A.

Anatomy and Physiology of Joints

Joints are a hinge that keeps the limbs moving properly, also a liaison between
one bony segment and the other, so that the two bones can be moved
according to the type of joint it mediates.
Most of our joints are synovial joints. Bony jointed surfaces are covered with
soft, slippery cartilage. The entire area of the joint is surrounded by a kind of
pouch, formed from a fibrous tissue called a capsule. This tissue is coated
with synovial membranes that produce synovial fluid to "oiling" the joints.
The outside of the capsule is reinforced by fibrous ligaments attached to the
bone, holding it firmly in place and limiting the movement that can be
performed.
Prone joints that coat the ends of bone have a dual function that is to protect
the end of the bone so as not to wear out and allow the movement of the joints

1
smooth / slippery, and as a bridge load and dampening impact. In order to be
prone to functioning well, a good matrix is needed.
Matrix consists of two types of macromolecules, namely:
1. Proteoglycans: which include 10% dry weight prone to joints, contain 70-
80% water, this is what causes resistance to pressure and allows elastic
joint prone
2. Collagen: these components include 50% of the dry weight of the joint,
highly resistant to traction. The more the end of the vulnerable joints
become thicker, so the thickness of the joints will be resistant to collagen
resistant to pull
Joints are a meeting place of two or more bones. Joints can be divided into
three types, namely:
1) Fibrous joints in which there is no cartilage layer, between the bones
connected to fibrous connective tissue, and divided into two subtypes
namely sutures and sindemosis;
2) The cartilaginous joint where the tip is enclosed by hyaline cartilage,
supported by the ligaments, slight movement, and subdivided into
subtypes of syncondrosis and simpisis; and
3) Synovial joints. Synovial joints are joints that can experience
movement, have a joint cavity and the joint surface is covered by
hyaline cartilage. The joint capsule wraps the tendons across the joints,
not widened but folded so they can move fully. Sinovium produces
synovial fluid that is yellowish, clear, not frozen, and contains
leucocytes. Hyaluronidase is responsible for the viscosity of the
synovial fluid and synthesized by the synovial wrap. Synovial fluid
has a function as a source of nutrition for the joint-prone. Types of
synovial joints :
3.1 Ginglimus: flexion and extension, monoaxis.
3.2 Selaris: flexion and extension, abd & add, biaxila;

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 3.3 Globoid: flexion and extension, abd & add; multi-axial sync
rotation;
3.4 Trochoid: rotation, mono axis;
3.5 Elipsoid: flexion, extension, lateral flexion, circumflex, multi axis.
Physiologically the joints are lubricated synovial fluid at the time
of moving pressure occurs which causes the fluid to shift to a
smaller pressure. As movement moves forward, the fluid shifts
preceding the load when the fluid pressure decreases back to back.
(Price, 2005; Azizi, 2004).

B. The Background Theory of Gout Arthtritis

1. Definition
Gout is a disorder that causes errors of purine metabolism that cause
hypersemia (serum uric acid> 7.0 mg / 100ml). This can affect the joints
(legs). Typically, the first metatarsafalangeal joint of the big toe is the
primary side involved. Other joints involved can include knees and ankles.
(Medical Surgical Nursing Care Plan, volume 2)
Gout Arthritis is a clinical syndrome that has a special picture of acute
arthritis. Gout arthritis is more prevalent in men than in women. In men
often about middle age, whereas in women usually approaching the
menopause. (Kapita Selekta Medicine, 3rd edition vol 1).
Gout Arthritis is a clinical syndrome that has a special picture, namely
acute arthritis. It is a type of rheumatic disease whose management is easy
and effective. In contrast to inadequate treatment, gout can cause joint
destruction. This disorder is associated with uric acid kinetic disorder that
is hyperuricemia. (Instructional Science Book of Volume 1, 3rd ed.).

3
2. Etiology
2.1 Symptoms Acute arthritis is caused by a tissue inflammatory reaction
to the formation of monosodium monohydrate crystalline crystals.
Therefore seen from the cause of this disease included in the class of
metabolite abnormalities.
2.2 Factors that play a role in the development of gout are:
2.2.1 Surgery
2.2.2 Trauma
2.2.3 Drugs
2.2.4 Alcohol
2.2.5 Emotional stress
2.2.6 High purine diet
2.3 Excessive formation of uric acid
2.3.1 Gout primary metabolically due to the increased direct
synthesis.
2.3.2 Secondary metabolic gout caused by excessive uric acid
formation due to disease.
2.3.3 Secondary metabolic gout caused by excessive uric acid
formation due to disease.
2.4 Lack of uric acid expenditure
2.4.1 Gout primer renal occurs due to impaired uric acid excretion
distal renal distal
2.4.2 Secondary renal gout is caused by kidney damage.

3. Clinical Manifestation
There are four stages of untreated gout clinical travel: (Silvi A. price)
3.1 The first stage is asymptomatic hyperuricemia. At this stage male
serum uric acid is elevated and asymptomatic aside from elevated
serum uric acid.

4
 3.2 The second stage of acute gout arthritis occurs sudden onset of
swelling and extreme pain, usually in the joints of the toes and
metatarsophalangeal joints.
3.3 Stage three after an acute gout attack is an intercritical stage. There
are no symptoms at this stage, which can last from months to years.
Most people experience recurrent gout attacks in less than 1 year if
left untreated.
3.4 The fourth stage is a chronic gout stage, with a buildup of uric acid
that continues to expand for several years if treatment does not begin.
Chronic inflammation of uric acid crystals results in pain, pain, and
stiffness, as well as enlargement and protrusion of swollen joints.

4. Classification
According to (Ahmad, 2011) type of uric acid that is:
4.1 Primary gout
In primary gout, 99% of the cause is unknown (idiopathic).
4.2 Secondary gout
In secondary gout is caused among others due to increased production
of uric acid due to nutrients, ie eating foods with high purine levels.

5. Complication
5.1 Erosion, deformity and inability of activity due to chronic
inflammation and tofi causing joint degeneration.
5.2 Hypertension and albuminuria.
5.3 Renal tubular damage leading to chronic renal failure.

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6. Pathophysiology
The presence of impaired purine metabolism in the body, intake of
substances containing high uric acid, and urinary acid excretion system
will result in excessive accumulation of uric acid in the blood plasma
(Hyperurecemia), resulting in uric acid crystals accumulate in the body.
This accumulation raises local irritation and generates an inflammatory
response.
Hyperurecemia is the result:
6.1 Increased production of uric acid due to abnormal purine metabolism.
6.2 Decreased uric acid excretion.
6.3 Combination of both.
When uric acid becomes accumulated in blood and other body fluids, the
uric acid crystallizes and will form the uric salts that will accumulate or
accumulate in the connectiv tissue throughout the body, this buildup is
called tofi. The presence of crystals will trigger an acute inflammatory
response and neutrophils release the lysosome. Lysosomes not only
damage the tissues, but also cause inflammation.
In acute gout disease no symptoms are present. Serum urate increased but
will not cause symptoms. Over time this disease will cause hypertension
due to the buildup of uric acid in the kidneys.
The first acute attack is usually very painful and quickly peaked. This
attack includes only one joint. This first attack is very painful that causes
joints become soft and hot, red. Metatarsophalangeal joint bones are
usually the first to be inflamed, then the ankles, heels, knees, and lumbar
joints. Sometimes the symptoms are accompanied by a mild fever. It
usually progresses quickly but tends to recur and with irregular intervals.
The intercritical period is a period in which there are no symptoms during
a gout attack. Most patients experience a second attack on the 6th to 2nd
month after the first attack. The next attack is called polyarticular which

6
 invariably attacks the joints of the foot and arms usually accompanied by
fever. The final stage of chronic gout or gout attacks is characterized by
polyarthritis that goes sick with a large tofi on the cartilage, synovial
membrane, tendon and fine tissue. Tofi is formed in the fingers, hands,
knees, feet, ulnar, helices on the ear, achilles tendons and internal organs
such as the kidneys. The outer skin undergoes ulceration and emits liming,
an exudate made up of uric acid crystals.

7. Pathway

7
8. Diagnostic Examination
8.1 Laboratory examination
Increased levels of uric acid in the blood (> 6 mg%)
8.2 Examination of enzymatic uric acid levels.
8.3 There was mild leukocytosis
8.4 LED rises slightly
8.5 Urine examination
High uric acid levels (500 mg% / liter per 24 hours)
8.6 Tofu fluid examination
8.7 See the response of symptoms in the joints to the administration of
Cholasin. Cholacin is a drug that inhibits the phagocytic activity of
leukocytes to give it a change so as to give dramatic changes and
quickly relieve symptoms.

9. Management
Gout handling is usually divided into the handling of acute and chronic
attacks. There are 3 stages in the treatment of this disease:
9.1 Overcoming an acute attack
9.2 Reduce uric acid levels to prevent accumulation of urate crystals in
the tissues, especially joints
9.3 Preventive therapy using hypouresemic therapy
a. Non-pharmacological therapy
Non-pharmacological therapy is an essential strategy in gout
management. Interventions such as adequate rest, use of cold
compresses, diet modification, reduced alcohol intake and weight
loss in overweight patients are proven effective.

8
b. Pharmacological therapy
1. Acute attacks
Rest and prompt treatment with NSAIDs, such as indomethacin
200 mg / day or diclofenac 159 mg / day, is the first-line therapy in
dealing with acute gout attacks, provided there is no
contraindication to NSAIDs. Aspirin should be avoided because
aspirin excretion is competent with uric acid and may aggravate
acute gout attacks. Drugs that lower serum uric acid levels
(allopurinol and uricosuric drugs such as probenesid and
sulfinpyrazone) should not be used in acute attacks.
Treatment of NSAIDs, cyclooxigenase-2 (COX 2) inhibitors,
colchicine and corticosteroids for acute attacks are discussed
below:
1.1 NSAIDs are an effective first-line therapy for patients who
experience acute gout attacks. NSAIDs should be given at
full dose in the first 24-48 hours or until the pain is gone.
Common NSAIDs used to treat acute gout episodes are:
1.1.1 Naproxen-early 750 mg, then 250 mg 3 times / day
1.1.2 Piroxicam- an early 40 mg, then 10-20 mg / day
1.1.3 Diclofenac - initial 100, g, then 50 mg 3x / day
1.2 COX-2 inhibitors; Etoricoxib is the only COX-2 licensed to
deal with acute gout attacks. These drugs are effective but
quite expensive, and are particularly beneficial for patients
who are not resistant to the non-selective gastrointestinal
effects of NSAIDs. COX-2 inhibitors have a lower risk of
upper gastrointestinal side-effects than non-selective
NSAIDs.
1.3 Colchicine is a specific and effective therapy for acute gout
attacks. However, compared to NSAIDs are less popular

9
 because they work more slowly and side effects are more
common.
1.4 Steroids are alternative strategies other than NSAIDs and
colchicine. This method can ease the attack quickly when
only 1 or 2 joints are affected. However, careful differential
diagnosis of atrithis sepsis and acute gout should be
carefully considered.
2. Chronic attacks
Long-term control of hyperuriesmia is an important factor to
prevent acute gout attacks, kidney involvement and uric acid
stones formation. The use of allopurinol, urikourik and
feboxsotat for chronic gout therapy is described below:
2.1 Allopurinol; the preferred hypoutesemic drug for chronic
gout is alluporinol, in addition to symptom control, it also
protects kidney function. Allopurinol decreases uric acid
production by inhibiting the enzyme xanthine oxidase.
2.2 Uricosuric drugs; most patients with hyperuresmia who
slightly excrete uric acid may be treated with uricosuric
drugs. Uricosuric as probenecid (500 mg-1 g 2x / day).

C. The Basic Theory of Nursing Care Report

1. Assessment
1.1. Identity
Name, age (about 50 annual), address, religion, gender (usually 95%
of gout sufferers are men), etc.
1.2. Main complaint
In general, clients feel tremendous pain in the joints of the big toe
(other joints)
1.3.Disease History Now

10
 P (Provocative): Assess the cause of pain
Q (Quality / quality): Assess how often clients feel pain
R (Region): Assess the joints that feel pain (usually at the base of the
thumb)
S (Saverity): `Does it interfere with motor activity?
T (Time): Assessing when the pain is felt? (Usually happens at night)
1.4. Past Medical History
Ask clients whether they have kidney disease?

1.5.Family Disease History

Ask if ever a family member of a client suffers the same illness as the
client is currently suffering.
1.6.Psychosocial and Spiritual Assessment
1.6.1 Psychology: Usually clients experience increased stress
1.6.2 Social: Tend to pull away from the environment
1.6.3 Spiritual: Assess what the patient's religion is, how the patient
carries out the worship according to his religion
1.7.Daily Needs Fulfillment
1.7.1 Nutritional needs
1.7.2 Eat: Assess the frequency, type, composition (taboo of protein-
rich foods)
1.7.3 Drinking: Assess frequency, type (abstinence alcohol)
1.7.4 The need for elimination
1.7.5 Urination: review the frequency, amount, color, odor
1.7.6 Defecate: review the frequency, quantity, color, odor
1.7.7 Activity needs
1.7.8 Usually clients are inadequate / unable to perform their daily
activities independently due to pain and swelling

11
2. Physical Examination
2.1 General situation:
2.1.1 Level of consciousness
2.1.2 GCS
2.1.3 Vital Signs
2.2 Improved sensing
2.2.1 System integument
Skin appears red or purplish, toned, smooth, and felt warm
2.2.2 Sensing system
Eyes: Assess vision, shape, visus, color sclera, eyeball movement
Nose: Assess the shape of the nose, there is a disturbance of smell
or not
Ears: Assess of hearing, there is a hearing loss or not, usually there
is a tofi on the ear
2.2.3 Cardiovascular system
Inspection: Is there a jugular vein enlargement
Palpation: Assess pulse frequency (takhikardi)
Auscultation: Is the heart sound normal S1 + S2 single / there is
additional sound
2.2.4 Digitizing system
Inspection: Assess abdominal shape, presence or absence of
enlargement in the abdomen
Palpation: Is there any tenderness on the abdomen
Percussion: Is bloated / not
Auscultation: Is there an increase in bowel sounds
2.2.5 Muskuluskeletal system
Usually there is a sudden swelling (on the thumb) and extreme
pain and can also form crystals in the peripheral joints, deformity
(joint enlargement)

12
2.2.6 Urinary system
Nearly 20% of people with gout have kidney stones

3. Nursing Diagnosis
3.1 Joint pain related to joint inflammation, crystal accumulation on
synovial membrane, articular cartilage, cartilage erosion, synovia
prolifera and panic formation.
3.2 Barriers to physical mobilization related to decrease in range of
motion, muscle weakness, movement, and stiffness in the foot joint
secondary to cartilage erosion, synovial proloferation, and panic
formation.
3.3 Self image disturbance related to changes in the shape of the feet
and the formation of tofus.

4. Intervention
4.1 Joint pain related to joint inflammation, crystal accumulation on
synovial membrane, articular cartilage, cartilage erosion, synovia
prolifera and panic formation.
Goals : Pain is reduced, lost, resolved.
Results criteria:
 Client reported pain search.
 Show more relaxed behavior.
 Demonstrating pain reduction skills.
 Pain scale 0 - 1 or resolved.

13
 Intervention Rational
1) Assess location, intensity, and 1) Pain is a subjective response
type of pain. Observe progress of that can be studied using a
pain to new area. Assess pain pain scale. Clients report
with a scale of 0 - 4. pain usually above the level
2) Assist clients in identifying of injury.
trigger factors. 2) Pain is affected by anxiety
3) Explain and help clients relate to and inflammation in the
non-invasive and non-invasive joints.
pain relief measures. 3) Approach by using
4) Teach relaxation: techniques relaxation and
related to skeletal muscle tension pharmacologilain shows
that can reduce pain intensity. effectiveness in reducing
5) Teach methods of distraction pain.
during acute pain. 4) Will launch blood
6) Increase the knowledge about the circulation so that oxygen
cause of the pain and the requirement in network is
relationship with how long the fulfilled and reduce pain.
pain will last. 5) Multiply the client's
7) Avoid clients drinking alcohol, attention to pain to the fun.
caffeine, and diuretic 6) Such knowledge helps to
medications. reduce pain and can enhance
8) Collaboration with medical team client adherence to
for administration of allopurinol therapeutic plan.
7) The use of alcohol, caffeine,
and diuretic medications will
increase uric acid levels in
serum.

14
 8) Alopurinol inhibits uric acid
biosentesis resulting in lower
serum uric acid levels
4.2 Barriers to physical mobilization related to decrease in range of
motion, muscle weakness, movement, and stiffness in the foot
joint secondary to cartilage erosion, synovial proloferation, and
panic formation.
Goals : the client is able to carry out physical activity in
accordance with its ability.
Result criteria:
 Clients participate in the training program
 Have no joint contractures
 Muscle strength increases
 The client demonstrates actions to improve mobility and
maintain optimal coordination.

Intervention Rational
1) Review existing mobility and 1) Knowing the level of ability
observe increased damage. of clients in performing
2) Teach clients to exercise active activities.
motion on the non-painless 2) Active movement gives a
ekstermities. period of tone, and muscle
3) Help clients perform ROM strength, as well as improve
exercises and self-care according heart and respiratory
to tolerance. function.
4) Monitor progress and 3) To maintain the flexibility of
development of the client's ability the joints according to the
to perform activities ability.

15
5) Collaboration with 4) To detect client development.
physiotherapists for physical 5) The ability to mobilize
exercise of the client. ekstermitas can be enhanced
by physical exercise from the
physiotherapy team.
4.3 Self image disturbance related to changes in the shape of the feet
and the formation of tofus.
Goals : The client's self-image increases
Results criteria:
 The client is able to say or communicate with the person
closest to the situation and the changes that occur
 Able to express acceptance of self to the situation
 Recognize and combine self-conceptualization in self-concept
with an accurate way without feeling negative self-esteem.

Intervention
1) Assess the change in perspective
and its relationship with the degree
of inability.
2) Reclaim the reality that you can
still use the diseased side and learn
to control the healthy side.
3) Help and advise good care and
improve habits.
4) Advise people closest to allow
clients to do as much as possible
for themselves.
5) Together with clients looking for
Rational
1) Determining individual
assistance in preparing a
treatment plan or selection of
interventions
2) Help clients see that the
moment of receiving both
parts of the whole body and
start accepting new situations.
3) Help improve feelings of self-
worth and control more than
one area of life.
4) Reinvigorate the feeling of

16
 positive coping alternatives.
6) Support the behavior or effort of
enhancing interest or participation
in rehabilitation activities.
7) Collaboration with
neuropsychologists and counseling
experts when indicated.
self-help and help in the
process of self-esteem and
affect the rehabilitation
process.
5) Nursing support to clients can
increase the client's
confidence.
6) Clients can adapt to change
and understand the role of
individuals in the future.
7) Can facilitate important role
changes for the development
of feelings..

5. Implementation
According to Carpenito (2009, p. 57). components of implementation in
the nursing process include the application of the skills necessary to
implement nursing interventions. Skills and knowledge needed for
implementation are usually focused on :
1) Doing activities for clients or helping clients.
2) Conduct a nursing assessment to identify a new problem or monitor
the status of an existing problem
3) Provide health education to help clients gain new knowledge about
their health or management disorders.
4) Help clients make decisions about their own health services
5) Consult and make referrals to other health professions to get the right
direction.
6) Provide specific actions to eliminate, reduce, or resolve health issues.

17
7) Help clients do their own activities
8) Help clients identify risks or problems and explore available options.
6. Evaluation
Evaluation is the last step of the nursing process by identifying the extent
to which the goal of the nursing plan is achieved or not. In evaluating the
nurse should have knowledge and ability to understand the response to the
nursing intervention, the ability to describe the conclusions about the
objectives achieved and the ability to link the nursing actions to the
outcome criteria (Hidayat, 2008. p. 124).

18
 Bibliography

Muttaqin, Arif. 2008. Buku Aajar Asuhan Keperawatan Klien Gangguan

Muskuloskeletal. Cet.1. Jakarta : EGC.

Price, Sylvia.A. 2006. Patofisiologi : Konsep Klinis Proses-proses Penyakit. Ed.6 ;

Cet.1 ; Jil.II. Jakarta : EGC.

Setiadi. 2007. Anatomi dan Fisiologi Manusia. Cet. 1. Yogyakarta : Graha Ilmu.

Carpenito, L.J. (2009). Diagnosis Keperawatan: aplikasi pada praktik klinis. Edisi ke
Sembilan. Jakarta : EGC.

Hidayat, A.A,. (2008). Pengantar Konsep Dasar Keperawatan, edisi kedua. Jakarta :
salemba medika.

Persatuan Ahli Penyakit dalam Indonesia.1996.Buku Ajar Ilmu Penyakit Dalam. Jilid
I edisi III. Jakarta: Balai Penerbit.

Doengoes, Marilynn E , dkk. 1999. Rencana Asuhan Keperawatan. Edisi 3. Jakarta:

Buku Kedokteran EGC.

Fakultas Kedokteran UI.2000. Kapita Selekta Kedokteran. edisi 3, Jilid I. Jakarta:

Media Aescul

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