EMRGI LECTURE 2: RHEUMATOLOGY

○ Pathophysiology
DEFINITION OF TERMS
■ Synovial inflammation → venous distention →
capillary obstruction → neutrophilic infiltration of
● Arthritis/Arthropathy - any pathologic disease affecting the joints
arterial walls (to fight inflammation) → areas of
of the musculoskeletal system
thrombosis and hemorrhage → hypertrophy
● Related Connective Tissue Diseases - because some
(thickening of synovial joint) → proliferation of
arthropathies are systemic in origin, some connective tissue
blood vessels → granulation tissue formation
disease are usually physiologically related to these arthropathies
(pannus)
■ As a consequence of inflammation, the synovium
TYPES OF ARTHROPATHIES because hypertrophic from proliferation of blood
vessels and synovial fibroblasts and from
multiplication and enlargement of synovial lining
SEROPOSITIVE
layers
■ Leads to formation of granulation tissue called
Seropositive Arthropathies are due to a tendency to have the presence of Pannus
an immunoglobulin M (IgM) factor (Rheumatoid Factor). Conditions under ● Extends to the articular cartilage as it
this type of arthropathy include the following: dissolves the collagen
1. Rheumatism and Rheumatoid Arthritis ● Actively invades and destroys the
2. Systemic Lupus Erythematosus (SLE) periarticular bone and the cartilage at the
3. Still’s Disease (Juvenile RA) margin between synovial and bone
4. Progressive Systemic Sclerosis (Scleroderma) ● Will eventually result in adhesions and
5. Dermatomyositis - Polymyositis fibrous or bony ankylosis in joint
6. Sjoregen’s Syndrome ○ Adhesions make synovial joint stick
together
RHEUMATISM & RHEUMATOID ARTHRITIS ○ Fibrosis is scar formation all over
the joint causing limitation of motion
● Destructive element of RA
● Rheumatism - chronic, inflammatory, systemic disease that
○ Damages cartilage & periarticular
produces its most common and most prominent manifestations in
bone
the diarthrodial joints
● Responsible for most of the deformities in
○ Rheumatoid arthritis
RA
● Rheumatoid arthritis - a common, chronic, polyarthritis which may
● Hallmark of RA
be classified as a diffuse, multi-system, connective tissue disease
○ Clinical manifestations
○ Affects multiple joints (mainly small joints in the hands &
■ Extra Articular
wrist)
● Rheumatoid nodules - most common extra
○ Not only affects the musculoskeletal system but other
articular manifestation
systems as well
○ All are RF positive
○ Hallmarks:
○ Common in:
■ (+) Rheumatoid Factor
■ Extensor surfaces of FA
■ Bilateral, usually symmetrical
■ Olecranon
■ Erosive changes in radiography
■ Achilles tendon
● Observed in the progression of the disease
■ Ischial area
especially in the severe & terminal
■ Over MTP Joints
presentations
■ Flexor surface of fingers
■ Persistent inflammatory synovitis
● Vasculitic lesions - most common lesions
■ Pannus
are:
● Granulation tissue resulting from an
○ Leukocytoclastic vasculitis
autoimmune cycle of inflammation & repair
○ Palpable purpura
● Peripheral neuropathies - usually found in
elderly RA Pt.
● Ocular involvement - keratoconjunctivitis
sicca in association with Sjogren's
syndrome
○ Scleritis has worse prognosis

○ Epidemiology
■ Population ~1%
■ Age predilection: 20-60 y.o.
● Majority between 35-40 y.o
■ Sex Predilection:
● F > M (3:1)
● After 65 y.o, equal distribution
○ Etiology ○ Hematologic - anemia is most common
■ Unknown ■ Felty's syndrome - characterized by
■ Believed to be autoimmune because individuals ● Splenomegaly - enlargement of spleen 2° to
with RA produces antibodies to their own twice the effort trying to clear the body of
immunoglobulin waste products of blood
■ Rheumatoid Factor (RF) - autoantibodies with ● Neutropenia - abnormal ↓ of neutrophils
specificity for the FC fragment of IgG are found in ● Thrombocytopenia - abnormal ↓ of platelets
60% of RA Pts.
 ● Anemia in long standing RA
of the metatarsals); foot may look like broader
○ Systemic and pointing out
■ Malaise and low grade fever
■ Anorexia MTP ● Metatarsalgia – pain over the metatarsal head;
■ Weight loss like stepping on pebbles
● MC deformity: Hammer Toes- PIP flexion, DIP
■ Fatigue
extension
○ Intraarticular ● May affect the push-off phase of gait (apropulsive
■ Always bilateral symmetrical gait)
■ Can affect any diarthrodial joint ● Orthosis: high toe box + Rocker bottom shoes to
■ Characteristics: aid push off
● Morning stiffness ● Hallux Valgus - present on RA & OA
● Flat foot - collapse of the medial longitudinal arch
○ Universal feature of synovial
inflammation Ankle ● Pronation of hindfoot
○ Lasts for more than 2 hours
● Tenderness TMJ ● LOM upon mouth opening
● Structural damage and crepitus - caused by
cartilage loss and erosion of periarticular
Hand Deformities
bone
● Swan Neck - PIP hyperextension, DIP flexion; failure of lateral
● Flexor contractures
slip (extends DIP); advised to use palm in gripping
● Finger deformities
● Boutonniere deformity - PIP flexion, DIP hyperextension; failure
○ Swan neck deformities - more
of central slip
common
○ Osteophytes - bony outgrowths at the end of the joint;
○ Boutonniere deformity
these osteophytes are common in OA but are unrelated
to RA.
○ Herbenden’s node (DIP); Bouchard’s node (PIP)
● Z-deformity/Zigzag Deformity - radial deviation of the wrist
○ MCP deviates ulnarly (Ulnar drift) as a compensation
Structures of the ulnar side are stretched
○ ● Mutilans Deformity (Opera Glass Hand) - Grossly deformed
● Usually affects hands, wrist, shoulder, knee, thumbs and severely deformed phalanges
C1-C2 joint and midcervical joint ○ Like holding a wine glass
● Vaughn-Jackson Deformity - Rupture of the extensor tendons
Joint Symptoms of the ring and small finger
○ Affects the 4th & 5th digits
Cervical spine ● C1-2 affectation
● LOM in rotation
● Subluxation of transverse ligament (may lead to ○ Diagnosis
SCI) ■ Erythrocyte Sedimentation Rate (ESR)
● Anterior atlantoaxial subluxation (pain in ■ Rheumatoid Factor (RF - IgM)
retroorbital, temporal or occipital during neck ■ CBC
flexion) ■ Synovial Fluid Analysis
● Staircase appearance if subluxations occur below
● Normal: transparent, yellowish, viscous with
C2
● Management: Soft Cervical Collar clots
● With inflammation - cloudy, less viscous,
Shoulder ● Atrophy (due to disuse & eventual subluxation) will clot
● Joint surfaces are eroded ■ Radiography
● Limitation in IR & adduction
● Marginal erosion with juxta articular
Elbow ● Inflammation, capsular & ligamentous distention osteoporosis
● Joint instability
● Flexion contracture
Classification of Progression of RA
● Loss of pronation & supination
Stage I No destructive changes observed upon radiographic
Wrist ● Early synovitis of the eight carpal bones and the
(Early) examination; radiographic evidence of osteoporosis is
ulna leads to
possible
● Rapid flexion contracture
● Loss of power grasp Stage II Radiographic evidence of periarticular osteoporosis, with
(Moderate) or without slight subchondral bone destruction; slight
MCP ● Ulnar drift & volar subluxation of MCP
cartilage destruction is possible; joint mobility is possibly
PIP ● Swelling in the PIP joints produces a fusiform or limited but no deformities are observed; adjacent muscle
“sausage like” appearance in the fingers atrophy is present; extra articular soft tissue lesions (e.g.
● There are 2 characteristic deformities seen in PIP nodules, tenosynovitis) are possible
of the individuals with RA:
Stage III Radiographic of cartilage and bone destruction in
○ Swan Neck Deformity
(Severe) addition to periarticular osteoporosis; joint deformity (e.g.
○ Boutonniere Deformity
subluxation, ulnar deviation or hyperextension) without
○ Z-deformity or Zigzag Deformity
fibrosis or bony ankylosis; muscle atrophy is extensive;
○ Mutilans Deformity (Opera Glass
extra articular soft tissue lesions (e.g. nodules,
Hand)
tenosynovitis) are possible
○ Vaughn-Jackson Deformity
Stage IV Presence of fibrous or bony ankylosis, along with criteria
Hip ● Less commonly involved in RA
(Terminal) of stage III
● Severe inflammatory destruction of femoral head
& acetabulum may lead to “Protrusio Acetabuli”
● May lead to LLD ○ 1987 Revised Criteria for Classification of RA
■ Morning stiffness
Knee ● Flexion contracture due to pain and immobility
● Subluxation of patella to lateral side ■ Arthritis of 3 or more joints
■ Arthritis of hand
Ankle & Feet ● May develop Splayed Foot Deformity (spreading ■ Symmetric arthritis
 ■ Rheumatoid nodule
STILL’S DISEASE (JUVENILE RA)
■ Serum RF
■ Radiographic changes
● Definition
● RA = at least 4 out of 7 criteria
○ An uncommon crippling disease of children associated
○ 1-4 must be present for at least 6
with fever and enlargement of lymph nodes and spleen
weeks
● Types
○ 2-5 observed by physician
○ Systemic onset
○ 6-7 laboratory findings
■ (+) of extra articular manifestations in addition to
○ Prognosis
arthritis
■ Individuals with RA may live less longer
■ Boys>girls; median age of onset: 5 y.o
■ Almost 50% will eventually have marked
■ (+) cardiac involvement
restrictions in ADL or will be incapacitated
■ Pt. may experience polyarthritis, anemia,
■ Elderly onset, better functional outcome than those
leukocytosis
with early onset
■ (+) high fever especially in the afternoon and
○ Pharmacological Management
evening
■ Salicylates
○ Pauciaarticualr arthritis
■ NSAIDS - 1st line of defense
■ 30% of JRA Pts.
■ Antimalarial drugs
■ Most frequent types
■ D-penicillamine
■ Girls>boys; early age of onset of 2-4 y.o.
■ Steroids-exogenous glucocorticoids
■ Involvement of 1 or few joints; common in knees &
ankles
American College of Rheumatology Revised Criteria for ■ Has mild arthritis; good prognosis
Classification of Functional Status in RA
■ May lead to cataract irritation, loss of vision and
Class I - independent Completely able to perform usual ADLs band keratopathy
○ Polyarticular arthritis
Class II - able to Able to perform usual self-care and vocational ■ 25% of Pts.
perform with pain activities but limited in avocational activities
■ Predominantly girls at younger age
Class III - able to do Able to perform usual self-care activities but ■ Has relatively good prognosis
some limited in vocational and avocational activities ■ Onset is insidious
■ Initial involvement of small joints
Class IV - unable to Limited in ability to perform usual self-care
● Epidemiology
perform vocational, and avocational activities
○ Boys = girls
○ Most common in childhood
SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) ○ 1st degree relatives and 40% of monozygotic twins may
be affected
● Clinical Manifestations
● Definition
○ Growth retardation
○ Systemic immune-mediated disorder characterized by
○ Abnormal speech
presence of a number of antibodies to nuclear
○ Rapid loss of ROM & contractures
components
○ Small mandible (micrognathia)
● Epidemiology
● Pharmacologic Management
○ Females (8:1) increase in women in child bearing age
○ Salicylates - 1st drug of choice
○ 15-45 y.o
○ Gold salts - be given if salicylates not effective
○ 2-4x greater in blacks and hispanics than in whites
○ Antimalarials
○ May be hereditary or genetically determined greater in
○ Systemic glucocorticosteroids (inflammation)
identical twin
● Etiology
○ Unknown PROGRESSIVE SYSTEMIC SCLEROSIS (PSS)
○ (+) of regulatory mechanisms in immune response
● Clinical Manifestations ● Definition
○ SHIN ROAD MAP ○ Scleroderma or systemic sclerosis
■ SHIN ○ Uncommon connective tissue disease with the most
■ Serositis - pericarditis & pleuritis prominent feature which is thickening or fibrosis of skin
■ Hematologic - Felty's syndrome ○ Heterogenous, both involving the internal organs and
■ Immunologic joints
■ Neurologic - psychosis & epilepsy ● Epidemiology
■ ROAD ○ Common in females (3:1)
■ Renal - lupus nephritis ○ Rare in children and in men under 30 y.o.
■ Oral - ulcers ○ Slightly more common in black women in child bearing
■ Arthritis - non-erosive non-deforming years
(Jaccoud's) ○ Common in coal & gold miners, especially those exposed
■ Discoid rash - ant. Neck & scalp area to silica dust
■ MAP ● Etiology
■ Malar rash - butterfly flash ○ Etiologic agent is obscure and no strong hypotheses
■ Anti-nuclear Antibody (ANA) - laboratory exists to its nature
hallmark of SLE ● Pathophysiology
■ Photosensitivity - can't tolerate light ○ Abnormal deposition of collagen in the CT of the
● Pharmacologic Management microvessels causing obliteration and permeability
○ Immunosuppressive drugs may be helpful changes (edema), platelet activation and perimuscular
○ Salicylates mononuclear cell infiltration leading to inflammation
○ Corticosteroids ○ Injury to endothelial cell lining of vessels makes the organ
damaged since there is the disturbance which activates
the clotting system releasing vasoactive peptides
 ○ Thus smooth muscles migrate in, proliferate and deposit to the muscle and skin leading to weakness in skeletal and
CT to a proliferative vascular lesion of PSS articular muscles
● Clinical Manifestations ● Clinical Manifestations
○ Raynaud's Phenomenon ○ Profound weakness of skeletal muscle
■ Caused by spastic blood vessel in the extremities ○ Weakness of respiratory and swallowing muscles
especially in the digits ○ Joint diseases are rare but bony erosions are common
■ Presence of pain and numbness especially on toes ● Types
and fingers of involved extremity
■ Ulcerations
Type Manifestations
■ Webbing conditions
■ Compromised blood supply to digits 1 - Primary, ● Insidious onset, moderate-severe arthritis,
○ Skin idiopathic PM Raynaud's phenomenon is present
■ Early disease - swollen fingers and hands, forearm, ● Pelvic girdle > shoulder girdle and neck muscle >
feet, lower legs, and face are affected dysphagia and dysphonia
■ Edema (pitting or non-pitting)
2 - Primary, ● Acute onset, proximal muscle weakness and
■ Skin thickening with arthritis in area
idiopathic DM heliotropic rash and Grottron's papules
■ Often shiny & bound down
● Muscles tenderness, systemic-fever, malaise,
○ GIT
weight loss
■ Esophageal hypomotility leads to dysphagia or
heartburn 3 - DM-PM ● More common in M > 40 y.o., muscle weakness
■ Gastric hypomotility leads to bloating & abdominal associated with usually progressive
pain malignancy ● Dysphagia and respiratory weakness
○ Pulmonary ● Death due to pneumonia or respiratory failure
■ Extertional dyspnea caused by deposition of
4 - DM/PM ● Disease of childhood
collagen in interstitium
associated with ● Rapid and progressive muscle weakness with
■ Often accompanied by non-productive cough vasculitis dysphagia, dysphonia, and respiratory weakness
○ Cardiac
● Contracture and atrophy is high
■ Pericarditis with or without effusions, heart failure,
● Calcinosis is present
and varying degrees of heart blocks or arrhythmias
■ May experience angina pectoris 2° to systemic 5 - Associated ● RA, SLE, PSS
hypertension with other ● Functional problems associated with the
○ Renal collagen individual collagen diseases often dominates the
■ Renal failure will manifest as increased fluid vascular clinical picture
diseases
retention
○ Neurologic 6 - Inclusions ● One of the rarest type of PM-DLM
■ Encephalopathy, severe headache, retinopathy, body myositis ● Overlaps with some other types
seizures
○ Complications
○ Complications
■ Pleuritis, interstitial fibrosis, pulmonary
■ Aspiration pneumonia
hypertension, weight loss, constipation, dysphagia
■ Lung dysfunction
■ May result to CREST syndrome
● Diagnosis
■ SubCutaneous phenomenon
○ Evaluation of serum muscle enzymes
■ Raynaud's phenomenon
■ Damage to muscle tissues (cardiac, smooth,
■ Esophageal dysfunction
skeletal muscles)
■ Sclerodactyly
○ Muscle biopsy (for Type 6)
■ Telangiectasia
○ EMG
● Pharmacologic Management
● Pharmacologic Management
○ Drug therapy
○ Steroids & anti-inflammatories are not effective
■ Penicillamine - 250 mg/day to ↓ collagen
production
■ Antiplatelet SJOGREN’S SYNDROME
■ Glucocorticoid - for inflammatory myositis &
pericarditis ● Definition
○ For Raynaud's phenomenon (Reserpine, ○ A chronic, slowly progressive inflammatory autoimmune
Phenoxybenzamine) exocrinopathy which is characterized by dry eyes
(keratoconjunctivitis sicca) and dry mouth (xerostomia)
DERMATOMYOSITIS - POLYMYOSITIS ○ Triad: Dry mouth, dry eyes, arthritis
● Epidemiology
○ Second most common immune-mediated disorder
● Definition
○ Most common in females, 50 y.o (9:1)
○ Inflammatory disease of muscle and skin often associated
● Etiology
with profound weakness of skeletal muscle, including
○ Unknown
heart, with or without the presence of rash
○ Associated with other autoimmune diseases such as RA,
● Epidemiology
SLE, PSS
○ Most common in 40-60 y.o.
● Pathophysiology
○ Children of 5-15 may acquire it
○ 2 main autoimmune phenomena are
○ Males = Females
■ Lymphocytic infiltration of exocrine glands
● Etiology
■ Lymphocytes attack exocrine glands,
○ Unknown cause
yielding them to be unable to produce
○ Theories: due to viral infection and autoimmune
excretions necessary to keep eyes, mouth
disturbances
& other areas moist
● Pathophysiology
■ B-lymphocyte hyperactivity
○ There is abnormal recognition of the self in which
antibodies of the individual attacks itself causing damage
 ● Clinical Manifestation
○ Keratoconjunctivitis sicca - dryness of eyes ● Clinical Manifestations
○ Xerostomia - dryness of mouth ○ Sacroiliitis
○ Arthritis ■ Hallmark of AS
○ Dyspareunia - pain during sexual intercourse ■ 1st initial symptom
○ Parotid gland enlargement ■ Dull pain felt in the lower lumbar with back morning
○ Raynaud's phenomenon stiffness
○ Fever/fatigue ○ Low back pain (due to SIJ involvement)
○ Lymphoma and Waldenstrom's macroglobulinemia ○ Bony tenderness
(non-Hodgkin’s lymphoma characterized by presence of ○ Enthesitis - inflammation of ligamentous tendinous
macroglobulin) insertions
● Complications ○ Peripheral arthritis - usually in shoulder and hip joints
○ Dry nose, throat, and trachea ○ LOM in hip and shoulder joints
○ Esophageal mucosal atrophy ○ Extraskeletal manifestation
○ Atrophic gastritis ● Diagnosis
○ Fatigability ○ Criteria
○ Renal involvement ■ History of inflammatory back pain
○ Nephritis, vasculitis ■ (+) sacroiliitis
● Tests ■ LOM of lumbar spine (Schober’s test)
○ Schirmer's test - test for keratoconjunctivitis sicca ■ Limited chest mobility (Chest Expansion
○ Rose Bengal test - test for presence of blood hallmarks of Measurement)
Sjogren’s disease Sacroiliitis + 1 of the other 3 criteria is (+) AS
○ Test for Xerostomia ○ Complications
● Medical/Surgical Management ■ Spinal fracture (most serious)
○ Goal - aimed at symptomatic relief and limit damaging ■ Bones of axial skeleton become weaker,
effects of chronic xerostomia and keratoconjunctivitis more prone to fracture
sicca ■ Can occur even with micro trauma to rigid
○ Management osteoporosis spine
■ Fluid replacement ■ Leads to quadriplegia
■ Avoid diuretics, antihypertensive and ● Differential Diagnosis
anti-depressant drugs ○ AS is differentiated from LBP causes by
■ Eye patching and boric acid ointments ■ Age of onset ( < 40 y.o.)
■ Glucocorticosteroids and immunosuppressive ■ Duration > 3 months, before medical attentions is
agents brought
■ Improvement with exercise & activity
■ Insidious onset
SERONEGATIVE
■ Morning stiffness
● Pharmacological Management
Seronegative Arthropathies are due to IgM or RF that are not found on
○ Indomethacin - most common
blood serum testing. Conditions under this type of arthropathy include
○ NSAIDs
the following:
○ Local corticosteroids
1. Ankylosing Spondylitis
● Medical/Surgical Management
2. Reiter’s Syndrome
○ Indications for surgery
3. Psoriatic Arthritis
■ Hip pain & stiffness
4. Arthritis due to inflammatory bowel disease

REITER’S SYNDROME
ANKYLOSING SPONDYLITIS

● Definition
● Definition
○ Presents as a clinical triad of
○ Systemic, chronic, inflammatory disorder of axial skeleton,
■ Non-gonococcal urethritis
affecting SI joints and spine
■ Conjunctivitis
○ Also known as
■ Arthritis
■ Von Bechterew's disease
● Epidemiology
■ Strumpell-Marie disease
○ Males are more commonly affected
■ Rheumatoid disease
○ Almost 100% HLA-B27 positivity
○ Prototype of spondyloarthropathies
● Etiology
● Epidemiology
○ Believed to be triggered by infection of genitourinary tract
○ More common in males (3:1)
caused by
○ 20-40 y.o.
■ Chlamydia
○ 90% with HLA-B27 positive (genetic predisposition)
■ Campylobacter
● Etiology
■ Salmonella
○ Unknown
■ Shigella
○ Hereditary
■ Yersinia
● Pathophysiology
● Pathophysiology
○ No specific exogenous agent has been identified to trigger
○ Triggering organisms invade host cells and survive
the disease
intracellularly
○ Implicate immuno-mediated mechanisms
○ Antigens of chlamydia, yersinia, salmonella persists in the
○ Inflammatory processes tend to start or originate in
synovium for long periods following acute attack
ligamentous and capsular sites of attachment to bones
○ CD+4 T-cells that respond to antigens of the inciting
(enthesitis), juxta-articular ligamentous structures, and the
organisms are typically found in inflamed synovium but
synovium, articular cartilage and subchondral bones of
not in peripheral blood
involved joints
○ Remains to be determines where the primary process is
an autoimmune response against antigens of triggering
organisms that have disseminated to the target tissue
● Clinical Manifestation ● Pharmacologic Management
○ Constitutional symptoms: fatigue, fever, malaise, and ○ Hydroxychloroquine - exacerbate psoriasis
weight loss ○ Gold therapy - being reevaluated
○ Triad: Conjunctivitis, Urethritis, Oligoarthritis ○ Immunosuppressive therapy (Methotrexate) - control the
○ Musculoskeletal symptoms disease
■ Spinal & LBP are common; may be caused by ○ Steroids, local skin treatment
infection, inflammation, muscle spasm, acute ○ Goeckerman regimen - may alleviate skin manifestations
sacroiliitis, or arthritis in IV articulations but do not seem to alter the course of joint disease
■ Tendonitis & fasciitis produces pain especially
Achilles insertion, plantar fascia sites along axial
ARTHRITIS DUE TO INFLAMMATORY BOWEL DISEASE
skeleton
○ Urethritis
● Definition
○ Discharge is mucopurulent, prostatitis is common
○ General term for a group of chronic inflammatory disorders
○ Conjunctivitis and iritis
of unknown cause involving the GIT
○ Arthritis which begins in the weight bearing joints (knees,
○ 2 Major Groups of Chronic IBD
ankles, feet, wrist)
■ Chronic non-specific ulcerative colitis (ulcer at the
○ Arthritis of hands and fingers may give sausage-digit
colon at the latter end of the GIT)
appearance
■ Crohn's disease (affectation of small intestine &
○ Skin involvement may include
mesentery)
■ Keratoderma blennorrhagica
● Epidemiology
■ Balanitis circinata
○ Whites > Blacks & orientals
● Pharmacological Management
○ Males = Females
○ NSAIDs - incomplete response
○ Peak age: 15-35 y.o.
○ Indomethacin - initial treatment of choice
● Etiology
○ Systemic glucocorticoids
○ Unknown cause
○ Azathioprine - immunosuppressive agent
○ Immune mechanism may be involved
○ Sulfasalazine - with persistent RS
○ Psychological features suggested that patients with IBD
● Surgical Management
have characteristic personality which renders susceptible
○ Synovectomy - for severe joint pain
emotional stressors which may precipitate their symptoms
○ Excision arthroplasty for metatarsalgia
● Pathophysiology
○ Tenosynovectomy
○ Chronic ulcerative
■ Inflammatory reaction in colonic mucosa and
PSORIATIC ARTHRITIS extends proximal in a continuous fashion
■ Backwash ileitis on the entire colon
● Definition ■ Inflammatory reaction with neutrophilic infiltration
○ Benign inflammatory skin disease with genetic which may cause eventual destruction
predisposition ■ Deeper layers of the bowel beneath the
○ Arthroplasty associated with combined features of both submucosa usually are not involved
RA and seronegative spondyloarthropathies ○ Crohn's disease
○ Polyarthritis with psoriasis ■ Characterized by chronic inflammation of intestinal
○ Red patches of skin topped with silvery scales wall and its mesentery
● Epidemiology ■ Bowel walls is pliable during the early stage
○ Male = Female ■ As progress, it appears greatly thickened and
○ 1% prevalence leathery with tis lumen narrowed
○ 30-50 y.o. onset ■ Mesentery appears with fingerlike projections
● Etiology ■ Granulomas are usually present and is often
○ Skin lesions usually antedate with arthritis and discontinuous
exacerbation and remissions of psoriatic arthritis are ● Clinical Manifestations
poorly correlated with the course of skin lesions Ulcerative Colitis Crohn's Disease
● Pathophysiology
○ Arthritis may affect 1 digit causing an inflammatory Diarrhea ++ ++
dactylitis
Rectal bleeding ++ +
○ Severe osteolysis at the opposing articular surfaces may
occur in peripheral and in proximal joints Abdominal pain + ++
○ Tendency to bony fusion may typically be seen and may
Palpable mass 0 ++
manifest to patients with generalized psoriatic
erythroderma Fistulas +/- ++
○ Severe resorptive arthroplasty in which loss of bonestock
Small bowel movement +/- ++
and joint surface is extensive that he skin overlying the
fingers or wrists may fold upon itself - so called Main en Rectal involvement ++ (95%) ++ (50)
Lorgnette syndrome
● Clinical Manifestations Toxic megacolon + +/-
○ Asymmetric oligoarthritis or monoarthritis Recurrence after
○ Symmetric polyarthritis resembling RA 0 +
colectomy
○ Auspitz sign (bleeding after scraping skin)
○ Nail findings including stippling and onycholysis Malignancy + +/-
○ Severely deforming arthritis known as arthritis mutilans ● Medical Management
causes shortening of fingers secondary to excessive bone ○ General measures
resorption plaques ■ Bed rest
○ Enthesis ■ Proper diet
○ Psoriatic lesions are seen ○ Local treatment of joints
○ In radiographic features: pencil-in-cup deformity ■ Heat
■ Active exercises
 ■ Immobilization ■ Dietary excess of purine
○ Prevention of deformity ■ Trauma
■ Splinting ■ Drugs
■ Exercises ■ Radiation therapy
● Pharmacologic Management ● Pathophysiology
○ Salicylates - ASA drug of choice ○ Probable cause
○ NSAIDs ■ Sustained hyperuricemia leads to development of
○ Steroids microphi (tophi are pathognomonic features of
○ Gold salts gout) into synovial lining cells
○ Antimalarials ■ Accumulation of monosodium urate in the cartilage
○ Methotrexate in proteoglycans that has higher affinity
● Surgical Management ■ Episodic release of urate crystals in the synovial
○ Synovectomy fluid due to several mechanisms involving
■ Performed in RA to relieve pain & inflammation disruption of microtophi turn over of cartilage
associated with chronic swelling proteoglycans
■ To alleviate or restore ROM in contracted joints ■ Lower temp. in joint space on an unequal
○ Tenosynovectomy distribution of water and urate in the synovial fluid
■ Most frequently in extensor-flexor tendons of hand may accelerate precipitation
and TA ● Clinical Manifestations
■ Major C/I ○ Recurrent acute monoarticular pain (early stage)
■ Very active polyarticular disease ○ Chronic deforming articular changes (late stage)
■ Poor general medical condition ○ Inflammation
■ Poor motivation of Pt. ○ Attacks precipitated by excessive protein intake, drugs,
■ Stage 4 in Joint destruction fasting, alcohol abuse, and trauma
○ Arthrodesis ○ Rapid onset
■ Surgical fusion of bony surfaces of a joint; usually ○ Symptom free between attacks
done in cases of severe joint pain & instability in ○ Most involved joints is foot (1st MTP), hand, wrist, knee,
which mobility of a joint is a lesser concern and elbow
■ Indications ○ Acute attacks: red, swollen, warm, tender & painful upon
■ Relieve persistent pain movement
■ Provides stability where there is mechanical ○ (+) tophi (chalky deposits of sodium urate surrounded by
destruction of joint and to halt progress of foreign body inflammatory reaction)
disease ● Diagnosis
■ C/I ○ X-ray
■ Significant bilateral joint disease ■ Early stage: no joint changes
○ Tendon transfer ■ Later stage: typical small punch-out areas
■ Common in RA for the ff containing uratic deposits at the ends of joints
■ Ruptured tendons of the body ○ Laboratory findings
■ Tendon release ■ Elevated blood uric acid (early stage)
○ Osteotomy ● Pharmacologic Management
■ Help to correct valgus deformity in JRA ○ Colchicines - aid metabolism of urine; helps in reducing
○ Joint Replacement inflammation & inflammatory process that attack gouty
■ Indications arthritis
■ Persistent pain ○ Phenylbutazone
■ LOM ○ Indomethacin
■ Loss of function ○ Ibuprofen
○ Other NSAIDs
○ Prevention of tophaceous deposits:
CRYSTAL-INDUCED
■ Xanthine oxidase inhibitor
■ Allopurinol
Crystal-induced Arthropathies are due to deposition of specific
■ Uricosuric agent
crystalline substances towards the joints affected. Conditions under this
■ Increase fluid intake - increase in solute so blood
type of arthropathy include the following:
will have greater solvent than solute, solution
1. Gouty Arthritis
becomes less concentrated
2. Pseudogout Arthritis
■ Alkalinization of urine

GOUTY ARTHRITIS
PSEUDOGOUT ARTHRITIS

● Definition
● Definition
○ A familial disorder of purine metabolism in which uric acid
○ Deposition of calcium pyrophosphate dihydrate (CPPD)
is involved
crystals in the joints characterized by acute inflammatory
○ Characterized by hyperuricemia (early stage) and
joint disease
deposition of Na+ urate in joints (late stage)
■ Chondrocalcinosis or Calcium pyrophosphate
● Epidemiology
deposition disease (CPDD)
○ Occurs after 30 y.o.
● Epidemiology
○ 90% of Pt. are male
○ Affects older individuals and their 4th-5th decade
○ Rare in blacks
○ Affects both genders
○ Affects single joint
○ Usually over 50 y.o.; Prevalence increases with age
○ Affects primarily the big toe
○ Ratio of pseudogout with gout in incidence is 2:3
■ Podagra

● Etiology
○ May be due to
■ Alcohol intake
 ● Etiology
OSTEOARTHRITIS
○ Unknown cause
○ Associated with metabolic disorders:
● Definition
■ Hyperparathyroidism
○ Slowly progressive musculoskeletal disorder affecting the
■ Parathyroid produces parathormone which
joints of
increases level of calcium in the blood
■ Hands (involved with pinch grip)
■ Hypothyroidism
■ Spine
■ Produces calcitonin, which decreases level
■ Weight bearing joints (hip, knee)
of calcium in the blood
○ Most common articular disorder
■ Hemochromatosis
○ Other names
■ Hypophosphatasia
■ Osteoarthrosis
■ Hypomagnesemia
■ Degenerative joint disease
■ Gout
■ Hypertrophic arthritis
■ Ochronosis
■ Degenerative disc disease (DDD in spine)
■ Wilson’s disease
■ Generalized OA (Kellegren's syndrome)
● Pathophysiology
○ Progressive loss of cartilage with remodeling of
○ Crystals in the synovial fluid are believed to be shed from
subchondral bone & progresseive joint deformity
the crystal in the cartilage: 3 possible mechanisms
● Epidemiology
■ Lowering of either calcium or pyrophosphate ions
○ Associated with increased age
in the synovial fluid may loosen and shed crystals
○ More common in women than men
from cartilage into the synovial fluid
○ Radiographic evidence in > 50-80% for those 65 y.o.
■ Crystals may enter synovial secondary to
○ Estimated 2-3% of audit population has symptomatic OA
mechanical destruction of cartilage resulting from
● Etiology
microfractures of subchondral bone
○ Systemic Factors
■ Release of crystals from degradation of cartilage
■ Age
by enzymes
■ Gender
● Clinical Manifestation
■ Race
○ Patterns of joint involvement
■ Genetics (Heredity “OA of DIP jts)
■ Pseudogout
■ Metabolic/endocrine
■ Occurs in 25% of cases
■ High bone density
■ Onset is rapid and reaches peak in 12- 36
■ Nutritional status
hours
■ Congenital/developmental
■ Involved joint is edematous, swollen, warm
■ Obesity
and painful
○ Local Factors
■ Usually confined in a single joint
■ Obesity
■ Attacks may be provoked by trauma,
■ Major joint trauma
surgery or medical illness
■ Repetitive stress
■ (+) radiographic evidence of
■ Muscle weakness
chondrocalcinosis
■ Altered joint biomechanics
■ Pseudorheumatoid disease
■ Excessive knee varus - compression on
■ Occurs ~5% of cases
med. side
■ Multiple joint involvement
■ Excessive knee valgus - compression on
■ Subacute attacks last to weeks or months
lat. side
■ Complains of morning stiffness & fatigue
■ Joint malalignment
■ Develops synovial proliferation, LOM &
■ Proprioceptive impairments
flexor deformities
● Risk Factors for OA
■ Chronic
○ Obesity
■ More in women
○ Heredity (esp. OA for DIP joints)
■ Progressive degenerative of multiple joints
○ Age
■ Joint involvement is usually symmetrical
○ Previous Joint Trauma
■ Affects mostly in knees followed by wrist,
○ Abnormal Joint mechanics (Excessive knee varus or
MCP, hips, shoulders, elbows, and ankles
valgus)
■ May resemble neuropathic arthropathy
○ Smoking (may contribute to DJD)
● Classifications
● Pathologic features of OA
○ Hereditary type
○ Early
○ CPDD associated with metabolic disease
■ Swelling
○ Idiopathic CPDD
■ Loosening of collagen framework structure
○ CPDD concomitant with OA
restraint
● Pharmacologic Management
■ Chondrocytes increase proteoglycan synthesis but
○ Phenylbutazone
also release more degenerative enzymes
○ Indomethacin
■ Increase cartilage water content
○ NSAIDs
○ Later
○ Glucocorticoids
■ Degradative enzymes break down proteoglycans
○ Salicyaltes
faster than it can be produced by chondrocytes,
resulting in diminished proteoglycan content in the
DEGENERATIVE cartilage
■ Articular cartilage thins and softens (joint space
Degenerative Arthropathies are due to degenerative processes that affect narrowing will be seen eventually)
joint and bone tissue. Conditions under this type of arthropathy include ■ Fissuring and cracking of cartilage; repair
the following: attempted but inadequate
1. Osteoarthritis ■ Underlying bone is exposed, allowing synovial fluid
2. Cervical Spondylosis to be forced by the presence of weight into the
3. Avascular Necrosis bone (shows up as a cyst or geos on radiographs)
 ■ Remodeling and hypertrophy of subchondral Involve fewer joints Involves many joints at
sclerosis and osteophytes (spurs) formation particular time
● Classification of OA
○ Primary (Idiopathic) W=M W>M
■ Localized OA (1 or 2 joints)
■ Generalized OA includes 3 or more areas
(Kellgren-Moore) ● OA is sometimes difficult to differentiate with RA because
○ Secondary sometimes the 2 may coexist
■ Trauma ● OA mayne stipulated by gouty, neuropathic or tuberculous joint
■ Congenital or developmental disease
■ Metabolic - ↑ or ↓ of collagen/hormones ● Medical Management
■ Endocrine - thyroid & parathyroid hormones ○ General measures
■ Malalignment due to fractures ■ Reassurance
■ Congenital subluxation of hips ■ Rest/modification of activity
■ Calcium deposition diseases ○ Local treatment
■ Other bone and joint diseases ■ Splints/braces
■ Neuropathic (Charcot joints) ■ Massage
■ Endemic ■ Exercise
■ Miscellaneous ● Pharmacologic Management
● Clinical Manifestations ○ Aspirin - drug of choice
○ Pain in involved joints ○ NSAIDs
○ Pain worse activity, better with rest ○ Corticosteroid
○ Morning stiffness (if present) < 30 mins ● Surgical Management (last resort)
○ Stiffness after a period of immobility (gelling) ○ Indications
○ Joint enlargement ■ Severe pain
○ Joint instability ■ Loss of function
○ Limitation of joint mobility ■ Progression of deformity
○ Periarticular muscle atrophy ○ Soft tissue procedures
○ Crepitus ■ Synovectomy
○ Most seen in hands, hips, knees, cervical & lumbar spine ■ Soft tissue release
○ Presence of nodes in hand ■ Tendon transfer
■ DIP - Heberden’s Nodes ○ Bone and joint procedures
■ PIP - Bouchard’s Nodes ■ Arthrodesis - relieve pain, result to a very stable
● Radiographic features joint but sacrifices freedom of motion
○ No ankylosis ■ Osteotomy - improve joint alignment
○ Alignment may be abnormal ■ Arthroplasty - joint replacement to relieve pain and
○ Bone mineralization restore function
○ Bone subchondral sclerosis
○ Bony spurs (osteophytes)
CERVICAL SPONDYLOSIS
○ No calcification in cartilage
○ Cartilage space narrowing which is non-uniform (occurs in
area of maximal stress in weight bearing joints) ● Definition
● Laboratory findings ○ Degenerative changes which occur to the IV disc and
○ ESR normal (no inflammatory process systematically) vertebral bodies
○ RF negative ● Epidemiology
○ ANA not present ○ Common in an advancing cage (esp. cervical spine)
○ Synovial fluid ○ Less than 40 y.o. (asymptomatic), 25% have DJD, 4%
■ High viscosity with good string sing have foraminal stenosis
■ Color is yellow & clear ○ More than 70 y.o.: 70% have degenerative spine changes
○ WBC counts typically <1,000-2,000/mm3 ● Etiology
○ No crystals and negative cultures ○ No specific cause
● Differential Diagnosis ○ Factors contributing to degenerative changes of spine
■ Aging
■ Trauma
Osteoarthritis Rheumatoid Arthritis
■ Work activities
Non-systemic Systemic ■ Genetics
● Pathophysiology
Non-inflammatory Associated with cutaneous and ○ IV discs loses hydration with age, leading to cracks and
inflammatory changes fissures
Affects weight bearing joints Small joints ○ Disc subseqeuntly collapses owing to biomechanical
incompetence causing annulus to bulge outwards
○ Surrounding ligaments also lose their elastic properties
(-) RF (+) RF but not all and develop traction spurs
(-) subcutaneous nodes (+) subcutaneous nodes ○ Uncovnertable spurring occurs as a result of the
degenerative process in which the facet joints lose
Normal ESR & Serologic test ↑ ESR; Leukocytosis with cartilage, becomes sclerotic and develop osteocytes
Eosinophilia ○ Stenosis due to spur formation, disc protrusion,
Clear synovial fluid; high Turbid synovial fluid; low ligamentum hypertrophy
viscosity viscosity & few cells with many ● Clinical Manifestation
polymorphonuclear cells ○ Morning neck pain
○ Stiffness
(+) osteophytes (-) osteophytes ○ Neck fatigue late in the day
○ Loss of neck ROM
DIP affectation Terminal joints not usually
○ Pain at extremes of ROM extension ROM is affected first
affected (ex. DIP)
 ○ Sometimes crystallization
● Complications
○ Neurological deficits
○ Vertebral artery injury
■ Due to facet osteophyte formation
○ Myelopathy
■ If arthritis is combines with disc degeneration or
post disc herniation
○ Cervical spinal stenosis
● Diagnosis
○ Plain films - later radiograph
○ CT scan - to rule out fracture
○ MRI - Most sensitive; can visualize soft tissues (IV discs)
● Medical Management
○ Long hot shower for morning stiffness
○ Soft cervical collar
● Pharmacologic Management
○ NSAIDS
■ Posses unacceptable medical risk for complication
○ Acetaminophen

AVASCULAR NECROSIS

○ Definition
■ Also called Osteonecrosis, Bone Infarction, Aseptic
Necrosis, Ischemic Bone Necrosis, AVN
■ Bone death resulting from blood supply deprivation in the
absence of pyogenic and tuberculous infection
■ Osteonecrosis is the term currently used recognizing the ● Three Stages (Taking about 2 years)
fact that bone may die because of reasons other than loss ○ Stage of Necrosis
of circulation ○ Stage of Fragmentation
■ If Avascular Necrosis involves bones of a joint, it often ■ Dead bony trabeculae may fx by body weight.
leads to destruction of the joint articular surfaces ■ Epiphysis may become collapsed and fragmented.
○ Epidemiology ○ Stage of Regeneration
■ New blood vessels enter the epiphysis and new
bone is laid down on the dead trabeculae
Sites of Predilection
● Clinical Manifestations
Femoral head ● 20 - 30% of all femoral neck fractures ○ General
(SCAFE) ● Infancy to late adulthood ■ Local swelling
● Men 30 – 60 years old ■ Tenderness
■ Thickening over affected bone
Carpal bones ● Uncommon
■ Limited ROM
(Keinbock’s ● Usually affects adolescents & men, 20-40 y.o.
disease & ● Keinbock’s disease - Spontaneous necrosis of ■ Muscle atrophy
Preiser’s the lunate bone ○ Specific
disease) ● Preiser’s disease - Spontaneous necrosis of the ■ Carpal bone osteonecrosis
scaphoid bone ■ LOM of wrist extension
■ Hip avascular necrosis
Metatarsal head ● Mostly in adolescents
(Freiberg’s ● Commonly affecting 2nd metatarsal bone ■ Pain in groin & thigh
disease) ■ Tenderness over hip joint
■ LOM in FAbIR
Tarsal navicular ● Uncommon ■ Antalgic gait
bone (Kohler’s ● Usually bilateral
■ X-ray shows "Crescent Sign"
disease) ● Occurs in childhood 4 – 6 years old

Talus Stage Findings

Segmented ● A fragment from the shaft of a long bone may 0 Incidental Finding (No symptom)
fractures be separated and undergo necrosis
1 Pain in Proximal Thigh and LOM
Other locations ● Capitulum of the humerus
(less common) ● Radial head 2 Symptoms are worse; X-ray shows sclerosis/cystic changes
● Lateral femoral condyle
3 Crescent-shaped subchondral fx line appears, followed by
subchondral collapse
○ Etiology
■ Any condition that cuts off blood supply to the bone 4 Radiographic evidence of OA
■ Trauma
■ Fractures ● Complications
■ Dislocations ○ Gout
■ Surgery ○ Traumatic arthritis
■ Excessive stripping of the periosteum ○ Renal transplantation
■ Organ transplantation ○ Sickle cell disease and other hemoglobinopathies
■ Prolonged corticosteroid intake ○ Caisson's disease - decompression sickness; diver's
■ Radiation exposure paralysis
■ The bones are important in terms of the storage of
fat, and in alterations of the bone, there would be
 embolisms, and that’s why it might cause paralysis Read:
or decompression syndromes Pathology Implications for PT, Goodman & Fuller 4th Ed.
● Diagnosis Differential Diagnosis for Physical Therapists: Screening for Referral,
○ X-ray Goodman 6th Ed.
■ Thin radiolucent line beneath joint surface Braddom’s Physical Medicine & Rehabilitation, Braddom 5th Ed.
■ "Crescent sign" in hip avascular necrosis Physical Medicine & Rehabilitation: Principles & Practice, De Lisa 5th Ed.
■ Denser area
■ Fragmentation
■ Thickening over fragmented area
○ Scintigraphy using radioactive technetium diphosphate
■ "Cold" initially
■ With time & revascularization becomes "hot"
● Differential Diagnosis

Hip Avascular Necrosis Hip Hemarthrosis

Pain Pain in the groin & thigh Pain in the groin & thigh (over
Location the greater trochanter)

Palpation Tenderness over the hip Fullness in the hip joint both
joint anterior to the groin & over
greater trochanter

LOM FAbIR FAbER

Gait Antalgic

● Prognosis
○ May progress into OA
○ Kohler's disease - good prognosis; little or no permanent
disability
● Medical/Surgical Management
○ Femoral head
■ Medical management (children)
■ Conservative protection of hip joint in
abduction for prolonged period until
reconstitution of femoral head is complete
■ Surgical Management (older patients)
■ Intramedullary or muscle-pedicle bone
grafting
■ Interposition or replacement arthroplasty
■ Arthrodesis
■ Total hip replacement
■ For older patient and other patients
with activity restrictions
○ Carpal bones (Keinbock's & Presiser's disease)
■ Medical management
■ Wrist immobilization in short dorsiflexion
splint
■ Surgical management
■ Reserved only if immobilization give
unsatisfactory healing
■ Simple excision
■ Total bone replacement
■ Arthrodesis
○ Metatarsal head (Freiberg's disease)
■ Medical management
■ Immobilization in a plaster boot or anterior
arch pad
■ Surgical management
■ Reserved only in late painful cases
■ Simple excision with use of anterior
arch support post-op
○ Tarsal navicular bone (Kohler's disease)
■ Medical Management
■ Use of longitudinal arch support &
restriction of activity
■ Immobilization with foot in slight inversion
by plaster cast for 6-8 weeks
■ If much pain upon weight bearing
■ Surgical management
■ Usually not applicable