Connective Tissue Disease Pptvo


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  • Connective Tissue Disease Pptvo

    1. 1. Connective Tissue Disease Peggy D. Johndrow 2009
    2. 2. Connective Tissue Diseases <ul><li>Common disorders such as Rheumatoid Arthritis (RA), Osteoarthritis (OA) or more rare conditions such as systemic lupus erythematosum (SLE) & Scleroderma </li></ul><ul><li>Commonly referred to as Autoimmune Diseases </li></ul><ul><li>Can be life threatening or merely inconvenient </li></ul><ul><li>Problems cause limitations in mobility and activities of daily living as well as systemic effects that can lead to organ failure and death </li></ul>
    3. 3. Autoimmune Disease <ul><li>May be primary or secondary health problems </li></ul><ul><li>May be acute or chronic with remission and exacerbations </li></ul><ul><li>Permanent changes may result from these conditions </li></ul>
    4. 4. Rheumatology <ul><li>Connective tissue disease (CTD) major focus of rheumatology </li></ul><ul><li>Rheumatic disease any disease or condition involving musculoskeletal system </li></ul><ul><li>Arthritis means inflammation of one or more joints </li></ul><ul><li>Non-inflammatory arthritis not systemic </li></ul><ul><li>Inflammatory arthritis </li></ul><ul><ul><li>Rheumatoid arthritis </li></ul></ul><ul><ul><li>Systemic lupus erythematosus </li></ul></ul>
    5. 5. Diagnostic Studies <ul><li>Arthrocentesis: needle aspiration of synovial fluid to obtain fluid & relieve pain; fluid cloudy instead of clear </li></ul><ul><li>X-rays: diagnose & monitor disease; show cartilage abnormalities, joint erosion, abnormal bone growth & osteopenia (decreased bone mineralization) </li></ul><ul><li>Arthrography: detect connective tissue disorders; radiopaque substance injected into joint cavity, outline joint contour </li></ul><ul><li>Bone and joint scans: reflect crystal lattice of bone “takes up” radioactive isotope; uptake considered abnormal </li></ul>
    6. 6. Diagnostic Studies <ul><li>Biopsy: muscle biopsy myositis, arterial biopsy arteritis/vasculitis, skin biopsy confirm inflammatory connective tissue disease lupus and scleroderma </li></ul><ul><li>Serum labs </li></ul><ul><li>No one test used in isolation sufficiently diagnoses a rheumatic disease </li></ul>
    7. 7. Serum Laboratory Studies <ul><li>Erythrocyte sedimentation rate (ESR) : increase CTD; indicates rising inflammation; used to monitor long-term inflammatory disease process; higher ESR greater inflammatory activity </li></ul><ul><li>Hematocrit: decrease in chronic inflammation </li></ul><ul><li>  RBC: decrease seen in RA, SLE </li></ul><ul><li>WBC: decrease in SLE </li></ul><ul><li>Serum Immunology </li></ul><ul><ul><li>  ANA Titer: positive with SLE, RA, Scleroderma, Raynaud’s disease, Sjogren’s syndrome, necrotizing arteritis; higher titer greater inflammation </li></ul></ul><ul><ul><li>Complement levels: decrease in RA and SLE[ indicates autoimmune/inflammatory activity </li></ul></ul>
    8. 8. Serum Laboratory Studies <ul><li>C-Reactive Protein: positive indicates active inflammation; often positive for RA, disseminated lupus erythematosum </li></ul><ul><li>Tissue Typing: HLA antigen; measures presences of HLA Antigen used for tissue recognition; found in 80-90% of clients ankylosing spondylitis and Reiter’s syndrome </li></ul><ul><li>Immunoglobulin Electrophoresis: increased levels with autoimmune disorders </li></ul><ul><li>Rheumatoid Factor (RF): determines presence of abnormal antibodies seen in CTD; positive in 80% with RA; positive may also suggest CTD; higher titer greater inflammation </li></ul>
    9. 9. Implications <ul><li>Diagnostic studies not clear-cut </li></ul><ul><li>Observe signs and symptoms over time to diagnose </li></ul><ul><li>Referred to rheumatologist for management </li></ul>
    10. 10. Gerontological Considerations <ul><li>May be primary or secondary </li></ul><ul><li>Clinical course can be different </li></ul><ul><li>Pharmacological treatment in older clients increased risk for ototoxicity, cumulative effect, altered metabolism of certain medication </li></ul><ul><li>More prone to side effects </li></ul>
    11. 11. Assessment <ul><li>Health history </li></ul><ul><li>Physical Exam </li></ul><ul><li>Functional Assessment of Musculoskeletal </li></ul><ul><li>Diagnostic studies </li></ul>
    12. 12. Pharmacological Management <ul><li>Salicylates: action anti-inflammatory, analgesic, antipyretic, platelet aggregation inhibitor; first line treatment </li></ul><ul><li>Nonsteroidal Anti-inflammatory Drugs (NSAIDs): action anti-inflammatory, analgesic, antipyretic, platelet aggregation inhibitor; alternate to salicylates for first-line therapy in several rheumatic diseases </li></ul><ul><li>Cox-2 Inhibitors: action inhibit cyclooxygenase-2 (COX-2) enzymes, produced during inflammation & spare COX-1 enzymes, protective stomach & kidneys </li></ul><ul><li>Disease Modifying Antirheumatic Drugs (DMARDs): anti-inflammatory, inhibit lysosomal enzymes; onset 2-4 months </li></ul><ul><li>Additionally: short-term low dose anti-depressants prescribed to re-establish sleep patterns, provide better pain management. </li></ul>
    13. 13. Degenerative Joint Disease <ul><li>Osteoarthritis (OA) </li></ul><ul><li>Most common disability joint disorder </li></ul><ul><li>Idiopathic, seen with increasing age; increasing age directly related to degenerative changes, as ability of articular cartilage unable to resist microfracture with repetitive low loads diminishes </li></ul><ul><li>Begins in 30’s and peaks in 50’s and 60’s </li></ul>
    14. 14. Osteoarthritis (OA) <ul><li>Affects articular cartilage, subchondral bone & synovium </li></ul><ul><li>Hereditary, congenital & developmental disorders predisposes to OA of hip </li></ul><ul><li>Obesity associated with OA </li></ul><ul><li>Mechanical factors such as joint trauma, sports activities, and occupations </li></ul><ul><li>IW Consider older adults; genetic considerations p 323 </li></ul>
    15. 15. Assessment <ul><li>History (IW Bullets p 324) </li></ul><ul><li>Physical assessment and clinical manifestations </li></ul><ul><ul><li>Joint involvement </li></ul></ul><ul><ul><li>Heberden's nodes </li></ul></ul><ul><ul><li>Bouchard’s nodes </li></ul></ul><ul><ul><li>Joint effusions </li></ul></ul><ul><ul><li>Atrophy of skeletal muscle </li></ul></ul><ul><li>Psychosocial </li></ul><ul><li>Diagnostic Studies </li></ul>
    16. 16. Clinical Manifestations <ul><li>Pain, stiffness, and functional impairment </li></ul><ul><li>Stiffness in morning or after awakening usually last less than 30 minutes & decrease with movement </li></ul><ul><li>Affects weight bearing joints hips, knees, cervical, lumbar spine, proximal and distal fingers </li></ul><ul><li>Characteristic bony nodes may be present; are usually painless </li></ul><ul><li>Compare to RA (I&W Table 20-1 p 325) </li></ul>
    17. 17. Diagnosis <ul><li>Tender enlarged joints, inflammation not destructive type </li></ul><ul><li>Characterized by progressive loss of joint cartilage, appears on x-ray as narrowing joint spaces, osteophytes, when combined with narrowing joint spaces are sensitive and specific findings </li></ul><ul><li>Serum studies not useful in diagnosis of disorder </li></ul>
    18. 18. Management <ul><li>Preventive measures </li></ul><ul><ul><li>Weight reduction, prevention of injuries </li></ul></ul><ul><ul><li>Health Promotion (I&W Bullets p 324; Chart 20-7 p 336) </li></ul></ul><ul><li>Conservative Treatment </li></ul><ul><ul><li>Heat, weight reduction, joint rest and avoidance of overuse, orthotic devices to splint and brace, OT, PT, isometric and postural exercises </li></ul></ul><ul><ul><li>I&W Chart 20-1 p 327; Bullets p 327; Chart 20-6 p 336 </li></ul></ul>
    19. 19. Pharmacological Therapy <ul><li>Tylenol if not relieved, add NSAIDs, ongoing reassess and reduce dose of NSAIDs and use only intermittently with joint pain exacerbation </li></ul><ul><li>Intra-articular injections of corticosteroids for immediate short term relief </li></ul><ul><li>IW Chart 20-2 p 328 </li></ul>
    20. 20. Surgical Management <ul><li>Only when pain is intractable and function has been lost (IW Bullets p 328) </li></ul><ul><li>Arthroplasty: replacement of affected joints </li></ul><ul><ul><li>I&W Table 20-2 p 330 </li></ul></ul><ul><ul><li>Knee replacement: continuous passive motion machine (CPM) I&W Fig 20-3 p 333; Chart 20-5 p 334 </li></ul></ul>
    21. 21. Total Hip Arthroplasty <ul><li>Preoperative care </li></ul><ul><li>Operative procedures </li></ul><ul><li>Postoperative care </li></ul><ul><ul><li>Prevention of dislocation, infection & thromboembolic complications </li></ul></ul><ul><ul><li>Assessment of bleeding </li></ul></ul><ul><ul><li>Management of anemia </li></ul></ul>
    22. 22. Care of Total Hip Arthroplasty <ul><li>Assessment for neurovascular compromise </li></ul><ul><li>Management of pain </li></ul><ul><li>Progression of activity </li></ul><ul><li>Promotion of self-care </li></ul><ul><ul><li>I&W Chart 20-3 p 330; Fig 20-2; Chart 20-4 p 332 </li></ul></ul>
    23. 23. Rheumatoid Arthritis <ul><li>A most common connective tissue disease & most destructive to joints </li></ul><ul><li>Chronic, progressive, systemic inflammatory autoimmune disease primarily affecting synovial joints </li></ul><ul><li>Autoantibodies (rheumatoid factors) formed that attack healthy tissue </li></ul><ul><li>Affects synovial tissue of any organ or body system </li></ul>
    24. 24. Rheumatoid Arthritis Pathophysiology <ul><li>Occurs in synovial tissue </li></ul><ul><li>Phagocytosis produces enzymes within joint, enzymes breakdown collagen, causes edema, proliferation of synovial membrane, and ultimately pannus formation </li></ul><ul><li>Pannus destroys cartilage and bone </li></ul><ul><li>Results in loss of articular surface, joint motion, muscle elasticity and contractile power lost </li></ul><ul><li>Genetics (I&W p 337) </li></ul>
    25. 25. Clinical Manifestations <ul><li>Classic: edema, pain, swelling, warmth, erythema & lack of function classic </li></ul><ul><li>Initially involves small joints as disease progresses involve larger joints; bilateral and symmetrical </li></ul><ul><li>Classic sign joint stiffness in morning lasting more than 30 minutes; stiffness improves later in day </li></ul><ul><li>Joint deformities (I&W Fig 20-4 p 338) </li></ul><ul><li>I&W Chart 20-8 p 337 </li></ul>
    26. 26. Other Manifestations <ul><li>Immobility for extended periods leads to contractures leading to deformity; deformities common in rheumatoid arthritis </li></ul><ul><li>Systemic: fever, weight loss, fatigue, anemia, lymph node enlargement, arteritis, neuropathy, scleritis, pericarditis, splenomegaly, Sjogren syndrome (dry eyes and dry mucous membranes) and Raynaud’s phenomenon (IW Bullets p 338) </li></ul><ul><li>Nodules non-tender and movable in subcutaneous tissue; appear over bony prominences </li></ul><ul><li>I&W Chart 20-8 p 337 </li></ul>
    27. 27. Diagnostic Studies <ul><li>Rheumatoid factor present in 80% of clients, ESR elevated, RBC & C4 complement component decreased; CRP & ANA may be positive </li></ul><ul><li>Arthrocentesis fluid cloudy; X ray reveals bony erosion & narrowed joint spaces </li></ul><ul><li>IW Chart 20-9 p 339 </li></ul>
    28. 28. Assessment <ul><li>Physical assessment and clinical manifestations </li></ul><ul><ul><li>Early disease manifestations </li></ul></ul><ul><ul><li>Late disease manifestations </li></ul></ul><ul><ul><li>Joint involvement </li></ul></ul><ul><ul><li>Systemic complications </li></ul></ul><ul><ul><li>Associated syndromes </li></ul></ul><ul><li>Psychosocial assessment </li></ul><ul><li>Diagnostic studies </li></ul>
    29. 29. Management Mild Symptoms <ul><li>Begin with salicylates or first generation NSAIDs; dosage to maintain consistent blood level </li></ul><ul><li>Second generation NSAIDs: COX-2 inhibitor blocks enzyme involved in inflammation without block enzyme involved in protecting stomach lining; less toxic than first generation </li></ul><ul><li>I&W Chart 20-10 p 341-342 </li></ul>
    30. 30. Management Moderate Symptoms <ul><li>DMARDs initiated early in treatment within 2 years improves symptoms control and management </li></ul><ul><li>Methotrexate used successfully </li></ul><ul><li>Physical therapy and add cyclosporine (immunomodulator) to enhance effects of methotrexate </li></ul>
    31. 31. Management Severe Symptoms <ul><li>Erosive effects </li></ul><ul><li>Reconstructive surgery, corticosteroids </li></ul><ul><li>Biological response modifiers such as etanercept, infiximab, adalimumab, anakinra </li></ul><ul><li>Immunosuppressive agents; high dose methotrexate, cyclophosphamide, and azathioprine </li></ul><ul><li>Highly toxic and can produce bone marrow suppression </li></ul>
    32. 32. Nonpharmacological Treatment of RA <ul><li>Plasmapheresis </li></ul><ul><li>Complementary and alternative therapies (I&W Bullets p 345) </li></ul><ul><li>Promotion of self-care </li></ul><ul><li>Management of fatigue (I&W Bullets p 346; Chart 20-11 p 346) </li></ul><ul><li>Enhancement of body image </li></ul><ul><li>Health teaching </li></ul>
    33. 33. Nursing Care <ul><li>I&W Plan of Care p 359 </li></ul><ul><li>Number 1&2; Bullets p 325 </li></ul>
    34. 34. Systemic Lupus Erythematosus <ul><li>Chronic, progressive, inflammatory connective tissue disorder can cause major body organs and systems to fail </li></ul><ul><li>Many clients with SLE have some degree of kidney involvement; increasing renal involvement has poor prognosis (I&W Bullets p 347) </li></ul>
    35. 35. Assessment <ul><li>History (IW Culture & Genetic p 348) </li></ul><ul><li>Physical assessment and clinical manifestations </li></ul><ul><ul><li>Skin involvement </li></ul></ul><ul><ul><li>Musculoskeletal changes </li></ul></ul><ul><ul><li>Systemic manifestations including pleural effusions or pneumonia and Raynaud’s phenomenon </li></ul></ul><ul><li>Psychosocial results can be devastating </li></ul><ul><li>Diagnostic studies </li></ul>
    36. 36. Clinical Manifestations <ul><li>Insidious or acute </li></ul><ul><li>Involves multiple body systems </li></ul><ul><li>I&W Chart 20-12 p 349 </li></ul>
    37. 37. Musculoskeletal <ul><li>Arthralgia and arthritis (synovitis) </li></ul><ul><li>Joint swelling, tenderness </li></ul><ul><li>Pain on movement </li></ul><ul><li>Morning stiffness </li></ul>
    38. 38. Integument <ul><li>Polycystic lesions </li></ul><ul><li>Chronic rash </li></ul><ul><li>Butterfly rash (“wolf mask”) </li></ul><ul><ul><li>IW Fig 20-7 p 349 </li></ul></ul><ul><li>Oral ulcers occurring in crops </li></ul><ul><li>I&W Chart 20-13 p 350 </li></ul>
    39. 39. Vascular and Lymphatic <ul><li>CV; pericarditis </li></ul><ul><li>Inflammation of arterioles </li></ul><ul><li>Papular, erythematous, purpuric lesions on the fingertips, elbow toes, forearms, and hands </li></ul><ul><li>May progress to necrosis </li></ul><ul><li>Lymphadenopathy </li></ul>
    40. 40. Renal <ul><li>Renal involvement affecting glomeruli </li></ul><ul><li>Can result in renal failure </li></ul><ul><li>Prognosis poor if this occurs </li></ul>
    41. 41. Neurological and Behavioral <ul><li>Widespread Neurological involvement </li></ul><ul><li>Changes in behavior and cognitive function </li></ul><ul><li>Depression and psychosis </li></ul>
    42. 42. Management <ul><li>Control disease activity or exacerbations </li></ul><ul><li>Prevent progressive loss of organ function </li></ul>
    43. 43. Pharmacological therapy <ul><li>NSAIDs for minor clinical manifestations </li></ul><ul><li>Corticosteroids : single most important medication available for treatment </li></ul><ul><li>Use topically for cutaneous; low oral doses; high doses for major disease activity IV corticosteroids </li></ul><ul><li>Antimalarials used for cutaneous, musculoskeletal & mild systemic features </li></ul><ul><li>Immunosuppressive agents with serious forms unresponsive to conservative therapies </li></ul>
    44. 44. Progressive Systemic Sclerosis <ul><li>Systemic scleroderma, meaning hardening of the skin </li></ul><ul><li>Diffuse cutaneous scleroderma </li></ul><ul><li>Limited cutaneous scleroderma </li></ul><ul><li>Pharmacotherapy slows disease progression but often unsuccessful </li></ul>
    45. 45. Scleroderma Pathophysiology <ul><li>Begin skin involvement, mononuclear cells cluster on skin, stimulate lymphokines to stimulate pre-collagen; insoluble collagen formed & accumulates excessively in tissue </li></ul><ul><li>Initial inflammatory response, edema formation, results in taunt, smooth & shiny skin </li></ul><ul><li>Skin undergoes fibrotic changes, leads to loss of elasticity & movement; eventually tissue degenerates, becomes nonfunctional </li></ul><ul><li>Occur in major blood vessels, major organs & body systems potentially resulting in death </li></ul><ul><li>IW Bullets p 351 </li></ul>
    46. 46. Clinical manifestations <ul><li>Starts insidiously with Raynaud’s phenomenon and swelling in hand </li></ul><ul><li>Skin and subcutaneous tissue hard & rigid </li></ul><ul><li>Skin dry: secretion suppressed </li></ul><ul><li>Extremities stiffen & lose mobility; IW Fig 20- p 351) </li></ul><ul><li>Condition spreads slowly </li></ul><ul><li>Face mask like appearance, immobile & expressionless, mouth becomes rigid </li></ul>
    47. 47. Other Manifestations <ul><li>Left ventricle with heart failure </li></ul><ul><li>Esophagus hardens interfering with swallowing </li></ul><ul><li>Lung scarring impeding respirations </li></ul><ul><li>Digestive disturbances because of hardening of intestinal mucosa </li></ul><ul><li>Progressive renal failure occurs </li></ul><ul><li>I&W Bullets p 351-352 </li></ul>
    48. 48. CREST <ul><li>Calcinous (calcium deposits in the skin) </li></ul><ul><li>Raynaud’s phenomenon </li></ul><ul><li>Esophageal hardening </li></ul><ul><li>Sclerodactyly (scleroderma of the digits) </li></ul><ul><li>Telangiectasis (capillary dilation that forms a vascular lesion) </li></ul>
    49. 49. Assessment and Diagnosis <ul><li>Skin changes </li></ul><ul><li>Skin biopsy </li></ul><ul><li>Abnormal ventilation perfusion studies </li></ul><ul><li>Abnormal esophageal studies </li></ul><ul><li>Positive ANA </li></ul>
    50. 50. Client Education <ul><li>Medication instructions </li></ul><ul><li>Encourage independence as possible </li></ul><ul><li>Information about the disease process </li></ul><ul><li>Therapeutic regimen </li></ul>
    51. 51. Management <ul><li>Penicillamine decreases skin thickening & reduces rate of new visceral organ involvement </li></ul><ul><li>Capoten (captopril) effective hypertension control </li></ul><ul><li>Anti-inflammatory to control arthralgia, stiffness, & general musculoskeletal discomfort </li></ul>
    52. 52. Nursing Interventions <ul><li>Common problems impaired skin integrity; self care deficits, altered nutrition, and body image disturbance </li></ul><ul><li>Focus on impaired gas exchange, decreased cardiac output, impaired swallowing and constipation </li></ul><ul><li>I&W Chart 20-14 p 352 </li></ul>
    53. 53. Gout <ul><li>Also called gouty arthritis, a systemic disease in which urate crystals deposit in joints and other body tissues, causing inflammation </li></ul><ul><li>Primary gout: most common type; cause by several errors of metabolism; uric acid production greater than ability of kidneys to excrete </li></ul><ul><li>Secondary gout: excess uric acid caused by another disease/medication (renal disease, diuretics, chemotherapy) </li></ul>
    54. 54. Clinical Manifestations <ul><li>Acute gout: joint inflammation caused by uric acid deposits </li></ul><ul><li>Chronic gout: presence of tophi (deposits of sodium urate crystals; IW Fig 20-9 354); ear, joints of arms, fingers; hard to palpation, irregular shape; renal calculi, renal dysfunction </li></ul><ul><li>Diagnosis: serial measurements serum uric acid levels; urine uric acid levels </li></ul>
    55. 55. Management <ul><li>Acute gout: combination of Novocolchicine (colchicine), NSAID, Motrin (ibuprofen); IV colchinicine effect in 12 hours, take orally for 4-7 days </li></ul><ul><li>Chronic gout: Zyloprim (allopurinol), Benemid (probenecid), ColBenemid (probenecid/colchicine) </li></ul><ul><li>Diet Therapy: usually avoid foods that cause gouty attacks; increase fluid intake </li></ul><ul><li>Avoid aspirin & diuretics; extreme stress, excessive physical exercise </li></ul>
    56. 56. Lyme Disease <ul><li>Reportable systemic infectious disease caused by spirochete Borrelia burgdorferi, resulting from bite of infected deer tick </li></ul><ul><li>Stages I, II and III </li></ul><ul><li>If not treated in early stages, chronic complications such as arthralgias, fatigue, memory & thinking problems present in later stages; permanent damage to joints & nervous system </li></ul>
    57. 57. Clinical Manifestations <ul><li>Stage I: Large “bulls eye” circular rash, flu-like symptoms (malaise, fever, H/A, joint/muscle pain); symptoms within 3-32 days of tick bite </li></ul><ul><li>Stage II: occur 2-12 weeks after tick bite; carditis, dysrhythmias, dyspnea, dizziness, palpitations; meningitis, facial paralysis ( ) , peripheral neuritis </li></ul><ul><li>Stage III (chronic persistent): occur weeks to years after tick bite; only sign may be arthritis, disease not respond to antibiotics, permanent damage to joints and nervous system </li></ul>
    58. 58. Pharmacological Therapy <ul><li>Stage I: Vibramycin (doxycycline), Amoxil (amoxicillin), Ceftin (cefuroxime) taken for 10-21 days </li></ul><ul><li>Stage II: if severe, IV antibiotics, Rocephin (ceftriaxone), Claforan (cefotaxime) </li></ul><ul><li>Stage III: treat symptoms; damage may be permanent </li></ul><ul><li>Prevention best therapy (I&W Chart 20-16 p 356) </li></ul>
    59. 59. Fibromyalgia Syndrome <ul><li>Chronic pain syndrome, not an inflammatory disease (I&W Fig 20-10 p 357) </li></ul><ul><li>Pain typically located at trigger points (neck, upper chest, trunk, low back, extremities) </li></ul><ul><li>Other symptoms (I&W Bullets p 358) </li></ul><ul><li>Exacerbated by stress, increased activity, change weather conditions </li></ul><ul><li>Secondary disease may develop r/t RA, SLE </li></ul>
    60. 60. Management <ul><li>Physical therapy treatment </li></ul><ul><li>Pharmacotherapy with NSAIDs, muscle relaxants, sedatives for sleep </li></ul><ul><li>Home exercises, including walking, swimming, rowing, biking, and water exercise </li></ul><ul><li>Stress management </li></ul>
    61. 61. Other Related Disorders <ul><li>Polymyositis/Dermatomyosis </li></ul><ul><li>Systemic Necrotizing Vasculitis </li></ul><ul><li>Polymyalgia Rheumatica; Temporal Arteritis(I&Wchart 20-15 p355) </li></ul><ul><li>Ankylosing Spondylitis </li></ul><ul><li>Reiter’s Syndrome </li></ul><ul><li>Sjogren’s Syndrome </li></ul><ul><li>Ankylosing Spondylitis (IW Genetics p 355 </li></ul><ul><li>Marfan Syndrome </li></ul><ul><li>Infectious Arthritis </li></ul><ul><li>Pseudogout </li></ul><ul><li>Psoriatic Arthritis </li></ul><ul><li>Chronic Fatigue Syndrome(I&W Bullets p 358) </li></ul><ul><li>Local inflammatory </li></ul><ul><li>Mixed Connective tissue disease </li></ul><ul><li>Psoriatic arthritis (IW Table 20-3 p 357 </li></ul>
    62. 62. Generalized Nursing Interventions
    63. 63. Pain Relief <ul><li>Medications for short-term acute pain </li></ul><ul><ul><li>Non-opioid analgesics </li></ul></ul><ul><ul><li>NSAIDS </li></ul></ul><ul><li>Disease modifying medications </li></ul>
    64. 64. Non-Pharmacological Pain Relief <ul><li>Superficial heat applied form of warm tub baths, showers, warm moist compresses </li></ul><ul><li>Paraffin baths (dips) for concentrated heat for wrist and small-joint involvement Maximum benefit with 20 minutes of application </li></ul><ul><li>Heat may increase pain </li></ul><ul><li>If inflammatory process acute may try cold compress </li></ul><ul><li>Muscle relaxation techniques, self-hypnosis, and distraction </li></ul>
    65. 65. Joint Support <ul><li>Use of braces, splints, and assistive mobility devices to ease pain from weight bearing </li></ul><ul><li>Splints may be applied to rest inflamed joints, support the joint and relieve spasms </li></ul>
    66. 66. Decrease Fatigue and Promote Sleep <ul><li>Acute or chronic </li></ul><ul><li>Modify and reduce fatigue </li></ul><ul><li>Periods of rest, splints, conditioning exercise to build endurance; recommended walking, swimming, bicycling </li></ul><ul><li>Sleep-inducing routine, medications, and comfort measures </li></ul>
    67. 67. Improve Mobility <ul><li>Proper body positing to prevent deformity </li></ul><ul><li>Support joints </li></ul><ul><li>Firm mattress supine position with a footboard and one pillow under the head. </li></ul><ul><li>Lie prone several times a day </li></ul><ul><li>Active range of motion; passive ROM if unable to perform active </li></ul><ul><li>Assistive devices </li></ul>
    68. 68. Exercise and Activity <ul><li>Maintain and improve joint function </li></ul><ul><li>Active inflammatory process: passive ROM </li></ul><ul><li>Subacute inflammatory process: active assistive ROM or active ROM within pain tolerance </li></ul><ul><li>Inactive, remission: active ROM, isometrics </li></ul>
    69. 69. Facilitate Self Care and Self-Concept <ul><li>Adaptive equipment to increase independence </li></ul><ul><li>Demonstrate use and positive attitude </li></ul><ul><li>Encourage verbalization of feelings, perceptions, and outlook </li></ul><ul><li>Active listening </li></ul><ul><li>Acceptance </li></ul>
    70. 70. Monitor and Manage Potential Complications <ul><li>Avoid drug-induced complications </li></ul><ul><li>Recognize and deal with side effects </li></ul><ul><ul><li>Side Effects: GI bleeding or irritation, bone marrow depression, mouth sores, rashes, changes in vision, bruising, breathing problem, dizziness, jaundice, dark urine, black or tarry stools, diarrhea, nausea and vomiting and headaches </li></ul></ul><ul><li>Corticosteroids can mask systemic and local infections </li></ul>