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Inflammatory and Crystal Arthropathy Flashcards

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1
Q

What is rheumatoid arthritis?

A

RA is an autoimmune disorder characterized by a deforming bilateral symmetrical arthritis affecting the peripheral joints.

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2
Q

What is the clinical presentation of rheumatoid arthritis?

A
  1. Articular manifestations
    1. Pain and stiffness of small joints
    2. Morning stiffness (>1 hour unlike other similar inflammatory arthropathies)
    3. Disturbed sleep
  2. B-symptoms (fatigue, anemia etc)
  3. Non-articular manifestations
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3
Q

What are the non-articular manifestations of rheumatoid arthritis?

A

Non-articular:

  1. Eyes: sicca syndrome, scleritis/episcleritis
  2. Lungs: Bronchiectasis/ILD
  3. Heart and peripheral vessels: Pericarditis, endocarditis, raynaulds
  4. Abdomen: Splenomegaly: Felty’s syndrome)
  5. Neuro: mononeuritis multiplex, cord compression from atlantoaxial subluxation, Compression neuropathies from synovitis
  6. NCNC inflammation
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4
Q

What are the orthopedic complications of RA?

A
  1. Synovitis
  2. Deformities
  3. Tendon rupture
  4. Late arthritis
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5
Q

What are the presentations for RA?

A
  1. Typical RA
  2. Episodic (one to severel joints, symptoms last weeks to months)
    1. Monoarthritis (Can have trauma preceding, persistent single joint arthritis) - important to ruel out septic arthrits and crystal arthritis)
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6
Q

What are the risk factors of RA?

A
  • Demographics
    • Female
    • 30-50
  • Genetics: family history,
  • Exposure/Lifestyle
    • Smoking
    • Occupation (Asbestos, silica)
  • Protective: estrogen
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7
Q

What investigations would you do in RA?

A
  1. Diagnosis
    1. Inflammatory markers: ESR, CRP
    2. Serology: ACPA, ANA, RF
  2. Rule out differentials
    1. Joint aspiration
  3. Complications
    1. X-Ray: Erosion, subluxation
    2. HRCT - pulmonary embolism
    3. ECG
  4. Management (before immunosuppression
    1. TB
    2. Hep B/C
    3. LFT (methotrexate is toxic)
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8
Q

How do you diagnose RA?

A

ACR classification 2010

This requires the presence of synovitis in at least 1 joint, the absence of an alternative that better explains the synovitis and a score of 6/10.

  • Number of joints
  • Serology (RF, ACPA)
  • Acute phase reactants (CRP, ESR)
  • Duration of symptoms
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9
Q

How do you manage RA?

A

Conservative:

  1. Education
  2. Lifestyle Management
    1. Exercise
    2. Weight loss
    3. Smoking cessation
    4. Rest (during acute flare)
  3. Physiotherapy
  4. Counselling - psycho-social issues, improve Self-esteem
  5. Job/home modification

Medical:

  1. NSAIDS
  2. Anti-inflammatories (Glucocorticoids)
    1. Prednisolone 5-15mg/day
  3. Disease-modifying anti-rheumatic drugs
    1. Methotrexate (1st line)
    2. Sulfasalazine
    3. Leflunomide
    4. Hydroxychloroquine
  4. TNF-Alpha blockers
    1. Etanercept
    2. Infliximab
  5. Biologics
    1. Rituximab (attack B cells)

Manage Complications

  1. Vitamin D and calcium (prevent bone loss)
  2. Surgery
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10
Q

How do you assess the effectiveness of your RA management?

A

Disease Activity Score

  1. Number of tender and swollen joints in the upper limbs and knees
  2. Involves ESR
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11
Q

What is the pathophysiology of RA?

A
  1. Autoimmune response by autoantibodies to igG and citrullinated proteins lead to inflammation and deposition of immune complexes systemically, but mostly in the synovium
  2. Infiltration of immune cells into the synovium (main site of pathology) leads to synovitis, producing a boggy swelling, thickened synovium and infiltration of inflammatory cells.
  3. This forms a pannus that spreads to the cartilage surface and damages it (cytokine action and blocking nutrient route)
  4. Cartilage is worn away and cytokine production and joint disuse combine to cause juxta-articular osteoporosis during active synovitis
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12
Q

What is gout?

A

Gout is a disorder of purine metabolism, resulting in hyperuricemia from overproduction or undersecretion of uric acid, resulting in deposition of urate crystals in the joints, tendons or bursae.

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13
Q

What is the clinical presentation of gout?

A
  1. Asymptomatic hyperuricemia
  2. Acute arthritis
    1. Acute monoarthritis of 1st MTPJ
    2. Pain, swelling, exquisite tenderness, peaks within hours, lasts for days
  3. Chronic recurrent arthritis
  4. Tophaceous gout
  5. Uric acid nephrolithiasis/nephropathy
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14
Q

What are the risk factors for gout?

A
  1. Underlying risk
    1. Advanced age, male
    2. Genetic factors
  2. Increased production
    1. Diet: Alcohol, seafood, red meat
  3. Decreased excretion
    1. Dehydration, fasting
    2. Kidney disease
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15
Q

What investigations would you do for a patient with gout?

A

To aid in diagnosis:

  • Joint aspiration to look for negatively birefringent crystals

To assess for complications:

  • X-Rays to check for erosive arthropathy

To aid management:

  • Baseline uric acid levels to check for efficacy of medication
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16
Q

How is gout diagnosed?

A

Diagnosis can be made by finding of negatively birefringent crystals in the joint fluid

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17
Q

How do you manage gout?

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A

Non-medical

  1. Patient Education
  2. Lifestyle modification
    1. Alcohol cessation
    2. Low-purine diet
    3. Weight loss
    4. Medication changes
  3. PTOT to restore function if ROM limited

Medical:

Acute Attack:

  1. Resting, applying ice
  2. NSAIDS
  3. Colchicine
  4. Intra-articular steroids
    1. Systemic (pred 20-30/day)

Long-Term Management:

  1. Urate lowering drugs
    1. Types
      1. Xanthine Oxidase inhibitors
        1. Allopurinol (Purine analogue)
        2. Febuxostat
      2. Uricosuric acid agents
        1. Probenecid/sulfinpyrazone
      3. Target SU level: <300 for tophaceous, <360 for non-tophaceous
  2. Never start urate lowering drugs until acute attack has passed or it may prolong or precipitate an attack. Cover with anti-inflammatories and NSAIDS.
  3. Surgery can be done to remove the tophi
18
Q

What is the clinical presentation of CPPD?

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A
  1. Asymptomatic CPPD disease
  2. Acute CPP crystal arthritis
    1. Intense pain, redness, warmth, swelling, joint disability
    2. Cluster attacks – several adjacent joints
    3. Knee most common, followed by wrists, shoulders, ankles, feet, elbows
  3. Chronic CPP crystal inflammatory arthritis
    1. Severe morning stiffness, fatigue, synovial thickening, localized edema, restricted joint motion
  4. OA with CPP
  5. Severe joint degeneration
  6. CPPD with nerve/spinal cord compression
19
Q

What is the etiology/risk factors of CPPD?

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A
  1. Demographics
    1. Older patients
  2. Genetics
    1. Familial chondrocalcinosis
  3. Metabolic/endocrine disorders
    1. Hemochromatosis
    2. Hyperparathyroidism
    3. Gout
20
Q

What investigations would you do in CPPD?

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A
  • Joint aspiration
  • Conventional X-Rays
    • Cartilage calcification: punctate and linear radiodensities in articular cartilage
    • Degenerative changes
21
Q

What is the management of CPPD?

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A

Conservative:

  1. Supportive measures
    1. Rest (Restrict weightbearing/routine joint use)
    2. Immobilization (splints if necessary)
    3. Cool (ice)
  2. Anti-inflammatory medications
    1. Joint aspiration and intraarticular glucocorticoid injections
    2. Oral (if more than 2 joints) – NSAIDS, Colchicine (can also be used for prophylaxis)
22
Q

What is the pathophysiology of CPPD?

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A
  1. Excessive cartilage pyrophosphate produced by chondrocytes in cartilage leads to CPP crystal formation
  2. Leads to acute and subacute joint inflammation
  3. Generally self-limited
23
Q

What is ankylosing spondylitis?

Study These Flashcards
A

Chronic multi-systemic inflammatory disorder of the SIJ and axial skeleton with effects mainly in spine and SIJ, leading to progressive stiffening and fusion.

24
Q

What are the clinical features of ankylosing spondylitis?

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A

Articular

  • Axial: Inflammatory back pain, SI joint tenderness (buttock/hip pain)
    1. Stiffness/Loss of ROM
    2. Postural abnormalties: Kyphosis
  • Peripheral Arthritis: (ankles, hips, knees)

Periarticular

  • Enthesitis
  • Dactylitis
  • Tendonitis

Extraarticular:

  • IBD (blood/mucus in stools, stomach pain)
  • Psoriasis (pink scaly rash)
  • Uveitis (pain, blurring of vision, photophobia)
  • CVS: Conduction abnormalities, Aortic regurgitation,

Systemic: Constitutional symptoms

25
What are the clinical signs of ankylosing spondylitis?
**Documentation of progression**: 1. Loss of horizontal gaze 2. Finger floor distance 3. Schober's test 4. Occipital-wall distance 5. Chest expansion (costovertebral joints) – normally 4cm **Posture**: Loss of lumbar lordosis, increased thoracic kyphosis, and forward thrust of neck, posture maintained by flexed hips and knees **Palpation**: Sacroilitis (Faber’s test) **Limited ROM**: Loss of extension earliest and most severe
26
What are the complications of AS?
* **Joint-related** * Osteopenia and fractures * Neurological manifestations from spinal cord injury/atlanto-axial subluxation * **Cardiovascular disease** (Increased levels of systemic inflammation), aortic regurgitation, arrthymias * **Pulmonary compromise** due to restrictive changes caused by disease (chest wall changes) and by lung changes themselves.
27
What are the risk factors for AS?
* Demographics: Male 4:1 * Genetics: HLA-B27
28
What investigations would you do for AS?
1. Labs: 1. Serology (ACPA, RF, ANA) 2. Inflammatory markers (CRP, ESR) 2. Radiology 1. Lumbar spine 1. Syndesmophyte ankylosis – flowing ossification (bamboo spine) 2. Interspinous ligament ossification 3. Ossification of spinal ligaments, joints and discs 4. Vertebral body squaring 2. Sacroilitis
29
How do you diagnose AS?
**Rome Criteria**: Bilateral sacroilitis \> grade 1 and any of the following * LBP+stiffness \>3 months not relieved by rest * Thoracic pain or stiffness * Decreased lumbar spine ROM * Decreased chest expansion * Hx of uveitis Alternatively can use the NY criteria.
30
How would you manage AS?
**Conservative** * Education, genetic counseling, chronic disease, fall prevention, smoking cessation * Lifestyle mod: Physio (spinal extension, postural training, breathing exercises, exercise, avoid rest) **Pharmacological:** 1. NSAIDS 2. Disease-modifying antirheumatic drugs (DMARDS): Sulphasalazine 3. Biologic DMARDS 1. Anti-TNF alpha 2. IL-17 inhibitor 4. Local glucocorticoid injections *Monitoring of disease activity with Bath Ankylosing Spondylitis Disease Activity Score (BASDAI)*
31
What is the pathophysiology of AS?
1. The primary pathology in ankylosing spondylitis is enthsitis (where ligaments, tendons and capsules attach to the bone.) 2. Inflammation at the entheses leads to bone erosion and formation of subcondral granulation tissue 3. Fibrosis and ossification of granulation tissue leads to ankylosis of joint and formation of syndesmophytes
32
What are the types of peripheral seronegative spondyloarthropathy?
1. Psoriatic arthritis 2. Reactive arthritis 3. Enteropathic arthritis
33
What is the clinical presentation of seronegative spondyloarthropathy?
1. Arthritis 1. Generally polyarthritis 2. Other possible clinical presentations 1. Asymmetric oligoarthritis 2. Symmetric polyarthritis 3. Arthritis mutilans (deforming and destructive arthritis) 2. Periarticular symptoms 1. Enthesitis 2. Tenosynovitis 3. Dactylitis 3. Non-articular features: 1. Psoriasis: Psoriatic plaques 2. Enteropathic: IBD (bloody, mucoid stools) 3. Reactive: recent infection 4. Pitting edema 5. Ocular inflammation: Uveitis and conjunctivitis 4. B-Symptoms (fatigue)
34
What is the gene most commonly associated with seronegative spondyloarthropathies?
HLA-B27
35
What are the physical signs of psoriatic arthritis?
* **Nail changes** * Nail pits – Sharply defined depressions in the plate caused by shedding of nail plate cells * Onycholysis * Nail bed hyperkeratosis – Separation of the nail from its bed * Splinter hemorrhages * Leukonychia * **Periarticular** * Enthesitis * Dactylitis * **Non-Articular** * Psoriatic plaques * Eye (uveitis)
36
What is the diagnostic criteria of Psoriatic arthritis?
CASPAR Study: * At least 3 points from the following * Skin Psoriasis * Nail lesions * Dactylitis * Negative RF * Juxta-articular bone formation
37
What is the management of peripheral seronegative spondyloarthritis?
**Conservative:** 1. Patient education 2. Exercise 3. Weight reduction 4. Physical and occupational therapy **Medical management:** 1. NSAIDS (Ibuprofen, diclofenac, ketoprofen) 2. DMARDs (Methotreate, leflunomide) 3. Biologics (TNF-Alpha inhibitor)
38
What are some common causative pathogens of reactive arthritis?
1. Chlamydia trachomatis 2. Yersinia 3. Salmonella 4. Shigella 5. Campylobacter 6. E. Coli 7. Clostridioides difficile 8. Chlamydia pneumoniae
39
How do you diagnose reactive arthritis?
Clinical diagnosis based on pattern of findings. 1. Characteristic MSK findings 2. Evidence of preceding extra-articular infections 3. Lack of better cause
40
How do you manage reactive arthritis?
1. Treatment of underlying infection 2. Treatment of arthritis 1. Acute reactive: NSAIDS, Intrarticular glucocorticoids, systemic glucocorticoids) 2. Chronic reactive arthritis: Non-biologic DMARD (Sulfasalazine, Methotrexate), biologic DMARD (TNF inhibitor)
41
How do you manage enteropathic arthritis?
1. Control the underlying IBD 2. Treat the spondyloarthritis 1. NSAIDS 2. DMARDS (peripheral arthritis resistant to initial therapy) 3. Biologics (TNF inhibitors)
42

Orthopedics (9 decks)

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