ARTHRITIS

By :
Dr. Bambang SN, Sp.PD
Departement of Internal Medicine
dr. Soedarso General Hospital
Pontianak
 Would healing
Resolution of
Inflamation

COX-2 Inhibitor

Stomach Disease Targets :

Kidney Artritis
Intestine Pain
Platelet Cancer
 Fungsi Golongan Prostaglandin
Meningkatkan Proses Radang Meredam Proses Radang

Pengaturan aliran darah dan pefusi

organ
PGE, PGE2 menghambat produksi
dari macrophage migration inhibiting
factor (MIF) oleh sel-sel T
Vasodilatasi (PGE2, pGI2, pgd2,
PGII)
PGE2 menghambat proliferasi
limfosit T

Menekan proliferasi sel sinovial

Menekan pembentukan plasminogen
Meningkatkan permeabilitas vaskular
(interaksi dg Ca5, LTB4, dan
Menghambat produksi dari radikal
oksigen dan pengeluaran enzim oleh
Histamin) neutrofil,
Potensi nyeri (interaksi Bradikinin)
Mengaktifkan limfosit dan produksi
dari limfokin PGI
Agregasi trombosit. Pengeluaran PAF
dan PGI2
Desuppressor T suppressor cells dan
meningkatkan RF
Resopsi dari tulang
 Nyeri somatik
Nyeri Nosiseptif
Nyeri viseral

Nyeri
Nyeri neuropatik

Nyeri non-nosiseptif
Nyeri psikogenik
 Rangsang

Rangsang Sistem imun bawaan INFLAMASI

Dihilangkan (alami) diaktifkan AKUT

INFLAMASI
KESEMBUHAN Rangsangan tak KRONIK
dihilangkan

Rangsang Sistem imun

Dihilangkan Penyesuaian diaktifkan

Menghasilkan Amplifikasi / JARINGAN

Sel-sel pengikat Pengerasan RUSAK
spesifik
 Radang (inflamasi) dan Respons Tubuh
Alami (tak spesifik) Didapat
(Penyesuaian Spesifik)
Sel-sel Netrofil Sel B dan T
Eosinofil APC
Basofil Sel sel dendritik
Trombosit Sel sel Langerhans
Makrofag
Monosit
Sel Mast
Sel NK
Faktor-faktor Lisosom sitokin ANTIBODI
yang larut INF ANTIBODI
Komplemen IgG & subklas, Ig M
Protein fase akut Ig A, Ig E, Ig D
Limmfokin
 ARTHRITIS

JOINT PATTERN EXTRA ARTICULAR

MANIFESTATION

Inflammation How Many Joint What Joint

Redness Warmth Swelling Morning Painfull

Stiffness
 Diagnostic value of the joint pattern
Characteristic Status Representative
Disease
Inflammation Present RA, SLE, gout
Absent OA
Number of Monoarticular Gout, trauma, septic arthritis,
involved joints Lyme disease
Oligoarticular Reiters disease, psoriatic
(2-4 joints) arthritis, IBS
Polyarticular RA, SLE
( 5 joint)
Site of Joint Distal Interphalangeal OA, psoriatic arthritis (not RA)
involvement
Metacarpophalangeal, RA, SLE (not OA)
wirsts
First metatarso Gout, OA
phalangeal
 OSTEOARTHRITIS
(Degenerative Joint Disease)

Essensial of Diagnosis
Commonly secondary to other articular disease
Degenerative disorder without systemic manifestations
Pain relieve by rest
Morning stiffnes : brief
Articular inflammation : minimal
NORMAL versus. SENDI OA
Lutut normal Lutut OA

Kapsul menebal
Kapsul
Pembentukan kista
Rawan sendi Sklerosis
Tulang subkhondral
Sinovium
Fibrilasi rawan sendi

Tulang Hipertrofi sinovium

Pembentukan osteofit

ACRFP
Hereditary and mechanical factors may be
involved in the pathogenesis

Arthropathy is characterized :
Degeneration of cartilago
Hypertrophy of bone at the artricular margin
Minimal inflammation
Clinical Findings :
The oncet is insidious
Articular stiffness < 15 minutes
Pain in motion
- Worse by activity / weight bearing
- relieved by rest
Deformity maybe absent or minimal
Bony enlargement of the interphallangeal occasionaly
prominent
Limitation of motion of affected joint is common
Joint effusion and other articular signs of inflammation
are mild
No systemic manifestation
Laboratory Findings :
Elevated sedimentation rate and other laboratory signs of
inflammation are not present.

Imaging :
Radiographs may reveal :
Narrowing of the joint space
Sharpened articular margin
Osteophyte formation
Lipping of marginal bone
Thickened, dense subchondral bones
Bone cysts may also be present
Treatment
A. Weight Loss can improve the symptoms
B. Analgesic and Antiinflammatory Drugs
- Acetaminophen
- Glucosamine
- Chondroitin sulphate
- NSAID
- Intraarticular Injection of Sodium
Hyaluronate or triamcinolone
- Capsaisin cream
- Diacerein
C. Surgical
Prognosis
Marked disability is less common than in
rheumatoid arthritis, but symptoms may be
quite severe and limit activity considerably
(especially with involvement of the hips,
knees, and cervical spine).
 Gouty Arthritis
(Crystal Deposition Arthritis)
Essentials Of Diagnosis
Acute onset, typically nocturnal and usually
monoarticular, often involving the first
metatarsophalangeal joint
Postinflammatory desquamation and pruritus
Hyperuricemia in most; identification of urate
crystals in joint fluid or tophi is diagnostic
Dramatic therapeutic response to NSAID or
colchicine
With chronicity, urate deposits in subcutaneous
tissue, bone, cartilage, joint, and other tissues
 Origin of hyperuricemia

Primary hyperuricemia
A. Increased production of purine :
1. Idiopathic
2. Specific enzyme defects (eg, Lesch-
Nyhan syndrome, glycogen storage
diseases)
B. Decreased renal clearence of uric acid (idiopathic)
Secondary hyperuricemia
A. Increase catabolism and turnover of purine :
1. Myeloproliferative disolders
2. Lymphoproliferative disolders
3. Carcinoma and sarcoma (disseminated)
4. Chronic hemolytic anemias
5. Cytotoxic drugs
6. Psoriasis
B. Decreased renal clearence of uric acid :
1. Intrinsic kidney disease
2. Functional impairment of tubular transport :
a. Drug-induced (eg, thiazides, probenecid)
b. Hyperacticacidemia (eg, lactic acidosis,
alcoholism)
c. Hyperketoacidemia (eg, diabetic ketoacidosis,
starvation).
d. Diabete insipidus (vasopressin-resistant)
e. Bartters syndrome
Clinical Findings :
Acute arthritis is characterized by sudden, nocturnal,
either without aparrent precipitating cause or following
rapid fluctutation in serum urate levels, from alcohol
excess or medication changes
Metatarsophalangeal joint of the great toe is the most
susceptible joint (podagra)
Feet, ankles, knees, are commonly affected
Hips and shoulders are rarely affected
Gouty attacks may develop in periarticular soft tissues
The involved joint are swollen and exquisitely tender and
overlying skin tense, warm, and dusky red
Fever is common and may reach 39oC
Tophi may be found in the external ears, hands, feet,
olecranon, and prepatellar bursas
Laboratory Findings :
Serum uric acid is elevated (> 7.5 mg/dL) in 95% cases
During an acute attack, the erythrocyte sedimentation
rate and white cell count are frequently elevated
Material aspirated from a tophus shows the typical
crystals of sodium urate

Imaging
Early in the disease, radiographs show no changes. Later,
punched-out erosions with an overhanging rim of cortical
bone (rat bite) develop. When these are adjacent to a
soft tissue tophus, they are diagnostic of gout.
Treatment :
1. NSAID
2. Colchicine
3. Corticosteroids
4. Analgesics, at times the pain of an acute attack may
require opioids
5. Bed rest, is important is the management of the acute
attack and should be continued for about 24 hours
Management Between Attacks
1. Diet (low : purine, alcohol)
2. Weight Loss
3. Avoidance of hyperuricemic medications (thiazide,
furosemide, aspirin)
4. Colchicine
5. Rednetion of serum uric acid
to maintain below 6mg/dL
uricosuric drugs
- Probenecid
- sulfin pyrazone
Allopurinol, a xanthine oxidase inhibitor

Prognosis
Without treatment, the acute attack may last from a few days to
several days
The younger of the onset, the greater the tendency to a
progressive course
Destructive arthropathy is rarely seen in patient whose first attack
is after age 50
Must be thought to have an increased incidence of hypertension,
Renal disease (eg, nephrosclerosis, interestitial nephritis,
pyelonephritis), dibetes melitus : hypertriglyceridemia and
atherosclerosis
 RHEUMATOID ARTHRITIS
(Auto immune Desease)
ESSENSIALS OF DIAGNOSIS
Prodromal systemic symptoms are malaise, fever,
weight loss and morning stiffness
Onset usually ansidious and small joints
Progression is centripetal and symmetric deformities
common
Radiographic findings : Juxtaartticular osteoporosis, joint
erosions, and narrowing joint spaces
Rhematoid factor usually present
Extra articular manifestation : subcutaneous nodules,
pleural effusion, pericarditis, lymphadenopathy,
splenomegali with leukopenia, and vasculitis
CLINICAL FINDING :
Clinical manifestation are highly variable
Onset of articular signs of inflammation is
usually insidious
Prodromal symptoms : malise, weight loss,
vague periarticular pain or stiffness
The trigger of acute onset by infection,
surgery : trauma, emotional strain or post
partum period
There is characteristically symmetric joint
swelling with associated stiffness, warmth,
tenderness and pain
 Stiffness persisting for over 30 minutes is
prominent in the morning & subsides during the
day
Any joint may be affected, the proximal
interphalangeal & Metacarpophalangeal joints of
the fingers as well as the wrists, knees, ankles
and toes are most often involved
Monoarticular is occasionally seen early
Synovial cysts and rupture of tendons may occur
Palmar erythema is noted occasionaly, as are
tiny hemorragic
Infarct in the nail folds or finger pulps, which are
signs of vasculitis
LABORATORY FINDINGS
Abnormal serum protein : rheumatoid factor,
antinuclear antibody
Esr elevated
Gamma globulins elevated
Hypochromic normocytic anemia
White cell count is normal or slightly elevated
Leukopeni may occur
IMAGING
The first 6 months normal
Soft tissue swelling and juxta articular
demineralization
Later : joint space narrowing, errosions
TREATMENT
A. Non Pharmacologic
1. Education & emotional factors
2. Physical & occupational therapy
3. Weight Loss
B. NSAID
C. Additional Drugs
- Methotrexate - TNF inhibitor
- Anti malarials - Corticosteroids
- Sulfazalazine - Leflunomide
- Azathioprine - Minocycline
- Gold Salts and Penicellinamine
D. Surgical Measures
PROGNOSIS
Patiens whose persist beyond 2 years,
the outcome is not so favorable
- can die, on average 10-15 years earlier,
than normal people
most common causes of death are
infection, heart disease, respiratory failure,
renal failure, & gastro intestinal disorder