N3 Exam 2

How many bones are there in the body

206 bones

What are all the types of bones

•Long bones

•Short bones

•Flat bones

•Irregular bones

Osteoblasts

Function in bone formation

Osteocytes

Mature bone cells that function in bone maintenance

Osteoclasts

Multinuclear cells that function in destroying, resorbing, and remodeling bone

Osteophytes (bone spurs)

Protrude into the joint space

Osteogenesis

process of bone formation

Ossification

the process of formation of the bone matrix and deposition of minerals

Regulating factors

Stress and weight bearing

Vitamin D (check)

Parathyroid hormone and calcitonin

Blood supply

Osteoarthritis (OA)

Slowly progressive noninflammatory disorder of the diarthrodial joints

Why are OA numbers expected to increase?

Because the population is aging

Is OA more common in men or women?

More common in women

More common in women (reason not fully established — hormonal factors, especially estrogen decline after menopause, are thought to play a role) (claude ai)

Which types of OA are especially common in women?

Especially hand OA and knee OA (after menopause)

When are most men affected by OA?

Most men affected by 70 to 80 years, except for traumatic arthritis

Which joint is OA more common in overall

Hip OA more common

OA: Etiology & Pathophysiology

 Gradual loss of articular cartilage

 Formation of osteophytes at joint margins

 Not normal part of aging process

Cartilage destruction causes 

narrowing of joint space

By what age are most adults affected by OA

Most adults affected by age 40

When do symptoms of OA typically manifest?

manifest after age 50 to 60

Pathologic changes in OA — what happens to the color and texture of cartilage?

Cartilage becomes:

• Dull, yellow, and granular

• Softer and less elastic

Less able to resist wear with heavy use

OA and Osteophytes

are formed resulting in uneven weight distribution; bones rub together leading to increasing pain in later stages

OA: Risk Factors

 Older age, female gender, and obesity

 Certain occupations (e.g., those requiring laborious tasks)

 Engaging in sport activities

 History of previous injuries, muscle weakness, genetic predisposition, and certain diseases

 Most prominent modifiable risk factor for OA is obesity

 Diet and exercise can help minimize symptoms of OA in patients with obesity

Most prominent modifiable risk factor for OA

• OA is obesity

• Diet and exercise can help minimize symptoms of OA in patients with obesity

OA: S/S

Joint pain = Pain worsens with joint use

• Early stages: rest relieves pain

• Later stages: pain with rest and trouble sleeping due to increased joint pain

 Pain contributes to disability and loss of function as OA progresses

• Pain may be referred to groin, buttock, or outside of thigh or knee

• Sitting down becomes difficult, as does getting up from a chair when hips are lower than knees

• Local pain and stiffness

 Crepitation (grating sensation)

 OA affects joints asymmetrically

When does joint stiffness occur in OA?

• after periods of rest or unchanged position

• Early morning stiffness usually resolves within 30 minutes

How does OA morning stiffness compare to rheumatoid arthritis?

rheumatoid arthritis cause Fatigue, fever, and organ involvement which is not present in OA

What effect does overactivity have on OA joints?

Leads to mild joint effusion, temporarily increasing stiffness

Joints most affected by OA

 Hips

 Knees

 Metatarsophalangeal (MTP)

 Cervical vertebrae

 Lumbar vertebrae

 Distal interphalangeal (DIP)

 Proximal interphalangeal (PIP)

 Metacarpophalangeal (MCP)

OA: S/S Joint Deformity

 Specific to joint involved

 Heberden’s nodes: DIP

 Bouchard’s nodes: PIP

• Appear red, swollen, and tender

 Varus deformity (bowlegged): medial knee

 Valgus deformity (knock-kneed): lateral knee

 One leg shorter than the other: hip

Thinking Nurse

The nurse is discussing the symptomology of

osteoarthritis (OA) with a patient. The nurse

would describe which common initial symptom

of the disease?

A. A fine red rash on the elbow that is constant.

B. Painful stiffness in the joints of the fingers

C. Popping sensation in the wrist joint when

typing.

D. Knee pain when the leg is at rest.

OA: Diagnostic Studies

• Bone scan, CT scan, MRI

• X-rays

• No specific lab tests or biomarkers

• Synovial fluid analysis

OA: Bone scan, CT scan, MRI

 Diagnosis of OA; show early joint changes

OA: X-rays

Detect joint space narrowing, increased bone density, and osteophytes

OA: No specific lab tests or biomarkers

Baseline labs may be done before starting treatments or for screening for related conditions

Is there a cure for OA

no cure

what does OA Tx focus on

 Managing pain and inflammation

 Preventing disability

 Maintaining and improving joint function

• Nondrug interventions are the basis for OA management = PT

 Drug therapy supplements nondrug treatment

OA: Treatment: Non-Pharm

 Balance rest and activity

 Rest during acute inflammation

 Modify activities to decrease joint stress

 Avoid prolonged standing, kneeling, or squatting

 Assistive device as needed

Heat and Cold Applications

Weight-reduction

Exercise

OA: Rest during acute inflammation

 Functional positioning with splints or braces

 Avoid increased stiffness by limiting immobility to less than 1 week.

OA Tx: Heat and Cold applications

 May help reduce pain and stiffness

 Ice for acute inflammation

 Heat therapy for stiffness

OA Tx: Wt reduction

critical if over weight

OA Tx: Exercise

Aerobic, Range of motion, & Muscle strengthening

OA Treatment: Surgery — Arthroscopic surgery

 For patients with loss of function, unmanaged pain, and decreased independence

 Common for patients with knee OA

 May provide no additional benefit over PT and medical treatment

OA: Treatment: Pharm based on

severity of patient’s symptoms

OA: Pharm Mild to moderate joint pain

 Acetaminophen

 Topical agent (e.g., capsaicin cream)

 OTC creams containing camphor, eucalyptus oil, and

menthol (e.g., BenGay, ArthriCare)

 Topical salicylates (e.g., Aspercreme)

 OTC Balm eg. Tiger balm

OA: Treatment: Pharm Moderate to severe joint pain

• Nonsteroidal antiinflammatory drug (NSAID); start low

dose, increase if needed

 Ibuprofen 200 mg up to four times per day TAKE WITH FOOD

 Misoprostol to decrease GI side effects

 Arthrotec (combination of misoprostol and NSAID diclofenac)

 Diclofenac gel

 Avoid both oral and topical NSAIDs together

• COX-2 inhibitor celecoxib (Celebrex)

Intraarticular corticosteroid injections

Hyaluronic acid injection

DMOADs—disease-modifying OA drugs

OA: Colecoxib (Celebrex)

Take the medication with food or milk

OA: Treatment: Pharm Intraarticular corticosteroid injections

 4 or more injections without relief suggest need for additional intervention

 Corticosteroids should not be given systemically

OA: Hyaluronic acid injection

• knee OA

• Viscosupplementation

OA: DMOADs—disease-modifying OA drugs

 No drugs approved to modify OA progression

Thinking Nurse

The nurse should include all of the following teaching for

the client with osteoarthritis EXCEPT?

A. Avoid aerobic exercise because it fatigues the joints

B. Take prescribed anti-inflammatory medications with

meals.

C. Alternate hot and cold packs to affected joints.

D. Rest during acute inflammation period for no more

than 1 week to prevent joint stiffness.

OA Nursing Assessment

 Joint pain and stiffness

 Type, location, severity, frequency, and duration;

aggravating or alleviating factors

 Impact on ability to perform ADLs

 Pain management practices

 Assess affected joints (compare to

unaffected)

 Tenderness, swelling

 Limitation of movement

 Crepitation—What is it?

OA Patient teaching

 Nature and treatment of disease

 Pain management

 Body mechanics

 Correct use of assistive devices

 Joint protection and energy conservation

 See Table 64-4 in the textbook

 Nutrition

 Weight and stress management

 Exercise WHAT TYPE?

The nurse determines that teaching about

management of osteoarthritis of the feet and hands has

been effective when the patient says:

a. “I will be careful to avoid crowds.”

b. “I can use heat to relieve the stiffness when I wake up in

the morning”

c. “I should exercise my hands every day, especially if they

are painful and inflamed.”

d. “I should avoid the use of glucosamine as it does not

have any therapeutic value.”

OA Take Home — What type of disease is OA often described as?

A disease of "wear and tear"

Are there biomarkers or lab abnormalities in OA?

No — there are no biomarkers and no lab abnormalities

What does synovial fluid look like in OA?

Basically normal

what is the range of joint disability seen in OA?

Mild to significant joint disability

In early-stage OA, what relieves pain?

Rest

Distiguishing feature of OA

early morning stiffness

RA: Pathophysiology & Etiology

Chronic, systemic autoimmune disease; inflammation of connective tissue in diarthrodial (synovial) joints

What is the disease course pattern of RA?

Periods of remission and exacerbation = Disabling form of arthritis

What may be needed if RA treatment is inadequate?

Mobility aids or joint reconstruction may be needed

What ethnic groups dfoes RA affect

all ethnic groups

How does RA incidence change with age?

Increases with age, peaks between 20 and 40

How does RA prevalence compare between women and men?

Three times as many women as men

check if we need to know

Rheumatoid arthritis. A, Early pathologic change in rheumatoid arthritis is rheumatoid synovitis. The synovium is

inflamed. There is a great increase in lymphocytes and plasma cells.

B, With time, there is articular cartilage destruction; vascular granulation tissue grows across the surface of the cartilage

(pannus) from the edges of the joint, and the articular surface shows loss of cartilage beneath the extending pannus, most

marked at the joint margins.

C, Inflammatory pannus causes focal destruction of bone. At the edges of the joint there is osteolytic destruction of bone,

responsible for erosions seen on x-rays. This phase is associated with joint deformity

cause of RA

Cause unknown, believed autoimmune etiology

Genetic factors: have increased human leukocyte antigen (HLA)

What does the triggering antigen cause in RA?

formation of abnormal immunoglobulin G (IgG)

What develops against the abnormal IgG in RA?

• Autoantibodies 

• Rheumatoid factor (RF)

What increases RA risk when your genetically predisposed

smoking

How much more often does RA occur in women vs. men?

RA occurs 2-3 times more often in women than in men

The nurse is preparing a flyer on rheumatoid arthritis (RA) for

distribution during a community health fair. Which

information should the nurse include? Select all that apply

A. Rheumatoid arthritis typically affects weight-bearing

joints.

B. Onset generally occurs between 20 and 40 years of age

C. Rheumatoid arthritis is the most common form of arthritis.

D. Women are more likely to be affected than men

E. Rheumatoid arthritis appears to have a genetic

component

RA: Diagnostic tests

4 OF THE FOLLOWING MUST BE PRESENT WITH 1 THROUGH 4 PRESENT A MINIMUM OF 6 WEEKS

• Moring stiffness equal to or greater than 1 hour

• Arthritis of 3 or more of the following joints: right or left PIP, MCP, wrist, elbow, knee, ankle, and iTP joints

• Arthritis of wrist, MCP, or PIP joint

• Symmetric involvement of joints

• Rheumatoid nodules over bony prominences, or extensor surfaces, or in juxtaarticular regions

• Positive serum rheumatoid factor

• Radiographic changes including erosions or bony decalcification localized in or adjacent to the involved joints

RA: Inflammatory Disease Lab Work

 WBC-elevated in stress, infection, inflammation, trauma

 C-reactive protein (CRP)-detects inflammation

 ANA-antinuclear antibody, suggest possible presence of

autoimmune disease

 Rheumatoid factor (RF)- autoantibody, present in RA

• Seronegative RA Factor

• Can still have RA-antibodies non-existent or too low to detect

 Vectra- advanced blood test for adults with rheumatoid

arthritis (RA). Measures 12 markers of disease activity

• Reports level of RA activity: High, Moderate or Low

RA: S/S

 Onset subtle eg fatigue, anorexia, weight loss, generalized stiffness that becomes localized stiffness with progression

 May report history of precipitating stressful event eg Infection, stress, exertion, childbirth, surgery,

 Specific joint involvement

 Symptoms occur symmetrically

 Often affects small joints (PIP, MCP, MTP)

 Larger joints & cervical spine may be involved

Typical Deformities of

Rheumatoid Arthritis

RA: Affects all body systems

 Firm, nontender masses found on bony areas exposed to pressure

 Cataracts and vision loss

 Nodular myositis

 Pleurisy, pleural effusion, pericarditis, pericardial effusion, and cardiomyopathy

Drug Therapy for RA-DMARDS

• DMARDS

• Methotrexate

RA: DMARDS

Disease modifying ant rheumatic drugs prescribed aggressively

RA: Methotrexate

• Drug of first choice

• Less expensive

• Lower toxicity

• Therapeutic effects in 4 to 6 weeks

Methotrexate Side Effects

 Sore mouth

 Low blood cell counts (bruising/bleeding, swollen lymph nodes)

 bone marrow suppression and hepatotoxicity

 monitor with CBC, chem panel, and LFT’s

 Liver & lung damage (follow with CXR and blood tests)

 Risk for Infection is high

DMARDS type

• Sulfasalazine and antimalarial drug

• Hydroxychloroquine (Plaquenil)

• Corticosteroids

• Leflunomide (Arava)

Hydroxychloroquine (Plaquenil)

• for mild to moderate cases (mechanism of action unknown)

• Rapid absorption & Relatively safe

• Well tolerated

• Need eye exam

Corticosteroids

daily prednisone

Leflunomide (Arava)

*newer, blocks immune cell overproduction

 Blocks immune cell overproduction

 Not used during pregnancy; teratogenic

Sulfasalazine Side Effects

 Changes in blood counts

 Nausea/Vomiting

 Sensitivity to sunlight

 Yellow/Orange color of urine, tears, sweat- stains clothes/contacts

 Avoid if allergic to Sulfa drugs

 Also used for IBD, Ankylolosing spondylitis (AS)

Hydroxychloroquine (Plaquenil) — What risk comes with high dose over time?

increase risk of damage to the retina-- follow with eye exam Q 6 months

what is Hydroxychloroquine (Plaquenil) taken with

Used with other DMARDS and steroids

Hydroxychloroquine (Plaquenil) uses

Used for early RA and SLE

Hydroxychloroquine (Plaquenil) originally developed for

malaria

Hydroxychloroquine (Plaquenil) side effects

Pt may have hair loss or hair becomes lighter

Tofacitinib (Xeljanz)

 JAK (Janus kinase) inhibitor: interferes with enzymes that cause joint inflammation

 Moderate to severe active disease

 No live vaccines

Janus kinase (JAK) inhibitors

 another type of DMARD, are the first in a class of treatments for moderate to severe RA.

XELJANZ, a JAK inhibitor, has been shown to help

reduce pain and swelling in the joints, and to slow the progression of joint damage.

XELJANZ works

alone

XELJANZ proven to reduce

RA pain, swelling, and joint damage without the need for methotrexate.

XELJANZ is also available a

a once-daily pill called XELJANZ XR.

Biologic Response Modifiers (BRMs/"Biologics")

target the underlying disease process, including specific parts of the immune system, to help reduce moderate to severe RA symptoms.

Biologic Response Modifiers (BRMs/"Biologics") have been shown to help

reduce pain, swelling, and stiffness in the joints, and the progression of joint damage

What do biologics block?

TNF