Tendinopathy Flashcards
(40 cards)
What is a tendon made up of
❖ Made up of collagen
❖ Collagen have a ‘wave-like’ appearance
❖ That configuration allows it to stretch and re-coil
❖ ‘Mid Portion’ can be a trouble portion or the origin
what is the function of the enthesis organ
➢ Compression of the tendon against the bone
reduces tensile load on insertion–>there is a wedge between the tendon and bone which gets pressed when tendon is pulled on which is normal, however when it occurs repeated times, causes a problem
➢ Confers a mechanical advantage to the muscle-tendon unit
what is the SSC
-Stretch -shortening cycle
❖ Tendon gets elongated–>stores potential energy/elastic energy and then releases this energy
❖ Function of muscle is intrinsically related to function of tendon
❖ Muscle contribute half of the passive extensibility of the MTU
what is the spring function in the LL
➢ Runners use Achilles as a spring
➢ More dynamic stuff–>use the knee as a spring
what is the tendon’s response to load at 24hrs
net catabolic–> normal
LOOK AT GRAPH
what determines whether it is an overload and development tendinopathy
fluctuations of greater than 10% in tendon response to load–> considered a pathology
what is the histopathology of tendinopathy
❖ Loss of fine fibre structure ❖ Loss of parallel fibre arrangement ❖ Reduction in tenocyte numbers, with rounded nuclei, more resemblant of chondrocytes ❖ Increased cellularity ❖ Increased vascularity ❖ Absence of inflammatory cells
what is the histopathology of
the extracellular matrix in tendinopathy
➢ Loss of collagen organisation
➢ Fibrocartilaginous change
➢ Glycosaminoglycan deposition
what is the histopathology of
chronic inflammation in tendinopathy
- higher levels of inflammatory cells in tendinopathic tissue v/s healthy control tendons
- tissue and cells derived from tendinopathic and ruptured achilles tendons show evidence of chronic inflammation
what is the histopathology of
poor colagen fibril structure in tendinopathy
➢ Poor collagen fibril structure of the tendon causes the pain and dysfunction
➢ Disorganisation of collagen is related to worsening clinical status
➢ Pain and function significantly improve with loading programs
➢ Tendon structure and dimensions remain unchanged
Why does tendon thickening occur
❖ Thickening of the tendon as a result of trying to repair itself but not doing a very good job
what is the presentation of reactive tendinopathy
➢ Acute severe pain
➢ Significant loss of function
➢ Thickening of tendon
➢ No hyperechoic areas on US or increased signal on MRI
What is the presentation of degenerative tendinopathy
➢ Mild to moderate pain
➢ Mild/moderate loss of function
➢ Thickening
➢ Hyperechoic regions on US and abnormally increased signal on MRI
➢ Often managing to run/walk for a long time with symptoms
➢ Pain is local
➢ Pain ‘warms up’–>The ability for it to warm up during exercise is a tendinopathy sign
➢ Pain and stiffness next morning
what is the presentation of reactive-on-degenerative tendinopathy
an acute flare in pain with history of mild to moderate ‘grumbly’ Achilles tendon pain
what factors affect load sensitivity
❖ Genetics
❖ Gender
❖ Metabolic syndrome/diabetes
❖ Antibiotics
how does genetics affect load sensitivity
❖ COL5A1 gene mutation increases type 5 collagen
how does gender affect load sensitivity
❖ Post menopausal women are equal to the male risk of tendinopathy
❖ Active women have higher incidence of tendon abnormality and thicker tendons than healthy inactive women
how does metabolic syndrome affect load sensitivity
❖ Insulin resistance = fatty infiltration in muscle tension
❖ Pain associated with fatty infiltration in tendon
❖ Waist circumference associated with tendinopathy
how does antibiotics affect load sensitivity
❖ Ciprofloxacin and levofloxacin were most commonly implicated fluoroquinolones
❖ Mean time of onset of symptoms was 16days following first FQ dose
What are the common subjective features of achilles tendinopathy
❖ HPC
➢ Gradual onset of symptoms
➢ Preceded by ‘increase’ in training (volume/intensity/nature)
➢ May be long-standing
❖ Relevant history intermittent over many years
❖ Symptom behaviour
➢ Aggravated by SSC activities–>warms up
➢ Morning stiffness
❖ Local muscle atrophy–> atrophy of PF muscles
What are some objective features of achilles tendinopathy
-PROM–> VISA-A
❖ Different diagnosis tests–> can be ligaments, joints or other muscle soft tissue that could be the problem, so need to cancel that out
❖ Palpate
➢ Achilles tendinopathy–>mid-portion, 2-4cm proximal to calcaneus
❖ Assess spring (carefully)–> what is their ability to so SSC
❖ Assess local muscle strength look at gastrocnemius for achillies (calf raise)
❖ Assess strength through the rest of leg (leg press)
❖ Assess spring maximal hop test
What are the common subjective features of patella tendinopathy
❖ HPC
➢ Gradual onset of symptoms
➢ Preceded by ‘increase’ in training (volume/intensity/nature)
➢ May be long-standing
❖ Relevant history–>intermittent over many years
❖ Symptom behaviour
➢ Aggravated by SSC activities–>warms up
➢ Morning stiffness
What are some objective features of patella tendinopathy
❖ Subjective history including factors influencing load sensitivity (Tendon Q)
❖ PROM–> VISA-A
❖ Different diagnosis tests
❖ Palpate
❖ Assess spring (carefully) what is their ability to so SSC
❖ Assess local muscle strength look at gastrocnemius for achillies
❖ Assess strength through the rest of leg (leg press)
❖ Provocation testing pain at inferior pole of patella
what is the pathogenesis of PHT
- Excessive compression of hamstring tendon in hip flexed positions
- internal compression= repeated hip flexion
- external compression = lots of sitting time
- relative increase in load in hip flexed positions
- degenerative changes occur at under surface of hamstring/ pain
