Tendon Pathology Flashcards

1
Q

what are tendons made up of

A

collagen bundles arranged around a central elongated collection of tenocytes (tendon fibroblasts) and capillaries

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2
Q

what are tendons composed of at birth

A

cellular and vascular

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3
Q

what are tendons composed of in an adult

A

collagen fibrils form 80% of dry matter

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4
Q

what is the structure of collgen fibrils in collagen type 1

A

form a zigzag waveform in longitudinal orientation

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5
Q

what are tenocytes

A

elongated tendon fibrocyte/fibroblast

longitudinal rows alongside the collagen fibrils

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6
Q

how do tenocytes communicate

A

via gap junctions and respond to mechanical signals

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7
Q

what are the function of tenocytes

A
  1. synthesize and degrade all of the collagenous and non-collagenous matrix
  2. repair the tendon matrix when injured
  3. slow turn-over in normal tendon
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8
Q

what are the predisposing changes in the injury and repiar of tendon

A

cartilaginous metaplasia, ischemia, fibroblast proliferation

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9
Q

what are the predisposed sites for injury and repair of a tendon

A

anatomic weakness or disproportionate stretch

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10
Q

what are stretch lesions (3)

A
  1. fibrils pulled out of kink register
  2. ruptured collagen fibres
  3. rupture of capillaries
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11
Q

how are tendons repaired (3)

A
  1. tenocytes and peritenon cells form myofibroblasts
  2. collagen type III (immature collagen)
  3. maturation over time (collagen type I)
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12
Q

how are large lesions repaired

A

more necrosis, fibrin, malaligned, scar collagen, adhesions

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13
Q

what occures in the acute phase of injury

A

inflammatory cells

pro-inflammatory mediators and cytokines

commonly asymptomatic horses

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14
Q

what occurs in the subacute phase of injury

A

3-6 weeks post injury

inflammatory cells replaced by fibroblastic cells and small blood vessels (granulation tissue)

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15
Q

what cells are responsible for repair of tendons

A

fibroblastic cells (tenocytes)

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16
Q

what two sites do fibroblasts migrate into the tendon from

A
  1. tendon sheath (extrinsic repair)
  2. epitenon/endotenon (intrinsic repair)
17
Q

what are the chronic phase of injury and repair

A

more than 3 months post injury

scar tissue

disorganized collagen fibrils

increased numbers of fibroblasts

enlarged endotendon

18
Q

what occurs with maturation over time

A

decreased cellularity

alignment of collagen fibrils

19
Q

what problems occur in tendon healing

A
  1. no regeneration: fascicles stuck together and destroyed by scar tissue
  2. ruptures may occur at margins of normal and scar tissue
  3. persistence of inflammatory cells (and blood vessels) in endotenon
20
Q

what are the tendon pathologies

A
  1. vascular
  2. inflammatory
  3. traumatic
  4. anomaly
  5. metabolic/toxic
  6. idiopathic/iatrogen
  7. neoplastic
  8. degenerative
21
Q

where are SDFT injuries most common

A

usually mid-metacarpal region

22
Q

what occurs after a SDFT injury

A

microdamage

microscopic level

subclinical changes to the tendon

naturally present in tendons of older horses

accelerated accumulations in tendons of horses <10 years due to high intensity exercise

23
Q

how does exercise accelerate the levels of microdamage

A
  1. mechanical overload
  2. hyperthermia
  3. hypoxia
  4. death or dysfunction of tenocytes –> poor tendon healing –> further presence/increase of microdamage
24
Q

what occurs during mechanical overload in SDFT

A

high levels of force break collagen fibrils and alter microscopic structure of the tendon –> microdamage

25
Q

how does the SDFT improve locomotion efficiency

A

SDFT converts both potential and kinetic energy into elastic energy

reduces muscle energy expenditure –> increases effeciency of locomotion

low mechanical safety marigin

26
Q

what is hyperthermia in the tendon core

A

not all elastic energy is returned during recoil of tendon

5-10% lost as heat

inefficient dissipiation of heat within the tendon core due to its poor vascular supply

high temp leads to tenocyte death

27
Q

what are the features of early microdamage in SDFT due to ageing

A
  1. decrease crimp angle (core) > 10 years
  2. decrease cellularity
  3. decreased gap junction communication
  4. increase in % type 1 tenocytes (and length)
28
Q

what are the features of early microdamage in the SDFT due to exercise

A
  1. decreased crimp angle (core) < 10 years
  2. decreased collagen fibril diameter (core)
  3. decreased glycosaminoglycan content
29
Q

what are the features of advanced microdamage in the SDFT

A

red core lesion

no clinical signs, no swelling

more type III collagen = immature (smaller, weaker fibrils)

30
Q

what are parasitic diseases of tendons

A

horse and cattle

adult worms in tendon, tendon sheaths, connective tissue of brisket or abdominal walls

microfilariae migrate to skin, picked up by blood sucking parasite

low grade or no tissue reaction; asymptomatic

31
Q

what is suspensory desmitis

A

degenerative diseases of tendons

changes in proteoglycan decomposition –> abnormal decorin and aggrecan

32
Q

what occurs during suspensory desmitis

A

hyperextension of metacarpophalangeal/tarsophalangeal joint

33
Q

what are the histological features of the tendon

A

tenocytes

vessels

not very cellular

34
Q

what are these cells

A