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suarjana In. Reumatoid artritis. Dalam Sudoyono AW,Setiyohadi B, Alwi I, dkk Buku Ajar Ilmu
Penyakit Dalam Edisi V. Jakarta:Interna Publishing: 2009
Patophysiology
• X-ray
– Shows
Erosion,
little
swelling or
damage in
the joint
Management
Pharmacology
• Symptom-modifying anti-rheumatic drugs (SMARDs) (in the
form of analgesics such as NSAIDs and glucocorticoids with only
Simptom)
– NSAID
– Glucocorticoids
• Disease-modifying anti-rheumatic drugs (DMARDs) (First Line,
given the first 3 months after symptoms appear)
– Methotrexate
– Leflunomide (10 mg per day for 3 days)
– Hydroxychloroquine (200-300 mg)
Gcelu, A., and Kalla, A.A., 2011, Current Diagnosis And Treatment
Strategies In Rheumatoid Arthritis, CME, August 2011, Vol.29, No.8.
management
• Biological DMARDs (Biological therapy is the
genetic technique of protein molecules that
block proinflammatory TNF-alpha and IL-1
cytokines, reduce peripheral B cells, or bind to
CD80 / 86 in T cells to prevent the co-
stimulation needed to complete T cell
activity).
• infliximab, etanercept, adalimumab, IL-1
inhibitors namely anakinra,
Gcelu, A., and Kalla, A.A., 2011, Current Diagnosis And Treatment
Strategies In Rheumatoid Arthritis, CME, August 2011, Vol.29, No.8.
Non-Pharmacological
• Quit smoking
• Perform joint replacement surgery
• Have a healthy diet
• Maintain body weight to remain ideal
• Do regular exercise
• Perform occupational therapy
• Hydrotherapy
• Provide education to patients
Gcelu, A., and Kalla, A.A., 2011, Current Diagnosis And Treatment
Strategies In Rheumatoid Arthritis, CME, August 2011, Vol.29, No.8.
Prevention
• Screening and
follow-up of
people with RA
risk factors
• Screening with
genetic factors
(expensive)
• Modification of
environmental
factors
NCBI
Rehabilitation and promotive
• Psychological support
• Education for self management
• Multidisciplinary care
CLASSIFICATION
Acute
Sub Acute
chronic
EPIDEMIOLOGY
Acute: Increases in children, adults rarely
Male: Female = 4: 1
Sub Acute: Children and adolescents
ETIOLOGY
Staphylococcus Aureus Hemolithicus (coagulation +)
90%
Haemophilus influenza (50%) => often in children <4
years
Streptococcus Hemoliticus, E. Colli, B. Aerogenus
capsulata, Penumococcus, Salmonella Tifosa,
Pseudomonas Aerogenus, Proteus Mirabilis, Brucella,
and anaerobic bacteria namely bacteroides fragilis
RISK FACTOR
Age and gender
Trauma
Location
Poor nutrition, immunity, and environment
PATHOPHYSIOLOGY
Bacteremia => Septicemia => Embolus infection into
epiphyseal in the area of long bone metaphysis =>
hyperemia and edema metaphysis area => formed pus
=> causes pressure in the bone to increase => this
disturbs circulation and thrombosis arises in bone
blood vessels = > bone necrosis.
In addition, there is an extensive process of new bone
formation in the interior of the periosteum along the
diaphysis (especially in children) => involucrum with
the sequestral tissue in it.
When pus penetrates the bone => drainage of pus
(discharge) from involucrum exits through a hole called
the cloaca or through the sinuses in the soft tissue and
skin.
CLINICAL MANIFESTATIONS
Acute:
Progressive (fast) => signs of visible inflammation, fever
(febrile), malaise, decreased appetite.
Tenderness
Joint movement disorders due to swelling of the joints
and will get worse if local spasms occur.
Sub Acute:
muscle atrophy
local pain and swelling
limp
normal temperature
Chronic:
The fluid comes out of the wound / sinus
Local fever & pain disappear
DIAGNOSIS
Anamnesis
History of trauma, fever, history of autoimmune disease
Physic Examinaion
Supporting investigation
Acute
Laboratory examination
Blood: Leukocyte increases> 30,000, ESR increases, Anti-
Staphylococcus antibody titers, Blood cultures => bacterial etiology,
CRP increases
Radiology Check
The first 10 days => radiological abnormalities cannot be seen, but
there is soft tissue swelling
> 10 days => description of bone destruction: diffuse bone
rarefaction with the formation of new bone under the elevated
periosteum.
Ultrasound => see effusion in the joint.
Sub Acute
Blood => Normal leukocytes and increased ESR
CRP => does not increase
X-ray examination => there is a 1-2 cm diameter cavity
in the metaphysical area of the tibia and femur.
Chronic
Blood => ESR and leukocytes increase, anti-
Staphylococcus antibody titers increase
Culture and sensitivity tests to determine the causative
organism and determine treatment.
Plain photos => signs of bone porosis and sclerosis,
thickening of the periosthes, elevation of periosthes,
sequestrum.
CT and MRI => see the extent of bone damage and
treatment plan.
TREATMENT
• Initial IV antibiotic should be based on result of
Gram stain of bone aspiration ,blood culture,
age associated disease.
• Initial IV antibiotic should cover S.aureus
(oxacillin,nafcillin methicillin, clindamycin)
• Possibility of methicilin –resistant staph
should be considered .
• The response to appropriate IV antibiotic
usually occur in 48 hr .
• Lack of improvement in fever and pain after
this time indicates that surgical drainage may
be necessary or an unusual pathogen may be
present .
• surgical drainage may be appropriate at
earlier time if :
1. sequestrum is present
2. disease is chronic or atypical
3. the hip joint is involved
4. Presence of spinal cord compression.
standard therapy usually consist of antibiotic
for 4-6 weeks
After initial inpatient treatment and a good
clinical response, including decreases in CRP
or ESR, consideration may be given for home
therapy with IV antibiotics or oral antibiotics,
COMPLICATIONS
Joint contractures
Amyloid disease
Pathological fracture
Local spread of infection
Decreased limb and joint function
PROGNOSIS
After getting therapy, generally acute osteomyelitis
shows satisfactory results. The prognosis for chronic
osteomyelitis is generally poor even with surgery,
abscesses can occur up to several weeks, months or
years afterwards.
REFERENCE
STANDARDS OF GENERAL DOCTORS COMPETENCE = III-
B
OSTEOARTHRITIS
DEFINITION
• Direct correlation
• Aging process
RISK FACTORS FOR PRIMARY OA
• Age
• Sex
• Obesity
• Genetics
• Trauma (daily)
SECONDARY OSTOARTHRITIS
• Trauma
• Previous joint disorders;
• Congenital hip dislocation
• Infection: Septic arthritis, Brucella, Tb
• Inflammatory: RA, AS
• Metabolic: Gout
• Hematologic: Hemophilia
• Endocrine: DM
ETIOLOGY OF OA
• Cartilage properties
• Biomechanical problem
Morphology of Primary OA
Primary Generalized OA
STRUCTURE OF JOINT CARTILAGE
• Collagen (Type 2)
• Proteoglycan
- Hyaluronic acid
- Glycoseaminoglycan
• Water
• Condrocyte
Regeneration and Degeneration
PATHOLOGY OF OA
• Fibrillation
• Eburnation
• Osteophytes
• Subcondral cysts
LABORATORY FINDINGS OF OA
• Osteophytes
• Bone cysts
RADIOLOGIC GRADE OF OA
• G1 Normal
• G2 Mild
• G3 Moderate
• G4 Severe
CLINICAL FINDINGS
Joint pain
+
RADIOLOGIC FINDINGS
Osteophytes
CLINIC OF OA
SIGNS AND SYMPTOMS
• Other factors
ETIOPATHOGENESIS OF OA
• Cell destruction
• Membrane phospholipids
• Arachidonic acid
• Cox-1, Cox-2
• IL-1 and metalloproteases have been found
to play an important role in cartilage
destruction.
• Symptomatic treatment
• Surgical treatment
STRUCTURE MODIFYING TREATMENT
• Regular exercises
• Weight control
• Prevention of trauma
AIMS OF OA TREATMENT
• Pain relief
• Education
Non-Pharmacologic Treatment of OA
• Patient education
• Weight loss (if overweight)
• Aerobic exercise programs
• Physical therapy
• Range-of-motion exercises
Muscle-strengthening exercises
• Assistive devices for ambulation
Patellar taping
Appropriate footwear
Lateral-wedged insoles (for genu varum)
• Bracing
• Occupational therapy
• Joint protection and energy conservation
PHARMACOLOGIC TREATMENT OF OA
• Intraarticular agents:
Hyaluronan
Glucocorticoids (effusion)
• Topical agents
HAND OA - RESTING SPLINT
SYMPTOMATIC TREATMENT OF OA
• Joint lavage
• Arthroscopy
• Cartilage grefting- genetic engineering
• Surgery
Osteotomy
Joint replacement