W09 - GROWTH, INJURY, REPAIR X2 Flashcards

1
Q

ANTERIOR and DORSAL roots

A

MOTOR NERVE FIBRES = ANTERIOR/VENTRAL

SENSORY NERVE FIBRES. POSTERIOR/DORSAL

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2
Q

Motor efferent unit

A

Found in ANTERIOR HORN CELL (grey matter)

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3
Q

Sensory unit

A

Cell bodies in POSTERIOR ROOT GANGLIA outside the SCord

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4
Q

Structural makeup of the nerve

A

AXONS (endoneurium) > FASCICLES (perineurium) > NERVE (epineurium)

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5
Q

Fiber types

A

Aa (largest) = muscle stretch and tension

Aß = touch pressure vibration proprio

Aγ = efferent motor

Aδ = sharp pain, light touch, temp

B = symp pre-gang motor

C = dull aching burning pain and temp

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6
Q

Axonotmesis

A

The axons and their myelin sheath are damaged in this kind of injury, but the endoneurium, perineurium and epineurium remain intact.

*followed by WALLERIAN DEGENERATION

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7
Q

neurotmesis

A

complete transection of a peripheral nerve

*no recovery unlessrepaired by SUTURING or GRAFTING
* miswiring risk during regeneration
= poor prognosis

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8
Q

Neurapraxia

A

Blockage of conduction = slight loss

*reversible

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9
Q

Classic Conditions of Compression

A

CARPAL TUNNEL SYNDROME = median nerve at wrist

SCIATICA = spinal root by IV disc

MORTON’S NEUROMA = DIGITAL NERVE IN 2ND OR 3RD WEB SPACE OF FOREFOOT)

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10
Q

Direct nerve injury

A

Blow laceration = resection

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11
Q

Indirect nerve injury

A

Avulsion, traction

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12
Q

Closed and Open Neve Injuries

A

CLOSED

  • nerve injuries in continuity (epineurium preservation)
  • recovery or sx after 3mos
  • nil recovery = electromygraphy

•typical stretching of nerve

OPEN

  • nerve division = neurotmetic injuries
  • early sx
  • wallerian degeneration
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13
Q

Clinical features of Nerve Injury

A

-DYSAETHESIAE

  • PARESIS
    +paralysis
    + dry skin (nil stim of sweat glands)
  • Diminished/absent reflexes
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14
Q

Healing of Nerve Injury

A

Axonal death distally > then to site
Proximal axon budding

  • pain to return first
  • Tinel’s sign = tap over site of nerve and paraesthesia will be felt as far distally as regeneration has progressed
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15
Q

Rule of 3

A

Immediate surgery within 3 days for clean and sharp injuries

Early surgery within 3 weeks for blunt/contusion injuries

Delayed surgery, performed 3 months after injury, for closed injuries.

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16
Q

UMN Lesion Findings

A

⇩strength

⇧tone, deep tendon reflexes

+Babinski’s sign, Cnus

17
Q

LMN Lesion Findings

A

⇩strenght, tone, reflexes

nil Clonus, Babinski’s Sign
+ATROPHY

18
Q

Cortical V Cancellous (Trabecular) Bone

A

CORTICAL = lamellae, concentric, outer layer
* resists BENDING, TORSION

CANCELLOUS = metaphysis, sute of physis
* resists COMPRESSION

19
Q

Stages of Bone Fracture

A

(1) INFLAMMATION: immediate
* mediators are released = attract repair cells
* angiogen.

> NSAIDs can reduce ability to repair
Loss of haematoma as aprt of Hx reduce biological drive to repair
Replacing platelet concentrates to promote repair drive

(2) SOFT CALLUS, collagen matrix being laid down
* end-point = fragments united by cartilage/fibrous tissue

> Demineral. Bone Matrix can replace cartilage
Replace bone to skip this step via bone graft

(3) HARD CALLUS = convt to woven bone
limit movement, endochrondral bone form.

(4) BONE REMODELLING = conv to lamellar bone, medullary canal reconstituted

20
Q

Significance of Autogenous Cancellous Bone Graft

A

GOLD STANDARD OF BONE GRAFT

21
Q

Allograft Bone

A
Allograft bone (bone banks) osteoconductive but not osteoinductive
*mechanism of substitution rather than synthesis
22
Q

Delayed Union

A

failure to heal in expected time d/t disruption to repair

  • distraction, instability
  • infection
  • steorids
  • smoking
  • warfarin, NSAID, ciproflox.

(non-union where bone fails to heal)

23
Q

Ligament v Tendon

A

Ligaments = ⇩%collagen, ⇧proteoglycans and water, less organised collagen fibres, rounder fibroblasts

Collagen fibre (type 1)

24
Q

Damage to Ligaments

A

When forces exceed strength ligament,

25
Q

Healing of Ligament Injuries

A

Hamorrhage: blood clot then resorbed, replaced with cellular infiltrate, hypertrophic vascular response

Proliferative phase
* scar tiss.; disorg. collagenous connec. tissue

Remodelling:
Matrix becomes more ligament like

> often conservative Tx
Repair; Augmentation; Replacement

26
Q

Structure of Tendon

A

COLLAGEN BUNDLES (endotenon) > Fascicles (paratenon) > Tendon (epitenon)

*Tendon sheath connected to tendon via VINCULA + synovial lining

27
Q

Significance of Vinculum

A

band of connective tissue, similar to a ligament, that connects a flexor tendon to a phalanx bone. They contain tiny vessels which supply blood to the tendon.

28
Q

Tendon Degeneration

A

e.g

Achilles tendinosis is a condition in which very small tears form and inflammation occurs in the Achilles tendon. Otherwise known as degenerative tendinopathy, this disorder frequently affects athletes and happens when too much stress is placed on the tendon.

=> progression to rupture

29
Q

Tendon Inflamm

A

e.g. de Quervain’s stenosing tenovaginitis

swollen, tender, red
+Finklestein’s test
* enthesiopathy at muscle origin rather than insertion

-tennis elbow (lateral humeral epicondylitis)

30
Q

Tendon Injury

A

traction apophysitis
- OSGOOD SCHLATTER’S DISEASE = patella tendon insers into ant. tibial tuberosity: pain @ apophysis
young active boys, recurrent load, inflamm

> rest

31
Q

Avulsion+bone fragment

A

failure @ insertion with excess load

MALLET FINGER: forced flexion of extended finger

> conservative
operative: reattachment tendon through bone, fixation

32
Q

Intrasubstance Rupture

A

Follows degeneration, achilles common where load exceeds failure strength

ACHILLES TENDON RUPTURE
+Simmond’s Test (plantar flexion squeeze)

> conservative: splint/cast
operative: risk of rerupture, high activity, ends cannot be opposed

33
Q

Musculotendinous Junction Tear

A

Plantaris Syndome, often partial, where medial head of gastroxnemius at musculotendinous junction tears

34
Q

Laceration of Tendons

A

common, M>F, young adults

>early Sx