CONNECTIVE TISSUE DISEASE

OSTEOARTHRITIS (OA)
Degeneration articular cartilage
Affects synovial joints
Stays confined to joints
 Joint pain
 Stiffness
 Limited ROM

TWO TYPES OA
Primary or Idiopathic

Secondary
 trauma
 fractures
 infection
 congenital deformities

ETIOLOGY/PATHOLOGY
Hyaluronidase (synovial fld.)
Thickening subchondral bone
1. Deformity
2. Denuded joints
3. Bone spurs (osteophytes)
4. Pain

PREDISPOSING FACTORS: OA
Excessive use/stress
Congenital defects (e.g. bow legs)
Metabolic problems
Hemophilia (intra-articular hemorrhage)
Septic arthritis
Neuropathic

CLINICAL MANIFESTATIONS: OA
No systemic manifestations Loss function
Joint pain Stiffness
Subluxation Crepitation
Asymmetric joints Malum coxae senilis
Nodules: Heberden s & Bouchard’s Chondromalacia patellae
Sleep disturbances Vertebral column
COLLABORATIVE MANAGEMENT:OA
Diagnostic studies:
 H&P
 X-rays
 No specific lab studies
 Synovial fluid
 ESR

COLLABORATIVE MANAGEMENT:OA
Supportive Care:
 Drugs
 Rest/Immobilization
 Positioning
 ROM
 Heat/Cold
 Nutrition

PHARMACOLOGICAL AGENTS: OA
ASA
NSAIDS
COX-2 INHIBITORS (suppress cyclooxygenase)
 Celecoxib (Celebrex) side effects still under study
 Rofecoxib (Vioxx) withdrawn 2004 (􀃅 stroke risk)
 Valdecoxib (Bextra)withdrawn 2005 (􀃅 cardiac risk)
Contraindications
Adverse reactions
 CORTICOSTEROIDS

LONG-TERM COLLABORATIVE MANAGEMENT:OA

MONITOR:
S&S
Pain control
 meds
 TENS
Exercise
Home & work safety
RHEUMATOID ARTHRITIS
(RA)

Chronic, SYSTEMIC disease

Symmetric joint inflammation
Periods remissions &
exacerbations
Shorter life-span
75% women
Geographic/racial
Age
Chronic disability

ETIOLOGY/PATHO: RA
􀁨 True cause unknown
􀁨 Genetic predisposition
 Antigen HLA-DR4
􀁨 Environmental
 Epstein-Barr
􀁨 Autoimmunity

AUTOIMMUNITY: RA
1. Inflammatory response
2. Impaired normal tissue function
3. Rheumatoid factors
4. Immune complexes
5. Deposited in joints, blood vessels, pleura
6. Release proteolytic enzymes
7. Damage articular cartilage, membranes, vessels, pleura
8. Joint changes
9. Systemic manifestations

PATHOLOGY: RA

1ST STAGE: synovitis

2nd STAGE: pannus

3rd STAGE: fibrous tissue

4th STAGE: calcificatiion/ankylosis

CLINICAL MANIFESTATIONS: RA
Insidious onset (usually)
Nonspecific manifestations
Tender joints
Vasculitis:
 periph. neuropathy
 myositis
 cardiac
Morning joint stiffness
Spindle shaped fingers
Ulnar drift
Swan neck & Boutonniere
Rheumatoid nodules
Potential complications:
 Sjogren’s
 spinal cord comp.
Caplan’s Syndrome

DIAGNOSTICS: RA
H&P
No specific test
Moderate anemia
ESR
Serum Rheumatoid factor
Latex agglutination
Antinuclear antibody (ANA)
Serum complement
WBC
X-Ray

COLLABORATIVE MANAGEMENT: RA
Education
Physical/Occupation therapy

Pharmacologic Management:
NSAIDS
Cox-2 Inhibitors (controversy regarding side effects)
Corticosteroids (intraarticular)
P.O. steroids- hydrocortisone, methylprednisolone, dexamethasone, prednisone
PHARMACOLOGIC MANAGEMENT:RA
CYTOTOXIC/IMMUNOSUPPRESSIVE DRUGS
 Methotrexate (Rheumatrex)
 Azathioprine (Imuran)
 Cyclophosphamide (Cytoxan)
 Adalimumab (Humira)

PHARMACOLOGIC MANAGEMENT
Gold salts (antiinflammatory)
 gold sodium thiomalate (Myochrysine) IM
 Auranofin (Ridaura) PO
Minocycline (antibiotic)
Etanercept (Enbrel) (biological response modifier/antiarthritic)
Infliximab (Remicade) [class: as above]

NUTRITIONAL MANAGEMENT
Diet
General nutrition
Selected studies: omega-3 fatty acids: fish, plant oils
Disability may impair appetite

SURGERY: RA
Correction of deformities
Relief of pain
Restoration function
Orthopedic aids

GOUT
PODAGRA

GOUT PATHOLOGY
Hyperuricemia
Uric acid levels
Gouty arthritis

Primary Gout:
1. Overproduction uric acid
2. Poor renal excretion uric acid

Secondary Gout:
Drugs Prolonged fasting
Diseases Others
Ethyl alcohol
ACUTE MANIFESTATIONS: GOUT
Acute pain
Swelling
Erythema
Great toe; other joints
Renal damage
Tophi/tophaceous deposits (monosodium urate)

COLLABORATIVE MANAGEMENT:GOUT
Diagnostics:
Serum uric acid >6 mg/dl
Urinary uric acids
Renal function
Definitive:
Aspiration synovial fluid
aspiration of tophus

COLLABORATIVE MANAGEMENT: GOUT

Control & prevention: Acute Gout
Uricosuric therapy:
Colchicine (colsalide)
NSAIDS
Indomethacin (Indocin)
Ibuprofen (Motrin)

COLLABORATIVE MANAGEMENT: GOUT

Chronic Gout

Allopurinol (Zyloprin)
Probenecid (Benemid)
Colbenemid (Probenecid & Colchicine)
Losartin (Cozaar)

COLLABORATIVE MANAGEMENT: GOUT

Teaching Points
Nature of disease
Medications
Lose weight
Control hypertension
Fluids 2000-3000 ml/day
Avoid excessive intake purines
LUPUS ERYTHEMATOSUS
Autoimmune disease
Unknown cause

Two Forms:
Systemic Lupus Erythematosus (SLE)
Discoid Lupus Erythematosus (DLE)

SYSTEMIC LUPUS (SLE)

Systems Affected:
Musculoskeletal
Cutaneous
Renal
Nervous
Cardiovascular

ETIOLOGY/PATHO. SLE
Theoretical Causes:
Genetic
Familial
Environmental factors
Susceptibility to viruses
Immune system dysfunction

PRECIPITATING FACTORS (SLE)

FLARES/EXACERBATIONS
Sun exposure/sunburns
Anticonvulsants
Cardiovascular meds
Oral contraceptives
Menarche
Pregnancy & Post-partum

CLINICAL MANIFESTATIONS(SLE)
Systemic
Musculoskeletal
CNS
Hematologic
Cutaneous
Genitourinary
Cardiopulmonary
Raynaud’s Phenomenon
G.I.
ASSESSMENT (SLE)
Family Hx
Physical exam
Psychosocial

DIAGNOSTICS (SLE)
Rheumatoid factor (RF)
ESR
Lupus cell prep. (LE cell prep)
Anti-DNA antibody (usually only in SLA)
Anti Sm antibody (only in SLA)
Anti-Antinuclear antibody (est. some type autoimmune disease)
Serum protein electrophoresis
Immunoglobins
CBC

COLLABORAT MANAGEMENT (SLE)

NSAIDS
Salicylates
Topical steroids
Corticosteroids (systemically)
Antimalarials (chloraquine)
Anticonvulsants
Immunosuppresant/cytotoxic: azathioprine, cyclophosphamide

COLLABORATIVE MANAGEMENT (SLE)

Renal dialysis
Renal transplant
Physical therapy

Home Care
Medications/disease management
Medic Alert bracelet
Family planning
Complication prevention
Arthritis & Lupus Foundations

DISCOID LUPUS ERYTHEMATOSUS (DLE)

Skin condition
 All races
 4th decade
Precipitating Factors
 Trauma
 Stress

Manifestations/Patho. (DLE)
 Erythematous “butterfly” rash
 Approx. 5-10% develop SLE
 No cure
 Diagnosis: skin biopsy

COLLABORATIVE MANAGEMENT (DLE)

 Palliative Measures
 Topical steroids
 Antimalarials
 Sunscreen