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Pathophys of MSK Flashcards

1
Q

What type of arthritis is a normal process of aging

A

osteoarthiritis

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2
Q

The term “gout” should make you think immediately of “too much ____ _____”

A

uric acid

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3
Q

Where does gout commonly first present?

A

First MTP joint

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4
Q

Who is more often affected by rheumatoid arthritis: men or women?

A

women

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5
Q

Articulations aka joint is the site where

A

two or more bones meet

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6
Q

The articular cartilage covers end of each bone to reduce what?

A

friction and distribute weight; composed of chondrocytes which manufacture a matrix of collagen, protein and water

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7
Q

What are cartilage components

A

Chrondrocytes

Water

Ground Substance (hydrated, semi-solid gel)

Proteoglycans (elasticity and some stiffness)

Collagen (tensile strength/support)

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8
Q

Proteoglycans act as a pump to regulate _______ and provides ________ and ________

A

synovial fluid flow, provide elasticity and some stiffness

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9
Q

OA is a disorder of _____ joints

A

moveable

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10
Q

OA is considered a _________ disease

A

noninflammatory

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11
Q

OA is defined as a process of cartilage degeneration, characterized primarily by:

A

focal loss of cartilage

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12
Q

_____________ is the most common form of arthiritis

A

OA

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13
Q

OA is associated with _______ impairment and prevalence increases with age.

A

functional

Over 65 years: 80% of U.S. population

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14
Q

In OA, you can have the development of ____________ due to osteocyte overgrowth

A

bone spurs

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15
Q

In OA, there is abnormal cartilage repair and remodeling. How does this occur?

A

Chondrocytes produce proteolytic enzymes and these Proteolytic enzymes destroy cartilage. Once cartilage is destroyed, further joint destruction can more easily occur

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16
Q

In OA, chondrocytes overproduce _________ and ________, but breakdown is also in onedrive so you see a net loss of these substances.

A

proteoglycans, cartilage

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17
Q

In OA, alterations of collagen mix occur along with what?

A

biochemical/biomechanical changes, liberation of proinflammatory cytokines

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18
Q

In OA, what structures are affected?

A

Synovium, subchondral bone, periarticular muscles/ligaments affected

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19
Q

What is the end result of OA?

A

Asymmetric joint cartilage loss

Subchondral sclerosis (bone density increased)
Process called: eburnation

Subchondral cysts

Marginal osteophytes

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20
Q

What are the two types of OA?

A

Primary (idiopathic): not associated with any risk factors; a function of aging; likely genetic component.

Secondary: associated with risk factors such as trauma; long-term mechanical stress; joint instability; neurologic, skeletal, hematologic or endocrine disorders.

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21
Q

What is radiographic OA ?

A

when the XR appears to be “bone on bone” can see joint space between them = cartilage however, when you see that there isnt much space at all= radiographic appearance of OA. a lot of people have the latter. these people may not have clinical s/s

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22
Q

Clinical S/S of OA

A

joint tenderness, pain, stiffness, Heberden’s or Bouchard’s nodes, joint crepitus, ↓ range of motion

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23
Q

Manifestations of OA

A

Morning stiffness of short duration (<30 minutes) as they get going they no longer have stiffness anymore

Pain on motion – worsens with increasing joint usage

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24
Q

What is the progression of OA?

A

Initial high-use joint pain relieved with rest
Next, pain is constant on affected joint usage
Eventually pain occurs at rest and at night

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25
What does NOT present in OA?
no systemic manifestations no fatigue no generalized weakness
26
In OA, what are the associated symptoms?
muscle spasm, contractures and atrophy
27
Symptoms of OA are uncommon before the age of ________
40
28
Bouchard nodes presents in the
pip joints
29
Hebderden nodes are present in the
dip joints
30
What is RA?
A chronic inflammatory disorder with articular and extra-articular features
31
For RA, incidence increases with age (peak_______)
40-60
32
In RA, Sustained joint inflammation leads to
destructive joint disease and disability
33
What is the cause of RA?
generally unknown; thought to be a combination of genetics (HLAs DR1 and DR4) and environment (i.e. viral infection)
34
In RA, Long-term or intensive exposure to antigen causes
an immunologic response in which normal antibodies such as immunoglobulins become autoantibodies
35
The transformed antibodies in RA are called ______________
rheumatoid factors
36
In RA, the changes vary from mild inflammation to infiltration and destruction of bone. What are the initial inflammatory stages?
Neutrophils, T-cells activate in synovial fluid, degrades surface layer of articular cartilage Cytokines (IL-1, TNF-alpha) cause chondrocytes to attack cartilage Synovium digests nearby cartilage, releasing more cytokines → inflammation B-lymphocytes release rheumatoid factor Microvascular damage develops; synovium swells with fluid & cellular debris Inflammation causes formation of thickened layers of granulation tissue known as pannus; this covers and invades cartilage, destroying joint capsule & bone Result: bone atrophy, misalignment, immobility
37
What are common S/S of RA?
fatigue, soreness, stiffness, joint swelling
38
Most people with RA experience (unilateral/bilateral) joint discomfort at hands, wrists, feet
bilateral
39
Where do you commonly see RA nodules?
at pressure points and disseminated (i.e. organs)
40
Swan Neck Deformity (RA)
Hyperextension of the PIP joint, flexion of the DIP joint, and sometimes flexion of the MCP joint.
41
Boutonnière deformity (RA)
- can result from tendon laceration, dislocation, fracture, osteoarthritis, or rheumatoid arthritis. Classically, the deformity is caused by disruption of the central slip attachment of the extensor tendon to the base of the middle phalanx, allowing the proximal phalanx to protrude (“buttonhole”) between the lateral bands of the extensor tendon.
42
Ulnar deviation of fingers (RA)
slippage of the extensor tendons off the metacarpophalangeal joints in an ulnar direction
43
Is it much more common to have adjacent structure involvement in RA or OA?
RA
44
What other diseases can people with RA present with?
Anemia of chronic disease (AOCD) Sjogren’s syndrome Extra-articular changes associated with advanced disease
45
Most cases of RA are (self limited, minimally, progressive)
progressive
46
What is the early damage from RA?
Two Years from onset: Joint space narrowing and erosions in 50% Ten years from onset: Young working patients are disabled: 50%
47
How is RA diagnosed?
Labs: Rheumatoid factor (not exclusive for RA) Erythrocyte sedimentation rate (ESR) Synovial fluid analysis Radiological changes American College of Rheumatology (ACR) criteria
48
What is gout
A syndrome characterized by ↑ in serum uric acid concentration (hyperuricemia) or in other body fluids (i.e. synovial fluid)
49
What population does gout mostly affect?
men
50
What are the two types of gout?
Primary (overproduction vs.↓ excretion) Secondary (2° to another disease or drug)
51
Normally, uric acid is mainly excreted by _________ and then some via __________
kidneys, GI tract
52
Most patients with gout have ______ uric acid clearance so it is retained
decreases
53
If uric acid reaches certain concentrations, it crystallizes and where would it deposit?
into connective tissues and synovial fluid
54
What is stage I gout
asymptomatic hyperuricemia; no pain, approximately 20% go to stage II
55
What is stage 2 gout?
acute gouty arthritis; very painful swelling and tenderness of great toe and metatarsophalangeal joint most commonly with phagocytic and inflammatory responses "sheet of paper can cause pain"
56
What is stage 3 gout?
intercritical stage; no symptoms noted but most patients have another attack within one year if untreated *goal is to not have the pt go beyond this stage*
57
What is stage 4 gout?
chronic gout stage; urate pool continues to expand with development of tophi on Achilles, forearm, bursa, ear helix -commonly leads to renal involvement (glomerular disease, stones)
58
What are the most common risk factors for gout?
Obesity Alcohol use High purine diet (meats, seafood) Diuretic therapy including Thiazide Diuretics
59
What is the gold standard for gout dx?
tap joint- get sample of synovial fluid in affected joint Test Sensitivity: 84% Test Specificity: 100% May also evaluate tophi and/or study symptoms alone
60
What are extra-arricular manifestations of RA?
-Rheumatoid nodules are present in 30% of patients *granulomas consisting of a central necrotic area surrounded by palisaded histiocytic macrophages, all enveloped by lymphocytes, plasma cells, and fibroblasts (can lead to rheumatoid lung, vasculitis, Raynaud’s) -Anemia of chronic disease (AOCD) -Sjogren’s syndrome
61
IN RA, extra articular changes is associated with
advanced disease
62
What are proteoglycans?
mucopolysaccharides bound to protein chains occurring in the extracellular matrix of connective tissue act as a pump to regulate synovial fluid flow, provide elasticity and some stiffness
63
Dx of OA
See osteocyte formation, cartilage loss, joint space narrowing on radiologic exam
64
Most people with RA experience _________ joint discomfort at hands, wrist, feet
bilateral
65
Gout Dx
urate crystals in synovial fluid is the primary way
66
What type of joints are most affected in OA?
weight bearing joints

Patho (16 decks)

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