Inflammatory Joint and Rheumatoid arthritis Flashcards

1
Q

What are the 4 cardinal signs of inflammation?

A
  • calor (heat)
  • rubor (redness)
  • tumour (swelling)
  • dolor (pain)
  • Functio laesa (loss of function)
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2
Q

What age / demographic would you expect to see an inflammatory arthritis compared to a degenerative arthritis?

A

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.

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3
Q

What is the speed of onset for inflammatory and degenerative arthritis?

A

Inflammatory - rapid (weeks to months)

Degenerative - slow (over years)

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4
Q

What joint distribution would you expect to see in inflammatory vs degenerative arthritis?

A

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.

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5
Q

Duration of morning stiffness for inflammatory vs degenerative arthritis? Does pain increase or decrease with use?

A

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
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6
Q

Would we expect to see systemic symptoms in inflammatory or degenerative arthritis?

A

Inflammatory - fatigue, fever, night sweats

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7
Q

What is the difference in the response to NSAIDs between inflammatory and degenerative arthritis?

A

Inflammatory - responds well to NSAIDs

Degenerative - does not respond as well to NSAIDs

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8
Q

What questions would you ask if someone presents with joint pain?

A
  1. Is it inflammatory?
    • Visible joint swelling
    • Elevated CRP
    • Variable symptoms with flares
  2. Joint pattern?
    • Pattern of joints involved
    • Is it symmetrical or asymmetrical
  3. 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.
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9
Q

What do we always need to exclude in anyone presenting with an acutely inflamed joint? How do we exclude it?

A

Septic arthritis - exclude with joint aspiration

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10
Q

What is rheumatoid arthritis? Pattern of joint distribution?

A

RA is an autoimmune chronic systemic inflammatory disease of synovial joints.
It is characterised by symmetrical deforming, peripheral polyarthriris

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11
Q

Pathophysiology of rheumatoid arthritis?

A
  • 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
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12
Q

How is a pannus formed in rheumatoid arthritis?

A
  • 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.
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13
Q

Why do extra-articular symptoms occur with rheumatoid arthritis?

A

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.

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14
Q

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?

A

1%
More common in females (2-3x)
Family history and smoking are main risks
Peak onset - 5-6th decade

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15
Q

What is the typical presentation of someone with RA?

What are the common joints affected?

A
  • 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
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16
Q

What are some later joint signs we can see in someone with RA?

A

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

17
Q

Extra-articular manifestations of RA?

A
  • 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
18
Q

Investigations for RA? What would we expect to see in bloods and X ray?

A

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
19
Q

How do we manage RA?

A
  • 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.
20
Q

What are the 7 similarities between seronegative arthritis?

A
  1. All negative for rheumatoid factor and positive for HLA-B27
  2. Axial arthritis - pathology in the spine and sacroiliac joints
  3. Asymmetrical, large joint oligoarthritis (<5 joints) or monoarthritis
  4. They all can cause enthesitis (Achilles tendonitis, Plantar fasciitis, Costochondritis)
  5. Dactylitis - (sausage digit) due to soft tissue oedema and tenosynovial and joint inflammation
  6. 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
  7. All have good response to NSAIDs and elevated CRP
21
Q

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?

A

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.

22
Q

What can precipitate a gout attack?

A
Trauma
Surgery
Starvation and dehydration
Infection
Diuretics 
Alcohol or shellfish binge
Most attacks are spontaenous
23
Q

Risk factors for gout?

Reduced urate excretion and excess urate production causes

A

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)
24
Q

Investigations for gout

A

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
25
Q

Treatment for gout

A

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.

26
Q

Prevention of gout?

A

Weight loss, avoiding prolonged fasting

Avoid excess alcohol and purine rich foods and low dose aspirin

27
Q

Prophylaxis for gout? when do we start this treatment?

A

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
28
Q

What is pseudogout? Who does it most commonly affect, what other condition does it commonly overlap with?

A

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

29
Q

Areas affected by pseudogout?

A

Knees>Wrists>Shoulders>Ankles>Elbows

30
Q

Risk factors for pseudogout?

A
  • Old age
  • Hyperparathyroidism
  • Haemochromatosis
  • Hypophosphataemia
  • Hypothyroidism
  • Acromegaly
31
Q

Tests for pseudogout? What do we see on xray?

A

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
32
Q

Acute and chronic pseudogout management?

A
  • 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.