Rheumatology - For BPTs

Rheumatology for BPTs
An introduction
Dr Leanne Alblas
2nd year Rheumatology trainee
Acknowledgment to Dr Claire Owen for

many of the slides
Outline
PMR and GCA
Monoarthritis
Polyarthritis
Back pain Inflammatory vs. Mechanical
PMR and GCA
Previous Exam Question

GCA vs PMR
A 75-year-old woman is evaluated for a sudden loss of vision in the left eye that began 30
minutes ago. She has a 2-week history of fatigue; malaise; and pain in the shoulders, neck, hips,
and lower back. She also has a 5-day history of mild bitemporal headache.
On physical examination, temperature is 37.3 C (99.1 F), blood pressure is 140/85 mm Hg,
pulse rate is 72/min, and respiration rate is 16/min. BMI is 31. The left temporal artery is tender.
Fundoscopic examination reveals a pale, swollen optic disc. Range of motion of the shoulders
and hips elicits moderate pain.
Laboratory studies:
Hemoglobin
9.9 g/dL (99 g/L)
Leukocyte count 7300/L (7.3 109/L)
Platelet count
456,000/L (456 109/L)
Erythrocyte sedimentation rate 116 mm/h
Which of the following is the most appropriate next step in this patients management?
A) Brain MRI
B) High-dose intravenous methylprednisolone
C) Low-dose oral prednisolone
D) Temporal artery biopsy

GCA
Which of the following clinical features confers the
highest likelihood for the presence of Giant Cell
Arteritis?
A. Diplopia
B. Headache
C. Jaw Claudication
D. Large Joint Synovitis
E. Proximal Myalgia
Polymyalgia Rheumatica
Polymyalgia Rheumatica (PMR) is a chronic,
inflammatory disorder of unknown cause

Characterised by sudden-onset shoulder and pelvic
girdle pain, and prolonged early morning stiffness

Affects men and women over the age of 50 years
Most common inflammatory rheumatic disease of the
elderly:
Ranks second only to Rheumatoid Arthritis in terms of lifetime
incidence risk (2.43% for women and 1.66% for men)

Kermani, TA (2013). Polymyalgia rheumatica. Lancet; 381:63-72.
Crowson, CS et al. (2011). The lifetime risk of ault-onset rheumatoid arthritis and other inflammatory autoimmune rheumatic diseases. Arthritis &
Rheumatism;63(3):633-9.
Figure 1: Typical sites of pain in patients with PMR. Shaded areas demonstrate
the distribution in the a) shoulder and b) pelvic girdle.
Salvarani, C. et al. Clinical features of polymyalgia rheumatica and giant cell arteritis. Nature Reviews Rheumatology;8(9):509-21.
Heterogeneity in the clinical features and disease
course is well recognised:

Distal manifestations eg. Synovitis, tenosynovitis,
pitting oedema, carpal tunnel syndrome (~50%)

GCA (16-21%):
Up to 50% of GCA diagnoses have musculoskeletal symptoms
consistent with PMR
Polymyalgic-onset Rheumatoid Arthritis and
spondyloarthritis
Dasgupta, B et al (2012). Provisional classification criteria for polymyalgia rheumatica: a EULAR/ACR collaborative initiative. Arthritis &
Rheumatism; 64(4):943-54.
Salvarini, C et al. Polymyalgia rheumatica and giant cell arteritis. Lancet; 372(9634):234-45.
Bilateral subacromial bursitis is the hallmark lesion
of PMR on imaging:
Sensitivity 92.9%, specificity 99.1%
Ultrasound:
Preferred imaging technique
Findings of biceps tenosynovitis and trochanteric
bursitis are similarly consistent with PMR
Camellino, D et al. (2012). Imaging of polymyalgia rheumatica: indications on its pathogenesis, diagnosis and prognosis. Rheumatology; 51(1):77-86.
Diagnosis is based upon a clinical construct and raised
inflammatory markers:
Dasgupta, B et al (2012). Provisional classification criteria for polymyalgia rheumatica: a EULAR/ACR collaborative initiative. Arthritis &
Rheumatism; 64(4):943-54.
Glucocorticoids remain the mainstay of treatment
The British Society for Rheumatology Guidelines for
Management of PMR represent a recently

developed consensus-based regimen:
PNL 15mg daily for 3 weeks
PNL 12.5mg daily for 3 weeks
PNL 10mg daily for 4 weeks, wean by 1mg every 4
weeks thereafter
The role of steroid-sparing agents is unclear
Dasgupta, B et al. (2010). BSR and BHPR guidelines for the management of polymyalgia rheumatica. Rheumatology;49(1):186-90.
Kermani, TA (2013). Polymyalgia rheumatica. Lancet, 381:63-72.
Giant Cell Arteritis

Also known as Temporal Arteritis
Giant Cell Arteritis (GCA) is a large-vessel vasculitis
with a predilection for the aorta and its branches

The aetiology is unknown
Characterised by temporal headache (80%), scalp
tenderness and jaw claudication

Most common vasculitis in men and women over 50
years of age
GCA: history & examination features
1. Smetana GW, Shmerling RH. Does this patient have temporal arteritis? JAMA 2002;287:92101

Ischaemic events are the most feared complication:
Anterior Ischaemic Optic Neuropathy (up to 20%)
Stroke (rare)
Long-term, GCA patients can develop large vessel
aneurysms or stenosis
Figure 3: Stenosis of the left subclavian

artery on MRA in a GCA patient.

Temporal artery biopsy is the diagnostic gold
standard:
Sensitivity ranges from ~70% to >90%
Breur, GS (2009). Rate of discordant findings in bilateral temporal artery biopsy to diagnose giant cell arteritis. Journal of Rheumatology; 36(4): 794.
Hunder, GG et al. (1990). The American College of Rheumatology 1990 criteria for the classification of giant cell arteritis. Arthritis & Rheumatism;
33:1122-8.
Figure 4: Temporal artery biopsy demonstrating segmental destruction of internal

elastic lamina and granulomatous vessel inflammation with giant cells.
American College of Rheumatology (2014). Available from: http://images.rheumatology.org

The lack of a non-invasive diagnostic tool has
promoted the use of imaging modalities

Ultrasound:
Arterial wall oedema, seen as the halo sign, can be
demonstrated in some patients with GCA:

Sensitivity 42%, specificity 94%
Figure 5: Colour duplex ultrasound

demonstrating the halo sign.
Black, R et al (2013). The use of temporal artery ultrasound in the diagnosis of giant cell arteritis in routine practice. International Journal of
Rheumatic Diseases; 16:352-7.

Treatment should not be withheld prior to temporal
artery biopsy
Glucocorticoids similarly remain the mainstay of
treatment:
Uncomplicated GCA (no visual loss) PNL 50mg daily
Evolving visual loss Methylprednisolone 1g IV for 3
consecutive days
Aspirin is also recommended in all patients with
GCA without a major contraindication

Ghosh, P et al. (2010). Current understanding and management of giant cell arteritis and polymyalgia rheumatica. Expert Review Clinical
Immunology; 6(6): 913-28.

A steroid-sparing agent should be considered
following recurrent relapse or failure to wean PNL
Ghosh, P et al. (2010). Current understanding and management of giant cell arteritis and polymyalgia rheumatica. Expert Review Clinical
Immunology; 6(6): 913-28.
Take Home Message

Condition
Manifestations
Temporal
headache
Scalp tenderness
Jaw claudication
Visual loss
Investigations
CRP elevated
ESR elevated
Temporal artery
biopsy
When to Refer
Immediately
Monoarthritis

Monoarthritis
A 78-year-old man with a 15-year history of osteoarthritis is evaluated for severe pain and swelling of the left
knee of 4 days' duration. He also has hypertension, type 2 diabetes mellitus, and chronic kidney disease.
Medications are glyburide, lisinopril, and low-dose aspirin.
On physical examination, vital signs are normal. He is unable to bear weight on the left leg because of pain. The
left knee is swollen and warm, and range of motion of this joint is limited and elicits pain. There are no tophi.
Laboratory studies reveal leukocyte count 15,600/L (15.6 109/L) (90% polymorphonuclear cells, 10%
lymphocytes), glucose (random) 210 mg/dL (11.7 mmol/L), serum creatinine 2.2 mg/dL (167.9 mol/L),
serum uric acid 10.7 mg/dL (0.63 mmol/L) and normal urinalysis.
Arthrocentesis of the left knee is performed. Synovial fluid leukocyte count is 24,000/L (90%
polymorphonuclear cells, 10% lymphocytes). Polarized light microscopy reveals intra- and extracellular
monosodium urate crystals. Gram stain is negative.
Q: Which of the following is the most appropriate treatment for this patient?
A. Allopurinol
B. Colchicine
C. Ibuprofen
D. Intra-articular methylprednisolone
E. Prednisone
DDx of acute monoarthritis

Septic arthritis
Haemarthroses
Crystal arthritis:
Gout
Pseudogout
BBC- Bugs, Blood, Crystals
Acute Monoarthritis
Can be the initial manifestation of many joint
disorders
Chokkalingam, S et al. (2003). Diagnosing acute monoarthritis in adults: a practical approach for the family physician. American Family Physician;
68(1):83-90.
Acute Monoarthritis
Can be the initial manifestation of many joint
disorders
68(1):83-90.
Acute Monoarthritis
Arriving at the correct diagnosis is crucial for
appropriate treatment
Serious management errors can arise from:
Failing to perform a joint aspirate
Starting treatment before aspirating the joint
Basing a diagnosis purely on laboratory results eg.
Serum urate level
68(1):83-90.
Synovial Fluid Analysis
Lingling, M et al. (2009). Acute monoarthritis: what is the cause of my patients painful swollen joint?. CMAJ; 180(1):59-65.
Septic Arthritis
Acute joint infection
Staphylococcus aureus is the most common
organism
Risk factors include:
Age >80 years
Diabetes mellitus
Rheumatoid arthritis
Recent joint surgery
Hip or knee prosthesis

Skin infection
Septic Arthritis
Characterised by joint pain (85%), swelling (78%)
and limited range of motion

Fever may be absent (sensitivity 57%)
A synovial fluid leucocyte count >50000/mm3 is the
most useful finding in making an early diagnosis:

Positive likelihood ratio 7.7 (CI 5.7 11.0)
Rapidly progressive joint destruction is seen on
plain x-ray in untreated cases

Gout and sepsis may co-exist
Margaretten, ME et al. (2007). Does this adult patient have septic arthritis?. JAMA; 297:1478-88.
Zhang, W et al (2006). EULAR evidence based recommendations for gout: part 1: diagnosis. Annals of Rheumatic Disease; 65:1301-11.
Past Exam Question

RA and septic arthritis
Which of the following DMARDs is most likely to
increase risk of septic arthritis in patients with
Rheumatoid Arthritis?
A. Corticosteroids
B. Etanercept
C. Leflunomide
D. Methotrexate
E. Sulfasalazine
Infection Risk in Rheumatology

Inflammatory conditions increase susceptibility to
infection due to:

Underlying immune modulation of the disease process
Frequent use of glucocorticoids and immunosuppressive
therapies
Prednisolone is associated with one of the highest
overall infection risks

Most evidence suggests a neutral effect of synthetic
DMARDs
Infection risk with TNF inhibitors is highest at
commencement (RR 4.6 in first 90 days)
Gout
Monosodium urate deposition in peri-articular soft
tissues
Male sex
Diabetes mellitus
Hypertension
Metabolic syndrome
Obesity
Cardiovascular disease
Chronic renal failure
Diuretic use
Purine-rich diet
Alcohol consumption
Past Exam Question

Purine metabolism
QUESTION 16
What is the most common mechanism for primary
hyperuricaemia?
A. Increased gastrointestinal absorption of uric acid
B. Increased cell turnover
C. Inherited defects in purine synthesis
D. Inherited defects in adenosine triphosphate (ATP)
metabolism
E. Reduced uric acid urinary excretion
Past Exam Question

Purine metabolism
QUESTION 16
What is the most common mechanism for primary
hyperuricaemia?
A. Increased gastrointestinal absorption of uric acid
B. Increased cell turnover
C. Inherited defects in purine synthesis
D. Inherited defects in adenosine triphosphate (ATP)
metabolism
E. Reduced uric acid urinary excretion
Gout
If polyarticular, typically asymmetrical in
distribution
Tophi have high clinical diagnostic value:
Positive likelihood ratio 40.0 (95% CI 21.1-75.8)
The serum urate level neither confirms nor
excludes the diagnosis

Needle-like, negatively birefringent
crystals are seen on synovial fluid analysis

Figure 8: Tophi seen in the
helices of the ear.
Gout
Long-term, plain x-ray changes include juxta-
articular punched-out erosions
Figure 9: A gouty erosion seen along the medial

margin of the first metatarsal head.
Past Exam Question

Gout Treatment
62 yo man with hx of gout presents with acute painful
arthritis of his 1st right MTP joint. He has mild renal
impairment Cr. 136. What is the best treatment
option?
A. NSAID's
B. Allopurinol
C. Colchicine
D. Probenecid
E. Corticosteroids
Gout
Management of an acute attack:
NEVER stop prophylaxis
Non-pharmacologic: ~15% decrease in serum urate level
Dietary modification (alcohol, purine-rich foods, fructose)
Weight loss and exercise (metabolic syndrome)
Pharmacologic:
Young and eGFR >50ml/min NSAIDs
Elderly and eGFR >50ml/min Colchicine 500mcg BD
Elderly and eGFR <50ml/min Prednisolone
Monoarticular (not MTP) intra-articular corticosteroid
Polyarticular PNL 25-30mg
Gout
Prophylaxis:
Indications:
Recurrent attacks
Tophi
Erosive change on plain x-ray
Nephrolithiasis
Commence 1-2 weeks after acute attack (consider ongoing
medication)
Review every month and treat to target serum urate level
<0.36
Allopurinol
(Uricosuric agents eg. Probenicid)

Febuxostat (xanthine oxidase inhibitor)
Pseudogout
Calcium pyrophosphate dihydrate crystal
deposition disease
Typically affects the knee and wrist joints
OA
Hypercalcaemia
Hyperparathyroidism
Hypomagnesaemia
Hypothyroidism
Haemochromatosis
Past Exam Question

CPPD distribution
QUESTION 37
Which of the these joints is most likely to be involved in
pseudogout (calcium pyrophosphate deposition disease)?
A. Ankle
B. Knee
C. 1st Metacarpophalangeal
D. 1st Carpometacarpal
E. Wrist
Past Exam Question

CPPD distribution
QUESTION 37
Which of the these joints is most likely to be involved in
pseudogout (calcium pyrophosphate deposition disease)?
A. Ankle
B. Knee
C. 1st Metacarpophalangeal
D. 1st Carpometacarpal
E. Wrist
Pseudogout
Rhomboid, positively birefringent crystals are seen
on synovial fluid analysis

Chondrocalcinosis may be seen on plain x-ray:
Figure 10: Calcification of the menisci and articular cartilage that is typical of
chondrocalcinosis.
Pseudogout
Management of an acute attack:
Young and eGFR >50ml/min NSAIDs
Elderly and eGFR >50ml/min Colchicine 500mcg BD
Elderly and eGFR <50ml/min Prednisolone
Take Home Message

Condition
Acute Monoarthritis
Manifestations
Joint pain
Joint swelling
Limited range of
movement
Investigations
Joint aspirate
Blood cultures
When to Refer
Immediately
Polyarthritis
Rheumatoid Arthritis
Chronic autoimmune disease that causes
inflammation and deformity of the joints

Prevalence 1%, twice as common in women as men
Precise aetiology remains unknown
Smoking is the best defined risk factor
Timely diagnosis is critical to prevent uncontrolled
disease leading to irreversible joint damage
Ngian, G. (2010). Rheumatoid arthritis. Australian Family Physician; 39(9):626-628.
Typically, characterised by a symmetrical arthritis
affecting the wrists and, metacarpophalangeal and

proximal interphalangeal joints of the hands
ESR and CRP are usually elevated at diagnosis and
correlate with disease activity and treatment response

Testing for both rheumatoid factor and anti-CCP is
recommended
Aletaha, D et al. (2010). 2010 Rheumatoid Arthritis Classification Criteria. Arthritis & Rheumatism; 62(9):2569-81.
Rheumatoid Factor
About 1% of the normal population has a detectable
rheumatoid factor
In Rheumatoid Arthritis (RA), 70% of patients are
rheumatoid factor positive:

Its role in the pathogenesis of RA is unknown

Persistent high-titre rheumatoid factor predicts more
severe disease
Karsten, K et al (2010). Profiling of rheumatoid arthritis associated auto-antibodies, Autoimmunity Reviews; 9:431-5.
Anti-Citrullinated Peptide Antibodies

Pathogenic auto-antibodies of RA
Similar sensitivity to rheumatoid factor, but
superior specificity:
Detected in sera of patients years before
symptom onset
Best prognostic indicator for erosive RA
Karsten, K et al (2010). Profiling of rheumatoid arthritis associated auto-antibodies, Autoimmunity Reviews; 9:431-5.
Anti-Nuclear Antibody
13-25% of the normal population have a
detectable ANA, 2.5% at high titre

Found in both systemic and organ-specific
autoimmune disease eg. Graves disease (50%)

Pattern correlates poorly with diagnoses, except
anti-centromere
If high titre, also check eNA and dsDNA
Satoh M. et al (2012). Prevalence and sociodemographic correlates of antinuclear antibodies in the United States. Arthritis and
Rheumatism;10:1002/art.34380.
Anti-Nuclear Antibody
Referrals to a tertiary centre Rheumatology Clinic for
positive ANA:
232 patients
2.1% had Systemic Lupus Erythematosus, 9.1% had other
ANA associated disease

No disease identified in patients with ANA <1:160
Abeles, A.M. & Abeles, M. (2013). The clinical utility of a positive Antinuclear Antibody Test Result. The American Journal of
Medicine : 126:342-8.
Rather than relying on surrogate markers of
inflammation, imaging is increasingly being utilised to

assess disease activity
Plain x-ray:
Historical gold standard of erosion assessment
Marginal erosions, peri-articular osteopaenia and joint space narrowing
are classic features

X-Rays are abnormal at presentation in only 15-30% RA patients
Most useful for monitoring progression of joint damage over time
Yearly repetition is common practice
McQueen, F (2013). Imaging in early rheumatoid arthritis, Best Practice and Research Clinical Rheumatology; 27:499-522.
Figure 11: Typical plain x-ray changes in RA including marginal erosions, peri-articular
osteopaenia and joint space narrowing.
American College of Rheumatology (2014). Available from: http://images.rheumatology.org
Ultrasound:
Visualises both inflammatory disease activity and
structural joint damage

Greyscale synovitis correlates highly with DAS28 and
radiographic progression at 1 year

Detects 6.5-fold more erosions in early disease
compared with plain x-ray

Power Doppler signal predicts clinical relapse (OR 6.3
95% CI 2.0-20.3)
Thiele, RG (2012). Ultrasonography applications in diagnosis and management of early rheumatoid arthritis, Rheumatic
Diseases Clinics of North America; 38:259-75.
MRI:
Ideally suited to image bony structures and cartilage,
as well as soft tissues and fluid
Detects erosions involving <20% bone volume loss of
metacarpal head
Unique capacity to image bone marrow oedema
In undifferentiated arthritis, predicts RA onset with
sensitivity of 100% and specificity of 78%

Availability, cost and contraindications problematic
McQueen, F (2013). Imaging in early rheumatoid arthritis, Best Practice and Research Clinical Rheumatology; 27:499-522.
Aggressive treatment to achieve clinical
remission is imperative:
Symptomatic:
Simple analgesia
NSAIDs/omega 3 fatty acids
Low-dose glucocorticoids eg. PNL 15mg daily
Disease modifying agents:
Methotrexate
Combination DMARD therapy eg. MTX + HCQ + SSZ
Biologics eg. TNF inhibitors
Take Home Message

Condition
Inflammatory
Polyarthritis
Manifestations
Joint pain
Joint swelling
Extended early
morning stiffness
Investigations
ESR elevated
CRP elevated
Rheumatoid
factor
Anti-CCP
ANA
Plain x-ray hands
When to Refer
Urgent outpatient
referral
Back pain: Inflammatory vs. Mechanical
Past Exam Question

An 18 year old has a two year history of recurrent
swelling of the knees and ankles which usually settles
after 1-2 weeks. They have also had intermittent crampy
abdominal pain and diarrhoea for the last 6 months. The
timing of the arthritis and diarrhoea do not appear to be
related. Which test is most likely to make the diagnosis?
A. Colonoscopy
B. HLA-B27
C. Plain XR of the joints
D. Rheumatoid factor
E. Stool culture
Back pain features:

Inflammatory vs. Mechanical
Golder, V & Schachna, L (2013). Ankylosing spondylitis: an update. Australian Family Physician; 42(11):780-4.
Spondyloarthritis
Encompasses a group of rheumatic disorders that
share clinical, genetic and radiographic features
Ankylosing Spondylitis
Chronic inflammatory condition of the sacroiliac
joints and spine

Affects 1 in 200 individuals
Male:female ratio 2:1

Extra-axial features include peripheral arthritis (up
to 50%), enthesitis, dactylitis and anterior uveitis

(40%)
Reduced spinal mobility is seen on examination
ESR and CRP are elevated in only 50-70% of
cases
HLA-B27:
Between 5-15% of the general population are HLAB27 positive, but only 5% of these develop AS
In AS patients, HLA-B27 occurs in 85-90%
Consequently, HLA-B27 has no role as a general
screening test for spinal pain
Diagnosis requires inflammatory back pain and
changes on plain x-ray of the pelvis
Figure 13: Radiographic grading of sacroiliac joints.

Non-Radiographic Axial SpA

Early presentation of AS,
prior to plain x-ray changes

50% of patients will evolve
into AS
A tailored exercise and stretching program is
recommended
NSAIDs are first-line therapy for symptomatic AS
Traditional DMARDs play no role in axial disease
TNF inhibitors can be initiated in patients with an
inadequate response to NSAIDs
Case 4
Management?
Tailored exercise and stretching program:
www.nass.co.uk/exercise
Celecoxib 200mg daily
Semi-urgent outpatient Rheumatology referral
Axial involvement non-responsive to above:
TNFi incl. Golimumab, Humira, Infliximab
Non-axial involvement
Methotrexate, Sulfasalazine
Past Exam Question

A 23 yo male presents with 1 week of arthralgias and
2 days of arthritis of the left wrist and right knee. On
examination there is tenosynovitis of the extensor
tendons of the left forearm, and a pustular rash on the
palm of his left hand. The most likely diagnosis is:
A. Ankylosing Spondylitis
B. Enteropathic arthritis
C. Gonococcal arthritis
D. Psoriatic arthritis
E. Reactive arthritis
Take Home Message

Condition
Inflammatory Low
Back Pain
Manifestations
Low back pain

Extended early
morning stiffness
Peripheral
arthritis
Enthesitis
Dactylitis
Anterior uveitis*
Investigations
ESR ?elevated
CRP ?elevated
Plain x-ray pelvis
HLA-B27
When to Refer
Semi-urgent
outpatient referral
Thank-you! Questions?

Rheumatology - For BPTs

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Rheumatology for BPTs

Acknowledgment to Dr Claire Owen for

Back pain Inflammatory vs. Mechanical

PMR and GCA

Previous Exam Question

Previous Exam Question

inflammatory disorder of unknown cause

girdle pain, and prolonged early morning stiffness

Most common inflammatory rheumatic disease of the

incidence risk (2.43% for women and 1.66% for men)

course is well recognised:

pitting oedema, carpal tunnel syndrome (~50%)

bursitis are similarly consistent with PMR

Management of PMR represent a recently

PNL 10mg daily for 4 weeks, wean by 1mg every 4

Giant Cell Arteritis

with a predilection for the aorta and its branches

tenderness and jaw claudication

GCA: history & examination features

Giant Cell Arteritis

Long-term, GCA patients can develop large vessel

Figure 3: Stenosis of the left subclavian

Giant Cell Arteritis

Giant Cell Arteritis

Figure 4: Temporal artery biopsy demonstrating segmental destruction of internal

Giant Cell Arteritis

promoted the use of imaging modalities

demonstrated in some patients with GCA:

Figure 5: Colour duplex ultrasound

Giant Cell Arteritis

GCA without a major contraindication

Giant Cell Arteritis

following recurrent relapse or failure to wean PNL

Take Home Message

Previous Exam Question

DDx of acute monoarthritis

Serum urate level

Synovial Fluid Analysis

Hip or knee prosthesis

and limited range of motion

most useful finding in making an early diagnosis:

Rapidly progressive joint destruction is seen on

plain x-ray in untreated cases

Past Exam Question

Infection Risk in Rheumatology

infection due to:

Prednisolone is associated with one of the highest

overall infection risks

commencement (RR 4.6 in first 90 days)

Past Exam Question

Past Exam Question

The serum urate level neither confirms nor

excludes the diagnosis

crystals are seen on synovial fluid analysis

articular punched-out erosions

Figure 9: A gouty erosion seen along the medial

Past Exam Question

Commence 1-2 weeks after acute attack (consider ongoing

(Uricosuric agents eg. Probenicid)

Past Exam Question

Past Exam Question

on synovial fluid analysis

Take Home Message

inflammation and deformity of the joints