A CASE PRESENTATION ABOUT

OSTEOARTHRITIS,
RHEUMATOID
ARTHRITIS,
AND GOUT

Presented by: Ryunosuke C. Aguilar

Topic Outline
I. DEFINITION
II. EPIDEMIOLOGY
III. ETIOLOGY
IV. ANATOMY
V. PATHOPHYSIOLOGY
VI. DIFFERENTIAL DIAGNOSIS
VII. DIAGNOSTIC PROCEDURE
VIII. LAB PROCEDURE
IX. PHARMACOLOGICAL TREATMENT

TODAY'S
DISCUSSION
 1. JOINT
Articulation", any adjacent bones or bone and cartilage bones
or bone and cartilage.

2. SYNOVIAL MEMBRANE
A connective tissue that lines the inside of the capsule, which
produces a fluid that also helps to reduce friction and wear in a
joint.

ANATOMY & 3. SYNOVIAL FLUID

synovia = “a thick fluid”), a thick, slimy fluid that provides
PHYSIOLOGY lubrication to further reduce friction between the bones of the joint.

4. TENDON SHEATH
A connective tissue sac that surrounds a muscle-tendon at
places where the tendon crosses a joint.

5. CARTILAGE
Covers the surface of a bone at a joint which reduce the
friction.
 6. LIGAMENTS
Surround the joint to give support and limit the joint's
movement Ligaments connect bones together.

7. TENDONS
Attach to muscles that control the movement of the joint.
Tendons connect muscles to bones

ANATOMY & 8. ARTICULAR/ JOINT CAPSULE

Completely envelopes the freely movable joints. Absorb shock
PHYSIOLOGY and reduce friction during movement.

9. BURSA .
Fluid-filled sacs, between bones, ligaments, or other nearby
structures. They help cushion the frictionin a joint.

10. MENISCUS
Curved partof cartilage in the knees and other joints.
JOINT CLASSIFICATIONS:
JOINT CLASSIFICATIONS:
JOINT SUBCLASSIFICATIONS:
SYNOVIAL JOINTS
CARDINAL SIGNS OF ORGAN SYSTEM
INFLAMMATION INVOLVED

RADICULOPATHY
ARTHRITIS CLASSIFICATION:
 OSTEOARTHRITIS

Aka osteoarthrosis or degenerative joint disease

Progressive destruction of articular cartilage and the
formation of bone at the margins of the joint.
Disease involving the entire jointincluding the
periarticular musculature
 ETIOLOGY
Aging - strongly associated but does not itself causes it
Genetic factors - 39% hand OA, 65% hip knee in women, and 70% OA of the
spine.
Trauma - before adulthood, initiate remodeling of bone - alters joint mechanics
and nutrition Occupational tasks - heavy lifting (hip OA); kneeling and heavy
lifting (knee OA).
Malalignment and Limb Length Discrepancy Varus malalignment -
strongest predictor of dse progression in the knee
Femoroacetabular impingement (FAI) - mechanical mismatch between the
femoral head and acetabulum.

Obesity - most evident in the knee incidence is women>men

 EPIDEMIOLOGY
Most common form of arthritis
Extremely prevalent among individuals over 40 y/o
Widespread in adults older than 65 y/o
Affects more men than women before age 50,
but reverses after age 50.
 PATHOPHYSIOLOGY
Repeated excessive loading of normal cartilage and subchondral bone,
or normal loading of biologically deficient cartilage and subchondralbone
-> microcracksand uneven distribution of chondrocytes.

Affects the entire joint, including the articular cartilage, synovium,

subchondral bone and surrounding connective tissues.

The degenerating, thinning cartilage is less able to redistribute forces,

causing hardening and the formation of osteophytes (bone spurs) at
joint margins.

As the joint surface deteriorates, the joint capsule may become lax,
leading to joint instability.

The most affected joints are the weight-bearing synovial joints of the
lower extremity, the spine and the CMC and DIP joints of the hand.

Factors contributing to OA include aging, excess body weight,

occupational or sport joint injury, and metabolic or endocrine disorders.
 CLINICAL S/SX

Upper extremity - commonly involved are DIP, HANDS & FINGERS DIP & PIP
PIP and CMC joints.
Cervical and lumbar spine, hips, knees, and LOM, poor grip strength, bony nodes, and joint
MTP of great toe. angulation
MCP, wrist, elbow, and shoulder -usually (+) Bouchard's and Heberden's
pared n primary OA. nodes - tender in early stages, restricted ROM
No bilateral, symmetrical presentation (except and fine motor skills later
w/ generalized OA) 1st CMC - pain or aching at the base of the
No systemic complaints (fatigue, morning thumb, dec. pinch strength and squaring of the
stiffness, fever, or loss of appetite thumb (due to thenar mm weakness and
May have (+) stiffness in awakening particular contracture)- abd, ext, opposition
joints similar to felt after inactivity during day
but not >30 minutes. Crepitus is common.
HIP
Pain – worsens with motion, except in later
Limp and LOM - flexed, abducted and ER
stage when it is present at rest and with
position
activity. Pain - groin, buttocks, trochanteric or knee
region
Decreased walking speed, stride length,
poor balance and increased energy
expenditure.
 SPINE

KNEE Lower cervical and mid to lower

lumbar - most susceptible to OA
Early: pain with weight-bearing activities Facet joint osteophytes - lateral
Late: pain and stiffness after prolonged
sitting
and central lumbar stenosis and
Joint locking and buckling – increased risk subsequent nerve root
of falling impingement
Medial joint - medial joint space narrowing
leading to psuedolaxity of the MCL,
Pain from the facet joint OA
stretching LCL and genu varus deformity. increases with
spinal extension, rotation,
FEET & TOES standing or sitting.
Lying and spinal flexion -
First MTP - MC site of OA - hallux valgus
or hallux rigidus deformity pain relief
Other MTP joint - hammertoes
Forefoot involvement - poor push-off in
the terminal stance phase of gait
and balance problems.
 DIAGNOSIS
1.Kellgren and Lawrence's Classification
Grade 0: Normal radiograph
Doub tful narrowing of the joint sp ac e an d po ssible osteophytes
Grade 1:
ab se nt or qu es tiona ble narrowing of the joint space
Grade 2:Definite osteophytes and
yte s an d joint sp ace narro wing , some scler osis, and possible
Grade 3: Moderate osteoph
deformity
rked na rro wi ng of joint sp ac e, se ve re sc ler osis, and definite
Grade 4: Large osteophytes, ma
deformity
by a na rro wing of the sp ac e be tw ee n the bo nes in your joint. An
2. X-rays. Cartilage loss is revealed
X-ray can also show bone spurs around a joint.
tailed im ag es of bo ne an d so ft tissu es , includ ing cartilage.
Magnetic resonance imaging (MRI) - de
dia gn os e os teo ar thr itis bu t ca n he lp pr ov ide more information in
An MRI isn't commonly needed to
complex cases.
oth er ca us es of joi nt pa in, su ch as rheu ma toid arthritis.
Blood tests - Rule out pa in is
inf lam ma tion an d to de ter mi ne wh ether yo ur
Joint fluid analysis - The fluid is then tested for
caused by gout or infection rather than
 DIFFERENTIAL DIAGNOSIS
1. Periarticular structure derangement: Periarticular pain that is not
reproduced by passive motion or palpation of the joint should
suggest an alternate etiology such as bursitis tendonitis, or
periostitis.

2. Inflammatory arthritis: If the distribution of painful joints includes

MCP, wrist, elbow, ankle, or shoulder, OA is unlikely, unless there
are specific risk factors (such as occupational, sports-related, history
of injury).

3. Other inflammatory/systemic conditions: Weight loss, fatigue,

fever, and loss of appetite suggest a systemic illness such as
polymyalgia rheumatica, rheumatoid arthritis, lupusor sepsis, or
malignancy.
 TYPES OF
OSTEOARTHRITIS

PRIMARY (Idiopathic) - involves the

hands in a more symmetrical fashion
and has a stronger genetic
association. Localized (one or two
joints affected). Generalized
(affecting three or more joints).

SECONDARY - caused by (e.g.,

trauma, bio mechanical factors,
congenital malformation, or another
musculoskeletal disease).
 COURSE/ PROGNOSIS

Insidious and may progress undetected some individuals.

Initial stage - episodic pain triggered by specific activity

Late-stage – pain is chronic, dull ache accentuated with

episodic severe pain. No systemic feature such as
fatigue, fever, or malaise. A slowly progressive condition
Prognosis is variable and not necessarily bad. Co-
morbidities contribute to increasing disability
ORAL ANALGESICS, NSAIDS, AND CORTICOSTEROID
INJECTIONS

Acetaminophen, an oral analgesic, is usually the drug of the

first choice.

Intra-articular corticosteroid injections are often used for acute

episodes with a moderate effect for pain relief. The knee is the
most common site. Viscosupplementation or intra-articular
injections of the knee.

Topical agentsinclude analgesics andanti- inflammatory

preparations.

MANAGEMENT:
PHARMACOLOGICAL
 MANAGEMENT:
PHYSICAL THERAPY

Deep healing modalities, such as ultrasound,

may affect the viscoelastic properties of
collagen and providing modest improvements
in function in individuals with knee OA.

Electrical agent - TENS

Orthoses, Splints, and Braces Cardiovascular

Training

Rom, strengthening, stretching and relaxation

exercise
 MANAGEMENT:
SURGICAL

ARTHROSCOPY, ARTHROPLASTY, AND ANGULATION OSTEOTOMY

May provide symptomatic relief, improved motion, and improved joint
biomechanics.

ARTHRODESIS - to relieve pain, result to a very stable joint but sacrifices

freedom of motion.

OSTEOTOMY - improve joint alignment.

ARTHROPLASTY - joint replacement to relieve pain and restore function

 MANAGEMENT:
SURGICAL

HIP AND KNEE REPLACEMENTS

The most common major orthopedic procedure performed in the elderly
is hip surgery.

SOFT TISSUE PROCEDURES

Synovectomy
Soft tissue release Tendon transfer
RHEUMATOID ARTHRITIS

Is primarily a disease of the synovium

systemic inflammatory disease autoimmune and
inflammatory disease.
 ETIOLOGY
An autoimmune disease of unknown
complex etiology

Main histocompatibility complexes - HLA-

Dw4 and DR4 are present Infection by
viruses and organisms – synovitis
 OGY
IOL
IDEM
EP
F>M, 2:1
Whites >African Black, Japanese, and Chinese Approximately
40 per 100,000 persons in the United States and northern
European countries.
Begin at any age, but the likelihood increases with
age. Patients most commonly are first affected in the
third to sixth decades.
Estimated prevalence of 1 to 2%- worldwide
5%in women over age 55
 PATHOPHYSIOLOGY
Inflammation of the synovium, peripheral articular cartilage,and
subchondral marrow spacesleading to granulationtissue
(pannus) forms -> erosion of articular cartilage.
Synovial inflammation leads to pain, stiffness, and limited
mobility.
The joint capsule becomes inflamed and immune cells degrade
the cartilage.

Rheumatic factor - antibody specific to IGg

Seropositive RF
(+) RF, (+) RA, 70% more severe disease association
(+) rheumatoid nodules = necrotic cell
Seronegative FR
(-) RF
Better prognosis
 CLINICAL S/SX

1 . Morning stiffness - hallmark clinical feature

2. Swelling (3 or more joints) erythema
3. Bilateral and symmetrical synovial joint
involvement. Limited mobility and signs of
inflammation including pain, redness, swelling,
crepitus, and warm joints. The most common joints
involved are the hands, feet, and cervical spine with
the hands generally affected early in the disease
course.
4. Systemic features of RA include weight loss, fever,
and extreme fatigue.
 CERVICAL SPINE
Occipito atlantal and Atlantoaxial joints frequently affected due to their
extensive synovial tissue.
Mid cervical - region is also a common site of inflammation inflammation
LOM – rotation
Ankylosing (i.e., fusion) of one or more vertebrae of the spine can lead to
loss of ROM and function of the involved joints.
TMJ
Limitation of mouth opening
Lag Phenomenon - the difference between active and passive ROM
SHOULDERS
Joint surface degeneration, pain, and loss of ROM (GH, SC, or AC joints).
Subluxation, tendinitis, and bursitis
LOM – Internal rotation
ELBOWS
LOM – Pronation and Supination
Flexion contracture
Effusions between the lateral epicondyle and olecranon prominence
Bilateral swelling of the olecranon bursa
Rheumatoid nodules on the olecranon or ulna
 WRISTS
Flexion contracture – diminishes the ability to grasp
Carpal tunnel syndrome – compressed median nerve
Ulnar deviation or drift – due to chronicinflammation causing movement of
the wrist toward the ulna
Volar subluxation – due to chronic inflammation of the proximal row of
carpals
HANDS - MCP
Ulnar drift of the MCP
Bowstring effect
Zigzag effect Trigger finger
HANDS - PIP & DIP
Swan neck deformity – PIP hyperextension and DIP flexion Boutonniere
deformity –DIP extension and PIP flexion
Bouchard nodes- osteophytes found at the PIP
Mallet finger – DIP extension; rupture of the EDC tendon
Heberden’s nodes – osteophytes found at the DIP
HANDS - THUMB (CMC)
Flail IP – loses the ability to flex the Ips
Mutilans deformity – opera-glass hand
 KNEE
Synovitis – accumulation of a large amount of fluid
Baker’s cyst – posterior accumulation of fluid in the knee; produces
pain, swelling, and heat in the posterior calf when ruptured
Anterior synovitis, Anterior synovitis
HIP
Pain in the groin and medial thigh, Pain due to trochanteric bursitis
Protrusio acetabuli –femoral head and the acetabulum may push the
acetabulum into the pelvic cavity
Trendelenburg and LE is positioned to FABER LOM - IR
DECONDITIONING
Significant clinical feature of RA Demonstrated with diminished:
cardiorespiratory status
muscular strength and endurance flexibility altered body composition
Direct Impairments:
loss of type II muscle fibers
systemic fatigue, cachexia (wasting of lean mass)
Shortening of contractile tissue
Indirect Impairments:
Deconditioning secondary to inactivity
Elevated resting energy expenditure
OCULAR COMPLICATIONS CARDIOPULMONARY
Episcleritis and Scleritis COMPLICATIONS
Ischemic heart disease
RHEUMATOID NODULES atherosclerosis
(+) in 20-25% with seropositive RF found in Pericarditis
subcutaneous areas subjected to repeated Pulmonary involvement
mechanical Pressure: (men>women) Pleuritis
Olecranon bursa Pulmonary nodules
Extensor surface of the Forearm
Achilles tendon DEATH FREQUENT CAUSE:
Infection
VASCULAR & NEUROLOGIC COMPLICATIONS Ischemic heart disease
VASCULITIS Renal disease Respiratory
discoloration of nail beds, purpura (red or disease
purple discoloration), and petechiae (red or GI disease
purple spots).
Peripheral neuropathies such as wrist or foot
drop, CTS, and tarsal tunnel syndrome
Rheumatoid arteritis
malnutrition, infection, CHF, and GI bleeding
 DIAGNOSIS
1. The 1987 Revised Criteria for the classification of Rheumatoid Arthritis
2. American College of Rheumatology Revised Criteria for Classification of Functional Status
in RA
Class I - independent
Class II - able to perform with pain
Class III - - able to do some
Class IV - unable to perform
3. The 2010 American College of Rheumatology (ACR and European League Against
Rheumatism (EULAR)
LABORATORY TESTING
1. Erythrocyte Sedimentation Rate (ESR) & C-Reactive Protein (CRP)
Indicate the presence of active inflammation

2. Rheumatoid Factor (RF)

Presence or absence alone can neither confirm nor rule out a dx of RA. Nearly 25% do
not have positive RA (seronegative RA)
3. Complete Blood Count (CBC)
RBC - decreased (anemia), found in 20% with RA
WBC - normal
Thrombocytosis - not uncommon in active RA
4. Synovial Fluid Analysis
Normal - transparent, yellowish, viscous, and without clots b. Inflammation - cloudy, less
viscous owing toa change in hyaluronate proteins, and will clot
5. Mucin Clot Test (viscosity of the synovial fluid)
Discriminates between infectious and inflammatory
Poor clotting - acute infectious arthritis
Fair clotting - rheumatoid arthritis
 DIFFERENTIAL
DIAGNOSIS
1.Viral polyarthritis
2.Other systemic rheumatic diseases - Stenosing tenosynovitis
Systemic lupus erythematosus (SLE), 1. Carpal tunnel syndrome
Sjögren's syndrome, dermatomyositis 2. Reactive arthritis and
(DM). arthritis of inflammatory
3. Osteoarthritis - can be confused with bowel disease
RA in middle aged or older patients when 3. Psoriatic arthritis
the small joints of the hands are involved 4. Crystalline arthritis
5. Hypermobility syndrome
and fibromyalgia
 COURSE/ PROGNOSIS
Exacerbating and remitting disease curse
Onset isaccompanied with generalized joint pain and
stiffness in multiple small joints (polyarthritis)
Symptoms may appear spontaneously or over a
prolonged period of time, same with remission
Abrupt onset and large joint involvement, particularly
of the shoulder-girdle, were more common in older
adults
Elderly-onset RA - Better functional outcomeand less
activity limitation and participation restrictions. Associate
with polymyalgia rheumatica - shoulder and pelvic
musculature leading to muscle inflammation.
Early-onset RA, Almost 50% will eventually have marked
restriction in ADL or will be incapacitated
 COURSE/ PROGNOSIS
Loss of income – major consequence of RA and
directly attributed to work disability.
Smoking Tobacco - can adversely affect the
progression of RA. Smoking causes
furtherinflammation, which can worsen the
progression of RA.
Early Detection - can lead to a significant difference in
a person’s outlook. Receiving the
appropriatetreatment early can prevent permanent
joint damage and minimizing the impact of RA on
quality of life.
Age - usually develops in older people, but it can
affect people of any age
 NON-STEROIDAL ANTI-
INFLAMMATORY DRUGS MANAGEMENT:
NSAIDS - Analgesic and anti-inflammatory
PHARMACOLOGICAL
DISEASE-MODIFYING
ANTIRHEUMATIC DRUGS
The primary class of drugs for managing
disease progression

BIOLOGICAL RESPONSE MODIFIERS (BRMS)

Biologically engineered to reduce or block
inflammatory process; treat moderate to
severe RA that is non- responsive to
traditional therapy

CORTICOSTEROIDS
Powerful anti-inflammatory drugs creating
rapid and potent supression of inflammation.
 MANAGEMENT:
SURGICAL

ARTHROCENTESIS/JOINT ASPIRATION
Procedure to remove fluid from a joint
with a needle.It may help ease the pain.
JOINT REPLACEMENT
May be needed to replace a damaged
joint with an artificial one. It may help SYNOVECTOMY
maintain function. The most common Removes inflamed synovium. This is the tissue
joints replaced are the hip and knee. that is around a joint. It may be done with other
surgery methods to ease pain and slow
damage. The tissue will grow back in time.
ARTHRODESIS
May be done when other methods do not help.
This surgery fuses two bones together. It may
ease pain, but the joint will no longer be able to
move.
MANAGEMENT:
PHYSICAL Therapeutic exercise - prevent deformity and loss of
motion and muscle strength.
THERAPY Strengthening - shoulder, hand, knee and whole-
body exercise at low intensities.
ROM - Active and passive, pain-free isometrics,
proper positioning, andposture should be performed
regularly to achieve functional goals
Aquatic therapy - the water temperatures
need to be higher than usual.
Splints and assistive devices
Gentle stretching andrelaxation exercises -
oftenhelp to decreasemuscle tension and stress.
 GOUT

Group of disorders that involve deposition of uric

acid crystals in joints and soft tissues, resulting in
articular and periarticular inflammation and injury.
 EPIDEMIOLOGY
Males > females, 3:1 to 10:1
AGE: 30 - 50 y/o
Prevalence of gout ranges from 1–4% worldwide
and incidence ranges from 0.1– 0.3%.

ETIOLOGY
Factors that can cause an acute gout attack: Injury
or recent surgery.
Fasting or overeating consuming excessive
amounts of alcohol.
Taking medications that can increase blood levels of
uric acid can include diuretics and daily low dose
aspirin.
 PATHOPHYSIOLOGY
PROBABLE CAUSES:
1. Sustained hyperuricemia leads to development of microphi (tophi
are pathognomonic features of gout) into synovial lining cells.
2. Accumulation of monosodium urate in the cartilage in proteoglycans
that has higher affinity.
3. Episodic release of urate crystals in the synovial fluid due to
several mechanisms involving disruption of mircrotophi turn over of
cartilage proteoglycans.
4. Lower temp. in jt, space on an unequal distribution of water and
urate in the synovial fluid may accelerate precipitation.

RISK FACTORS:
Obesity, high blood pressure, injury or recent surgery.
Consuming excessive amounts of alcohol on a
regular basis.
Diets high in meat, shellfish, and beverages
sweetened with high-fructose corn syrup Taking
medications that can increase blood levels of uric acid
(especially diuretics).
 CLINICAL S/SX
1. Asymptomatic Hyperuricemia
2. Acute intermittent → Acute Gouty arthritis
Pain, warm tenderness swelling - 1st MTP joint
(Podagra)
3. -Mono-articular
4. Chronic Tophaceous Gout
Tophi from after several years of attacks
5. Polyarticular Gout
Sites of involvement:
Olecranon Bursa, wrist, hands, renal
parenchyma w/ uric acid nephrolithiasis
PATTERN: Asymmetric
MC SITE: 1st MTP joint (Podagra) OTHER SITES:
LE: midfoot, heels, ankles, knees
UE: fingers, wrists, elbows
 DIAGNOSIS
1. Joint Fluid test
2. Blood test
3. X-ray imaging, Ultrasound and Dual energy
CT scan
LABORATORY FINDINGS:
a. Hyperuricemia
b. Joint aspiration: monosodium urate
RADIOGRAPHIC FINDINGS:
Acute gouty arthritis
Soft tissue swelling around affected joint
Chronic tophaceous
Tophi appear as nodules in lobulated soft
tissue masses
Bone erosions near tophi
Joint space preserved
No osteopenia
 DIFFERENTIAL DIAGNOSIS
1. Acute Gouty Arthritis:
2. Trauma
3. Cellulitis
4. Septic Arthritis
5. Pseudogout (calcium pyrophosphate crystals)
6. Reactive arthritis
7. Acute rheumatic fever
8. Sarcoidosis
9. Other crystalline arthropathies
10. Chronic Gouty Arthritis
11. Pseudogout
12. Rheumatoid or other inflammatory arthritis
13. Osteoarthritis
14. Lyme disease
 COURSE & PROGNOSIS
The symptoms of an acute gout attack are sudden, severe
joint pain with redness, swelling, and tenderness of the joint.
The joint may feel quite warm to the touch. Progressive gout
can cause bone destruction and deformity.
When someone has many attacks over years, tophaceous
gout can develop. This means that large amounts of uric
acid crystals have accumulated
into masses called tophi.
 MANAGEMENT:
PHARMACOLOGIC
ACUTE: Colchicine, NSAIDs, corticosteroids
CHRONIC: allopurinol, probenecid

Physical Therapy
Heat and Cold therapy Splints for immobility
PROM & AROM, stretching and strengthening ex.
Bracing; assistive device
Surgery - joint replacement surgery -in severe cases
REFERENCES:
O’Sullivan, S.B.,Schmitz, T.J.,& Fulk, G. D.(2014). Physical rehabilitation (6th ed). F.A. Davis Co.
A Comprehensive Guide to Geriatric Rehabilitation: [Previously entitled Geriatric
Rehabilitation Manual. (2014). Elsevier Health
Sciences UK.
Arthritis: An Overview - OrthoInfo - AAOS
Diagnosis anddifferential diagnosis of rheumatoid arthritis - UpToDate
Reactive Arthritis (Reiter's Syndrome) - American Family Physician (aafp.org)
Psoriatic Arthritis - Physiopedia (physio-pedia.com)
https://www.aafp.org/afp/2007/0715/p247.html#:~:text=The%20differential%20diagnos
is%20of%20fibromyalgia,tender%20area
s%20in%20the%20muscles
Diseases andConditions Vasculitis (rheumatology.org)
Surgical andMedical Procedures for Rheumatoid Arthritis | Winchester Hospital
Rheumatoid Arthritis (RA) |Arthritis | CDC
Lupus (rheumatology.org)
Systemic lupus erythematosus: MedlinePlus Medical Encyclopedia
Lupus (Systemic Lupus Erythematosus) Diagnosis & Treatments (hss.edu)
https://pubmed.ncbi.nlm.nih.gov/18028042/
https://www.vasculitis.org.uk/about-vasculitis/treating-vasculitis
https://www.mayoclinic.org/diseases-conditions/vasculitis/symptoms-causes/syc-
20363435 https://www.mayoclinic.org/diseases-conditions/pseudogout/diagnosis-
treatment/drc-20376988 https://www.assh.org/handcare/condition/pseudogout
https://www.kidneyfund.org/kidney-disease/chronic-kidney-
diseaseckd/complications/gout/
https://www.versusarthritis.org/about-arthritis/conditions/gout/
THANK
YOU FOR
LISTENING !