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MBBS VI Medicine > Rheumatology handbook > Flashcards

Rheumatology handbook Flashcards

1
Q

What is the clinical features of gouty arthritis?

A

Acute gout (monoarticular, polyarticular)
Chronic tophaceous gout
Uric acid calculi
Gouty nephropathy

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2
Q

What is the dx of gout?

A

Definitive gout: intracellular negative birefringement urate crystal on joint fluid microscopy
Presumed gout: classical history of episodic acute arthritis rapidly resolved with NSAID (or colchicine) + history of hyperuricemia

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3
Q

What is the management of acute gouty arthritis?

A

1. NSAID/COX2 inhibitors (Note! Check patient’s drug allergy)
High dose, tapering over 5 days, reduce dose in renal impairment: a) indomethacin 50 mg TDS25 mg TDS25 mg BD
b) naprosyn 500 mg STAT250 mg TDS250 mg BD
c) Celecoxib 200 mg BD (if high GI risk)
2. Colchicine
0.5 mg TDS for 1–2 days (stop if nausea/diarrhoea) Renal impairment – caution and reduce frequency Not recommend Q1HQ2H for 10 doses regime
3. Corticosteroid
a)** Intra-articular steroid** injection after septic arthritis ruled out
b) Prednisolone 20 to 40 mg daily within 1 week, rapid tapering
(consider for patients with NSAID or colchicine contraindications, or renal failure)

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4
Q

What is the urate lowering therapy for gout?

A

1. Xanthine oxidase inhibitors (Do NOT use with azathioprine!)
a. Allopurinol (usual dose 300 mg daily)
 Start with low dose 100 mg daily; increase weekly to your target dosage; inform patients to stop if skin reaction (~5%) and seek medical attention early
 Further reduce dose in renal impairment, step up slowly
 Start allopurinol only when acute gout has subsided
 Prophylaxis: add regular colchicine 0.5 mg daily or bd, or
NSAID, for 3 to 6 months, to prevent acute gout attacks
 Titrate dose to target serum uric acid < 0.36 mmol/L
 FDA approved maximal dose is 800 mg daily
 Severe cutaneous adverse reactions are associated with
HLA B*5801 in Han Chinese
b. Febuxostat – a new non-purine selective xanthine oxidase inhibitor
 Alternative for patients with allopurinol cutaneous adverse reaction
 Usual dose 40 mg to 80 mg daily
 Caution in patients with high cardiovascular thromboembolic risks
2. Uricosuric drugs
Probenecid 250 mg BD to 1000 mg TDS
(Contraindications: moderate renal impairment, urate renal stone, tophaceous gout, and high 24-hour urine uric acid excretion) Benzbromarone – licensed in HK but not under HA formulary Sulfinpyrazone – not licensed in HK
3. Uricase
Rasburicase, a recombinant urate-oxidase enzyme, is for pre- chemotherapy prevention of acute tumour lysis syndrome. Caution in G6PD deficiency.

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5
Q

What is the 2010 ACR/EULAR classification criteria for RA?

A
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6
Q

What are the investigations for RA?

A

 ESR and C-reactive protein (CRP)
 RF (sensitivity ~70%)
 Anti-cyclic citrullinated peptide antibody (anti-CCP) – highly
specific for RA, helpful in undetermined situations
 Plain X-ray of the hands and feet for erosion
 MRI or USG may be useful for detecting early bony erosion

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7
Q

What is the DMARD management of RA?

A
  1. Conventional DMARDs
     Start DMARDs early! All take time to act.
     Usually start with methotrexate monotherapy, but step-up combination may be considered early in patient with severe disease
     Titrate up to optimal doses according to RA disease activity
     Switch or add-on another DMARD promptly if target not met
     Counsel patients on DMARD effects and side effects and their slow action
     Anchor drug is methotrexate
     Other examples: sulphasalazine, hydroxychloroquine, leflunomide, low dose prednisolone (less than 10 mg/day), less commonly used are cyclosporin A, tacrolimus, azathioprine, intramuscular gold
  2. Biologics
     E.g. anti-TNF (Etanercept, Adalimumab, Infliximab, Golimumab, Certolizumab), IL-6 receptor blocker (Tocilizumab), co- stimulation molecule blocker (Abatacept), anti-CD 20 (Rituximab)
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8
Q

What is the ASAS criteria for axial spondyloarthritis (SpA)?

A

a. Imaging evidence of sacroiliitis (XR, MRI or CT) plus one SpA features*
b. HLA-B27 positivity plus 2 other SpA features*
SpA features:
 Inflammatory back pain age of onset < 40  Arthritis
 Enthesitis
 Psoriasis
 Uveitis
 Dactylitis
 Crohn’s/colitis
 Good response to NSAIDs
 Family history for SpA
 Elevated C-reactive protein (CRP)  HLA-B27

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9
Q

How to measure decreased spinal mobility in AS?

A

a. Modified Schober test – spinal forward bending (excursion of two points: PSIS level and 10 cm above; normal excursion > 5 cm).
b. Note: finger floor distance may be apparently normal when good hips flexion compensates limited spinal flexion
c. Occiput-to-wall: normal 0 cm
d. Tragus-to-wall: normal < 14 cm
e. Chest expansion
f. Cervical rotation
g. Intermalleolar distance

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10
Q

What are the investigations for ankylosing spondylitis?

A

a. XR sacroiliac joints and spine
b. MRI SI joints in doubtful cases
c. HLA-B27 (role refers to ASAS criteria)

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11
Q

What is the diagnostic criteria for psoriatic arthritis?

A
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12
Q

What are the features distinguishing PsA from RA?

A

 Presenceofpsoriasis
- Hidden lesions common, e.g. scalp, hairline, behind the ear and
inside ear cannel, guttate lesions on back, under the breasts,
around umbilicus, around the perineum or even natal cleft  Nail dystrophy
- Onycholysis, pitting, ridging, etc
 Distal phalangeal joint involvement
 Spondylitisorsacroiliitis
 Enthesitis(inflammationofjunctionofligament,tendonorjoint
capsule to bone)
 Dactylitis

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13
Q

What is the ACR criteria for classification of SLE?

A

> 4 criteria
1. Malar rash
2. Discoid rash
3. Photosensitivity
4. Oral ulcers
5. Arthritis
6. Serositis (pericarditis, peritonitis, pleuritis)
7. Renal disease (proteinuria > 0.5 g/day, or +++ by dipstick, or
cellular casts)
8. Neurological (seizure, or psychosis)
9. Haematological (haemolytic anaemia, or leucopenia < 4×109/L,
lymphopenia < 1.5×109/L, on two or more occasions, or
thrombocytopenia < 100×109/L)
10. Immunological (anti-dsDNA, or anti-Sm, or false +ve VDRL for
more than 6 months, or the presence of the antiphospholipid
antibodies)
11. Positive anti-nuclear antibody (ANA)

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14
Q

What is the immunologic criteria for SLE?

A
  1. ANA above laboratory reference range
  2. Anti-dsDNA above laboratory reference range (except ELISA: twice
    above laboratory reference range) 3. Anti-Sm
  3. Antiphospholipid antibody: e.g. lupus anticoagulant, false-positive test for syphilis, anticardiolipin antibody (at least twice normal or medium-high titre), anti-β2 glycoprotein 1 antibody
  4. Low complement: e.g. low C3, low C4, low CH50
  5. Direct Coombs test in absence of haemolytic anaemia

Anti ENA antibodies
Anti: Ro causing congenital heart block so prenatal counselling and UV light protection is advised
Anti ENA antibodies seldom sero-convert and repeating tests is not necessary

Antiphospholipid antibodies
Lupus anticoagulant, anti-cardiolipin (aCL) antibody associated with thrombocytopenia, livedo reticularis, valvular heart lesions, recurrent miscarriages, arterial and venous thrombosis
Twice positive tests 12 weeks apart necessary for dx of antiphospholipid syndrome.

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15
Q

How do we monitor disease activity of SLE?

A

 Clinical assessment (signs and symptoms of disease flares)
 Serology: C3 and C4 level, anti-dsDNA titre

ANA titer does not correlate with disease activity and is not reliable for disease monitoring. No need to repeat ANA if it is already positive.
CRP is usually not elevated with active SLE. An elevated CRP in SLE may indicate infection, persistent synovitis/arthritis, serositis. Infection has always to be considered before augmentation of immunosuppressive therapy.

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16
Q

What is the treatment of SLE?

A

General: Patient education and counselling, sun-screening (avoid strong sunlight, frequent application of SPF 15+ sun lotion), screening and treatment of cardiovascular risk factors and osteoporosis, vaccination and infection prevention, early recognition and prompt treatment
Hydroxychloroquine should be considered for every lupus patient:
 Overall stabilizing SLE
 Decreases infection, some anti-thrombotic and lipid lowering effect  Stabilises pregnant SLE patients and improves foetal outcome
 Recommend < 5 mg/kg/day
Mild SLE manifestations
 NSAIDs – arthritis, serositis, fever
 Hydroxychloroquine – arthritis, skin lupus
 Methotrexate – persistent and refractory arthritis and skin
 Topical steroid – skin lupus
 Smalltomoderatedosesofprednisolone–fever,systemicupset,mild
cytopenias, more severe serositis and skin lupus
 Azathioprine – haematological, mild renal disease, steroid sparing
 Belimumab (Benlysta) – as an alternative for arthritis, skin lupus,
serositis, haematological

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17
Q

What are severe SLE manifestations?

A

Glomerulonephritis, neuropsychiatric lupus, severe cytopenias, thrombotic thrombocytopenic purpura, pulmonary haemorrhage, myocarditis, pneumonitis, pulmonary arterial hypertension

18
Q

What are the neuropsychiatric syndromes of neuropsychiatric lupus according to 1999 ACR classification?

A
19
Q

What is the presentation of cervical subluxation in RA?

A

 Commonly presents with neck pain radiating towards the occiput, clumsiness, abnormal gait, spastic quadriparesis, sensory and
sphincter disturbances. May cause cord compression and death.
 4 forms in descending order of frequency: anterior, posterior, lateral,
vertica

20
Q

What are the investigations for cervical subluxation in RA?

A

 Plain AP and lateral XR of cervical spine with flexion and extension views
 Anterior subluxation: distance between the posterior aspect of the anterior arch of the atlas and the anterior aspect of the odontoid process (Atlanto-dens interval, ADI) ≥ 4 mm
 Dynamic (flexion-extension) MRI (if surgery indicated)

21
Q

What is the medical and surgical managementfor cervical subluxation?

A

Medical: high impact excercises and spinal manipulation are contraindicated. Stiff cervical collars may provide marginal benefit but compliance is a problem.

Surgical (refer to ortho surgeons or neurosurg if signs of cord compresion)
Surgical options: Craniocervical decompression, cervical or occipito-cervical fusion (alone or in combination)

22
Q

What is the presentation of giant cell arteritis?

A

Presentation: At least 3 of the following 5 criteria
1. Age ≥50 years
2. Localized headache of new onset
3. Tenderness or decreased pulse of the temporal artery 4. ESR >50 mm/hr
5. Biopsy revealing a necrotizing arteritis with a predominance of mononuclear cells or a granulomatous process with multinucleated giant cells.

 Polymyalgia Rheumatica (PMR) is characterized by aching and morning stiffness in the shoulder and hip girdles, occurring in 40–50% of GCA patients.
 Other presentations: jaw or arm claudication, weight loss, PUO
 Complications: Ischaemic optic retinopathy (visual loss 15–20%).
Blindness is abrupt and painless, may be preceded by amaurosis fugax.
 Aneurysms, dissections, stenotic lesions of the aorta and its major
branches

23
Q

What is the investigations of giant cell arterieis?

A

 Elevated ESR, often >100 mm/hr (5% of GCA has ESR< 40mm/hr)
 Ultrasound of temporal artery to look for “halo” sign
 Temporal artery biopsy of the affected side

24
Q

What is treatment for giant cell arteritis?

A

 High dose prednisolone (1 mg/kg/day)
 For visual symptoms or signs (eg, amaurosis fugax, partial or
complete visual loss), start empirical steroid before temporal artery
biopsy result
 Acute visual changes - consider IV pulse methylprednisolone (250–
1000 mg) daily for 3 days
 Consider anti-IL 6 (Tocilizumab) for refractory cases (used by
specialist only)

25
Q

What are the investigations for ANCA vasculitis pulmonary renal syndrome?

A

 Check anti-GBM and ANCA (anti-neutrophil cytoplasmic antibody)
 Check for Anti-PR3 ANCA (proteinase 3) or anti-MPO ANCA
(myeloperoxidase) if ANAC is positive
 Raised ESR/CRP
 Renal biopsy to show pauci-immune glomerulonephritis
 CXR, HRCT, bronchoscopy etc for pulmonary haemorrhage

26
Q

What are common causes of polyarthralgia and monoarthritis?

A
27
Q

What are the relevant Ix done for inflammatory arthritis?

A
28
Q

When should septic arthritis be suspected?
What are essential initial Ix done?

A
  • Hot, swollen and tender joint should be dx as septic arthritis until proven otherwise, even in the absence of fever, leukocytosis, elevated ESR or CRP. Delay in dx can result in irreversible joint destruction or septicemia
  • Prompt aspiration of joint is warranted. Synovial fluid should be sent for DC: usually >50,000 WBC/ml and oftne >100,000ml, predominantly neutrophils. Gram stain. Culture and sensitivity. Polarizing microscopy for crystals
  • CBC with DC, RFT, LDT, blood culture, X ray of joint, swabs of pharynx, urethra, cervix and anorectum if gonococcal infection suspected
  • Start empirical IV anitbiotics immediately according to suspected organisms and results.
  • Therapeutic joint aspiration to dryness
  • Consult ortho surgeon for drainage especially for infected prosthetic joint.
  • Start PT early
  • NSAIDs for pain relief
  • IV antibiotics for at least 2 weeks or until signs improved for non gonococcal arthritis, then orally for an additional 2-4 weeks
29
Q

What are the suggested antibiotics depending on pathogen causing septic arthritis?

A
30
Q

What is the disease assessment of ankylosing spondylitis?
What is the treatment?

A
31
Q

What are the clinical features of psoriatic arthritis?

A

 30%psoriasispopulationhasarthritis
 60% psoriasis precedes arthritis, 20% arthritis precedes psoriasis,
20% concurrent
 Also watch out for associated metabolic syndrome e.g. overweight, DM, HT, HL, hyperuricaemia etc

32
Q

What is the treatment of psoriatic arthritis?
Skin psoriasis?

A
33
Q

What is the disease activity scoring system for SLE?

A
34
Q

How to classify lupus nephritis?
What is the management?

A
35
Q

How to make a dx of neuropsychiatric SLE?

A
36
Q

What is the treatment of neuropsychiatric SLE?

A
37
Q

What is the clinical presentaion of renal crisis in scleroderma?
What is treatment?

A

Symptoms are sudden onset and usually not preceded by significant prodromal symptoms
Life threatening condition
Clinical presentation: malignant hypertension, acute renal failure, less often MAHA
Treatment: ACEI +/- dialysis
Consult specialis

38
Q

What are the usage guidelines for NSAIDs?
What are AE?

A
39
Q

What are the RF for GI toxicity in use of NSAIDs?

A

a. Chronically disabled
b. Age >60 years
c. Previous history of proven peptic disease
d. Co-administration of high dose prednisolone or anticoagulation
e. Higher dosage of NSAIDs
f. Extent of inflammatory disease for which NSAIDs is prescribed

40
Q

What are adv and AE of using COX 2 inhibitors?

A
41
Q

What are the recommendations for patients recieving NSAIDs?

A

MBBS VI Medicine (92 decks)

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