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HOME ASSIGNMET

1. Synovial Fluid Comosition and


Physiology
Ultrafiltrate of plasma
• Hyaluronic acid, lubricin, proteinase, collagenases, and
prostaglandins
• Nourishes and lubricates cartilage
• Non-newtonian fluid: “shear thinning” (thixotropic)
◦ Viscosity decreases with increased shear rate.

• Normal knee has approximately 2 mL.


• Normally contains no RBCs, WBCs, clotting factors, or
hemoglobin (Hb).
• Joint fluid analysis: evaluate effusions
Synovial Analysis
Normal Non- Inflammatory Septic Traumatic
Inflammatory
Clarity Transparent Transparent Translucent Cloudy to Bloody
opaque
Colour Clear Straw Color Yellow-green Dirty / Yellow Red
tinged
Viscosity High Normal High Low viscosity Variable Variable

WBC/mm3 <200 <200 2000 to 50,000 to 200-2000


75,000/mL 80,000/ml
PMNs % <25% 25% <50% >75% 50-75%
2. Joint Lubrication and Wear Mechanism
Purpose
 Studies have shown that fluid-film lubrication dominates in synovial joints. In practical terms,
all types of fluid-film lubrication and boundary lubrication occur in synovial joints, depending
on the specific joint in question and the particular type of loading applied

 Consequences of wear particles:


 Synovitis.
 Aseptic osteolysis and loosening.
 Systemic distribution.
 Immune reaction.
 Increased friction of the joint.
 Misalignment of the joint and catastrophic failure
Friction and Lubrication
• Friction: resistance between two objects as one slides over the other
Not a function of contact area
Coefficient of friction: 0 = no friction
• Lubrication: decreases resistance between surfaces
Articular surfaces, lubricated with synovial fluid, have a coefficient of friction 10 times better than the best synthetic
systems.
• Coefficient of friction for human joints: 0.002 to 0.04
• Coefficient of friction for metal-on-UHMWPE joint arthroplasty: 0.05 to 0.15
Not as good as human joints
• Elastohydrodynamic lubrication
Primary lubrication mechanism for articular cartilage during dynamic function
Coefficients of Friction of Various
Articulations
3. Muscle Healing
• Torn myofiber and Basal Lamina.

• Contraction band and demarcation membrane seal the


torn fiber ends. Satellite cells (SC) begin to proliferate
and inflammation reaction begins.

• SCs differentiate into myoblasts and fibroblasts begin to


produce collagens and form scar tissue.

• Myoblasts fuse into myotubes.

• Myotubes fuse with the surviving parts of the torn fibers


and start to form new MTJs.

• Fully regenerated fiber with organized scar tissue and


MTJs attached to it.
Muscle Repair
Muscle needs :
◦ Blood supply
◦ Stimulation in the form of a nerve supply.

Muscle regeneration can occur without a nerve supply-> permanent muscle atrophy will develop
if reinnervation fails. Note the following:

◦ More proximal the belly tear,


◦ worse the prognosis, as more bulk is denervated.
◦ Muscle laceration results in dense brous scar tissue formation
◦ Myotubes regenerate across scar tissue in small numbers only.
4. Types of Muscle Contraction

Isotonic – muscle tension is constant throughout the range of motion, length changes.
Isometric – muscle tension is generated while length remains constant.
Isokinetic – muscle contracts maximally at a constant velocity throughout the range of
movement.

Muscle contraction associated with change of length (i.e. isotonic or isokinetic contractions) may
be either concentric, when the muscle shortens with contraction, or eccentric, where the external
load exceeds the muscle force generated so the muscle lengthens during contraction.
Example

Post-operative protocol of ACL reconstruction:


◦ Day 1: Isometric quadriceps & hamstring exercise

Postoperative management protocol after


fixation of femoral shaft by K- nail
◦ Day 1: Isometric quadriceps exercise
5. Energy sources for muscle activity

Energy sources for muscle activity.


ATP, Adenosine triphosphate
CP, creatine phosphate
 ATP–creatine phosphate system
(phosphagen system) converts stored carbohydrates to energy without the use of oxygen and no lactate
production. For intense muscle activities lasting up to 20 seconds Example: sprinting in a 100- or 200-m dash
 Lactic anaerobic system (lactic acid metabolism)
For intense muscle activities lasting 20 to 120 seconds
Example: a 400-m sprint
Involves hydrolysis of one glucose molecule to ultimately produce lactic acid plus energy
 Aerobic system
The body depends on this system for muscle activities of longer duration and lower intensity with
replenishment of ATP through oxidative phosphorylation and the Krebs (or citric acid or tricarboxylic acid)
cycle. Glucose or fatty acids are used to produce ATP.
6. Pathophysiology OA

Articular cartilage changes in osteoarthritis and


aging. Proteoglycan aggregate and aggrecan
molecule
7. Characterstics/Features of Cartilage
Layers
8. Judgement of muscle tissue viability
 Colour
Surface tissue may be discoloured due to contusion or local vasoconstriction, non viable muscle will have
dark coloured, however this sign has a least realibilty
 Consistency
The ability of rebound to initial shape after grasping with forceps, this sign is most realible early signs (non
viable muscle: mushy and soft)
 Contractility
 Contractility is assesed by observing retraction by pinch forceps or stimulus observation by electrocautery.
 Capability of bleed (circulation)
This sign maybe difficult to be detected early due vasospasm, non viable muscle will have no bleeding when
its cut.
9. The difference between
sprain and strain
 Sprain: It is a tear in the ligaments. The severity varies from grade I to grade III. Mild sprains
are more common and heal by conservative treatment, whereas grade III sprains cause joint
instabilities and need to be repaired surgically. Sprains are commonly encountered in knee joints
and ankle joints. They are discussed in detail in appropriate sections.
 Strain: It is a tear in the muscles, is more common in young athletes, and usually heals by
conservative methods.
Refferences
Miller, Mark D, and Stephen R. Thompson. Miller's Review of Orthopaedics. , 2016
Ramachandran, M., & Nunn, T. (2017). Basic Orthopaedic Sciences (2nd ed.). CRC
Press.

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