Osteoartritis dan Rhematoid artrtitis

7/30/2019 Osteoartritis dan Rhematoid artrtitis

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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


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.



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.


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




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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.





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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.


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




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Criteria ad must be present

for at least 6 weeks. Criteria

be must be observed by aphysician.


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.


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


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


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SIGNS & SYMPTOMS OF OA &


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SIGNS & SYMPTOMS OF OA &

RA





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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.


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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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Osteoartritis dan Rhematoid artrtitis