Rheumatic Disorders Part I

Autoimmune Disorders Part I: Rheumatoid Arthritis, Osteoarthritis, &

Gouty Arthritis

Maria Carmela L. Domocmat, RN, MSN

Instructor, School of Nursing

Northern Luzon Adventist College

IMMUNE TOLERANCE:

ability to recognize or distinguish self (self-

antigens) from non-self (foreign antigens) like

bacteria or viruses.

immune system is tolerant to the host‘s tissues

but is able to reject foreign tissues and destroy

infectious agents.

Autoimmune Disorders

failure of the tolerance mechanism

immune reaction against self-antigens

usually occurs after destruction of some of the

body‘s tissues release of ‗self antigens‘ that

circulate in the body acquired immunity

(activated T cells or antibodies)

Why does the immune system attack the body that

it‘s supposed to protect?

Failure to recognize some cells as ―self‖

in rheumatic fever, the streptococcus antigen is very similar to a

protein in heart tissue, so the body mistakenly identifies heart

tissues as foreign

When the immune system sees ―self‖ antigens as ―nonself‖

cells seen as foreign are attacked and destroyed

may be only a few select cells or organs (organ-specific) – e.g.,

multiple sclerosis, juvenile diabetes, rheumatic fever

may be systemic - e.g., systemic lupus erythematosus, rheumatoid

arthritis

Incidence

~ 3.5 % of people have autoimmune diseases

On average, women are 2.7 times more likely to

develop these diseases than men

Cause:

most have no known cause

may be due to genetic factors, infectious agents,

gender, and age

Effect:

The autoimmune response results in tissue damage

Some damage occurs in only one or a few organs, in

other cases it may be body-wide (systemic)

Treatment

No Cure

Symptomatic treatment

CONNECTIVE TISSUE: A

REVIEW

Connective tissue

is a type of tissue made up of fibers forming a

framework and support structure for body

tissues and organs.

Connective tissue

is the material between the cells of the body that

gives tissues form and strength.

This "cellular glue" is also involved in delivering

nutrients to the tissue, and in the special

functioning of certain tissues.

surrounds many organs. Cartilage, blood and bone are specialized forms of connective

tissue.

Connective tissue

is made up of dozens of proteins,

including: collagens (a fibrous protein building block)

proteoglycans (a group of proteins that maintain

tissue stiffness)

glycoproteins (composed of a protein and a sugar)

The combination of these proteins can vary between

tissues.

Connective tissue disorders (CTD)

Is the major focus of rheumatology

The study of rheumatic disease

rheumatic disease

is any disease or condition involving the

musculoskeletal system

CTDs are discussed separately from other

musculoskeletal disorders bcoz most CTDs are

classified as autoimmune disorders

Connective tissue disorders (CTD)

Many rheumatic related

conditions are also

connective tissue disorders

including:

Lupus (Systemic Lupus

Erythematosus)

Psoriasis

Scleroderma (Systemic

Sclerosis)

Ankylosing Spondylosis

Reactive Arthritis

Fibromyalgia

Dermatomyositis

Polymyositis

Bursitis

Vasculitis

Polymyalgia rheumatica

Giant Cell Arteritis

Mixed Connective Tissue

Disease (MCTD)

Lyme disease

Sarcoidosis

Rheumatic diseases or disorders

Comprise autoimmune and inflammatory

disorders

‗the primary crippling disease‖

Rheumatic diseases or disorders

Primary reason for work-related disability

Leading cause of disability among 65 yrs old

and above

More than 40M in US have at least 1 of more

than 100 types of arthritis

Arthritis – means inflammation of one or more joints

Rheumatoid Arthritis (RA)

chronic systemic autoimmune disease

- anti-self antibodies that react with the constant regions of other

antibodies (rheumatoid factor)

onset of disease occurs most often between the ages of 25-55

women are 3 times more likely to develop this than men

symptoms include weakness, fatigue, and joint pain

infections, hormones and genetic factors may be involved

X-ray shows severe arthritis

affecting the joints and

limiting mobility

Rheumatoid arthritis (RA) affects peripheral

joints and may cause destruction of both cartilage

and bone. The disease affects mainly individuals

carrying the DR4 variant of MHC genes.

Treatment

ACR Clinical Classification

Criteria for Rheumatoid Arthritis using history, physical examination, laboratory

and radiographic findings:

ACR Clinical Classification

Criteria for Rheumatoid Arthritis

http://img.medscape.com/slide/migrated/editorial/cmecircle/2004/3415/images/moreland/slide07.gif

Initial Laboratory work-up

Complete blood count

Comprehensive metabolic panel

Urinalysis

Sedimentation Rate

Rheumatoid Factor

Anti-nuclear Antibody

Other diagnostic tests

Radiologic exam

X-ray, Bone scan or joint scan, MRI

Help confirm disease activity and monitor treatment

results

Early stage: Increased shadowing around the affected

joint: indicates soft tissue swelling

Radiology

early in the disease

show nothing other than soft tissue swelling.

periarticular osteopenia may develop.

With progression of disease

narrowing of the joint space is caused by loss of

cartilage, and juxta-articular erosions appear, generally

at the point of attachment of the synovium.

end-stage disease

large cystic erosions of bone may be seen. Bony

proliferation may occur because of degenerative

changes that follow inflammation.

Other diagnostic tests

Arthrocentesis

Aspirate sample of synovial fluid; analyzed for inflam

cells and immune complexes

Synovial fluid is milky, cloudy, or dark yellow fluid (normal:

transparent)

Arthroscopic examination: show pale, thick, edematous

synovial villi, cartilage destruction, and fibrous scar formation

(pannus)

Nrg care: use ice and rest the affected joint for 24 hrs

Acetaminophen

Clinical manifestations

http://nobelprize.org/medicine/laureates/1996/illpres/implications.html

Typical visible changes

include ulnar deviation of

the fingers at the MCP

joints, hyperextension or

hyperflexion of the MCP

and PIP joints, flexion

contractures of the

elbows, and subluxation

of the carpal bones and

toes (cocked -up).

Extra-Articular Disease

Rheumatoid Nodules

Cardiopulmonary Disease

Ocular Disease

Neurologic Disease

Felty's Syndrome

Rheumatoid Vasculitis

Sjogren's Syndrome

Rheumatoid Nodules

subcutaneous nodule

the most characteristic extra-articular lesion of the

disease.

occur in 20 to 30% of cases, almost exclusively in

seropositive patients.

located most commonly on the extensor surfaces of the

arms and elbows but are also prone to develop at

pressure points on the feet and knees.

Rheumatoid Nodules

http://images.rheumatology.org/vi

ewphoto.php?imageId=3011201

&albumId=75692

Rheumatoid Nodules

commonly form near

extensor surface of elbow

can be fixed to underlying

periosteum or can be

freely mobile.

There are several pulmonary manifestations

including pleurisy with or without effusion,

intrapulmonary nodules,

rheumatoid pneumoconiosis (Caplan's syndrome),

diffuse interstitial fibrosis, and rarely,

bronchiolitis obliterans pneumothorax.

Caplan‘s Syndrome

Presence of rheumatoid nodules in lungs

pneumococcus (noted in among coal miners and

asbestos workers)

http://images.rheumatology.

org/image_dir/album75692/

md_99-05-0096_1.tif.jpg

Pericarditis is the most common cardiac

manifestation.

Neurologic Disease

most common - mild, primarily sensory peripheral

neuropathy, usually more marked in the lower

extremities.

Entrapment neuropathies (e.g., carpal tunnel

syndrome and tarsal tunnel syndrome) sometimes

occur because of compression of a peripheral

nerve by inflamed edematous tissue.

Neurologic Disease

Cervical myelopathy secondary to atlantoaxial

subluxation (partial dislocation) is an uncommon

but particularly worrisome complication potentially

causing permanent, even fatal neurologic

damage.

Felty's Syndrome

is characterized by splenomegaly, leukopenia -

predominantly Granulocytopenia and leg ulcers

rare complication

Recurrent bacterial infections and chronic

refractory leg ulcers are the major complications.

Rheumatoid Vasculitis

most common clinical manifestations a

small digital infarcts along the nailbeds.

Sjogren's Syndrome

• is the most common ocular manifestation of

rheumatoid arthritis.

Autoimmune destruction of the lacrimal, salivary and vaginal mucus producing glands

which leads to impaired secretion of saliva

and tears and results in the sicca complex:

dry mouth (xerostomia)

dry eyes (keratoconjunctivitis sicca)

dry vagina (rare)

Sjogren's Syndrome

Associated with RA and fibromyalgia

Insufficient tears cause inflammation and

ulceration of the cornea

insufficient saliva cause decreased digestion of

CHO, promotes tooth decay and increases

incidence of infections

Vaginal dryness cause infection and

dyspareunia

NO CURE!!!

Criteria for Diagnosis of Sjögren's Syndrome

Four or

more of

following

criteria

must be

present

Keratoconjunctivitis, Sicca

PROGNOSIS

Disability is higher among patients with

rheumatoid arthritis with 60% being unable to

work 10 years after the onset of their disease.

Recent studies have demonstrated an increased

mortality in rheumatoid patients.

Median life expectancy was shortened an average

of 7 years for men and 3 years for women

compared to control populations.

Patients at higher risk for shortened survival are

those with

systemic extra-articular involvement,

low functional capacity,

low socioeconomic status,

low education, and

prednisone use.

(updated April, 2002)

ACR Guidelines for Medical

Management of Rheumatoid

Arthritis

Management

goals of treatment

aim toward achieving the

lowest possible level of arthritis disease activity

and remission if possible,

the minimization of joint damage, and

enhancing physical function and quality of life.

Reduce pain and inflammation

Protect Articular surface

› Reduction of joint stress

Maintain function

› ROM exercises

› Physical and occupational therapy

Surgical intervention

REDUCE PAIN AND

INFLAMMATION

Pharmacologic treatment

1. Non-steroidal Anti-inflammatory Agents

(NSAIDs)

2. Disease Modifying Anti-rheumatic Drugs

(DMARDs)

3. Corticosteroids

NSAIDs and corticosteroids

have a short onset of action while DMARDs can

take several weeks or months to demonstrate a

clinical effect

NON-STEROIDAL ANTI-

INFLAMMATORY AGENTS

(NSAIDS) Maria Carmela L. Domocmat, RN, MSN

NSAIDs

major effect - reduce acute inflammation thereby

decreasing pain and improving function.

have mild to moderate analgesic properties

independent of their anti-inflammatory effect.

Note: these drugs alone do not change the course

of the disease of rheumatoid arthritis or prevent

joint destruction.

OTC NSAIDs

Aspirin

ibuprofen (Advil ®, Motrin®, Nuprin ®)

naproxen (Alleve®, Flanax)

ketoprofen (Actron, Orudis KT)

Aspirin - oldest drug of the non-steroidal class

but because of its high rate of GI toxicity, a narrow

window between toxic and anti-inflammatory serum

levels, and the inconvenience of multiple daily doses,

aspirin's use as the initial choice of drug therapy

has largely been replaced by other NSAIDs.

Prescription NSAIDs include

meloxicam (Mobic®),

etodolac (Lodine®),

nabumetone (Relafen®),

sulindac (Clinoril®),

tolementin (Tolectin®),

choline magnesium

salicylate (Trilasate®),

flurbiprofen (Ansaid),

dexibuprofen (Seractil)

diclofenac (Cataflam®,

Voltaren®, Arthrotec®),

diflusinal (Dolobid®),

indomethicin (Indocin®),

ketoprofen (Orudis®,

Oruvail®),

oxaprozin (Daypro®),

piroxicam (Feldene®).

Beware of NSAID-induced ulcers

How to Prevent NSAID-Induced

Ulcers

If NSAID-induced ulcers are identified, the

following steps have been suggested:

Switch to alternative pain relievers.

proton-pump inhibitors (PPIs).

misoprostol or Arthrotec.

L-arginine

If cannot change drugs, then should use lowest

NSAID dose possible

Prevention NSAID-Induced Ulcers

proton-pump inhibitors (PPIs).

Can reduce NSAID-ulcer rates by as much as 80%

compared with no treatment.

omeprazole (Prilosec)

esomeprazole (Nexium)

lansoprazole (Prevacid),

rabeprazole (Aciphex),

pantoprozole (Protonix).

Prevention NSAID-Induced Ulcers

Try misoprostol or Arthrotec.

If other agents are inappropriate, misoprostol protects against

the major intestinal toxicity of NSAIDs.

the first drug approved for preventing NSAID-induced ulcers.

It is equally or even more effective than some of the PPIs, but it

does not heal existing ulcers and has more side effects than

PPIs. Patients tend to stop using it.

Arthrotec - a combination of an ulcer protective

agent called misoprostol and the NSAID

diclofenac.

L-arginine supplement

an amino acid found in health stores

may help protect against damage from NSAIDs.

an alternative agent

not government regulated and more research is

needed to confirm its benefits.

Topical NSAIDs

delivered in gels, creams, or patches are proving

to reduce arthritic pain and pose less of a risk for

gastrointestinal complications associated with

oral NSAIDs.

diclofenac (Pennsaid, Oxa Sat)

eltenac, ibuprofen, or ketoprofen.

$63.07

NSAIDS: COX-2 inhibitor

includes COX-2 inhibitors

also effective in controlling inflammation.

Only one of these agents is currently available in

the United States (celecoxib, Celebrex®) while

additional compounds are available in other

countries (etoricoxib, Arcoxia®; lumiracoxib,

Prexige®).

or COX-2 medications

COX-2 inhibitors

designed to decrease the gastrointestinal risk of

NSAIDS,

but concerns of possible increases in

cardiovascular risk with these agents has led to

the withdrawal of two of these drugs from the

market (rofecoxib, Vioxx®; valdecoxib, Bextra®).

CORTICOSTEROIDS

Corticosteroids

anti-inflammatory & immunoregulatory activity.

PO, IV, IM or can be injected directly into the joint.

useful in early disease as temporary adjunctive

therapy while waiting for DMARDs to exert their

antiinflammatory effects.

Corticosteroids

also useful as chronic adjunctive therapy in

patients with severe disease that is not well

controlled on NSAIDs and DMARDs.

Weight gain and a cushingoid appearance

(increased fat deposition around the face, redness

of the cheeks, development of a ―buffalo hump‖

over the neck) is a frequent problem and source of

patient complaints

cushingoid appearance

Prevent osteoporosis due to steroid

use adequate calcium and vitamin D supplementation

Bisphosphonates

alendronate (Fosamax®)

risedronate (Actonel®)

ibandronate (Boniva®)

Patients with and without osteoporosis risk factors

on low dose prednisone should undergo bone

densitometry (DEXA Scan) to assess fracture risk.

Intra-articular corticosteroids

(e.g., triamcinolone or

methylprednisolone and others)

are effective for controlling a local

flare in a joint without changing the

overall drug regimen.

http://www.mayoclinicproceedings.com/content/84/9/831.full

DISEASE MODIFYING ANTI-

RHEUMATIC DRUGS

(DMARDS) Maria Carmela L. Domocmat, RN, MSN

Disease Modifying Anti-rheumatic

Drugs (DMARDs) Can alter the disease course and improve

radiographic outcomes.

DMARDs have an effect upon rheumatoid arthritis

that is different and may be more delayed in onset

than either NSAIDs or corticosteroids.

when the diagnosis of rheumatoid arthritis is

confirmed, DMARD agents should be started.

DMARDs

Methotrexate (Rheumatrex®, Trexall®)

Hydroxychloroquine (Plaquenil ®)

Sulfasalazine (Azulfidine®)

Tumor Necrosis Factor Inhibitors

etanercept (Enbrel®

adalimumab (Humira ®)

infliximab (Remicade®)

Leflunomide (Arava®)

T-cell Costimulatory Blocking Agents

abatacept (Orencia®)

DMARDs

B cell Depleting Agents

rituximab (Rituxan®)

Interleukin-1 (IL-1) Receptor Antagonist Therapy

anakinra (Kineret®)

Intramuscular Gold

Other Immunomodulatory and Cytotoxic agents—

azathioprine (Imuran®),

cyclophosphamide, and

cyclosporine A(Neoral®, Sandimmune®)

Nursing Mgmt

Note: DMARDs are toxic to multiple body organs

including liver, kidneys, GIT, lungs, bone

marrow, eyes, and must be monitored closely

These drugs suppress the bone marrow and

place clients at risk for infection, anemia, and

bleeding

Methotrexate

the first-line DMARD agent

Has rapid onset of action at therapeutic doses (6-

8 weeks)

good efficacy

favorable toxicity profile

ease of administration

and relatively low cost.

http://www.muabannhadat123.com/forum/showthread.php?p=3477

Hydroxychloroquine

an antimalarial drug

relatively safe and well-tolerated agent for the

treatment of rheumatoid arthritis.

have limited ability to prevent joint damage on

their own, their use should probably be limited to

patients with very mild and nonerosive disease.

Hydroxychloroquine

is sometimes combined with methotrexate for

additive benefits for signs and symptoms or as

part of a regimen of ―triple therapy‖ with

methotrexate and sulfasalazine.

Sulfasalazine

Azulfidine®

effectiveness - somewhat less than

that methotrexate,

reduce signs and symptoms and

slow radiographic damage.

given in conjunction with

methotrexate and

hydroxychloroquine as part of a

regimen of ―triple therapy‖

Leflunomide (Arava®)

efficacy is similar to methotrexate in terms of signs

and symptoms

viable alternative - failed or are intolerant to

methotrexate.

Tumor necrosis factor (TNF)

inhibitors Tumor necrosis factor alpha (TNF)

is a pro-inflammatory cytokine produced by

macrophages and lymphocytes.

found in large quantities in the rheumatoid joint and is

produced locally in the joint by synovial macrophages

and lymphocytes infiltrating the joint synovium.

TNF is one of the critical cytokines that mediate joint

damage and destruction due to its activities on many

cells in the joint as well as effects on other organs and

body systems.

TNF antagonists

first of the biological DMARDS to be approved for

the treatment of RA

have also been referred to as biological

response modifiers or “biologics” to

differentiate them from other DMARDS such as

methotrexate, leflunomide, or sulfasalazine.

TNFs or Biological Response

Modifiers (BRMs) Etanercept (Enbrel®)

Infliximab(Remicade®)

Adalimumab (Humira®)

Etanercept (Enbrel®)

Etanercept is effective in reducing the signs and

symptoms of RA, as well as in slowing or halting

radiographic damage, when used either as

monotherapy or in combination with methotrexate.

Infliximab(Remicade®)

Infliximab, in combination with methotrexate, is

approved for the treatment of RA, and for the

treatment of psoriatic arthritis, and ankylosing

spondylitis, as well as psoriasis and Crohn‘s

disease.

Adalimumab (Humira®)

Adalimumab is a fully human anti-TNF monoclonal

antibody with high specificity for TNF.

Anakinra (Kineret™)

a human recombinant IL-1 receptor antagonist (hu

rIL-1ra)

can be used alone or in combination with

DMARDs other than TNF blocking agents

(Etanercept, Infliximab, Adalimumab).

T-cell Costimulatory blockade

Abatacept (Orencia®)

first of a class of agents known as T-cell

costimulatory blockers.

interfere with the interactions between antigen-

presenting cells and T lymphocytes and affect

early stages in the pathogenic cascade of events

in rheumatoid arthritis.

Intramuscular Gold

Myochrysine® and Solganal®

have been replaced by

Methotrexate and other DMARDS

as the preferred agents to treat RA.

rarely used now due to their

numerous side effects and

monitoring requirements, their

limited efficacy, and very slow

onset of action.

Plasmapheresis

Alternative treatments

glucosamine sulfate

chondroitin sulfate

are dietary supplements usually taken in pill form that

are thought to protect and possibly help repair

cartilage cells.

NURSING MANAGEMENT

Chronic pain r/t inflammation and swelling from

pressure on surrounding tissues, joint deformity

and joint destruction

Teach about meds

Promote comfort with nonpharmacologic measures

Manage stiffness

Promote sleep and rest

Promote comfort with

nonpharmacologic measures

Manage stiffness

Promote sleep and rest

Encourage to sleep at least 8 hrs at night, take

daily naps

Promote a quiet envt

Provide warm beverages before retiring to sleep

Administer hypnotics or relaxants as prescribed

REDUCTION OF JOINT

STRESS

Reduction of joint stress

Because obesity stresses the musculoskeletal

system, ideal body weight should be achieved and

maintained.

Rest, in general, is an important feature of

management.

When the joints are actively inflamed, vigorous

activity should be avoided because of the danger

of intensifying joint inflammation or causing

traumatic injury to structures weakened by

inflammation.

Readiness for enhanced self-care r/t complex

medication schedules, high risk of S/E of meds,

health maintenance, and self-care

Promote balanced diet

Promote decision-making

Promote hope

Promote coping

Self-care

Use china or heavy plastic cup with handle

which is easier to manipulate rather than

styrofoam or paper cup which may bend or

collapse

When fine motor activities become impossible –

use larger joints or body surfaces

Ex: use palm of hand to press the toothpaste to

toothbrush rather than the fingers

Use devices – long-handed brushes to brush hair or

dressing sticks for facilitite wearing of pants

Reduction of joint stress

urge to maintain a modest level of activity to

prevent joint laxity and muscular atrophy.

Splinting of acutely inflamed joints, particularly at

night and the use of walking aids (canes, walkers)

are all effective means of reducing stress on

specific joints.

Assistive devices

Arthritic's Pen

Computer Keyboard Aid

Phone & Cup Holder with

Hook and Loop Strap

Arthritis in your hands

causes your finger joints

and knuckles to become

stiff and sometimes

painful and swollen.

Protect your hands by

avoiding pushing, pulling

and twisting motions.

Avoid making a tight fist

or pinching objects tightly.

Instead, use a grasp that

aligns your knuckles

evenly along the handle

of the tool or utensil.

This makes grasping the

tool more comfortable

and requires less effort to

use the tool.

For instance, a built-up

handle made of foam can

make it easier for you to

grasp your toothbrush.

For tasks that require to pinch

objects tightly, look for

assistive devices that can help

hold the object with less force.

special key holder may help

turn keys more comfortably

without putting strain on hand.

This type of holder aligns knuckles

evenly along the handle of the tool

or utensil, allow use a larger grip

to turn the key.

Use assistive devices to

help you open jars. This

spares your fingers from

the twisting motion

required to open a jar.

To protect your finger joints,

avoid tightly pinching with

your fingers.

For example, use a button

aid to help you grasp and

fasten buttons on your

clothes. Choose clothes with

easy-to-close fasteners,

such as zippers, large

buttons or hooks.

Promote balanced diet Good oral hygiene b4 and after meals

Small, frequent feedings

High-caloric snacks

If with xerostamia – moisten foods, extra fluids with

Eliminate spicy or acidic foods

Sit upright to eat

Take all meds with food and full glass of water – to

ameliorate GI distress

Use assistive device if with stiffness

Sjogren‘s syndrome mgmt

Symptomatic treatment Artificial tears and saliva

Lubricants

Moisturizers

Systemic pilocarpine – for dry mouth

Blockade of tear outflow

NSAIDS – for pain

Promote decision-making

Exercise healthy control over the disease

Client should be able to verbalize cause of illness

Educate the client

Increase participation in decision-making

allow as many choices as possible

Decide on own ADL

Promote hope

Avoid false reassurance

Help set realistic goals

Praise for accomplishments (no matter how

small)

Active listening

Be sensitive to changes in mind and affect

Promote coping

The client would be able to integrate disease

into the demands of daily living

Sign that the client has healthy approach

strategies

Seek out info and assistance

Find strength through spiritual support

Verbalize feelings and concerns

Set goals

Express positive thoughts

Maintain realistic independence

Signs of less adaptive strategies

Avoidance strategies – ex: denial

Excessive sleeping

Other passive behaviors

Depression

FATIGUE

Management of Fatigue:

For muscle atrophy – aggressive PT to

strengthen muscle and prevent further atrophy

Management of Fatigue

Principles of energy conservation

Pacing activities- do not plan too much activity for one

Allow rest periods

Set priorities – determine which activities are most

important and do them first

Obtain assistance when needed – delegate

responsibilities

balance activity and rest

Plan ahead to prevent last minute rushing and stress

Learn own activity tolerance and do not exceed it

BODY IMAGE DISTURBANCE

Enhance body image

Body image may be affected by both the disease

process and drug therapy

Ulnar deviation, swan-neck deformity, boutonnière

deformity, rheumatoid nodules

Steroid side effect – cushingoid syndrome

Determine client‘s perception of the changes

and impact of reaction of the SO

Most impt Ix – communicate acceptance of the

client ; establish and maintain trusting

relationship to encourage the client to express

feelings Maria Carmela L. Domocmat, RN, MSN

Let the client wear own clothes rather than the

hosp gown, brush own hair, use make-up if

desired

Use colored hair accessories , nail polish,

perfume

SURGICAL INTERVENTIONS

Surgical interventions

Tendon transfer and osteotomy

Synovectomy

Arthrodesis

Joint arthroplasty or replacement

Tendon transfer and osteotomy

Nodules or benign bony tumors (exostoses) –

surgically removed and flexion contractures

surgically relieved

Osteotomies

Excision or cutting through bones

Synovectomy

Surgical removal of synovia – elbow, wrist, fingers,

Synovectomy

ordinarily not recommended for patients with

rheumatoid arthritis, primarily because relief is

only transient.

synovectomy of the wrist - an exception

recommended if intense synovitis is persistent despite

medical treatment over 6 to 12 months.

Persistent synovitis involving the dorsal compartments

of the wrist can lead to extensor tendon sheath rupture

resulting in severe disability of hand function.

Synovectomy

Arthrodesis

Operation that produce bony fusion of joint

used for clients with bone loss after joint

infection , tumors, musculoskeletal trauma,

paralysis

Immobilize the joint but eliminate some

discomfort or arthritic process

Ankle - most common

Joint arthroplasty or replacement

particularly of the knee, hip, wrist, and elbow, are

highly successful.

Arthroplasty of the metacarpophalangeal (knuckle)

joints also can reduce pain and improve function.

Hip Replacement

Other operations include

release of nerve entrapments (e.g., carpal tunnel

syndrome)

arthroscopic procedures

removal of a symptomatic rheumatoid nodule

Complementary/ Alternative

therapies

Pain relief – hypnosis, acupuncture, magnet

Good nutrition

Omega-3 fatty acids

Found in coldwater fish (salmon, sea bass, tuna)

May help reduce inflam

But amount needed is impractical to human consumption

Fish oil capsules

Complementary/ Alternative

therapies

Antioxidant vitamins (A,C, E) to help maintain

normal function of the immune system

Trace elements for joint health

Zinc, Selenium, Copper, Iron

Osteoarthritis associated with the

aging process and

can affect any joint.

The cartilage of the

affected joint is

gradually worn

down, eventually

causing bone to rub

against bone.

Bony spurs develop

on the unprotected

bones, causing pain

and inflammation.

Bouchard‘s nodes

Heberden‘s nodes

WHAT’S THE DIFFERENCE

BETWEEN RA AND OA?

Osteoarthritis is a deterioration of cartilage and

overgrowth of bone often due to "wear and tear."

Rheumatoid arthritis is the inflammation of a

joint's connective tissues, such as the synovial

membranes, which leads to the destruction of

the joint's cartilage.

Known as the ―wear-and-tear‖ kind of arthritis

a chronic condition characterized by the

breakdown of the joint‘s cartilage. Cartilage is the

part of the joint that cushions the ends of the

bones and allows easy movement of joints. The

breakdown of cartilage causes the bones to rub

against each other, causing stiffness, pain and

loss of movement in the joint.

degenerative joint disease,

ostoarthrosis,

hypertrophic arthritis

degenerative arthritis.

stages of osteoarthritis

Cartilage loses elasticity and is more easily

damaged by injury or use.

Wear of cartilage causes changes to underlying

bone. The bone thickens and cysts may occur

under the cartilage. Bony growths, called spurs or

osteophytes, develop near the end of the bone at

the affected joint.

stages of osteoarthritis

Bits of bone or cartilage float loosely in the joint

space.

The joint lining, or the synovium, becomes

inflamed due to cartilage breakdown causing

cytokines (inflammation proteins) and enzymes

that damage cartilage further.

The main problem in

knee OA is degeneration

of the articular cartilage.

Articular cartilage is the

smooth lining that covers

the ends of bones where

they meet to form the

joint. The cartilage gives

the knee joint freedom of

movement by decreasing

friction.

The articular cartilage is

kept slippery by joint fluid

made by the joint lining

(the synovial membrane).

The fluid, called synovial

fluid, is contained in a soft

tissue enclosure around

synovial joints called

the joint capsule.

An important substance

present in articular

cartilage and synovial

fluid is called hyaluronic

acid. Hyaluronic acid

helps joints collect and

hold water, improving

lubrication and reducing

friction. It also acts by

allowing cells to move

and work within the joint.

When the articular

cartilage degenerates, or

wears away, the bone

underneath is uncovered

and rubs against bone.

Small outgrowths called

bone spurs,

or osteophytes, may form

in the joint.

Changes in the cartilage and bones of the joint

can lead to pain, stiffness and use limitations.

Deterioration of cartilage can:

Affect the shape and makeup of the joint so it doesn‘t

function smoothly. - limp when walk or have trouble

going up and down stairs.

Cause fragments of bone and cartilage to float in joint fluid

causing irritation and pain.

Cause bony spurs, called osteophytes, to develop near

the ends of bones

Mean the joint fluid doesn‘t have enough hyaluronan,

which affects the joint‘s ability to absorb shock.

Causes and Risk factors

there is no single known cause of osteoarthritis

there are several risk factors that should be

considered

Obesity

Injury or Overuse

Genetics or Heredity

Muscle Weakness

Other Diseases and Types of Arthritis

Treatment

Acetaminophen

Nonsteroidal anti-inflammatory drugs (NSAIDs) or

COX-2 medications

Capsaicin

Tramadol

Narcotic pain relievers

glucosamine sulfate and chondroitin sulfate

Acetaminophen

Tylenol, Anacin-3, Panadal, Phenaphen,

Valadol, and others)

for mild to moderate osteoarthritis.

usually the first choice

Nonsteroidal anti-inflammatory

drugs (NSAIDs)

for moderate to severe arthritic pain.

OTC NSAIDs

Prescription NSAIDs include

Drugs for Prevention NSAID-

Induced Ulcers

If NSAID-induced ulcers are identified switch to

alternative pain relievers.

Topical NSAIDs

$63.07

Capsaicin (Zostrix)

is an ointment prepared from the active

ingredient in hot chili peppers that has been

helpful for relieving painful areas in other

disorders.

SALONPAS PAIN PATCH WITH CAPSAICIN

Tramadol (Ultram)

is a pain reliever that has some properties that

are similar to narcotics.

not as addictive, however, and may be an

alternative for patients who do not respond to

NSAIDs or less potent agents.

Narcotic pain relievers

oxycodone, oxymorphone, or morphine

may be necessary for severe pain that does not

respond to less potent pain relievers.

http://differncebetween.infoloommedia.netdna-cdn.com/wp-

content/uploads/2009/11/oxycodone.png Maria Carmela L. Domocmat, RN, MSN

Management

Same with RA

Let‘s Exercise

http://www.medicinenet.com/rheumatoid_arthritis

_exercises_slideshow/article.htm

Gouty arthritis

is a disease characterized by an abnormal

metabolism of uric acid, resulting in an excess of

uric acid in the tissues and blood causing

inflammation

People with gout either produce too much uric

acid, or more commonly, their bodies have a

problem in removing it.

the disease of kings

the king of diseases

Gouty arthritis

2 major types

Primary

Secondary

Gouty arthritis

Primary

Inherited X-lined trait

Caused by several inborn errors of purine metabolism

Uric acid- is the end-product of purine metabolism; excreted

in urine

Production of uric acid exceeds the excretion

capability of kidneys

Sodium urate is deposited in the synovium and other

tissues which results in inflammation

Males, 30‘s and 40‘s

Gouty arthritis

Secondary

Hyperuricemia

Excessive uric acid in blood casued by anoterh disease

Affects all ages

Renal insufficiency

Diuretic therapy

Multiple myeloma

Carcinomas

Causes:

decreased normal excretion of uric acid and other waste

products

Increased production of uric acid

Four Stages Of Gouty Arthritis

Asymptomatic Hyperuricemia

Acute Gout / Acute Gouty Arthritis

Interval / Intercritical

Chronic Tophaceous Gout

Asymptomatic Hyperuricemia:

Asypmptomatic but with elevated blood uric acid

levels

Serum uric acid level (mg/dl) Incidence of gout

>9.0 7.0-8.9

7.0-8.9 0.5-0.37

<7.0 0.1%

Acute Gout / Acute Gouty Arthritis

hyperuricemia has caused deposits of uric acid

crystals in joint spaces, leading to gouty attacks.

Excruciating pain and inflammation of one or more

joints – esp metatarsophalangeal joints of the great

toe (podagra)

Increased ESR, WBC

http://cdn.nursingcrib.com/wp-content/uploads/gouty-arthritis.jpg

http://img.medscape.com/slide/migrated/e

ditorial/cmecircle/2004/3689/images/cohen

/slide019.gif

Interval / Intercritical

the periods between acute gouty attacks – may be

months or years after the 1st attack

Asymptomatic period

No abnormality in joints

Chronic Tophaceous Gout:

the disease has caused permanent damage

Deposits or urate crytals under skin and within major

organs (i.e., urate kidney stone formation)

Tophi – deposits of sodium urate crystals

May occur anywhere; common in outer ear

http://www.hopkins-arthritis.org/images/gout_fig7.gif

http://www.cdaarthritis.com/images_slides/40_gout_b_toe1_360.jpg

http://img.medsca

pe.com/slide/migr

ated/editorial/cme

circle/2004/3689/i

mages/cohen/slid

e019.gif

http://img.medscape.com/slide/migr

ated/editorial/cmecircle/2004/3689/i

mages/cohen/slide019.gif

http://msnbcmedia1.msn.com/i/ms

nbc/Components/Interactives/Healt

h/MiscHealth/GOUT.gif

http://img.medscape.com/slide/migrated/editorial/cmecircle/2004/3689/images/cohen/slide019.gif

Dx tests

Synovial fluid analysis (shows uric acid crystals)

Uric acid - blood

Joint x-rays (may be normal)

Synovial biopsy

Uric acid - urine

Management

Drug therapy

Diet therapy

Management

Drug therapy

acute gouty arthritis – inflammation subsides

spontaneously within 3 to 5 days

But if cannot tolerate pain

Colchicine (Colsalide, Novocolchicine) and NSAIDs

Taken for 4-7 days

(NSAIDs) -Indomethacin (Indocin), ibuprofen (Advil),

and naproxen (Aleve), celecoxib (Celebrex)

painkillers such as codeine, hydrocodone,

and oxycodone

Corticosteroids

Management

Drug therapy

Chronic or repeated acute episodes

Allopurinol (Zyloprim)

A xanthine oxidase inhibitor – prevents conversion of xanthine

to uric acid

Probenecid (Benemid, Benuryl)

Uricosuric drug – promotes excretion of excess uric acid

drink at least 2 liters of fluid a day while taking this medication

(to help prevent uric acid kidney stones from forming).

Combination drug

Probenecid and Colchicine (ColBenemid)

Note: avoid aspirin – it inactivates the drug

Febuxostat (Uloric)

first new medication developed specifically for the

control of gout in over 40 years.

Decreases formation of uric acid by the body and is a

very reliable way to lower the blood uric acid level.

can be used in patients with mild to moderate kidney

impairment.

should not be taken with 6-mercaptopurine (6-MP), or

azathioprine.

http://www.emedicinehealth.com/gout/page7_em.htm#Medications

Management

Diet therapy

Avoid alcohol, anchovies, sardines, oils, herring,

organ meat (liver, kidney, and sweetbreads), legumes

(dried beans and peas), gravies, mushrooms,

spinach, asparagus, cauliflower, consommé, and

baking or brewer's yeast.

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001459/

Limit meat

Avoid fatty foods such as salad dressings, ice

cream, and fried foods.

Eat enough carbohydrates.

If losing weight, lose it slowly. Quick weight loss

may cause uric acid kidney stones to form.

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001459/

http://s1.hubimg.com/u/1184832_f496.jpg

Avoid all forms of aspirin and diuretics – may

precipitate attack

Excessive physical or emotional stress- can

exacerbate disease

Prevention of kidney stone

formation

Increase fluid intake – prevent stone formation

Dilute urine and prevent sediment formation

Alkaline ash diet

Citrus fruits, juices, milk and certain dairy products

Uric acid is more soluble in high pH urine – less likely

to form urinary stones

Complications

Chronic gouty arthritis

Kidney stones

Deposits in the kidneys, leading to chronic

kidney failure

Rheumatic Disorders Part I

acr clinical

narcotic pain

alternative

prescription

soft tissue

disease modifying

connective

connective

Documents

Medical Nutrition Therapy for Rheumatic Disorders

Hair Disorders Part 1

Neurological Disorders part 1

Rheumatic Disorders Part IV

Rheumatic heart disease: Acute Rheumatic Fever

Rheumatic,Connective tissue disorders

Obsessive-Compulsive Spectrum Disorders and Rheumatic Fever:...

Musculoskeletal Disorders Part II

Breast Disorders Part II

Rheumatic Disorders of Eye

rheumatic conditions in the northern part of central java an...

Treating rheumatic disorders successfully using the Bicom...

Rheumatic fever & acute rheumatic heart disease Rheumatic.....

Gastrointestinal Disorders - Part II

Thyroid disorders Part 1

Arthritis and Other Rheumatic Disorders ICD-9-CM to ICD-10.....