4. What are the differential diagnose of the scenario ?

ANSWER:

1. Gouty arthritis
2. Osteoarthritis
3. Rheumatoid arthritis
4. Pseudogout

GOUTY ARTHRITIS

A. DEFINITION OF GOUTY ARTHRITIS

Gouty arthritis or arthritis piral is an inflammation of the joints as a
manifestation of the accumulation of monosodium urate crystals precipitate, which is
collected in the joint as a result of the high levels of uric acid in the blood
(hyperuricemia). Not everyone with hyperuricaemia is piral arthritis sufferer or are
suffering from arthritis piral. However, the risk is greater with arthritis piral
meningatnya blood uric acid concentration.

B. EPIDEMIOLOGY
Gout is a dominant disease in older men. As it is stated by Hippocrates that
gout is rare in men prior to adolescence and in women, rarely before menopause. In
1986 the reported prevalence of gout in the United States is 13.6 / 1,000 men and 6.4 /
1,000 women. The prevalence of gout increases with increasing standard of living.
The prevalence among African American men is higher compared with Caucasian
men. (Edward Stephen, 2010).
In Indonesia there are many publications about artitis gout epidemiology (AP).
In 1935 a Dutch national physician named Van der Horst has reported 15 patients with
gout artitis disability of an area in Central Java. Another assessment found that the
treatment of gout patients on average had suffered from the disease for more than five
years. This may be due to a lot of gout patients who treat themselves. One study long
in Massachusetts received more than 1% of the population with uric acid levels of less
than 7 mg / 100ml've got artitis acute gout attacks.

C. ETIOLOGY
Factors that influence as a cause of gout are:
a. Hereditary factors with a history of gout in the family tree
 b. Increased levels of uric acid as a diet high in protein and other foods rich in purine
compounds. Purines are compounds that will be reformed into uric acid in the
body
c. Excessive alcohol consumption, because alcohol is one of the sources of purines
also can inhibit the discharge of urine through the kidneys.
d. The resistance of the removal of uric acid due to certain diseases, especially renal
impairment. Patients are advised to drink plenty of fluids in the number .minum
much as 2 liters of water or more each day to help disposal veins, and minimize
deposition of urate in the urinary tract.
e. Use of certain medications that increase uric acid levels, especially diuretics
(furosemide and hydrochlorothiazide)
f. Other factors such as stress, diet, injury to the joints, high blood pressure and
excessive exercise. (VitaHealth, 2007)

D. PATHOPHYSIOLOGY
Increased serum uric acid levels can be caused by excessive formation or a
decrease in the secretion of uric acid, or both. Uric acid is the final product of purine
metabolism.
Normally, the metabolism of purines into uric acid can be explained as
follows:
1) De novo pathway involves purine synthesis and then uric acid precursor
nonpurin. The substrate initially is ribose-5-phosphate, which is converted
through a series of intermediates into mukleotida purine (sinosinat acid, guanilat
acid, acid cyclase). This pathway is controlled by a series of complex
mechanisms, and there are several enzymes which catalyze reactions are: 5-
fosforibosilpirofosfat (PRPP) synthetase and amidofosforibosiltransferase
(amido-PRT). There is a mechanism of feedback inhibition by purine nucleotides
formed, whose function is to prevent excessive pembenukan.
2) Austerity pathway is the path through the formation of purine nucleotides
purines free acid, nucleic solver, or food intake. This path is not through
intermediaries such substances lane de novo.basa free purines (adenine, guanine,
hypoxanthine) berkondenasi with PRPP to form a purine nucleotide precursors
of uric acid. This reaction is catalyzed by two enzymes: hypoxanthine guanine
phosphoribosyltransferase (HGPRT) and adenine phosphoribosyltransferase
(APRT).
 Uric acid is formed from the purine metaolisme will freely filtered by the
glomerulus and reabsorbed in the proximal tubule of the kidney. A small portion of
uric acid is reabsorbed and then excreted in the distal nephron and excreted through
the urine.

In gout arthritis, there is interference with metabolic balance (formation and

excretion) of gout include the following.

a. Decrease in uric acid excretion in idiopathic

b. Decrease in uric acid excretion secondary, such as kidney failure.
3) Increased production of uric acid, for example caused by a tumor (which
increases cellular turnover) or increased synthesis of purines (for defect enzymes
or inhibitory feedback mechanisms that play a role).
4) Increasing the intake of foods containing purines
Increased production or barriers will increase the excretion of uric acid levels
in the body. Uric acid is a substance whose solubility is so low that tend to form
crystals. Uric acid accumulation at most pinned in the form of monosodium urate
crystals, the mechanism is still unknown.

The presence of monosodium urate crystals will cause inflammation in several

ways, as follows.

1. The crystals are activating the complement system mainly C3a and C5a, this
complement is emotaktik and will recruit neutrophils into the tissue (joints and
synovial membrane). Crystal triggers phagocytosis against toxic free radicals and
leukotrienes, primarily leukotriene B. Death of neutrophils cause the release of
lysosomal enzymes that destructive ends.
2. Macrophages were also recruited to the deposition of urate crystals in the joint
will perform phagocytosis activity, and also issued a number of proinflammatory
mediators such as IL-1, IL-6 IL-8 and TNF. Mediator mediator will reinforce the
inflammatory response, in addition to activating cells sinuviumdan cartilage cells
to produce protease. Protease this will cause tissue injury.

Accumulation of crystals of uric urate crystals and recurrent attacks will cause
the formation of deposits such as white limestone called tophi / tofus (tophus)
ditulang cartilage and joint capsule. In the capsule sediment will trigger
granulomatous inflammatory reaction, which is characterized by masses of uric
tamorf (crystal) surrounded by macrophages, limfosis, fibroblasts, and foreign body
 giant cells. Persiste chronic inflammation can cause fibrosis of the synovium,
cartilage erosion, and may be followed by fusion joints (ankylosing). Tofus can form
in other places (eg: tendons, bursa, soft tissue). Deposition of uric acid crystals in the
renal tubules can lead to blockages and nephropathy gout.

E. CLINICAL MANIFESTATIONS
Clinical manifestations divided into two types: the typical gout arthritis and gout
arthritis atypical.
a. Typical gout arthritis
Clinical picture really has the following properties:
1. Weighing arthritis attack has the properties can not walk, can not meemakai
shoes and disrupt sleep. The pain is described as extruciating paint and peaks
in 24 hours. Without pengbatan at the beginning of the attack can recover
within 3-4 days.
2. The attack is usually a sign of inflammation monoartikuler with red is like ,
swollen, painful, hot, and painful when moved. A predilection for the firts
metatarsophalangeal (MTP-1).
3. Remission perfectly between acute attacks.
4. Hiperurisemia. Usually associated with acute gouty arthritis attack, but the
diagnosis of arthritis does not have to be accompanied hiperurisemi.
Fluctuations in serum uric acid precipitate gout attacks
5. Precipitant. Precipitant is alcohol, medicine and surgery. Usually these factors
are kwon sufferers.

b. Atypical gout arthritis

Typical clinical features such as severe arthritis, monarticular, and complete
remission was not found. Tofi which typically occur several epidemic after an
acute attack. This atypical type rarely found. In the face of the atypical cases of
gout, diagnosis should be done carefully. For this diagnosis confirmed by
performing puncture dpat joint fluid and further microscopically dihat urate
crystals.
In gout arthritis evolus obtained four phases, as follows.
1. Arthritis acute gout
Manifestations of acute attacks give a distinctive and can immediately
make a diagnosis. The joints most affected are the first
metatarsophalangeal joint (75%). In the affected joint is clearly visible
symptoms of inflammatory complete.
2. Arthritis gout interkritikal
 This phase is the phase and no clinical symptoms of acute attacks.
Even without symptoms, crystals of monosodium can be found in the fluid
that can be aspirated from the joints, these crystals can be found on sinevia
cells, the synovial cell vacuole, and the cell vacuole mononuclear
leukocytes.
3. Hyperuricaemia asymptomatic
This phase is not identikdenagn gout arthritis. In patients denag this
situation should also be checked for blood cholesterol levels because of the
elevation of blood uric acid is almost always accompanied by elevation
koleserol.
4. Arthritis chronic gout with tofi
Tofi is hoarding crest subcutaneous veins occur at the joints and
chronic gouty arthritis, which biasaya longstanding approximately between
5-10 years.

F. INVESTIGATIONS
a) Laboratory
1. Examination of synovial ciran obtained their intracellular monosodium urate
crystals.
2. Examination of serum uric acid increased> 7 mg / dL.
3. Urinalysis obtained 24 hours excretion> 800 mgasam uric
4. Urinalysis to detect the risk of uric acid stones.
5. Examination of blood chemistry to detect kidney function, liver,
hipertgigliseridemia, high LDL, and the presence of diabetes mellitus
6. leukocytosis obtained in the acute phase.

b) Radiodiagnostic
1. radiography to detect calcification of joints.
2. Radiographs obtained erosion on the surface of the joint and the joint capsule.

OSTEOARTHRITIS

A. DEFINITION OF OSTEOARTHRITIS
Osteoarthritis is a degenerative disease of the joints which is caused by a
number of factors. This disease has characterized by damage to joint cartilage
(cartilage). Cartilage is a hard tissue surrounding the slippery nature around
the latter part of the hard bone in the joints. This network serves as
smoothing the movement between the bones and as a damper (shock absorber) at the
time joint activity or movement.
B. EPIDEMIOLOGY
Osteoarthritis is the leading cause of disability among American adults. The
prevalence of osteoarthritis in Europe and America is bigger than the prevalence in
other countries. The National Arthritis Data Workgroup (NADW) estimates that 9 of
osteoarthritis in the United States in 2005 as many as 27 million are between ages 18
and over. Data from 2007 to 2009 the prevalence rose about 1 in 5 or 50 million
people who suffer from osteoarthritis doctors diagnosed (Murphy and Helmick,
2012). Estimates of the incidence of osteoarthritis in Australia is greater in women
than in men of all age groups is 2.95 per 1000 population compared to 1.71 per 1000
population (Woolf and Pfleger, 2003). In Asia, China and India ranked as the top two
countries with the highest osteoarthritis epidemiology consecutive 5650 and 8145
souls who suffer from osteoarthritis of the knee (Fransen et. Al, 2011). Data Basic
Health Research (Riskesdas) in 2013 the results of the interview at age 15 years the
average prevalence of joint disease / arthritis was 24.7%. East Nusa Tenggara (NTT)
was the province with the highest prevalence of OA which is around 33.1% and the
lowest prevalence invitation provinces are Riau which is about 9%, while in East Java
prevalence rate is high at around 27% (Riskesdas, 2013). Approximately 32.99% of
the elderly in Indonesia complained of degenerative diseases such as gout,
rheumatism / arthritis, high blood pressure, low blood, and diabetes (Center for Data
and Information Ministry of Health, 2013). 56, 7% of patients in the clinic of
rheumatology RSUPN Dr. Cipto Mangunkusumo diagnosed with osteoarthritis
(Soenarto, 2010). Symptoms of knee OA is higher in women than in men which is
13% female and 10% male. Murphy, et.al estimate the risk of progression of knee OA
about 40% in men and 47% in women. Oliveria reported an average incidence of OA
of the hip, knee and hands about 88, 240, 100 / 100,000 each year. The incident will
be increased at the age of 50 years and above and decreased at the age of 70 years
(Zhang and Jordan, 2010). Framingham cohort study, 6.8% of people aged 26 years
and older have symptoms of osteoarthritis of the hand with an average of 3.8% of men
and 9.2% women. NADW estimated 13 million of the US population aged 26 years
and older have symptoms of OA of the hand, knee OA was estimated at 9.3 million
(4.9%) and OA of the hip as much as 6.7%. Johnston Country Osteoarthritis (OA
JoCo) Project, a study of knee and hip OA in 43.3% of patients complain of pain and
 stiffness in the joints. This is due to a thickening of the joint capsule and deformation
of osteophytes (Murphy and Helmick, 2012).

C. ETIOLOGY
Some etiologic factors that have known to be associated with the occurrence of knee
osteoarthritis include:
1) Age
The more elderly person, in general, the greater the risk factor for knee
osteoarthritis. This is because the knee joint which is used as a fulcrum weight
often experience a compression or tension and friction, which can cause the
cartilage that lines the hard bone in the knee joint will eventually eroded and
susceptible to degeneration.

2) Obesity
It is obvious that being overweight or obese can be a risk factor for knee
osteoarthritis. Excess weight would add compression or pressure or load on the
knee joint. The greater the load ditumpu by the knee joint, the greater the risk of
damage to the bone.

3) Hereditary or congenital factor

The structure of cartilage and laxity in the joints, as well as the joint surfaces
are irregular one has as a risk factor for congenital factor occurs Osteoarthritis of
the knee.

4) Trauma to the joint and damage to the joints previous

Trauma, collision or injury to the knee joint can also cause damage or
abnormalities in the bones forming the joint.

5) Collinear leg
The angle between the femur and tibia were> 180 degrees can result in load
pedestal supported by the knee joint becomes uneven and localized on one side
only, where the side loads greater tumpuannya be at greater risk of damage.

6) The work and activities of daily living

Employment and akifitas which involve the movement of the knee is also one of
the causes of osteoarthritis of the knee.

D. PATHOPHYSIOLOGY
The development of osteoarthritis is divided into three phases, as follows:
 1) Phase 1: proteolytic degradation in the cartilage matrix. Chondrocyte metabolism
becomes affected and increase the production of enzymes such as
metalloproteinases that was later destroyed in martiks cartilage. Chondrocytes also
produce protease inhibitors that would affect proteolysis. These conditions give
manifestation to thinning of the cartilage.

2) Phase 2: in this phase occurs fibrillation and erosion of the cartilage surface,
accompanied by the release of proteoglycans and collagen fragments into the
synovial fluid.

3) Phase 3: the decomposition of cartilage product that induces inflammatory

responses in synovial. The production of synovial macrophages such as
interleukin 1 (IL-1), tumor necrosis factor-alpha), and metalloproteinases be
increased.(TNF These conditions give back to the cartilage manifestation.
Molecules such as pro-inflammatory nitic oxide (NO) is also involved. These
conditions provide a manifestation of joint architectural changes, and have an
impact on the growth of bone due to the stability of the joint. Architectural
changes and stress joints inflammatory effect on the articular surface makes the
condition progressive disorder.
E. CLINICAL MANIFESTATIONS
Shown osteoarthritis clinical presentation depends on the extent of the impact
of osteoarthritis causes damage to the cartilage (cartilage). Genue osteoarthritis
symptoms are progressive, where the complaint occurred slowly and gradually get
worse. On history clinical conditions commonly obtained are as follows:
Unchecked will grow worse and cause pain each perform certain movements,
especially when weight bearing, but could be improved if rested. In some
patients, joint pain can occur after a long break, for example, sitting in a chair
or in a car seat on a long journey. Sometimes also felt after waking up in the
morning.
The presence of swelling / inflammation in the joints.
Joints pain reddish color.
Fatigue accompanying joint pain.
Difficulty using joints.
Beep on every joint (crepitus). These symptoms do not cause any pain, just
discomfort at each joint (usually the knee).
Changes in bone shape. This is due to the network getting damaged cartilage,
bone began to change shape and become inflamed, causing extreme pain.
SOURCE:

Noor, Zairin. 2012. Gangguan muskuloskeletal 2th edition. Jakarta : salemba medika.
Page 302-317
Soeroso, Joewono. 2015. Ilmu Penyakit Dalam 6th edition Jilid III. Jakarta : interna
publishing. Page 3187-3200.