Patho-UNIT 2_OA

kms013's version from 2016-02-03 20:01


Question Answer
OA- whats another name for it?Degenerative Jt/Disc disease...she doesn't like to use this bc then pts say "my bones are disintergrating!!"
How any people have OA?>20 mil in US
more than ____% of ppl over the age of ____ suffer from OA50, 65
Do women suffer more from OA or men? And what age?women > men, over age 55
prevalance for OA incr dramatically above what age?50
General articular anatomy: list the layers from internal to external:Bone - Perichondrium/periosteum (hyaline) - Hyaline - jt space/cavity - synovial embrane - jt capsule
what type of cartilage is perichondrium?Hyaline
what is the outermost layer of a jt called?perichondrium/periosteum
What is in an articular jt space/cavity?synovial fluid
_____ continues with the articular cartilage (what layer of the jt?)Synovial
what has vessels & nerves w a tough fibrous outer layer?jt capsule
Is cartilage avascular or vascular?avascular
how is cartilage nourished?by diffusion from vessels in perichondrium and from synovial fluid
What is a chondrocyte?a mature cell in articular cartilage
what are the fx of chondrocytes?fluid/nutrient exchange 2. create, maintain, and repair the cartilage matrix (secretion of substances such as proteoglycans/GAGs)
chondroblasts -- what are they?progenitors
what do chondroblasts do?secrete chondrin (rubbery protein in ECM)
what is chondrina rubbery protein in ECM secreted by chondroblasts
where are chondroblasts found?in the outermost layers of cartilage as they secrete ECM and become trapped & mature
Proteoglycans are long chains of _____GAGs (GlycosAminoGlycans)
____ --> GAGS --> ______glucosamine, proteoglycans
wha are the 4 main groups of GAGs?Hyaluronan, synovial fluid, proteoglycans, aggrecans
what is hyaluronan?(hyaluronic acid) - made by an enzye complex at the cell surface; long chain WITHOUT sulphated sugars (not a proteoglycan) absorbs a lot of H20
what is a major component of synovial fluid?hyaluronan
_____ is a chondroitin sulphateaggrecan
Hyaluronan combines with ____ to form large complexes (aggregates) that are neg. charged and asorb wateraggrecan
What content contributes to "shock absorbing" qualities (resisttance to compression)?water
What is viscosity in regards to ECM/Ground substance ?slow movments
what is elasticity in regards to ECM/Ground substance?fast movements
___% water and what _________% proteoglycan (mainly aggrecan) are chondroblasts & chondrocytes in ECM?75%, 10%
What are the 3 main components of chondroblasts & chondrocytes in ECM?water, proteoglycan (mainly aggrecan), collagen fibrils & other components
Hyaline is what type of cartilage?articular
What type of appearance does hyaline cartilage have?Bluish-white, glossy appearance
What type of collagen is present in hyaline cartialge?Type II
Fibrocartilage -- give some examples of where this is in the body?discs, menisci, TMJ, pubic symphysis
What type of appearance does fibrocartilage have?white, fibrous appearance
what type of collagen is present in fibrocartilage?Type I & Type II
Describe fibrocartilage.very tough, fibrous -- dense collagne iriented in the direction of jt stresses
scar tissue after cartilage injury is composed of ____fibrocartilage
what are 2 principle mechanisms that initiate the process of OA (Pathogenesis)?1. physical forces/traumatic injury to articular surfaces 2. fundmentaly inadequate cartilage
there are 2 mechanisms to initate the process of OA. The first is physical forces/truamatic injury to articular surface. Tell me 3 major bullet points about this.this refers to 1. major event OR repeated microtrauma 2. includes mechanical irregularities causing uneven wear 3. chondrocytes react to injury by releasig degradative enzymes and attempting to repair the damage 4. regenerated cartilage has altered biomechanical properites
there are 2 mechanisms to initate the process of OA. THe second is fundamentally inadequate cartilage. Name 3 bullet points about this.Type II collagen genetic defect 2. falls in response to normal loads/stresses 3. less common
There are 3 stages of pathogenesis: what are they?1. proteolytic breakdown of cartilage matrix 2. erosion of cartilage surface 3. synovial inflammation
What happens in the 1st stage of pathogenesis of OA?1. proteolytic breakdown of cartilage matrix. This includes cartilage "swelling" due to incr synthesis of proteoglycans, efforts of the chondrocytes to repair cartilage damage, and early OA- years to decades
What happens in the 2nd stage of pathogenesis of OA?2. erosion of cartilage surface --> as OA progressions, proteoglycan concentration decreases, causing cartilage to soften and lose elasticity (further compromising jt surface integrity), microscopically, flicking and fribrillations (vertical clefts)..ultimately, loss of jt space
What happens in the 3rd stage of pathogenesis of OA?3. synovial inflammation --> synovial cells phagocytose to breakdown product & produce proteases & proinflammatory cytokines
_____ is a class of zinc-containing enzymes that contribute significantly to degradation of cartilage and development of OAmetalloproteases (MPs)
what is inhbited by tissue inhibitons of Metalloproteases (TIMPs)Metalloproteases (MPs)
What is a cytokines?inflammatory signaling molecule
are IL-1 and TNF-a catabolic or anabolic?catabolic
are IGF-1 & TGF-b catabolic or anabolic?Anabolic
____ results in low grade systemic inflammationObesity
____ are formed w incr level in jts w OA, but its unclear if ac ause and/or effect of cartilage damage occursCalcium crystals
____ may have a direct pathogenic role in OACalcium crystals: it promotes articular cart. damage by causing synovial proliferations or induce the secretion of metaloproteinases or local inflammatory mediators
Calcium Crystals: Familal CPPD associated with early onset & progression to severe degenerative OA...didn't know how to make this a ? lol
what are 4 examples of things that can change physically from a result of pathogenesis of OA?1. Bony changes 2. sclerosis 3. subchondral cysts 4. osteophytes
what are bony changes assoc. w OA?erosion of cart. continues until underlying bone is exposed
what is sclerosis assoc. w OA?increasing stresses on bone (due to cart. failure) --> exceeds in the iomechanical strenght of the denuded bone; subchondral bone responds to the excessive stress w incre vascularity and cellularity; bone becomes thickened and dense area of pressure
what are subchondral cysts associated with OA?pattern of bony degeneration due either to boy necrosis resulting from chronic impaction or to intrusion of synoival fluids
what are osteophytes associated wiht OA?irregular outgrowht of new bone along the articular margin; vascularization of subchondral marrow; osseous metaplasia of synovial CT, and ossifying cartilagious protrusions
Clinical manifestions of OAstiffness, p!, decr ROM, jt effusion, crepitus, structural alterations
subclinical manifestions of OAerosion of articular cart.; altered cart biomechanial properites, subchondral sclerosis/thickening (XRAY); subchondral cysts
P! mechanism in OA: a combination of what mechanism?Osteophytic periosteal elevation, vascular congestion of subchondral bone ( incr intraosseous pressure), synovitis & activation of synovial membrane nociceptors, overal jt contractures, jt effusion & stretching of the jt capsule, bursitis, torn menisci, mm fatigue, periarticular mm spasm; psychological factors; central p! sensitization
Are bone spurs a p! mechanism in OA?NOOOOOOOOOO
what are risk factors for OA?AGE & OBESITY PRIMARILY; but others include trauma, genetics, reduced levels of sex hormones, mm weakness, repetitive use, infection, crystal deposition, acromegaly, previous inflammatory arthritis, heritable metabolic cuases, hemoglobinopahtes, neuropahtic disorders leading to a charcat jt; underlying morphologicl risk factors; disorders of bone, previous surgical procedures (meniscectomy)
Why is quadricep weakness a risk factor of OA?may be related to kne OA due to incr impact Fs transitted to articular cartilage bc of decr control of deceleration during swing phase (incr Fs @ heelstrike)
why is arthrogenous mm inhibition a risk factor for OA?altered sensory input (P!) from osteoarthritic knee thought to result in efferent inhibition of the quadriceps group, contributing to insufficient activiation
In the animal study, what were the findings?decr proprioception PLUS ligamentous instability significantly increases risk of OA
what are 3 examples of "systemic" changes of aging?loss of mm mass, lower hormone levels, impaired proprioception
When people age, you have a lower number of ____chondrocytes in articular cartilage (decreased proliferation & synthetic capacity)
When people age, they have a decr in size in what molecule?Decrease in molecular weight (size) of HYALURONAN molecule, with decrease in water-absorbing capacity of cartilage
in context of pathogenesis, what are 2 tx for OA?glucosamine (precursor to GAGs) 2. Chondroitin (a GAG) 3 NSAIDS (topical, oral--> decr in inflammatory cascade leading to a less catabolic state) 4. Tylenol (elevates p! threshold, unclear if it has any significant effect on inflammation inhibits PG synthesis but overall effect is not clear 5. injections (steroids & hyaluronic acid)
what is glucosamine?precursor to GAGs
what is chondroitin?a GAG
what do NSAIDS do?decr inflammatory cascade leading to a less catabolic state
what does tylenol do?elevate p! threshold, unclear if it has any sig. effect on inflammation; inhibits PG synthesis but overall effect is not clear
What do steroid injections do?"cortisone" ---> decr inflammatory cascade in favor of a less catabolic state
what do hyaluronic acid injections do?"viscosupplementation" -->Hyaluronan is the major component of synovial fluid; made from rooster combs
(dog study) what does moderate running do to cartilage?incr cart. thickness, stiffness, and proteoglycan content
(dog study)what does strenuous running do to cartilage?decr cartilage thickness and stiffness
(dog study)what does chronic strenous running do to cartilage?subchondral bone remodeling
In humans, moderate exercise does what?incr GAG content in knee cartilage (measured by MRI)
Jt unloading (experimentally casting limbs) yielded what 3 things?reduced proteoglycan content and synthesis, decr cartilage thickness and stiffness, amputation causes decr cartilage thickness in proximal jt of residual limb- indicating WB is the essential element, not ROM

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