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Rheumatoid Arthritis

Chronic inflamation that commonly


cause by progressive autoimmune
disease in the joint. Characterized as
joint swollen.
Etiology
Stiil not well known.
Immune system that used to against the infection
but attack the normal cell in joint instead. it’s
make stiffnes, swelling and pain in the joint

Suspected, there is connection between:


• Genetic factor: complex produc
histocompatibility class II (HLA-DR)
• Environmental Factor: Obesity, Smoking,
Age,infection
resource: Buku Ajar Ilmu Penyakit Dalam UI Edisi V ; Gibofsky, 2012, Overview of Epidemiology,
Pathophysiology, and Diagnosis of Rheumatoid Arthritis, The American Journal of Managed Care,
VOL. 18, NO.13, pp: 295-302
Epidemiology
• in Indonesia, RA incident in
adult (above 18 th) around 0,1-
0,3%.
• Child and adolescent found
1:100.000.
• Most found in female, ratio
between female : male = 3:1.

suarjana In. Reumatoid artritis. Dalam Sudoyono AW,Setiyohadi B, Alwi I, dkk Buku Ajar Ilmu
Penyakit Dalam Edisi V. Jakarta:Interna Publishing: 2009
Patophysiology

Gambar 1. Pembentukan kompleks


imun (Immunopaedia.org, 2010)
Gambar 2. Aktivasi jalur
komplemen klasik
(Immunopaedia.org, 2010)
Gambar 3.Inflamasi pada
sel target
(Immunopaedia.org, 2010)
Clinical Manifestation
• swelling, heat, erythema
• muscle and joint pain and stiffness. Ordinary in
the morning (knee, shoulder, elbow, wrist and leg
area)
• Systemic symptoms:
• Fatigue
• lack of appetite
• low grade fever
• Inflammation may occur: swollen lesions called
rheumatic nodules.
resource: Buku Ajar Ilmu Penyakit Dalam UI
Edisi V
Diagnosis
Anamnesis
– Main complaint :
• pain and stiffness in several joints, such as wrist joints, PIP
(proximal interphalanges joints), and meta
carpopphalanges joints.
– Morning stiffness lasts up to 1 hour
– swelling, heat, erythema
– Past illness history
– Current illness history
– History of family illness
• A family history of Rheumatoid Arthritis
– Pregnancy (causes RA remission), breastfeeding or
not (in breastfeeding the risk is lower)
Physical Examination
• Pain
• swelling, heat, erythema
• stiffness more than 1 hour in the morning
• Boggy swelling (in PIP)
• Arthralgia
• Fatigue
• Weight loss
• Low grade fever
Boggy Swelling
Supporting Examination
• ACPA
• Rheumatoid Factor (less specific, because it can
also increase in hepatitis C)
• ANA (Anti nuclear antibody)
• CRP (usually increases)
• Erythrocyte sediment (usually increases)
• CBC (Complete Blood Count)
• Renal physiology and liver function (to choose the
prescribe, whether it can be given NSAIDs or not)
Imaging

• 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

R.N.,ASSOCIATE HEAD OF NURSING ANESTHESIOLOGY DEPARTMENT & PAIN THERAPY


“SISMANOGLEIO”GENERAL STATE HOSPITAL OF ATHENS,GREECE, POST GRADUATE STUDENT,
MSC, MEDICAL SCHOOL UNIVERSITY OF ATHENS, GREECE.
Complication

Mechanisms of Disease The


Pathogenesis of Rheumatoid Arthritis
Iain B. McInnes, F.R.C.P., Ph.D., and
Prognosis
• Patients with RA live 3 to 12 years less than
the general population.
• Increased mortality in these patients is mainly
due to accelerated cardiovascular disease,
especially in those with high disease activity
and chronic inflammation.
• Relatively new biological therapy can reverse
the development of atherosclerosis and
prolong life in those with RA.
SLE
Definition
• Systemic Lupus Erythematosus (SLE) is an
autoimmune disease of the connective tissue.
Epidemiology
• In the world: 2.9 / 100,000 - 400 / 100,000
cases
• Many in races: Negro, Chinese, Filipino
• Many at age: 15-40 years (reproductive
period)
• Woman: male = 5.5-9: 1
Etiology
• Idiopathic, but there are risk factors:
Genetic factors
Immunological factors
Hormonal factors
Environmental factor
Factor of medicine
Patogenesys
Clinical manifestation
• At first, the disease has non-specific clinical
symptoms, including weakness, extreme
fatigue, prolonged lethargy, heat, fever,
nausea, decreased appetite, and weight loss.
This non-peculiar initial symptom is similar to
some other diseases. Therefore the symptoms
of this disease are very broad and not typical
at first.
More specific symptoms:
• Skin: butterfly rash
• Musculoskeletal: muscle pain (myalgia), joint
pain (arthralgia), or is an arthritis where there
is clear evidence of joint inflammation.
Diagnosis
• Diagnosis of LES can be established based on clinical and laboratory
images. The American College of Rheumatology (ACR), in 1997, proposed
11 criteria for the LES classification, where if 4 criteria were obtained, the
diagnosis of LES could be established
• (1) Butterfly rush,
• (2) Discoid rush,
• (3) Photosensitivity,
• (4) Mouth Ulcer,
• (5) Arthritis,
• (6) Serositis,
• (7) Proteinuria
• (8) Neurological abnormalities,
• (9) Blood disorders
• (10) Immune disorders,
• (11) ANA test (Antiniclear antibodies) is positive
3. fotosensitivitas 4. Ulkus mulut
2. discoid rash
Treatment
• Conservative therapy: simple analgesics
(NSAIDs), for example:
– Diclofenac
– Paracetamol
– Ibuprofen for arthritis, arthralgia and myalgia.
• Follow-up Plan
– 1. Refer to secondary services for definitive diagnosis
– 2. Continuous laboratory and follow-up tests are
needed to monitor the patient.
– 3. The involvement of various organs in LES requires
treatment from various fields such as rheumatology,
neurology, nephrology, pulmonology, cardiology,
dermatology, and hematology specialists.
• Counseling and Education
– 1. Psychosocial interventions and direct counseling
– 2. Advise patients to join the group with lupus
– 3. Suggest that you don't get too much sun exposure
and always use sunblock, long sleeves and umbrellas.
– 4. Monitoring and explanation of the effects of long-
term steroid use on patients.
– 5. To get regular treatment
Complication
• Hemolytic anemia
• Thrombosis
• Cerebral lupus
• Lupus nephritis
• Secondary infection
Prognosis
• 25% of patients can experience remission for
several years, but this is rare
Osteomyelitis
DEFINITION
Osteomyelitis is an infection of the bone due
to both pyogenic and non-pyogenic infections
such as mycobacterium tuberculosis.

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

• Osteoarthritis OA is a degenerative disease


of diarthrodial (synovial) joints,
characterized by
• Breakdown of articular cartilage
• and proliferative changes of surrounding
bones
EPIDEMIOLOGY
• Osteoarthritis(OA) is the most common joint
disease
• OA of the knee joint is found in 70% of the
population over 60 years of age
• Radiological evidence of OA can be found in
over 90 % of the population
LIMITED FUNCTION
• OA may cause functional loss
• Activites of daily living
• Most important cause of disability in old age

• Major indication for joint replacement surgery


CHARACTERISTICS OF OA
• OA is a chronic disease of the musculoskeletal
system, without systemic involvement
• OA is mainly a noninflammatory disease of
synovial joints
• No joint ankylosis is observed in the course of
the disease
CLASSIFICATION OF OA
• Primary OA Secondary OA

Etiology is unknown Etiology is known


AGE
• Primary OA > 40 years

• 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

• There are no pathognomonic laboratory


findings for OA

• Laboratory analysis is performed for


differential diagnosis
RADIOLOGIC FINDINGS OF OA
• Narrowing of joint space
(due to loss of cartilage)

• Osteophytes

• Subchondral (paraarticular) sclerosis

• Bone cysts
RADIOLOGIC GRADE OF OA

• G1 Normal
• G2 Mild
• G3 Moderate
• G4 Severe

• Kellgren Lawrence Classification


DIAGNOSIS OF OA

CLINICAL FINDINGS
Joint pain
+
RADIOLOGIC FINDINGS
Osteophytes
CLINIC OF OA
SIGNS AND SYMPTOMS

• Joint pain - degenerative


• Stiffness following inactivity – 30 min
• Limitation of ROM – later stages
• Deformity – restricition of ADL
OA OF KNEE JOINT (GONARTHROSIS)

• More common in obese females


• over 50 years of age
• Joint stiffness (<30 minutes)
• Mechanical pain
• Physical examination findings: Crepitus
• Pain on pressure
• Painful ROM and functional limitation
• Limitation of ROM in later stages of OA (first extension)
• Laboratory analysis within normal limits
GENU VALGUM - ORTHOSIS
RADIOLOGIC FINDINGS?
GRADE 1 - 4?
OA OF HIP JOINT
• More common in males over 40 years of age
• Joint stiffness
• Pain of hip, gluteal and groin areas radiating to
the knee (N obturatorius)
• Mechanical pain
• Limited walking function
COXARTHROSIS
Physical examination:
• Antalgic limping
• Limitation of ROM (first internal rotation)
• Painful ROM
• Trendelenburg test positivity
• Leg length discrepancy
Laboratory analysis within normal limits
BIOMECHANICS
X-RAY OF HIP OA
Peripheral Joints
• Hands
• Feet
ETIOPATHOGENESIS OF OA
• Age,gender
Local
• Genetic OA biochemical
effects

• Other factors
ETIOPATHOGENESIS OF OA

• Dysfunction of joint cartilage


• Condrocyte function: 1- Degredative enzymes
(metalloproteases)
2- Inhibitors
Degeneration and regeneration functions are
balanced
• IL-1  , degredative enzymes + synovial
inflammation results: Breakdown of cartilage
PATHOGENESIS OF OA

• Cytokines IL-1, IL-6, TNF-

• 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.

• Local growth factors, especially


transforming growth factor (TGF) are
involved in the formation of osteophytes
TREATMENT OF OA

• Symptomatic treatment

• Structure modifying treatment

• Surgical treatment
STRUCTURE MODIFYING TREATMENT

• Hyaluronic acid injection (HA)

• Glycose amino glycans (GAG)


PRIMARY PREVENTION OF OA ??

• Regular exercises

• Weight control

• Prevention of trauma
AIMS OF OA TREATMENT

• Pain relief

• Preservation and restoration of joint


function

• 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

• Oral Systemic Medical Agents


- Analgesics (acetaminophen)
- NSAIDs
- Opioid analgesics

• Intraarticular agents:
Hyaluronan
Glucocorticoids (effusion)

• Topical agents
HAND OA - RESTING SPLINT
SYMPTOMATIC TREATMENT OF OA

• Decrease of joint loading


- Weight control
- Splinting
- Walking sticks
• Exercises
- Swimming
- Walking
- Strengthening
• Patient education
INDICATIONS OF SURGICAL
INTERVENTION

• Severe joint pain,


resistant to conservative treatment
methods
• Limitation of daily living activities
• Deformity, angular deviations, instability
INVASIVE METHODS

• Joint lavage
• Arthroscopy
• Cartilage grefting- genetic engineering
• Surgery
Osteotomy
Joint replacement

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