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4. HDS Multisystem > Arthritis > Flashcards

Arthritis Flashcards

1
Q

Synovial Joint

Anatomy

A
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2
Q

Synovial Fluid

Analysis

A
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3
Q

Acute Arthritis

Pathogenesis

A
  • Acute inflammation
    • Peaks in about 3 hours
    • Cyclooxygenase products produced ⇒ innate immunity mech.
    • T_hree main processes occur:_
      • Increased blood flow
      • Increased permeability of the capillaries
      • Migration of neutrophils
  • Chronic inflammation takes at least 6 weeks ⇒ acquired immunity mech.
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4
Q

Acute Arthritis

Differential Diagnosis

A
  • Infection – Always need to consider this dx in acute mono-articular arthritis
    • Disseminated Gonococcal Infection
    • Non-gonococcal bacterial infection
    • Fungal, Mycobacterial, Viral
    • Lyme Disease
  • Inflammation
    • Crystalline arthropathies (Gout, Pseudogout)
    • Systemic Inflammatory Arthritis (at onset)
      • RA, spondyloarthropathy, SLE, sarcoidosis, etc.
  • “Exacerbations” of Osteoarthritis
  • Trauma
    • Tears of meniscus/ligaments, hemarthroses
  • Cancers
    • Can present as acute arthritis
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5
Q

Gonococcal

Septic Arthritis

A
  • Gonorrhea tends to infects joints
  • Can result in less inflammation than non-gonoccal infections e.g. S. aureus
  • ± Skin pustules w/ disseminated gonorrhea
    • Usually a few lesions
    • Usually found on extremities
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6
Q

Non-Gonococcal

Septic Arthritis

A
  • Most dangerous/destructive form of arthritis
  • Cartilage and joint can be destroyed rapidly if not drained and tx with abx
  • 30% have residual pain/⇓ ROM post treatment
  • 5-15% mortality; up to 50% in polyarticular disease
  • 80-90% monoarticular presentation
  • Polyarticular can be seen in patient with preexisting polyarticular arthritis, IVDU
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7
Q

Bursitis

A
  • Swelling of the bursa
  • See erythema and tenderness
  • Septic Olecranon bursitis and septic prepatellar bursitis common
  • If it looks ugly, tap it
  • Tx w/ aspiration, steroids, and ± abx
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8
Q

Septic Arthritis

Diagnosis

A
  • Purulent synovial fluid
    • 50 to 100K WBC/mm3
    • > 90% PMNs
    • May see lower fluid WBC if peripheral WBC is low (Oncologic patient)
  • Send fluid for:
    • Cell count and diff
    • Gram stain (60-80% positive)
    • Culture (>90% positive)
    • Crystal analysis
  • Blood Cultures (50% are positive)
  • X-rays to establish baseline; r/o adjacent osteomyelitis
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9
Q

Septic Arthritis

Treatment

A
  • Parenteral antibiotics for at least 2 weeks or longer
    (depending on the organism/clinical situation)
    • 4 to 6 weeks for S. aureus, GNR
    • For Gram Positives:
      • Vancomycin initially
      • Narrow coverage when sensitivities return
  • Serial Drainage (repeat arthrocentesis) may be necessary
  • Follow WBC, culture results
  • Surgery if persistent infection, poor access, prosthetic joint
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10
Q

Hyperuricemia

A

Elevated uric acid in the blood

Uric acid (and/or sodium urate) is the end product of the breakdown of nucleoproteins

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11
Q

Uric Acid Synthesis

A
  • First step is rate limiting:
    • 5-phosphoribosyl -1- pyrophosphate (PRPP) plus glutamine
      • By PRPP amidotransferase
  • Nucleotides recycling back into synthetic pathway requires hypoxanthine guanine phosphoribosyl transferase (HGPRT)
  • Humans w/ 1° disorders of ↑ uric acid in blood and urine
  • Humans & great apes excrete uric acid in the urine
    • Other mammals degrade it to allantoin
  • ↑ Levels of uric acid ⇒ ± Gout
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12
Q

Hyperuricemia

Causes

A
  • Overproduction
    • Secondary:
      • Myeloproliferative disorders, drugs, enzyme defects
    • Idiopathic (primary?): Defect unknown
  • Under-excretion
    • Secondary: Renal defect or failure
    • Idiopathic: Defect unknown
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13
Q

Gout and Uric Acid Levels

A
  • Above 7 mg% in men over 6 mg% in females usually lower
  • Minute to minute blood level of uric acid does NOT reflect TOTAL BODY POOL
  • Complications are associated with an increase in TOTAL BODY POOL
  • Gout is a disease caused by the precipitation of urate crystals
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14
Q

Gout

Clinical Manifestations

A
  • Acute Gouty arthritis
    • Podagra = gout of the big toe
  • Urate urolithiasis
  • Tophi
  • (Intercritical gout)
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15
Q

Tophi

A
  • Appear rather late in gout
  • Aspirate tophus and visualize on a slide
  • Multiple birefringent crystals will be seen on polarized microscopy
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16
Q

Gout

Diagnosis

A
  • History:
    • Gouty arthritis ⇒ acute inflammatory reaction
      • Peaks in three hours
      • Lasts 2 to 3 weeks
    • Tophi are not inflamed
    • Kidney stones should be analyzed
  • Physical examination:
    • Acute inflammation (infection is the same)
    • Hip a problem to evaluate
  • Laboratory Diagnosis:
    • Monosodium urate crystals in synovial fluid during an acute attack
    • Needle-shaped, strongly ⊖ birefringent crystals under polarized light microscopy
      • Finding of urate crystals is virtually diagnostic BUT there may also be an infection
      • You should look for and find urate crystals at least one time ⇒ “crystal proven”
    • Looking at a tophus is just as good
  • Typical picture with response to therapy?
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17
Q

Gout

Treatment

A
  • The Acute Attack
    • Goal: Stop the acute Inflammation
  • The Hyperuricemia
    • Goal: Keep urate blood level below 6 mg%
      • Long-term causes tissue urate to mobilize ⇒ leave the body ⇒ ↓ total body pool
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18
Q

Acute Gout Attack

Treatment

A

Essentially 2 choices:

NSAIDS vs Steroids (intra-articular, oral)

  • Indomethacin 50 mg q4 hours for 3 days then 25 mg 4x/day for 2-3 days
  • Prednisone 20 mg stat then 20 mg the next day, then evaluate daily for cont. tx
  • Intra-articular steroids

Classic Colchicine 0.6 mg every hour x 8 is no longer used. Never give IV.

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19
Q

Hyperuricemia and Gout

Summary

A
  • Hyperuricemia ⇒ urate level > 7 mg% in a male, 6 mg% in a female
  • Blood level may not reflect total body pool
  • Gout is a disease with one or more of the following:
    • Acute Gouty Arthritis
    • Tophi
    • Uric acid nephrolithiasis
  • Acute attacks are treated with NSAIDs or steroids
  • Hyperuricemia is treated with Probenecid or Allopurinol
    • Asymptomatic hyperuricemia is not treated
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20
Q

Pseudo-gout

(CPPD Arthropathy)

A
  • Calcium Pyrophosphate Dihydrate Crystal deposition in joints ⇒ acute arthritis
    • Often mono- (knee, wrist) or oligo-articular arthritis that mimics gout
    • Can be polyarticular and with less intense inflammation
      • Pseudo-rheumatoid pattern
      • Pseudo-osteoarthritis pattern
  • Ass. with CPPD deposition in cartilage ⇒ chondrocalcinosis
  • Typically affects elderly > 65
  • Crystals are intracellular rod- or rhomboid-shaped w/ ⊕ birefringent under polarized light microscopy
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21
Q

Osteoarthritis (0A)

Overview

A

“Degenerative Joint Disease (DJD)”

  • Most common type of arthritis
  • 26.9 million Americans older than 25 y/o
  • Prevalence increases with age
  • Leading cause of long-term disability in U.S.
  • Lower extremity OA is the most common cause of difficulty walking and stair-climbing
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22
Q

Osteoarthritis

Pattern of Disease

A
  • Weight-bearing joints are often affected:
    • Spine, hips, knees
  • Hands (other UE joints rarely affected)
    • DIP > PIP > MCP involved
  • Symptomatic disease is more common in the knees
  • Incidental e/o OA joint involvement more common than symptomatic disease
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23
Q

Osteoarthritis

Characteristics

A
  • Wear and tear on synovials joint leading to joint failure
  • Can involve the entire joint including:
    • Subchondral bone
    • Ligaments
    • Joint capsule
    • Synovial membrane
    • Periarticular muscles
    • Articular cartilage
  • Non-inflammatory arthritis
    • No persistent warmth or erythema of the joint
    • No signs of systemic inflammation like fever or elevated inflammatory markers
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24
Q

Osteoarthritis

Pathophysiology

A

Initial trauma (micro or macro) ⇒ joint damage ⇒ failed repair ⇒ ∆ balance b/t synthesis and degradation of ECM ⇒ progressive loss of articular cartilage with subchondral bone remodeling ⇒ ∆ joint structure ⇒ OA

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25
Q

Osteoarthritis

Risk Factors

A
  • ↑ risk with ↑ age
  • Hand and knee OA are more common among women
  • Genetic predisposition
    • Esp. in women with nodular disease in hands
    • Strong family predilection
  • Obesity ⇒ ↑ stress on weight-bearing joints
  • Diseases that alter cartilage
    • Hemochromatosis, gout, pseudogout
  • Joint instability from neuro problem or ligamentous laxity
  • Prior infection of the joint
  • Trauma (micro-trauma/macro-trauma)
  • Abnormal joint anatomy
    • Congenital, Rheumatoid Arthritis, etc.
  • Hemophilia
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26
Q

Osteoarthritis

Clinical Features

A
  • Hallmark features are chronic joint pain and joint stiffness
    • Pain worsens w/ activity and relieved w/ rest
  • “Gelling” ⇒ joint stiffness brought on by rest and relieved rapidly with activity
  • Frequently monoarticular but multiple joints can be involved
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27
Q

Osteoarthritis

General Exam Findings

A
  • Bony enlargement
  • Crepitus ⇒ creaking /cracking of the joint heard or felt when palpating the joint during ROM
  • ↓ Range of motion (ROM)
  • No signs of inflammation or thickened synovium
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28
Q

Osteoarthritis

Hip Findings

A

Decreased ROM with internal rotation occurs before external rotation.

Groin pain with rotation may also be seen.

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29
Q

Osteoarthritis

Knee Findings

A
  • Crepitus
  • Tenderness along joint line
  • Varus or valgus deformity (due to asymmetric loss of cartilage)
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30
Q

Osteoarthritis

Hand Findings

A
  • Tenderness / bony enlargement @ 1st carpometacarpal joint
  • DIP > PIP > MCP involvement
  • Osteophytes at DIP ⇒ Heberden’s nodes
  • Osteophytes at PIP ⇒ Bouchard’s nodes
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31
Q

Osteoarthritis

Diagnosis

A
  • Distinguish from inflammatory joint diseases by H&P
  • Characteristic radiographic features include:
    • Subchondral sclerosis
    • Subchondral cysts
    • Narrowing of joint space
    • Osteophytes
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32
Q

Osteoarthritis

Treatment

A
  • Non-pharmacologic:
    • Weight loss
    • Avoid excessive use of joint
    • Physical therapy
    • Assistive devices ⇒ ↓ weight on joint
    • Knee brace and/or supportive footwear
  • Pharmacologic:
    • Alters symptoms not course of disease
    • Weigh pros and cons and potential issues with tx options
    • Potential options include:
      • Acetaminophen
      • NSAIDs ⇒ avoid in elderly and others with risk factors (kidney disease, CHF, etc)
      • Topical NSAIDs and capsaicin ⇒ limit systemic toxicity issues
      • Glucosamine/chondroitin sulfate ⇒ no clear evidence from trials but seem to be safe
        • Anecdotal reports of ↓ pain for some patients
      • Intra-articular corticosteroid injection ⇒ short-term benefit
      • Need to carefully consider narcotic/opioid use
  • Surgical options:
    • Arthroscopic surgery ⇒ probably ineffective
    • Total joint replacement
      • ↓ pain/disability and improves function
      • Should be delayed as long as possible ⇒ ↓ need for future revisions
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33
Q

Osteoarthritis

Conclusions

A
  • OA is the most common cause of arthritis
  • Consider it early when a patient present with a non-inflammatory joint complaint
  • Diagnosis is clinical, but can be confirmed with typical x-ray findings
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34
Q

Rheumatoid Arthritis

Definition

A

Systemic, symmetric inflammatory polyarthritis that leads to joint destruction, deformity and loss of function.

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35
Q

Rheumatoid Arthritis

Morphological Changes

A

Pathology of RA involves synovial membranes and periarticular structures of multiple joints.

Resulting in:

  • Pain
  • Swelling
  • Uncontrolled inflammation ⇒ irreversible damage and deformity
  • Stiffness
  • Functional limitation
  • Pannus formation
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36
Q

Rheumatoid Arthritis

Pathogenesis

A
  • Interaction between APCs, T-cells, and B-cells
  • ⊕ Helper T-cells ⇒ TNF-α and other soluble factors ⇒ ⊕ MΦ ⇒ secrete TNF-α, IL-1, and IL-6
  • TNF-α plays a central role in the inflammation process
  • Current therapies intervene at each one of these steps in the inflammation process
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37
Q

Rheumatoid Arthritis

Demographics

A
  • Prevalence is 1% of adults worldwide
  • Women affected 2-3x more than men
  • Peak age of onset is 30-50 y/o
  • Most pts are dx under 65 yrs of age
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38
Q

Rheumatoid Arthritis

Long-term Outcomes

A
  • Joint destruction
  • Functional and work disabilities
  • Treatment side effects
  • Psychosocial dysfunction
  • Comorbidities
  • ↓ quality of life
  • ↓ life expectancy
  • Total estimated annual cost in US ⇒ $9 billion
  • Lifetime costs for RA rival those of CVD or CVA
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39
Q

Rheumatoid Arthritis

Etiology

A
  • Etiology of RA is unknown
  • May be multifactorial
  • Genetic susceptibility?
    • HLA-DR4 and -DR1 Class II MHC leukocyte antigen types
    • Enhanced T-cell responses to inflammatory stimuli
    • Intrinsic abnormalities in synovial responses
  • Environmental factors?
    • Unclear if either environmental and/or genetic effects account for ethnic differences in prevalence of RA
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40
Q

Rheumatoid Arthritis

Clinical Presentation

A
  • Onset is:
    • Usually insidious ⇒ 70%
    • Subacute onset ⇒ 20%
    • Acute ⇒ 10%
    • Rarely episodic course w/ migratory involvement
  • Peripheral joints of the hands and feet are involved in almost everyone
    • Hands ⇒ MCPs, PIPs and wrists (DIPs are spared)
    • Feet ⇒ MTPs and ankles
    • Axial and central joints
      • C-spine (C1-2), hip, shoulder, TM
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41
Q

Rheumatoid Arthritis

Physical Findings

A
  • Early rheumatoid arthritis (RA)
    • Swelling of MCPs and PIPs joints
    • Fusiform or spindle-shaped enlargement of PIP joints
    • Tenderness and limited range of motion
  • Late rheumatoid arthritis (RA)
    • Massive diffuse swelling
    • Deformities such as the Boutonnière, swan neck, and unstable PIP joint
    • Caused by synovitis in that joint
  • Long-standing RA
    • Severe deformities resulting from joint destruction
    • Ulnar deviation
    • MCP joint subluxation
    • Rheumatoid nodules
42
Q

Rheumatoid Arthritis

Radiographic Features

A

Progression of disease includes:

  • Early in disease: peri-articular osteopenia w/ preserved joint space
  • Progression shows: joint space narrowing and irregularity
  • Later findings: joint erosions, ulnar deviation
43
Q

Rheumatoid Arthritis

Systemic Involvement

A
  • General – weight loss, fatigue, fever
  • Ocular – Keratoconjunctivitis Sicca, Episcleritis, Scleritis, Scleromalacia Perforans
  • Pulmonary – interstitial fibrosis, pulmonary nodules, pleuritis, pleural effusions, Brochiolitis obliterans, Caplan’s syndrome
  • Dermatologic – subcutaneous nodules, Leukocytoclastic vasculitis, palmar erythema, ischemic ulcers
  • Neurologic – peripheral neuropathy, entrapment syndromes, cervical myelopathy, mononeuritis multiplex
  • Hematologic – anemia, lymphoma, Felty’s syndrome
  • Cardiac – pericarditis, myocarditis, coronary vasculitis
44
Q

Rheumatoid Arthritis

Revised ACR Criteria

45
Q

Rheumatoid Arthritis

Mortality

A
  • Life expectancy ↓ by 10-15 yrs in pts w/ severe disease
  • Mortality may approach 50% over 5 yrs in cases of severe disability
  • Pts w/ extra-articular involvement 2x more likely to die vs those w/ articular disease only
  • Comorbid conditions and drug toxicity account for majority of deaths in RA
46
Q

Rheumatoid Arthritis

Initial Evaluation

A
  • Synovial fluid analysis ⇒ inflammatory
    • 5,000-50,000 WBC/mm3 (>50% PMNs)
    • No crystals
    • ⊖ cultures
  • ↑ ESR/CRP
  • ⊕ rheumatoid factor, anti-CCP
  • CBC, CMP, LFTs
  • ⊕ ANA in 30%
  • Hep B, Hep C, parvovirus if onset < 6 weeks
  • XR of hands, wrists, feet
47
Q

Rheumatoid Factor

A
  • 70% ⇒ ⊕ RF @ disease onset
    • 10-15% ⇒ become ⊕ w/in 2 yrs
    • 15-20% ⇒ remain seronegative throughout
  • RF not specific for RA
  • Can be ⊕ in many conditions including:
    • Hep B and C, HIV, chronic infections, SABE
      • RF present in 44% of HCV
      • 76% in HCV w/cryoglobulin
    • SLE, Sjogren’s, MCTD, PBC
    • Sarcoidosis, IPF, asbestosis, age > 65 years, malignancy
48
Q

Anti-Cyclic Citrullinated Peptide (CCP)

A
  • Citrulline ⇒ post-translationally modified arginine residue
  • Anti-CCP Abs as detected by ELISA ⇒ useful adjunct in RA dx
  • Sensitivity 47-90%
  • Specificity 90-98%
  • Low incidence of anti-CCP found in Hep C
  • ⊕ Anti-CCP early in course of RA predicted progression of radiographic joint scores at 5 yrs better than RF
49
Q

Juvenile Idiopathic Arthritis (JIA)

“Durban Criteria”

A

Classifies subtypes based on clinical features:

  • Systemic arthritis
  • Polyarthritis
  • Pauciarthritis or oligoarthritis
  • Enthesitis-related arthritis
  • Psoriatic arthritis
50
Q

Systemic-Onset JIA

A

Previously called Still’s disease

  • Least common JIA presentation
  • Men = women
  • Age of onset is < 17 y/o
  • Any joints may be involved
  • Ass. w/ destructive arthritis
  • Presents w/ fever, rash, lymphadenopathy, hepatosplenomegaly
  • Lab abnormalities include leukocytosis, anemia, ↑ ESR
  • ⊖ ANA
  • Rheumatoid Factor is rare
  • Treated w/ disease modifying drugs
51
Q

Pauciarticular-onset JIA

A
  • Most common JIA presentation
  • Female > male predominance
  • Peak onset is 2-3 y/o
  • Rare after age 10 yrs
  • Large joints affected but rarely hips
  • No systemic sx
  • ± Mildly ↑ ESR
  • ⊖ RF
  • Low titer ANA ⊕ is common
    • A subset of those w/ ⊕ ANA will have uveitis
52
Q

Polyarticular-onset JIA

A
  • Peak onset is 2-5 yrs and 10-14 yrs
  • More similar to adult RA ⇒ multiple joint involvement; destructive arthritis
  • Mild anemia
  • ± Mildly ↑ ESR
  • Low titer ANA ⊕ is common
  • 10-20% of those > 10 yrs have ⊕ RF
  • Disease modifying drugs used for treatment
53
Q

Juvenile Idiopathic Arthritis (JIA)

Laboratory Findings

A
  • ⊕ ANA, especially in pauciarticular
  • Ass. w/ ↑ incidence of uveitis
  • ESR/CRP usually normal
  • RF usually ⊖
54
Q

Rheumatoid Arthritis

Joint Erosions

A
  • Occur early in RA
  • Up to 93% of pts w/ < 2 yrs of RA ⇒ ± radiographic abnormalities
  • Erosions detected by MRI w/in 4 months of RA onset
  • Rate of progression is significantly more rapid in the 1st yr vs 2nd and 3rd yrs
  • Goal of early treatment is to prevent progression of disease
55
Q

Rheumatoid Arthritis

Management

A
  • Education
  • Build a cooperative long-term relationship
  • Use materials from arthritis foundation and ACR
  • Assistive devices
  • Exercise ⇒ ROM, conditioning, and strengthening
  • Medications
  • Analgesic and/or anti-inflammatory
  • Immunosuppressive, cytotoxic, and biologic
  • Balance efficacy and safety w/ activity
56
Q

Rheumatoid Arthritis

Treatment

A
  • Two drug classes used to ↓ inflammation ⇒ NSAIDs and glucocorticoids
    • ↓ inflammation but do not slow disease process
  • Long-term use of corticosteroids ⇒ weight gain, diabetes, cataracts, osteoporosis
  • Low dose corticosteroids ↓ joint destruction
  • Disease Modifying Anti-Rheumatic Drugs (DMARDS) can slow progression
57
Q

Disease Modifying Anti-Rheumatic Drugs

(DMARDS)

A
  • Slow disease progression
  • Take some time to exert their action
  • Fall into two major categories
    • Older agents ⇒ non-biologics
    • Newer agents ⇒ mostly, but not exclusively Ab’s or recombinant proteins (“biologics”)
58
Q

Spondylarthritis (SpA)

Definition

A
  • Group of inflammatory arthropathies
  • Share common clinical, pathophysiologic and immunogenetic factors
  • Related to and may form a disease spectrum w/ psoriasis and inflammatory bowel disease
59
Q

Spondylarthritis (SpA)

History

A
  • Originally thought to be variants of rheumatoid arthritis
  • Later defined as a distinct group
  • Named seronegative spondyloarthropathies
    • Lack of rheumatoid factor
  • Characteristic spinal involvement
60
Q

Spondylarthritis (SpA)

Diseases

A

SpA encompasses several identifiable diseases

Undifferentiated form or isolated features that suggest they fall into this group

Diseases include:

  • Ankylosing spondylitis (as)
  • Reactive arthritis (ReA)
  • Psoriatic arthritis (PA)
  • Arthritis associated w/ inflammatory bowel disease (EA)
  • Undifferentiated spondyloarthritis (UspA)
61
Q

Spondylarthritis (SpA)

Shared Characteristics

A

Features vary among the different entities and among individuals:

  • Inflammatory back pain or asymmetric synovitis
  • Enthesopathy ⇒ inflammation of tendon/ligament attachments
  • Dactylitis ⇒ swelling of a whole finger or toe
  • Asymmetric arthritis
  • Fhx of the same or a related disease
  • Ocular inflammation ⇒ uveitis or conjunctivitis
  • Psoriasis
  • Bowel inflammation
62
Q

Spondylarthritis (SpA)

Shared Pathophysiologic Features

A
  • Enthesitis ⇒ the attachment of ligaments and tendons to bone
    • Major site of inflammation in SpA
    • Enthesis attaches w/ a fibrocartilage component w/ fibers implanting in the bone
  • Synovitis different pathologically to RA
  • Bone erosion @ sites of inflammation
  • New bone formation can occur along the spine, fusing joints, or at tendon attachments
    • Unlike RA where erosion occurs w/o bone formation
63
Q

Spondylarthritis (SpA)

Immunogenic Associations

A

HLA B27 ⇒ major genetic marker

Not seen in all pts

Not associated w/ all conditions of SpA family

  • Ankylosing spondylitis ⇒ 90%
  • Reactive arthritis ⇒ 30-50%
  • Enteropathic spondylitis ⇒ 35-75%
  • Psoriatic spondylitis ⇒ 40-50%
  • Undifferentiated spondyloarthritis ⇒ 70%
  • Anterior uveitis ⇒ 50%
  • Aortic insufficiency/heart block ⇒ 80%
64
Q

Spondylarthritis (SpA)

Epidemiology

A
  • No diagnostic lab studies ⇒ estimates of incidence difficult
  • Overall incidents ~ 0.1-1.4
  • Influenced by ethnicity of the population
65
Q

Ankylosing Spondylitis

Definition

A

An inflammatory disease primarily of the axial skeleton

66
Q

Ankylosing Spondylitis

Epidemiology

A
  • Onset typically in early 20’s w/ rare exceptions starting before age 45
  • 2:1 M to F ratio
  • Incidence follows B27 incidence in population in the US
  • 1% of non-Hispanic of self-reported European ancestry
  • Includes non-radiographic axial spondylarthritis
67
Q

Ankylosing Spondylitis

Pathology

A
  • Inflammatory ∆ start in sacroiliac joints and at enthesis
  • Cytokine production @ inflammatory site
  • TNF ⇒ cartilage and bone erosion
  • Later development of ossification w/ new bone formation
    • Response to inflammation
    • Lack of inhibitors of signaling of bone formation
68
Q

Ankylosing Spondylitis

Clinical Features

A
  • Axial pain ⇒ key sx
    • Often described as stiffness
    • Worse in the morning for ≥ 1hour
    • Improves w/ activity
    • Worsens w/ rest
    • Pattern is called inflammatory back pain
    • Not exclusively seen in SpA but very suggestive
    • Important to recognize pts early in their course
    • Pain and involvement tends to start at the sacrum
    • Proceeds to involve the spine in an ascending fashion over a period that can be yrs ⇒ sacrum to cervical
  • Pts may complain of pain in the posterior leg
    • From irritation of the sciatic nerve by the piriformis muscle
  • Chest pain can occur from:
    • Referred pain from the thoracic spine
    • Involvement of the manubriosternal joint
  • Peripheral arthritis tends to involve shoulders or hips
    • Can occur in an asymmetric lower extremity pattern
    • Similar to that seen w/ ReA
69
Q

Ankylosing Spondylitis

Physical Examination

A
  • Early loss of motion of lumbar spine
    • Normally forward flexion L-spine ⇒ lordotic curvature reversal to kyphotic & an expansion of ~ 5 cm
    • Assessed w/ the Shoeber maneuver
    • Occurs before any XR ∆
  • ± Early loss of chest expansion
    • Normal chest expansion measured @ nipples is 2 inches or 5 cm
    • Easier to measure in men
70
Q

Ankylosing Spondylitis

Radiologic Features

A

Characteristic radiologic ∆ ⇒ necessary for dx of as until recently

∆ always bilateral in AS

  • Initial ∆ in sacroiliac joints (SIJ)
    • Smudging of the subchondral bone
    • Widening of the joint w/ cartilage erosions
    • Joint fusion
  • Ascending ∆ in spine w/ squaring of vertebral bodies
    • Subsequent ossification along spinal ligaments
    • Called Syndesmophyte on radiographs
  • Leads to fusion of the spine
    • XR appearance called bamboo spine
    • Progression varies and does not advance in all pts
  • Time from onset of sx → XR ∆ ~ 5-10 yrs
    • Led to delayed dx in the past
  • Inflammatory ∆ can be seen much earlier by MRI
  • Bone edema around the SIJs
  • Edema at ligament attachment sites or discs in the spine
71
Q

Ankylosing Spondylitis

Lab Abnormalities

A
  • No specific abnormalities
  • ± Anemia of chronic inflammation
  • ↑ ESR/CRP
    • ↑ CRP is the better marker
  • ~ 90% of pts of European ancestry w/ HLA B27
    • Never a dx test but ↑ likelihood of disease in the proper setting
72
Q

Ankylosing Spondylitis

Extra-Articular Features

A
  • Anterior uveitis (AU)
    • Occurs in ~ 25%
    • Feature of all SpA
    • Also associated w/ many other diseases and occurs idiopathically
    • ~ 50% of idiopathic AU pts are B27 ⊕ so likely is a “forme fruste” of SpA
    • A minor feature of a disease presenting in isolation
  • Heart block and aortic insufficiency
    • Results from inflammation @ aortic root involving the conduction system and aortic valve
    • Seen in ~ 3% at 10 yrs of disease and 10% at 30 yrs
  • Upper lobe pulmonary fibrosis
  • Cauda equine syndrome
    • Impingement of the spinal nerves past the end of the cord
    • Causes numbness over the sacrum (saddle anesthesia), leg weakness, and bowel and bladder sphincter dysfunction
  • Bowel inflammation
    • ~ 60% of pts have subclinical ∆ in terminal ilium consistent w/ Crohn’s disease
    • Some will eventually develop symptomatic inflammatory bowel disease
73
Q

Ankylosing Spondylitis

Diagnosis

A

Dx made from clinical features and radiologic findings:

  • Bilateral sacroiliitis by XR or MRI almost pathognomonic
  • ↑ CRP and ⊕ B27 can be suggestive
  • Uveitis and fhx can also suggest dx
  • Long delay in XR ∆ and MRI
  • ∆ can come and go
74
Q

Non-Radiographic Axial Spondyloarthritis

A
  • Long delay in XR ∆ and MRI & ∆ can come and go
  • Non-Radiographic Axial Spondyloarthritis now recognized
  • Defined by having inflammatory back pain and several other features including:
    • Family history
    • ↑ ESR/CRP, B27
    • Other SpA features such as psoriasis
  • By this definition, more pts identified w/ equal gender incidence
75
Q

Ankylosing Spondylitis

Course and Prognosis

A
  • Course very variable
  • From persistent sx w/o XR progression ⇒ non-radiologic axial spondyloarthritis
  • To complete fusion of the spine and potentially progressive deformity and disability
  • Complications of spinal fusion
  • Potential for fracture w/ trauma
  • Osteoporosis
76
Q

Ankylosing Spondylitis

Treatment

A
  • NSAIDs improve sx and may affect progression of fusion
  • TNF inhibitors have substantially ↓ sx and ↓ functional impairment of axial disease
  • Physical therapy ⇒ maintain function and prevent spinal deformity
77
Q

Reactive Arthritis (ReA)

Definition

A

Previously called Reiter’s syndrome

  • An inflammatory disease occurring following infection
  • Originally thought that organisms were not participating in the process but had provoked an Inflammatory response
78
Q

Reactive Arthritis (ReA)

Bacteriology

A
  • Urethritis which is sexually acquired ⇒ Chlamydia trachomatis
  • Bacillary dysentery
  • Shigella
  • Salmonella
  • Yersinia
  • Campylobacter fetus
79
Q

Reactive Arthritis (ReA)

Epidemiology

A
  • Generally M:F is 5:1 in post-urethritis
  • Equal incidence post-dysentery
  • Incidence and prevalence difficult to establish
  • Least common SpA
80
Q

Reactive Arthritis (ReA)

Features

A
  • Sx occur days to weeks and occasionally months after infection
  • Infectious event may be forgotten and at times sx were not dramatic
    • I.e., mild dysuria and discharge or diarrhea w/o fever or bleeding
81
Q

Reactive Arthritis (ReA)

Clinical Manifestations

A

Clinical features occur in variable combinations and time course:

  • Arthritis/enthesitis
    • Asymmetric joint involvement
    • Predominantly lower extremity w/ involvement of knees, ankles, toes
    • Most characteristic is enthesitis
      • @ Achilles attachment ⇒ achilles tendonitis
      • @ Attachment of the plantar fascia to the calcaneus ⇒ plantar fasciitis
    • ± Back pain from sacroiliitis (may be unilateral)
      • Other important causes of unilateral sacroiliitis is infection ⇒ bacteria, mycobacteria, and brucella
  • Urethritis
    • Urethra is the target & portal of entry of organism
    • Usually mild dysuria and discharge
  • Conjunctivitis/uveitis
    • Most typical eye involvement is conjunctivitis ⇒ erythema and discharge which may be mild
  • Anterior uveitis ⇒ same as seen w/ AS
  • Mucocutaneous disease
  • Painless mouth ulcers
  • Keratoderma blennorhagicum
    • Lesions typically on palms and soles
    • Histology is typical of psoriasis
  • Circinate balanitis
    • In circumcised men ⇒ hyperkerotic lesion on the glans
    • In uncircumcised men ⇒ shallow ulcers around the glans
    • Can occur in isolation from the rest of syndrome
82
Q

Reactive Arthritis (ReA)

Differential Diagnosis

A
  • After urethritis ⇒ disseminated Neisseria gonorrhea infection
  • Diarrhea and arthritis ⇒ inflammatory bowel disease
  • Initiating event unclear ⇒ other causes of acute arthritis and enthesitis
83
Q

Reactive Arthritis (ReA)

Lab Studies

A
  • No specific diagnostic study
  • If possible:
  • PCR for chlamydia from urethra or other mucous membrane site
  • Culture of a typical organism from stool
  • Synovial fluid is inflammatory w/ > 2,000 WBCs
  • HLA-B27 reported in 40-80% ⇒ supportive of dx in the proper setting
84
Q

Reactive Arthritis (ReA)

Course and Prognosis

A
  • Attacks last weeks to months and recurrences occur
  • Some pts (9- 19%) develop chronic sx
  • More common after Chlamydia > bowel infection
  • Over yrs, pts can develop symptomatic spondylitis & heart lesion as in as
85
Q

Reactive Arthritis (ReA)

Relation of Infection

A
  • Now known that chlamydia persists in a dormant intracellular form in synovia of pts w/ ReA
  • Ag from bowel organisms, but not intact organisms exist in the joints
  • Relation to enthesitis and other features is unknown
86
Q

Reactive Arthritis (ReA)

Treatment

A
  • NSAIDs are used for symptomatic therapy
  • Other agents have been used for ongoing sx
  • Methotrexate, sulfasalazine and TNF inhibitors
  • May be possible to eradicate chlamydia and disease w/ combo of doxycycline or azithromycin and rifampin
87
Q

Psoriatic Arthritis (PA)

Definition

A

A characteristic arthritis that occurs in pts w/ psoriasis

88
Q

Psoriatic Arthritis (PA)

Epidemiology

A
  • Occurs in 10-30% of pts w/ psoriasis
  • M:F ratio is 11:1
  • Age of onset typically 40-50s
  • Can occur in childhood or much later
  • Relationship to the skin disease varies
89
Q

Psoriatic Arthritis (PA)

Timeline

A
  • 70% ⇒ psoriasis (skin involvement) occurs before arthritis
  • ~15% ⇒ arthritis before skin findings
  • ~15% ⇒ skin findings dx @ the time of arthritis
  • No relation between extent of skin disease and arthritis
90
Q

Psoriatic Arthritis (PA)

Clinical Picture

A

Usually described by onset and pattern of joint disease

Patterns seen early, less distinct later in course

  • Asymmetric arthritis
    • Typically in hands and feet
    • Involved: DIPs, PIPs, MCPs, usually few joints
    • Can involve large joints
    • Inflammation of DIP joints
      • Very characteristic of PA > other SpA
      • DIPs not involved in RA
      • Common in OA in the hands
    • Characteristic psoriatic nail ∆ occur in the involved digit
  • Dactylitis (sausage digit) ⇒ almost pathognomonic
    • Swelling and pain in a whole digit from flexor tendon and multiple joint involvements
  • Enthesitis such as achilles tendonitis
  • Symmetric arthritis
    • Same appearance as RA but RF and cyclic citrullinated peptide Ab are absent
  • Spondylitis
    • Sacroiliitis and spondylitis similar to as
  • Arthritis mutilans
    • Highly destructive form of PA
    • Produces the characteristic XR ∆ known as “pencil and cup”
    • Joint destruction and telescoping of digits
  • Extra-articular features
    • Uveitis and subclinical bowel disease
91
Q

Psoriatic Arthritis (PA)

Pathophysiology

A
  • Relationship to psoriasis is unknown
  • Majority of inflammatory process occurs @ enthesis w/ less being actual synovitis
  • Synovial membrane in PA w/ ↑ vascularity and ↓ Mφ compared to RA
  • Multiple inflammatory cytokines including TNF ↑ in synovial fluid
  • Relationship b/t BMI to arthritis severity ⇒ ? Role of leptin and other adipose derived hormones
92
Q

Psoriatic Arthritis (PA)

Diagnosis

A

No lab abnormality characteristic of PA

  • ± ↑CRP/ESR
  • HLA B27 is ↑ to 50% w/ spondylitis but not w/ peripheral arthritis
  • Dx made w/ characteristic clinical findings and presence of psoriasis
  • Fhx is helpful in pts not exhibiting psoriasis at presentation
    • Psoriasis has a strong genetic component
93
Q

Psoriatic Arthritis (PA)

Course

A
  • PA tends to have remissions and exacerbations
  • 40-50% have destructive and deforming disease
  • 20-40% have spondylitis
94
Q

Psoriatic Arthritis (PA)

Treatment

A

TNF inhibitors

Best therapy for symptomatic disease and prevention of joint destruction

95
Q

Enteropathic Arthritis

Definition

A

Arthritis and spondylitis occurring in the presence of ulcerative colitis (UC) or Crohn’s disease (CD)

Occurs in ~ 10% of UC and CD

96
Q

Enteropathic Arthritis

Clinical Features

A
  • Usually involves a few joints in the lower extremities
  • Become symptomatic w/ activity of the bowel disease
  • More common w/ colonic involvement
  • Previously when colectomy was done for UC, it abolished the peripheral arthritis
  • Arthritis usually occurs in pts w/ established IBD
  • Can precede clinical bowel disease
  • Subclinical bowel inflammation common in other SpA’s
  • Spondylitis present in 10% of pts w/ IBD
  • A larger number have lower back pain related to sacroiliitis
  • Course of spondylitis independent of bowel disease
97
Q

Enteropathic Arthritis

Pathogenesis

A
  • HLA-B27 in 50% of pts w/ IBD and spondylitis, not ↑ in peripheral arthritis
  • Evidence that IL-23 stimulated by bowel bacteria may be a driver of arthritis
  • Multiple cytokines are ↑
  • TNF important in both bowel disease and arthritis
    • Given response to inhibition of TNF
98
Q

Undifferentiated SpA

A

Pts w/ features of SpA who do not fit a specific entity

  • Related to typical clinical features ⇒ dactylitis, asymmetric arthritis
  • ↑ frequency of HLA B27 ⇒ idiopathic anterior uveitis, chronic achilles tendonitis, or plantar fasciitis
  • 65% of pts w/ undifferentiated SpA have subclinical bowel inflammation
  • Led to another classification scheme for SpA ⇒ includes axial and peripheral spondyloarthritis
99
Q

Spondylarthritis (SpA)

HLA Associations

A
  • HLA-B27 ⇒ best recognized etiopathologic factor in SpA
    • All subtypes of B27 except 06 and 09 ass. w/ AS and other SpA
    • B27 frequency in populations determines frequency of SpA
    • No difference between B27 ⊕ and B27 ⊖ disease
    • Only a small proportion of B27 ⊕ people develop SpA
  • In AS, genetics account for 80-90% of susceptibility
    • 50-75% concordance rate in MZ twins and a 15% in DZ
    • Relative risk of disease is 94 for 1st-degree, 25 for 2nd-degree, and 34 for 3rd-degree relatives
    • B27 accounts for 30-50% of inheritance
  • Other candidate genes ⇒ endoplasmic reticulum amino peptidase 1 (ERAP1) and IL-23 receptor
100
Q

Spondylarthritis (SpA)

Non-HLA and Environmental Factors

A

IL-23/IL-17

  • IL-23/IL-17 axis ⇒ major driver of all the spondyloarthridities
  • Also important in psoriasis and inflammatory bowel disease
  • Bowel flora ⇒ ⊕ IL-23 from dendritic cells and Mφ ⇒ ⊕ IL-17 cells ⇒ ⊕ IL-17, IL-22, TNF and INF-𝛾
  • Associated w/ findings of SpA
101
Q

Spondylarthritis (SpA)

Treatment

A
  • Non-steroidal agents to ↓ pain and swelling
    • Useful, particularly in axial inflammation
  • Agents used to treat RA w/ limited or no benefit
    • Methotrexate, sulfasalazine, and lefunimide
  • TNF inhibitors ⇒ most effective agents
    • Infliximab, etanercept, and adalimumab
  • IL-12/23 and IL-17 inhibitors now available

4. HDS Multisystem (43 decks)

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