Osteoarthritis verses Rheumatoid Arthritis

prevalence

OA – 20.7 million

RA - 2.1 million

osteoarthritis

A degenerative disorder with minimal articular inflammation.

No systemic symptoms.

Pain relieved by rest; morning stiffness brief.

Radiographic findings: narrowed joint space, osteophytes

OA general information

non-inflammatory disease

characterized by progressive degeneration of joint cartilage with bone margin involvement and osteophyte formation

· Osteoarthritis is a chronic long-term, degenerative disease that causes the breakdown of cartilage in the joints leading to pain and stiffness.

cortical steroids (risk factor for osteoporosis)

Before the age of 45, osteoarthritis predominantly affects men. After 55 the condition is more frequent in women.

Fifty percent of people over 60 years of age are affected in at least one joint. It is estimated that everyone over the age of 75 suffers from osteoarthritis.

primary osteoarthritis

· an unknown cause but is generally associated with aging. It is sometimes referred to as "wear and tear" arthritis.

secondary osteoarthritis

the destruction of cartilage from a known cause. Conditions that lead to cartilage loss include repetitive trauma, obesity, crystal deposits, infection, congenital abnormalities, injury or joint surge (obesity, gonorrhea, gout)

joints most commonly affected include

hips and knees

joints where thumb meets hand (carpometacarpal joint/basal joint), two distal joints to the knuckle

OA signs and symptoms

Pain

Pain is the most common symptom of osteoarthritis and usually increases with joint use.

Pain can also restrict mobility.

Stiffness

Swelling

Deformity

Painless, irregular bony enlargements

Heberden's nodes

Bouchard's nodes

“Harley-Davidsons raise your Blood Pressure”

Crepitus

stiffness

Stiffness of the affected joint is often noticed first thing in the morning, and after resting. < 15 minutes

crepitus

Grating sound or sensation produced by friction between bone and cartilage

eroding cartilage

cartilage

osteoarthritis (image)

What symptoms can you see on an x-ray?

bone spurs, narrowing space

Why can't cartilage grow back?

it's avascular

Heberden's nodes

bony growths of DIP

Bouchard's nodes

bony growths of PIP

OA risk factors

Obesity

Trauma

Genetics - predilection for cartilage breakdown

Increased age (>40)

Repetitive movements (sports or employment - manual laborers)

radiograph "LOSS"

a. Loss of joint space

b. Osteophytes - spurs of bone

c. Subarticular sclerosis

Increased density of bone on joint line

d. Subchondral cysts

Small fluid filled holes in bone on the joint line

OA on left hip

OA labs

none

OA medical treatment

1.Acetaminophen – Tylenol

2. Nonsteroidal anti-inflammatory (NSAIDs)

Motrin

Advil

Celebrex

Intra-articular injections of triamcinolone ((corticosteroid) often

with lidocaine)

surgical intervention-joint arthroplasty

Total hip and knee replacements provide excellent symptomatic and functional improvement when involvement of that joint severely restricts walking or causes pain at rest, particularly at night.

What's a risk of arthroplasty?

infection

micro-fracture surgery

quick fix to help delay an arthroplasty, wet paint on knee, you can't weight bear for a 5 weeks. A lot of people

OA prognosis

a. No cure

b. Manage pain and minimize disability

c. Maintain quality of life

d. Encourage exercise - strength and joint function

e. Depression associated with chronic pain

DIP

distal interphalengeal

rheumatoid arthritis

a chronic, system, autoimmune inflammatory disease

RA essentials

Usually insidious onset with morning stiffness and joint pain.

Symmetric polyarthritis with predilection for small joints of the hands and feet; deformities common with progressive disease.

Rheumatoid factor and antibodies to cyclic citrullinated peptides (anti-CCP) are present in 70-80%.

Extra-articular manifestations: subcutaneous nodules, interstitial lung disease, pleural effusion, pericarditis

What is the most common inflammatory arthropathy?

rheumatoid arthritis

Are men or women more likely to get RA?

females (3:1 ratio)

When is RA onset?

4th or 5th decade

RA environmental factors

tobacco; known to be a major trigger both for new onset RA and as an exacerbating agent for existing RA

RA genetic factors

HLA DR beta 1 alleles - genetic trait that increases the incidence of the condition. There is a strong familiar relationship associated with RA. (can be passed on)

inflammatory response

chronic inflammation of the synovium (synovitis) erodes cartilage, bone, ligaments, and tendons.

Effusion and other manifestations of inflammation are common.

unbated

without any reduction in intensity or strength (disability becomes pronounced)

RA symptoms

Patients have flares (OA is constant) RA can get worst sometimes and have asymptomatic days

Usually insidious onset with morning stiffness and joint pain.

Symmetric polyarthritis with predilection for small joints of the hands and feet

Wt loss, fatigue, muscle weakness and vague m/s discomfort that eventually settles in joints

Morning stiffness that lasts about one hour

What joints are affected by RA?

Although any joint may be affected the most commonly involved joints are:

i. PIP joints of the fingers

ii. MCP joints

iii. Wrists

iv. Knees

v. Ankles

vi. MTPs

Stages of RA

it's a progressive disease-deformities caused by disruption/erosion of ligaments and tendons

Early RA -> Intermediate RA -> Late RA

Physical exam findings

1. Joint findings (we want to fend off inflammation with medication before deformities occur and we can't help them)

2. Rheumatoid nodules

3. Ocular symptoms

4. Systemic disease (must do a good pulmonary and cardiac exam)

joint findings

A. Polyarticular joint edema, erythema and pain, often at rest (red, painful, warm to touch)

B Swan-neck and Boutonniere deformities

C Ulnar deviation at MCPs

Swan neck deformity

hyperextension at PIP and Flexion at DIP

Buotonniere Deformity

flexion at PIP and hyperextension at DIP

ulnar deviation at MCPs

thickening of fingers-sausage fingers, edematous- important to take rings off so they don't have to be cut off

rheumatoid nodules

Twenty percent of patients have subcutaneous rheumatoid nodules, most commonly situated over bony prominences but also observed in the bursae and tendon sheaths

ocular symptoms

Dryness of the eyes, mouth, and other mucous membranes is found especially in advanced disease

systemic disease

A Interstitial lung disease -decreased ability to gas exchange

B Pericarditis -inflammation of the pericardial sac in which the heart sits

C Disease of the lung pleura

**because the immune system attacks more than joints - thus we must be

concerned with systemic manifestations

RA classic complaint

I woke up and my ____ was sore and I couldn't move it and I couldn't _____ but now it feels fine (they had a flare but it went away before we saw them)

RA labs

1 Anti-cyclic citrullinated peptide (anti-CCP)

Anti-CCP antibodies are the most specific blood test for rheumatoid arthritis

Anti-CCP is an autoantibody produced by the patient’s immune system that attacks the body. These attacks can produce inflammatory symptoms most commonly experienced in rheumatoid arthritis.

2 Rheumatoid factor

An antibody that is detectable in the blood of approximately 80% of adults with rheumatoid arthritis.

RA prognosis

Aggressive RA can shorten life by 10-15 years (cardiac/pulmonary issues)

Decreases quality of life = some depression involved

Early aggressive therapy is warranted by rheumatologist

RA treatment

“The primary objectives in treating rheumatoid arthritis are reduction of inflammation and pain, preservation of function, and prevention of deformity.”

“Early recognition and diagnosis of RA may allow intervention with appropriate medications with a decrease in the destructive arthropathy that can occur with the disorder.” JAAPA DiBaise and Kohn

If medications do not achieve the target of remission of symptoms or low disease activity, additional medications should be added to the therapeutic regimen.

Immunosuppressive agents increase a patient’s risk of infection including Hepatitis B and Hepatitis C. (should be the first in line for vaccines every year)

low-dose corticosteroids (prednisone)

produce a prompt anti-inflammatory effect and slow the rate of articular erosion. These should only be used for short term control for patients with acute "flares". (keep in mind they increase risk for osteoporosis)

disease-modifying antirheumatic drugs (DMARDs)

sulfasalazine, methotrexate, and biological response modifiers

sulfasalazine

similar to methotrexate in terms of medication category.

This medication is a good choice for women with RA who are interested in becoming pregnant. Sulfasalazine is not teratogenic and will allow her to safely become pregnant.

LFT should be obtained at the onset of medication and then every 3 months thereafter and after increasing the dose.

methotrexate

a long standing medication used to treat RA

Methotrexate increases adenosine levels. Adenosine

promotes an anti-inflammatory state.

Taken once per week - by mouth or IM injection (thigh)

Adversely impacts body's folic acid levels via GI tract - thus patients often take folic acid supplements along with methotrexate.

Known teratogenic effects make this medication CONTRAINDICATED in pregnancy.

Obtain a pregnancy test prior to starting the medication.

Adverse effect - possible liver damage - pts are often advised to avoid alcohol and monitor LFTs (liver function tests). LFT should be obtained at the onset of medication and then every 3 months thereafter.

Anencephaly

fetus taken to gestation but born without CNS (lack of folic acid)

spina bifida

spinal cord grown outside of skin (lack of folic acid)

What is needed in CNS production?

folic acid

biological response modifiers

newest class of disease-modifying antirheumatic drugs (DMARDs) used to treat rheumatoid arthritis.

They are genetically engineered to act like natural proteins in the patient’s immune system.

Biologics don’t cure RA, but they can dramatically slow its progression.

Generic Name Trade Name

A Etanercept Enbrel

B Adalimumab Humira

C Infliximab Remicade

*These are injectable medications*

info about DMARDs

All three of these drugs are tumor necrosis factor blockers. TNF is a protein in the immune system that contributes to inflammation and joint damage. TNF blockers block the action of TNF that leads to damage from abnormal inflammation.

Medications in this class cause the patient to be at increased for serious infections such as tuberculosis, herpes zoster and fungal infections

What are concerns about a patient on steroids for too long?

impaired immune system and bone density problems