Transcript 14.Joint.Brittanyx

CONNECTIVE TISSUE
STRESSORS
PART II
BRITTANY WARING, RN, BSN
WITH THANKS TO
PRITAM PANDIT RN, BSN, CCRN
FOR THE SLIDES
CONDITIONS
• SCLERODERMA
• FIBROMYALGIA
• GOUT
• OSTEOARTHRITIS
SCLERODERMA
SCLERODERMA
• A chronic autoimmune connective tissue disease characterized by hardening of the skin.
• Affects connective tissue of the skin, blood vessel walls, digestive tract, and internal organs.
• 3-5 x more common in females than males.
• Onset most frequently seen between ages 30 – 50.
SCLERODERMA
• There are 2 general types –
a) Localized = affects only cutaneous system (hands, arms and face); more common in children.
b) Systemic = affects large areas of skin and 1 or more internal organs (ex: kidney, esophagus, heart,
and/or lungs).
• Most deaths occur from lung, heart, and kidney complications.
SCLERODERMA
• Caused by genetic (HLA gene) and environmental (silica, welding fumes, chlorinated
solvents, etc.) factors.
•Is not contagious, infectious,
cancerous or malignant.
•There is no cure.
PATHOPHYSIOLOGY
1. Begins with a stimulant; creates damage to vascular structure (endothelium).
2. Adhesion molecules and cytokines attract leukocytes; B cells and T cells – autoimmune
component.
3. Lymphokines are stimulated, in turn stimulate procollagen (fibroblasts).
4. Excess collagen accrues in tissues.
PATHOPHYSIOLOGY
• Initially – edema; results in taut, smooth, shiny skin.
• Fibrosis occurs – loss of elasticity and movement.
• Tissue degenerates, becomes nonfunctional.
• Entire process from inflammation to degeneration – occurs in blood vessels, major organs,
and body systems.
SIGNS & SYMPTOMS
• Begins with Raynaud’s phenomenon and
swelling in hands.
• Skin becomes hard and rigid; dry – r/t suppression of sweat secretion at involved region.
• Extremities become stiff and lose mobility.
• Spreads slowly – may remain in hands and feet.
Over years, face becomes mask-like, immobile,
expressionless; mouth becomes rigid.
SIGNS & SYMPTOMS
• Cardiovascular: Raynaud phenomenon (affects ≅ 70%); skin/mucosal telangiectasis;
palpitations, irregular HR, HTN, CHF involving LV, digital ulcers.
• Digestive: r/t hardening of the intestinal mucosa – esophagus hardens (interferes with
swallowing), GERD, bloating, indigestion, diarrhea/constipation, loose teeth & hoarseness
(acid reflux).
SIGNS & SYMPTOMS
• Pulmonary: progressive worsening of SOB, chest pain r/t pulmonary artery HTN, dry/persistent
cough due to lung disease.
• Musculoskeletal: joint and muscle aches, decreased ROM, carpal tunnel syndrome, muscle
weakness.
• Genitourinary: ED, dyspareunia, kidney failure.
• Other: facial pain, headache, fatigue, weight loss, hand paresthesias.
SIGNS & SYMPTOMS
DIAGNOSTICS
• There is no conclusive diagnostic test.
• Assessment – GI, pulmonary, renal, cardiac symptoms.
• CT – pulmonary HTN
• ECHO – pericardial effusion
• Blood tests – ANA (antinulear antibodies—attack body’s own tissues) — usually positive
• Esophageal studies – decreased motility
MEDICAL MANAGEMENT
• Counseling
• Moderate exercise – prevent joint contractures
• GI: PPI (antacids) – gastric reflux
• Tums, rolaids, mylanta, protonix
• Cardiac:
• Ca+ channel blockers (amlodipine, nicardipine) – improve decrease symptoms of Raynaud’s
MEDICAL MANAGEMENT
• Aspirin and statins to reduce cardiovascular risk factors
• Flolan, sildenafil (viagra) – pulmonary HTN
• UV A irradiation – decrease synthesis of collagen
• Kidney crisis – ACE & ARB
• Immunosuppressant
• Methotrexate, cytoxan – teratogenic; risk to mother and child; reduced fetal wt.
• Can use hydroxychloroquine (DMARD) and low-dose corticosteroid (such as prednisone,
hydrocortisone)
NURSING MANAGEMENT
• Avoid extreme temperatures; use lotion for skin care/dryness
• Warm socks & proper fitting shoes (prevent ulcers)
• Patient education (Raynaud’s)
• Smoking cessation
• Balanced nutrition
• Improve functional ability (exercise)
FIBROMYALGIA
FIBROMYALGIA
• A disorder of pain processing due to abnormalities in how pain signals are processed in the
central nervous system – neurogenic disorder.
• The neurochemical imbalances and the activation of inflammatory pathways in the brain result in
abnormalities in pain-processing.
FIBROMYALGIA
• Literally means “muscle and connective tissue pain.”
• Characterized by chronic widespread pain and a heightened and painful response to
pressure.
• Women are more affected than men.
• 25% – 65% of those with fibromyalgia also have rheumatic conditions such as RA and SLE.
PATHOPHYSIOLOGY
• Ascending and descending pain pathways (CNS) function abnormally.
• Described as a high “volume control setting” (very low pain tolerance).
• Ex: increased sensitivity to touch.
• A disruption of dopamine transmission.
• Predisposing factors – anxiety, depression, stress, trauma, PTSD, lack of sleep, viral infections.
SIGNS & SYMPTOMS
• The defining symptoms are chronic widespread pain, fatigue, sleep disturbance, and
heightened pain in response to tactile pressure (allodynia).
• The cause is relatively unknown.
SIGNS & SYMPTOMS
DIAGNOSIS
1. Pain lasting more than three months—affecting all four quadrants of the body (both sides, and above and
below the waist).
2. Widespread pain index (WPI) – counts up to 19 body areas where pain experienced over the last two
weeks. WPI > 7.
3. Symptom severity scale (SS) – rates the severity of the person's fatigue, unrefreshed waking, cognitive
symptoms, and general somatic symptoms, each from 0 to 3; total score from 0 - 12.
SS > 5.
MEDICAL MANAGEMENT
• Anti-depressants: Cymbalta, amitriptyline
• Neuropathic pain: Lyrica
• Seizures: gabapentin, pregabalin
• Opioids: Ultracet (tramadol + Tylenol),
Tylenol #3 (codeine + Tylenol)
• Dopamine agonists: Mirapex, Requip
• NSAIDs – muscle aches and stiffness
MEDICAL MANAGEMENT
• Cognitive Behavioral Therapy (CBT)—greatest benefit if used alongside exercise
• Complementary Alternative Medicine (CAM)
• Acupuncture
• Massage
• Hydrotherapy
• Homeopathy
• Craniosacral and myofascial therapy
NURSING MANAGEMENT
• Education – antidepressant medications may take up to 6 months before having the desired effect.
• Exercise – improves fitness and sleep; long-term aquatic based combines cardiovascular exercise
with resistance training.
• Not degenerative or fatal.
NURSING MANAGEMENT
• Support/encouragement
• Listening
• Pain management
• Lifestyle modifications
GOUT
GOUT
• Most common form of inflammatory arthritis.
• 3-4x more common in men than women.
• Comorbid conditions include HTN, DM, dyslipidemia, OA, kidney disease.
• Caused by increased serum uric acid
levels (hyperuricemia).
PATHOPHYSIOLOGY
• Initial cause for attack is r/t macrophages in the joint space phagocytizing urate crystals.
• Underexcretion of uric acid by the kidney is the primary cause of hyperuricemia in about
90% of cases
• Uric acid is a by-product of purine metabolism (meats).
• Meats and ETOH contribute to increase in free fatty acid concentrations which can trigger
acute attacks.
PATHOPHYSIOLOGY
• Crystallization occurs (sudden increase) → crystals deposit in joints, tendons, and
surrounding tissues → initiates inflammatory response (IgG and interleukin).
• 2 types of hyperuricemia –
• Primary – severe dieting/starvation; increased intake of high purine foods.
• Secondary – leukemia, multiple myeloma, psoriasis; diuretics.
PATHOPHYSIOLOGY
• Repeated attacks result in accumulation of sodium urate crystals, called ‘tophi’.
• Usually deposited in peripheral areas such as hands, toe, ear.
• Kidney stones may develop 2º urate crystal deposition.
GOUT RISK FACTORS
• Age
• BMI
• ETOH intake
• HTN
• Diuretic use
• Fructose-rich beverages
SIGNS & SYMPTOMS
• Recurrent attacks of acute inflammatory arthritis – red, tender, hot, swollen joint.
• Most commonly affected area = the metatarsal-phalangeal joint (approximately 90%).
• Joint pain – at night due to lower temps.
SIGNS & SYMPTOMS
• Long-term hyperuricemia results in hardened, painless ‘bumps’ on toes called ‘tophi’.
• Fatigue
• High fever (rare)
• Kidney stones
• Very painful to touch; sensitive
• Decreased ROM r/t joint enlargement
SIGNS & SYMPTOMS
• Spontaneously subside over 3-10 days
• Symptom free until next attack (months-years)
• Over time attacks are more frequent, involve more joints, last longer
• Tophi also found in aortic walls, heart valves, nasal & ear cartilage, eyelids, cornea, sclera
DIAGNOSTICS
• Definitive – presence of uric acid crystals in the synovial fluid
• Plasma urate – > 7.0 mg/dl (m), > 6.0 mg/dl (f)
• CBC – WBC
• CMP – BUN/creat, electrolytes
• ESR
• X-rays, CT scan
MEDICAL MANAGEMENT
• Acute attacks:
• NSAIDs – 1st line treatment (indomethacin, ibuprofen)
• Corticosteroids (hydrocortisone, prednisone, methylprednisone)
• Colchicine (best if given within first 36 hrs of attack)
MEDICAL MANAGEMENT
• Uric acid lowering (after attack has subsided):
• Allopurinol and uloric – agents of choice
• Krystexxa (newly approved; lowers uric acid levels)
• Probenecid (inhibits renal absorption)
• Frequent attacks
NURSING MANAGEMENT
• Diet education – ↓ ETOH, meat, seafood, fructose drinks
• Disease process education
• Weight reduction
• Medication adherence importance
• Lifestyle – decrease trauma, stress
• Don’t abandon preventative behaviors if feeling well
• Early therapy effective in acute attacks
OSTEOARTHRITIS
OSTEOARTHRITIS
• The most common form of joint disease.
• A.K.A.: DJD.
• The protective cartilage on the ends of the bones wears down over time.
• Osteophytes (bone spurs).
OSTEOARTHRITIS
• Classification:
• Primary (idiopathic) – no prior event or disease is related.
• Secondary – from previous joint inflammation or injury.
• Most commonly affects joints in hands, knees, hips, and spine.
• Is limited to the affected joints.
OSTEOARTHRITIS
• No systemic symptoms associated with it.
• Begins in 3rd decade, peaks in 5th and 6th decades.
• No cure exists.
RISK FACTORS
• Older age
• Obesity (the most prominent modifiable risk factor).
• Repetitive motion jobs
• Trauma/anatomic deformities
• Genetics
RISK FACTORS
• Women – Hispanic or African-American.
• Hx of previous injuries.
• Sports.
SIGNS & SYMPTOMS
• Pain – main symptom.
• Tenderness – even with light pressure.
• Stiffness – mornings (resolves within 30 min).
• Bone spurs – hard lumps forming
around the affected joint.
• Heberden/Bouchard nodes.
SIGNS & SYMPTOMS
• Joint effusion
• Loss of flexibility – decreased ROM.
• Grating sensation.
• Insidious onset.
• Advanced hip OA can cause one leg to be shorter than the other.
DIAGNOSIS
• History and physical examination
• Functional assessment – pain , stiffness, swelling, muscle atrophy
• Early joint changes – bone scan, CT, MRI
• Progressive OA – joint space narrowing, bony sclerosis, osteophytes on x-ray
PHARMACOLOGICAL THERAPY
• Acetaminophen is recommended first line with NSAIDs used as add-on therapy.
• Cox-2 enzyme blockers - Celebrex
• Opioids
• Joint injections (cortisone)
• Topical analgesics (capsaicin,
methylsalicylate)
PHARMACOLOGICAL THERAPY
• Viscosupplementation – inject gel-like substances (hyaluronates) into joint;
supplements viscous properties of synovial fluid.
SURGICAL THERAPY
• Osteotomy – most commonly used (alters distribution of weight within the joint).
SURGICAL THERAPY
• Arthroplasty – joint components are replaced.
LIFESTYLE MANAGEMENT
• Weight loss
• Exercise
• Cardiovascular aerobic exercise
• Lower extremity strength training
• OT/PT
• Wedged insoles, knee braces
LIFESTYLE MANAGEMENT
• Walking aids
• CAM
• Massage
• Yoga
• TENS (pain relief)
• Diet
NURSING MANAGEMENT
Goals:
• Pain management (pharmacological, non-pharmacological)
• Optimal functional ability
• Achieve independence in self care (assistive devices)
• Alteration of modifiable risk factors
• Education
QUESTIONS?