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Patho Summer Test #1 > MSK 2 - Articular Structure and Pathology > Flashcards

MSK 2 - Articular Structure and Pathology Flashcards

1
Q

What is a synovial joint composed of?

A

Joint capsule: Fibrous joint capsule (outer layer) and synovial membrane (inner layer)

Joint space

Synovial fluid

Articular cartilage

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2
Q

What is the outer layer of the joint capusule?

A

Fibrous capsule or stratum fibrosum

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3
Q

What kind of blood supply does the fibrous capsule have?

A

Poor blood supply BUT rich in joint receptors (sensory receptors)

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4
Q

What is the function of the synovium?

A

produce synovial fluid

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5
Q

What do type B cells of the synovium do?

A

Secrete hyaluronate (HA) = gel that improves viscosity of synovial fluid and attracts H2O

Secrete lubricin (glycoprotein) = reduce friction

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6
Q

What do type A cells of the synovium do?

A

Secrete immunoglobulins

Secrete lysosomal enzymes

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7
Q

What is synovial fluid?

A

Clear viscous fluid

Provides lubrication for joint surface –> frictionless surfaces between bones

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8
Q

What are thixotrophic properties?

A

Viscosity varies inversely w/ velocity of movement:

Rest - synovial fluid resists movement of joint

Movement - synovial fluid provides less resistance to movement

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9
Q

What is hyaline articular cartilage?

A

Thin covering on the ends of most bones

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10
Q

What does hyaline articular cartilage do?

A

Reduces friction

Absorb/disperse compressive forces

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11
Q

What is articular cartilage composed of?

A

Cellular component

Extra-cellular matrix

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12
Q

What is the cellular component of articular cartilage?

A

Chondroblasts (chondrocytes)

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13
Q

What do chondrocytes to?

A

Produce/maintain extra-cellular matrix

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14
Q

How much of cartilage do chondrocytes make up?

A

2%

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15
Q

What makes up the non-fibrous component of the extra-cellular matrix?

A

Proteins

Proteoglycans

(makes up 5 - 10%)

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16
Q

What does the non-fibrous component of the extra-cellular matrix do?

A

Regulate fluid flow in/out of cartilage (water = 60 - 80% of cartilage)

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17
Q

What makes up the fibrous component of the extra-cellular matrix?

A

Collagen fibers

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18
Q

What do collagen fibers do in the extra-cellular matrix?

A

Arranged to absorb mechanical stress

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19
Q

How much of the cartilage is made of collagen?

A

10 - 30%

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20
Q

What is zone 1 of the cartilage-bone interface?

A

Smooth surface –> reduce friction of joint surface

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21
Q

What are zone 2 and zone 3 of the cartilage-bone interface?

A

Transitional zones –? absorb compressive forces

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22
Q

What is the tidemark of the cartilage - bone interface?

A

Interface between uncalcified and calcified layers

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23
Q

What is zone 4 of the cartilage-bone interface?

A

Calcified cartilage –> anchors cartilage to bone

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24
Q

What are the stimuli for matrix turnover?

A

Enzymes from chondrocytes

Hormones: GH/IGF

Mechanical Load: weight bearing

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25
Q

What does weight bearing activity do in healthy cartilage?

A

Push fluid (water/synovial fluid) out of cartilage

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26
Q

What happens to fluid flow during weight bearing activity in healthy cartilage as the cartilage becomes more compressed?

A

Fluid flow out becomes slower and resistnace becomes exponentially harder

**prevent ALL of the fluid from flowing out of the cartilage

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27
Q

What is responsible for regulating fluid flow in/out of cartilage?

A

Proteoglycans

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28
Q

What is the net result of fluid flow in/out of cartilage w/ compression?

A

Protects against compressive forces

Allows for nutrients to pass in/out of cartilage to reach chondrocytes

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29
Q

Does articular cartilage have blood/nerve supply?

A

No

**pain results from inflammation/swelling/irritation of pain sensitive tissues such as joint capsule/synovium, periosteum

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30
Q

How does articular cartilage heal after its been injured?

A

Poor ability to regenerate d/t poor blood supply

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31
Q

What is the most common joint disease?

A

Osteoarthritis

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32
Q

What is the primary defect of osteoarthritis?

A

Loss/disruption of articular cartilage –> matrix destruction involving chondrocytes, collagen and proteoglycans

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33
Q

What are the enzymatic changes seen in osteoarthritis?

A

Excessive enzyme secretion from chondrycytes –> matrix breakdown

Ezymes from synovium also contribute to matrix (collagen) breakdown

**loss of proteoglycans in cartilage disrupts fluid regulation (H2O flows in/out too easily)

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34
Q

What are the hormone changes seen in osteoarthritis?

A

Chondrocytes become less sensitive to GH/IGF

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35
Q

What are the cytokine changes seen in osteoarthritis?

A

Excessive production of IL-1 –> inhibition of normal cytokine regulation of matrix turnover

  • *IL-1 facilitates NO synthesis
  • *IL-1 = inflammatory cytokine
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36
Q

What is found in synovial fluid and synovium in the joints of pts w/ osteoarthritis that is not found in normal joints?

A

Nitric Oxide

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37
Q

What does nitric oxide do in the joints of pts w/ osteoarthritis?

A

Chondrycyte apoptosis

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38
Q

What are the fluid changes @ rest that occur w/ osteoarthritis?

A

Increased volume of water w/ in cartilage

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39
Q

What are the fluid changes during weight bearing activity that occur w/ osteoarthritis?

A

Fluid is pushed out rapidly

Cartilage is easily compressed w/o much resistance

**relase of wt bearing allows increased volume of fluid to re-enter cartilage

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40
Q

What is the net result of the fluid changes during weight bearing activity that occur w/ osteoarthritis?

A

Cartilage has limited ability to absorb foces and provide adequate nutrients to chondrocytes

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41
Q

How does osteoarthritis effect surrounding structures (besides articular cartilage)?

A

Cause bone sclerosis and bone cysts

Osteophyte formation –> irritation

Synovial thickening –> loss of gross movement

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42
Q

What are the risk factors of osteoarthritis?

A

Trauma/Genetics = largest risk

Joint/ligament laxity

Inflammatory conditions

Neurological disorders –> abnormal movements –> damage joints

Exercise –> high impact sports

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43
Q

What are the typical radiolgoical (X-ray) findings associated w/ osteoarthritis?

A

Heberden’s Nodes - DIP joints

Bouchard’s Nodes - PIP joints

44
Q

What are the pain patterns typical of osteoarthritis?

A

Morning pain

Pain following prolonged postural positions (same position for long periods of time)

45
Q

Describe how pain may refer in osteoarthritis?

A

Hip may refer to knee

Hip may refer to ankle

Knee may refer to hip

46
Q

How are the joints affected in osteoarthritis?

A

Joint capsule thickening –> deformation

Loss of function/mobility

47
Q

What is the conservative treatment for osteoarthritis?

A

Changes in exercise, joint mobility, lifestyle

48
Q

What are the pharmaceutical treatments for osteoarthritis?

A

Symptomatic relief –> over the counter to narcotics

49
Q

What are the surgical treatments for osteoarthritis?

A

Viscosupplementation

Cartilage “repair” strategies

Joint Replacement (arthroplasty)

50
Q

What is Viscosupplementation?

A

Inject hyaluronates (gel like substance) into joint space to improve viscous properties of synovial fluid

51
Q

What are the cartilage repiar strategies for osteoarthritis?

A

Arthroscopic lavage and debridement

Marrow stimulating techniques (microfracture)

Osteochondral autografts and allografts (OATS) –> make chondrocytes in lab from pts own bone and inject it into joint

52
Q

When would you do a joint replacement in a pt w/ osteoarthritis?

A

Last resort

If all other strategies have failed or are not appropriate

53
Q

What are infectious inflammatory joint disease?

A

Inflammation directly d/t bacteria, virus, fungi, protozoa etc

**Lyme dz, Rocky Mt Spotted Fever

54
Q

What are non-infectious inflammatory joint disease?

A

Inflammation d/t autoimmune reax

**Rheumatoid Arthritis, Juvenile Rheumatoid Arthritis, Gout, Ankylosing Spondylitis

55
Q

What is Rheumatoid Arthritis?

A

Systemic autoimmune disorder that causes chronic inflammation of connective tissues, primarily joints

56
Q

What are the primary tissues involve in Rheumatoid Arthritis?

A

Synovial membrane

57
Q

What are the secondary tissues involve in Rheumatoid Arthritis?

A

Chronic inflammation gradually destroys:

Articular Cartilage

Fibrous Joint Capsule

Menisci

Surrounding Ligaments/tissue

Bone

58
Q

What are the most common joints involved w/ Rheumatoid Arthritis?

A

Fingers, Wrist, Elbow

Knee, Ankle, Foot

59
Q

Which joints are usually the first to become symptomatic w/ Rheumatoid Arthritis?

A

MP Joints

PIP Joints

Wrists

60
Q

Who are most affected by Rheumatoid Arthritis, men or women?

A

Female:Male (3:1)

**Peak age = 35 - 45

61
Q

What is rheumatoid factor?

A

“New antibodies” –> combine w/ IgM, IgG and sometimes IgA and attack tissue

**called autoimmune complexes

62
Q

What is the stimulus of rheumatoid arthritis?

A

Antigen of unknown cause combined w/ genetic susceptibility

63
Q

What is the result of the stimulus of rheumatoid arthritis?

A

CD4 T helper cells and B lymphocytes are activated in the synovial fluid

64
Q

What do B lymphocytes do in rheumatoid arthritis?

A

Facilitate the formation of rheumatoid factor –> facilitates formation of autoimmune complexes that are deposited in joint tissue

65
Q

What do CD4 T helper cells do in rheumatoid arthritis?

A

Facilitate release of inflammatory enzymes that have destructive effect on structures (synovium, articular cartilage, joint capsule, tendons/ligaments)

Facilitates release of RANKL –> promotes osteoclastic activity, creating erosive lesions in the bone surrounding the joint

66
Q

What are the general systemic manifestations of inflammation in rheumatoid arthritis?

A

Fever

Fatigue

Weakness
Anorexia

Weight Loss

General Achiness/Stiffness

67
Q

What are the local manifestations of inflammation in rheumatoid arthritis?

A

Joint = paintful, tender and stiff

Morning stiffness

Progressive joint limitation d/t pain and gradual destruction

68
Q

What are the hand deformities that are typical of rheumatoid arthritis?

A

Z deformity

Swan-neck

Boutonniere deformities

69
Q

What does the z deformity of rheumatoid arthritis look like?

A

Radial deviation of the wrist

Ulnar deviation of the fingers

70
Q

What does the swan-neck deformity of rheumatoid arthritis look like?

A

Extended PIP

Flexed DIP

71
Q

What does the Boutonniere deformity of rheumatoid arthritis look like?

A

Flexed PIP

Extended DIP

72
Q

What is a pannus formation or cloth cover seen in rheumatoid arthritis?

A

Granulation tissue (scar tissue) that covers articular surface

73
Q

What happens if patients have an extra-articular manifestations of rheumatoid arthritis?

A

Have increased mortality rate

More severe disability

74
Q

What are the cardiac manifestations seen with high-titer rheumatoid arthritis?

A

Pericarditis

Cardiomyopathy

Valvular incompetence

**caused by nodules and interstitial fibrosis

75
Q

What are the eye manifestations seen with high-titer rheumatoid arthritis?

A

Scleritis –> suggests poor prognosis

76
Q

What are extrasynovial rheumatoid nodules seen with high-titer rheumatoid arthritis?

A

Nodules seen in cutaneous areas that are under pressure or exposed to trauma

**MC on elbows/fingers

77
Q

What are the nervous system manifestations seen with high-titer rheumatoid arthritis?

A

Neuropathies –> peripheral nerve compression

78
Q

What are the kidney manifestations seen with high-titer rheumatoid arthritis?

A

Amyloid deposition

79
Q

What are the hematopoietic system (Felty’s syndrome) manifestations seen with high-titer rheumatoid arthritis?

A

Anemia

Splenomegaly

Leukopenia

80
Q

What are the vascular manifestations seen with high-titer rheumatoid arthritis?

A

Vasculitis

81
Q

How is the diagnosis of rheumatoid arthritis made?

A

4 or more of following signs and symptoms and if symptoms are present for more than 6 weeks:

Morning stiffness > 1 hr

Arthritis of 3+ joints

Arthritis of hands

Symmetrical involvement

Rheumatoid nodules over extensor surfaces or bony prominences

Elevated rheumatoid factor present –> know this one!

82
Q

How is rheumatoid arthritis treated?

A

Activity modifications –> limit exercise

Meds –> reduce inflammation, inhibit immune responses, rheumatic disease modifying drugs

Surgery –> correct deformity, correct mechanical imbalances

83
Q

How many cases of adult rheumatoid arthritis begin in childhood?

A

5%

**F > M

84
Q

Is juvenile rheumatoid arthritis pain as severe as adult?

A

No

**kid may be able to walk on affected joint

85
Q

What are the the things that differ between juvenile rheumatoid arthritis and adult rheumatoid arthritis?

A

Antinuclear antibodies

Large joints affected

More often involves the cervical spine

86
Q

What is gout?

A

Result of hyperurcemia –> joint destructionsoft tissue deposits and kidney damage

87
Q

Who is affected more by gout, men or women?

A

M > F (7:1 to 9:1)

88
Q

Which part of the body is usually affected by gout?

A

Big toe

89
Q

Where does uric acid come from?

A

End product of purine metabolism

**excess synthesis or reduced elimination of uric acid = hyperurcemia

90
Q

Where does the excess uric acid in the blood deposit?

A

Connective tissues surounding joint –> bursae, ligaments, articular cartilage, synovial membranes

91
Q

What happens when uric acid saturates the synovial fluid?

A

Crystallizes

92
Q

What do the urate crystals do in the joint?

A

Provokes inflammatory response –> joint destruction

93
Q

What is tophus?

A

Subcutaneous deposits d/t chronic elevation of uric acid

94
Q

Where is the first attack of gout usually?

A

90% = MTP (metatarsal-phalageal) jointo f the first toe

95
Q

What are the signs/symptoms of a gout attack?

A

Joint = swollen and warm

Decreased weight bearing d/t pain

Fever, tachycardia, fatigue

96
Q

How long do gout attacks usually last?

A

2 - 3 days

**spontaneous remission w/ reoccurrence

97
Q

What happens to gout attacks as the disease progresses?

A

Get closer together

98
Q

Where do tophi (plueral of tophus) deposit?

A

Ears

Elbows

Patella

**subcutaneous regions

99
Q

What can happen to kindneys in pts w/ gout?

A

Kidney damaged by deposits of uric acid

Renal Stones

100
Q

What are some chronic diseases associated w/ gout?

A

Alcoholism

Obesity

HTN

Hypertriglyceridemia

CAD

101
Q

What are some other predisposing conditions for gout?

A

Increased dietary purine intake: organ meat, seafood, goose, bouillon, broth, yeast, gravy

Decreased purine biosynthesis (lack of uricase enzyme)

Prolonged use of diuretics (thiazides)

102
Q

What is ankylosing spondylitis?

A

Chronic inflammatory joint dz –> stiffening and fusion of the spine and SI joint

103
Q

What is the antigen that is associated w/ ankylosing spondylitis?

A

HLA-B27 (human leukocyte antigen) –> 90% of pts are (+) for this

104
Q

Describe the pathology of ankylosing spondylitis?

A

Immune/inflammation response attack fibrocartilage structures of the joints

105
Q

What structures of the joint are attacked in ankylosing spondylitis?

A

Joint capsule

Intervertebral discs

Etheses = attachment sites of tendon, ligament and joint capsule

Periosteum

Patho Summer Test #1 (8 decks)

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