Escolar Documentos
Profissional Documentos
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• Determine of Etiopathogenesis
• List of clinical symptoms
• Proposed supporting examination
• Make of List of diagnosis criteria
• Performe management
• DEFINITION OF SLE
– Systemic Lupus Erytemathosus (SLE) is a
chronic-progressive systemic disease
– Autoimmune disease that marked with
antibody to nuclear cell
• Epidemiology
– Mostly in female ( female : male = 9 : 1),
occurred in all age especially on 2nd – 4th
decade (reproductive period).
– Affect all race.
There is familial tendency
ETIOLOGY OF SLE
• Etiology of SLE still unknown
approximately interaction of genetic, environment, hormonal
and social factors.
– Genetic
approximately on HLA-DR2 or DR3,
there were C2, C3, and C4 complement deficiency
– Environment
approximately slow viral possible retroviral as a trigger
– Hormonal
Disorder of estrogen metabolism and hyperprolactinemia
– Other factors
Sun exposure (ultraviolet), drugs, stress, nutritional
imbalance and smoking, etc.
SLE Pathogenesis
Etiology
Genetic Virus ?
Factor
B Lym- T
T Helper phocyte Supressor
Antibody to DNA
•Nucleoprotein Immune
•Histon complex in
•Nuclear Ribonucleoprotein
•Others from nuclear whole organs
Clinical point of SLE
• Autoimmune and systemic
disease
• Systemic disorder (extra articular) :
dominants
• Articular disorder : rarely
Clinical symptoms
• Great a many variations,
there is no specific abnormality
• First stage usually unknown,
manifestation is not simultaneously
• Caustitutional symptoms:
– Febrile
– Anorexia
– Weakness or decreased body weight
Clinical Symptoms
• Skin:
– Facial Erythema (“butterfly rash”)
– Dermatitis caused by sensitive of sunshine
(photosensitive)
– Bulosa lesion.
– Annular and papulosquamouse lesion on
subacute condition
– Chronic condition: Discoid with central
atrophy, depigmentation or alopecia with or
without scar tissue (hair lupus)
– Ulcer could occurred on finger
– Raynaud complaint caused by
“acroscllerosis”.
Clinical symtoms :
• skin (cont) :
– Purpura or echymosis can occurred caused
by its’ disease or side effect of corticosteroid
– In mucous can occurred ulcer on pallatum or
perforation of septum nasalis
– Skin vasculitis can cause ulceration small to
big formed
– Bleeding and periungual erythema, livido
reticularis are mild vasculitis form which very
usual found
• Joints:
– Arthralgia, arthritis, rarely to make deformity or
myositis
– The most involved joint that affect are
interphalangeal joint, knee, wrist,
metacarpophalangeal, interphalangeal proximal
Cardiovascular :
Pericarditis
Coronary heart diseases due to artherosclerosis
Verucosa endocarditis.
• NSAID
• Corticosteroid
the very important drugs,
not all SLE need corticosteroid
• Antimalaria
• Other Immunosuppressants
Indication for Corticosteroid :
Autoimunne Process
humoral immunity (FR)
seluler immunity
mediator of inflammation
sitocynes
SYNOVITIS
Pathogenesis
• Autoimmune process,
• Viral infection is suspected as a
precipitating factor malfunction of T
Lymphosit producing abnormal Ab
against the body itself (nuclear).
• immuneComplex in circulation is
suspected causing local and systemic
pathological abnormalities.
Trimolecular complex
(HLA molc.,peptide Ag, T cell receptor)
APC
CD4 T cell
The inflammation products on RA after trimolecdular
complex (TMC)
Keadaan
Awal
TNF-a IL-2
IL-1 IFN-g
Regulasi IL-6 TNF-b
IL-8 IL-4
IL-10 INOS
Inflamasi /
TGF-b
Kerusakan Sendi
Sel B Synoviocyte Aktivasi Adhesion
Aktivasi Komplemen
• Radiology
– Early stadium : normal
– Soft tissue sweling
– Periartikular osteopenia
– Marginal erosion
• Astroscopy
– See directly macroscopis
– Biopsy – PA
RA Diagosis
CRITERIA OF RA
1. Morning Stiffeness of the hand joints 1 jam
2. Arthritis 3 joint
3. Arthritis joint of the hands
4. Symetrical Artritis
5. Rhuematoid Nodule
6. Rheumatoid Factor positive
7. Typical imaging picture
Artritis Rematoid: 4 criteria above;
criteria 1-4 6 weeks
RA PROGRESSION
Management of RA
• Goals :
– Education & Motivation
– Reducing inflammation
– Keeping joint function
– Correcting joint damage
– By :
• Education
• Physical treatment
• Medication treatment
• Surgery
• Others : alternatif
• Do by team (Ruematologist/Internist, Ortopedist,
Fisioterapist, Psikiater, Sosial worker and family)
Medical treatment :
• Symptomatic
– NSAID
• Cortikosteroid
– Antiinflammatory and Immunosupresant efect
– Without disease modication efect
• DMARD
(Disease Modified Anti Rheumatic Drug)
/Remitive drug
• Biologic response modifiers
– Beyond treatment
How to choose DMARD
• Traditional way (Pyramida system)
– Early step– QAINS
– 1 - 3 months no response/ more progresif
– add OR (eq klorokuin, garam emas, or sulfasalasin)
combination of Steroid oral or intra-artikuler.
• Multidrug combination: “ Step-down Bridge”
– Some OR together (Steroid oral, garam Emas,
Metrotreksat dan Klorokiun)
– Step by step stopping, begin from the most toxic OR
then OR that most mild toxicity effect (Klorokiun)
– Continou for few months or years.
• The Sawtooth Strategy
– Multidrug serial combination that given since the early
then switch to other serial combination if there is no
response therapy.
THE CHOICE OF DMARD
• Traditional way
(Pyramidal system)
• Multidrugs Combination :
“ Step-down Bridge”
• Sulfazalasin.
– Devide into 2 components in the gut, Sulfanamid (Sulfapiridin )
that has antiinflammatory effect.
– Dose Sulfazalasin 0,5 g a day and titrate 0,5 every week untill maximal
dose 2 g a day.
– If still no good response can increase 3 g a day after 3 month
– Response therapy shown in 1 - 2 months.
– If in 3 months there is no response therapy stop the medication.
– Maintance dose 1 g a day (maximal 2 g).
• Metrotrexat.
– Is an imunosupresant drug that starting wide using in RA treatment
– Unclearly therapeutic effect mechanism.
DMARD FOR RA TREATMENT
DRUGS ONSET DOSE TOXICITY