The document discusses rheumatoid arthritis (RA), a chronic autoimmune disease characterized by inflammation of the joints. It begins by defining RA and noting its prevalence. The etiology is unknown but involves genetic and environmental factors. The pathophysiology involves the immune system attacking the synovial tissue lining joints. Clinical features include symmetric joint pain and stiffness. Diagnosis involves evaluating symptoms, labs like rheumatoid factor, and imaging. Treatment aims to reduce inflammation and joint damage through medications like NSAIDs, DMARDs, corticosteroids, and biologics. Lifestyle changes like exercise and nutrition can also help manage symptoms.

1. RHEUMATOID
ARTHRITIS
PRESENTED BY
ANJALI RARICHAN
M.PHARM
1ST YEAR

2. CONTENTS
DEFINITION
OVERVIEW
ETIOLOGY
PATHOPHYSIOLOGY
CLINICAL FEATURES
DIAGNOSIS
TREATMENT
ALGORITHM

3. DEFINITION
 Rheumatoid arthritis (RA) is a chronic
and usually progressive inflammatory
disorder of unknown etiology
characterized by polyarticular
symmetrical joint involvement and
systemic manifestations.

4.  Rheumatoid arthritis (RA) is a chronic,
systemic autoimmune disease that
involves inflammation in the membrane
lining of the joints and often affects
internal organs. Most patients exhibit a
chronic fluctuating course of disease
that can result in progressive joint
destruction, deformity, and disability. RA
affects between 1 and 2 million
Americans. It occurs three times more
often in women, and peaks at age 35 to
50 years.

5. Rheumatoid arthritis is a chronic
disease, characterized by periods of
disease flares and remissions.
The cause of rheumatoid arthritis
is not known.
In rheumatoid arthritis, multiple
joints are usually, but not always,
affected in a symmetrical pattern.
Rheumatoid arthritis can affect
people of all ages.
Damage to joints can occur early
and does not correlate with the
severity of symptoms.
The "rheumatoid factor" is an
antibody that can be found in the
blood of 80% of people with
rheumatoid arthritis.

7. The cause of rheumatoid arthritis is unknown.. It is
believed that the tendency to develop rheumatoid
arthritis may be genetically inherited (hereditary). It is
suspected that certain infections or factors in the
environment might trigger the immune system to
attack the body's own tissues; resulting in
inflammation in various organs of the body such as the
lungs or eyes.
Environmental factors also seem to play some role in
causing rheumatoid arthritis. For example, scientists
have reported that smoking tobacco increases the risk
of developing rheumatoid arthritis.
ETIOLOGY

8.  The cause of RA is not fully understood
but appears to be multifactorial.
 It is considered an autoimmune disease
in which the body loses its ability to
distinguish between synovial and
foreign tissue. Other factors involved in
RA are as follows:
 1. Environmental influences, such as
infections or trauma, are thought to
trigger the development of RA.

9. 2. Genetic markers, such as human leukocyte
antigen DR4 (HLA-DR4), have been associated with
triggering the inflammatory process in RA. Such
markers, however, are not considered diagnostic
because 30% of people with HLA-DR4 never
develop RA.
3. Antigen-dependent activation of T lymphocytes
leads to proliferation of the synovial lining,
activation of proinflammatory cells from the bone
marrow, cytokine and protease secretion, and
autoantibody production.

10. 4. Anticitrullinated proteins and peptides are high
specific for RA.
5. Tumor necrosis factor & (TNF-&), IL-1, IL-6,
IL-8, and growth factors propagate the
inflammatory process, and agents found to alter
these cytokines show promise in reducing pain and
deformity.
6. Inflamed synovium is a hallmark of the
pathophysiology of RA. Synovium proliferates
abnormally, growing into the joint space and into the
bone, forming a pannus. The pannus migrates to
the articular cartilage and into the subchondral bone
leading to destruction of cartilage, bone,
tendons, and blood vessels.

11. Genetic and environmental factors play a part.
Gender. Women before the menopause are affected
three times more often than men. After the menopause
the frequency of onset is similar between the sexes,
suggesting an etiological role for sex hormones. The use
of the oral contraceptive pill has shown no affect on RA
overall, as previously thought, but it may delay the
onset of disease.
Familial. The disease is familial with an increased
incidence in first degree relatives and a high
concordance amongst monozygotic twins (up to 15%)
and dizygotic twins (3.5%). In occasional families it
affects several generations.

12. 12
Genetic factors are estimated to account for up to 60%
of disease susceptibility.
There is a strong association between susceptibility to RA
and certain HLA haplotypes. HLA-DR4, which occurs in
50–75% of patients, correlates with a poor prognosis, as
does HLA-DRB1. Individuals with HLA-DRB1 combined
with a positive rheumatoid factor are13 times greater
risk for developing bone erosions in early disease.

13. 13
Hands and wrists
Shoulders
Elbows
Feet
Knees
Hips
Cervical spine

15.  Chronic inflammation of the synovial tissue
lining the joint capsule results in the proliferation
of this tissue. The inflamed, proliferating
synovium characteristic of rheumatoid arthritis is
called pannus. This pannus invades the cartilage
and eventually the bone surface, producing
erosions of bone and cartilage and leading
to destruction of the joint. The factors that initiate
the inflammatory process are unknown.

16. The immune system is a complex network of checks
and balances designed to discriminate self from non-
self (foreign) tissues. It helps rid the body of
infectious agents, tumour cells, and products
associated with the breakdown of cells. In
rheumatoid arthritis, this system no longer can
differentiate self from non-self tissues and
attacks the synovial tissue and other connective
tissues.

19. Signs & Symptoms of RA
• Fatigue.
• Stiffness, especially in early morning and
after sitting a long period of time.
• Not relieved by pain
• Low Grade Fever, Weakness.
• Muscle pain and pain with prolonged sitting.
• Symmetrical, affects joints on both sides of
the body.
• Rheumatoid nodules.
• Deformity of your joints over time.
• Raynauds phenomenon.
• Pain

22.  1. Rheumatoid factor (RF) is found in
" 60% of patients with RA; however, as
many as 5% of healthy individuals will
have elevated titers of RF. If initially
negative, the test can be repeated in 6
to 12 months. RF is not an accurate
measure of disease progression.
LABORATORY ASSESSMENT

23. 2. Erythrocyte sedimentation rate (ESR) and C-
reactive protein (CRP) :
They are markers of inflammation and are usually
elevated in patients with RA. They can also help
indicate the activity of the disease, but they do not
indicate disease severity.
3. Anticyclic citrullinated peptide antibodies
(ACPA) :
These are found in most patients with RA and are
useful in predicting erosive disease.

24. Radiographic examination:
This can reveal the extent of bone
erosion and cartilage loss. An MRI can
detect proliferative pannus.

25. Rheumatoid Arthritis
 Symptom criteria
– Morning stiffness
– Arthritis of 3 or more joints
– Arthritis of hand joints
– Symmetric arthritis
– Rheumatoid nodules
– Serum rheumatoid factor
– Radiographic changes
 A person shall be said to
have rheumatoid arthritis
if he or she has satisfied
4 of 7 criteria, with
criteria 1-4 present for at
least 6 weeks

26. Diagnosis and clinical evaluation:
In 2010, EULAR (European League Against
Rheumatism) established a score-based algorithm
criteria aimed at diagnoses before joint damage
occurs. Definitive RA is defined as a score # 6/10
based on four domains:
1. Joint involvement (e.g., number and location of
involved joints)
2. Serology (e.g., RF, ACPA)
3. Acute phase reactants (e.g., CRP, ESR)
4. Duration of symptoms

28. Treatment objectives
 The goals in the management of RA are:
 1. To prevent or control joint damage
 2. To prevent loss of function
 3. To decrease pain
 4. To maintain the patient’s quality of life
 5. To avoid or minimize adverse effects of
treatment.
 6. Preservation of muscle and joint function.
 7. Return to a desirable and productive life.

29. ALGORITHM OF TREATMENT OF RA
Methotrexate Or other DMARD ± NSAID
± Prednisone within first 3 months
Poor response
Other DMARD mono Rx
(MTX if not used above)
Combo DMARD Rx Biologic DMARD
Mono or combo with DMARD
Poor response
Try other combination, triple drug (DMARD + Biologic), add low dose of
Prednisone for long term, consider second line DMARD.

30. Non pharmacological Treatment
 Diet
 Exercise
 Acupuncture
 Herbal Medicines
 Massage
 Stress Reduction Techniques –
prayer, meditation, hypnosis, yoga.

31. Nutrition
The most commonly observed vitamin and
mineral deficiencies in patients with RA
are:
o folic acid
o vitamin C
o vitamin D
o vitamin B6
o vitamin B12
o vitamin E
o calcium
o magnesium
o zinc
o selenium

32. Exercise
Being overweight strains joints and leads to further
inflammation.
4 times a week for
30 minutes
•Walking
•Light jogging
•Water aerobics
•Cycling
•Yoga
•Tai chi
•stretching

33. Medications
 There are four types of medications used
to treat RA:
– Non-steroidal anti-inflammatory drugs
(NSAIDs)
– Disease-modifying anti-rheumatic
drugs(DMARDS).
– Corticosteroids
– Biologic Response Modifiers
(“Bioligics”)
(Arthritis Foundation, 2012; Gulanick & Myers 2011)

34. Non-steroidal anti-inflammatory drugs (NSAIDs)
Examples General Use Side Effects Nursing
Considerations
Aspirin, ibuprofen,
naproxen, COX-2
inhibitors, propionic
acid, phenylacetic
acid
• anti-
inflammatory:
Used in the
management
inflammatory
conditions
•Antipyretic:
used to control
fever
•Analgesic:
Control mild to
moderate pain
•Nausea
•Vomiting
•Diarrhea
•Constipation
•Dizziness
•Drowsiness
•Edema
•Kidney failure
•Liver failure
•Prolonged
bleeding
•Ulcers
•Use cautiously in
patients with Rx
of bleeding
disorders
•Encourage pt to
avoid concurrent
use of alcohol
•NSAIDs may
decrease
response to
diuretics or
antihypertensive
therapy

35. Corticosteroids
Examples General Use Side Effects Nursing
Considerations
Cortisone,
hydrocortisone,
prednisone,
betamethasone,dex
a-methasone
• Used in the
management
inflammatory
conditions
•When
NSAIDS may
be
contraindicate
d
•Promptly
improve
symptoms of
RA
•Increased
appetite
•Weight gain
•Water/salt
retention
•Increased blood
pressure
•Thinning of skin
•Depression
•Mood swings
•Muscle
weakness
•Osteoporosis
•Delayed wound
healing
•Onset/worsenin
g of diabetes
•Take
medications as
directed (adrenal
suppression)
•Used with
caution in
diabetic patients
•Encourage diet
high in protein,
calcium,
potassium and
low in sodium
and
carbohydrates
•Discuss body
image
•Discuss risk for
infection

36. Disease-modifying anti-rheumatic drugs(DMARDS)
Examples General Use Side Effects Nursing
Considerations
Methotrexate
(the gold
standard)
, gold salts,
cyclosporine,
sulfasalazine,
azathioprine
•immunosuppressiv
e activity
•Reduce
inflammation of
rheumatoid arthritis
•Slows down joint
destruction
•Preserves joint
function
•Dizziness,
drowsiness,
headache
•Pulmonary
fibrosis
•Pneumonitis
•Anorexia
•Nausea
•Hepatotoxicity
•Stomatitis
•Infertility
•Alopecia
•Skin ulceration
•Aplastic anemia
•Thrombocytopeni
a
•Leukopenia
•Nephropathy
•fever
•photosensitivity
•May take several
weeks to months
before they
become effective
•Discuss
teratogenicity,
should be taken
off drug several
months prior to
conception
•Discuss body
image

37. Biologic Response Modifiers (“Biologics”)
Examples General Use Side Effects Nursing
Considerations
Etanercept, anakinra,
abatacipt,
adalimumab,
Infliximab
(Remicade)
• Used in the
management
inflammatory
conditions
•When
NSAIDS may
be
contraindicate
d
•Promptly
improve
symptoms of
RA
•Increased
appetite
•Weight gain
•Water/salt
retention
•Increased blood
pressure
•Thinning of skin
•Depression
•Mood swings
•Muscle
weakness
•Osteoporosis
•Delayed wound
healing
•Onset/worsening
of diabetes
•Take medications
as directed
(adrenal
suppression)
•Encourage diet
high in protein,
calcium,
potassium and
low in sodium and
carbohydrates
•Discuss body
image
•Discuss risk for
infection

39. Questions? 
?

40. • V
COMMENT ON THERAPY