Transcript Rheumatoid Diseases

Musculoskeletal: Autoimmune;
Inflammatory; Metabolic;
Infectious Disorders
Rheumatoid Arthritis; SLE; Paget’s
Disease; Gout; Osteomyelitis
Carolyn Morse Jacobs, RN,
MSN, ONC 10/ 24/ 04
Autoimmune and Inflammatory Disorders:
Rheumatoid Arthritis
Chronic systemic, inflammatory disease
characterized by recurrent inflammation of
connective tissue, primarily of joints
(diarthroidal) and related structures.
Pathophysiology Rheumatoid
Arthritis
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Normal antibodies (immunoglobulins)
become autoantibodies and attack
host tissues (RF)
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Neutrophils, T cells synovial fluid cells acitavted;
Cystokines, interleukin-1 and TNR (tumor necrosing
factor) alpha; chrondroytes attack cartilage;
Synovium digests cartilage; inflammatory molecules
released containing interleukin-1 and TNF alpha
Pathophysiology: Rheumatoid
Arthritis

Pathophysiology

IgG/RF (HLA)= antigen-antibody
complex
 Precipitates in synovial fluid
 Inflammatory response
Cartilage connective tissue primarily
affected!
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Rheumatoid arthritis: assessment:
manifestations and complications
Fatigue,
weakness, pain
 Joint deformity
 Rheumatic
nodules
 Multisystem
involvement
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How does Rheumatoid Arthritis Compare to
Osteoarthritis?

Definition: *wear and tear, progressive,
non-systemic, Degenerative Joint
Disease (DJD)
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Pathophysiology
Osteoarthritis (top slide
only)
Identify which joints
are primarily
affected with
osteoarthritis.
What factors
contribute to the
development of
osteoarthritis?
Ankylosing
spondylitis (what
type of arthritis is
this?)
Structural changes with Osteoarthritis
Early
Cartilage softens, pits, frays
Progressive
Cartilage thinner, bone ends hypertrophy,
bone spurs develop and fissures form
Advanced
Secondary inflammation of synovial
membrane; tissue and cartilage destruction; late
ankylosis
What signs and
symptoms does
the person with
osteoarthritis
experience?
Normal Knee
structure
Moderately
advanced
osteoarthritis
Advanced
osteoarthritis
What symptoms/assessment for
the patient with osteoarthritis?
Onset of pain is insidious, individual is
healthy!
Pain is aching in nature; relieved by rest!.
Local signs and symptoms: swelling,
crepitation of joint and joint instability,
asymmetrical joint involvement
Deformities with Osteoarthritis
Carpometacarpocarpal joint of
thumb with subluxation of the
first MCP
Genuvarus
Herberden’s nodes
Osteoarthritis (review
only)
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Diagnostic Tests
None specific
 Late joint
changes, boney
sclerosis, spur
formation
 Synovial fluid
inc., minimal
inflammation
 Gait analysis

Nursing diagnosis
Interventions
determined by
complications
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Supportive devices
Medications (no
systemic treatment
with steroids)
Dietary to dec. wt.
Surgical
Intervention (joint
replacement)

Teaching
Comparison of RA and OA
RA
Cause unknown; auto-immune factor
Onset sudden
Remissions
*Body parts affected, systemic, small joints, symmetrical
Causes redness, warmth, swelling of joints
Females, age 20-30; 3-1 ratio
OA
Cause “wear and tear”, develops slowly
Non-systemic, weight bearing joints
Middle-aged and elderly, males 2-1 affected
Does not cause malaise
Begins after 40
Manifestations of RA
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Systemically ill
Hematologic
Pulmonary/CV
Neurologic
Ocular symptoms
(Sjorgen’s)
Skin
Musculoskeletal
deformity, pain
Pain!
Pain!
Pain
Joints changes with RA

Early Pannus
• Granulation,
inflammation at
synovial
membrane,
invades joint,
softens and
destroys
cartilage
RA
Mod advanced Pannus
joint cartilage disappears,
underlying bone destroyed,
joint surfaces collapse
Fibrous Ankylosis
Fibrous connective tissue
replaces pannus; loss of joint otion
Bony Ankylosis
Eventual tissue and joint
calcification
Joint Changes RA
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Bilateral,
symmetrical,
PIP’s, MCP’s
Thumb instability
Swan neck,
boutonniere
deformity
Tensynovitis
Multans deformity
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Subcutaneous
nodules
Genu valgum
Pes plano valgus
Prominent
metatarsal heads
Hammer toes
Assessment RA
Deformities
that may
occur with
RA
Synotenovitis
Ulnar drift
Swan neck
deformity
Boutonniere
deformity
Mutlans deformity
(rapidly progressing
RA)
Hitch-hiker thumb
Genu valgus
Subcutaneous nodules
(disappear and appear
without warning)
Hammer toes
Diagnostic Tests RA
ESR elevated
+ RA, ^ RA titer
Sed rate increased
CBC
C-reactive protein
Dec. serum complement
Synovial fluid inflammation
Joint and bone
Swelling,inflammation
Interventions RA

Nursing
Diagnosis
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Comfort
Physical mobility
Self image
Goals
 Team Approach
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Pain
management
 Exercise
 Surgery
 Teaching
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Medications RA
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ASA & NSAIDS
Corticosteroids; low dose
DMARDs (diverse group) of remitting agents:
including antimalarial (hydroxychloroquine:plaquenil)
*eye effects; Penicillamine (empty stomach); Gold
(Auranofin) *dermatitis, blood dyscrasia; and
Immunosuppressive agents as methotrexate
and cyclosporine
Biologic response modifiers
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Adalimumab (Humira)
Infliximab (Remicade)
Joint Protection: Do’s and Don’t’s
Case Presentation; Mrs. Michaels with
Rheumatoid Arthritis
(PDS: Adult Health: Musculoskeletal Health: Mrs. Michaels)
Comparison to ‘usual’ course
 Diagnostic tests
 Nursing diagnosis
 Therapies
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Medications used
 Exercise
 Joint Protection
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Resources on the Web
Systemic Lupus
Erythematous (SLE)
Chronic multisystem disease
involving vascular and
connective tissue
Lupus
Foundation
Etiology and Pathophysiology
SLE
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Exact etiology unknown:
genes (HLA), hormones,
environment involved
Formation auto-antibodies;
immune complexes
deposited
Inflammatory response
triggered by deposition of
immune complexes
(kidney, brain)
Drug induced syndrome
similar to SLE (Procan-SR,
hydralazine, isonaiazid)
Pneumonia, infections,
*renal, CNS involvement!;
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Course of disease varies
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Mild
Episodic
Rapidly fatal
Manifestations/Complications
of SLE
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Types: Discoid, SLE
Incidence: 1:2000
Women 1-9, childbearing age, african
americans
Periods remission
and exacerbation
Stress
Environmental
factors
Assessment
 Low grade fever
 Integumentary
 MS involvement
 CV
 Respiratory
 Urinary Renal failure
 Neurologic CNS
 GI
 Hematologic
 Endocrine
 Reproductive
Characteristic
butterfly rash
associated with
SLE, especially
discoid lupus
erythematous
Barry’s
lupus
SLE characterized by periods of
remission and exacerbation.
Stimulated by sunlight, stress,
pregnancy, infections like strep and
some drugs. Some drugs like
apresoline, pronestyl, dilantin,
tetracycline, phenobarbital may cause
a lupus-like reaction which disappears
when drug is stopped.
Diagnostic Tests
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LE cell
Ant-DNA
ANA, titer
Anti-DNA
Complement
fixation decreased
ESR
Other (and CBC,
UA)
Kidney biopsy
Criteria to Dx.
malar, discoid
rash
 photosensitivity
 arthritis
 renal disorder
 immunological
disorder
 DNA, ANA
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Therapeutic Interventions/Management
SLE
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Medications
 NSAIDS
 (Disease modifying agents)
Antimalarial drugs
 Corticosteroids
 Immunsuppressive therapy
• Antineoplastic drugs
such as Imuran, cytoxan,
cyclosporine
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Avoid UV
Reduce stress
Monitor/manage to prevent
complications
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Nursing diagnosis
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See RA
• Impaired skin integrity
• Ineffective protection
• Impaired health
maintenance
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Goal: control inflammation
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Emotional support
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Life Planning
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Required Review
Case Study
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Clinical Background:
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18 year old patient admitted with recent
onset (3 months earlier) of malar rash
and constitutional symptoms (weakness
and malaise), now symptoms of renal
failure. She reported having a 5-year
history of Raynaud's phenomenon and
arthralgia.
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Abnormal results of laboratory studies
included the presence of ANA, antinDNA, anti-SS-A autoantibodies and a
proteinuria of approximately 10 g/d.
Renal biopsy revealed a Class IV lupus
glomerulonephritis.
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What assessment data is priority:
what additional date should you
collect?
What are the priority
interventions?
What are the priority nursing
problems?
What medications are
typically used and why?
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Scleroderma (Systemic sclerosis)
Definition: progressive sclerosis of
skin and connective tissue; fibrous
and vascular changes in skin,
blood vessels, muscles, synovium,
internal organs. become “hide
bound”
 Immune-mediated disorder; genetic
component
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Scleroderma (Systemic sclerosis)
Abnormal amounts of fibrous
connective tissue deposited in
skin, blood vissels, lungs, kidneys,
other organs
 Can be systemic or localized
(CREST) syndrome
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CREST Syndrome
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Calcinosis
Raynaud’s
phenomena
Esophageal
hypomotility
Sclerodactyl (skin
changes of fingers)
Telangiectasia
(macula-like
angioma of skin)
Crest Syndrome
More on
CREST
CREST Syndrome & scleroderma
Sclerodactyl (localized
scleroderma of
fingers)
Raynaud’s disease with
ischemia
Typical “hidebound” face of
person with
scleroderma
Tissue hardens;
claw-like
fingers; fibrosis
Manifestations & Complications
(systemic)
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Female 4:1
Pain, stiffness,
polyartheritis
Nausea, vomiting
Cough
Hypertension
Raynauld’s
syndrome
Skin atrophy,
hyperpigmented
Scleroderma cont.
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Esophageal
hypomotility leads to
frequent reflux
GI complaints common
Lung-pleural thickening
and pulmonary fibrosis
Renal disease...leading
cause of death!
Diagnosis/Treatment Scleroderma
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R/O autoimmune disease
Radiological: pulmonary
fibrosis, bone resorption,
subcutaneous
calcification, distal
esophageal hypomotility
ESR elevated
CBC anemia
Gammaglobulin lelels
elevaed; RA present
Skin biopsy to confirm
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What are the KEY
components of care
for the individual with
Scleroderma?
Scleroderma: Patient Care
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Do’s
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Avoid cold
Provide small,
frequent
feedings
Protect fingers
Sit upright post
meals
No fingersticks
Daily oral
hygiene
Resources
Scleroderma: Patient Care
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Medications: based
upon symptoms:
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Immunosuppressive
agents & steroids &
remitting agents
Ca channels blockers
& alpha-adrenergic
blockers
H2 receptor blockers
ACE inhibitors
Broad spectrum
antibiotics
Ankylosing Spondylitis
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Definitions: chronic
inflammatory
polyarteritis of
spine
Affects mostly
young men
Associated with
HLA-B27 antiget
positive antigen
(90%)
Pathophysiology &
Manifestations
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Like arthritis have
inflammatory changes; erosion
of cartilage, ossification of
joint margins; scar tissue
replaces
Morning backache, flexion of
spine, decreased chest
expansion
Diagnosis
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ESR elevation
Positive HLA-B27
antigen
Vertebral changes
Ankylosing
Spondylitis
Insidious
onset
Morning
backache
Inflammation
of spine; later
spine
ossification
Oh my back hurts!
Comparison
of changes
with
ospeoporosis
and
Ankylosing
spondylitis
Identify a
PRIORITY
nursing
concern
related to
ankylosing
spondylitis
Management Ankylosing
Spondilitis
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Do’s
Maintain spine
mobility
 Pain
management
 Proper
positioning
 Meds for pain,
inflammation
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Other Collagen Diseases
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Reiter’s Syndrome
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Reactive arthritis
associated with enteric
disease
Lyme Disease (mimics
rheumatoid disease)
 Caused by spirochete, borrelia
burgdorferi (tick)
 Inflammatory disorder
 3 stages
• Initial rash (target)
• Disseminated (arthitic like
symptoms)
• Late (neurologic symptoms)
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Diagnosis
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Culture (difficult)
Antibody detection
Treatment: antibiotics
(amoxicillin, vibramycin,
tetracycline, etc);
NSAID)
Prevention
Other Collagen Diseases
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Polymyositis
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Systemic connective
tissue disorder
characterized by
inflamation of connective
tissue and muscle fibers
Autoimmune; affecting
women 2:1
If muscle fiber
inflammation is
accompanied by skin
lesion disease known as
dermatomyositis
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Manifestations &
complications
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Muscle pain, tenderness,
rash; arthralgias; fatigue;
fever and weight loss;
Skeletal muscle weakness
most prominent
Dusky red rash over face
Raynaud’s phenomenon
Malignancy with
dermatomyositis
Diagnosis
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None specific
Elevated CK
Other Collagen Diseases cont
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Reiters syndrome
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Self-limited disease of
reactive arthritis
• such as shingles,
venereal diseas,
associated with HLA—
B27 antigen
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Polyarteritis Nodosa
• Collegan; diffuse
inflammation and
necrosis of wall of small
to medium sized arteries
especially in muscles ,
kidneys, heart liver, GI
and peripheral nerves like
SLE

Juvenile Rheumatoid
Arthritis