Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
83 Cards in this Set
- Front
- Back
osteoarthritis also known as
|
DJD (degenerative joint DZ)
|
|
Which joint does osteorthritis affect?
|
Diarthrodial (free moving synovial joint)
|
|
osteorthritis affects the articular cartilage as well as the
|
entire joint
-subchondral bone -ligaments -capsule -synovial membrane -periarticular muscles |
|
What is the most common joint dz of mankind?
|
osteorthritis
|
|
Who is OA most common in?
<50 yo >50 y/o |
age <50 M>F
age >50 F>M |
|
Prevalence osteorthritis in those greater than 65 y/o?
|
50% have radiographic knee OA
*2nd most common cause long-term disability us |
|
What is the most common reason for total hip and knee replacement?
|
osteorthritis
|
|
Is osteorthritis the inevitable consequence of aging?
|
no
-simply result of "wear and tear" *not treatable |
|
Key function articular cartilage
|
Distribute LOAD EVENLY over articular surface to prevent concentration of stress on the bone
*also helps bone GLIDE |
|
Normal articular cartilage is composed of?
|
Extracellular matrix (mostly)
Chondrocytes (fewer) |
|
Collagen (types II, IX, XI)
Hyaluronan Proteoglycans all are part of the? |
ECM (extracellular matrix)
|
|
What provides TENSILE strenght?
|
Collagen II mostly
IX, XI as well |
|
What binds proteoglycan
has a negative charge that retains water? |
Hyaluronan
|
|
What allows for the compressive stiffness of articular cartilage?
|
Proteoglycan
|
|
What is the core protein of proteoglycans?
|
Aggrecan
|
|
What are the side chains that stick to aggrecan in proteoglycans?
|
Glycosaminoglycan
|
|
What synthesizes the matrix components of normal articular cartilage?
|
Chondrocytes
-small percentage |
|
Does articular cartilage injury cause pain
|
Articular cartilage itself does NOT have pain receptors, no pain in cartilage
|
|
Regarding the structure of cartilage, what is the Tide mark?
|
Separates calcified vs non-calcified cartilage
|
|
What are the layers of collagen?
|
Superficial: parallel to articular surface
Middle: more random Deep: relatively lned up -TIDE MARK Calcified cartilage |
|
What is underneath the layers of collagen?
|
Subchondral bone
Cancellous bone |
|
How does cartilage structure (w/ chondrocytes) correspond to organization of collagen?
|
Similar
-organized near top -transitional zone -radial zone where stacked up -Calcified zone -Bony end plates |
|
In ECM, what deos hyaluronan interact w/?
|
binds Proteoglycan (aggrecan + glycosaminoglycan side chains)
|
|
Gross appearance of osteorthritis?
|
Surface irregularity
Then: ulceration of surface Then, then: may erode to bone |
|
Microscopic appearance of OA?
|
Fibrillation (irregularity)
Loss of Cartilage Matrix components (collagen, hyaluran, proteoglycan) -chondrocyte replication (clones) |
|
In the early stage of osteorthritis, what indicates an initial REPARATIVE response
|
Thickness in Proteoglycan content increases
|
|
What happens to the bone as a result of osteorthritis/
|
Remodeling and hypertrophy
-trabeculae thicken (sclerosis) -Eburnation (ivory appearnce of abraded bone under ulcer) -Osteophytes |
|
What causes visible new growth of bone w/ osteorthritis?
|
Osteophytes (bone spurs)
|
|
In the synovium, is there LOTS of inflammation?
|
NO - this is a key way to differentiate between inflammatory degenerative DZs like Rheumatoid arthritis
|
|
Since there's not a LOT of inflammation in synovium, what is there?
|
Mild, patchy, chronic inflammation
|
|
What happens to the joint capsule w/ osteorthritis?
|
Thickens
|
|
Where is osteorthritis most likely to occur
|
Weight bearing surfaces
|
|
Histopathology of osteorthritis observe?
|
Subchondral sclerosis
Fibrillation (cleft in cartilage) Focal loss of cartilage Osteophyte (new bone growth) |
|
Over course of osteorthritis, how does GAG (glycosaminoglycan content change?)
|
Initially increased then decreased
-also intial increase in cartilage water content |
|
What later degrades cartilage after initial increase in GAGs?
|
Matrix Metalloproteinases
-degrade cartilage |
|
What is Tissue Inhibitor of Metalloproteinase, and how do its levels change?
|
TIMP levels decrease
MMP (metalloproteinase levels increase) -stop inhibiting MMP, b/c TIMP levels decrease --> leads to cartilage degradation |
|
Normal cartilage is PINK (indicating high concentration of GAG and normal distribution chondrocytes), how does osteorthritis compare?
|
severe loss of GAG (safranin O staining)
-loss of chondrocytes -Tangential clefts causing surface irregularity -vertical clefts causing fibrillation) |
|
How do chondrocyte clones appear histologically?
|
Clusters
|
|
Which of the follwoing is NOT a histopathological feature of OA?
a. Fibrillation b. Intense synovial inflammation c. Loss of Glycosaminoglycan content d. osteophytes |
b. Intense synovial inflammation (typically this is MILD, recall, helps differentiate between inflammatory DZs like Rheumatoid arthritis)
|
|
In older individuals, hip osteorthritis more common in ?
|
men
|
|
Who is hand and 1st carpometacarpal (CMC) joint disease more common in?
|
women
|
|
What is the most common risk factor for knee and hip osteorthritis?
|
Obesity
(hereditary sometimes in hand and hip, but not as common) |
|
Be familiar w/ risk factors for osteorthritis such as
|
-vocational/avocational overload
-trauma (esp. to knee like previous periarticular fractures or meniscal tears/removal) -Neuromuscular (quadricep muscle weakness) -Metabolic (CPPD (calcium pyrophosphate dihydrate crystal deposition, hemochromatosis, acromegaly) |
|
Secondary osteorthritis is linked to?
|
Trauma: acute or chronic (sports)
Congenital/developmental: (legg-calve-perthe dz, congenital hip dislocation) -mechanical (leg lenth discrepancy, hypermobility, varus/valgus deformity) -endemic (Kashin-beck, Mselini) |
|
How is Varus different from Valgus?
|
Varus - bow-legged
Valgus - knock knee'd |
|
Secondary arthritis can also be associated w/ a number of metabolic, endocrine, neurpoathic joint, etc. dz's - don't know them, just be familiar
|
-metabolic (ochronosis, hemochromatosis, Wiilson's DZ, Gaucher's DZ)
-endocrine (acromegaly, hyperparathyroid_ -Calcium deposition dz's (calcium pyrophosphate, hydroxyapatite) -Neuropathic joint -other (fracture, osteonecrosis, RA, Paget's DZ, following an infected joint) |
|
Describe the pain in osteorthritis?
|
Deep
Aching Poorly localized pain in involved joints |
|
Can pain at rest occur w/ osteorthritis? how is it diff. from that w/ RA (rheumatoid arthritis)?
|
pain at rest can occur after long progression DZ
-diff. from RA b/c usually this will go away upon standing a little |
|
Can pain in the morning (morning stiffness) occur w/ osteorthritis? how is it diff. from that w/ RA (rheumatoid arthritis)?
|
minimal morning stiffness (<30 min), and stiffness after activity is mild
-RA has much longer joint stiffness in morning |
|
What can person w/ osteoarthritis experience in joint
|
-reduced range of motion
-giving way of weight bearing joints |
|
When there is inflammation (which is normally mild) w/ osteoarthritis, where does it occur?
|
typically in synovium or joint capusel (inflammation/distension)
|
|
What other postulates exist about apin?
|
Subchondral bone (medullary hypertension, microfractures)
Oteophytes (stretching of periosteal nerve endings) Ligaments (strectch) Muscle (spasm) |
|
Is there a strong correlation between pathologic and radiological severity of OA?
|
No - very poor correlation
-however, those w/ lower socioeconomic status more likely to be symptomatic |
|
What might you notice as a sign of osteoarthritis?
|
Tenderness on palpation joint
-pain on passive motion -joint enlargement due to cartilage and/or bony proliferation (osteophytes) -Restricted range of motion (joint surface incongruity, muscle spasm, mechanical block) |
|
What is joint crepitus?
|
grating/crunching on motion
-sign of osteoarthritis May be accompanied by joint instability |
|
Is there much fluid in the joint (effusion) w/ osteoarthritis?
|
some, but usually not large, if anyhting, knee might have some
|
|
What is antalgic gait?
|
limp
|
|
What joint deformity/subluxation might observe w/ osteoarthritis?
|
-Genu Varus (bow leg)
-Genu Valgus (knock kneed) -angular deformities fingers |
|
Enlargement of knees/joint usually due to?
|
Bony enlargement (osteophytes)
|
|
Which of the following is NOT consistent w/ a diagnosis of osteoarthritis?
a. Crepitus b. Joint enlargement c. Prolonged synovial proliferation/pain d. Effusion |
c. pain is NOT prolonged (as it would be w/ RA)
|
|
What is Heberden's Node?
|
DIP (distal interphalangeal joints) osteoarthritis
|
|
What is Bouchard's Node?
|
PIP (proximal interphalangeal joints) osteoarthritis
|
|
What is known as "squaring" of the joint?
|
CMC - First metacarpal (this is at the trapezium bone articulation w/ thumb)
|
|
What joints are primarily affected by osteoarthritis?
|
1. Hand joints (DIP, PIP, CMC)
2. Hips 3. Knees 4. Spine: cerical and lubar |
|
If there is suspected osteoarthritis in sites other than the primary sites of osteoarthritis, what should you suspect?
|
causes of secondary osteoarthritis
-from there you can try to figure out prob (ie: elbow pain in jack-knife operators) |
|
Is Heberden's (DIP) more common or is Bouchard's (PIP)?
|
DIP (Heberden's) > PIP (Bouchard's)
|
|
Who is more likely to get nodal generation of osteoarthritis (hand)
|
Mostly women
-onsent around time of menopause -familial predispostion -may get OA in knees, hips, and spien |
|
Who does Erosive inflammatory osteoarthritis mostly affect?
|
Postmenopausal women
|
|
Where is Erosive inflammatory osteoarthritis most common?
|
DIP and PIPs equally involved
-most joints affected at once |
|
What can erosive inflammatory osteoarthritis attacks of mild to moderate synovitis lead to?
|
Ankylosis
|
|
What specific changes occur as a result of Erosive inflammatory osteoarthritis?
|
Subchondral/central erosive changes
|
|
Match the name to the site
1. Heberden 2. Bouchard c. Squaring -PIP -1st CMC joint - DIP joint |
Heberden - DIP
Bouchard - PIP Squaring - 1st CMC joint |
|
Are laboratory tests effective in DXing osteoarthritis/
|
Not really
-one thing might note is elevated WBC count in synovial fluid, but still less than 2000, so characterized as noninflammatory *can measure cartilage degradation in serum and synovial fluid, but may not be useful |
|
Key radiographic feature of osteoarthritis?
|
-Joint space narrowing (cartilage loss)
-Marginal osteophytes (bone growth around region) -Suchondral sclerosis -Malalignment (varus/valgus) |
|
What is the most common location in hand of osteoarthritis
|
1st CMC joint (area appears squared)
then (DIP (Heberden's)> PIP (bouchard's) |
|
What are some underlying DZ assocations of osteoarthritis and CPPD dz (recall, CPPD is Calcium Pyrophosphate Dihydrate Crystal Depostion)
|
-Hemochromatosis
-Hyperparathyroidism -Hypothyroidism -Hypophophatasia -Hypomagnesemia -Neuropathic joints -Trauma -Aging, hereditary |
|
What is one way to distinguish osteoarthritis from RA, radiographically?
|
GULL WINGING
-resulting from central, not marginal erosions |
|
What does gull winging look like
|
an M "middle erosion is occurring)
|
|
What should prompt search for secondary causes of osteoarthritis?
|
osteoarthritis in atypical sites
|
|
Does presence of osteoarthritis exclude or preclude other arthritides or causes of pain?
|
No
- |
|
What should inflammatory symptoms, signs, and/or synovial fluid do w/ regard to one's dx?
|
Make one consider other diagnoses than osteoarthritis
|
|
Are tendonitis/bursitis necessarily responsible for osteoarthritis?
|
No - may be responsible for exacerbations of pain, not OA itself
|
|
What can often help imporove function, increase endurance and strength, and reduce fall risk w/ osteoarthritis/
|
Exercise program
-patient education as well: self help course, weight loss, heat/cold modalitites, shoes, cane |