Arthropathy Pathophysiology Flashcards
where do joints exist? what is their function? (3)
exist where 2 bones meet;
functions are:
1. movement: occurs because muscles originate proximal and corresponding tendons insert distal to a joint
2. load distribution
3. load absorption
describe joint structure in 2 categories
soft tissues/fluid:
1. joint capsule/synovium: intimal layer of capsule is a cell rich lining (synoviocytes), a subintima, and a fibrous joint capsule surrounding
2. ligaments: anterior and posterior cruciates
3. menisci
4. tendons
5. fluid
cartilage:
type II collagen
describe the synovium/joint capsule cell population (2) what happens to this population following trauma?
- synoviocytes: secretory cells; secrete
-hyaluronic acid (HA) and
-glycosaminoglycans (GAGs)
-substances which usually supplement to treat OA - macrophage-like cells
following trauma, the cell population increases
describe synovial membrane elasticity
allows flexion and extension of the joint; is why we flex and extend on exam to make inferences on the inherent presence or lack of elastic joint capsule properties
describe synovial fluid (plasma ultrafiltrate) (4)
- primarily water with a few solutes (glucose)
- negative pressure: assists joint movement and allows proprioception to occur
- does not clot due to absence of fibrinogen and other clotting factors
- NUMBER ONE ELEMENT is hyaluronic acid!: provide viscosity (0.5mg/ml) and reduces shear stress on articular cartilage; mucin clot is a qualitative assessment of HA polymerization
-boundary lubrication; absorbs shear stress from: synovium on synovium, synovium on articular cartilage and allows gliding between layers of the synovial membrane and fibrous joint capsule
describe evaluation of normal synovial fluid (2)
- cells: 500-2,000 nucleated cells per uL is normal
-few synoviocytes
-monocytes
-90% lymphocytes! primary cell type, inactive until problem
-PMNs/neutrophils (10%) - protein: should be less than 2g/dl
describe changes in synovial fluid seen with traumatic arthritis (4)
- glucose goes down: consumed by bacterial population
- cell count goes up (esp neutrophils)
- protein goes up (4-6g/dl, 2x normal)
- positive pressure in joint
describe menisci; what happens when sustains tears?
fibrocartilagenous semicircular disc interface between tibia and femur that functions as a shock absorber
can sustain a variety of tears, which is very bad because you cannot replace the meniscus and often tears are accompanied with a cruciate tear
describe articular cartilage composition (3)
- 70-80% water
- dry weight is
-50% type II collagen; hyaline, can sustain shear stress
-35% proteoglycans: chondroitin sulphate
-10% glycoproteins
-3% mineral
-1% lipid - chondrocytes are 1-12% by volume; which is very few cells relative to all that ECM they are responsible for secreting and maintaining; largely anaerobic metabolism (small number of cells relative to function plus anaerobic metabolism = slow cartilage turnover/highly deficient degeneration)
what are 2 distinct features of articular cartilage?
- avascular
- aneural: causes an issue with early detection of arthritis because animals are not often painful at disease onset, will be much later into progression before see pain and may not be able to treat as effectively
describe type II cartilage
85-90% of total articular collagens; provides tensile strength to cartilage
describe articular cartilage matrix turnover (5)
- driven by matrix metalloproteinases (MMPs)
- MMPs are produced by chondrocytes and degrade collagen over a long period of time
- MMPs also degrade proteoglycans over a shorter turnover time
- MMPs CANNOT replace collagen, will put fibrous tissue in its place = we all get arthritis as we age
- because collagen provides resistant to tensile loads, its replacement with fibrous tissue during turnover causes cartilage to FAIL IN TENSION
describe subchondral bone
the body foundation of articular cartilage with a trabecular pattern that functions as a shock absorber
describe arthritis; contrast to osteoarthritis
arthritis is a broad term covering a number of pathological entities of joints with 3 causes
1. traumatic
2. developmental
3. infectious
osteoarthritis is a specific term implying progressive and permanent deterioration of the articular cartilage; represents a group of disordered characterized by:
1. deterioration of articular cartilage
2. changes in subchondral bone
3. changes in soft tissues of joint
where does OA start?
we don’t know for sure, but we know metabolically active tissues play a role (synovial membrane, articular cartilage, subchondral bone)
describe synovitis/capsulitis; inclue pathogenesis
- acute inflammation of the synovium
- common in young horses/animals’ joints in training
- commonly accompanied by capsule injury
- results in synovial effusion leading to increased intra-articular pressure and PAIN, followed by lameness
pathogenesis:
joint insult results in release of inflammatory mediators and cytokines (IL-1 and TNF-alpha most common), inflam mediators cross talk with chondrocytes, leading to catabolism and damage to articular cartilage
-the inflammatory mediators cause cartilage damage, so early intervention is key! try to stop their release! can become a vicious cycle if not
what occurs following failure of the subchondral bone?
cartilage fibrillation (fuzziness) and cleft formation: microfractures of cartilage allow joint fluid to enter cartilage matrix and cause further degradation
what is a radiographic feature of OA?
osteophyte formation at the joint margin due to separation of bone fragments at the periphery
what are 5 clinical signs of OA?
- lameness and PAIN (one can cause the other and vice versa) that gets periodically worse, can be elicited by passive and active joint motion
- +/- effusion and joint enlargement
- decreased ROM
- often bilateral; occasionally unilateral
- no systemic clinical signs
how are pain receptors distributed in a joint?
- pain sensation in OA or joint pathology does NOT come from articular cartilage (aneural)
- pain receptors are distributed along collateral ligaments and the interior of the joint capsule; when stretched, causes lameness and pain
what causes the decreased ROM seen in OA? (4)
- joint surface incongruity
- contracture and spasm of surrounding soft tissues
- capsular fibrosis!!
- mechanical interference of osteophytes or loose bodies
describe diagnosis of OA
- lameness exam
- intra-articular anesthesia: gold-standard to isolate OA to a joint!
- imaging:
-radiology shows joint deterioration
-nuclear scintigraphy can show where problem is
