Inflammatory arthritis

• Rheumatoid arthritis is an autoimmune condition mainly affecting the joints of the body.

• Typical features are morning stiffness, joint pain relieved by movements and aggravated by rest.

• Basic investigations for patients with suspected rheumatoid arthritis/inflammatory arthritis
• FBE
• UEC
• LFT
• ESE
• CRP
• Anti CCP
• RA
• ANA
• ENA 

• DMARDs have made significant improvement in patients with RA. We don't see patients with RA with severe deformities anymore. The best outcome is when patients are started on DMARDs early, so refer early. 

• Methotrexate is the first line DMARD for RA at the moment. Cheap, relatively easy and safe to take. Common side effects: nausea and mouth ulcers. Monitor LFT and FBE monthly. 

Approach to tiredness/fatigue

Tiredness/chronic fatigue: diagnostic strategy model

Probability diagnosis

• Stress and anxiety
• Depression
• Viral/postviral infection 
• Sleep-related disorder (e.g. sleep apnoea)

Serious disorders not to be missed

• malignant disease
• cardiac arrhythmia (e.g. sick sinus syndrome)
• cardiomyopathy
• anaemia 
• hidden abscess
• haemochromatosis
• HIV infections 
• Hepatitis C

Pitfalls

• 'Masked' depression
• Food intolerance
• Coeliac disease
• Chronic infection (e.g. lyme disease)
• Incipient CCF
• Fibromyalgia
• Lack of fitness
• Drugs: alcohol, prescribed, withdrawal
• Menopause syndrome
• Pregnancy
• Neurological disorders
• post-head injury
• CVA
• Parkinson disease
• Kidney failure
• Metabolic (e.g. hypokalaemia, hypomagnesaemia)
• Chemical exposure (e.g. occupational)
• Rarities
• Hyperparathyroidism
• Addison disease
• Cushing syndrome
• Narcolepsy
• Multiple sclerosis
• Autoimmune disorders

Minimal investigations from John Murtagh General practice 5th edition:

• FBE
• ESR/CRP
• TFTs
• Coeliac serology
• LFT
• CMP
• BSLs
• Iron studies
• Urine MCS

Paget's disease

Paget's disease

• a chronic disorder of the adult skeleton in which new soft bone replaces localised areas of normal bone
• cause unknown 

Clinical features

• M:F ratio 2:1
• 95% asymptomatic 
• symptoms include joint pain and stiffness (e.g. hips, knees), bone pain (usually spine), deformity. headache and deafness
• Bone pain is typically deep and aching; it occurs at rest, particularly at night
• signs may include deformity, enlarged skull, bowing of tibia, waddling gait and hyper dynamic circulation 

Diagnosis

• Page's disease is diagnosed radiologically 
• early: lytic lesions or flame shaped, advancing lytic wedges in long bones
• late: mixed lytic and sclerotic areas, thickened trabecular, bone expansion, cortical thickening and deformity
• isotope bone scanning is more sensitive

Investigation (2)

• Plasma alkaline phosphatase
• Liver function tests
• Vitamin D levels
• Isotope bone scan
• Radiography of affected bones

Treatment 

• Asymptomatic disease dose not require treatment
• indications for treatment 
• pain 
• neurological complications 
• significant osteolytic lesions 
• involvement of long bones, vertebrae or base of skull 
• before surgery involving pagetic bones
• significant joint involvement 
• Recommended drugs
• zoledronic acid 5 mg single dose, given IV over 15 mins
• alendronate 40 mg daily, given orally for 3-6 months
• risedronate 30 mg daily, given orally for 2 months

References

1. John Murtagh p.747
2. http://www.racgp.org.au/afp/2012/march/paget-disease-of-bone/

Approach to pain in the arm and hand

Pain in the arm and hand: diagnostic strategy model

Probabiligy diagnosis

• Dysfunction of the cervical spine 
• Disorders of the shoulder
• Medial or lateral epicondylitis
• Overuse tendonitis of the wrist
• Carpal tunnel syndrome 
• Osteoarthritis of the thumb and DIP joints

Serious disorders not to be missed

• Cardiovascular 
• angina
• myocardial infarction 
• axillary vein thrombosis
• Neoplasia
• pancoast tumour
• bone tumours
• Severe infections
• septic arthritis (shoulder/elbow)
• osteomyelitis
• infections of tendon sheath and fascial spaces of hand 

Pitfalls (often missed)

• Entrapment neuropathies
• Pulled elbow 
• Foreign body 
• Rarities
• polymyalgia rheumatica
• Reflex sympathetic dystrophy
• Thoracic outlet syndrom e
• Arm claudication 
• kienbock disorder

Approach to neck pain

Neck pain: diagnostic strategy model

Probability diagnosis 

• vertebral dysfunction 
• traumatic strain or sprain 
• cervical spondylosis

Serious disorders not to be missed

• Cardiovascular
• angina
• subarachnoid haemorrhage
• arterial dissection 
• Neoplasia
• primary 
• metastasis --> breast, prostate and lung. also kidney, thyroid and melanoma.
• Pancoast tumour --> Horner's syndrome
• Severe infections
• osteomyelitis
• meningitis
• Vertebral fractures or dislocation

Pitfalls

• Disc prolapse
• Myelopathy
• Cervical lymphadenitis
• Fibromyalgia syndrome 
• Outlet compression syndrome 
• Polymyalgia rheumatica
• Ankylosing spondylitis
• Rheumatoid arthritis
• Oesophageal foreign bodies and tumours
• Paget disease

Red Flags

• History of major trauma
• Age > 50 years
• Constant pain (day and night)
• Fever > 38 
• Anterior neck pain 
• History of cancer
• Unexplained weight loss
• Neurological deficit
• Radicular pain in arm 
• Rheumatoid arthritis
• Down syndrome 

Sarcoidosis

Condition

• Sarcoidosis

Definitions

• Sarcoidosis is a multisystemic disorder of unknown aetiology which is characterised by non-caseating granulomatous inflammation that involves the lung in about 90% of affected patients. A characteristic feature is bilateral hillier lymphadenopathy, which is often symptomless and detected on routine chest x-ray (CXR). Radiological lung involvement can be associated with or occur independently of hillier lymphadenopathy. 

Main features

• May be asymptomatic (one-third)
• Onset usually third or fourth decade
• Bilateral hilar lymphadenopathy (on CXR)
• Cough
• Fever, malaise, arthralgia
• Erythema nudism
• Ocular lesions (e.g. anterior uveitis)
• Other multiple organ lesions (uncommon)
• Overall mortality 2-5%

Investigation

• diagnosis is usually made by biopsy
• Female with erythema nodosum with an acute swinging fever, malaise and arthralgia in a young adult female is diagnostic of sarcoidosis

Treatment

• Referral

Reference

• John Murtagh's general practice 5th edition 

Scleroderma (Systemic sclerosis)

Condition

• Scleroderma 

Definition

• Chronic systemic autoimmune disease characterised by hardening of the skin 
• 3 clinical variants
• limited cutaneous disease, for example, morphea
• cutaneous with limited organ involvement (CREST: calcinosis, raynaud phenomenon, oesophageal dysmotility, sclerodactyly, telangiectasia + anticentromere antibody)
• diffuse systemic disease (systemic sclerosis)

Main features

• Female to male ratio 3:1
• A progressive disease of multiple organs
• Raynaud phenomenon 
• Stiffness of fingers and other skin areas
• Bird like faces (mouth puckered)
• Dysphagia and diarrhoea 
• Respiratory symptoms 
• Cardiac symptoms such as pericarditis
• Look for tight skin on chest (Roman breastplate)

Murtagh diagnostic triad

• Finger discomfort + arthralgia + GORD +/- skin tightness = scleroderma

Investigations

• ESR may be raised
• Normocytic normochromic anaemia may be present t
• ANA test up to 90% positive
• Rheumatoid factor +ve in 30%
• Anticentromere antibodies - specific (positive in 90% with limited disease and 5% with diffuse)
• Antitopoisomerase (anti-Scl-70) antibody is specific but positive in 20% - 40% 
• Skin biopsy - increase in derma collagen 

Treatment

• Analgesics for pain 
• Avoid vasospasm (no smoking, beta blockers, ergotamine); calcium channel blockers such as nifedipine may help Raynaud
• Treat malabsorption if present, skin emollients
• D-penicillamine can help if there is significant systemic or cutaneous involvement 

References

1. John Murtagh's general practice 5th edition

Gout

Key points:

1. Gout is the most common inflammatory arthritis with a prevalence of about 2% in Australasia.
2. Key steps in the development of gout are 1)chronic hyperuricemia 2) monosodium rate monohydrate 3)interaction between the crystals and the inflammatory system, which is primarily responsible for the clinical features. 
3. Definition of hyperuricemia: serum rate level > 0.42
4. Hyperuricemia is caused by medications and genetic predisposition
5. Only 20% of patients with hyperuricemia develop gout 
6. Definite diagnosis can only be achieved via synovial fluid analysis. This needs to be done before recommending hypouricemic drug therapy.
7. Management of acute gout:
   
   8. There is an increase risk of gout when the patient is started on rate lowering therapy. Patients can be started on low dose colchicine 0.5 mg daily or daily NSAID or 5mg prednisolone. Usually prophylaxis is required for around 3-6 months.
   
   
   9. Serum rate target is less than 0.36 mmol/L, however for patients with a large rate crystal load (as reflected by the presence of tophi) erosions or chronic joint deformity due to gout, the target is a serum rate of less than 0.3 mol/L
   
   
   10. Diet and lifestyle modification alone usually is inadequate to lower serum urate level.
   
   
   11. Allopurinal hypersensitivity syndrome occurs with greater frequency in the setting of renal insufficiency, advanced age, HLA B58:01 positivity and higher initial doses but can occur in their absence. The syndrome usually occurs in the first 12 weeks of exposure, and thus the development of rash during this period should prompt immediate cessation of allopurinol, assessment of liver and renal function, and for the possibility of hypersensitivity. 
   
   
   12.Probenecid is another agent which can be used as rate lowering agent. But the patient needs to have renal function > 30-40ml/min. Because of the marked increase in urinary uric acid in the early phase of treatment, good hydration and urinary alkalisation are appropriate. 
   
   
   
   
   
   
   

Ankylosing spondylitis

Key features:

- Ankylosing spondylitis encompasses a group of rheumatic disorders that share clinical, genetic and radiographic features and includes psoriatic arthritis, reactive arthritis or inflammatory bowel disease.

- Affects 1 in 200 individuals and is usually diagnosed many years after onset of symptoms . Chronic back pain is common and recognition of early disease requires clinical experience and a high index of suspicion. Further, inflammatory markers are not invariably elevated and radiographic changes are often late findings.

  - The presence of inflammatory back pain (IBP), the archetypal feature of AS, increases the likelihood of SpA to approximately 14%.

- Two very specific features of IBP are alternating buttock pain and awakening only in the second half of the night with spinal pain or stiffness. Table listed the difference between inflammatory and mechanical back pain

- Examination findings:

• Reduced spinal mobility: modified schober's test, lumbar side flexion and occiput to wall distance.
• Extra axial features: 50% asymmetric oligoarthrits (< 4joints), often targeting the lower limb joins, enthesitis and dactylitis.
• Extra-articular features: uniocular anterior uveitis in 40% of patients (presents with acute painful red eye, blurred vision and photophobia)

- Investigation findings: 

• Lab test: CRP, ESR (Only 50-70% of AS patients), HLA-B27
• Imaging: x-rays

References:

- http://www.racgp.org.au/download/Documents/AFP/2013/November/201311golder.pdf

Fish Oil

Fish Oil

Key points:

- Fish oil has been reported to have anti-inflammatory and immunosuppressive effects, and it also result in decreased platelet activity. (beware of procedures)
- Long chain omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have anti-inflammatory properties when taken in doses greater than 2.7g daily.
- It is safe to use but compliance and cost is an issue as to have the inflammatory effect, patient needs to take quite many tablets per day. The following table is from therapeutic guideline:

References:
therapeutic guideline: rheumatology. Getting to know your drug.

NSAIDs - How to prevent GI bleed?

NSAIDs - How to prevent GI bleed?


I saw a young man today with likely ankylosing spondylitis. I started him on NSAIDs. He told me that he suffers from reflux, this brings up a question, how can I reduce the GI side effect?

How does it work ? (This is to remind myself, I seriously can't remember)

Key points:

1. No one NSAID is safer another. 

2. Use low dose NSAIDs for the shortest time possible. 

3. COX-2 NSAIDs seem to have less GI side-effects

4. Co-infection of H. Pylori and the use of NSAIDs increase the risk of GI ulcer by 60 folds and bleeding by 6 folds. 

5. Other drugs which can increase bleeding risks include: anti platelets, anti coagulants, anti depressants, corticosteroids, cigarette, smoking and excessive ETOH consumption.

6. Some other risk factors of GI bleed: 

7. Consider the use of PPI in high risk groups: 

Reference:

Australian therapeutic guideline 

Gout

Gout

Key points:

1. Gout is the most common inflammatory arthritis with a prevalence of about 2% in Australasia.
2. Key steps in the development of gout are 1)chronic hyperuricemia 2) monosodium rate monohydrate 3)interaction between the crystals and the inflammatory system, which is primarily responsible for the clinical features. 
3. Definition of hyperuricemia: serum rate level > 0.42
4. Hyperuricemia is caused by medications and genetic predisposition
5. Only 20% of patients with hyperuricemia develop gout 
6. Definite diagnosis can only be achieved via synovial fluid analysis. This needs to be done before recommending hypouricemic drug therapy.
7. Management of acute gout:
1. 
8. There is an increase risk of gout when the patient is started on rate lowering therapy. Patients can be started on low dose colchicine 0.5 mg daily or daily NSAID or 5mg prednisolone. Usually prophylaxis is required for around 3-6 months.
9. Serum rate target is less than 0.36 mmol/L, however for patients with a large rate crystal load (as reflected by the presence of tophi) erosions or chronic joint deformity due to gout, the target is a serum rate of less than 0.3 mol/L/
10. Diet and lifestyle modification alone usually is inadequate to lower serum urate level.
11. Allopurinal hypersensitivity syndrome occurs with greater frequency in the setting of renal insufficiency, advanced age, HLA B58:01 positivity and higher initial doses but can occur in their absence. The syndrome usually occurs in the first 12 weeks of exposure, and thus the development of rash during this period should prompt immediate cessation of allopurinol, assessment of liver and renal function, and for the possibility of hypersensitivity. 
12. Probenecid is another agent which can be used as rate lowering agent. But the patient needs to have renal function > 30-40ml/min. Because of the marked increase in urinary uric acid in the early phase of treatment, good hydration and urinary alkalisation are appropriate.