MCQs – Basic 3

Modern Study Review (AI-Generated)

High-Yield Summary

Nerve regeneration and peripheral nerve injury are high-yield topics in orthopaedic exams, focusing heavily on nerve fiber susceptibility, regeneration sequences, and functional recovery timelines. The critical clinical decision point is distinguishing between motor and sensory fiber involvement, as motor fibers fail and recover in a predictable order relative to sensory fibers. While classic teaching emphasizes the Schwann cell role and regeneration from 1 cm proximal to injury, modern practice increasingly incorporates microsurgical techniques to optimize axonal guidance and functional outcomes. Understanding gait kinematics and tendon healing mechanisms is also essential for comprehensive musculoskeletal assessment and rehabilitation planning.

High-Yield Decision Matrix

Active Recall Q&A

Nerve Regeneration and Fiber Susceptibility

Q: What is the primary cellular influence on nerve regeneration after injury?
A: Schwann cells are the biggest influence on nerve regeneration.
Related Pearl: Schwann cells occupy the endoneural tubes of the last centimeter of the proximal stump after axonal degeneration, guiding regrowth and remyelination.

Q: From where does nerve regeneration originate relative to the injury site?
A: Regeneration comes from the nerve substance 1 cm proximal to the injury.
Related Pearl: This proximal segment contains Schwann cells essential for axonal guidance and successful regeneration.

Q: Which nerve fiber types are more susceptible to injury: motor or sensory?
A: Motor fibers are more susceptible to injury than sensory fibers.
Related Pearl: Larger diameter and higher metabolic demand of motor fibers increase their vulnerability to trauma.

Q: Between large myelinated and fine/nonmyelinated fibers, which are more injury-prone?
A: Large myelinated fibers are more susceptible than fine or nonmyelinated fibers.
Related Pearl: Large myelinated fibers have higher conduction velocities but are mechanically more vulnerable.

Nerve Fiber Failure and Recovery Sequence

Q: What is the sequential order of nerve fiber failure after injury?
A: Motor ? Proprioception ? Pinprick/Temperature ? Pain.
Related Pearl: Pain fibers are thinnest and nonmyelinated, explaining their delayed failure compared to other fibers.

Q: What is the order of nerve fiber recovery following injury?
A: Pain returns first, then pinprick/temperature, then proprioception, and finally motor function.
Related Pearl: Recovery follows the reverse order of failure due to differential regeneration rates and fiber characteristics.

Axonal and Electrophysiological Properties

Q: How does the caliber and myelination of regenerated axons compare to normal?
A: Regenerated axons are smaller in caliber and less thickly myelinated.
Related Pearl: This results in decreased conduction velocity and may limit functional recovery.

Q: How is action potential propagation velocity related to nerve diameter?
A: Velocity is directly proportional to nerve diameter; larger diameter nerves conduct faster.
Related Pearl: This principle explains why large myelinated fibers transmit signals rapidly.

Q: What ions move during depolarization and repolarization of a nerve cell?
A: Depolarization: sodium (Na?) rushes in, potassium (K?) goes out; repolarization: sodium is pumped out, potassium is pumped back in.
Related Pearl: Ion pumps restore resting membrane potential, essential for repeated action potentials.

Q: How does myelin affect action potential initiation and conduction?
A: Myelin interferes with initiation but allows rapid conduction via nodes of Ranvier where voltage-gated sodium channels are concentrated.
Related Pearl: Saltatory conduction increases conduction velocity by jumping between nodes, optimizing energy efficiency.

Bone Marrow and Implant Biology

Q: How does bone marrow composition change from infancy to adulthood?
A: Red marrow is replaced by yellow marrow starting distally in appendicular skeleton, progressing proximally; by age 20, only upper humerus and femur retain red marrow.
Related Pearl: Marrow conversion impacts hematopoiesis and bone healing capacity in adults.

Q: What role does fibronectin play in orthopaedic implants?
A: Fibronectin binds to biomaterials and promotes bacterial adherence to implants.
Related Pearl: This facilitates biofilm formation, increasing risk of implant-related infections.

Tendon Composition and Healing

Q: Is reticulin found in tendons?
A: Reticulin is unlikely to be found in tendons.
Related Pearl: Tendons primarily contain elastin, parallel collagen fibers, and small amounts of proteoglycans, optimizing tensile strength.

Q: How does healing occur in a sheathed (avascular) tendon after laceration?
A: Controlled passive motion promotes intrinsic healing from the epitenon; immobilization leads to extrinsic healing via connective tissue ingrowth from the sheath and endotenon proliferation.
Related Pearl: Early mobilization improves tendon healing quality and reduces adhesions.

Q: How does healing occur in a paratenon-covered (vascular) tendon?
A: The wound fills with inflammatory products forming a callus that remodels over time.
Related Pearl: Vascular supply facilitates a robust inflammatory and reparative response, enhancing healing.

Hematology and Meniscus Biology

Q: What laboratory parameters indicate disseminated intravascular coagulation (DIC)?
A: Increased fibrin split products (FDPs), increased PT and PTT, decreased platelets, decreased antithrombin III, and decreased fibrinogen.
Related Pearl: These consumptive coagulopathy markers guide diagnosis and management of DIC.

Q: How does the proteoglycan and glycoprotein concentration in meniscus compare to hyaline cartilage?
A: Meniscus has only 10% of the proteoglycan and glycoprotein concentration of hyaline cartilage.
Related Pearl: This lower concentration contributes to the meniscus’s unique biomechanical properties, favoring load distribution over compressive resistance.

Q: Where is innervation located in the meniscus?
A: Innervation is restricted to the peripheral two-thirds of the meniscus.
Related Pearl: Peripheral meniscus injuries are more likely to be painful and have better healing potential due to vascularity and innervation.

Gait Kinematics

Q: When is the foot maximally dorsiflexed during gait?
A: During midstance and terminal stance phases.
Related Pearl: Dorsiflexion during stance aids in shock absorption and forward progression.

Q: At what gait phase is the knee maximally flexed?
A: At preswing, with approximately 40° flexion.
Related Pearl: Knee flexion during preswing prepares the limb for swing phase and foot clearance.

Q: When is the hip maximally flexed and extended during gait?
A: Maximal hip flexion occurs at initial contact (25°), and maximal extension occurs at terminal stance (20°).
Related Pearl: Hip extension during terminal stance contributes to propulsion and stride length.

Q: What are the approximate percentage durations of gait phases?
A: Initial Contact 0%, Loading Response 0-10%, Midstance 10-30%, Terminal Stance 30-50%, Preswing 50-60%.
Related Pearl: Precise phase timing is critical for gait analysis and rehabilitation protocols.

Q: What are the typical joint angles of ankle, knee, and hip during gait phases?
A:

• Ankle: 0° IC, 10° plantarflexion LR, 5° dorsiflexion MS, 10° dorsiflexion TS, 20° plantarflexion PS
• Knee: 0° IC, 15° flexion LR, 0° MS/TS, 40° flexion PS
• Hip: 25° flexion IC/LR, 0° MS, 20° extension TS, 0° PS

Related Pearl: These angles reflect normal kinematics essential for efficient and energy-conserving gait.

Classic Clinical Notes

• Probably the biggest influence on nerve regeneration is the Schwann cell. The regeneration comes from the nerve substance 1 cm proximal to the injury. “With transection, axonal degeneration occurs, leaving the endoneural tubes of the last centimeter of the proximal stump occupied only by Schwann cells”.

• As a general rule, motor fibers are more susceptible to injury than sensory fibers, and large myelinated fibers are more susceptible than fine or nonmyelinated fibers.

• Motor and sensory nerve fibers fail sequentially in the following order:
• Motor
• Proprioception
• Pinprick/temperature
• Pain – these are often the thinnest, nonmyelinated fibers, so it makes sense that they fail last.

• The order of recovery is then reversed (i.e., pain returns first, then pinprick/temp, then proprioception, then motor).

• At the completion of regeneration, the surviving axon will be smaller than normal caliber and will be less thickly myelinated, and hence the conduction velocity will be less.

• The velocity of action potential propagation is DIRECTLY related to the diameter of the nerve – if the nerve is bigger, the faster the action potential will move.

• During depolarization, sodium rushes into the cell, potassium goes out; during repolarization, the sodium is pumped back out of the cell, the potassium is moved back in.

• Myelin interferes with action potential initiation, but at the nodes of Ranvier there are high concentrations of voltage gated sodium channels – action potentials are evoked at the nodes and local currents flow quickly down the myelinated region to the next node. This salutatory conduction is a property of myelinated nerves.

• In the infant, the bones are filled with red marrow (hematopoetic); this is replaced by yellow marrow beginning with the appendicular (peripheral) skeleton and later the axial skeleton. The process begins in the distal ends of the long bones and extends up to the proximal part – by age 20, only the upper end of the humerus and femur still contain red marrow.

• Fibronectin is a ubiquitous serum and matrix protein that binds to a variety of common orthopaedic biomaterials, depending on the biomaterial’s composition. Bacteria can adhere to this fibronectin molecule – so the fibronectin has a role in promoting bacterial adherence to implants.

• Reticulin is a scleroprotein from the connective fibers of reticular tissue – it is unlikely that it is found in tendons. Tendons probably do consist of elastin; they definitely have very straight, parallel collagen, and they have small concentrations of proteoglycan.

Tendon Healing in a Sheathed (avascular) tendon

• In the proper environment, the lacerated tendon itself is capable of repair – in repaired tendons treated with controlled passive motion, this “intrinsic” response, originating from the epitenon, predominates. In the immobilized tendon, healing occurs through the ingrowth of connective tissue from the digital sheath and cellular proliferation of the endotenon.

Tendon Healing in a paratenon covered (vascular) tendon

• Wound fills up with inflammatory products and forms like a callus which remodels eventually.

• Laboratory parameters of DIC: increased fibrin split products (FDPs), increased PT, PTT, decreased platelets (consumptive), decreased antithrombin III (consumptive), decreased fibrinogen (consumptive).

• In the meniscus, the concentration of proteoglycans and glycoproteins is only 10% that of hyaline cartilage.

• In the meniscus, the innervation is restricted to the peripheral 2/3rds.

• During stance phase, the foot is maximally dorsiflexed during midstance / terminal stance.

• The knee is maximally flexed at preswing.

• The hip is maximally flexed at initial contact, maximally extended at terminal stance.

Last Updated on January 25, 2026 by Christian Veillette