Transcript 03.Joint1.2016x

Joint Disorders - Autoimmune
Zelne Zamora, DNP, R.N.
Rheumatic Diseases- Inflammatory
Process
Series of steps causing:
-swelling, pain and stiffness
-warmth, effusion, decreased ROM, increasing
pain
-increasing severity
-joint instability, contractures, systemic
complications (vessels, lungs, heart, kidneys)

Rheumatic Diseases-Inflammatory
Process


Immune system response to antigens or damaged
cells
T and B cells react to the antigen response
Rheumatic Diseases- Autoimmune
Process




Body reacts against own tissue
Treats as a foreign body
Can affect all systems
HLA genes (human leukocyte antigen)-linked to
immune response
Rheumatic Diseases-Degenerative
Process
Poorly understood
 Genetics?
 Hormones?
 Prior joint damage?
 Mechanical?
 Inflammation is a secondary process
 Degradation of joint

Rheumatic Diseases-affected sites






Skeletal muscles
Bones
Cartilage
Ligaments
Tendons
Joints
Rheumatic Diseases







Limitations in mobility
Pain
Fatigue
Altered self image
Sleep disturbance
Organ failure
Death
Rheumatic Diseases




Minor vs. life threatening
Primary vs. Secondary
Monoarticular vs. Polyarticular
Inflammatory vs. Non-inflammatory
Rheumatic Diseases-Clinical
Manifestations







Skin
Hair
Eyes
Ears
Mouth
Chest
Cardiovascular
Rheumatic Diseases-Clinical
Manifestations





Abdomen
Genitalia
Neurologic
Musculoskeletal
Surrounding tissue
Rheumatic Diseases




Acute
Insidious
Remissions
Exacerbations
Rheumatic Diseases

Diarthroidial /Synovial joints
Rheumatic disease - Arthritis








Ankylosing spondylitis
Rheumatoid arthritis
Osteoarthritis
Bursitis
Carpel tunnel
Fibromyalgia
Gout
Crohns’s disease








Juvenile arthritis
Lupus
Lyme disease
Marfan’s syndrome
Paget’s disease
Raynauds’s disease
Scleroderma
Myositis
Common Lab Studies-Rheumatic
Diseases
Creatinine-increase may indicate renal
disease (dz) in SLE, scleroderma
 ESR-increase in inflammatory dz
 Hct-decreased in anemia of chronic dz
 RBC-decreased in RA, SLE
 WBC-decreased in SLE
 VDRL-false positive in SLE

Labs (cont’d)




ANA-positive in SLE, RA\
CRP-positive indicative of
inflammation: RA and SLE
RF- positive in 80% of
those with RA. Positive in
SLE
Complement levelsC3 and
C4-decreased in RA and
SLE
Management goals for Rheumatic
Diseases
Decrease inflammation
 Control pain
 Maintain or increase mobility
 Maintain or increase function
 Increase client knowledge
 Promote self-management

Rheumatologic DiseasesGerontology Considerations




Disability
Cognitive changes
Co-morbid conditions
M/S conditions most
common
Rheumatoid Arthritis
Chronic, systemic,
inflammatory disease that’s
mediated by the immune
system
 Autoimmune disease
 Affects 1%
 Diffuse connective
tissue disease

Rheumatoid Arthritis:
Pathophysiology







Originates in synovial tissue
Breaks down collagen
Edema
Proliferation of synovial membrane
Pannus formation
Cartilage destruction
Bone erosion
Cartilage

Connective tissue
RA risk factors
Female: 2-3 times more likely
 Genetic disposition
 Can occur at any age
 Onset may be sudden
or gradual

Proposed causes of RA








Bacteria?
Virus?
Heredity?
Error in antigen
formation?
Environmental factors?
Diet?
All of the above?
Unknown cause
Rheumatoid Arthritis: Systems
Affected




Arterial walls
Endothelium
Nervous system
HDL production
Autoimmune process
Immune response to antigen
 Formation of IgG
 Rheumatoid factor;
autoantibodies
against IgG
 RF combines
with IgG

Autoimmune process



Deposit on synovial membranes
Activation of complement
Inflammatory response
Autoimmune process



Neutrophils to site of
inflammation
Proteolytic enzymes
released
Synovial lining thickens
Signs and symptoms of RA







Symmetric painful joints
Symmetric swollen joints
Movement does not relieve
symptoms
Warm joints
Spongey joints
Ulnar deviation
Swan neck deformity
Signs and symptoms of RA








Stiffness lasting > 1 hour in the a.m.
Fatigue, malaise, fever
Loss of ROM
Weight loss
Anemia
Lymphadenopathy
Typically starts in small joints
Advances to larger joints
Signs and Symptoms: RA
Disfigured joints-late
 Rheumatoid nodules
 Onset acute

Co-morbidities: RA





Arteritis
Neuropathy
Pericarditis
Splenomegaly
Sjogrens
Diagnosis of RA
H&P
 Rheumatoid factor (positive)
 CBC (anemia)
 ESR -elevated
 C4 complement –decreased
 Anti CCP- positive antibodies. 95%
diagnostic
 CRP- elevated

Diagnosis of RA
x-rays
Diagnosis of RA


ANA- positive
Synovial fluid- cloudy, yellow, +leukocytes,
+complement
Treatment goals/RA







Early intervention
Control inflammatory
disease
Prevent joint damage
Relieve pain
Find optimal drug
regimen
Improve function
Achieve remission
DMARD’s-disease modifying antirheumatic drugs – First line







Cyclophosphamide (Cytoxan)
Methotrexate (Rheumatrex)**
Sulfasalazine (Azulfidine)
Hydroxyxholoroquine
(Plaquenil)
Azathioprine (Imuran)
Cyclosporine (Prograf)
These are the gold standard of
care: early use!!
NSAIDs – now adjunctive therapy only
COX-1 vs COX-2
 COX-1 GI irritation is common; risk for ulcer
 COX-2 reduce swelling, no GI upset;
decreased risk of bleeding; increased risk of
CV disease
 NSAIDs used to control swelling and
inflammation

NSAIDs – now adjunctive therapy only


NSAID’s: Ibuprofen,
Naproxen
COX-2 inhibitors:
Celebrex
Gold salts (Less used DMARD’s)


Auranofin (oral
gold)/Ridaura
Gold sodium thiomalate
(inj)/Myochrysine)
Biologic response modifiers
Inhibits production of cytokines
 Etanercept (Enbrel): given SQ
 Inflisimab (Remicade): IV
 Dyridimine(Arava)

Opioids: long acting


OxyContin
Fentanyl patch
Corticosteroids



Prednisone: po, IM,
joint injections
Short duration
Lowest dose possible
CAM/Alternative







Copper bracelets
Devil’s claw
Gin-soaked raisins
Colonics
Coffee enemas
Shark cartilage
Snake venom
Prosorba therapy


Severe RA-not responsive to
DMARD’s
Device used during apheresis
therapy to bind IgG
Surgery




Arthroscopic
Joint fusion
Joint replacement
Tendon reconstruction
Nursing care considerations
Promote comfort
 Facilitate independence and self care
 Reduce fatigue
 Promote mobility
 Injury prevention
 Patient education
 Dietary considerations
 Assess for depression

Systemic Lupus Erythematosus (SLE)




Lupus is a chronic, autoimmune disease
Immune system becomes hyper active and attacks
normal tissue
Increased production of autoantibodies
Results in inflammation and brings about symptoms
Systemic Lupus Erythematosus



Combination of genetic,
hormonal, environmental and
immunologic interactions (B cells
and T cells)
Medications: Apresoline,
Pronestyl, INH, Thorazine
Onset insidious or acute
Systems Affected by SLE

Auto-immune disease
that can affect any
system
Who gets Lupus?



Can occur at any age
Nine out of ten people with
lupus are women
In women ages 15-44, lupus
strikes women 10-15 times
more frequently than men
Who gets Lupus?
African American women have a 3 times
higher incidence and mortality
 A.A. tend to develop disease at a younger
age and to develop increased severity of
complications
 Also more common in women of Hispanic,
Asian and Native American decent

Types of Lupus
Systemic lupus erythematosus
 Discoid lupus erythematosus-affects the skin
 Drug induced-caused by medication
 Neonatal lupus-rare, affects babies of
mothers with lupus.

Diagnosis of Lupus can be
Difficult
Thorough H&P
 Same blood tests as RA:
-increased Cr
-RF/positive
-increased ESR
-IgA, IgM, IgG-elevated
-anemia
-no one test confirms!!
-leukopenia
-results only support Dx
-ANA positive
-CXR/
-anti-DNA-titers elevated -echo
-compliment C3/C4-decreased

Classic Signs and Symptoms of
SLE
Fever
 Weight loss
 Arthritis
 Fatigue
 Pleurisy
 Pericarditis

Clinical Manifestations-Derm






Cutaneous lesions
Butterfly rash
Ulcers: mouth, buccal mucosa,
hard palate, clusters with
exacerbations
Alopecia
Lesions worsen during
exacerbations
May worsen with sun exposure
Clinical Manifestations-Derm


Sub acute cutaneous
lupus erythematosuspapular lesions
Discoid lupus
erythematosus-chronic
rash, erythematous
papules, scarring, in
some cases only this
occurs.
Clinical Manifestations-M/S
Musculoskeletal
-polyarthralgia with morning
stiffness/acute or slow
onset
-joint
swelling/tenderness/pain
-swan neck deformity
-ulnar deviation
-prolonged, extreme fatigue

Clinical Manifestations-cont’d
Musculoskeletal
-arthritis
-myositis
-synovitis

Clinical Manifestations: C/P
Cardiopulmonary
-tachypnea
-pleurisy
-dysrhythmias
-accelerated ASHD in women with SLE
-pericarditis-MOST COMMON
cardiac problem!!

Clinical Manifestations/Renal
Renal
-hematuria
-proteinuria
-glomerulonephritis
-early detection important to prevent
kidney damage
and HTN

Clinical
Manifestations/Hematology
Hematological
-anemia
-leukopenia
-antibodies against blood cells
-thrombocytopenia
-coagulopathy/clots
-lymphadenopathy
-spleenomegaly

Clinical Manifestations/GI
Gastrointestinal
-abdominal pain
-diarrhea
-dysphagia
-nausea/vomiting
-reproductive
-menstrual abnormalities

Clinical Manifestations/CNS
CNS
-widespread!!
-photosensitivity
-seizures
-peripheral neuropathy
-cognitive dysfunction
-subtle changes in behavior

Clinical Manifestations/Misc
Miscellaneous
-Raynaud’s syndrome
-persistent high fever >100
degrees F
-alopecia

Warning Signs of SLE Flare
Increased fatigue
 New or higher fever
 Increased pain
 Development or worsening of a rash
 Upset stomach
 Headache or dizziness
 Development of s/s client has not had before

SLE Flare Triggers
Overwork
 Emotional crisis
 Exposure to sunlight
 Infection
 Injuries or surgery

SLE Flare Triggers
Pregnancy/post partum
 Sudden withdrawal of medications
 Sensitivities or allergies
 Certain prescription drugs-sulfa
 OTC medications-herbs
 Immunizations-live vaccines

Treatment Goals/SLE
Prevent flares
 Treat flares when they occur
 Minimize complications/loss of organ function
 Minimize disabilities/improve functional
status
 Prevent complications from
therapy/treatment
 Promote self management
 Manage psychological implications

Treatment Goals of SLE
Management of acute and chronic disease
 Acute-controlling flares in disease to prevent
organ damage
 Chronic-periodic monitoring with recognition
of subtle changes in condition

Treatment/SLE

Treatment always
dependent on severity
Treatment/SLE

Corticosteroids: most important, beware of
side effects, topical for derm, low dose oral
for minor disease, high dose po, IM or IV for
severe
Treatment SLE

NSAID’S-used with steroids to allow for lower
dosage of steroid
Treatment SLE

Anti-malarials: Plaquenil. Used for mild
symptoms and/or systemic involvement.
Treatment SLE

Immunosuppressant Drugs: Imuran,
Cytoxan, Methotrexate. Reserved for severe
SLE. Suppress autoimmune response.
Treatment SLE

B cell Depleting
Therapies: Newer
treatment option.
Severe SLE. Rituxan.
CAM/Alternative Treatment SLE




Acupuncture
Biofeedback/ meditation
Massage
Herbs/Supplements
-flax seed, fish oil, DHEA,
calcium, Vit. D
Nursing Management/SLE
Patient education disease process
 Regular health screenings
 Self management
 Maintain skin integrity
 Body image disturbance
 Medications
 Diet: high in antioxidants, avoid refined
foods, red meat, coffee
