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Gout
Gouty Arthritis
Etiology/Pathophysiology
 Gout is a metabolic disease resulting from
an accumulation of uric acid in the blood
 It is an acute inflammatory condition
associated with infective metabolism of
purines.
 Gout can be primary , secondary, or
idiopathic.
 It affects men aproximately 4 times more
than women
Purine
A side note
 Purine is an organic compound commonly
found in the body and is metabolized by
the body into uric acid. People with
primary gout have either an increased
production of uric acid or an impaired
excretion of uric acid, or a combination of
both.
Etiology/Pathophysiology
 In this condition sodium urate crystals are
deposited on the articular cartilage of
joints and in the particular tissue like
tendons. This provokes an inflammatory
reaction of these tissues. These deposits
often increase in size and burst through
the skin to form sinuses discharging a
chalky white material.
Etiology/Pathophysiology
 Normally, the human bloodstream only
carries small amounts of uric acid.
However, if the blood has an elevated
concentration of uric acid, uric acid
crystals are deposited in the cartilage and
tissue surrounding joints. Elevated blood
levels of uric acid can also result in uric
kidney stones.
Etiology/Pathophysiology
 Of all people with gout, 85% have a
genetic tendency to develop the disease.
 Tophi (uric acid crystal deposits ) result in
inflammation of the joint; it is unclear why
this occurs.
 Typically the big toes are involved, but
other joints can be affected
Clinical Manifestations
 Onset occurs at night, with excruciating pain,
edema, and inflammation in the affected joint.
 The pain may be of short duration, or may be
saver and continuous for 5 to 10 days.
 The patient may have repeated attacks or only
one attack in a life time.
 Tophi are seen around the rim of the ear and can
disfigure the ear. Surgical removal may be
needed
Assessment/ Subjective
 Noting a complaint of pain occurring at
night involving the big toe.
 Dietary history, with specific questions
regarding alcohol and foods high in purine
such as organ meats
MMMM PIG Organs Its
what's for dinner
Assessment/Subjective
 Assessment of joints for signs of edema,
heat, discoloration, and limited movement
 Vital sign data may reveal an elevated
temperature and hypertension,
tachycardia, and tachypnea
 Tophi can form in the kidneys causing
impaired function.
Diagnostic tests.
 Serum and urinary uricacid levels
 C.B.C.
 Elevated E.S.R.(Erthrocyte sedimentation rate)
 X- Ray revel cysts and toe bone pockets.
 Synovial fluid will contain urate crystals
Medical management
 Acutely, first line treatment should be pain
relief. Once the diagnosis has been
confirmed, the drugs of choice are
indomethacin, other nonsteroidal anti-
inflammatory drugs (NSAIDs), or intra-
articular glucocorticoids, administered via
a joint injection.
Medical management
 Colchicine was previously the drug of choice in
acute attacks of gout. It impairs the motility of
granulocytes and can prevent the inflammatory
phenomena that initiate an attack of gout.
Colchicine should be taken within the first 12
hours of the attack and usually relieves the pain
within 48 hours. Its main side-effects
(gastrointestinal upset) can complicate its use.
NSAIDs are the preferred form of analgesia for
patients with gout.
Nursing Intervetions
 Interventions are aimed at giving
medications prescribed by the physician
for relief of pain and inflammation
 When giving colochicine it is important to
observe for side effects, such as diarrhea,
nausea, and vomiting.
 Increase fluid intake
 Careful documantation of I and O.
Nursing Intervetions
 Bed rest
 Joint immobilization
 Pt teaching is aimed at giving info about
the disease and stressing the importance
of keeping uric acid levels within normal
limits

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17.gout lecture.ppt

  • 2. Etiology/Pathophysiology  Gout is a metabolic disease resulting from an accumulation of uric acid in the blood  It is an acute inflammatory condition associated with infective metabolism of purines.  Gout can be primary , secondary, or idiopathic.  It affects men aproximately 4 times more than women
  • 3. Purine A side note  Purine is an organic compound commonly found in the body and is metabolized by the body into uric acid. People with primary gout have either an increased production of uric acid or an impaired excretion of uric acid, or a combination of both.
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  • 5. Etiology/Pathophysiology  In this condition sodium urate crystals are deposited on the articular cartilage of joints and in the particular tissue like tendons. This provokes an inflammatory reaction of these tissues. These deposits often increase in size and burst through the skin to form sinuses discharging a chalky white material.
  • 6. Etiology/Pathophysiology  Normally, the human bloodstream only carries small amounts of uric acid. However, if the blood has an elevated concentration of uric acid, uric acid crystals are deposited in the cartilage and tissue surrounding joints. Elevated blood levels of uric acid can also result in uric kidney stones.
  • 7. Etiology/Pathophysiology  Of all people with gout, 85% have a genetic tendency to develop the disease.  Tophi (uric acid crystal deposits ) result in inflammation of the joint; it is unclear why this occurs.  Typically the big toes are involved, but other joints can be affected
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  • 10. Clinical Manifestations  Onset occurs at night, with excruciating pain, edema, and inflammation in the affected joint.  The pain may be of short duration, or may be saver and continuous for 5 to 10 days.  The patient may have repeated attacks or only one attack in a life time.  Tophi are seen around the rim of the ear and can disfigure the ear. Surgical removal may be needed
  • 11. Assessment/ Subjective  Noting a complaint of pain occurring at night involving the big toe.  Dietary history, with specific questions regarding alcohol and foods high in purine such as organ meats MMMM PIG Organs Its what's for dinner
  • 12. Assessment/Subjective  Assessment of joints for signs of edema, heat, discoloration, and limited movement  Vital sign data may reveal an elevated temperature and hypertension, tachycardia, and tachypnea  Tophi can form in the kidneys causing impaired function.
  • 13. Diagnostic tests.  Serum and urinary uricacid levels  C.B.C.  Elevated E.S.R.(Erthrocyte sedimentation rate)  X- Ray revel cysts and toe bone pockets.  Synovial fluid will contain urate crystals
  • 14. Medical management  Acutely, first line treatment should be pain relief. Once the diagnosis has been confirmed, the drugs of choice are indomethacin, other nonsteroidal anti- inflammatory drugs (NSAIDs), or intra- articular glucocorticoids, administered via a joint injection.
  • 15. Medical management  Colchicine was previously the drug of choice in acute attacks of gout. It impairs the motility of granulocytes and can prevent the inflammatory phenomena that initiate an attack of gout. Colchicine should be taken within the first 12 hours of the attack and usually relieves the pain within 48 hours. Its main side-effects (gastrointestinal upset) can complicate its use. NSAIDs are the preferred form of analgesia for patients with gout.
  • 16. Nursing Intervetions  Interventions are aimed at giving medications prescribed by the physician for relief of pain and inflammation  When giving colochicine it is important to observe for side effects, such as diarrhea, nausea, and vomiting.  Increase fluid intake  Careful documantation of I and O.
  • 17. Nursing Intervetions  Bed rest  Joint immobilization  Pt teaching is aimed at giving info about the disease and stressing the importance of keeping uric acid levels within normal limits