Locomotion 2 Flashcards
1
Q
For patients with high energy trauma what is the priority
A
- For patients presenting with high energy trauma orthopaedic injury is NOT the priority
- Once the patient is stabilized, visual orthopaedic assessment, screening neurological examination and orthopaedic examination can take place:
○ All limbs and the spinal column should be evaluated
○ Watch the patient carefully when they are walking.
2
Q
What are the 3 natures of fractures and 3 energy levels
A
1) traumatic
2) stress
3) pathologic (underlying disease)
1) low energy - non-displaced fracture
2) high energy (comminuted fracture
3) very high energy (gunshot injury)
3
Q
What are the 4 different completeness categories of fractures
A
1) Complete - fracture involves the entire cortex; on a single radiograph both cortical lines are fractured
2) Incomplete - fracture doesn’t involve the entire cortex, with some cortex intact
○ Generally due to penetration
3) Greenstick fracture - immature bones, periosteum is intact
4) Stress fracture - due to repeated cycling, more common in performance animals
4
Q
What are the 4 different types in number of fracture lines
A
1) Simple - one fracture line - transverse or oblique
2) Multiple - >1 fracture line in a single bone, fractures are not continuous
○ spiral and segmental (directions)
3) Comminuted - complete fracture with multiple bone fragments
○ Can no longer reconstruct
4) Segmental - complete fracture, with a diaphyseal fragment with a complete cortex
5
Q
What are the 7 different direction of fracture lines
A
1) Transverse
2) Oblique
3) Spiral
4) Fissure
5) Avulsion
6) Depressed (flat bones)
7) “T” and “Y” fractures (elbows)
6
Q
Relationship of fracture fragments what need to describe
A
describe the location of major distal fragment, relative to proximal fragment
- Describe the location of major distal fragment
- Degree of end-to-end apposition
- Alignment
- angulation
- rotation
- Limb/bone shortening (over-riding)
- Luxations - combination of injury to both the bone and joint -> most commonly occur with the elbow and the hock
7
Q
What are the 2 different soft tissue injury
A
1) closed (skin remains intact)
2) open
- Gas opacity in soft tissues - communication with the outside world
- Bone fragments protruding through skin, and radiopaque debris within soft tissue
- Interposition of soft tissue
8
Q
what occurs with new bone formation, when is there a fibrous scar and the 3 stages
A
New bone forms and remodels –no fibrous scar tissue
- Fibrous scar tissue occurs when there is a failure in bone healing -> consequence of unfavourable mechanical environment such as instability
Stages:
1) Fracture-haematoma following a fracture (haemorrhage)
2) Cellular components such as activated platelets and components
3) Then heal via a variety of means
9
Q
What are the 2 types of bone healing and the types within
A
1) Direct bone union
1. primary and secondary
primary divided into contact and gap healing
2) indirect bone union - fracture callous forms
10
Q
Inter-fragmentary Strain Theory what is the equation and why is it important
A
strain = change in length of gap/ original length of gap
- Forming bone is intolerant of strain
- New bone can only form under conditions of < 2% strain
Strain is high when:
1. Change in length is high (instability)
2. The initial gap is small (large fracture gap can lead to a low strain environment)
11
Q
Direct Bone Union what does it require and does a fracture callus form
A
•Requires: - Anatomic alignment - Absolute stability of fragments (<2% strain) - Compression - ideally • Little to no fracture callus forms
12
Q
Contact healing when does it occur and how
A
Compression - occurs when bone fragments are in direct contact (no fracture gap) and fragments are stable
• Cutting cones (the way the osteoclasts come through)
- Simple transverse fracture, simple anatomically alignment
- Composed of Osteoclasts with trailing osteoblasts cross the fracture site
» Rate 50-80um/day
» Simultaneous resorption of old bone and deposition of new lamellar bone
13
Q
Gap healing when does it occur and how
A
- Occurs where small gaps (<1mm) present between fracture fragments but rigid stability is present
- Inter-fragmentary strain < 2%
- Vessels and loose connective tissue
- Woven bone deposited initially:’
- Orientation perpendicular to fracture ends (weak)
- 3 weeks –cutting cones remodel lamellar bone parallel to long axis
14
Q
What is the direction of inital bone formation for contact and gap healing and why
A
contact - parallel as lamellar bone initally deposited
Gap - perpendivular as woven bone initially deposited before cutting cones remodel to lamellar bone
15
Q
Secondary Osteonal Reconstruction when occur
A
- can occur with callus where stability less than absolute and deformation great to allow primary bone deposition
- widening of a gap to decrease strain
- callus formation to increase stability and decrease strain
16
Q
Indirect bone union reslt of what, what results in and the 4 phases
A
The result of:
- Instability (IFS>2%)
- Gaps between fragment ends >1mm
•Results in:
- Sequential and orderly deposition of tissues more tolerant of strain to those less tolerant
•Phases:
1. Inflammatory (haematoma, granulation tissue) - initiates fracture healing -> bleeding and platelet degranulation results in the delivery of cytokines and growth factors and an influx of inflammatory cells to clean up debris and damaged tissue
2. Soft Callus (Cartilage)
3. Hard Callus -> woven bone
4. Remodelling -> lamellar bone
•Callus deposition is a response to instability and results in increasing stability
17
Q
What are the 2 main forces created and their effect on bone and what has to occur for a fracture to occur
A
1) Weight bearing creates a ground reaction force
- This creates bending, compressive and rotational forces on the bone
2) Muscle contraction creates tension and rotation
- Forces create the fracture -> when the sum of forces that act on the bone exceeds its strength
- Act at the site once the fracture has been created -> Instability
18
Q
what is the bone, what is the amount of deformation proportional to, and what is the amount of soft tissue damage proportional to and what occurs with high and low energy fractures
A
Bone is viscoelastic
- Amount of deformation is proportional to rate of loading
- Energy stored during deformation released at time of yield (fracture)
- Amount of soft tissue damage is proportional to energy released
- Energy absorbed = area under curve= energy released at fracture
- Rapid loading -> high energy fracture (gunshot wounds) -> lots of soft tissue damage
Low loading -> low energy fracture -> less soft tissue injury
19
Q
Bone is anisotropic what does this mean and list the forces that act on it
A
- Stronger when loaded longitudinally vs transversely
- Stronger in compression vs tension
THEREFORE - The forces acting on bone determine the fracture conformation / morphology
- Compression
- Bending
- Torsion
- Tension / distraction
20
Q
What do compressive forces and bending forces lead to
A
compressive = oblique fractures
bending = transverse
- concave surface subject to compression
- convex surface subject to tension
- bone is weaker in tension - fracture starts here and propagates across the bone
21
Q
what do tensile forces and torsional forces lead to
A
= trasnverse fracture
- fracture is perpendicular to direction of tensile load
- often combination with bending
torsional = spiral cracks
22
Q
Bending + compression what does it lead to, how does it occur
A
= butterfly fracture
- starts similar to pure bending -> propagates along transverse line -> compression causes an oblique fracture on the other side
23
Q
What are the 3 aims of the surgeon in fracture repair
A
1) Provide stability against forces acting at the fracture site - Choose appropriate implant system
2) Preserve the vascular supply of the healing bone
3) Limb alignment and alignment of fracture ends
24
Q
What are the 3 factors that result in different prognosis for fractures
A
1) Mechanical factors - what breed (large or small), how many limbs, compression what number of fragments
- High score if single limb, small breed, compression needed
2) Biological factors - health of the patient, age, co-current injuries
- High score if young, healthy, closed fracture etc,
3) Patent/owner factors - risk tolerance, compliance, economic state
- High score if good compliance for client and patient
25
carpenters approach what type of approach, positives and negatives and what suitable to
Carpnter’s Approach
- Historical approach - not used as much
- Rigid anatomic reconstruction of bone column
- Functional load sharing
NEGATIVE
- Extensive dissection:
- Loss of soft tissue attachment
- ↓ Blood supply
- Remove fracture haematoma
- Longer time taken therefore higher chance of infection
•Suitable for simple transverse fractures
26
Gardener’s Approach what also called, positives and negatives and what suitable to
- Also known as Biologic Osteosynthesis
- Alignment of fragments to preserve length, angular and rotational alignment
- No attempt at anatomic reconstruction
- Preservation of fracture haematoma
- Preservation of soft tissue attachments and blood supply
- Closed or indirect fracture reduction
- Open but do not touch approach (OBDNT)
27
give examples of external and internal fixation
```
External coaptation
- Bandages
- Splints/Casts
Internal fixation:
- Intramedullary (IM) Pins / wires
- Interlocking nails (ILNs)
- Plates / Screws
- DCP vs Locking plates
```
28
External Coaptation what are the 4 ways it can be used, what forces are they good at preventing and which aren't they
1) Primary method of immobilisation - cast
2) Temporary immobilisation
3) Adjunctive support/immobilisation
4) To prevent weight bearing
- Only good at preventing BENDING
- Can Potentially reduce ROTATIONAL forces but only if the joint above and below the fracture are immobilised.
- Easily accomplished for metapodial and phalangeal fractures
- Difficult to accomplish/maintain for antebrachial or tibial fractures
Extremely difficult to achieve for humeral and femoral fractures
29
What are the 2 types of bandages and what are they good for
1) Robert jones bandage
- good for temporary support
- very bulky
2) modifies robert jones
- useful to limit soft tissue swelling
- not sufficient for fractures
30
How to increase resistance of material to bending forces
- AMI of a rod ∝ Radius 4
- Small increase in radius → large increase in AMI
- Choose larger pin size when possible to get increase resist to bending
- AMI of a plate ∝Height 3
- Thicker plate resistance to bending
31
Bending forces what best neutralised by
- Best neutralised by an implant placed in the neutral axis of the bone - In the medullary canal
- Pins - good with bending, not rotational, no compression
- Interlocking nails - combine pins with interlocking help with additional stability
Alternate Methods:
- Plate fixation within the bone
- External fixation
32
Torsional forces neutralised by
- Plate and screws
- Interlocking nail
- External skeletal fixation
•Poorly resisted by intramedullary pins
- Combine IM pin with plate or ESF
33
Cyclic stress and implant failure what occurs
- Stainless steel is very susceptible to cyclic stress
- Fracture management is a race between bone healing and implant failure
- Implants will almost always fail IF the bone does not heal
- Why regular follow-up is needed
34
Bone marrow how look different between adult and young
- Diffusely red in younger animals -> high amount of red marrow -> high haematopoiesis
- Atrophy of the fat within the bone marrow -> emaciated state of the animal, last area that fat would be used
35
What are the 3 general skeletal muscle responses
1) Innervation
○ Skeletal muscle need motoneuron to innervate muscle to get contraction
2) Necrosis and regeneration
○ necrosis parasitic, black leg disease, trauma
○ Doesn't matter the cause the healing is the same
3) Structural
○ Tends to be genetics
36
What are the 7 signs of muscle disease
1. Atrophy -> condition score decrease
2. Hypertrophy -> can be compensatory, special issue in the cardiac muscle
3. Swelling -> fluid accumulation
4. Weakness
5. Muscle spasm -> uncontrolled contraction
6. Abnormal gait -> muscular dystrophy first clinical sign
7. Esophageal dysfunction ->
37
Muscle dysfunction what are the 3 general causes and causes within
1) Physiological
- muscle rupture
- exercise induced damage
- loss of innervation
- loss of blood supply -> ischemic damage in muscle
- endocrine/electrolyte imbalance
2) genetic
- errors of metabolism
- genetic defects
- developmental defects
3) Nutritional/toxic
- deficiency of selenuim/vit E
- toxic plants
- feed additives
- toxins
38
What is a motor unit
Motoneuron + all muscle fibres innervated from the motoneuron
Muscle fibres just innervated by ONE motoneuron
39
What are the 2 fibre types and there function
Type 1 - rich in mitochondria, fatigue resistant, tend to be in posture related muscle
Type 2 fibres - white fibres
- Larger, fast-twitching fibres, not as much mitochondria, rely on glycolysis, fatigue quickly
40
What are the 5 causes f atrophy and the fibre type mainly affected
1) denervation - type 1 and 2
2) disuse - type 2
3) endocrine - type 2
4) malnutrition - type 2
5) congenital myopathy - type 1
41
Denervation atrophy what look like
Atrophic fibre surrounded by normal fibres
• Pressed into angular shape - physically swash the muscle fibres into the angular shape by the other muscles that aren't denervate
• Large group atrophy - nuclei have stayed in the periphery and look like they have increased, just closer proximity due to the fibre atrophy
• Generalised atrophy
• Increased concentration of nuclei
42
Reinnervation what occurs and what results in
- Neighbouring motoneurons will sprout and innervate the fibres that have been denervated
○ If the motoneuron that has branched was from another type of fibre, the fibres newly innervated will change to that fibre type -> FIBRE TYPE GROUPING
§ Generally have different fibre types within a muscle but with reinnervation will have more of the same fibres within an area
Influence speed and strength of contraction
43
Hypertrophy what is the response to
Compensatory in response to
- Loss of functional fibres (increased load on remainder)
Once get too big and cannot get perfusion from blood vessels as diffusion distance
Fibres split which lead to Alterations in normal metabolic processes
44
Neuromuscular junction what are examples of disruptions
- Neurotransmitters - acetylcholine
• Anything that affects the breakdown of acetylcholine will result in failure to relax of the muscle
Examples
1. Botulinum toxin
2. Tick paralysis
- Either don't get contraction or cannot relax, can be both
45
Arthrogyropsis what is the common name, what result from and what may lead to in calves, causes
- “Crooked joint”
- Defective innervation during development -> no flexion of the muscle or tendons -> don't grow properly
○ If severe cannot suckle or eat and may lead to death -> euthanise
- Histologically similar to denervation
Causes
- Genetic
- Teratogenic viruses
- Teratogenic toxins
- Nutritional. Vitamin A and manganese
46
Congenital Myasthenia gravis how inherited, where animals found in, what occurs and when do clinical signs develop
Congenital
- Inherited disorder
- Only described in humans, dogs and cats.
- Jack Russell, springer spaniels, few Siamese
- Defective NMJ with decreased membrane surface area
○ Efficiency of the NMJ is reduced
- Symptoms increase with rapid post‐natal growth
47
Myasthenia gravis cause, what occurs, leads to, what common animals and histological lesions
immune mediated - autoimmune disease
- Autoantibodies against Ach receptors
- Leads to severe decrease in number of functional receptors
○ Cannot contract properly -> floppy
- Dogs (German Shepard), infrequent in cats
- Histologically see denervation atrophy
48
List the neoplasia of the neuromuscular junction, how fast grow, arise from what cell is it common
Rhabdomyosarcoma
- Rapid growth, malignant
- Thought to arise from satellite cells or other precursors
- Not common
49
The following colours what can result from pale muscle, pale streaking and dark red muscle
```
• Pale muscle
- Necrosis or denervation
- Often localised
• Pale streaking
- Myofibre necrosis or mineralisation
- Infiltration by fat or collagen (scar tissue) - if the tissues give up with trying to repair properly
• Dark red
- Haemorrhage
- Inflammation
- Rhabdomyolysis - myoglobin out of the circulation -> end up with red or dark urine
```
50
What are the 2 types of necrosis within skeletal muscle
• Segmental
- Involvement of only one or several contiguous segments within the cell - one segment of muscle fibre
○ Muscular dystrophy this occurs
• Global
- Affects entire length. Only under extreme circumstances; pressure to the entire muscle such as crush injury or ischemia
51
Skeletal muscle regenerative what are the 5 steps
1) Damage to the muscle - MUST HAVE NECROSIS OR SOME DEGENERATIVE DAMAGE TO LEAD TO THIS
2) Inflammation occurs -> clears away necrotic tissue, anti-inflammatory macrophages
○ -> if doesn't occur get scar tissue
3) Satellite cells sits just outside the muscle fibre normally doesn't do much but now induced and proliferate
4) Migrate to site of damage, fuse together or damaged end of the muscle fibre
5) Regenerates the muscle
○ As long as they are there the muscle will keep regenerating itself
52
Satellite cells what activated by, are they resistant, when proliferate and how cause regeneration
- Resistant to most forms of damage
- Proliferate within remaining basal lamina ~ “sarcolemmal tube” - basement membrane - scaffold needed for regeneration
- Fuse to damaged ends or with each other to form myotubes within the sarcolemma tube
- Happens over days
53
What are the 2 things needed for successful muscle regeneration
1. Presence of intact basal lamina
| 2. Availability of viable satellite cells
54
What are the 2 things that lead to ineffective regeneration
1) Disruption to basal lamina
- Destructive lesions (trauma that transect fibres)
- Giant cells - histological (balloon of satellite cells at the end of the muscle fibre - clump together but not scaffold to be organised)
2) Decreased satellite cell viability
- Extensive injury (heat, extreme inflammation or infarction)
- “Healing” by fibrosis
55
Muscle ischemia what are the 4 causes
1. Occlusion of a major blood vessel
2. External pressure on a muscle (crush)
3. Swelling of muscle (compartment syndrome)
4. Vasculitis/vasculopathy
56
Muscle necrosis in recumbency what are the 3 results and the 2 main causes
• Decreased blood flow due to compression onto the leg muscles
○ Tends to affect back legs more than front
• Reperfusion injury (calcium influx)
• Increased intramuscular pressure (compartment syndrome)
1) Recumbency ‐ Down cows
2) Downer cow syndrome
- Complications that occur secondary to prolonged recumbency
- A cow unwilling or unable to stand for >12 hours
57
Complications of recumbency
1) compartment syndrome
2) musculoskeletal damage due to struggling to rise
- - Rupture of muscles
- Hip dislocation
- Fracture
3) Pressure sores
4) Lifting damage
5) Heat stress or hypothermia
6) Pain
- Mastitis
58
Compartment syndrome what are the 8 steps wtihin
1) Weight of the recumbent animal causes external physical compression of the leg
2) Each muscle surrounded by fascia
3) Pressure builds up in each compartment
4) Eventually pressure collapses the blood vessels
5) Muscle deprived of oxygen
6) Tissue starts to die
7) Fluid leaks and muscles swells
8) Pressure damages nerve
59
Complications of recumbency what is the rate at which damage occurs and in which limbs first
```
Rate at which damage occurs
– Depend on size of animal
– Weight of the animal
– Hardness of surface lying on
– Ability of animal to shift it’s weight
• Hindlimbs > forelimbs
Most of the front weight supported by brisket
```
60
Nutritional deficiency what lead to muscle necrosis and exertional myopathy
Selenium/vitamin E deficiency
• Myofibre degeneration (mainly due to selenium)
• Common in livestock especially neonates
• Oxidative damage (muscle is especially susceptible)
• White Muscle Disease ~ necrosis
Exertional Myopathy
• Capture myopathy -> capturing a wild animal, try to escape
• Exercise induced
- Exertional rhabdomyolysis in horses - muscle can go black
- Exercise with underlying condition
61
Inflammatory myopathies what are the 2 main types and causes within
```
Bacterial Myopathies
• Bacterial
- Suppurative and necrotising
- Suppurative and fibrosing
- Hemorrhagic
• Clostridial
- Damage to myofbres
- Vasculature
- Toxemia
EG - black leg
Inflammatory Myopathies
• Viral
• Parasitic
- Sarcocystis
- Trickinella
- Trypanosoma
```
62
What is a congenital inherited disorder of skeletal muscle. what results in and what breeds more susceptible
Muscular Dystrophy
- Tear in muscle fibres, calcium moves in, necrosis and degeneration
- No resolution of inflammatory -> satellite cells stop working as overworked, cannot get regeneration
○ Muscles just waste away -> lose function, contractions of tendons and muscles
- Labradors, beagle more susceptible
63
Malignant hyperthermia what can it result in
- skeletal muscle
- Unregulated release of Ca++ -> Excessive contraction
- Generation of heat (increase body temp)
- Can be triggered by halothane or stress (pigs highly susceptible)
64
Post-operatively we use the four A’s to describe the repair what are they
1. Alignment (Rotational, angular)
2. Apposition (Relationship of the bone ends to one another)
3. Apparatus (Are the selected implants appropriate and are they positioned appropriately)
4. Activity (Evidence of one healing or lack thereof)
65
What are the general functions of bones, hyaline cartilage, fribrocartilage, ligaments, tendons, muscles, fascia, fat, tissue fluid
BONES support the body
HYALINE CARTILAGE - provides low friction surface, shock absorbance
FIBROCARTILAGE - provides resilient support
LIGAMENTS - tie bones together
TENDONS - tie muscles to bones
MUSCLES - contract to move the skeleton
FASCIA - wraps around to hold things in place
FAT provides padding and reduces weight
TISSUE FLUID provide hydrostatic support
66
What are the composition of bones, cartilage, ligaments/tendons, muscles, fascia, fat
Bones - colagen stifened with minearl
cartilage - collagen filled with glycoproteins that hold water (no sensory nerves)
Ligaments/tendons - collagen (+/- elastin) aligned into ropes
Muscles - collagen bags of cells filled with contractile proteins
Fascia - collagen not otherwise named
Fat = collagen (fascia) + adipose stuffed with triglycerides
67
What are the 4 components that allow the body to move
* Muscles provide the movement
* Joints allow the movement -> flexion and extension, adduction and abduction, pronation (inwards) and supination (outward), sliding
* Posture of the body and the length, position and stiffness in ligaments and tendons determine how that movement is directed.
* Elasticity within ligaments and tendons, along with connections between them, smooths movements and helps balance
68
Ligaments what can you do to them and what if you don't
Ligaments can only be stretched
1) If never stretched they passively (slowly) contract, become stiffer & maybe less strong
2) If continuously stretched, they lengthen and may become sloppy and cease to provide support
3) If used within an active balanced system they will be elastic and strong and supportive
69
What occurs with balancing and unbalancing ligaments
- Balancing ligament tone allows the spinal muscles to strengthen evenly.
- Unbalanced ligament tone means that certain muscles are overused and movements through the joints are no longer optimal.
- Joints then become painful and/or damaged which restricts joint movement and causes more imbalance in the system.
70
What are the 4 joint types and examples of where found
1) fibrous - skull sructures
2) cartilagenous - intervertebral discs, costochondral/ sternal
3) synocial - most limb joints
4) muscular - pectoral girdle to trunk
71
List the potential movements of the spine and where occur
1) flexion and extension -> nodding -> skull and atlas mainly, neck and lumbosacral joints
2) Axial rotation around C1 and C2
3) lateral bending occurs C1-7 and some through rib cage
72
Name the 3 sesamoid bones within the horse forelimb
Medial and lateral proximal pamar sesamoids - fetlock joint
| navicular bone
73
Meniscus what is it and 2 places in which they are found
- Fibrocartilage (soft-tissue density)
a. Left and right temporomandibular
b. Left and right femorotibial
74
What are the 4 main types of ligaments and examples
1) extracapsular - joint capsule thickening - collateral ligmanet
2) intracapsular - eg - cruciate lig
3) fascial thickening eg - annular
4) spanning many joints eg - interosseous or nuchal lig
75
Fascia what composed of and what does thick fascia do
- Consists of thin sheets of ligamentous material which wraps regions of the body and groups of muscles like cling film
- Thick fascia distributes the force of contraction of any muscle within its surrounds to connective tissue and other structures within the fascia
76
function of fat
- Provides padding, cushioning, insulation and acts as an energy store
- Minimal blood and nerve supply and slow turnover rate
- Holds its shape and used to fill spaces in many places within the body
- When elastic padding is required (digital cushion within dog poor or deep to the frog within the hoof) then fat is contained within a strong meshwork of collagen
77
Patellar ligaments in the horse what are they and where located and how compare to dog
```
Hold patella onto teh tibia
3 in the horse
1) lateral
2) medial
3) medial
Medial hooks over the medial femoral condyle
Dog only 1 patella ligament
```
78
What type of levers are most muscles and what does this mean
3rd order levers
- Distance/speed multiplier
- Muscles attach close to joint to get weight of the limb further away to move fast and a long distance
79
What are the 2 types of muscle contraction and what determines a muscles function note
1) isometric
2) isotonic
1) Cross sectional area (power) of whole muscle -> how many fibres and the length, hence the power of the muscle
○ Powerful -> short sharp bursts
○ As muscle gets larger the muscle becomes less strong as not increasingly the cross-sectional area
2) Length (range) of whole muscle - gives you the range of movement
3) Size, relative length and direction of the muscle fibres.
4) Position relative to the skeleton.
5) Points of attachment to the skeleton - form and strength.
6) Other attachments or constraints (annular ligaments, strength and attachments of muscle sheath; length, size, shape and position of any extra tendinous or fascial attachments.
80
What is the normal function of joint capsule and articular ligaments and what are potential consequences of injury to these structures
stability during movement
- because of their relatively poor vascularisation and limited distensibility, the joint capsule and ligaments have limited repair capacity (but they can undergo complete repair) and they display only mild changes in inflammatory joint disease
- excessive or prolonged tension on the capsule or ligaments may cause irreversible stretching
- may predispose to subluxation/luxation of joints
81
What is the transitional zone of synovial joint and why is it important
where the synovium is reflected on intra-articular bone and merges with the periosteum
- Synovial membrane
Extends a little way into the non-weight bearing areas of the cartilage (transitional zone of the synovium -> where generally see reactive lesions)
82
Synovial fluid, gross appearance, cytologically, how produced and what is its function
- normally viscous (should be able to move fingers away 2-3cm before breaks), clear and colourless (to slightly yellow in horses)
- there is a low total nucleated cell count in synovial fluid in health, with most cells present being small lymphocytes and monocytes/macrophages, with a few synoviocytes; neutrophils normally comprise less than 10% of the nucleated cells
- functions to lubricate joints and nourish the articular cartilage
- produced by synoviocytes
83
How is articular cartilage nourished in a juvenile versus a mature animal
- in immature animals, the articular cartilage can also be nourished by diffusion from blood vessels in the underlying epiphyseal growth cartilage and subchondral bone
- in mature animals, synovial fluid is the chief source of nourishment of the articular cartilage
84
What is meant by the term epiphyseal growth cartilage
articular-epiphyseal complex (AEC) (articular cartilage + epiphyseal growth cartilage (has blood vessels present))
the epiphyseal growth cartilage undergoes endochondral ossification and thereby contributes to the growth of the epiphysis
85
What does articular cartilage look like grossly in a juvenile animal
appears grossly smooth, moist, bluish and semi- transparent; looped blood vessels may be grossly visible in the underlying epiphyseal growth cartilage
86
what is the tidemark or blueline of articular cartilage
- Demarcation between articular cartilage and subchondral bone
- mineralised zone
87
what are the key components of articular cartilage and what maintains the cartilage matrix
produced and maintained by chondrocytes and is approximately 70-80% water, with the remainder type II collagen, with small amounts of type IX collagen, proteoglycans and hyaluronan
88
What happens to articular cartilage during the lifespan of an animal and What does articular cartilage look like grossly in an aged animal
- proteoglycan content of articular cartilage slowly decreases from birth
chondrocytes can synthesise collagen throughout life but the rate of synthesis is low and cannot compensate for wear and tear in mature animals
cellularity of the articular cartilage decreases with age (thinning)
○ with advancing age, articular cartilage grossly becomes yellow-tinged, opaque and superficially roughened, and has reduced elasticity
89
What is the most important function of subchondral bone
necessary to support the articular cartilage
rticular cartilage protects the subchondral bone from fracture by deforming to produce a large contact area when loaded and by more evenly distributing stress at the level of the subchondral bone than at the articular surface
defects in one layer therefore have the potential to cause defects in the other
90
How do superficial injuries to articular cartilage typically heal
- cartilage matrix may also flow into the defect, facilitated by load-bearing and joint movement
- superficial defects usually do not heal completely but they do not necessarily progress
91
How do deep injuries to articular cartilage typically repair
heals via the fibrocartilaginous “scar” may persist indefinitely and does not perform as well as the original articular cartilage when subjected to mechanical loading
92
What is the source of pannus and why is ti significant
- from marrow spaces of subchondral bone
SIGNIFICANCE
- pannus interferes with diffusion of nutrients into articular cartilage
- it can also cause erosion/ulceration and destruction of cartilage and bone because of its collagenolytic activity
- formation of metaplastic bone within pannus can -> permanent bony ankylosis -> permeant restriCted joint mobility
93
what are the sources of chemical mediators of articular cartilage degeneration and what broad types of joint injury can result in release
1) lysosomal enzymes
2) prostaglandin E2
3) interleukin -1
4) reactive oxygen species
injured and/or inflamed synovial joints, various mediators released by leukocytes, synoviocytes and/or chrondrocytes may cause degeneration of articular cartilage
94
What are subchondral bone cysts and In which domestic animal species are these
most commonly diagnosed
most commonly seen in horses and are usually associated with osteochondrosis
○ however, some may result from traumatic injury to the articular cartilage with seepage of synovial fluid into microfractures and fissures in the subchondral bone
95
What disorders triggers degeneration of articular cartilage and the typical sequence
cartilage damage in degenerative joint disease, septic arthritis, immune-mediated arthritis, joint trauma and haemarthrosis
1) Loss of proteoglycans from the cartilage matrix
2) the collagen fibres condense, fray -> cartilage fibrillation
3) eburnation of subchondral bone
4) synoviocyte hypertrophy and synovial villous hyperplasia are common in diseased joints -> velvety or frond-like membrane appearance
5) synovitis
6) periarticular osteophytes that persist as spurs and possible joint mouse
7) subchondral bone cysts
96
what is meant by the term end-stage joint
the exposed subchondral bone, periarticular osteophytosis, synovial villous hyperplasia, variable synovitis and fibrous thickening or laxity of the joint capsule
- EVERYTHING GOING WRONG
97
What is meant by degenerative joint disease and what are the potential causes
= degenerative arthropathy, osteoarthritis, osteoarthrosis
- virtually any insult that structurally damages the articular cartilage or the subchondral bone or the supporting structures of a joint can lead to DJD (e.g. joint trauma, previous joint inflammation or infection, repeat episodes of haemarthrosis, metabolic or nutritional bone disease etc)
- primary - no apparent cause
- secondary - predisposing causes
98
List 2 examples of degenerative joint diseases in animals
1) Arthopathy of the bovine stifle
| 2) arthropathy of the canine shoulder
99
What is meant by the term joint sprain and What causes a sprain? What is the prognosis following a sprain?
- wrenching or twisting of a joint with partial tearing of ligaments +/- joint capsule
- multiple, minor, traumatic injuries to joints
- minor sprains usually heal rapidly with no permanent damage
- severe sprains tend to heal with persistent joint laxity -> DJD
100
What happens to dislocated ends of bone in joint luxations?
○ if the dislocated end lies against bone, it will provoke periosteal reactivity
○ if there is no or only slight movement, fibrous or bony ankylosis may develop
○ if there is continuous movement, a new false joint will develop, with the articulating surfaces covered by fibrous tissue or eburnated bone or even fibrocartilage
101
What causes haemarthrosis, and the potential consequences of repeated episodes of haemarthrosis
- haemarthrosis may result from joint trauma, neoplasia or inflammation
- a single episode of haemarthrosis has no effect on the articular cartilage
- repeated episodes of haemarthrosis (e.g. haemophilia A or B) -> decreased proteoglycans and cartilage erosion -> DJD
