OSTEOARTHRITIS

Osteoarthritis (OA) merupakan penyakit sendi degeneratif yang berkaitan dengan kerusakan
kartilago sendi, vertebra, panggul, lutut, dan pergelangan kaki paling sering terkena OA.
Osteoartritis merupakan kelainan sendi non inflamasi yang mengenai sendi-sendi penumpu berat
badan dengan gambaran patologis yang berupa memburuknya tulang rawan sendi, yang
merupakan hasil akhir dari perubahan biokimiawi, metabolisme fisiologis maupaun patologis
yang terjadi pada persendian.

Faktor Risiko Umur, obesitas, pekerjaan yang diulang, trauma tulang sendi, kerusakan tulang
rawan secara berlebihan, keturunan

Etiologi
Primer (idiopatik) OA  tidka diketahui
Sekunder OA  trauma (kerusakan tulang rawan secara berlebihan), penyakit metabolic dan
endokrin, dan factor konginental
Yang paling utama yaitu disebabkan oleh faktor biomekanik  kegagalan mekanisme protektif,
antara lain kapsul sendi, ligamen, otot-otot persendian, serabut aferen, dan tulang-tulang.
Patofisiologi
  Kerusakan tulang rawan akan meningkatkan aktivitas kondrosit untuk memperbaiki
kerusakan, dengan peningkatan sintesis matriks konstituen dengan cartilage
swelling.Tulang Subchondral yang berdekatan dengan tulang rawan artikular mengalami
perubahan patologis dan peptida vasoaktif rilis dan membentuk matriks logamprotein
(MMPs).
 Neurovaskularisasi dan terjadi peningkatan permeabilitas tulang rawan yang
berkontribusi pada penghilangan dan apoptosis kondrosit. Kehilangan tulang rawan
menyebabkan penyempitan dan nyeri pada sendi serta kerusakan sendi. Sisa tulang rawan
akan melembutkan dan mengembangkan fibrillations.
 Perubahan inflamasi dapat terjadi pada kapsul tulang rawan dan synovium. Kristal atau
rusaknya kartilago dalam cairan sinovial dapat menyebabkan peradangan melalui
pelepasan IL-1, prostaglandin E2, tumor necrosis factor-α (TNF-α) dan nitrat oksida.
Perubahan inflamasi mengakibatkan pleura sinovial dan penebalan. nyeri disebabkan oleh
peningkatan cairan synovial.
Terapi farmakologi
Analgesik  Asetaminofen (lini pertama), tramadol, hidrokodon, oksikodon.
NSAID (menghambat pembentukan prostaglandin)  ibuprofen, indometasin, asam mefenamat,
ketoprofen, piroxicam, naproxen
NSAID inhibitor COX-2 selektif  celecoxib
Pompa Proton Inhibitor (PPIs) dan misoprostol  preventif ganggguan GI pada pasien yang
mengkonsumsi NSAID
NSAID topical  Capsaicin 0.025% or 0.075%, diklofenak gel 1% untuk nyeri (> 75 tahun)
apabila penggunaan analgetik oral kurang berefek
Intra artikular (IA) kortikosteroid suntikan  untuk kedua pinggul dan lutut OA ketika analgesia
dengan acetaminophen atau NSAID suboptimal.
DMARDS  nonbiological (methotrexate, hydocloroquine, sulfasalazine, leflunomide),
biological (etanercept, infliximab, adalimumab, certolizumab, golimumab) atau kombinasi
keduanya

Nonfarmakologi
 Menjaga pola makan, olahraga ringan, dan program penurunan berat badan untuk pasien
kelebihan berat badan.
 Terapi fisik  dengan perawatan panas atau dingin
 Menggunakan alat bantu (tongkat, pejalan kaki, kawat gigi, tumit cangkir, Sol) dapat
digunakan
 selama kegiatan olahraga atau setiap hari.
 Prosedur bedah (misalnya, osteotomi, artroplasti, fusion

PARKINSON
Tanda dan gejala jika penyakit mulai menjadi serius adalah:
● Tangan atau jari‐jari agak bergetar adalah gejala awal. Pertama kali diketahui ketika cara
menulis mulai berubah atau orang memiliki masalah pada pergerakan motorik halus (misalnya
saat mengancingkan baju). Getaran terjadi pada salah satu atau kedua tangan, terutama saat
beristirahat
● Otot kaku
● Gerakan melambat secara bertahap
● Kesulitan berjalan (terutama saat memulainya)
● Sulit menelan
● Masalah keseimbangan
● Sering kali kehilangan ekspresi wajah dan sulit berbicara dan menulis.

Etiologi
Infeksi oleh virus yang non-konvensional (belum diketahui), reaksi abnormal terhadap virus
yang sudah umum, pemaparan terhadap zat toksik yang belum diketahui, serta terjadinya
penuaan yang prematur atau dipercepat
Parkinson idiopatik  factor lingkungan (xenobiotic, pekerjaan, infeksi, diet, ras , trauma
kepala, stress dan depresi

Faktor risiko
Umur: anak muda jarang terkena penyakit Parkinson, tapi sering terjadi pada orang paruh baya
atau lanjut usia lebih dari 60 tahun.
Bawaan: faktor risiko penyakit ini meningkat jika ada anggota keluarga yang juga mengidap
penyakit ini.
Jenis kelamin: pria lebih banyak terpengaruh daripada wanita.
Kontak dengan zat kimia: kontak terus‐menerus dengan pestisida dan herbisida dapat
meningkatkan risiko.

Patofisiologi
Neuron/sel saraf dalam otak  substansia nigra (menghasilkan dopamine) mati atau melemah 
kekurangan dopamine  tingkat kehilangan dopamin (nigrostriatal ) berkorelasi positif dengan
tingkat keparahan gejala motor  Mengurangi aktivasi reseptor dopamine1 dan dopamine 2 
mengurangi aktivasi korteks motor.

Terapi farmakologi
Nonfarmakologi
Gaya hidup dan pengobatan rumahan di bawah ini mungkin membantu mengatasi Penyakit
Parkinson:
● Minum obat sesuai resep dokter.
● Berolahraga secara teratur, misalnya berjalan, membantu menjaga otot tetap lentur dan kuat.

Permasalahan Kasus
R/ Sifrol SR 0,75 mg (1xsehari)  Pramipexole
Metotrexate (3x sehari)
Mefenamic acid 500 mg (2x sehari)
Interaksi  MTX-Asmef meningkatkan toksisitas methotrexate (diberikan asam folat)
Efek samping  MTX (Nausea) dan Asmef (gangguan GI), pasien memiliki piwayat gangguan
GI sehingga risiko terjadi efek samping (nyeri ulu hati)  diberikan antacid atau PPI atau
misoprostol
Pasien Parkinson tremor dan bradykinesia (perlambatan/hilangnya gerakan spontan dan rutin)
serta perasaan kaku
OSTEOARTHRITIS
Osteoarthritis (OA) is a degenerative joint disease associated with damage to the cartilage of
joints, vertebrae, pelvis, knees, and ankles are most often affected by OA. Osteoarthritis is a non
inflammatory joint disorders affecting joints penumpu weight with pathological picture of
worsening of cartilage in the joints, which is the end result of Biochemistry, metabolism changes
of physiological maupaun pathological happening in joints.
Etiology
Primary (idiopathic) OA, the most common type, has no known cause.
Secondary OA is associated with a known cause, such as trauma (damage to articular cartilage
through injury), metabolic or endocrine disorders, and congenital factors.
The main thing that is caused by biomechanics factor the failure of the protective mechanism,
among others, joint capsule, ligaments, joints, muscles, afferent fibers and bones.
Risk factors include increasing age, obesity, repetitive use through work or leisure activities,
joint trauma, damage to articular cartilage through injury and genetic predisposition.
Pathophysiology
• Damage to the cartilage will increase the activity of the kondrosit to fix the damage, with
increased synthesis of cartilage matrix constituents with swelling. Subchondral bone adjacent to
the articular cartilage experience pathological changes and peptide vasoaktif release and form the
matrix logamprotein (MMPs).
• Neurovaskularisasi and an increase in the permeability of the cartilage that contributed to the
disappearance and apoptosis kondrosit. Loss of cartilage causes constriction and pain in the
joints and joint damage. The rest of the cartilage will soften and develop fibrillations.
• inflammatory Changes can occur in cartilage and synovium capsules. Crystal or destruction of
cartilage in the synovial fluid can cause inflammation through the release of IL-1, prostaglandin
E2, tumor necrosis factor-α (TNF-α) and nitric oxide. Inflammatory changes lead to pleural
thickening and synovial. the pain caused by the increase of synovial fluid.
Pharmacology theraphy
Analgesic  Acetaminophen (first-line), tramadol, hidrokodon, oksikodon.
NSAIDS (inhibit the formation of prostaglandins) ibuprofen, indomethacin, mefenamic acid,
ketoprofen, piroxicam, naproxen
COX-2 inhibitor NSAIDS selective  celecoxib
Proton pump Inhibitor (PPIs) and misoprostol  preventive GI problem in patients who taking
NSAIDS
NSAID topical  Capsaicin 0025% or% 0075, diclofenac gel 1% for pain (> 75 years) if the
use of oral analgetik less effect conferring
Intra articular corticosteroid injections (IA)  for both hip and knee OA when analgesia it has
with acetaminophen or NSAID suboptimal.
DMARDS  nonbiological (methotrexate, leflunomide, sulfasalazine, hydocloroquine),
biological (etanercept, infliximab, adalimumab, certolizumab, golimumab) or a combination of
both
Nonphrmacology
• Educate patient about disease process and extent, prognosis, and treatment. Promote
dietary counseling, exercise, and weight loss program for overweight patients.
• Physical therapy—with heat or cold treatments and an exercise program—helps
maintain range of motion and reduce pain and need for analgesics.
• Assistive and orthotic devices (canes, walkers, braces, heel cups, insoles) can be used
during exercise or daily activities.
• Surgical procedures (eg, osteotomy, arthroplasty, joint fusion) are indicated for functional
disability and/or severe pain unresponsive to conservative therapy.

PARKINSON
Parkinson’s disease (PD) has highly characteristic neuropathologic findings and a clinical
presentation, including motor deficits and, in some cases, mental deterioration
Signs and symptoms of the disease start being serious if it is:
● Hand or finger form the finger rather vibrate is an early symptom. First known when writing
began to change or have problems with fine motor movements (for example when buttoned up
shirt). The tremor occurred in one or both hands, especially when resting
● Rigid Muscles
● Movement slows down gradually
• Difficulty walking (especially when started it)
● Difficult swallowing
● Balance problems
● Often lose facial expressions and it is difficult to speak and write.
Etiology
Infection by viruses that are non-conventional (not yet known), abnormal reaction to the virus
that was already public, exposure to toxic substances which are not yet known, as well as the
occurrence of premature aging or idiopathic Parkinson's accelerated environmental factor (
xenobiotic, occupation, race, diet, infections, head trauma, stress and depression
Risk factors age: young children are rarely affected by Parkinson's disease, but often occurs on
middle-aged people or seniors over 60 years old.
Default: risk factors of this disease increases if there are family members who also suffered from
this disease.
Gender: men are more affected than women.
Contact with chemicals: terus‐menerus contact with pesticides and herbicides can increase the
risk.
Pathophysiology
Neurons/nerve cells in the brain  substantia nigra (dopamine produce) dead or weakened 
dopamine deficiency levels lost dopamine (nigrostriatal) correlated positively with the severity
of the symptoms of motor  Decrease receptor activation dopamine1 and dopamine 2  reduce
activation of the motor cortex.
Pharmacological therapy (diatas)
Non Pharmacology
Nonfarmakologi lifestyle and home remedies below may help overcome Parkinson's disease:
● Take medication accordingly prescribed.
● Exercise regularly, for example walking, helps keep the muscles remain supple and strong.
R/Sifrol SR 0.75 mg (1xsehari)  Pramipexole
Metotrexate (3 x daily)
Mefenamic acid 500 mg (2 x a day)
Interaction  MTX-Asmef increase the toxicity of methotrexate (given folic acid)
Side effects of MTX  (Nausea) and Asmef (GI Disorders), patients have piwayat GI Disorders
so that risk occurring side effects (heartburn)  given antacid or PPI or misoprostol
Parkinson Patientstremor and bradykinesia (slowing/loss of spontaneous movement and
routine) as well as a feeling of stiffness