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 Dermatomyositis
conditions are also Polymyositis
connective tissue disorders Bursitis
including:
Vasculitis
Lupus (Systemic Lupus
Erythematosus) Polymyalgia rheumatica
Psoriasis Giant Cell Arteritis
Scleroderma (Systemic Mixed Connective Tissue
Sclerosis) Disease (MCTD)
Ankylosing Spondylosis Lyme disease
Reactive Arthritis Sarcoidosis
Fibromyalgia


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
the
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.


ACR Guidelines for Medical
Management of Rheumatoid
Arthritis
(updated April, 2002)

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)

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®), diclofenac (Cataflam®,
etodolac (Lodine®), Voltaren®, Arthrotec®),
nabumetone (Relafen®), diflusinal (Dolobid®),
sulindac (Clinoril®), indomethicin (Indocin®),
tolementin (Tolectin®), ketoprofen (Orudis®,
choline magnesium Oruvail®),
salicylate (Trilasate®), oxaprozin (Daypro®),
flurbiprofen (Ansaid), piroxicam (Feldene®).
dexibuprofen (Seractil)


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


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)

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®
IM
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

Computer Keyboard Aid

Arthritic's Pen


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
meals
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
day
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

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,
knees


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


Surgical intervention


Surgical intervention
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

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.


AKA
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
(OA),
there are several risk factors that should be
considered
Age
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

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.
AKA
gout
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
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

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Rheumatic Disorders Part I