osteoporosis?

A

testosterone

54
Q

What is Z score adjusted for? (DEXA)

A

age, gender and ethnic factors

55
Q

Where does septic arthritis most commonly occur in adults?
tx?

A

the knee
IV flucloxacillin

56
Q

old man, bone pain, raised ALP =

A

think Paget’s!

57
Q

With abx should never be prescribed alongside methotrexate?

A

trimethoprim - may cause bone marrow suppression and severe or fatal pancytopaenia

58
Q

What should you do before starting bisphosphonates?

A

correct hypocalcemia/vitamin D deficiency

59
Q

What feature might help you to differentiate psoriatic arthritis from other inflammatory arthridities on examination?

A

nail changes - pitting and onycholysis

60
Q

acute joint pain + sterile synovial fluid with a high WCC on aspiration =

A

reactive arthritis!!

‘Can’t see, pee or climb a tree’

tx = analgesia, NSAIDS, intra-articular steroids

61
Q

How should oral bisphosphonates be taken?

A

swallowed with plenty of water while sitting or standing on an empty stomach at least 30 minutes before breakfast (or another oral medication)

the patient should stand or sit upright for at least 30 minutes after taking

62
Q

Low serum calcium, low serum phosphate, raised ALP and raised PTH =

A

osteomalacia

Y3 Medicine (9 decks)

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