GOUT ARTHRITIS
This can
 is a type of arthritis due to the
accumulation of uric acid in the blood.
1. Over production of Uric acid (10 % of cases
It is a disorder of PURINE
characterized by ELEVATED URIC
LEVELS and deposition of Urates
(usually crystal form) in JOINTS and
other tissues
2. Underexcretion of Uric Acid (90% of cases)
 This causes uric acid crystals to form in
the joints and the patient will
experience severe pain, inflammation,
redness, and limited mobility.
 More common in men but may affect
postmenopausal women especially
those taking diuretics.
WHAT CAN CAUSE GOUT?
What is URIC ACID?
 It is a waste product created from the
purine breakdown during digestion. It
enters the blood stream and is filtered
through the kidneys and excreted out
in the urine. The kidneys play a role in
keeping the uric acid levels within
normal range….therefore, if the kidneys
are damaged there is a high risk of uric
acid levels increasing.
What is PURINE? It’s a chemical compound
used as a building block for nucleic acid (DNA
and RNA) in our body. Foods that are rich in
purine include:
 Internal organ meats (liver, kidneys,
sweetbreads (thymus and pancreas)
 Alcoholic beverages (all types)
 Some fish, seafood and shellfish,
including anchovies, sardines, herring,
mussels, codfish, scallops, trout and
haddock.
 Some meats, such as bacon, turkey,
veal, venison and organ meats like
liver.
PATHOPHYSIOLOGY AND ETIOLOGY
 Results from overabundant
accumulation and deposition of
monosodium urate crystals in joints
and other connective tissue.
occur in TWO WAYS:
 Inherited enzyme defects
 Certain diseases- myeloproliferative
disorders, cancer chemotherapy,
hemolytic anemias, Psoriasis
 due to renal disease, endocrine
disorders, medications (diuretics,
low dose of aspirin, pyrazinamide,
and nephrogenic diabetes
insipidus
 High consumption or intake of purine
rich foods like Internal organ meats
(liver, kidneys, sweetbreads (thymus
and pancreas), high fructose corn syrup
drinks (fruit juice and soda drinks)
 Alcohol…WHY? Alcohol and uric acid
compete within the kidneys, and the
kidneys choose to excrete alcohol
rather than uric acid, which leads to the
buildup of uric acid.
 Kidney problems: kidneys (nephrons)
are unable or not working properly to
filter out the uric acid in the blood so it
accumulates in the blood as in
conditions such as Chronic Kidney
Disease
 Dehydration: urine becomes
concentrated allowing uric acid crystals
to form
 Overweight: increases uric acid levels…
losing weight helps decrease level
 Medications- aspirin (increases uric
acid levels…. niacin, cyclosporine
(immune suppressor) and loop and
thiazide diuretics…WHY? They can
cause dehydration and reduce the
kidney’s ability to excrete urate, which
is part of uric acid.
 Physical stress on the body:
hospitalization due to an illness,
 surgery… stress increases uric acid white/yellowish nodules that can
levels found under the skin (helix of the ear,
fingers, elbow etc.), within the joints,
cartilage, soft tissues or bones . Tophi
CLINICAL MANIFESTATIONS
can lead to bone erosions and
ACUTE GOUT ATTACKS deformity and joint damage.
 happen suddenly or randomly…may  Patients with gout are educated to
only happen a few times or once in a follow a diet that is low in purines,
person’s lifetime and lasts 1-2 weeks. alcohol, and high fructose corn syrup
Some patients may have several drinks. Food high in purines include
months or a year between attacks.
seafood, organ meats, red meat, and
 The joints tend to not become
alcohol (especially beer).
damaged.
 The sudden swelling, redness and pain HYPERURICEMIA
in a joint tends to awake the patient  Produces no symptoms with persistent
from their sleep (middle of the night) elevated uric acid
and tends to affect the big toe (knee,
 Renal calculi of uric acid may develop
elbow, wrist, fingers, heels and toe can
and deposition of this uric acid in the
also be affected).
kidney can cause nephropathy.
 The affected joint will present with
swelling, inflammation, fever and
severe pain, warm to the touch, and
the patient will be unable to tolerate
even the slightest pressure on the site.
 Patient may have flu-like like
symptoms…body aches.
 As the day progresses, the pain
intensifies (4-24 hours), and the patient
may have joint stiffness. The affected
area is VERY sensitive and the slightest
pressure on the joint causes intense
pain.
 Duration of symptoms is self limiting
and last 3-10 days without treatment
CHRONIC TOPHACEOUS GOUT
 is due to constant elevated uric acid
levels that leads to repeated acute
gout attacks or if acute gout is  Complications include itching and
skin peeling and uric acid kidney
inadequately treated or untreated.
stones.
 Joints become permanently damaged
because urate crystals start to form
together in large masses called Tophi.
 In chronic gout, tophi tend to
develop. Tophi are large masses of
uric acid crystals that have formed DIAGNOSTIC EVALUATION
into large clumps. They are
  SYNOVIAL FLUID ANALYSIS- It can
identify monosodium urate crystals
under polarized microscopy
 Synovial WBC Count -Can range from
2000 to 10,000/uL.
 ESR- Elevated due to inflammatory
condition. A test that determines the
rate at which RBC fall out of unclotted
blood in 1 hour.
 24 Hours Urine for uric Acid to
determine overproduction and
underexcretion of uric acids
 Xray- shows joint changes consistent
with diagnosis of gout
Nursing Assessment
 Obtain history for factors predisposing
to Gout such as alcoholism, renal
insufficiency and malignancy
 Perform physical examination.
Inspecting redness, swelling, warm,
effusion and level of pain
 Observe for Tophi over pinna of the ear,
olecranon bursa, big toes, wrist
Nursing Diagnosis
 Acute Pain related to disease process
 Impaired Physical Mobility related to
disease process.
Medical Management as prescribed by the
physician to treat gout:
Acute Management
 NSAIDs-to decrease pain inflammation
 Corticosteroids- intra articular if attack
confined to one or two joints, oral if
attacks involves many joints or other
treatment are contraindicated
COLCHICINE
 Used for both acute attacks and
prevention of further attacks
 IV usually effective for acute attacks
 It decreases swelling and lowers uric
acid levels
 NURSE’S ROLE: Monitor for GI
upset, neutropenia (sore throat, slow
wound healing etc.), and
toxicity muscle pain, tingling/numbness
in finger or toe, gray lips, easy bleeding,
bruising.
 NO grapefruit juice….increases risk of
toxicity
Chronic Management
Anti hyper-urecemic Agents
 Urate lowering agents to prevent
progressive articular damage in case of
asymptomatic hyperucemia and chronic
tophaceous gout
Examples
Probenecid (Benemid) and Sulfinpyrazone
(Anturane)
 Interfere with tubular reabsorption of
uric acid
Allopurinol (Zyloprim):
 Interfere with conversion of
hypoxanthine and xanthine to uric acid
 Works by decreasing the production of
uric acid, hence preventing gout
attacks.
 Used for prevention of gout
attacks doesn’t relieve an acute attacks
 Most commonly taken with colchicine
or NSAIDs
 NURSE’S ROLE: patient needs regular
eye exams to monitor for vision
changes and to avoid vitamin C
supplements while taking due to risk for
renal calculi formation.
Adverse Reactions of Anti Hyper-urucemic
 Headaches, anorexia, NV, allergic
reaction and other blood dyscrasias
and worsening of gout
Nursing Interventions for Gout
RELIEVING PAIN
 Assess patient joints, especially toes,
fingers, elbows for warmth, redness, or
pain
 Assess for a history of gout (especially if
hospitalized) because remember illness
can cause a gout attack
 Assess events leading up to the flare-up
to help patient avoid these type of
events in the future (example: diet…did
the patient recently consume an
excessive amount of food rich in
purine?)
 Cold and warm compresses, if tolerated
by the patient (alternate between cold
and warm)
 Stay hydrated 2-3 liters per day, unless
contraindicated : remember
dehydration further increases uric acid
levels. In addition, staying hydrated
helps prevent uric acid crystals from
forming within kidneys. It assist with
excretion of uric acid and to decrease
stone formation
 Bed rest with affected extremities in a
foot board or cradle to keep area from
pressure (bed linens and accidental
bumps).
 Administer and teach self
administration of pain medications
 Instruct patient to take prescribed
medications CONSISTENTLY because
interruptions in therapy can precipitate
acute attacks
FACILITATING MOBILITY
 Elevate and protect affected joint
during acute attacks
 Assist with ADLs
 Encourage exercise and maintenance of
routine activity in chronic gout except in
during acute attacks
 Protect draining tophi by covering and
applying antibiotic ointment as needed
Health Education and Health Maintenance
 Diet: Low Purine diet to reduce serum
uric acid level
 EDUCATE  patient to determine what is
causing their attacks so they can avoid
future attacks. Every patient varies with
the cause of gout. Some patients will
only have a gout attack when they
consume high amount of alcohol or
seafood while others experience gout
due to an illness where they become
dehydrated.
 Avoidance of obesity and fluctuations of
weight
 Avoid alcohol can precipitate gout
attacks through over production and
decreased excretion of urates
 Avoid, diuretics, and cyclosporins and
Aspirin…it increase uric acid level
 Avoid rapid Weight loss
 Avoid foods rich in purine: red meats,
internal organ meats, seafood, alcohol
(beer), sardines, shellfish, anchovies
Points to remember include:
 The patient has issues with HIGH URIC
ACID levels in the body because the
patient is producing too much uric
acid or not excreting it normally.
 Sharp needle-like urate crystals form
around the joints causing intense
inflammation along with pain
and redness.
 It tends to most commonly occur in
the BIG TOE, but can affect the fingers,
elbow, knee, small toes, wrist.
 Diet management and losing weight
plays a role in managing gout attacks.
Complications
 Uric acid renal calculus
 Urate nephropathy
 Erosive, deforming arthritis
References:
 1. “Gout | Arthritis Basics |  a fixed tightening of muscle, tendons,
CDC.” Cdc.gov. N.p., 2017. Web. ligaments, or skin. It prevents normal
31 July 2017. movement of the associated body part.
 defined as the lack of full passive range
2. What Is Gout?. Bethesda:
of motion (ROM) of a joint resulting
National Institute of Arthritis and
from structural changes of non-bony
Musculoskeletal and Skin
tissues, such as muscles, tendons,
Diseases, 2014. Web. 31 July
ligaments, joint capsules and/or skin. 
2017.
 Contractures develop when normal
elastic connective tissues are replaced
RHEUMATOID ARTHRITIS with inelastic fibrous tissue
  An autoimmune condition that causes  This is cause by muscle or bone injury,
inflammation in the joints. nerve damage, brain injury (stroke or
 This inflammation specifically affects cerebral palsy), muscular dystrophy
the membrane lining of the joint called Etiology
the synovium. Rheumatoid arthritis can  Unknown, but a combined effects of
eventually lead to bone fusion. environmental, infectious and genetics
 What is a joint? It is where two bones Rheumatoid Arthritis Stages:
meet together.
 Common among women than men
 Can happen at any age…most
commonly 20-60 years old….not just in
older adults as in osteoarthritis.
 Cases vary: some patient have severe
chronic cases that last for life time.
While others may have for a short time
and it goes into remission. RA can come
on suddenly or gradually over years.

Pathophysiology

 Due to immunologic response (antigen)

resulting to inflammation of synovium
leading to destruction of articular
cartilage, edema and production of
granular tissue called PANNUS.
 Granulation tissue forms adhesions that
leads to decreased joint mobility. Such
adhesions can occur in supporting
structures such as ligaments and
tendons and cause contractures and
ruptures that affects joint mobility.
CONTRACTURES
1. Synovitis: inflammation of the synovium
 WBCs invade the synovium, which
causes it to become inflamed. This
inflammation leads to thickening, and
the formation of a pannus.
2. Formation of a Pannus:
 A pannus is a layer of vascular fibrous
tissue. The pannus will grow so large it
will damage the bone and cartilage
within the joint. The space in between
 the joints will disappear and anklyosis In the late stages bone deformity occurs (note
will develop. the image below how the fingers are curved at
3 Fibrous ankylosis  the tops and it is symmetrical):
 is a fibrous connective tissue process or
fusion of joints together which results in
decreased range of motion.
4. Bony Ankylosis:
 This is the fusion of the bones. The
patient will have major stiffness and
immobility of the joint.

Clinical Manifestations

 Bilateral Symmetric arthritis most

commonly affects the fingers and wrist.
It can also affect the neck, shoulders,
elbows, ankles, knee, and feet.
Signs and Symptoms of Rheumatoid Arthritis
However, it can extend to the heart,
Seven S’s
skin, eyes, mouth, lungs, and cause
 Sunrise Stiffness (severe pain)
anemia.
 Soft feeling in the joints
 Swelling in the joint (warm)
 The patient will have soft, tender,
 Symmetrical it affects the joint
warm, and swollen joints.
bilaterally
 They will feel very tired (this leads them
 Synovium (affected and inflamed)
to be inactive) and have a fever.
 Systemic (affects not only the joints…
 Hallmark signs: RA affects the same
patient will feel achy, tired, and it can
joint bilaterally. Stiffness and pain will
affect the lungs, heart, anemia etc)
be worst in the mornings (>30 minutes
 Stages (synovitis, pannus, anklyosis)
of stiffness) or after long periods of
inactivity and all types of joints can be
Diagnostic Evaluations
affected.
Rheumatoid Factor (RF)
 A test for macroglobulin found in the
blood of patients with RA. RF has
properties of an antibody and may
directed against immunoglobulin
 Positive 70-80% with RA
ESR and C- reactive protein
- Elevated due to active inflammation
X RAYS
 Changes develops within 2years
 Hands and wrist- marginal erosions and
generalized osteopenia
 Cervical- erosions that produce
atlantoaxial subluxation
 shows joint deterioration
Synovial biopsy
 To detect inflammatory cells assoc. with
RA
Nursing assessment
 Perform joint examination to affected
joints such as ROM of each joint,
 Inspection: Note for presence of heat,
redness, swelling, and possible joint
effusion
 Note for presence of Swan neck (PIP
joint extended, Boutonniere (PIP joint
flex), ulnar deviation (fingers point
toward ulna
 Assess pain level such as the pain rating
scale
 Ask patient questions to help determine
early on if this is RA: does it affect the
symmetrical joints, when is the stiffness
the worst?
 assess patient’s understanding about
RA because management (exercise,
medications) help improve quality of
life and prevent further joint
deterioration.
Assess functional status using the American
College of Rheumatology
Class 1- completely able to perform usual
activities of daily living
Class 2: Able to perform usual self care and
vocational activities but limited to avocational
activities
Class 3: able to perform usual self care activities
but limited to vocational and avocational
activities
Class 4: limited ability to perform usual self care
vocational and avocational activities
Nursing Dx:
 Chronic Pain related to disease process
 Impaired physical mobility r/l to pain
and limited joint motion
Planning
 To reduce and pain and to improve joint
mobility
Nursing Interventions
Pain (need to know how to treat the pain)
 Apply local heat or cold to the affected
joints 15-20 minutes 3-4 times a day.
Heat is best for stiffness using heating
pads or hot showers
 Use of splints
 Encourage pain control measures
muscle relaxation, meditation,
transcutaneous electrical serve
stimulation acupuncture and relaxation
techniques
 Administer pharmacologic agents as
prescribed
Preserving the joints
 improving function and mobility, using
assistive devices)
 Education (medications and
nonpharmacological treatment, the
disease itself)
 Mental status (dealing with depression
and improving self-esteem, pain, alters
life, no cure)
Optimizing Mobility/ Taking care of joints and
decreasing fatigue:
 During flare-ups rest the joints that are
inflamed (no exercise on the joint
 Encourage warm bath or hot shower in
the morning to decrease morning
stiffness. heat (best for stiffness)…
heating pad or hot showers. cold (best
for pain….helps reduce inflammation)
 Use splints, perform ROM or assist in
ADL if necessary to protect the affected
joints
 Refer to PT. Patient needs to maintain
physical exercise as tolerated. This
improves the fatigue and prevents a
decrease in muscle strength. In
addition, it prevents contractions by
keeping the joints in motion.
 Patient needs to schedule times for rest
and to never overexert themselves.
 Monitor for signs and symptoms of
anemia (pale, fatigue, short of breath
on excretion, palpations)….may be
 ordered supplements to promote RBCs  Dexamethasone (Decadron),
production like iron, folic acid, vitamin Methylprednisolone (Medrol),
b 12…at risk for GI bleeding due to Prednisone
medications NSAIDs….watch for dark,  Can be given by mouth, topical, IV,
tarry stools injection into the joint or IM
 Multidisciplinary approach: Physical  Skin become thins and fragile, bruises
therapy and occupational therapy will and tears easily….meticulous skin care
be part of the patient’s care to help  Watch for hyperglycemia, especially
assist with treatment plans. in diabetic patients
 Patient needs to perform routinely  At risk for infection
ROM (range of motion) exercises and
DMARDs (disease-modifying antirheumatic
low impact aerobic exercise (stationary
drugs): 
bike, walking, water aerobics)
 Use assistive devices such as shower
 suppresses immune system from
chair, cane, walkers etc. (make sure the
attacking the joint along with helping
patient is using them correctly to
slow down the destruction of the
promote safety…at risk for injury).
disease on the joints and bones.
These devices help alleviate stress on
 Hydroxychloroquine (Plaquenil)
the joints. These devices include raised
(monitor for vision changes…retinal
toilet seat, tools to help grab items,
damage), Leflunomide (arava),
tools to help button or zip shirts.
Methotrexate (Trexall), Sulfasalazine
(Azulfidine)
Non Pharmacological Management with:
 Lifestyle changes (developing plans for
DMARDS (biologic response modifiers)
rest and exercise)
 Joint support: splints, using assistive
 These drugs are still part of the
device
DMARDs drug category but
 Stay healthy and low stress (cause flare-
are genetically engineered and used in
up)
very severe cases.
MEDICAL MANAGEMENT
 Abatacept, Adalimumab
 No live vaccines, avoid infection
There is no cure for RA. This key is to catch it
(handwashing, avoid crowds and sick
early to prevent the progression of joint
people), keeping appointments to
damage. Use in combination of therapy may be
measure blood levels (wbcs), injection
used depending on the patient’s case
site will be sore…common to have site
reaction
Treatment includes:
NSAIDs
Surgery
 to relieve pain and inflammation
- Synovectomy -replacing the joint with
 Ibuprofen”: may cause GI distress…
an artificial one, removal of the
needs to be taken with food
synovium
- Arthrodesis” (joint fusion) where the
joint is removed and the bones are
fused together with a bone graft.
Corticosteroids
- Total Joint Replacement
 decreases inflammation
It leads to the destruction of the joint within 2
years of the development of the disease, so it
happens fast