Ra Oa Gout

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Osteoarthritis

Back 1

Most common type of arthritis
progressive deterioration and loss of cartilage in one or more joints
May cause osteophytes-bone spurs
Eventually cartilage disintegrates and pieces of bone and cartilage "float" in the diseased joint=crepitus
Usually pain with activity that decreases with rest

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Assessment of OA

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History: older than 60 years of age, type of work they do, smoking hx
Physical: joint pain/stiffness, crepitus, Heberden's nodes, Bouchard's nodes, joint effusions, atrophy of skeletal muscle
Psychosocial: severe pain may cause depression/anxiety
Laboratory: ESR, nsCRP-may be elevated when secondary synovitis occurs
Radiographic: MRI (to determine vertebral or knee involvement), CT

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Priority problems with OA

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Chronic pain r/t cartilage deterioration
Decreased mobility r/t joint pain and muscle atrophy

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Drug therapy for OA

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Tylenol: primary drug of choice to reduce pain caused by cartilage destruction, muscle spas, and/or secondary joint inflammation
Short term use: NSAIDS-careful of GI irritation, look for bleeding
Topical drug applications such as lidoderm patches
Cortisone injection into joint may help--->maybe no if DM; no more than 4 times a year or once every 3 months
COX inhibitor (Celebrex)--->no if have CAD or HTN

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Nonsurgical interventions for OA

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analgesics, rest, positioning, thermal modalities, weight control, and integrative therapies
Canes should be used on the strongest side of the body
Position joints in their functional position
Ice or heat to affected area

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Complementary and alternative therapies for OA

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Glucosamine may decrease inflammation
Chondroitin may play a role in strengthening cartilage
Contraindications: HTN, pregnancy, concurrent use with anticoagulants (watch for bleeding), DM (monitor blood sugars)
Acupuncture, massage, distraction

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Surgical management of OA

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Total joint arthroplasty (TJA)
Osteotomy (bone resection) to correct joint deformity
Arthroscopy may be used to remove damaged cartilage

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Indications for TJA in OA

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Osteonecrosis-bony necrosis secondary to lack of blood flow, usually from trauma or chronic steroid therapy

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Contraindications for TJA in OA

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Active infection anywhere in the body
Advanced osteoporosis

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Converting from heparin to coumadin in OA

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Have to have overlap until therapeutic level of coumadin
Check INR and PT/PTT levels

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Neurovascular Assessments in OA

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Check for movement, sensation, warmth, color, pulses, and capillary refill

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Post Op Care for OA

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Hip dislocations
VTE-compression devices, anticoagulants
Infection-monitor surgical incision and vital signs
Anemia-assess for bleeding
Neurovascular compromise-check extremities

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Rheumatoid Arthritis

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Ages 20-50
Common connective tissue disease, destructive to joints
Chronic, progressive, systemic inflammatory autoimmune disease
Affects primarily synovial joints
Transformed autoantibodies form, attack healthy tissue causing inflammation
Vasculitis-blood vessel involvement, organ supplied may be affected

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Assessment for RA

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History:
Physical: joint stiffness, swelling, pain, and fatigue; generalized weakness and morning stiffness, low-grade fever, fatigue, anorexia, paresthesias, deformities; Baker's cysts-enlarged popliteal bursae behind the knee
Psychosocial: can be crippling if not controlled, fear of becoming disabled and dependent, altered body image
Laboratory: rheumatoid factor (RF) measures the presence of unusual antibodies of the IgG and IgM, antinuclear antibody (ANA) measures the titer of unusual antibodies that destroy the nuclei of cells and cause tissue death in patients with autoimmune disease, serum complement are usually decreased in autoimmune disease, elevated ESR confirms inflammation or infection, hsCRP measures inflammation, CBC-for a low hemoglobin, hematocrit, and RBC count/increase in WBC count may indicate inflammatory process
Diagnostic: X-ray to see joint changes, CT for degree of cervical spine involvement

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Drug therapy for RA

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Anti-inflammatories
DMARDS (methotrexate): taking 4-6 weeks to begin; monitor decreased WBCs and platelets, or elevations in liver enzymes-no alcohol; pregnancy contraindicated; may have mouth sores
NSAIDS: do not take on empty stomach
BRMs: not for people with MS or TB, watch CBC
Steriods: suppress immune response, also increase blood sugars; chronic use may lead to DM or infection, even maybe HTN; also maybe osteoporosis

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Non pharmacologic interventions for RA

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Plasmapheresis: plasma is treated to remove the antibodies causing the disease

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Promoting self management of RA

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Encourage independence in completing ADLs
Energy conservation
Improve body image: use personal items

Front 18

Lupus

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Chronic, progressive, inflammatory connective tissue disorder
Can cause major body organs, systems to fail
Spontaneous remissions and exacerbations
Autoimmune
Tends to be attracted to the glomeruli of the kidneys

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Clinical manifestations for Lupus

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Skin involvement-butterfly rash
Age 15-40
Polyarthritis
Osteonecrosis-bone necrosis from lack of O2
Muscle atrophy
Fever and fatigue
Anorexia
Pleural effusion
Raynaud's syndrome-poor perfusion to the extremities
Pericarditis
Neurologic changes: seizures, migraines, psychosis, cranial nerve palsy

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Assessment for Lupus

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Psychosocial: disfiguring and embarrassing, chronic fatigue and weakness may prevent from being active
Laboratory: skin biopsy, immunologic tests, CBC shows pancytopenia (a decrease of all cell types)***, RF will be positive, ESR will increase, serum complement will decrease, may have a false positive syphilis test

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Drug therapy for Lupus

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Anti-malarial agent to decrease the absorption of UV light
Topical cortisone
NSAIDS
Steroid therapy
Immunosuppressive therapy: Methotrexate-monitor for bone marrow suppression, risk of infection/risk of bleeding

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Interventions for lupus

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Monitor for HTN
Monitor I and Os-at least 30 ml/hr
Look for diminished breath sounds
Look for pericarditis-pain with inspiratory breath
Small meals, with supplements in between meals
Protect from the sun: cleanse skin with mild soap, dry skin thoroughly by patting, apply lotion liberally to dry skin areas, avoid powder and other drying agents, use cosmetics that contain moisturizers, avoid direct sunlight, wear a large-brimmed hat/long sleeves/long pants, use a sun-blocking agent of at least SPF 30, inspect your skin daily for open areas and rashes

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Scleroderma

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Chronic, inflammatory, autoimmune connective tissue disease
Not always progressive
Hardening of the skin
Classifications: diffuse cutaneous (trunk, face, proximal and distal extremities), limited cutaneous (face, neck, and distal extremities)
Affects respiratory
May see HTN
Renal disease r/t scleroderma can lead to death

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Clinical manifestations of scleroderma

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CREST syndrome: calcium deposits, raynaud's syndrome, esophageal dysmotility (may need swallow study), sclerodactyly, telangiectasis (spider-like hemangiomas)
First symptom is pitting edema of the hands and forearms
Can be associated with carpal tunnel
GERD is commonly present in patients with either type of the disease
Peristalsis is diminished-representing similar symptoms of a partial bowel obstruction--->leading to malabsorption and malodorous diarrheal stools

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Drug therapy for Scleroderma

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High doses of steroids and immunosuppressants are given but do not work very well
Find the organ that is involved and treat the symptoms r/t that organ

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Interventions for scleroderma

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Elevate HOB during meals and for at least 1 hr after meals
Soften food
Small frequent meals
Avoid foods that increase gastric secretions such as caffeine, pepper, and other spices
GIve antacids or histamine antagonists as needed
Monitor for EKG changes
Turn patient frequently
Educate on signs and symptoms of medications--->at MUCH higher risk for infection and decreased platelets

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Gout

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Also called gouty arthritis
Urate crystals deposit in joints and other body tissues, causing inflammation
Primary gout r/t inborn metabolic disorder
Secondary gout-hyperuricemia
Most common in middle age to older men; peak time is 40 to 50 years of age
Producing uric acid too fast to excrete it
Chemotherapy, diuretic therapy, renal insufficiency, and crash diets can cause this

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Drug therapy for Gout

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Colchicine with NSAID for acute gout
Allopurinol is the drug of choice for chronic gout-take after meals and drink a full glass of water with each dose to decrease GI upset

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Assessment for Gout

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History: age, gender, family hx
Physical: inflammation in prominent joints (toes, knees), painful to touch
Laboratory: serum uric acid levels if greater than 6.5, urinary uric acid, renal function tests, synovial fluid aspiration to determine needle-like crystals in fluid
Chronic=signs of renal calculi, Tophi: deposits of sodium urate crystals on the skin (fingers and ear; hard and irregular shape)

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Interventions for Gout

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Fluid intake
Diet education
Medication side effects and use

Front 31

Fibromyalgia

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Most common in women between 30 and 50 years of age
Precipitating factors: CFS, lymes disease, trauma, flu-like symptoms, and lack of sleep

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Assessment of fibromyalgia

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Physical: pain, stiffness, tenderness at specific sites, GI and abdominal pain, diarrhea, constipation, heartburn, genitourinary, dysuria, polyuria, blurred vision, dry eyes, decreased concentration, forgetfulness, dyspnea, CP, dysrhythmias =
Psychosocial: frustrated with no diagnosis, depression, isolation, anxiety, decreased sleep

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Interventions for fibromyalgia

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Limit caffeine, alcohol, or other substances that interfere with deep sleep
Exercise regularly
Complementary interventions such as massage, acupuncture, tai chi

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Drug therapy for fibromyalgia

Back 34

Antidepressants
NSAIDs
Trazadone
Tramadol
CAM

Front 35

Hyperthyroidism

Back 35

Excessive thyroid hormone secretion
Manifestations are called thryotoxicosis
Exaggerates normal body functions
PRoduces hypermetabolism and increased sympathetic nerous system activity
Thyroid hormones stimulates heart (increased heart rate and stroke volume), affects protein/lipid/carb metabolism, glucose tolerance decreased leading to hyperglycemia, increased libido
Changes secretions from hypothalamus and anterior pituitary
Causes: Graves' disease, toxic multi-nodular goiter, excessive use of thyroid replacement hormones
Most common in women 20-40 years old
Thyroid storm--->life threatening: fever and hypertension; result of uncontrolled hyperthyroidism

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Assessment for hyperthyroidism

Back 36

History: do not do a thyroid scan if: pregnancy, medical hx, iodine allergy, birth control contrast media--->false increase of Thyroid hormones
Physical: hyperactivity, nervousness, decreased attention span, fatigue, weight loss, insomnia, warm/sweaty/flushed skin, tremors, hyperkinesia, hyper-reflexia, vision changes, staring gaze, hair loss, goiter, increased HR, increase BP, S3 heart sounds
Laboratory: TSH (decreased in graves), TSH increased in secondary and tertiary, FTI and T3 increased, TRH stimulation test failure to increase TSH
Diagnostic: radio-iodine uptake and thyroid scan to clarify size of gland and detect hot/cold nodules