Rheumatic Diseases

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Rheumatic Diseases

Commonly called arthritis (inflammation of the joint)

I. General
46 Approximately 200 diseases
47 Affects skeletal muscle, bones, ligaments, tendons & joints
48 Males and females of all ages are affected
49 Impact may be life threatening or an inconvience
50 Acute or insidious onset with periods of exacerbation and remission
51 No real cure; only advanced treatments
52 About 1 in 7 Americans complains of some arthritic signs and symptoms

II. Problems encountered include:


53 Chronic pain
54 Mobility limitations
55 Alterations in ADLs
56 Self-image disturbances
57 Systemic effects which may lead to organ failure or death

III. Age related changes of Muscloskeletal system: Gerontological


Considerations
58 Age related changes: Muscle atrophy; slow mobility; decrease in posture and
height; Joint cartilage erosion; Muscle weakness; decreased muscle mass; bone
Demineralization; S/s increase with age (Clients over 60 have some degree of
DJD)
59 Arthritis is commonly a secondary diagnosis as other medical complications take
Precedence (Old CVAs; Cancer; DM)
60 However, arthritis accounts for more disability
61 Osteoarthritis is the most prevalent activity limitation among elderly leading to
Disability.

IV. Osteoarthritis
a. A degenerative rheumatic disease
b. mainly affects: hips/ knees but can also affect fingers and small joints
c. Risk factors
1. Heredity: Defect in genes responsible for making collagen (a major component
of cartilage)
2. Obesity: Increased risk for DJD of the knee
3. Injuries: Knee related injuries; sever back injury; broken bones/ joint margins
4. Overuse: Repeated knee bending; a “wear and tear” arthritis associated with
the aging process.
d. Pathophysiology
1. Joint cartilage and underlying bone deteriorates resulting in microfractures of
the subchondral bone
2. Thickened subchondral bone absorbs weight poorly, damaging articular
cartilage –synovial cells release enzymes further degrading the cartilage.
3. Articular cartilage becomes rough and cracked –bone rubs against bone
4. Changes in bone structure (hypertrophy)
5. DJD causes the cartilage in joint to become stiff, losing elasticity, increases
susceptibility to damage
6. Cartilage wears away over time decreasing its ability to act as shock absorbers
7. As cartilage wears away, tendons and ligaments stretch causing pain.
e. Clinical manifestations
1. Deep aching joint pain and soreness accentuated by use and weight bearing.
2. Enlarged joints, mild tenderness
3. Changes in alignment of joints – decreased mobility and ROM – contractures
4. Heberden and Bouchard’s nodes – bony proliferations over distal and proximal
Interphalangeal joints (PIP)
-Characteristic clinical manifestations of osteo:
62 Heberden nodes: distal interphalangeal joint (of hand)
b. Bouchard’s: (PIP) Proximal interphalangeal joints
f. Diagnostic evaluation
1. Physical assessment of musculoskeletal system: ROM, tenderness, swelling,
etc; presents asymmetrically
2. Location and pattern of pain: relief, onset, time
3. X-ray- osteophytes and narrowing of joint spaces: overgrowth in joint capsule
4. Arthrocentesis: draw fluid from joint to look for debris; cartilage decreasing
enzymes; inflammatory cells
5. No specific useful serum study: May have increased Sed Rate (shows
inflammation)
g. Therapeutic Management: Goals of treatment
1. Decrease joint pain/ stiffness
2. Improve joint mobility/ stability
3. Increased ability to perform ADLs
**Remember, pain management and maintenance of joint function are essential in
accomplishing the goals of treatment.**
h. Conservative measures of treatment:
1. Heat or cold: which ever works best because it is chronic
2. Weight control: decrease added pressure on joints
3. Rest joint/ no overuse: to decrease inflammation
4. Supportive devices: splint for support
5. Exercise: increase circulation and mobility; strengthen joins and muscles;
increase coordination. (low impact)
6. Occupational and physical therapy
i. Pharmacotherapy:
1. Salicylates: Aspirin; “the grandfather”; (Needs to be enteric coated)
2. Ibuprofen: Advil, Motrin, Nuprin (take with food – can cause GI distress)
3. NSAIDs (non steroidal anti-inflammatory drugs): Celebrex – the “Super
Aspirins”; The older drugs: Aleve, Indosen, Napersin (The older drugs can cause
GI distress; Do not drink ETOH; Potential for GI bleed)
4. Glucosamine and Chondroitin: Nutritional supplements – help build cartilage
5. Tramadol (Ultram): narcotic-related pain reliever
6. Intra-articular corticosteriod injections: relieves pain due to decreasing
inflammation; lasts approx. 6 months
j. Nursing Management:
1. Chronic pain r/t joint degeneration- give meds as order
2. Impaired physical mobility related to restricted joint mobility
3. Body image disturbance related to visible body changes
4. Self-care deficit related to immobility
5. Knowledge deficit related to lack of knowledge of disease process
6. Ineffective individual/ family coping related to stress of managing disease.
k. Preventive measures: Joint protection
1. Correct body mechanics
2. Avoid grasping actions that strain finger joints
3. Spread weight of an object over several joints
4. Maintain good posture
5. Use strongest muscles and favor large joints.

V. Rheumatoid Arthritis
a. chronic, systemic disease with periods of exacerbations and remission
b. Progressively deteriorating connective tissue disease that is characterized by
inflammation of the synovial membrane of the Diarthrodial Joint (freely moveable)
63 A systemic disease that can affect all connective tissue including nonarticular
connective tissue.
64 It attacks the collagen; which is the protein in the connective tissue that is found
in the lungs, heart, muscles, blood vessels, and tendon.
o May also cause lesions of vasculature, nervous system, and other major
organs of the body.
65 Progressive in nature
66 OA has interactions in the joint capsule that lead to inflammation and RA
the inflammation occurs first**

ETIOLOGY AND INCIDENCE


67 Could be an autoimmune disorder
68 Could be a metabolic factor that causes an abnormal function in the production of
the collagen.
69 Usually diagnosed at 35-45 (family and careers)
70 May be a genetic predisposition

PATHOPHYSIOLOGY
71 Synovium becomes inflamed
o Edema with vascular congestion increases production of synovial fluid
o Continued inflammation with thickening of the synovium and granulation
tissue (pannus) begins to form over cartilage which results in necrosis of
the cartilage
o If areas of cartilage are lost this will result in formation of adhesions,
ankylosis, and weakening of tendons and ligaments
o Destruction leads to dislocation of joints and deformities
72 Joint involvement is usually bilateral and symmetrical.
73 Process often starts in fingers and toes, however all joints can become involved
(hips, knees, wrists, elbows, shoulders, jaws)
o Cartilage – Absorbs the load (cushion) of weight bearing
o Nourished by the synovial fluid; if there is a problem with the synovial
membrane it cannot nourish the joint capsule.

CLINICAL MANIFESTATIONS
74 Local
o Inflammation Heat
o Swelling Erythema - Redness
o Pain Decreased ROM
75 Systemic
o Fever Weight loss
o Fatigue Generalized aching
o Edema
o Lymph node enlargement
§ You have a problem
o Joint tissue becomes spongy
o Presents bilaterally and symmetrically
o Onset may be acute (OA slowly)
o Hands, hips, and feet are involved and can progress to shoulders,
knees, elbows, spine, and also temporal mandibular joint
o Joint stiffness in the a.m. lasting longer than 30 minutes (OA Feel stiff
at first but can work the pain out)
76 Complications – Structural Deformities
o Z-thumb deformity
§ Overflex or hyperextention of the thumb
o Ulnar deviations
§ Fingers deviate toward the ulnar side of hand (pinky)
§ Metacarpal phalengeal joints are swollen – Spongy moveable
nodules (OA are hard)
o Genu Valgun
§ Knock knees
§ May tend to sublux (dislocate)
o Hallux melleus
§ Hammertoes with lower arch
§ Some cannot walk – wide toed shoes
These people are on prednisone and things that mask infection and lot of times
they can get infection from attempting surgery.
o Swan-neck deformity
§ Hyperextension of the PIP joint and flexion of the distal joint
o Boutonniere’s deformity
§ Hyperflexion of the PIP joint and extension of the distal joint
DIAGNOSTIC EVALUATION
77 Full History and Physical
78 Increase in Sed rate – ESR
o Only looking for inflammation
79 C-Reactive Protein – Shows abnormal glycoprotein due to inflammatory process
and active inflammation. Coming in periodically to see if this is beginning to rise
the MD may increase medication to combat the inflammation
80 ANA – Anti nuclear antibodies – Measuring antibodies that react to nuclear
antigens
81 Rheumatoid Factor Test (RF) or Latex Fixation
o Specifically for RA; Positive indicates RA; keep in mind you may get a
false positive so assess all the other manifestations
82 Decreased in RBC’s - RA can cause anemia
83 C3 and C4 Complement Components
84 Athrocentesis
o Fluid should be clear, viscous, straw colored, that would be normal
o RA the fluid would be cloudy, milky, or dark yellow
85 X-Ray - Will show narrowing of joint space; could help diagnose what stage of
disease
86 Physical assessment
MEDICAL MANAGEMENT

Relief of Inflammation with Medications


87 If you decrease inflammation you will decrease pain; then you would have
possible functioning of the joint for that individual.
88 Every thing you do revolves around joint protection
89 There are 3 stages of RA: Early, Moderate, Persistent or Erosive RA
o Now they begin with large doses of medications while they still have the
opportunity to combat the autoimmune process and prevent deformities

DRUG THERAPY
90 DMARD’s – Disease Modifying Anti Rheumatic Drug
o Plaquenil – Anti-malarial
§ Reduces the inflammation
o Gold Salts
§ Myochrysine, Solganal, Radura
§ Decrease breakdown
o Penicillamine – Cuprimine, Depen
§ Inhibits T-Cell function
§ Decreases inflammation
91 NSAID’s – Non Steroidal Anti Inflammatory Drug
92 Corticosteroids
o Prednisone
o Reduce inflammation and slow joint damage; given short term
o Carry side effects: Weight gain, retaining fluid, cushings, Increase BP,
Increase blood glucose, causes sodium retention, can lead to
Osteoporosis by reducing bone mass, Masks S/S of infection, slows
down healing.
93 Immunosuppressive
o Because it is an autoimmune process; they tame the immune system
o Methotrexate, Imuran, Sandimmune, Neoral, Cytoxan, Arava
94 Antidepressant - Depressed, change in alteration of lifestyle

Relief of Pain
95 Pain, decreased ROM, Fatigue, and sleep disturbances are the most common
problems associated with RA.
96 Traditional Methods of Pain Management
o Medications
o Splinting
§ To decrease inflammation. Support optimal position of function
o Exercise, keep mobile
o Positioning
o Heat / Ice
o Emotional Support
o Rest body – “systemic disease”
Fatigue
o Make sure they rest
o Don’t over do it
Sleep Disturbance
o Medication – sleep aids
Maintenance of Optimal Function
o Good posture
o Exercise
o Splinting
§ Some will have splints made specifically for them.
§ To rest and support the joint in its most optimal position
o Joint protection
o Energy conservation
o Assistive devices
§ Cane
o Surgeries

Education of Patient
o Sitting in firm chair with arm rest and help with getting up
o Good posture
o Isometric / Isotonic exercise
o Therapy for daily routine
o Balance activity with rest
o Plan ahead, Set priorities, Pace activity, Learn activity
o Assistive devices
§ Increase independence
§ Simplify task
§ Utilize available function in pain free and atraumatic manner
o Shoe low heel with wide toe (may have shoes fitted)
o Develop realistic acceptance of disease
o Help client strive for independence

NURSING DIAGNOSIS
97 Altered Comfort: pain R2 inflamed joints
98 Impaired Physical Mobility R2 pain and deformity
99 Self care Deficit R2 fatigue, pain or deformity
100Body image disturbance R2 deformities
101Powerlessness R2 loss of independence and change in life-style
102Knowledge deficit

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