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UM - MSK > Synovial joint > Flashcards

Synovial joint Flashcards

1
Q

List the components of a synovial joint

A

Joint capsule
Synovium
Synovial fluid
articular cartilage

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2
Q

T or F: Capsular redundancy occurs in all joints

A

False - it only occurs in highly mobile joints and is a source of dysfunction

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3
Q

What is the joint capsule?

A

A cuff around the joint of Type I collagen fibers organized in parallel bundles that varies in thickness and attachment and completely encloses the joint, covering all surfaces EXCEPT articulating/contact surfaces

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4
Q

What are the 3 types of mechanoreceptors

A

Muscle
Skin
Joint

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5
Q

What are joint mechanoreceptors?

A

Sensory receptors on the joint capsule and articular ligaments that respond to velocity, position, and changes in movement (mechanical P or deformation)

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6
Q

List the 4 types of joint mechanoreceptors

A 
Ruffini Corpuscles (Warm)
Pacinian Corpuscles (Pressure)
Golgi-type (length change)
Nociceptors (pain)
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7
Q

Ruffini Corpuscles

A. Location?
B. Threshold, stim, adaptation?
C. Provide info on?
D. Responds by?

A

A. superficial jt capsules, ligaments and menisci
B. low threshold, easy stim, slow to adapt
C. Static or dynamic position (Postural Receptors), sense of velocity & direction and amplitude of movement
D. Increase tone in stretched mm, relaxing antagonistic mm

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8
Q

Pacinian corpuscles

A. Location?
B. Threshold, stim, adaptation?
C. Provide info on?
D. Responds by?

A

A. joint capsule, ligaments, fat pads and menisci
B. low threshold, oscillation to stim, rapidly adapting
C. Provide info on DYNAMIC sudden changes in movment or dynamic presssure changes in the joint (Accel/decl)
D. Increase tone in mm being stretched and relaxes antagonistic mm

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9
Q

Golgi-Type Endings

A. Location?
B. Threshold, stim, adaptation?
C. Provide info on?
D. Responds by?

A

A. joint capsule, ligaments, and menisci
B. High threshold, velocity stim, and slowly adapting
C. stim by stretch at end range –> DYNAMIC movement
D. Reflexively inhibits mm

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10
Q

Nociceptors

A. Location?
B. Threshold, stim, adaptation?
C. Provide info on?
D. Responds by?

A

A. Capsule, ligaments, articular fat pads, periosteum, walls of blood vessels
B. High threshold, movement stim, non adaptive
C. Burning, aching pain difficult to localize from excessive movement or pain (Static and dynamic)
D. Tonic receptors - respond by producing a tonic mm contraction to increase tone

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11
Q

Which two mechanoreceptors respond to both static and dynamic movement?

Which are static only?

A

Both: Nociceptors and Ruffini Corpuscles

Dynamic only: Golgi-type endings and Pacinian Corpuscles

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12
Q

Which joint mechanoreceptors need an outside stimulus to turn them off?(non-adapting)

A

Nociceptors

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13
Q

What are two types of joint capsule injury and what do they both have a potential to lead to?

A

Effusion
Capsular fibrosis

Adhesion formation

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14
Q

What is joint effusion (S/S)?

A

Signs: Joint moves to position of comfort
Symptoms: Tight in joint

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15
Q

What is capsular fibrosis?

A

Injury to capsule where it becomes thickened, and collagen fibers have decreased extensibility
Signs: Dec ROM in a capsular pattern

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16
Q

What pop is more prone to capsular fibrosis?

A

Elderly bc there is already not enough protein/water in joints so it all sticks together

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17
Q

What is adhesive capsulitis? (S/S)

A

Gradual loss of AROM and PROM w/capsular end feel and pain at the end range w/general aching around the hsoulder

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18
Q

What is frozen shoulder?

A

The most common type of adhesive capsulitis w/ ER > Abd > IR

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19
Q

T or F: Synovium covers all surfaces of joint capsule

A

False - it does not cover the weight bearing surfaces of the joint

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20
Q

What are synovicytes

A

A specialized layer of connective tissue cells that form the synovium

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21
Q

What are the two layers of the synovium

A

Intima and subsynovial tissue

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22
Q

What is the intima?

A

The inner synovial layer composed of specialized fibroblasts that contain macrophage and fibroblast cells which help lubricate the joint and secrete the matrix

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23
Q

What is the subsynovial tissue?

A

The second layer of the synovium that is fibrous, areolar, and adipose tissue that produces the collagen matrix and has lymph and blood vessels that vary w/in each joint

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24
Q

Which components of the subsynovial tissue have greater vascularity? Lowest?

A

Greatest: areolar and adipose

Lowest: fibrous subsynovial tissues

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25
Q

What are the functions of the synovium?

A

Joint lubrication (secretes GAG)
Transportation (nutrition)
Stability

May: regulate intra-articular temp and antimicrobial effect

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26
Q

What is the reaction to injury in the synovium?

A
  1. Proliferation of surface cells
  2. Increase in vascularization
  3. Gradual fibrosis of subsynovial tissues
  4. Granular surface appears
  5. Alteration in synovial fluid
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27
Q

List some common diseases and disorders of the synovium

A
  • PT Synovitis
  • Hemarthrosis
  • Pigmented Villanodular Synovitis (PVNS)
  • Rheumatoid Arthritis (RA)
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28
Q

What is Post-Traumatic Synovitis?

Pathophys and S/S

A

Patho: Intima increases to 8-15 layers (from 1-3) and an increase in lymphatics and protein synthesis occurs

S/S: joint effusion w/tight sensation around the joint

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29
Q

What is hemarthrosis? (S/S)

What do you need to rule out?

A

Rule out a fracture 1st

Signs: rapid swelling w/in 15 min - 2hrs after injury and dec. ROM from swelling (blood entering joint)
Symptoms: inc. pain and tight sensation (dec. ROM and swelling)

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30
Q

What is pigmented Villonodular Synovitis?

A

Possible autoimmune response or benign neoplastic process in which nodules are formed in synovial tissue due to attachment of blood clots that causes a lot of pain and discomfort and further hemorrhage during movements due to crushing of the nodules

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31
Q

What are s/s of PVNS and treatment?

A

Inflammatory s/s w/pain w/compression of joint surfaces

To treat it you do a synovectomy

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32
Q

Define RA

A

Chronic systemic inflammatory autoimmune disorder which causes symmetrical polyarthritis of large and small joints w/unknown etiology

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33
Q

Risk factors for developing RA?

A

Woman (lower if have kids or contraceptives)

Age 30-40

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34
Q

What is the key antibody present to dx RA

A

Anti Citrullinated Peptide Antibodies (ACPA) –> 80% have this

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35
Q

What are the symptoms of RA

A
  • joint pain
  • fatigue 4.5 hours after rising
  • weakness unproportional to activity
  • joint stiffer after inactivity and better w/activity
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36
Q

What are the signs of RA

A
  • Swell in small jts of hands,wrists, and forefeet is most common
  • palmar erythema is common
  • cool, moist skin
  • atrophy of hands and feet mm (late stages)
  • joint contractures (late stages)
  • symmetrical
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37
Q

How is RA dx?

A

W/lab tests, history, and phys exam

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38
Q

Treatment goals of RA (PT)?

A
  • dec. pain
  • maintain mobility
  • min nstiffness and edema
  • min jt destruction
  • NOTHING AGGRESSIVE
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39
Q

What is synovial fluid

A

Blood plasma w/additions of proteins and hyaluronic acid

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40
Q

What is arthrocentesis

A

The surgical withdrawal of fluid from the joint cavity for analysis

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41
Q

What are the categories of arthrocentesis findings?

A 
0: Normal
I: Non-inflamm
II: Inflamm
III: Purulent (Pus)
IV: Hemorrhagic
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42
Q

What happens to x of the fluid as you progress through the stages?

a. clarity
b. viscosity
c. WBC amount

A

a. from transparent to translucent to opaque
b. very high viscosity to very low
c. less than 200 to greater than 75,000

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43
Q

What stage of synovial fluid is OA? RA?

A

OA will not progress past Group I/Stage I: Non-inflammatory

RA is stage I and stage II

44
Q

At what quantity of WBC in synovial fluid are we concerned about inflammatory disease?

A

2000 WBC causing cloudy appearance

45
Q

What des fat in a synovial fluid indicate?

A

A fracture

46
Q

What is the function of hyaline articular cartilage

A
  • distribute F across bones (Shock absorb)
  • transmit loads and sheer forces evenly to the bone
  • ptorect the subchondral bone
  • permit frictionless movement
47
Q

how many zones are in articular cartilage?

A

4

48
Q

What is zone 1 of the articular cartilage?

A

Superficial Tangential Zone

10-20% of thickness that protects and maintains the deeper layers by resisting shear, tensile and compressive forces

49
Q

What is zone 2 of the articular cartilage?

A

Middle or Transitional Zone

40-60% of the thickness that contains proteoglycans and collagen fibers that is the first line of defense in resisting compressive forces on the joint

50
Q

What is zone 3 of the articular cartilage?

A

Deep Zone

30% of articular cartilage that provides the best defense against compressive forces w/cells lined up perpendicular to the joint and the tidemark

51
Q

What is zone 4 of the articular cartilage?

A

The calcified cartilage that anchors the cartilage to the bone

52
Q

What is the tidemark

A

A boundary b/t the articular and calcified cartilage that lays in zone 3: deep zone

53
Q

What is the extracellular matrix of hyaline articular cartilage made of?

A

Water (HIGHEST PERCENT), Collagen, and Proteoglycans (ground substance) that is more of a gel than a liquid

54
Q

How does hyaline articular cartilage get its nutreients?

A

W/diffusion and osmosis through the porous surfaces as it is pushed in and out via WB activities

55
Q

What is the histological composition of hyaline articular cartilage

A
  • chondroblasts
  • fibroblasts
  • fibrocytes
  • chondrocytes
56
Q

What are chondrocytes

A

(multinucleated) Cells that synthesize the matrix of articular cartilage w/anabolic and catabolic activity and contain a receptor for bFGF (basic fibroblast growth factor)

57
Q

What are the 3 As of the extracellular matrix of HAC

A

Avascular
Aneural
Alymphatic

58
Q

What are the 3 main proteoglycans of HAC

A

Aggrecan
Leucine-rich Proteoglycans
Cell-surface proteoglycans (lubrican)

59
Q

What is aggrecan

A

proteoglycan of HAC that is negatively charged and expands w/o stress and compresses w/stress to push out water to sustain high compressive forces

60
Q

What are leucine-rich proteoglycans

A

one or two GAG chains that bind to the matrix to regulate development of fibrils and stabilize the cartilage

61
Q

What are cell-surface proteoglycans

A

proteoglycans of the HAC that maintain the tissue structure, utilize molecular signaling, and act as reservoirs and receptors for growth factors

62
Q

List the 3 variables for lubrication (HAC)

A
  1. surface compliance/elasticity (harder surface = higher friction)
  2. load (light load –> min congruency)
  3. thixotrophic (low velocity –> low viscosity)
63
Q

What is thixotrophic

A

viscosity changing w/velocity changes (thicker w/higher velocities)

64
Q

What are the 3 models of joint lubrication

A
  1. Boundary
  2. Fluid Film
  3. Mixed Mode
65
Q

What is boundary lubrication?

A

W/low load prevents direct surface contact, eliminates surface wear, and is dependent on lubricin

66
Q

What is fluid film lubrication?

A

When there is a high load: can be squeeze film or hydrodynamic

67
Q

What is squeeze film lubrication

A

A type of fluid film lubrication w/perpendicular forces, high loads, and short durations where the fluid in the HAC is forced into the joint cavity

68
Q

What is hydrodynamic lubrication

A

A type of fluid film lubrication caused by tangential (rolling) movement, lifting pressure and weeping ahead of the load occurs

69
Q

What are the 2 types of mixed mode lubrication

A 
Elastohydrodynamic (high load)
Boosted lubrication (low load)
70
Q

What is elastohydrodynamic lubrication

A

A type of high load mixed mode lubrication w/both boundary, squeeze film and hydrodynamic lubrication (perpendicular and tangential forces)

71
Q

Which type of cartilage operates under elastohydrodynamic lubrication?

A

Articular cartilage

72
Q

What is boosted lubrication

A

A type of low load mixed mode lubrication w/both boundary and squeeze film lubrication (perpendicular forces)

73
Q

What are some age related initial changes to HAC

A

Fibrillation (fx of collagen fibers)

& depletion of ground substance

74
Q

what are possible causes of injuries to HAC

A
  • mechanical injuries blunt trauma
  • penetrating wound
  • frictional abrasion
  • biomechanical stress (alt. in WB)
75
Q

When does the cycle of degeneration of HAC begin

A

After fibrillation and loss of ground substance occurs leading to softening of surface layer of cartilage, death of local chondrocytes leading to the release of proteolytic enzymes

76
Q

What are some factors that influence healing in HAC

A
  • depth of injury (partial vs full thickness)
  • Volume and SA of articular cartilage involved
  • immobilization (delays healing)
77
Q

What is the cycle of degeneration in a joint?

A
  1. fibrillations occur
  2. cause death of chondrocytes
  3. release proteolytic enzyme
  4. leads to inflamed joint
  5. leads to change in normal jt mechanics
  6. start cycle over & even develop osteophytes as bone tries to stabilize in any way it can
78
Q

Define OA

A

A non-inflammatory degen. jt disease characterized by loss of articular cartilage w/secondary changes in subchondral bone

79
Q

What is primary osteoarthritis (ideopathic)

A

OA that develops spontaneously (w/o any pre-existing jt disease) in middle age and progresses slowly

80
Q

What is secondary osteoarthritis

A

most common type of OA following jt trauma due to abnormal stresses placed on the joint, associated w/obesity, inc. PA, and physical disabilities

81
Q

What is the prevalence of OA

A

21 mil people in US accounting for 24% of all visits to PCP and 50% of all NSAID prescriptions

82
Q

How much of the pop has radiographic OA by age 65

A

80% but does not mean it will be symptomatic (only 60%)

83
Q

Which joints are commonly affected in OA?

A

hip, knee, cervical and lumbar spine, and first MTP (from load from walking)

84
Q

Theories for why OA occurs

A
  • defect in articular cartilage matrix = premature failure

- primary abnormality is in bone and cartilage failure is secondary

85
Q

Onset of OA

A

age 40 (where water dec in jt) and women > men

86
Q

Pathology of OA

A

cartilage is worn, thin, and frayed and subchondral bone is exposed and compressed causing shape changes

87
Q

What are the radiographic features of OA

A
  • joint space narrowing
  • bone cyst formation
  • periarticular sclerosis
  • ostephyte development (sclerosing of a hook)
88
Q

What kind of nodes are seen in the hand w/

OA?

RA?

A

OA: Herberden’s nodes (distal segments of fingers w/more prox. swelling)

RA: Bouchards nodes (nodes at the PIP)

89
Q

S/S of OA

A

Sympt: dull aching pain relieved w/rest
Signs: Stiffness lasting 30 min or less, crepitus, joint deformity and LOF

90
Q

What is grade 0 OA

A

Normal joint w/smooth bone and good separation

91
Q

What is grade 1 OA

A

macroscopic changes w/softening of cartilage but no change in jt space and possible osteophytes

92
Q

What is grade 2 OA

A

Fragmentation and fissuring cartilage w/osteophyte development at edge of joint and possible narrowing (<0.5in diameter of involvement)

93
Q

What is grade 3 OA

A

Moderate multiple ostephytes, definite narrowing, some sclerosis and possible deformity of bone ends (w/area of involvement >0.5 in diameter)

94
Q

What is grade 4 OA

A

Full thickness injury w/exposed bone characterized by large osteophytes, marked narrowing, severe sclerosis, and definite deformity of bone ends

95
Q

What is eburnation

A

Degenerative proces of bone w/subchondral bone changing into a dense substance w/ a smooth surface (like ivory)

96
Q

What is non-operative MGT for OA

A

Possible in early stages (1 &2) as chondroitin sulfate and glucosamine supplements or Injections of hyaluronic acid i

97
Q

What exercises should be avoided w/OA

A

Eccentric exercises from large compressive forces

98
Q

What type of exercises are good w/HAC and OA

A

PROM w/tracction
Static isometric of Low Load Short Duration after low load high velocity mvmts
load bearing exercise is necessary for health of the cartilage

99
Q

Pharmacological interventions for OA

A
  • NSAIDS to inc. ROM and dec warmth and relieve pain BUT can cause GI bleeding
  • possible COX II drugs
100
Q

What are the types of surgery for HAC?

A

Cartilage repair
Autologous chondrocyte implantation
OATS
Hemi/Total Joint Replacements

101
Q

When is cartilage repair indicated (HAC)

A

If it is a small injury in the HAC you can fill the it in w/stem cells or other material

102
Q

What is autologous chondrocyte implantation

A

Part of cartilage removed from NWB area, sent to a lab for chondrocytes to be sep, allow them to be cultures and then implanted into WB joint

103
Q

What are the downsides to autologous chondrocyte implantation

A
  • Time consuming (culture for 4-5 weeks then NWB for 12)
104
Q

What is osteoarticular transfer system (OATS)

A

A one-stage mosaicplasty where cylindrical osteochonrdral pieces are removed from NWB areas of the AC and transferred into debrided full thickness defects

105
Q

What are the benefits of OATS over autologous chondrocyte implantation?

A
  • lower cost
  • not lab dependent
  • minimally invasive
106
Q

What are the downsides to OATS

A

only effectiveness for small and medium-full thickness

ST only

107
Q

What joints are most typical for hemi or total joint replacement

A

Knees, Shoulders, Hips and hands

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