CARE OF PATIENTS WITH

GOUT AND PAGET’S DISEASE

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Nizza Asfaar
Instructor RCN
OBJECTIVES
By the end of the session, learners will be able to:

 Discussgout and paget’s disease with its

pathophysiology

 Listclinical manifestation and causes of gout

and paget’s disease

 Explain medical and nursing management of

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gout and paget’s disease
GOUT
 Itis a heterogenous group of conditions related to a
genetic defect of purine metabolism that results in
hyperuricemia.

 Over secretion of uric acid or a renal defect resulting

in decreased excretion of uric acid, or a combination
of both occurs.

 Its incidence increases with age and body mass index.

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GOUT
Primary hyperuricemia:

Elevated serum urate levels or manifestation of

urate deposition appear to be consequences of
faulty uric acid metabolism.

Itis caused by severe dieting or starvation,

excessive intake of foods high in purine (shell fish,
organ meat) or heredity.
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GOUT
Secondary hyperuricemia:

Gouty features secondary to any of a number

of genetic or acquired processes, including
conditions in which there is an increase in cell
turnover and increase in cell breakdown.

Altered renal tubular function and some drugs

(ATT) can contribute to uric acid under
excretion. 5
PATHOPHYSIOLOGY OF GOUT

Sudden increase in uric acid levels

Urate crystal precipitate within a joint

An inflammatory response occurs

Attack of gout begins

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CLINICAL MANIFESTATION OF
GOUT
 Acute gouty arthritis (recurrent attacks of severe
articular and periarticular inflammation)
 Tophi (crystalline deposits accumulating in articular
tissue, osseous tissue, soft tissue and cartilage)
 Gouty nephropathy (renal impairment)
 Uric acid urinary calculi
 Trauma, alcohol ingestion, dieting, medications,
surgical stress or illness may trigger acute attack
 Abrupt onset occur at night, awakening the patient
with severe pain, redness, swelling and warmth of
the affected joint. 7
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STAGES OF GOUT
 Asymptomatic hyperuricemia:
Very common biochemical abnormality
Majority of people with hyperuricemia never
develop symptoms of uric acid excess

 AcuteIntermittent Gout (Gouty Arthritis):

Episodes of acute attacks. Symptoms may be
confined to a single joint or patient may have
systemic symptoms
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STAGES OF GOUT
 Intercritical
Gout:
Symptom free period interval between attacks.
May have hyperuricemia and MSU
(monosodium urate) crystals in synovial fluid
 Chronic Tophaceous Gout:
Results from established disease and refers to
stage of deposition of urate, inflammatory
cells and foreign body giant cells in the
tissues. Deposits may be in tendons or
ligaments.
Usually develops after 10 or more years of
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acute intermittent gout.
MEDICAL MANAGEMENT FOR
GOUT
 Polarized light microscopy of synovial fluid to
diagnose gouty arthritis.(visualize the crystal)
 Colchicine: (anti-gout agents) lowers uric acid
deposition and interferes with leukocyte infiltration,
thus reducing inflammation
 Uricosuric agents:( probenecid, benzbromarone and
sulfinpyrazone). inhibits renal reabsorption of urates
and increases urinary excretion of uric acid. It also
prevents tophi formation
 Xanthine oxidase inhibitor ( allopurinol): interrupts
breakdown of purines before uric acid is formed.
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 Corticosteroids: if no response to other therapy
NURSING MANAGEMENT FOR
GOUT
Encourage patient to:

 Restrictconsumption of foods high in purines

and to limit alcohol intake.

 Maintain normal body weight.

 Management of pain and avoidance of factors

that increases pain and inflammation.
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PAGET’S DISEASE (PD)
 It is a disorder of localized rapid bone turnover.
 It is a chronic, progressive bone disease that can
affect one bone (monostotic) or several bones
(polystotic).
 It is the second most common bone disorder after
osteoporosis in the United States.
 Its incidence is slightly greater in men than
women and increases with aging (>50 years).
 Its cause is unknown but evidence suggests that it
may have genetic and environmental influences. 13
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PATHOPHYSIOLOGY OF PD
Primary proliferation of osteoclasts produce bone
resorption(breakdown)

Compensatory increase in osteoblastic activity that

replaces the bone

As bone turnover continues, a classic mosaic

(disorganized) pattern of bone develop

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Increase risk of pathologic fracture
CLINICAL MANIFESTATIONS OF PD
 PD is insidious but asymptomatic.
 Some patients are asymptomatic but have
skeletal deformity whereas few have
symptomatic deformity and pain.
 Mostly identified on X-rays studies.

 Sclerotic changes, skeletal deformities (bowing

of femur and tibia, enlargement of skull,
deformity of pelvic bones) and cortical
thickening of long bones occur.
 Pain, tenderness and warmth over the bones. 16
ASSESSMENT AND DIAGNOSTIC
FINDINGS OF PD
 Elevated serum alkaline phosphatase concentration
and urinary hydroxyproline( a neutral heterocyclic
amino acid) excretion because of increased
osteoblastic activity
 X-rays confirms the diagnosis (mosaic pattern and
irregularities in bones)
 Bone scan demonstrate extent of disease

 Bone biopsy aid in differential diagnosis

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MEDICAL MANAGEMENT FOR PD
 NSAIDs for pain
 Walking aids, shoe lifts and physical therapy for
gait problems.
 Weight control to reduce stress on weakened bones
and malaligned joints.
 Diet adequate in calcium and vitamin D and
periodic monitoring for asymptomatic patients.
 Antiosteoclastic therapy, calcitonin,
biphosphonates and cytotoxic antibiotics to reduce
bone turnover, reverse the course of disease, relieve
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pain, and improve immobility.
 Management of complications (fractures, arthritis ).
PATIENT EDUCATION FOR PD
 Counseling patient about preventing falls and
fractures.
 Avoiding heavy lifting

 Weight control to reduce pain related to weight

bearing.
 Maintaining good bone health is also important
to prevent fractures.
 Encourage patient to stay physically active.

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 Advice patient to adhere to medication regimens
to improve outcomes and prevent disease
complications.
 Advise patient to report any worsening
symptoms that could be a sign of disease
worsening, fracture, or sarcomatous
development.

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