Inflammatory Joint and Rheumatoid arthritis Flashcards
What are the 4 cardinal signs of inflammation?
- calor (heat)
- rubor (redness)
- tumour (swelling)
- dolor (pain)
- Functio laesa (loss of function)
What age / demographic would you expect to see an inflammatory arthritis compared to a degenerative arthritis?
Inflammatory - any age, young, those with psoriasis, those with family history
Degenerative - usually occurs later in life, older patients, relates to prior occupation or sports.
What is the speed of onset for inflammatory and degenerative arthritis?
Inflammatory - rapid (weeks to months)
Degenerative - slow (over years)
What joint distribution would you expect to see in inflammatory vs degenerative arthritis?
Inflammatory - symmetrical polyarthritis & synovial swelling
- Small joints of hands and feet
Degenerative - initially asymmetrical monoarthritis, then involving more bones. Bony swellings
- Weight bearing joints: knees, hips, thumb base, big toe.
Duration of morning stiffness for inflammatory vs degenerative arthritis? Does pain increase or decrease with use?
Inflammatory
- worse in the morning and at rest lasting >1hr
- pain eases with use
Degenerative
- stiffness <1hr and worse at end of the day or after activity
- pain increases with activity/use
Would we expect to see systemic symptoms in inflammatory or degenerative arthritis?
Inflammatory - fatigue, fever, night sweats
What is the difference in the response to NSAIDs between inflammatory and degenerative arthritis?
Inflammatory - responds well to NSAIDs
Degenerative - does not respond as well to NSAIDs
What questions would you ask if someone presents with joint pain?
- Is it inflammatory?
- Visible joint swelling
- Elevated CRP
- Variable symptoms with flares
- Joint pattern?
- Pattern of joints involved
- Is it symmetrical or asymmetrical
- Associated symptoms and risks?
- Extra-articular features (rashes or photosensitivity - SLE)
- Dry eyes and mouth (Sjorgens)
- Psoriasis (particularly with nail involvement)
- Inflammatory eye or bowel symptoms
- Family history (psoriasis, autoimmune disease) and smoking history (RA)
- Social history - occupation, age, sex, ability to function (dressing), smoking.
What do we always need to exclude in anyone presenting with an acutely inflamed joint? How do we exclude it?
Septic arthritis - exclude with joint aspiration
What is rheumatoid arthritis? Pattern of joint distribution?
RA is an autoimmune chronic systemic inflammatory disease of synovial joints.
It is characterised by symmetrical deforming, peripheral polyarthriris
Pathophysiology of rheumatoid arthritis?
- Chronic inflammatory reaction where T cells enter the joint space and secrete cytokines which recruit macrophages which produce even more cytokines
- Infiltration of lymphocytes, macrophages & plasma cells
- These cytokines stimulate synovial cells to proliferate
How is a pannus formed in rheumatoid arthritis?
- Tumour like mass ‘pannus’ is formed which is a thick, swollen synovial membrane with granulation tissue made up of fibroblasts, myofibroblasts and inflammatory cells
- Over time, the pannus causes damage to cartilage and erodes the bone causing joint space narrowing.
- Activated synovial cells secrete proteases which break down cartilage and therefore, the bones are exposed and can rub against eachother.
- Antibodies also enter the joint space (rheumatoid factor and anti-CCP) and these bind to their targets and form immune complexes which accumulate in the synovial fluid & activates the complement system promoting joint inflammation and injury.
Why do extra-articular symptoms occur with rheumatoid arthritis?
Inflammatory cytokines do not stay in the joint space but they enter the blood stream and affect other organs of the body such as skeletal muscle, skin (nodules), blood vessels (atheroma), liver, lung (effusions), brain (fever) etc.
What percentage of the population is affected by RA? Is it more common in males or females?
What are the main risk factors?
Peak age of onset?
1%
More common in females (2-3x)
Family history and smoking are main risks
Peak onset - 5-6th decade
What is the typical presentation of someone with RA?
What are the common joints affected?
- Symmetrical, swollen, painful and stiff small joints (hands and feet), worse in the morning or after periods of inactivity
- There can be a loss of function of those joints and the pt can present with general fatigue & malaise.
- Extra-articular involvement
Common joints affected - usually affects >5 joints symmetrically - Small joints (metacarpophalangeal MCP) Proximal interphalangeal (PIP) Metatarsophalangeal (MTP) No DCP involvement
What are some later joint signs we can see in someone with RA?
Joint damage, deformities
Ulnar deviation and sublaxation of the wrist and fingers
Boutonniere and swan neck deformities or Z-finger of thumbs
Larger joints can begin to become involved
Atlanto-axial joint sublaxation may threaten the spinal cord (rare) and cause instability of the cervical spine
Extra-articular manifestations of RA?
- Nodules
- lymph nodes may be palpable and spleen may be enlarged
- Lungs - pleural disease and effusion
- Cardiac - IHD, pericarditis, pericardial effusion
- Eye - episcleritis, scleritis (corneal ulceration), scleromalacia, dry eyes
- Carpal tunnel syndrome
- Peripheral neuropathy
Investigations for RA? What would we expect to see in bloods and X ray?
Rheumatoid factor positive in 70% patients
Anticyclic citrillinated peptide antibodies (anti-CCP) - positive in 70% patients
Bloods
- anaemia with chronic disease
- increased platelets, ESR, CRP
X-ray
- Soft tissue swelling
- Periarticular osteopenia (decreased bone density)
- joint space narrowing
- bony erosions
How do we manage RA?
- refer to rheumatology
- DMARDs to suppress inflammation - methotrexate, hydroxychloroquine)
- Biological response modifiers - Rituximab suppresses B cells
Abatacept suppresses T cells - Acute flares: steroids for exacerbations (intra-articular)
- NSAIDs good for symptom relief but no effect on disease progression
- Manage other risk factors - RA = increase in CVD and cerebrovascular disease, stop smoking etc.
What are the 7 similarities between seronegative arthritis?
- All negative for rheumatoid factor and positive for HLA-B27
- Axial arthritis - pathology in the spine and sacroiliac joints
- Asymmetrical, large joint oligoarthritis (<5 joints) or monoarthritis
- They all can cause enthesitis (Achilles tendonitis, Plantar fasciitis, Costochondritis)
- Dactylitis - (sausage digit) due to soft tissue oedema and tenosynovial and joint inflammation
- Extra-articular symptoms
→ IBD - gastrointestinal involvement
→ GI infection
→ Eye inflammation
→ Psoriasis - nail involvement
→ Dactylitis, nail pitting and whitening & lifting of nail from nail bed
→ Percarditis or aortic regurgitation - All have good response to NSAIDs and elevated CRP
What is gout? What is the typical presentation? What causes the pain? Does it affect men or women more commonly? What condition do we need to exclude on presentation?
Inflammatory disease where monosodium urate crystals deposit in the joints making them red, hot, tender & swollen.
Typically presents with acute monoarthropathy with severe joint inflammation and intermittent episodes. 50% occur at metatarsophalangeal joint of the big toe (podagral) where pt wakes up feeling like big toe is on fire.
Pain is felt due to WBCs infiltrating the joint to remove uric acid and releasing pro-inflammatory cytokines.
Affects men x6 more than women.
Exclude septic arthritis.
What can precipitate a gout attack?
Trauma Surgery Starvation and dehydration Infection Diuretics Alcohol or shellfish binge Most attacks are spontaenous
Risk factors for gout?
Reduced urate excretion and excess urate production causes
Reduced urate excretion
- Impaired renal function
- Diuretics (thiazide)
- Aspirin
- Elderly
- Men
- Post-menopausal women
- HTN
- Metabolic syndrome
- Antihypertensives
Excess urate production
- Dietary (alcohol, seafood, organ meat)
- Genetic disorders
- Psoriasis
- tumour lysis syndrome (tumour broken down rapidly & causes increased uric acid)
- Drugs (alcohol, warfarin, cytotoxics)
Investigations for gout
Routine bloods
- inflammatory markers
- uric acid (between attacks)
- joint aspiration confirms diagnosis (negatively birefringent urate crystals)
- x ray shows soft tissue swelling and later shows punched out erosions
Treatment for gout
Rest and elevate joint
High dose NSAID or colchicine is NSAID contraindicated
(NSAIDs and colchicine both problematic in renal failure)
Steroids - prednisolone may be used directly into joint or oral.
Prevention of gout?
Weight loss, avoiding prolonged fasting
Avoid excess alcohol and purine rich foods and low dose aspirin
Prophylaxis for gout? when do we start this treatment?
Started if more than 1 episode per year or if renal stones
- allopurinol - xanthine oxidase inhib stops production of uric acid
- get uric acid level <300
What is pseudogout? Who does it most commonly affect, what other condition does it commonly overlap with?
Type of arthritis which causes similar symptoms to gout yet is formed by different crystal types (calcium pyrophosphate) which triggers the reaction.
Predominantly a disease of the elderly and overlap with osteoarthritis
Areas affected by pseudogout?
Knees>Wrists>Shoulders>Ankles>Elbows
Risk factors for pseudogout?
- Old age
- Hyperparathyroidism
- Haemochromatosis
- Hypophosphataemia
- Hypothyroidism
- Acromegaly
Tests for pseudogout? What do we see on xray?
Tests
- Routine bloods - iron, PTH, PO4, Mg, TSH
- Inflammatory markers
- Uric acid
- Joint aspiration is diagnostic
- Polarised light microscopy of synovial fluid shows weakly positive birefringent crystals.
- Soft tissue calcium deposition on x ray
Acute and chronic pseudogout management?
- Acute attacks*
- Cool packs, rest, aspiration, intra-articular steroids, NSAIDs (+PPI) used with caution may prevent acute attacks.
- Chronic*
- Long term low dose of pred or colchicine might be used in chronic
- Methotrexate and hydrocholoroquine may be considered for chronic CPP inflammatory arthritis.
