MS1 Rheuma: Common Representative

Rheumatic Diseases
Osteoarthritis/degenerative joint disease
-

Most common joint disease

Joints that are commonly used
Wear and tear disorder
Slowly progressive, non-inflammatory
Involves
o Progressive deterioration and loss of
articular cartilage
o Formation of new cartilage and new bone
at the margins of the joints (osteophyte
formation)

Epidemiology
2-3% of the adult population has symptomatic OA
Associated with increased age
o Almost universal in persons 65 yrs. above
(though only 2-3% will complain of pain)
More common in women (2:1)
Radiographic findings in >50-80%
Risk Factors
Obesity joint has more weight-bearing stress
Heredity increased risk of developing even with
proper lifestyle
Age
Previous joint trauma accidents
Abnormal joint mechanics
smoking
Types
-

Primary or idiopathic
o Most common
o Has no identifiable underlying etiology or
predisposing cause
o Types: localized or generalized (Kellgrens
syndrome)
Secondary
o Has an underlying cause
o Pathologically indistinguishable from
primary OA
o Regardless of type, pt will still complain of
the same sx associated with both primary
and secondary
o Causes

Metabolic calcium crystal

deposition, hemochromatosis,
acromegaly

Anatomic leg length inequality

(one leg has more stress),
congenital hip location

Traumatic major hip trauma

Inflammatory

Phase 3: erosion swelling, cracking,

Sx and symptoms
Use-related pain
Asymmetrical pain doesnt have to be in both
sides
Morning stiffness is <30-60mins.
Gelling phenomenon when resting in a short
period of pain results into pain when moved again
Loss of movement
Feeling of instability
Tenderness around the joint
Crepitus cracking sound when moving the joint
Bony swelling
Mild inflammation
Functional limitation
Periarticular muscle atrophy
Hand OA
Heberdens nodes DIP joint affectation; spur
formation at dorsolateral and medial aspects of the
DIP joint
Bouchards nodes PIP joint affectation
1st CMC involvement
Knee OA
Most common joint affected
Strong association with obesity
Chondromalacia patella
Genu varus and valgus
Hip OA
-

Most disabling form of OA

Insidious onset of pain limp
Groin, thigh, knee or buttock pain
Men affected slightly more than women
(+) FAbERes positive pain in the ff areas:
o Flexion
o Abduction
o External Rotation

Spine OA
Results from involvement of the intervertebral discs,
vertebral bodies or posterior apophyseal
articulations
Spinal canal stenosis
Can present with neurologic symptoms because of
joint space narrowing which could squish the
nerves; and osteophyte formation
o Would cause nerve damage if osteophyte
formation occurs on the nerve canals
Lumbar spine L3 to L4

Pathophysiology
Imbalance between chondrocytes and formation of
cartilage
Failure of chondrocytes within the joint to synthesize
a good-quality matrix
Failure to maintain balance between synthesis

Uncommon jts affected in primary OA

MCP joints of the hands
Wrist
Elbows
Shoulders
Ankles
2-5th MTP

OA joint
Phase 1: edema and microcracks
Phase 2: fissuring and pitting

Diagnosis
Primarily based on history and physical examination
Also on symptoms, location of pain

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If joints such as the elbow or shoulder are involved,

etiology other than OA should be entertained
X-ray can confirm diagnosis
o Primary imaging method used to confirm
the diagnosis of OA, stage its severity and
follow its progression
o Severity of x-ray findings might not be
equal to the complaints

Ex: mild x-ray, severe pain

o Although more than 90% of people over
age 40 have some radiographic evidence
of OA joint changes, only 30% have
symptoms
Osteophyte extra bones/fibrous cartilage

Laboratory Findings/Other Tests

Routine lab tests are normal; useful for:
o Screening for associated conditions or
secondary causes of OA
o To establish a baseline for monitoring
therapy
Only request lab tests to confirm other conditions,
not just diagnosis of OA
Synovial fluid analysis
o Slight increase in the number of WBCs,
usually less than 1000-2000 WBC/mm3
with less than 30% polymorphonucleocytes
(PMNs)
General Principles of OA treatment
Relieving symptoms
Maintaining or improvement of fxn
Nonpharmacologic therapy
Avoid medications that can exacerbate
Patient education
o Self management programs

Ex: Plan your activities

Avoid flexion of the knee

o Social support
Physical therapy
o Exercises

ROM, muscle strengthening,

aerobic conditioning
o Modalities
o Assistive Devices
Occupational therapy
o Assessment of ADLs
o Assistive devices
Weight loss
***Management table from Sullivan
Pharmacologic Therapy
Start with a low form of drugs such as paracetamol
or ibuprofen
Systemic
o Analgesia agents

Non-narcotic analgesics

Narcotic analgesics
o Anti-inflammatory agents

Nonsteroidal anti-inflammatory
drugs

Specific cyclooxygenase-2
inhibitors
Local topical analgesics

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Intraarticular

Corticosteroid injections could

produce osteoporosis

Viscosupplementations series of
injections that aim to increase
lubrication in the joints; lasts for
one year usually but depends;
can be injected only twice a year

Closed tidal lavage

Topical therapy

Other treatment options

Surgery
Alternative medicine
o Supplements

Glucosamine collagen

Chondroitin
o Acupuncture

Rheumatoid Arthritis
-

Chronic, inflammatory, systemic disease that

produces its most common and most prominent
manifestations in the synovial jt
Synovial membrane affectation
Etiology: unknown; autoimmune

Rheumatoid Factor
Found approximately 70 percent of patients with RA
Antibodies specific to IgG; the target of RF is igG
One can still have RF even without RA
Increased frequency of subcutaneous nodules
1987 Revised Criteria for the Classification of RA
Criterion if you have at least 4, you are diagnosed with
RA; the jt. sx and symptoms described from 1-4 must have
lasted for at least 6 weeks
1. Morning Stiffness morning stiffness in and
around the jts, lasting at least one hour before
maximal improvement
2. Arthritis of three or more jt areas at least 3 jt
areas simultaneously have had soft tissue swelling
3. Arthritis of hand joints
4. Symmetric arthritis both left and right hand will
have; might not happen at the same time
5. Rheumatic nodules found in the extensor
surfaces
6. Serum rheumatoid factor
7. Radiographic changes
2010 Criteria
Swollen or tender
jt
0
1
2
3
4
5

1 large joint
(shoulder, elbow,
hip ankle)
2-10 large joints
1-3 small jts(not
including DIP, first
MTP, or first CMC)
4-10 small joints
>10 jts

Epidemiology

Lab studies
Negative RF +
CCP IgG (ACPA)

Low positive RF
or CCP IgG
Highly positive RF
+ CCP IgG

Acute Phase
reactant
Normal CRP and
ESR
Abnormal CRP
and ESR

Affects women more than men, 2-4x more at all

ages
Peak incidence is between 4th-6th decades
General increase in prevalence for both sexes with
increasing age
Race: native american>caucasian>blacks
o Lower incidence in Asians

Pathophysiology
1. Inflammation begins in the synovium
2. Synovium begins to proliferate and forms pannus, a
rough grainy tissue that erodes cartilage
3. Cells in the pannus release enzymes that eat into
the cartilage, bone, soft tissues
4. Tendons and the joint capsule may become
inflamed causing pain, instability, deformity,
weakness and loss of motion; tendon rupture or
joint fusion may follow
Manifestations in Specific Joints
1. Cervical Spine
a. Atlantoaxial jts and midcervical region
b. Could cause cord compression
c. Rare in thoracic and lumbar spine
d. Neck stiffness with limited ROM especially
rotation
e. Tenosynovitis of C1 and C2 -> C1-C2
instability -> cord compression
2. Temporomandibular jt
a. Results in limited mouth opening
3. Shoulders
a. Loss of ROM -> frozen shoulder syndrome
b. Tendinitis and bursitis
4. Elbow
a. Flexion deformity
b. Ulnar compression neuropathy
5. Wrists
6. Hand
a. z-hand deformity
b. Boutonniere and swan neck deformity
c. Piano-key sign floating ulnar head
i. Ulnar collateral ligament is
raptured
ii. Proliferating synovium leads to
rupture or destruction of the ulnar
collateral ligament
iii. Pseudobenediction sign
1. Stretched radioulnar
ligaments
d. Mutilan deformity (opera glass hand)
i. Digits look like sausages
ii. Digits are shortened and
phalanges appear retreated with
skin folds resorptive and
arthropathy
iii. Telescoping appearance of the
digits
iv. Most serious arthritic involvement
*for patients with RA give splints
*for patients with (+) RF --splints
7.

Hip
a.
b.
c.
d.

Symptom is not apparent

Less commonly involved in RA
Loss of ROM
(+) FABERes

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8.

9.

Knee
a.
b.

One of the most commonly involved

Bakers cyst
i. Cyst located on the posterior
aspect of the knee
ii. Rupture
Foot and ankle
a. Cock-up deformity of MTP
b. Hallux valgus
c. Lateral deviation of the toes

Extraarticular Manifestation
1 Skin
a Rheumatoid nodule (25-50%) over
olecranon, ext. of forearm, Achilles tendon
and ischial area
i Seen in extensor surfaces
2 Ocular
a Keratoconjunctivitis sicca (Sjogrens)
dryness of the eye
b Scleritis, episcleritis
3 Respiratory
a Inflammation of cricoarythenoid jt
laryngeal pain and dysphonia
b Caplan syndrome
4 Cardiovascular
a Inflammation of blood vessels
5 Gastrointestinal
a No specific GI system in RA
b Gastritis PUD secondary to NSAID and
steroid use
6 Renal
a Related to drug use
7 Neurologic
a Myelinopathies related to cervical spine
instability
b Entrapment neuropathies
c
Ischemic neuropathies related to vasculitis
8 Hematological
a Feltys syndrome (splenomegaly,
leucopenia and leg ulcers) related to joint
pain and RA
b Hypochromic-microcytic anemia
Laboratory
There is no laboratory text, histologic, radiographic
finding that conclusively indicates a definitive
diagnosis of RA
Rheumatoid Factor
o Autoantibody against IgG
o In 70-85% of RA; 5-20% of healthy adults
o Correlate with severe unremitting disease,
nodules and extraarticular lesion
o Presence of RF indicates has the severe
type of RA
ESR and C-reactive protein
o Presence indicates acute inflammation
(these are acute phase reactants meaning
if they are elevated, then an acute process
is on going

Course and Prognosis

Intermittent mild disease with partial/complete
periods of remission
Long clinical remission

Proposed Criteria for Clinical Remission of RA

5 or more symptoms are present for 2 consecutive
months
Symptoms:
o Duration of morning stiffness not
exceeding 15 minutes; or lasts for less
than 60 minutes

Active
o ESR less than 30mm/hr. for females or
20mm/hr. for males

Acute phase reactant (ESR)

o No soft tissue swelling in joints or tendon
sheets
o No tenderness of pain on motion
o No joint pain
o No fatigue

Exercise
Joint mobility
o Gentle grade I and II distraction and
oscillation techniques inhibit pain and
minimize fluid stasis
o Stretching are not performed when joints
are swollen
Strengthening
Endurance training
Functional training
Gait training

Poor Prognosis
Early age of onset
High RF
Presence of rheumatoid nodules
Persistent sustained dse of more than one year
duration (if it does not undergo remission)
HLA-DR4 haplotype

Splinting
RA
Ulnar deviation splints
Siris silver ring splints
o Allows flexion but blocks hyperextension
o Figure of 8 rings; brings fingers into a more
functional form

Class I
Class II

**Management Guidelines Sullivan

Class III
Class IV

Completely Able to do ADL

Able to do self-care and
vocational activities but
limited avocational activities
Able to do self-care but
limited vocational and
avocational activities
Limited to ADL

Treatment
1 Patient education
a Learn things that would concern their joints
b Joint protection
c
Energy conservation techniques
i Since there is complaint of easy
fatigability
ii Planning their activities
2 Symptomatic medical therapy
a Non-steroidal anti-inflammatory drugs
b Corticosteroids
c
Biological response modifiers
d Slow acting anti-rheumatic drugs
(SAARDS)
3 Surgery
a Soft tissue: synovectomy, tendon transfers
and soft tissue release
b Bone and joint: osteotomy, arthroplasty
and arthrodesis
4 Rehabilitation
a Pain modalities
b Exercise
c
Splinting
d Orthotic or assistive devices
Pain Modalities
Superficial heat hot moist packs, dry heating
pads/lamps, paraffin and hydrotherapy
Ultrasound should not be used in the acute stage
Deep heating modality ultrasound
Cold done in extreme swelling in the joint; except
in those with Raynauds and cryoglobulinemia

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Raynauds patients who have sensitivity

to cold; terminal vasospasm of the digits
TENS pain modality which uses electricity;
transcutaneous electrical nerve stimulator
o

Subacute and Chronic Stages

Intensity of pain, joint swelling, morning stiffness
and systemic effects diminish
o Cardiopulmonary endurance
o Flexibility and strength
o Joint protection and activity modification
Crystal-induced arthropathy pain brought about by
deposition of crystals
Monosodium urate (MSU)
Calcium pyrophosphate dihydrate (CPPD)
Pseudogout
Gout
-

a metabolic disease associated with deposition of

MSU crystals (tophi) in and around the joints,
connective tissue and kidneys
Hyperuricemia serum urate concentration more
than 2 SD above the mean
o Increase in uric acid to more than a
standard deviation of 2 above the mean
o Men - 7.0mg/dL
o Women - 6.0mg/dL
o Measured in the blood

Epidemiology
More common in males, with peak incidence of 50
y/o
M>F; 2-7:1
Postmenopausal women
o Estrogen promotes renal excretion of uric
acid
Mechanism responsible for hyperuricemia
Urate overproduction
o More than 800 mg of uric acid excreted
o Occurs in

Excessive purine diet

Enzyme deficiency

Increased nucleotide turnover

Accelerated degradation

Hyposemia
Uric acid underexcretion
o More than 90% of people with gout present
with this type of pathology
o Pharmacologic agents
o Medical conditions

Hyperparathyroidism/hyperthyroid
ism

Renal disease

Diabetic ketoacidosis
Combined overproduction and underexcretion
o Due to alcohol

Increases production and

decreases excretion
o Inborn errors of metabolism

Glucose-6-phosphatase
deficiency

Fructose-1-phosphate aldolase
deficiency

Unusual forms of Gout

Lesch Nyhan Syndrome
o Choreoathetosis, spasticity, self-mutilation
mental retardation, gout
o Complete deficiency of HGPRTase
Kelly Seegmillar Syndrome
o Without neurological problems
o Same with Lesch Nylan
Risk factors for gout
Alcohol ingestion
Dietary excess of purine
Exercise
Trauma
Surgery (post-operative 3-5 days)
Hemorrhage
Infections
Drugs (diuretics, etc.)
Radiation therapy
Risk factors
Familial occurrence is reported by about 20% of
affected patients
o Hyperuricemia has been demonstrated in
first degree patients
Commonly affected joints in gout
LE > UE
1st MTP joint swelling (potagra)
pain in Ankles
pain in Heels
pain in Knees (gonadra)
pain in wrists (chirargra)
fingers
elbows
Stages of Classic Gout
Asymptomatic Hyperuricemia increase in uric
acid but no symptoms
Acute intermittent gout severe pain, warmth,
swelling; presence of acute signs of inflammation
Intercritical stage resolution of pain but blood
uric acid is elevated
Chronic tophaceous gout

o
o

Usually develops the unremitting form of

gout
10 or more years of acute intermittent gout
transition occurs when the intercritical
periods are no longer free of pain

Always acute
patients have tophi, polyarticular
involvement becomes much more frequent

Deposition of crystals

Tophi formation
Is a function of the duration and severity of
hyperuricemia
o Early age of onset
o Long periods of active but untreated gout
o An average of four attacks per year
o Greater tendency toward UE involvement
(fingers, wrist, knees, ears, and ulnar
aspect of the forearm and the Achilles
tendon)
o Polyarticular episodes
Laboratory diagnosis
Blood uric acid test
Diagnosis should be confirmed by needle aspiration
of acutely or chronically inflamed joints or
tophaceous deposits
Differential diagnosis
o Acute septic arthritis
o Psoriatic arthritis
MSU crystals
o Strongly birefringent, needle-shaped
o With negative elongation
o Largely intracellular
Synovial fluid
o Cell counts are elevated (2000-60000)
Bacterial infection can coexist with urate crystals in
sF
Radiographic features
Cystic changes
Well-defined erosions
o Martels signs
Soft tissue swelling
Preserved joint space
Treatment
Acute gouty arthritis
o NSAIDS
o Colchicine acute gouty attack; promotes
excretion of uric acid
o Steroids
Chronic hypouricemic therapy
o Probenecid undersecretors
o Allopurinol over
o Febuxostat

Calcium Pyrophosphate Dihydrate Deposition

Disease
-

Most common in elderly

o 10-15% of 65-75yo
o 30-60 of those more than 85 years old
asymptomatic
Cause is uncertain

Commonly affected joints

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Knee
Wrist
Shoulder
Ankle
Elbow
Hands
Rarely, TMJ
Trauma, stress on joints (such as injections)
Acute attacks may be precipitated by trauma,
arthroscopy
In as many as 50% of cases it is associated with
fever synovial analysis with microbial cultures is
essential

Diagnostic test
Clinical and radiographic evidence indicates that
CPPD deposition is polyarticular in at least 2/3 of
patients

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Chondrocalcinosis is presumptive of CPPD

deposition (linear radiodense deposit in joint
meniscus)
Synovial fluid has inflammatory qualities
o WBC count can range from several
thousand cells (100000 cells/microliter)
o Cells will look rhomboid

Treatment
NSAIDs
Colchine
Steroid
For persistent synovitis
o Radioactive synovectomy
o Antimalarial agents
Joint replacement