Ra Oa

Rheumatoid
Arthritis
Anisyah Achmad, S.Si., Apt., Sp.FRS

Department of Clinical Pharmacy, Major of Pharmacy
FKIK - UNSOED
Rheumatoid arthritis (RA) is an

autoimmune disease that causes
chronic inflammation of the joints
patients may experience long
periods without symptoms
the disease can also cause

inflammation and injury in other
organs in the body
The prevalence of rheumatoid arthritis in most

Caucasian populations approaches 1% among
adults 18 and over and increases with age,
approaching 2% and 5% in men and women,
respectively, by age 65
The incidence also increases with age, peaking
between the 4th and 6th decades
The annual incidence for all adults has been
estimated at 67 per 100,000
Both prevalence and incidence are 2-3 times

greater in women than in men
African Americans and native Japanese and
Chinese have a lower prevalence than
Caucasians
Several North American Native tribes have a
high prevalence
Genetic factors have an important role in the
susceptibility to rheumatoid arthritis
Rheumatoid arthritis is an autoimmune disease

in which the normal immune response is
directed against an individual's own tissue,
including the joints, tendons, and bones,
resulting in inflammation and destruction of
these tissues
The cause of rheumatoid arthritis is not known
Investigating possibilities of a foreign
antigen, such as a virus
Description
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
Morning stiffness*
Arthritis of 3 joint areas*
Arthritis of hands*
Symmetric arthritis*
Sero +ve
Radiological changes
* for greater than 6 weeks
Complications include:
Carpal tunnel syndrome, Bakers
cyst, vasculitis, subcutaneous
nodules, Sjgrens syndrome,
peripheral neuropathy, cardiac and
pulmonary involvement, Feltys
syndrome, and anemia
Medications
NSAIDS - Usually, only one such NSAID should
be given at a time. Can be titrated every two weeks

until max dosage or response is obtained. Should
try for at least 2 to 3 wk before assuming
inefficacy.
Slow acting - Generally, if pain and swelling
persist after 2 to 4 mo of disease despite treatment
with aspirin or other NSAIDs, can add a slowacting or potentially disease-modifying drug (eg,
gold, hydroxychloroquine, sulfasalazine,
penicillamine) Methotrexate, an
immunosuppressive drug is now increasingly also
used very early as one of the second-line
potentially disease-modifying drugs.
Corticosteroids offer the most effective short-term

relief as an anti-inflammatory drugs. Long-term
though improvement diminishes. Corticosteroids do
not predictably prevent the progression of joint
destruction, although a recent report suggested that
they may slow erosions. Severe rebound follows the
withdrawal of corticosteroids in active disease.
Immunosuppressive drugs These drugs (eg,
methotrexate, azathioprine, cyclosporine) are
increasingly used in management of severe, active RA.
They can suppress inflammation and may allow
reduction of corticosteroid doses. Major side effects can
occur, including liver disease, pneumonitis, bone
marrow suppression, and, after long-term use of
azathioprine, malignancy.
Symptom relief
Some slowing of radiological progression
Prednisolone > 10mg/d is rarely indicated
Avoid using without a DMARD
Use to bridge effective DMARD therapy
Minimise duration and dose
Always consider osteoporosis prophylaxis
Oral 7.5mg - ^ by 2.5mg every 6w to max 25mg. ONCE

WEEKLY (allows liver to recover)
Is an anti-metabolite, cytotoxic drug, which inhibs
DNA synthesis & cellular replication
Lower dose in elderly & renal impairment as its renally
excreted
Folic acid (3d after methotrexate) thought to decrease
toxicity
Avoid cotrimoxazole, trimethoprim, XS ETOH, live
vaccines
Give annual flu jab
Can be given subcut if oral absorption poor
SEs: oral ulcers, nausea, hepatotoxicity, bone

marrow suppression, pneumonitis
All respond to dose reduction except
pneumonitis
Stop 3/12 before pregnancy remember males
Pre-Rx: FBC, U+E, LFT, CXR, Pt education
Monitoring:
every 2/52 for 1st 2/12.

then every 1/12
Withhold and d/w rheumatologist if;

WBC < 4
Neuts <2
Plts< 150
> x2 ^ AST, ALT
Unexplained low albumin
Rash or oral ulcers
New or ^ing dyspnoea
Ix if MCV > 105 (B12/ Folate)
Deterioration in renal func decease dose
Abnormal bruising or sore throat stop and check FBC
500mg/day - ^ by 500mg weekly to 2-3g/d

Pre-Rx: FBC, LFT, U+E
Monitor:
FBC, LFT every 2/52 for 8/52
then 1/12 for 10/12
Then every 3/12 after 1ys treatment
Stop and d/w rheumatologist as indicated

before
Headaches, dizziness, nausea decrease dose
Least toxic
Is an anti-malarial
Yearly optician review retinal toxicity
200-400mg/d
Often used in combo with other DMARDs
Check U+E prior to starting
Avoid in eye related maculopathy, diabetes or
other significant eye disease
Consider stopping after 5 years
Yearly bloods
100mg for 3 days, then 20mg/d, can decrease

to 10mg/d
2nd line treatment. Is a new drug.
Should not be used with other DMARDs
May inhibit metab of warfarin, phenytoin,
tolbutamide
Long elimination half life so may react with
other DMARDs even after stopping it
Must not procreate within 2y of stopping. Do
serum levels.
SEs: blood dyscrasias, hepatotoxicity, mouth

ulcers, skin rash (inc stevens-johnson & toxic
epidermal necrolysis), mild ^BP, GI upset, wt
loss, headaches, dizziness, tenosynovitis, hair
loss.
If severe SEs elim with cholestyramine 8g or
activated charcoal
Pre-Rx: FBC, U+E, LFT, BP
Monitor: FBC, LFT, U+E, BP
Every 2/52 for 6/12
Then every 8/52
1mg/kg/d - ^ after 4-6/52 to 2-3mg/kg/d

Immunosuppressant, antiproliferative, inhibits DNA
synthesis
Lower dose in hepatic or renal impairment
If on allopurinol cut dose by 25%
Avoid live vaccines
Give pneumovax and flu jab
Passive immunisation for varicella zoster in nonimmune pts if exposed to chicken pox or shingles
Pre-Rx: FBC, U+E, LFT
Monitor:
Every 2/52 for 2/12 & after every dose change

Then every 1/12
10mg im test dose (done in clinic) then 20mg,

then weekly 50mg to dose of 1g then reassess
Pre-Rx: FBC, U+E, LFT, urinalysis
Monitor:
FBC and urinalysis at each injection

Results to be available at next dose
Each time ask about oral ulcers & rashes
Withhold as above
Is an immunosuppressant
2.5mg/kg/d in 2 divided doses. ^ after 4/52
by 25mg to max 4mg/kg/d
Avoid in renal impairment or uncontrolled BP
Numerous drug interactions -> BNF
Need to dose of diclofenac
Avoid colchine & nifedipine
Use k-sparing diuretics with care
Avoid grapefruit juice & live vaccines
Pre-Rx: FBC, U+E X2, LFT, lipids, BP X2, 24 hour

creatinine clearance
Monitor: FBC, LFT, ESR, BP
2/52 till on stable dose for 3/12
Then 1/12
LFTs every 1/12 until on stable dose for 3/12 then
every 3/12
Serum lipids every 6/12 1 year
Withhold and d/w rheumatologist;
^ by 30% of baseline creat
Anormal bruising
^K
^BP
^lipids
Plts < 150
>X2 ^ of AST, ALT, ALP
Use for highly active RhA in adults who have failed at

least 2 DMARDs, including methotrexate
Etanercept 25mg subcut twice a week
Infliximab 3-10mg/kg iv every 4-8 weeks
Adalimumab 40mg subcut alternate weeks
Rapid onset (days to weeks)
Disadvantages: cost & unknown long term effects,
infections, demyelinating syndromes
Should be given with methotrexate
High risk atypical infections low threshold for abx
prophylaxis
Not commonly used yet!

Anakinra 100mg/d subcut
In combo with methotrexate
Slower onset than anti-TNF
SE; injection site reactions, pneumonia (esp in
elderly with asthma)
Surgery: video
Removal of inflamed
synovium
Arthroplasty
Physical therapy
Hello
friend.
Most common rheumatic disease and

is characterized by progressive
loss of cartilagreactive changes at
the margins of the joint and in the
subchondral bonee and
The disease usually begins in ones
40s
Prevalence increases with age and the
disease becomes almost universal
in individuals aged 65 and older
Primarily affects weight-bearing
joints such as the knees, hips, and
lumbrosacral spine
The pathology reflects the result

of and response to joint failure,
with loss and erosion of
articular cartilage, subchondral
bone alterations, meniscal
degeneration, a synovial
inflammatory response, and
bone and cartilage growth
(osteophytes).
reported that OA cartilage produces

inflammatory mediators such as nitric
oxide, prostaglandin E2 and other pro
inflammatory cytokines locally which
leads to joint deterioration
Cause is unclear
Considered to be a wear and tear arthritis
and is thought to occur as a consequence of
some earlier damage or overuse of the joint
Obesity is frequently associated with it
Genetic factors play a role in the development
that is sex-influenced and dominant in females,
resulting in an incidence 10 times greater than
in men
The final outcome is full-thickness loss of
cartilage down to bone
In early disease, pain occurs

only after joint use and is
relieved by rest
As the disease progresses,

pain occurs with minimal
motion or even at rest
Nocturnal pain is commonly
associated with severe
disease
Limited use of the involved joint

Walking and transfer activities may be
impaired
Generally, ADLs will not be significantly
impaired
Medications
Early PT/exercises
Heat/cold therapy
Joint protection
Surgery
Osteoarthritis is a slowly progressive disease
The eventual outcome is complete destruction
of the joint, and ultimately surgical
intervention is required
Can continue in present job unless it requires

dexterous or heavy use of the involved joint
Heavy lifting should be avoided
Light to medium work should be possible
Climbing, balancing skills, stooping, and
kneeling may be impaired
Returning to work after surgery requires
intensive postop rehab and continued exercise
to maintain muscle strength
Most individuals are able to sustain gainful
employment and a normal level of activity

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Rheumatoid

Anisyah Achmad, S.Si., Apt., Sp.FRS

Rheumatoid arthritis (RA) is an

the disease can also cause

The prevalence of rheumatoid arthritis in most

Both prevalence and incidence are 2-3 times

Rheumatoid arthritis is an autoimmune disease

A person shall be said to

be given at a time. Can be titrated every two weeks

Corticosteroids offer the most effective short-term

Oral 7.5mg - ^ by 2.5mg every 6w to max 25mg. ONCE

SEs: oral ulcers, nausea, hepatotoxicity, bone

every 2/52 for 1st 2/12.

Withhold and d/w rheumatologist if;

500mg/day - ^ by 500mg weekly to 2-3g/d

Stop and d/w rheumatologist as indicated

100mg for 3 days, then 20mg/d, can decrease

SEs: blood dyscrasias, hepatotoxicity, mouth

1mg/kg/d - ^ after 4-6/52 to 2-3mg/kg/d

Every 2/52 for 2/12 & after every dose change

10mg im test dose (done in clinic) then 20mg,

FBC and urinalysis at each injection

Pre-Rx: FBC, U+E X2, LFT, lipids, BP X2, 24 hour

Use for highly active RhA in adults who have failed at

Not commonly used yet!

Most common rheumatic disease and

The pathology reflects the result

reported that OA cartilage produces

In early disease, pain occurs

As the disease progresses,

Limited use of the involved joint

Can continue in present job unless it requires

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