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Case:
Perempuan 60 tahun dibawah ke RSdengan keluhan nyeri pada lutut
sebelah kiri sejak 6 bulan yang lalu,
terutama saat berjalan, dan sakit saathendak berdiri dari posisi jongkok.
Penderita mengeluh sakit pada pagi
hari dan kaku selama 20 menit. Pada
pemeriksaan fisik ditemukan bengkak
pada lutut kiri dan tidak ada tanda-
tanda trauma.
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1st step: Identify key words
and sentences
perempuan 60 thn nyeri pd lutut sebelh kiri, sejak 6 bln
lalu
saat berjalan nyeri sakit pada pagi hari, kaku slm 20
menit
tanda trauma (-) bengkak pd lutut kiri
nyeri dirasakan pada waktu berdiridari posisi jongkok
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2nd step : Define the problems
1. Bagaimana mekanisma terjadi pebengkakan pada lutut kiri pasien ?
2. Bagaimana mekanisme timbulnya nyeri pada lutut sebalah kiri pasien
3. Mengapa kaku dirasakan sejak pagi hari dan kaku selama 20menit ?
4. Bagaimana penatalaksanaannya ?
5. Adakah hubngan fak. Usia dan gejalah klinis ?
6. Apa yang menyebabakan pasien merasa nyeri setelah berdiri dariposisi jongkok ?
7. Apa diagnosis dari pasien ini ?
8. Bagaimana penegakan diagnosis terhadap pasien ini ?
9. Bagaimana prognosis dari penyakit ini ?
10. Mengapa pasien mengeluhkan nyeri teteapi tidak ada tanda2 trauma?
11. Apa DD dari penyakit ini?
12. Bagaimana penceghan dari penyakit ini?
13. Faktor resiko apa saja yang dapat menyebabakn keluhan pada
pasien ini ?
14. Adakah komplikasi dari penyakit ini ? jelaskan !
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3rd step : Analyse the problems
1. Bengkak diakibatkan karena adanya
suatu peradangan pada sendi pasien
yang di awali dengan adanya jejas
yang mengundang proses inflamasi
sehingga bermanifestasi menjaditanda-tanda peradangan.
2. kondisi di mana sendi terasa nyeri
akibat inflamasi ringan yang timbulkarena gesekan ujung-ujung tulang
penyusun sendi. (kartilagonya telah
menipis/injury)
Sudoyo Aru W, setiyohadi B, dkk. Buku Ajar Ilmu
Penyakit Dalam. Ed 2. Jil III. Jakarta:InternaPublishing. 2009
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3. Kaku pada pagi hari. Pada beberapa pasien
mengalami hal ini, termasuk pasien ini dapat
timbul akibat setelah imobilitasi dalam wktuyang cukup lama.
4. lihat slide penatlaksanaan OA
5. Ada. Usia tua (monopause) pada pasienwanita ini berkaitan dengan hormon estrogen
yang sudah menurun di masanya. Dimana
estrogen dibutuhkan tulang untuk
pembentukan osteoblas untuk kondrosit.
Selain itu juga sudah terjadi penurunan
kemampuan sintesis matriks tulang pada
usianya. Sehingga mempunya resiko cukup
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6. Ketika berdiri, tubuh betumpuh pada lutut.
Sedangkan pada lutut terjadi peradangan
sendi, hal ini mengakibatkan nyeri. Selainitu,imobilitas (duduk) lama juga
menyebabkan nyeri.
7. Berdasarkan gelajah klinis dapat disuspekterkena osteoartritis (OA)
8. Diagnosisnya : anamnesis, pemeriksaan
fisik, laboratorium & radiologi.9. Prognosis baik. Tidak menyebabkan
kematian hanya menurunkan kualitas hidup.
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10.Akibat adanya infeksi dari dalamsendi.
11. Dilihat dari gejalah klinis, Ddnya
Rheumatoid artritits12. Menghindari faktor resiko atau
meminimalisir faktor resiko.
13.Ageing, gender, genetic/racial,Obesity, Injury, Overuse of joint
congenital
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14. Bisa mengalami komplikasi karena
terapinya. Penggunaan obat NSAIDmenyebabakn gangguan GI, dkk.
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Anatomi
Bone is a tissue composed of
matrix
and several types of cells:
osteocytes,osteoblasts, osteoprogenitor cells,
and
osteoclasts
Joint is a place to conect two or more
bones.One of the sinovia joints
Martini, Frederic. Fundamentals of anatomy & physiology.
9th ed. United State: Pearson Education; 2012. p173, 254
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NO. BASED ON ITS FUNCTIONS NO. BASED ON ANATOMICAL
ORGANIZATION OF THE
JOINT
1. synarthrosis ( an immuvable
joints)
1. Bone
Cartilago
2. amphiarthrosis (A slightly movable
joint)
2. Fibrous
3. diarthrosis (A f reely movable) 3. cartlago
Martini, Frederic. Fundamentals of anatomy & physiology.
9th ed. United State: Pearson Education; 2012. p254
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Next...
cartilago is a specialized form of connectivetissue derived from mesenchyme and it consistsof cells (chondrocytes and chondroblasts) andthe extracellular matrix.
Cartilago is avascular so it takes nutrients fromthe extracellular matrix through the diffusionprocess.
There are chondrocytes and chondroblastswhich synthesize extracellular matrix.
Ereschenko, Victor P. Atlas deFiore dengan korelasi
fungsional/Victor P. Eroschenko. Ed 11. Jakarta: EGC,201O. p75
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Matriks ekstraselulernya terdiri dari :
organik
inorganik
Ereschenko, Victor P. Atlas deFiore dengan korelasi
fungsional/Victor P. Eroschenko. Ed 11. Jakarta: EGC,201O. p75
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Componen of cartilago
inorganicorganic
cellMatrix celluler
type 1 collagen
fiber
asam hialoronat
glicosaminoglicansulfat phosphat
calcium
osteoclas
ostheocytes
ostheoblast
ostheoprogenitor
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OSTEOARTHRITIS (OA)
Osteoarthritis (OA) is defined by the American College of
Rheumatologyas a heterogeneous group of conditions
that lead to joint symptoms and signs which are associated
with defective integrity of articular cartilage, in addition to
related changes in the underlying bone at the joint
margins.
Primary
Secondary
Bronner F. Bone and osteoarthritis. 4th Vol.Farmington: Verlag London . 2007. p1
Idiopathic, when there is no
obvious predisposing cause.
there is some clearly defined
predisposing Pathology . Such as;
metabolic disorders, endocrine
disorders, ect.
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Bronner F. Bone and osteoarthritis. 4th Vol.Farmington: Verlag London . 2007
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RISK FACTOR
ageing
Gender
Genetic/racial
Obesity, Injury, Overuse of join
congenital
Sudoyo Aru W, setiyohadi B, dkk. Buku Ajar Ilmu
Penyakit Dalam. Ed 2. Jil III. Jakarta:InternaPublishin . 2009
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1. Ageing
Age is the most potent risk factor for OA,
with prevalence and incidence of diseaserising dramatically with age..
can because of this failure to synthesize
matrix with loading, cartilage thins withage, and thinner cartilage experiences
higher shear stress at basal layers and is
at greater risk of cartilage damage.
Fauci Antony S (eds). Harrisons Rhaumatology.
2nd ed. US: The McGraw-Hill Companies, Inc.2010. p226
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2. Gender
Older women are at high risk of OA in all
joints, a risk that emerges as womenreach their sixth decade. While hormone
loss with menopause may contribute to
this risk, there is little understanding of thevulnerability of olderwomens joints to OA.
Because estrogen in menopause are
decrease. So, osteblast cant be realase.
Fauci Antony S (eds). Harrisons Rhaumatology.
2nd ed. US: The McGraw-Hill Companies, Inc.2010. p226
FRZB d l h t k
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3. Genetic/racial OA in blacks more often than whites Emerging evidence suggests that people with
mutations in proteins that regulate genetranscription Major cartilage molecules athigh risk of OA. One Gene involved is FRZB.
or there are mutation in the type 2procollagen gene or other structural geneselements such as cartilage type 9 &12collagens, like binding protein or
proteoglycans play a role in the onset offamilial tendency in certain OA.
FRZB adalah gen untuk
Protein yang merupaka antagonis ligan Wnt
ekstraseluler, dan jalur sinyal Wnt memainkan peran
penting
dalam sintesis matriks dan pembangunan bersama.
Fauci A. S, Langfor E. H (eds). HARRISONS. Rheumatology. 2nd ed. USA: The
McGraw-Hill Companies, 2010. p.226
Sudoyo Aru W, setiyohadi B, dkk. Buku Ajar Ilmu Penyakit Dalam. Ed 2. Jil III. Jakarta:
InternaPublishing. 2009
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4. obesity, injury, overuse
Excessive weight gain can increase the loadof the knee joint to bear the brunt of our
body. So.
Sudoyo Aru W, setiyohadi B, dkk. Buku Ajar Ilmu
Penyakit Dalam. Ed 2. Jil III. Jakarta:
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PATHOGENESIS
Already known about thepathogenesis.
Normally, cartilage undergoes a
remodeling process, stimulated by
joint movement or use.
In OA, this process is altered by a
combination of mechanical, cellular,
and biochemical processes, resulting
in abnormal reparation of cartilage and
an increase in cartilage degradationKori A. Dewing, DNP, FNP, ARPN, dkk. Osteoarthritis andrhematoid arthritis 2012: pathofphysiology, diagnosis andtreatment. NPHF: 2012
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Egloff, C., dkk. The European Journal of medical scinces;
Biomechanics and pathomechanisms of ostheoarthritis. [online
may 23th, 2013][cited july 19th, 2012].
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DIAGNOSIS
Anamnesis
Physical exemination
Radiologi
Laboratory (darah tepi).
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TREATMENT1. Hand OA
Nonpharmacolog ic modal it ies. (
(Marc C. Hochberg, Roy D. Altman, ect.American College of
rheumatology 2012 recommendation for use of nonpharmacology
and pharmacology therapies in Astheortritis of the hand, hip, and
knee. 4th vol. American college of rheuatology: 2012
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Pharmaco logic modal it ies.
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2. Knee OA
Nonpharmacologic m odal it ies
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Pharmaco log ic modal i ties.
1 Hip OA
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1. Hip OA
Nonpharmacolog ic modal it ies
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Pharmaco logic modal it ies
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Acetaminophen, option for mild-to-moderate pain, is the preferred first-
line agent for the management of OA.
At recommended doses (less than3000mg/day), acetaminophen is
associated with fewer risks than non-
steroidal anti-inflammatory drugs(NSAIDs), and can be effective at
controlling OA painKori A. Dewing, DNP, FNP, ARPN, dkk. Osteoarthritis and
rhematoid arthritis 2012: pathofphysiology, diagnosis and
treatment. NPHF: 2012
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NSAID, work by reducing production ofpro-inflammatory and pain-related
prostaglandins.17 They inhibit twocyclooxygenase (COX) enzymes: COX-1is important in the normal regulation ofthe gastrointestinal (GI) tract; COX-2 is
upregulated at sites of inflammation,among other functions, and may beresponsible for inflammation.17Therefore, NSAIDs are effective intreating pain, immobility, andinflammation associated with OA
Kori A. Dewing, DNP, FNP, ARPN, dkk. Osteoarthritis and
rhematoid arthritis 2012: pathofphysiology, diagnosis and
treatment. NPHF: 2012
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Glucocorticoids, If an OA patient fails
NSAID therapy, intra-articular corticosteroidinjections are another option.MCorticosteroidinjections may provide pain relief over short-term periods (one to four weeks), but there isno evidence that these injections improve
function. Current ACR guidelines recommendthe use of glucocorticoid injections for kneeand hip OA if other pharmacologic therapiesdo not provide sufficient relief. The
guidelines do not recommendcorticosteroid injections in the treatmentof hand OA.
Kori A. Dewing, DNP, FNP, ARPN, dkk. Osteoarthritis and
rhematoid arthritis 2012: pathofphysiology, diagnosis and
treatment. NPHF: 2012
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Rheumatoid Arthtrits
is an inflammatory disease. It largelyaffects synovial joints, which arelined with a specialised tissue calledsynovium.
RA typically affects the small joints ofthe hands and the feet, and usuallyboth sides equally and symmetrically,
although any synovial joint can beaffected. It is a systemic disease andso can affect the whole body,including the heart, lungs and eyes.
Fauci Antony S (eds). Harrisons Rhaumatology.
2nd ed. US: The McGraw-Hill Companies, Inc.2010. p91-92
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ETIOLOGI
The exact cause of RA is unknownand, as yet, there is no cure.
autoimun
It is different from osteo-arthritis,which is caused by wear and tear in
the joints
American College of rheumatology: Rhematoid arthtritis. 2012
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Phatophysiology
RA is multifactorial in origin with agenetic predisposition including aclear association with MajorHistocompatibility Complex (MHC).
A large part of the MHC comprisesthe Human Leucocyte Antigen (HLA)genes.
These encode an individuals tissuetype and are divided into class I (HLA-A, HLA-B, HLA-C) and class II(HLA-DR, HLA-DQ, HLA-DP) genes
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Symptoms & Signs
Inflammation at thejoints
Pain and loss ofstrength
Movement limitationaround joints of thehands, feet, elbows,knees and neck
Feeling generally
unwell and fatigued Stiffness in the
morning and aftersitting still for a long
time
Classification of RA
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Classification of RA
Fauci Antony S (eds). Harrisons Rhaumatology.
2nd ed. US: The McGraw-Hill Companies, Inc.2010. p91
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Criteria ad must be present
for at least 6 weeks. Criteria
be must be observed by aphysician.
Fauci Antony S (eds). Harrisons Rhaumatology.
2nd ed. US: The McGraw-Hill Companies, Inc.
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DIAGNOSIS
Anamnesis Physical exemination
Radiologi
Laboratory
The American college of rheumatologyarthritis recommend to test pheriperalblood, rhematoid factor, LED, CRP
if RF adn anti-CRP are negatife,confirm with anti-RA33 test todifference RA patian with the high risk.
Sudoyo Aru W, setiyohadi B, dkk. Buku Ajar Ilmu
Penyakit Dalam. Ed 2. Jil III. Jakarta:InternaPublishin . 2009
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Rheumatoid arthritis erosions on X-ray
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TREATMENT
GENERAL PRINCIPLES The goals oftherapy for RA are :
(1) relief of pain,
(2) reduction of inflammation,(3) protection of articular structures,
(4) maintenance of function,
(5) control of systemic involvement
Fauci Antony S (eds). Harrisons Rhaumatology.
2nd ed. US: The McGraw-Hill Companies, Inc.
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There is no cure for RA.
The goal of treatment is to lessen your symptomsand poor function by starting proper medical
therapy as soon as possible, before your jointshave lasting damage.
No single treatment works for all patients. Manypeople with RA must change their treatment atleast once during their lifetime.
Good control of RA requires early diagnosis and,at times, aggressive treatment.
Thus, patients with a diagnosis of RA shouldbegin their treatment with disease-modifyingantirheumatic drugs referred to as DMARDs.
These drugs not only relieve symptoms but alsoslow progression of the disease. Often, doctorsprescribe DMARDs along with nonsteroidal anti-inflammatory drugs or NSAIDs and/or low-dosecorticosteroids, to lower swelling, pain and fever.
DMARDs have greatly improved the symptoms,
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Drugs Therapy :Two major types of drug are used :
1. NSAIDsThe NSAIDs have a rapid suppresive effectthrough blokade of enzyme cyclo-oxygenase(Cox) and the inhibition of prostaglandins,thereby reducing pain, stiffness andinflammation. The NSAID do not influencecytokine
2. DMARDsThe DMARDs act by a variety of means :
inhibition of pro-inflammatory cytokines
reduced cytokine-driven inflammation,decrease disease activity, produce asecondary reduction in joint damage,preservation of functional capacity,
National Institute for health and clinical
excellence. The Management of Rheumatoid
Arthrtitis. 2009
7/30/2019 Osteoartritis dan Rhematoid artrtitis
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Kori A. Dewing, DNP, FNP, ARPN, dkk. Osteoarthritis and
rhematoid arthritis 2012: pathofphysiology, diagnosis and
treatment. NPHF: 2012
SIGNS & SYMPTOMS OF OA &
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SIGNS & SYMPTOMS OF OA &
RA
Kori A. Dewing, DNP, FNP, ARPN, dkk. Osteoarthritis and
rhematoid arthritis 2012: pathofphysiology, diagnosis and
treatment. NPHF: 2012
7/30/2019 Osteoartritis dan Rhematoid artrtitis
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Kori A. Dewing, DNP, FNP, ARPN, dkk. Osteoarthritis and
rhematoid arthritis 2012: pathofphysiology, diagnosis and
treatment. NPHF: 2012
7/30/2019 Osteoartritis dan Rhematoid artrtitis
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Kori A. Dewing, DNP, FNP, ARPN, dkk. Osteoarthritis and
rhematoid arthritis 2012: pathofphysiology, diagnosis and
treatment. NPHF: 2012
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Prognosis
Bad cos it can make complication.
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REFRENCE
Martini, Frederic. Fundamentals of anatomy& physiology. 9th ed. United State: PearsonEducation; 2012.
Bronner F. Bone and osteoarthritis. 4th Vol.Farmington: Verlag London . 2007.
Ereschenko, Victor P. Atlas deFiore dengankorelasi fungsional/Victor P. Eroschenko. Ed11. Jakarta: EGC, 2010.
Sudoyo Aru W, setiyohadi B, dkk. Buku Ajar
Ilmu Penyakit Dalam. Ed 2. Jil III. Jakarta:InternaPublishing. 2009
Fauci Antony S (eds). HarrisonsRhaumatology. 2nd ed. US: The McGraw-HillCompanies, Inc. 2010.
7/30/2019 Osteoartritis dan Rhematoid artrtitis
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Marc C. Hochberg, Roy D. Altman, ect.American College of rheumatology 2012recommendation for use of nonpharmacology
and pharmacology therapies in Astheortritis ofthe hand, hip, and knee. 4th vol. Americancollege of rheuatology: 2012
Kori A. Dewing, DNP, FNP, ARPN, dkk.
Osteoarthritis and rhematoid arthritis 2012:pathophysiology, diagnosis and treatment.NPHF: 2012
Egloff, C., dkk. The European Journal ofmedical scinces; Biomechanics and
pathomechanisms of ostheoarthritis. [onlinemay 23th, 2013][cited july 19th, 2012].
American College of rheumatology: Rhematoidarthtritis. 2012
National Institute for health and clinicalexcellence. The Management of Rheumatoid
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THANK YOU........
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