Joint pathology Flashcards
Primary/ idipathic osteoarthritis?
aging phenomenon
appears insidiously without cause
oligoartiuclar (few joints affected)
Secondary osteoarthritis?
younger individuals
history of predisposing conditions
-previous injury, congenital deformity, systemic disease
usually affect the predisposed joint
Clinical course osteoarthritis?
insidious deep, achy pain morning stiff crepitus limit ROM impingment on spinal foramina causing radiular pina, muscle spasm, muscle atrophy, and neuro deficits
Commonly seen with/ joints of osteoarthritis?
hips, knees, cervical and lumbar vertebrae, PIP, DIP
herberden nodes common in women
no preventive treatment, cannot halt progression
Genetic factors osteoarthritis?
genes involved with prostaglandin metabolism and WNT signaling
Environmental factors osteoarthritis?
Aging, 80-90% have evidence of OA by 65 yo Biochemical stress (joint stability, muscle strength)
Path mechanism of OA?
chondrocyte injury cause proliferation and form clusters
water content increases and concentration of proteoglycans decreases
Cracking of the matrix occurs as the supporing catilage and type II collage are degraded
Gross morphology of OA?
exposed subchonral surface
subchondral cyst
residual cartilage (destruction of)
Eburnation?
dectructive process of cartialge that exposes the bone
Rheumatoid arthritis?
chronic, systemic, inflammatory disorder
affects many tissues and organs
women more than men
nonsuppurative, profilerative and inflammatory synovitis
clinical course Rheumatoid arthritis?
slow and insidious
maliase, fatigue, generalized MSK pain
joint involvement ensuses after several weeks to months, small before large/symmetrical
(joints swollen, warm, painful, stiff from inactivity)
Lab indicators of Rheumatoid arthritis?
Rheumatoid factor- may appear in other conditions
Anti-CCP antibody (both tests together are sensitive)
synovial fluid shows:
neutrophils, high protein content, low mucin content
Diagnose Rheumatoid arthritis? (four of following)
morning stiffness arthritis in 3 or more joints arthritis of hang joints symmetric arthritis rheumatoid nodules serum rheumatoid factor typical radiographic changes
Pathogenesis Rheumatoid arthritis?
genetic susceptibilty associated with HLA-DRB1
Environment arthritogen microbial agents: EBV, retrovirus, mycobaterium citrullinated proteins
autoimmunity
What causes bone/cartilage destruction?
antigen is picked up by MHC class II, present to CD4+ T cell, release cytokines activate macrophages, B cells, and recruit leukocytes
leads to pannus formation, destroy bone, catilage
fibrosis, ankylosis
Histology of Rheumatoid arthritis?
formaiton of villi
proliferative synovium
dense lymphoid aggregate
Rheumatoid nodule?
most common cutaneous lesion
usually in areas subjected to pressure (elbows, forearm)
less common in lungs, spleen, heart
What is a Rheumatoid nodule?
central zone of fibrinoid necrosis surrounded by palisading granuloma and numerous lymphocytes and plasma cells
Herberden’s nodes?
at the DIP
Bouchard’s node?
at the PIP
Boutonniere deformity?
hyperflexion of the PIP, hyperexternsion of DIP
Swan neck deformity?
hyperflexion of DIP, hyperextension of PIP
Juvenile idiopathic arthritis?
before 16 yo, persist for min 6 wks
no nodules
JIA from RA?
oilgoarthritis is more common
systemic disease more frequent
large joints affected more often than small joints
rhuematoid nodules and RF are usually absent
ANA seropositivity is common
Crystal induced arthritis?
gout, pseudogout
Gout?
monosodium urate crystals accumulate in the joint, due to overproduction or underexcretion of uric acid
hyperuricemia
clin course gout?
asymptomatic hyperuricemia acute gouty arthritis (hyperemic, warm, painful joint) (rule out septic arthritis) intercritical gout chronic tophasceous gout
Classify gout?
primary or idiopathic (usually)
secondary (increased nucleic acid turnover) (leukemia, cancer) Metabolic disease (Lesch-Nyhan deficient HGPRT)
renal disease
Uric acid crystals?
need shaped, negatively birefirngent, water soluble crystals
Path of Gout?
crystals phagocytized by macrophage, release IL-1beta other cytokines to cause release of proteases, to cause tissue injury and inflammation
crystals also activate complement, neutrophil chemotaxis, phagocytosize crystals by neutrophils,lysis of neutrophils, release of lysosomal enzymes, tissue injury and inflammation
Gross morph gout?
synovium is endematous and congested
Histo of gout?
dense neutrophilic infiltrate with uric acid crystals in synovium
scattedered lymphocytes, plasma cell and macrophages
Thophus?
pathognomonic lesion of gout
gross- urates from visible depositis in the synovium, Hyperplastic and fibrotic synovieum
Histo- large aggregates of urate crystals
intense inflammatory reaction
Pseudogout (chondrocalcinosis)?
calcium pyrophosphate crystals accumulate and deposit in the joint, can be seen on xray
over 50, common knee
weakly bifringent, rhomboid/geometric shaped crystals
Pseudogout assoc with?
diabetes, hypothyroidism, hyperparathyroidism, hemochromatosis
Infectious arthritis?
potential serious, can cause deformatities
routes of infection
-hematogenous dissemination (via blood)
-direct inocculation
-contiguous spread from soft tissue abcess or focuse of osteomyeltitis
Etiologic agents for infectious arthritis?
Bacteria
Mycobacterium TB
sprichete: Borrelia burgdorferi
virus
bacterial arthritis?
suppurative arthritis, cloudy synovial fluid
acute onset on painful and swollen infected joint
systemic symptoms, fever, leukocytosis, increased ESR
etiologic agents by group
etiologic agents of bacterial arthritis?
<2 yo— H. influenza
older children and adults— S.aureus
Sex active women– Gonococcus
all ages with sickle cell disease— salmonella
Lyme disease?
Tick borne (Ixodes dammini) disease Borrelia burgdroferi skin rash migratory arthritis involving the knees, shoulder and elbows CNS and cardiac involvement
Erythema Chronicum Migrans?
target lesion from lyme disease
not allergy but actual infection
Seronegative Spondyloarthropathies?
develop in genetically predisposed individuals
HLA-B27 (prevalent in caucasians)
immuno Seronegative Spondyloarthropathies?
immune mediated manifestations triggered by a T cell response towards an antigen that cross=reacts with native molecules of MSK system
peripheral or azial inflammatory oligoarthritis
Seronegative Spondyloarthropathies? (ex)
Anklyosing spondyloarthritis
Reiter syndrome
Enteritis-Associated Arthritis (GI infection)
Psoriatic arthritis (chronic inflammatory arthropathy develeops in more than 10% of this pop)
Anklyosing spondyloarthritis?
rehuamtoid spondylitis
destruction of articular cartilage and resultant bony ankylosis esp sacroiliac joint (LBP)
men are affected more than women
HLA-B27
(complications) fracture spine, uveitis, aortitis, and amyloidosis
Reiter Syndrome?
Form of reactive arthritis
waxes/wanes over period wks-months
caused by autoimmune rxn by previous infection
HLA-B27 pos
Reiter Syndrome previous intiated by?
GI infection (Shigella, Salmonella, Campylobacter) GU (Chlamydia)
Reiter Syndrome triad of?
nongonoccocal urethritis or cervititis
conjunctivitis
Extra-articular symptoms of Reiter Syndrome?
inflammatory balanitis, cardiac conduction abnormalities and aortic reguritation
