RHEUMATOID

ARTHRITIS
GROUP 2
Bagares, Jared
Bonifacio, Dayanara A.
Delos Santos, Techie E.
Gutierrez, Yvette
Inguito, Ella
Jagolino, Rhein A.
Ramirez, Alyssa N.

DEFINITION OF TERMS:
Arthritis any disorder that affects
joints, it can cause pain and inflammation
Articular Cartilage tough slippery
covering on the ends of the bone which
allows smooth joint movements
Ankylosis fusion or growing together
of bones in the joint

DEFINITION OF TERMS:
Cytokines substances secreted by
certain cells of the immune system and
have an effect on other cells
Pannus an inflammatory exudate
overlying synovial cells on the inside of a
joint capsule, usually occurring in
rheumatoid arthritis or related articular
rheumatism

DEFINITION OF TERMS:
Synovial Membrane surrounds
moveable joints
Synovial Fluid lubricates and
nourishes joint tissue such as cartilage

EPIDEMIOLOGY
1% of population worldwide with females
being 2-3 times more common

increase with age in both sexes; nearly 5%

of women and 3% of men over the age of 65
years

peak age: 30-50 years (women) & slightly

older (men)

also affects young children -- classification

and treatment differs slightly from adults

JOINT

Immoveable
Joints

Slightly
moveable
joints

Freely
moveable
joints

FEATURES
OF JOINTS
Flexibility
Precision of
movement
Supports weight

RHEUMATO
ID
ARTHRITIS
2nd most
common type
of arthritis

RHEUMATOID
ARTHRITIS
Autoimmu
ne
response

PATHOPHYSIOLOGY

PATHOPHYSIOLOGY

CLINICAL MANIFESTATIONS
Disease onset is usually insidious with the
predominant symptom being pain, stiffness
and swelling. Typically, the
metacarpophalangeal and proximal
interphalangeal joints of the thumbs, the wrists,
and metatarsophalangeal joints of the toes are
affected during early stages of the disease.

Remission has been reported in a small

proportion of patients but usually is very rare
without disease-modifying anti-rheumatic drugs

DIAGNOSIS
A clinical diagnosis is made based on the
patients history, family history, presenting
symptoms and clinical findings.
Investigations which includes blood tests,
ultrasound for the presence of synovitis
and X-rays are also useful.
X-rays are used to demonstrate joint
destruction which indicates a late
manifestation of the disease.

THE AMERICAN RHEUMATISM

ASSOCIATION
o design for the disease classification in
patient with established disease and are
not sensitive for patients in early stages
of rheumatoid arthritis
*refer to Box 53.2 page 833

THE DISEASE ACTIVITY SCORE

(DAS28) AND AMERICAN
COLLEGE OF RHEUMATOLOGY

to assess disease activity and to

monitor the patients response to
treatment

*refer to Boxes 53.3 and 53.4

Inflammatory markers:
erythrocyte sedimentation rate
(ESR)
C-reactive protein (CRP)
Usually but not always elevated in active
disease
Useful for monitoring response to treatment
Blood tests may be used to detect
rheumatoid factor, which is an antibody
produced by a reaction in your immune system.

Anti-cyclic citrullinated peptide

antibodies (anti-CCP antibody)
Useful for early detection of
rheumatoid arthritis in a patient with
inflammatory arthritis
Antinuclear antibodies (ANA) and
extractable nuclear antigens (ENA)
Useful for establishing the differential
diagnosis such as other connective tissue
diseases

TREATMENT FOR
RHEUMATOID
ARTHRITIS

PRIMARY GOALS:
Symptom

relief

including

pain

control

Slowing

or

prevention

of

joint

damage

Preserving and improving functional

Four Main Categories of Drugs:

Non-Steroidal
Anti-Inflammatory
Drugs (NSAIDs)

Disease

Modifying Anti-Rheumatic

Drugs (DMARDs)

Glucocorticoids
Biological Therapies

Non-Steroidal Anti-Inflammatory
Drugs
(NSAIDs)

Used to reduce joint pain and swelling

Provide symptomatic treatment only

must be

used in combination with other agents

Non-selective
Voltaren),
(Flanax)

COX-2

NSAIDs: Diclofenac (Cataflam,

Ibuprofen (Advil), and Naproxen

inhibitors:
Etoricoxib (Arcoxia)

Celecoxib

(Celebrex)

and

Non-Steroidal Anti-Inflammatory
Drugs
(NSAIDs)

Rofecoxib (Vioxx)
COX-2 inhibitor
Withdrawn from

the market due to the high risk

of thrombotic events

All

patients taking a non-selective NSAID or COX-2

inhibitor should receive concomitant treatment
with a PPI to minimize GI effects.

Disease Modifying Anti-Rheumatic

Drugs
(DMARDs)
Fewer Adverse Reactions
inflammatory cytokines (TNF-,
interleukin-1,
interleukin-2,
and
interleukin-6)
Slow onset of action and Must be
taken for 8 Weeks

Disease Modifying Anti-Rheumatic

Drugs
(DMARDs)
Combination

DMARD therapy as a first-line

therapy, ideally (within 3 months)

The

combination
therapy
must
be
METHOTREXATE and at least one DMARD,
usually
Sulphasalazine
or
Hydroxychloroquine

KEY POINTS REGARDING DMARD

THERAPY:
Early (within 3 months ideally)
Use Combination DMARD involving
and at least one other DMARD

Use Monotherapy
Withdraw cautiously

methotrexate

Methotrexate
Gold standard DMARD
Folic acid antagonist: reversible
inhibitor
reductase

of

once

dihydrofolate

weekly dose via orally or

parenterally (IM or subcutaneous)

Parenteral therapy

Methotrexate
Doses

for oral and parenteral

therapy
are
similar,
Bioavailability in parenteral
route is greater
Oral folic acid reduces
adverse effects
2.5mg and 10 mg strengths

Sulphasalaz Hydroxychloroq
uine
ine
Least toxic
Slows
joint

erosion
and
suppresses
inflammatory
activity in RA
Blood
dyscrasias

Milder

cases of

RA

Symptomatic
relief only

May

be
prescribed for
pregnant
women

Leflunom
ide
2 weeks
Loading

dose

Hepato-

and

Omitted

hemato-toxicity

Gold
Intramuscular

gold

(sodium
aurothiomalate) Oral
gold (auranofin)

Proteinuria
Blood Disorders
Rashes
GI upset or Bleeding

OTHER DMARDS
D-Penicillamine:

Rashes, Taste loss and

Vomiting)

Azathioprine

and Ciclosporin: Refractory

Rheumatoid Arthritis

Glucocorticoids
Oral, intramuscular or intra-articular route
Act by inhibition of cytokine release

and giving rapid

relief of symptoms and inflammations

Prednisolone most commonly used oral steroid

steroids
(Triamcinolone
Intra-articular

and

Methylprednisolone)
Inflamed joints for local anti-inflammatory action, pain
relief and to reduce deformity

Glucocorticoids
Should be reserved for short-term
Can induce osteoporosis prophylactic
therapy with vitamin D and calcium
supplementation and biphosphanates

Gastroprotection

with H2 antagonists and

PPIs

Diabetes,

Increased Risk of Infection, HTN

and Weight gain

Biologic Therapies
Anti-TNF agents

Infliximab

Adalimumab

Etanercept

Certolizumab pegol

Golimumab

Anakinra and tocilizumab target the interleukins

Abatacept and rituximab act on the T-cells and B-cells

Treatment Algorithm:
DMARD (combination therapy where appropriate)
+
Symptom relief using glucocorticoid, NSAID or simple analgesia

Anti TNF agent

Rituximab

No specific recommendation on choice of agent if patients fails or cannot

tolerate rituximab. Available options include high dose steroids,
tocilzumab,abatapt, anakinra or alternative anti TNF agent

Non
Pharmacological
Physical Therapy
Occupational Therapy
Low impact Exercise

CASE STUDY

PATIENT DEMOGRAPHICS

Patient name: A.U.

Age: 58 y.o.
Sex: Female
Wt: 144 lb
Ht: 66

CHIEF COMPLAINT
I have pain in all my joints, a swollen
left knee and stiffness every
morning.

HISTORY OF PAST ILLNESS

A.U. presents to her rheumatologist with
generalized arthralgias, a swollen left knee,
and morning stiffness.

Symptoms have been occurring with

increasing severity for the past week.

Presented the same symptoms when she

came to the clinic 2 months ago.

PAST MEDICAL HISTORY

RA x 6 years
S/P hysterectomy 4 years ago
HTN x 10 years

FAMILY HISTORY
Father: died form complications after a traumatic fall
at age 65

Mother: died of hip fracture and pneumonia at age

78

No siblings

SOCIAL HISTORY
Housewife
No rash, nausea, vomiting or diarrhea
Decrease ROM on hands
Denies HA, chest pain, SOB, bleeding episodes or syncopal attacks
Fatigue experienced daily during afternoon hours
Denies loss of appetite or weight loss
Reports minor visual changes corrected with stronger prescription glasses

ALLERGIES
Penicillin (rash 25 years ago)

MEDICATIONS
HCTZ 25mg po qam
Norvasc 10mg po qd
Relafen 750mg 2tabs qhs
Prednisone 5mg tab po qam
Patient receives medications at a local community pharmacy.
Medication profile indicates that she refills her medications on time.

PHYSICAL EXAMINATION
GEN: pleasant middle aged Caucasian women in moderate distress
due to pain and swelling in knee

VS: no rashes, normal turgor, no break down or ulcers

HEENT: atraumatic, moon facies, PERRLA, EOMI, A-V nicking visible
bilaterally, pale conjunctiva bilaterally, TMS intact, xerostomia

NECK or LN: supple, no JVD or Thyromegaly, no bruits, palpable

lymph nodes

CHEST: CTA
CV: RRR, normal S1, S2: no m/r/g

MS/EXT:

HANDS

ELBOWS
SHOULDERS
HIPS
KNEES
FEET
NEURO

Mild RA changes, swelling 3,4,5 PIP joints

bilaterally, pain 3,4 MCP joints on L, Boutonierre
deformity 3,4 bilaterally, ulnar deviation
bilaterally, decreased grisp streght , L>R(patient is
left handeed)
WRIST: good ROM

Good ROM, slight permanent contracture on

R, fixed nodule at pressure point
Decreased ROM(especially abduction)
bilaterally
Decreased ROM on R, Atrophy of quadriceps,
L>R
Pain bilaterally, decreased ROM on L,
effusion/edema on L
No edema, full plantar flexion and
dorsiflexion: 3+ pedal pulses
CN ii-Xii grossly intact, muscle streght 5/5 UE,
4/5 LE, DTRs 2/4 biceps & triceps 1/4 patella

LABORATORY RESULTS
Na

135 mE/qL

Plts

356 x 103/mm3

4.1 mE/qL

Ca

9.1 md/dL

Cl

101 mE/qL

Urate

5.1 mg/dL

CO2

22 mE/qL

T. chol.

219 md/dL

BUN

12 mg/dL

CK

<20 IU/L

SCr

0.8 mg/dL

ANA

NEGATIVE

Glu

103 mg/dL

Wes ESR

47 mm/hr

Hgb

10g/dL

RF positive

1:1280

Hct

31%

TSH

0.74 IU/mL

WBC

13.5 x 103/mm3

SOAP

SUBJECTIVE
Patient verbalized, I have pain in all my
joints, swollen left knee and stiffness every
morning.

OBJECTIVE
Data

Lab result
(pt.)

Normal value

Hgb

10.0g/dl

12.1-15.1g/dl

Hct

31%

36.1-44.3%

13.5 x
103/mm3

4-10 x
103/mm3

Vital signs
BP

138/80mmHg

PR

82bpm

RR

14bpm

Temp

98.8F/ 37.11C

History revealed generalized

anthralgia, swollen left knee
and morning stiffness with
increasing severity in the
past week.
Past medical history
presented RA for 6 years and
HTN for 10 years.

WBC
RF

1:1280( POSI
TIVE)

ESR

47mm/hr

ANA

NEGATIVE

0-30mm/hr

Synovial fluid: from knee, white cells

23.0x10^3mm3, turbid in
appearance.

OBJECTIVE
PATIENT A.U., 58 YR. OLD FEMALE IS SEEN TO HAVE
MODERATE DISTRESS DUE TO PAIN AND SWELLING OF
KNEE. S/S ARE AS FOLLOWS:
Visible A-V nicking, moon facies, pale bilateral conjunctiva
HAND: Swelling 3,4,5 PIP joints bilateral, pain 3,4 MIP on L, Boutonniere
deformity 3,4 ulnar deviation bilaterally, decrease strength on LE
ELBOWS: slight contracture on R
SHOULDER: decrease ROM on bilateral shoulders
HIPS: decrease ROM on R, presence atrophy on L quadriceps,
KNEES: pain bilaterally, decrease ROM on L, edema/effusion on L
NEURO-CN: cranial anomaly, muscle strength 4/5 LE, DTR 2/4 biceps &
triceps and patella

ASSESSMENT
Patient A.U., 58 yrs old Female
positive for RA, Hypertensive,
became unresponsive on current
medication use in managing RA.

PLAN
Non-Pharmacologic

PASSIVE ROM
EXERCISES

DEEP BREATHING
EXERCISES

DIVERT ATTENTION TO
DECREASE PAIN

INCREASE FLUID INTAKE

LOW CALORIE DIET
PROPER POSITIONING

Pharmacologic
Continue steroid-prednisone,
Amlodipine(Norvasc), & HCTZ
Discontinue Nabumetone
(Relafen)
Start Methotrexate 2.5mg tablet
Start Folic acid (Folart) 5mg
tablet

PDAA
R

PROBLEM
DRUG-DRUG INTERACTION

DATA
HYDROCHLOROTHIAZIDE + FOLIC
ACID

ASSESSMEN
T
Hydrochlorothiazide decreases level of folic
acid by increasing renal clearance. Minor or
not significant interaction.

ACTION
Take each with 2-3 hours interval

PROBLEM
DRUG-DRUG INTERACTION

DATA
METHOTREXATE + FOLIC
ACID

ASSESSMEN
T
Folic acid decreases the effects of
methotrexate by pharmacodynamic
antagonism. Minor or non-significant
interaction. Vitamin preparation containing
folic acid or its derivatives may decrease
responses to systemically administered
methotrexate

ACTION
Not administered on the same days as
methotrexate

PROBLEM
DRUG-DRUG INTERACTION

DATA
PREDNISONE +
HYDROCHLOROTHIAZIDE

ASSESSMEN
T
Pharmacodynamic synergism. Risk of
hypokalemia, especially with strong
glucocorticoid activity.

ACTION
Monitor potassium levels

PROBLEM
DRUG-DRUG INTERACTION

DATA
PREDNISONE +
AMLODIPINE

ASSESSMEN
T
Prednisone will decrease the level or effect
of amlodipine by affecting
hepatic/intestinal enzyme CYP3A4
metabolism. Minor or non-significant.

ACTION
Take each with 2-3 hours interval

Answers to
Questions

1. WHAT NON-PHARMACOLOGICAL MODALITIES

MAY BE BENEFICIAL TO THIS PATIENT?

Passive ROM exercises

Deep breathing exercise, divert attention to
decrease pain

Increase fluid intake, low calorie and carbohydrate

intake

Proper positioning

2. WHAT PHARMACOLOGICAL
ALTERNATIVES ARE AVAILABLE FOR THE
TREATMENT OF RA?
Anti-TNF Agents
DMARDs

Infliximab

1L Inhibitors T&B cells Inhibitors

Anakinra

Abatacept

Sulphasalazine

Adalimumab

Tocilizumab
Hydrochloroquine

Certolizumab
Etanercept

Rituximab
Leflunomide
Gold

3. WHAT DRUG, DOSAGE FORM, DOSE,

SCHEDULE AND DURATION OF THERAPY
ARE BEST FOR THIS PATIENT?

Methotrexate (Zexate) 2.5mg tablet once

daily

Amlodipine (Norvasc) 10mg tablet daily

Prednisone 5mg tablet every morning
Folic acid (Folart) 5mg tab every other day

END
OF
PRESENTAT
ION