Pathophysiology-Progressive Deterioration and Loss of

Here's what me and Sherilynne Have for chapter 20, let us know if
we are missing anything important.
I. Osteoarthritis- unilateral disease

1. Pathophysiology- progressive deterioration and loss of
cartilage in one or more joints. (common weight bearing
places such as: in hips, knees, vertebral column, and hands)
Primary (idiopathic) normal part of aging. Secondary
(degenerative changes) lead to by Rheumatoid Arthritis.
2. Etiology- initiated by developmental, genetic, metabolic, and
traumatic factors. AGE is strongest RISK Factor. Obesity
contributes, heavy manual occupations(carpet installation,
construction, farming)
3. Assessment- pain is most common assessment
a Heberden nodes- at distal joints, Bouchard node-at proximal
joints(nodes appear on both hands, painful and red.)
b High-sensitivity C reactive protein (HsCRP)-slightly
elevated with synovial inflammation.
c ESR Erythrocyte Sedimentation Rate- normal or slightly
elevated
1. 4. Intervention
a Non-Surgical
1) Nutrition – Omega-3 fatty acids, fish oil capsules
2) Pharmacology
a) Drug class of choice- NSAIDs- Salicylates- watch GI
side effects.
-drug of choice(primary): Tylenol, 4000mg daily
3) Non-pharmacological
a) Rest(local rest(immobilize joint), system rest(immobilize
entire body), and psychological rest(relief from daily stress that
enhance pain), Positioning(elevate, use pillows), Heat(use heat
instead of cold to reduce pain)
b) Complementary and Alternative Therapies-acupuncture,
acupressure, tai chi, therapeutic touch, hypnosis, magnets…
c) Promotion of Self Care
d) Management of Fatigue
1. a. Surgical- any arthroplasty do frequent neurological
assessments
-Total joint arthroplasty-TJA- surgical creation of joint (infection)
with infection in older patient assess MENTAL STATUS
-Osteotomy- less invasive, bone resection
-Total hip arthroplasty-most common joint replaced, common
complication is dislocation (subluxation) Life threatening
complication is DVT!
1. Nursing Diagnoses (NANDA)

1. Impaired Physical Mobility
2. Chronic Pain
3. Fatigue
4. Disturbed Body Image
5. Self-Care Deficit
6. Outcomes
1. Reduction in Joint Pain
2. Ambulate Independently
3. ADL’s with or without assistive devices
4. II. Rheumatoid
Arthritis
Etiology: female 15-40 y.o, AA descent, Asian descent,
and Native American descent.
Dry, scaly, raised rash (butterfly rash)
1. Pathophysiology- chronic, progressive, systemic inflammatory
autoimmune disease process that primarily affects synovial
joints.
2. Rheumatoid factors (RF) consist mainly of immunoglobulin M
and G. B and T lymphocytes are stimulated and increase
inflammatory response. Cytokines (interleukin-1 and TNF)
cause chrondrocytes to attack cartilage. TNF effects lipid
metabolism, coagulation, insulin, resistance, and endothelial
function. Increase WBCs and RF is Present.
3. Assessment: onset is more in winter months than summer
months.
-Early manifestations: joint stiffness, swelling, pain and fatigue,
anorexia, wt loss of 2 or 3 lbs, weakness, low grade fever and
inflammation. Late manifestations: moderate to severe pain and
morning stiffness, osteoporosis, anemia, renal disease, peripheral
neuropathy, TMJ (creptitus-continous grading)
1. Common complications from rheumatoid arthritis- extreme
weight loss, fatigue, and fever.
Associated Syndromes
-Sjogren’s Syndrome- dry eyes, dry mouth, and dry vagina
-Felty’s syndrome- hepatosplenomegaly (enlarged spleen) decrease
in WBC’s
Caplan’s syndrome- presence of rheumatoid nodules in lungs
1. Labs: Rf(present), ANA increase(unusual antibodies that
destroy nuclei of cells, causes tissue death) ESR increases
which confirms infection and inflammation, 20-40 mild, 40-
70 moderate, 70-150 severe.
1. Nursing management of RA
b) Disease Modifying Agents
i. Plaquenil- antimalarial, helps decrease joint and
muscle pain. Used for mild disease, Eye Examine every 6-12
months.
ii. Aszulfidine-(mild to moderate) minimizes GI side
effects; check for sulfa allergy or kidney/liver disease (toxicities),
failure to drink lot of fluids may cause crystals in urine. Drug can
lower sperm count in men.
c) Moderate to Severe disease
i. Methotrexate- Rheumatrex- avoids crowds and
people with infections. Causes bone marrow suppression(increases
risk for infection) and alopecia. Monitor for decrease WBC’s and
platelets. Folic acid is given.
ii. Leflunomide (Arava)- strict birth control, Labs done
usually 6 to 8 weeks, improves mobility. Questran(Chlostyramine)-
Blocks action
d) Biological Response Modifiers-neutralize biologic
activity of TNF by inhibiting binding with TNF receptors.
i. Embrel- Monitor SITE INJECTIONS, monitor CBC,
creatinine and liver panel drawn Q 4-8 weeks.
ii. Remicade- Do Not Refrigerate (prevents drug
composition) Acetaminophen and Benadryl is given before drug is
started.
iii. Humira-first fully human TNF inhibitor.
iv. Kineret- inhibits interleukin-1, can be given to
clients with MS or TB, which patient with these diseases can’t
take TNF inhibitors.
e) Adjunctive therapy
i. Glucocorticoids- prednisone- high dose for short
duration( pulse therapy)
ii. Immunosuppressive agents- cyclophosphamide- may
cause sterility, given to control RA vasculitis.
f) Gold therapy
g) Analgesics
1. III. Lupus Erythematosus

-SLE- chronic, progressive, inflammatory connective tissue
disorder that can cause major body organs and systems to fail.
Some degree of kidney involvement- leading cause of death.
-lupus affects women age 15-40 about ten times as much as men,
black women more than white.
-Manifestations: butterfly rash, alopecia is common, muscle pain
(myalgia)
-Labs- DLE-skin biopsy, SLE: Rheumatoid Factor, ANA, ESR, may
also give a false positive syphilis test which is common with lupus.
Drug Therapy- immunosuppressant
1. IV. Scleroderma- hardening of the
skin, generalized, systemic disease. Chronic inflammatory,
autoimmune connective tissue disease, not always
progressive. Hypertension and respiratory involvement are
common.
-Pathophysiology- diffuse- trunk, face, proximal and distal
extremities. Limited- distal to elbows and knees may be involved
face and neck.
CREST syndrome- Calcinosis-Raynauds-Esophageal dysmotility-
Sclerodactaly-Telangiectasia
-Assessment- arthralgia, acute inflammation is uncommon;
deformities are rare, painless symmetric pitting edema of hands
and fingers
-Labs- similar to SLE
-Interventions- steroids and immunosuppressant, skin protection,
drug therapy similar to RA
1. V. Gout-
Pathophysiology- primary most common, error in purine
metabolism, end product is uric acid that exceeds excretion
capability of kidneys. Secondary- hyperuricemia caused by other
diseases.(crash diets, renal insufficiency, diuretic therapy)
-Etiology- primary gout is for some patients is an
inherited X-linked trait, peak onset 40-50 years in men. Increased
ESR.
-Assessment-
-Acute- uric acid levels checked- 8.5mg/dl,
- Urinary uric acid levels 750mg/24hr
-definitive test (arthocentesis)
-Chronic- check for tophi (outer ear, arms and
fingers near joints)
-Drug therapy- acute gout- NSAIDS (indomethacin, and
ibuprofen), colchicines (colsalide) chronic gout- allopunnol-drug of
choice, xanthine oxidase inhibitor. AVOID ASPIRIN
Risky foods: artichovies, sardines, mushrooms, asparagus,
mussels, kidney, liver, heart, brain, sweetbread, gravies, and
alcohol.

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Here's what me and Sherilynne Have for chapter 20, let us know if

we are missing anything important.

I. Osteoarthritis- unilateral disease

1. Nursing Diagnoses (NANDA)

1. III. Lupus Erythematosus

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