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Patho > Pathophys of MSK > Flashcards

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
Q

What does NOT present in OA?

A

no systemic manifestations
no fatigue
no generalized weakness

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26
Q

In OA, what are the associated symptoms?

A

muscle spasm, contractures and atrophy

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27
Q

Symptoms of OA are uncommon before the age of ________

A

40

28
Q

Bouchard nodes presents in the

A

pip joints

29
Q

Hebderden nodes are present in the

A

dip joints

30
Q

What is RA?

A

A chronic inflammatory disorder with articular and extra-articular features

31
Q

For RA, incidence increases with age (peak_______)

A

40-60

32
Q

In RA, Sustained joint inflammation leads to

A

destructive joint disease and disability

33
Q

What is the cause of RA?

A

generally unknown; thought to be a combination of genetics (HLAs DR1 and DR4) and environment (i.e. viral infection)

34
Q

In RA, Long-term or intensive exposure to antigen causes

A

an immunologic response in which normal antibodies such as immunoglobulins become autoantibodies

35
Q

The transformed antibodies in RA are called ______________

A

rheumatoid factors

36
Q

In RA, the changes vary from mild inflammation to infiltration and destruction of bone. What are the initial inflammatory stages?

A

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
Q

What are common S/S of RA?

A

fatigue, soreness, stiffness, joint swelling

38
Q

Most people with RA experience (unilateral/bilateral) joint discomfort at hands, wrists, feet

A

bilateral

39
Q

Where do you commonly see RA nodules?

A

at pressure points and disseminated (i.e. organs)

40
Q

Swan Neck Deformity (RA)

A

Hyperextension of the PIP joint, flexion of the DIP joint, and sometimes flexion of the MCP joint.

41
Q

Boutonnière deformity (RA)

A
  • 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
Q

Ulnar deviation of fingers (RA)

A

slippage of the extensor tendons off the metacarpophalangeal joints in an ulnar direction

43
Q

Is it much more common to have adjacent structure involvement in RA or OA?

A

RA

44
Q

What other diseases can people with RA present with?

A

Anemia of chronic disease (AOCD)
Sjogren’s syndrome
Extra-articular changes associated with advanced disease

45
Q

Most cases of RA are (self limited, minimally, progressive)

A

progressive

46
Q

What is the early damage from RA?

A

Two Years from onset:
Joint space narrowing and erosions in 50%

Ten years from onset:
Young working patients are disabled: 50%

47
Q

How is RA diagnosed?

A

Labs:
Rheumatoid factor (not exclusive for RA)
Erythrocyte sedimentation rate (ESR)
Synovial fluid analysis

Radiological changes
American College of Rheumatology (ACR) criteria

48
Q

What is gout

A

A syndrome characterized by ↑ in serum uric acid concentration (hyperuricemia) or in other body fluids (i.e. synovial fluid)

49
Q

What population does gout mostly affect?

A

men

50
Q

What are the two types of gout?

A

Primary (overproduction vs.↓ excretion)
Secondary (2° to another disease or drug)

51
Q

Normally, uric acid is mainly excreted by _________ and then some via __________

A

kidneys, GI tract

52
Q

Most patients with gout have ______ uric acid clearance so it is retained

A

decreases

53
Q

If uric acid reaches certain concentrations, it crystallizes and where would it deposit?

A

into connective tissues and synovial fluid

54
Q

What is stage I gout

A

asymptomatic hyperuricemia; no pain, approximately 20% go to stage II

55
Q

What is stage 2 gout?

A

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
Q

What is stage 3 gout?

A

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
Q

What is stage 4 gout?

A

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
Q

What are the most common risk factors for gout?

A

Obesity
Alcohol use
High purine diet (meats, seafood)
Diuretic therapy including Thiazide Diuretics

59
Q

What is the gold standard for gout dx?

A

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
Q

What are extra-arricular manifestations of RA?

A

-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
Q

IN RA, extra articular changes is associated with

A

advanced disease

62
Q

What are proteoglycans?

A

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
Q

Dx of OA

A

See osteocyte formation, cartilage loss, joint space narrowing on radiologic exam

64
Q

Most people with RA experience _________ joint discomfort at hands, wrist, feet

A

bilateral

65
Q

Gout Dx

A

urate crystals in synovial fluid is the primary way

66
Q

What type of joints are most affected in OA?

A

weight bearing joints

Patho (16 decks)

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