MSK Mod 2 Flashcards
1
Q
what is the outer layer of the joint capsule
A
fibrous capsule aka stratum fibrosum
2
Q
characteristics of outer layer of joint capsule
A
poor blood supply but rich in joint receptors (sensory receptors)
CT of joint capsule (connective tissue?)
3
Q
what is the inner layer of the joint capsule
A
synovium aka stratum synovium
4
Q
functions of inner layer of joint capsule
A
synovial fluid production immune function secrete immunoglobulins secrete lysosomal enzymes secrete hyaluronate (hyluronic acid) secrete lubricating glycoproteins reduce friction in joint ingest debris
5
Q
what is hyalurnate?
A
glycoaminoglycan gel to improve viscosity of synovial fluid
6
Q
what is the joint space
A
enclosed by capsule and filled with synovial fluid
7
Q
what is synovial fluid
A
- clear, viscous fluid
- provides lubrication for the joint surfaces to create “frictionless” surfaces bw bones
- thixotropic properties - viscosity varies inversely with velocity of movement
8
Q
thixotropic properties at rest and movement
A
- rest - synovial fluid resists movement of the joint
2. movement - synovial fluid provides less resistance to movement
9
Q
what is articular cartilage
A
hyaline articular cartilage
- thin covering on the ends of most bones
- reduces friction, absorb/disperse compressive forces
10
Q
composition of articular cartilage
A
- cellular component: chondroblasts
2. extracellular matrix: fibrous vs nonfibrous
11
Q
what are chondrocytes
A
produce and maintain extracellular matrix
- produce and secrete enzymes that assist in matrix turnover (collagen and PGs)
- forms 2% of cartilage
12
Q
what is the nonfibrous component of matrix
A
proteins, proteoglycans (5-10% cartilage)
-regulate fluid flow in/outcartilage
water (60-80% of cartilage)
13
Q
what is the fibrous component of matrix
A
collagen fiber (10-30% of cartilage)
- arranged to absorb mechanical stress
- collagen fibers play role in regulating amount of fluid flow in/out of cartilage and prevent proteoglycans from escaping out of cartilage
14
Q
what is the cartilage-bone interface
A
zone 1: smooth surface, reduce friction of joint surface
zone 2&3: transitional zones, absorb compressive forces
trademark: interface bw uncalcified and calcified layers
zone 4: clacified cartilage, anchors cartilage to bone
15
Q
what is matrix turnover
A
- optimal joint function requires consistent matrix turnover
- enzymes hormones and mechanical stimuli all play role in maintaining matrix turnover
16
Q
3 things that assist in matrix turnover
A
- enzymes
- hormones
- mechanical load
17
Q
how do enzymes help matrix turnover
A
chondrocytes - secrete enzymes to assist in breakdown and rebuilding of matrix
18
Q
how do hormones assist in matrix turnover
A
GH (growth hormone) and IGF (insulin growth like factor) stimulate chondrocytes and play role in regulating matrix turnover
19
Q
how does mechanical load assist in matrix turnover
A
normal weight bearing forces required to stimulate optimal matrix turnover
20
Q
function of articular cartilage
A
allow cartilage to absorb forces and provide nutrition to cartilage
21
Q
healthy cartilage and weight bearing activity
A
- wt bearing activity will push fluid (water/synovial fluid) out of cartilage
- fluid flow becomes slower and resistance becomes exponentially harder the more the cartilage is compressed
- proteoglycans are responsible for regulating fluid flow in/out of cartilage
- release of wt bearing force allows fluid to re-enter back into cartilage
22
Q
net result of healthy cartilage
A
this cycle protects against compressive forces and allow for nutrients to pass in/out of cartilage to reach chondrocytes
23
Q
what is the joint composed of
A
joint capsule (fibrous & synovial membrane)
joint space
synovial fluid
articular cartilage
24
Q
does articular cartilage have any nerve or blood supply
A
no
25
can pain associated with joint injuries/pathology be from articular cartilage
no
26
what is pain from in joint injuries/pathologies
results from inflammation/swelling/irritation of pain sensitive tissues such as joint capsule/synovium, periosteum, increased subchondral bone pressures, tendon/ligament insertion sites and protective muscle spasm
27
healing ability of articular cartilage
has poor ability to regenerate after injury because of poor blood supply
28
what is osteoarthritis
degenerative joint dz
| classified as non inflammatory joint dz however evidence exists that there is an inflammatory component in OA
29
what is the MC of joint dz
osteoarthritis
30
primary defect of OA
loss/disruption of articular cartilage
- multiple factors contribute to cascade of events leading to OA
- -matrix destruction involving chondrocytes, collage, and proteoglycans
31
gross articular cartilage changes in primary defect OA
smooth glossy surface becomes a dull yellow/brown gray color with surface flaking fissures and fibrillations
32
4 cellular changes in articular cartilage
1. enzymatic
2. hormones
3. cytokines
4. nitric oxide and apoptosis
33
what enzymatic changes occur in cellular changes in articular cartilage in OA
excessive enzyme secretion from chondrocytes to matrix breakdown
1. proteoglycans, collagen and glycoaminoglycnas broken down by lytic enzymes
2. loss of proteoglycans in cartilage disrupts fluid regulation (water flows in/out of cell too easily)
3. elevated PGs found in synovial fluid
enzymes produced from synovium also contribute to matrix collagen breakdown
34
what hormone changes in articular cartilage OA
chondrocytes becomes less sensitive to GH/IGF
35
cytokine role in cellular changes in OA
1. excessive production of IL-1 from synovium and chondrocytes leads to inhibition of normal cytokine regulation of matrix turnover
2. IL-1 facilitates NO synthesis
3. IL-1 is an inflammatory cytokine
36
NO and apoptosis role in cellular changes of OA
NO not normally found in healthy joint but is found in synvovial fluid and synovium of pts with OA
NO facilitates chondrocyte death (apoptosis)
--cartilage calcification also facilitates chondrocyte death (apoptosis)
37
articular cartilage function in OA
disruption of cartilage matrix allows fluid to flow in/out easier
- fluid changes:
1. rest: (non weight bearing) - increased volume of water within cartilage
2. wt bearing activity: fluid pushed out of cartilage rapidly and cartilage is easily compressed without much resistance
- release of wt bearing allows increased volume of fluid to re enter cartilage
38
net result of articular cartilage function in OA
cartilage has limited ability to absorb forces and provide adequate nutrients to chondrocytes
39
secondary gross pathological changes associated with OA
--OA effects surrounding structures and not just the articular cartilage
subchondral bone sclerosis and bone cysts
-may be asymptomatic unless severe
-potential to communicate with the fissures and release contents into synovial fluid of joint space
-osteophyte formation may lead to irritation of synovium may contribute to loss of gross movement
-synovial thickening - may contribute to loss of gross movement
40
etiologies of OA
1. multifactorial
| 2. exercise
41
multifactorial etiologies of OA
1. trauma & genetics = largest
2. joint/ligament laxity
3. inflammatory conditions
4. neurological disorders - abnormal movements
42
exercise etiology of OA
running, walking, = low to no additional risk
high impact sports tend to increase risk due to traumatic type forces or injuries
-shearing twisting high impact movements increase stress
43
pain patterns of OA
1. morning pain
2. pain following prolonged postural positions
3. relief of pain with easy activity increased pain with extreme activity
4. pain in extreme wt bearing movements (kneeling, squatting, stairs, sports)
5. may experience "good day/bad day" pattern but overall experience chronic episodes
44
referred pain in OA
1. spine: potential for nerve root entrapment
| 2. LE joints: hip may refer to knee, hip to ankle, knee to hip
45
joint deformation in OA
joint capsule thickening
46
loss of function/mobility in OA
limited ROM due to decreased congruency , osteophytes or secondary to pain
gradual loss in wt bearing ability if lower extremity (hip/knee)
47
conservative care for OA
appropriate exercise, joint mobility, lifestyle changes
48
pharmaceutical tx of OA
targeted at symptomatic relief (range from OTC to narcotic)
49
surgical tx of OA
1. viscosupplementation
2. cartilage repair strategies
3. joint replacement
50
what is viscosupplementation
hyaluronan injections - joint fluid therapy
-injection of gel like substances into the joint to improve the viscous properties of synovial fluid
FDA approved only for knee
51
cartilage repair strategies for OA
1. arthroscopic lavage and debridement
- technically not cartilage repair
2. marrow stimulating techniques
3. osteochondral autografts and allografts
4. cell based repairs including autologous chondrocyte implantation
52
joint replacement for OA
arthroplasty
- last resort if all other strategies failed or not appropriate
- criteria: elective procedure determined by pain and quality of life
53
infectious inflammatory joint dz
inflammation directly d/t bacteria virus fungi protozoa
| ex. Lyme, RMSF
54
noninfectious inflammatory joint dz
inflammation d/t autoimmune rxns
| ex. RA, JRA, gout, anklysosing spondylitis
55
what is RA
rheumatoid arthritis
| -systemic auto immune disorder that causes chronic inflammation of connective tissue primarily in joints
56
primary tissue involve in RA
synovial membrane is initial and primary tissue involved
57
secondary tissue involved in RA
chronic inflammation gradually destroys articular cartilage, fibrous joint capsule, menisci, surrounding ligaments/tissue, bone
58
MC joints involved in RA
fingers, wrist, elbow
knee, ankle, foot
most often presents with involvement in the feet and hands - MP joints, PIP joints, and wrists are first to become symptomatic
59
ratio of F:M in RA
3:1
60
peak onset of RA
35-45 yo
61
etiology of RA
cause not clear
- most autoimmune diseases often thought to be d/t:
- abn immune response to a virus or infection
- as body attack's initial virus/infections it is tricked into programming it's immune system to attack its own tissue
62
what is RF
rheumatoid factor = new antibodies
| classes of antibodies in RF present in RA
63
stimulus of RA
antigen of unknown cause combined with genetic susceptibility
64
result of RA
inflammation/destruction of synovium and other joint tissues
65
what cause the inflammation/destruction of synovium and other joint tissues in RA
CD4 T helper cells and B lymphocytes activated in synovial fluid
66
what do the B lymphs do in the inflammation/destruction of synovium and other joint tissues in RA
1. facilitate formation of RF
2. RF facilitates formation of autoimmune complexes that are deposited in joint tissue
3. macrophages/phagocytes consume autoimmune complexes and also release lytic enzymes that destroy synovium
67
what do the CD4 T helper cells do in the inflammation/destruction of synovium and other joint tissues in RA
1. facilitate release of inflammatory enzymes that have destructive effect on joint structures (synovium, articular cartilage, joint capsule, tendon/ligaments
2. facilitate release of RANKL which promotes osteoclast activity creating erosive lesions in bone surrounding the joint
68
what is the viscous episodic cycle of inflammation in RA
cycle continues of connective tissue autoimmune attack (autoimmune deposition) followed by inflammatory components which further damages connective tissue of joint structures
69
general systemic manifestations of inflammation
fever, fatigue, weakness, anorexia, wt loss, general achiness/stiffness
symmetrical polyarthralgias
70
local manifestations of inflammation in RA
1. joint is painful, tender and stiff
2. morning stiffness d/t swelling in and around joint
3. progressive joint limitation d/t pain and gradual destruction
4. palpation...joint feels warm
71
hand deformities in RA
1. Z deformity = radial deviation of the wrist + ulnar deviation of fingers
2. swan neck = extend PIP and flex DIP
3. boutonniere deformities = flex PIP and extend DIP
72
pannus formation in RA
aka cloth cover
| covers articular surface...granulation tissue (scar tissue)
73
extra articular manifestations of RA
1. increased mortality rate and severe disability
| 2. more common with high titer RF
74
cardiac manifestations of RA
pericarditis, cardiomyopathy, valvular incompetence caused by nodules and interstitial fibrosis
75
eye manifestations of RA
scleritis
| rheumatoid scleritis is the most common ocular complication of RA and suggests poor prognosis
76
extrasynovial rheumatoid nodules in cutaneous areas
areas of pressure or trauma
MC on elbows fingers
will see on knees, back, feet
77
nervous system manifestations of RA
neuropathies (peripehral nerve compression) - median nerev
78
kidney manifestations of RA
amyloid deposition
79
hematopoietic system manifestations in RA
Felty's syndrome
| -anemia, splenomegaly, and leukopenia
80
vasculitis in RA
d/t elevated levels of circulating immune complexes
| usually is a non necrotising arteritis of the small terminal arterials
81
diagnostic criteria for RA
1. made in presence of 4 or more of the following and if joint s/s are present for 6+ wks
1. morning stiffness >1hr
2. arthritis of 3+ joints
3. arthritis of hands
4. symmetrical involvement
5. rheumatoid nodules over extensor surfaces or bony prominences
6. elevated RF present
82
tx of RA - activity
1. activity modifications - limits exercise during periods of exacerbations
83
tx of RA - medical
2. medical
- meds to reduce inflammation, inhibit immune responses, and rheumatic dz modifying drugs
- surgical correct deformity and correct mechanical imbalances aka hand surgery
84
what is JRA
juvenile rheumatoid arthritis
85
how many cases of adult RA begin in childhood
5%
86
female to male occurrence in JRA
F>M
87
basic pathology of JRA
same as adult RA
- synovial proliferation/inflammation leads to joint destruction
- severe joint destruction is seen in only 5% of pts
88
clinical findings of JRA
1. joints may appear worse than symptoms
- joint pain not as severe as in adult type, joint effusion may be only finding
- child may walk on affected joint despite swelling, warmth and limitation of motion
89
differences bw JRA and adult RA
1. ANA in serum while RF not usually found
2. large joints effected in JRA
3. more often involves cervical spine - subluxation of C1-2 in spine
4. arthritis is generally less destructive
5. fever, rash, leukocytosis and lymphadenopathy with splenomegaly are common
90
what is gout
result of hyperurecemia that causes joint destruction, soft tissue deposits and kidney damage
91
M:F ratio of gout
7:1 to 9:1
92
age of onset of gout
begins 30-50
93
pathogenesis of gout
1. uric acid is end product of purine metabolism
- excess synthesis or a reduced elimination of uric acid results in hyperurcemia
- hyperurcemia deposits in connective tissues surround joint (bursa, ligaments, articular cartilage, and synovial membranes)
2. uric acid saturates the synovial fluid and crystallizes
3. urate crystals in the joint provoke inflammatory response
4. over time joint destruction occurs
5. chronic elevation of uric acid forms subcutaneous deposits known as tophus
94
clinical manifestations of gout
1. hyperurcemia: asymptomatic
2. acute and recurrent attacks of monoarticular arthritis
3. tophi deposits in subcutaneous regions
4. renal dz
5. formation of renal stones
95
acute and recurrent attacks of monoarticular arthritis in gout
1. 90% of cases the first attack is the MTP joint of the first toe
2. joint is swollen and warm
3. decreased wt baring d/t pain
4. systemic effects: fever, tachycardia, fatigue
5. attacks last 2-3 days: spontaneous remission, reoccurrence may occur as soon as few weeks but usually longer
6. gradually attacks ar closer together as dz progresses
96
where are tophi deposits found in gout
ears, elbow, patella
| --usually not painful
97
formation of renal stones in gout
elevated levels of uric acid int he urine increase the chance they will crystallize to form kidney stone
98
predisposing conditions in gout
1. common chronic dz associated with gout include alcoholism, obestiy, HTN, CAD, and hypertriglyceridemia
2. increased dietary purine intake
3. decreased purine biosynthesis (lack of serum enzyme uricase)
4. prolonged use of diruetics
99
what is anklylosing spondylitis
chronic inflammatory jnt dz resulting in stiffening and fusion of the spine and SI joint
100
etiology of ankylosing spondylitis
autoimmune but process unclear
| associated with HLA-B27 human leukocyte antigen
101
pathology of ankylosing spondylitis
1. classic theories suggest pathological destruction thought to occur at enthesis (attachment sites of ligaments, tendons and joint capsules
2. recent theories suggest cartilage and other structures are initial target of inflammatory immune response
3. immune/inflammation response attack fibrocartilage structures of the joints
4. inflammation damages these structures causing reparative reaction from fibroblasts
102
what fibrocartilage structures of the joints does ankylosing spondylitis affect
joint capsule
intervertebral discs
entheses
periosteum
103
how does fibroblasts repair inflamation of fibrocartilage structures in ankylosing spondylitis
1. fibroblasts secrete collagen forming scar tissue
2. scar tissue eventually becomes calcified and ossified resulting in fusion of spinal joints an obliteration of SI joint
