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most common disabling musculoskeletal disorder in the US
arthritis
almost 2/3 of adults in the US w/ arthritis are
of working age
18-64 years old
local disorders of joint function
osteoarthritis (know for test)
infectious arthritis
lyme disease
systemic disorders of joint function
immune-mediated (know for test)
post infectious
joint dysfunction secondary to other diseases
psoriatic
gout (know for test)
most common arthritis in the world
osteoarthritis
osteoarthritis
progressive disease of DIARTHROIDAL JOINTS
local degenerative joint disorder (DJD) associated w/
aging ( > 70 y/o)
wear & tear from repetitive stress
osteoarthritis is characterized by
LOSS OF ARTICULAR CARTILAGE
cartilage calcifies
wear of underlying bone
formation of bone spurs (osteophytes)
noninflammatory
weight-bearing joints
reason that osteoarthritis is noninfammatory
no immune system involvement; only mechanical damage
[osteoarthritis] factors that increase the likelihood of abnormal “wear & tear” on joins
obesity
joint trauma
congenital disorders
genu valgus/varus
hip dysplasia
etiology of osteoarthritis
lifestyle & occupation
abnormal stress to joins
genetic predispositions
hormonal status
postmenopausal
pathogenesis of osteoarthritis via initial injury causes
chondrocytes to release enzymes that breakdown matrix of proteoglycan & collagen
proteolytic
collagenolytic
collagen fatigue & microfractures
pathogenesis of osteoarthritis via progressive injury causes
structural breakdown of cartilage
osteophyte/spur formation
joint effusion
inflammation of synovial membrane = joint distention
clinical manifestations of osteoarthritis
localized
joint pain w/ function; relieved by rest but not at night
crepitus (creaking) w/ movement
bony enlargement
morning stiffness
hand deformity
morning stiffness in osteoarthritis
lasts < 30 minutes
improves w/ joint mobility
hand deformities related to osteoarthritis
Heberden (DIP joint involvement) = top joint in finger
Bouchard nodes (PIP joint involvement) = middle joint in finger
PIP
proximal interphalangeal (top joint in finger)
DIP
distal interphalangeal (middle joint in finger)
MCP
metacarpophalangeal
radiologic changes in osteoarthritis
bony proliferation at the joint margins (bony spurs/osteophytes)
ASYMMETRIC narrowing of joint space
subchondral bone sclerosis
malalignment of joints
cyst formation
mnemonic for radiologi changes in osteoarthritis
LOSS
Loss of joint pain
Osteophytes
Subchondral cysts
Subchondral sclerosis
treatment for osteoarthritis is aimed at
decreasing stress on the joint & protecting from additional trauma
treatment for osteoarthritis
acetaminophen (reduces pain)
nonsteroidal anti-inflammatory (NSAID) drug therapy
intraarticular injection of hyaluronan (joint lubrication)
physical therapy
surgery
most common cause for total hip & knee replacement
osteoarthritis (OA)
rheumatoid arthritis
systemic autoimmune inflammatory disease that involves synovial membranes, cartilage, joint capsule, & surrounding ligaments & tendons
characteristics of rheumatoid arthritis
greater in women
premenopausal age (40-50 y/o)
cause unknown
all races
caused by abnormal autoimmune response
rheumatoid arthritis is triggered by
bacterial or viral antigen in GENETICALLY susceptible individuals
HLA-DR4 in whites
HLA-DRB1
factors that increase the risk of rheumatoid arthritis
smoking
women who have never given birth
pathogenesis of rheumatoid arthritis (3 phases)
initial phase
inflammatory phase
destruction phase
initial phase of rheumatoid arthritis
immune response localizes in synovial tissue
activation of B cells, T cells, macrophages
B cells produce auto-antibodies
anti-IgG antibody (RF factor)
anti-Cyclic polypeptid antibodies antibodies (anti-CCP)
inflammatory phase of rheumatoid arthritis
immune cells activate the complement
cytokines & other immune mediators produced
STIMULATE & SPREAD INFLAMMATION IN THE JOINT
destruction phase of rheumatoid arthritis
escalating inflammatory response leads to PANNUS FORMATION
erode & destroy articular cartilage; results in
inflammation
subluxations (partial separation/displacement)
contractures (tightening of tissue around joint)
& deformities
pannus formation
vascularized tissue made up of lymphocytes, macrophages, histiocytes, fibroblasts, & mast cells
clinical manifestations of rheumatoid arthritis
BILATERAL SYMMETRIC polyarthritis involving smaller joints
malaise, fatigue
diffuse musculoskeletal pai
hands, wrists, knees, & feet are most commonly involved
swelling in hands (nodule)
joint deformity
abnormalities in gait & limitation of movement (hip involvement)
joint deformities in rheumatoid arthritis
ONLY MCP & PIP joint involvement
swan-neck deformity
boutonniere deformity
ulnar deviation
swan-neck joint deformity in rheumatoid arthritis
hyperextension of PIP
flexion of MCP & DIP due to contraction of muscle & tendon
boutonniere joint deformity
flexion of PIP
hyperextension of DIP due to excess laxity of extensor tendon
ex: top joint in finger makes u shape
clinical manifestations of rheumatoid arthritis
pericarditis
myocarditis
mitral valve disease
complete heart block
pulmonary manifestations
ophthalmic manifestations
pulmonary manifestations of rheumatoid arthritis
pleuritis
pulmonary effusion
ophthalmic manifestations of rheumatoid arthritis
scletitis
2˚ sjogren syndrome (dry eyes & mouth)
diagnosis of rheumatoid arthritis
at least one documented swollen joint
absence of alternative diagnosis that better explains the joint swelling
a total score on the criteria scale of ≥ 6
treatment goal for rheumatoid arthritis
alleviation of pain & swelling
prevention of structural damage
preservation of function
treatment for rheumatoid arthritis
anti-inflammatory medication
corticosteroids
disease-modifying antirheumatic drugs
biological agents – achieve long term control; recommended very early to minimize later damage
joint dysfunction secondary to other diseases
neurovascular, hematologic, & metabolic disorders associated disorders of joint function
most related to chronic diseases
gout
heterogenous disorder in which there is a disturbance of uric acid metabolism
deposition of uric acid crystals in joints
risk increases w/ age
characteristics of gout
hyperuricemia
urate crystal = induced arthritis
recurrent attacks of articular & periarticular inflammation
accumulation of tophi (urate crystal stones)
renal impairment / uric acid calculi
gouty arthritis is most common in
middle aged men
postmenopausal women
a diet involving food rich in purines can lead to
gout
clinical manifestations of gout
hyperuricemia
elevated serum urate levels
four phases of gout
asymptomatic hyperuricemia
acute gouty arthritis
intercritical goat
chronic tophaceous gout
acute gouty arthrits
weight bearing joints most commonly affected
warm, red, & tender joints
great toe
intitial attacks can last 1-14 days
later attacks become more frequent
intercritical gout
intervals between acute attacks
no symptoms
chronic tophaceous gout
advanced deforming gout
tophi develops
tophi appear 10yrs after initial onset of gout
tophi appear in synovium, bone, & tendons
can develop renal malfunction
diagnosis of gout
joint fluid test
blood test (uric acid / creatinine)
xray imaging to rule out other causes of joint inflammation
ultrasound to detect urate crystals in joint or tophus
treatment of gout
for acute gouty attack
colchicine
NSAIDs
corticosteroids
uricosuric agents / probenecid (increase uric acid secretion by kidneys)
block uric acid production / allopurinol