Orthopedic pathology 1 (general terminology) Flashcards
orthopedic pathology
study of injuries to, or conditions involving the musculoskeletal system
Orthopedic Surgery
branch of surgery that deals with the correction of injuries or disorders of the skeletal system
associated muscles,
joints and ligaments
sprain
Overstretch or tear injury to a ligament
ligament function
Control ROM
Taut at end ROM
Relaxed in midrange
sprain cause
Related to sudden twist or pulling of joint beyond its normal ROM
sprain other cause
Congenital ligament laxity
Hypermobile joints
Biomechanical instability
History of Sprains
CT pathologies
more than once
History of Sprains
Signs symptoms
SHARP
Pain
Swelling
Bruising
Loss of functional ability
A “pop” when the injury occurs
sprain severity
Mild – with only slight stress to the ligament
Severe – with total separation of the ligament that supports a joint
grade 1
A minor stretch and tear to the ligament
No joint instability on passive relaxed testing
Minimal pain and swelling
No loss of functional ability – person can continue ADLs with some discomfort
Able to weight bear on the affected joint
Bruising is absent or slight
Able to weight bear on the affected joint
1
bruising 1
absent or slight
grade 2 sprain
Partial tearing of a ligament
Bruising
Moderate pain and swelling
Usually some loss of function - due to pain
Trouble bearing weight on the affected joint
*
Snapping sound and joint gives way at time of injury
Joint is hypermobile yet stable on passive relaxed testing
2
Usually some loss of function - due to pain
Trouble bearing weight on the affected joint
partial tear
2
3
Complete tear or rupture of a ligament or an avulsion fracture
Pain, swelling and bruising are usually severe
Unable to put any weight on the affected joint
*
Snapping sounds and joint gives way
Significant instability and no end point on passive relaxed testing
Chronic – painlessly hypermobile in the direction ligament is intended to check
complete teart, avulsion fracture also possible
3
unable to put any weight
3
adl affected
joint effusion
Occurs when injury is severe enough to inflame the synovium
Increased production of synovial fluid causing joint capsule to swell
knee effusion
water on the knee
water on knee cause
joint injury
arthritis
hemarthrosis
Bleeding into the synovial space
diagnosis of sprain, joint injury
x ray to rule out bone injury, fracture
why heal slowly?
igaments are moderately vascularized
adhesions during healing of ligament
Adhesions can form between the ligament and surrounding tissue that can limit ROM
SCAR TISSUE FORMATION TIME FRAME IN LIGAMENTS
Scar tissue in a ligament takes 6 weeks to develop – but a full 6 months to mature and provide maximum strength to the affected joint
6 weeks 6 months
6 weeks to develop, 6 months to fully mature, provide max strength
3 sprain
Usually surgically repaired or treated by a conservative approach of immobilizing the joint in a cast or strapping
future sprain
After a sprain of any severity an individual has an increased risk of having future sprains in the area (future instability)
common sprain location
Ankle
Lateral ligaments most likely in inversion sprain
most common in ank.e
anterior talofibular
least common ankle
calcaneocuboid
Calcaneofibular
also common
eversion sprain?
affects deltoid lig. (but they are quite strong, thus if they rupture, they tend to avulse the bone, i.e. medial malleoli of tibia)
eversion sprain?
deltoid ligament
anteiro psoteior tibiotalar
tibiocalcaneal
tibionavilcular
knee
PCL, ACL
MCL
m/c due to pronated feet and knees coming together
Cause: repetitive strain, trauma from lateral side of leg
LCL
force from medial side of leg
most common knee
MCL
terrible traid
When foot is fixed on ground, and knee is struck by a valgus force (medially directed), affects three structures:
medial meniscus, ACL and MCL
wrist
Palmar radiocarpal – m/c
Dorsal radiocarpal
Ulnar collateral
Radial collateral
Intercarpal ligamentm
most common wrist
palmar radiocarpal FOOSH
shoulder
AC lig joint
conoid lig, trapeziud lig (coracoclavicular ligs)t
treat sprian
RICE (outdated…)
ice for acute and subacute
heat/ice for flared up chronic or subactue
heat for dormant chronic, with pain but no inflammation
rest is okay, but must remain as active as possible to accelerate healing, increase circulation and homrones contributing to healing
elevation ???
compression ???
when surgery?
grade 3, immobilize/brace for … 10 weeks
how long immobilize brace?
10 weeks
6weeks scar tissue form
6 months scar tissue complete
strain
verstretch injury to a musculotendinous unit
of a muscle, tendon, their osseous attachment and the musculotendinous junction
acute chronic strain
ACUTE - caused by a sudden overstretching of the muscle or an extreme contraction of the muscle against heavy resistance
CHRONIC strains are usually the result of overuse – prolonged repetitive movement of the muscles and tendons
why chronic strain?
overuse
two mucsle ocntaction type
concentric eccentri
eccentric
can CREATE greater forces within the muscle than concentric contractions
which more likely result in strain?
ecentric
what else risk for strian?
Single, explosive muscle contractions, either eccentric or concentric, can also result in a strain
note
“The weakest link in the muscultendinous unit at the time of injury is the structure that is damaged”
why young more likely fracture than strain
developing bone weaker than ligament/tendon structure
and children muscles genreally cannot produce the amount of force required to strain muscle (e.g. like powerlifter)
most common strain? upper body
supraspinatus
which part of body more common
lower body more common than upper body
e.g. common
hamstrings @ origin (Isch tub?)
gastroc @ insertion (CALCANEAL TENDON)
QUADRICEPS – belly
(esp RECTUS FEMORIS)
most common quad
rectus femoris
adductors strain
most common near groin @ pubic tubercle
biceps brachii,w hich head
most common LONG HEAD
the way it cross GH jt to supragelnodi tubercle
neck most common
ANTERIOR SCALENE
Levator Scapulae
SCM
Longis Colli
Infra/Suprahyoids
cause strain
Sudden overstretching of the muscle
Extreme contraction of the muscle against heavy resistance
Overuse
Inadequate warm-up
Limited flexibility
Fatigue
Biomechanical imbalnces
History of previous strains
HISTORY OF STRAINS?
more common
limimted flexibility ?
nmore common
hypomobility
overuse
can also cause strain
signs symptoms
SHARP
Pain
Muscle spasm
Muscle weakness
Localized swelling
Cramping
Inflammation
Loss of muscle function
1 strain mild
Mild strain in which only some muscles fibers have been damaged
Mild pain at the time of injury or within the first 24 hours
Mild local swelling
Minimal loss of strength
Localized tenderness and pain occur when the tissue is stressed
Can continue ADLs
Usually heals in 2-3 weeks
1 how long heal
2-3weeks
1 adl
not really affected
1 strength
not really affected
1 tenderness?
mild local tenderness
grad e 2 moderate
Moderate strain with more extensive damage to the muscle fibers
Muscle is not completely ruptured
May or may not have a snapping sound
Palpable gap at injury site
Moderate edema, pain and tenderness
Difficulty continuing ADLs
Loss of strength
Usually heals in 3-6 weeks
2 heal time
3-6 weeks
2 loss of strength
yes
adls affected
2 gap @ site
yes
grade 3 severe
Severe strain injury with complete rupture of the muscle
can avulsion factr
Snapping sensation/sound
Palpable and visible gap
Severe pain, edema, heat, bruising
Can not continue ADLs
Typically involves surgical repair of the muscle
Healing period can be up to 3 months
healing time 3
up to 3 months
3 adls
no
3 SHARP, pain
Severe pain, edema, heat, bruising
3 gap
palpable AND visible
treatment 1-2
Rest and rehab, then maintain and increase ROM across a joint
rtreatment 3
surgery
contusion
crush injury to muscle
resultant bleeding into the muscle, skin and subcutaneous tissue.
bruising (ecchymosis) ranging from a local, minor discolouration to a large, debilitating area. It can track along the fascial planes to appear at a distant site.
Bruising is red, black and blue.
ecchymosis
a discoloration of the skin resulting from bleeding underneath, typically caused by bruising.
ekkhumonathai –> ekkhumosis
“FORCE OUT BLOOD, ESCAPE OF BLOOD”
cause contusio-n
contact sport
MVA
Fall
location contusion MOST COMMON
quadriceps “Charlie horse”
other contusion site
any muscle, and other structure E>g. bone
E.g.
Deltoid, triceps, biceps, brachialis
Dorsum of foot
Anterior tibia periosteum
Sacrum and Iliac crest
Greater trochanter
Olecranon
Palmar wrist – pisiform/hook of hamate
severity
mild contusion
moderate
severe
mild ocntusion
minor crush
minimal bleeding
minimal NO strength loss
minimal ROM loss
continue ADLs, minor discomofrt
mild adl
continue, mild discm
mild, srength ROM
minimal, no
mild symptoms
Minimal local edema
Tenderness at site
Minor discomfort
5-20% loss of ROM and minimal or no loss of strength
Can continue ADLs
moderate contusion
Moderate crushing of muscle with bleeding and swelling
Difficulty continuing ADL’s
moderate symtpoms
SHARP
Moderate local swelling
Heat and bruising present
Moderate tenderness
20-50% loss of ROM and moderate loss of strength
Pain is moderate
Difficulty continuing ADL’s
moderate pain, adls, strength
yes
ADL challenging
moderate strength loss
moderate rom loss
20-50% rom loss
severe contusion
Severe crushing of tissue
With rapid bleeding and swelling
Significant pain and muscle weakness
Unable to continue ADL’s
severe symptoms
Marked rapid local swelling with increased heat, edema and bruising
Severe pain at site
> 50% loss of ROM and functional loss of strength
Cannot continue ADL’s
severe contusion, pain, ADLs, ROM, strength
significant pain
more than 50 loss of ROM
loss of strength
cannot ADL, with extreme difficulty
treatment contusion
1st 24 hours critical
Control bleeding if severe
Avoid alcohol, stretching, heat, massage, activity, blood thinners
see doctor
hematoma
large area of local hemorrhage following a trauma
Pooling blood causes swelling and pain as it compresses nearby nerve fibers
More rapid swelling than edema due to arterial pressure
Pain increases with movement or if pressure applied to site
why pain hematoma
pooling blood compress nerve
why more swelling than edema (hematoma)
arterial pressure
why pain increase when pressure
more pressure on nerves, nociceptors
myositis ossificans
occasional complication
following HEMATOMA
blood within muscle CALCIFIES
fibroblasts replaced with osteoblasts (from nearby bone?)
–> 6 weeks to devleop
“Some of the bone may be slowly reabsorbed” (??)
“May have attachment to an existing bone or within the muscle itself”
myositis ossificans ..
Strength of muscle decreases
Spasms and local inflammation may occur in the affected muscle tissue
myositis ossificans, surgery
Is done if the calcification is found within the muscle
Is not performed when attached to a bone
“trauma from surgery will cause more bone formation”
myositis ossificans….
“Myositis ossificans occurs when bone forms where it shouldn’t, usually in your muscles or other soft tissues. Usually, myositis ossificans develops after a traumatic injury. Rarer hereditary types of myositis ossificans cause more severe symptoms. There’s no cure for these types of myositis ossificans.”
myositis”
inflammation and degeneration of muscle tissue.
cruciate and meniscal injuries
Prior to treatment it is important to distinguish between cruciate or meniscal injuries and collateral ligament injuries
cruciate ligamnets
These ligaments check motion at the knee and are most taut when the knee is in extension
form cross
.
cruciate ligaments inside joint capsule?
They are within the joint capsule but not within the synovium
ie within fibrous joint capsule/membrane
not synovila membrane of capsule
ACL function
Functions to prevent knee extension, anterior movement of the tibia on the femur AND**** internal tibial rotation
acl which movement limit also?
INTERNAL TIBIAL ROTTATION
ANTAGONIST muscle of acl
quadriceps
acl injury cause
Blow to lateral knee,
forced hyperextension
with internal rotation of the tibia
blow to posterior tibia
most common mechanism of acl injury?
BLOW TO LATERAL KNEE
acl injury test
anterior drawer test
PCL
Functions to prevent posterior movement of tibia on the femur and** internal tibial rotation
PCL ALSO which rotation prevent
internal rotaiton of tibia
pcl antagonist mucsle
hamstrings
pcl stronger
than acl
less commonly injuryed
pcl injury mechanisms cause
Blow to anterior tibia
(MVA (dashboard injury))
ALSO EXCESS HYPERextneisonp
pcl test
posterior drawer
cruaciate injyr managemnet
Depends on degree of instability and any associated injuries, demands places on the knee and time/cost involved in treatment
Conservative approach
Rest, anti-inflammatories, splint, remedial exercise
surgery cruciate
Open or arthroscopic
Rupture may use the followin for reconstruction
Patellar tendon, IT band, gracilis, semitendinosus tendon
which structurestissue is used for cruciate ligament reoconstruction
Patellar tendon,
IT band,
gracilis,
semitendinosus tendon
crucaite rehbailitate
Keep moving
Knee brace – 18 months
aas much actiivty as possible to promote healing via vlood ciruclation increase, and hormone during exercise that influecen healing (E.g. testosterone)
menisici
why?
shock absorption
add increased gliding between the femur and tibia
(reduce friction)
what percentage of load is transmitted via menisci
30-55%
menisci difference between anterior vs posterior side
MORE MOBILE anteriorly
less mobile posteriorly
thick convex outer edge –> “attached to the joint capsule”
“thinner concave inner edge unattached”
which part of menisci avascular?
Middle and inner potions are avascular
medial meniscus, shape, and attachments
forms semi circle
where attached?
periphery to joint capsule
“to the outer margin of the medial tibial condyle by the coronary ligament”
“To the MCL”
which part of MCL most commonly injured?
POSTERIOR ASPECT
“Bucket handle tear”
(recall, anterior more mobile, posterior less mobile –> less mobile = more common to tear)
lateral meniscus
almost complete circle
“Attached to Periphery to the joint capsule and tibia”
“No attachement to LCL”
“More mobile [overall] than medial one and therefore less prone to damage”
“It is moved posteriorly during knee flexion by the tendon of the popliteus muscle”
medial vs lateral meniscus shape
medial is semi-circle
lateral is almost* complete circle
lateral meniscus, popliteus
It is moved posteriorly during knee flexion by the tendon of the popliteus muscle
meniscus, injury mechanism cause
Twisting injury while foot is weight bearing and anchored to the ground
meniscus injuries, tests
Tests
Apleys Compression
McMurray Reduction Click
Apley’s distraction
meniscus injury treatment
Rest, supports and remedial exercise
if severe, Surgery – open or arthroscopic
different meniscal tears
longitudanl tear
radial tear
horizontal tear
bucket handle tear
parrot beak tear
flap tear
meniscus injury and curicate lig injury, symptoms
SHARP
Pain, swelling and muscle guarding
Bruising or redness
Held in semi-flexed position due to swelling (reduce compression)
Have crutches, elastic bandages or splints to support joint
cruciate, acute, symptoms
grade 1-2
continue adls
grade 3
total rupture
no ADLs
cruciate, chronic, grade 2-3, acl/pcl
acl – no run forward
pcl – no squat
– no walk downstairs
– no run backward
meniscal injury, sx, acute/chronic
severe acute
Knee may “give way”, buckle or lock
Pain on side with injury and with knee flexion
Tenderness at joint line
**
CHRONIC
Clicking sounds
Knee may lock if torn meniscus prevents knee motion
Return of acute symptoms with activity
treatment, meniscal, curciate
Support, rest, exercise, medication, surgery
complications,
Reflex Sympathetic Dystrophy Syndrome
Complex Regional Pain Syndrome
”
“What is Reflex Sympathetic Dystrophy (RSD) Syndrome?”
“RSD is an older term used to describe one form of Complex Regional Pain Syndrome (CRPS).”
“Both RSD and CRPS are chronic conditions characterized by severe burning pain, most often affecting one of the extremities (arms, legs, hands, or feet).”
cause “
some conditions that can trigger RSD are sprains, fractures, surgery, damage to blood vessels or nerves and certain brain injuries.
mechanism “
“your sympathetic nervous system gets mixed signals. It turns on after an injury, but doesn’t turn back off. This causes a lot of pain and swelling at your injury site.”
CRPS
“Complex regional pain syndrome (CRPS) is a form of chronic pain that usually affects an arm or a leg. complex regional pain syndrome (CRPS) typically develops after an injury, a surgery, a stroke or a heart attack. The pain is out of proportion to the severity of the initial injury.”
spasm
Is an involuntary, sustained contraction of a muscle
Spontaneous motor unit activity
cramp
Cramp
Is a common or lay term for a painful, prolonged muscle spasm
Reflex Muscle Guarding
Describes a muscle spasm in response to pain
Functions to splint the area, reducing movement and preventing further injury
Guarding disappears when pain disappears
why reflex muscle guard?
Functions to splint the area, reducing movement and preventing further injury
when guarding go away?
Guarding disappears when pain (/injury) disappears
intrinsic muscle spasm
viscious cycle ?
“The prolonged contraction of a muscle in response to the local circulatory and metabolic changes that occur when a muscle is in a continued state of contraction.”
vicious cycle, intrinsic msucle spasm
pain –> tension –> lower circu –> more pain –> more tenson –> less circu –> more pain
why poor circulation = pain
“Poor circulation can cause pain in the legs, feet, arms, and hands. Cold hands and feet may ache or throb, especially as they start to warm and blood flow returns.”
“Also, when the blood does not circulate correctly, oxygen and nutrients cannot reach tissues effectively, resulting in stiffness and cramping.”
muscle tone
Is the resistance of a relaxed muscle to passive stretch or elongation
“Resistance of the muscles and connective tissue to palpation and the active, but not continuous, contraction of a muscle in response to the stimulation of the nervous system”
hypotonia
Decrease in muscle tone
Hypertonia
Increase in muscle tone
muscle tension
Is a muscle held in a sustained contraction
hypertonicity vs hypertonia ????
“Hypertonia of muscle: This term can refer to the same concept as hypertonicity, but it can also encompass a broader range of conditions involving increased muscle tone or tension. Hypertonia can include not only increased muscle tone at rest (hypertonicity) but also increased resistance to passive movement, spasticity, rigidity, or other abnormalities in muscle tone.”
FROM CHATGPT, may be incorrect
hypertonicity (neurologists)
As the abnormally high tone usually seen with upper motor neuron disorders
hypertonicty (osteopathic)
As an increase in tone that is present with painful, dysfunctional muscles
tone associated neuronal disorders
spasticity
rigidity
spasticity
Increased tone in response to stretch
Protective mechanism
Tries to keep muscle in it’s contracted state as it is being stretched to far
Looked after by GTO’s
rigidity
Continuous contraction
skeletal muscles
Fascicles, muscle fibers, myofibrils, thick and thin filaments, sarcomere
muscle spindles
Major sensory organs of muscles
Aid in the control of muscle movements
Measure both the degree to which a muscle is stretched and the speed
GTO
Are nerve receptors located in the tendons near their muscular attachments
Sensitive to tension in the muscle
They can inhibit contraction of a muscle protecting it from an overstretch injury
causes (???) (hypertonicity, spasms, spasticity?)
Pain
Trauma, infection, inflammation
Decreased circulation
Guarding, lock of movement, pathology
Increased gamma neuron firing (MUSCLE SPINDLE)
From stress, anxiety, fatigue, overstretch
Chilling of muscle
Nutritional deficiency
Calcium, magnesium, Vit D, sodium, potassium, water, protein
Pathologies
Muscular dystrophy, tetanus, thrombus/emboli, vascular diseases, Buerger’s disease, DVT, Raynauds, medications
buerger’s disease
Buerger’s disease (also known as thromboangiitis obliterans) affects blood vessels in the body, most commonly in the arms and legs. Blood vessels swell, which can prevent blood flow, causing clots to form. This can lead to pain, tissue damage, and even gangrene (the death or decay of body tissues).
myofascial triggerpoints
Is a hyperirritable spot, usually within a taut band of skeletal muscle or its fascia
It is point tender on site, often exhibits a predictable pain referral pattern and causes shortening of the affected muscle
Healthy muscles do not contain trigger points
TrP pathogenesis
not well known
“Believed that a taut band may be a contracture of muscle fibers that were damaged in the trauma that initiated the trigger point”
“Damage to SR allows calcium to spill out and cause an uncontrolled sustained contraction”
when TrP commonly develop?
In physically active years or with bouts of extremely vigorous exercise – active TrP
Sedentary – latent TrP
TrP development when sedentary (??)
Sedentary – latent TrP
causes, etiology
idiopathic
risk factors, TrP
Direct stimuli:
Trauma, muscle overload, fatigue, chilling of the muscle
Indirect stimuli:
Referred pain from other trigger points, referred visceral pain, emotional stress
Prolonged period where muscle is shortened
TrP other factors
Mechanical stresses/postural imbalances
Muscle constriction – backpacks, purse
Nutritional/metabolic imbalances
Depression and anxiety
Infection/inflammation
Impaired sleep
active vs latent TrP
.
active Trp
Painful at rest and with movement of the muscle containing it
Prevents muscle from fully lengthening and decreases its strength
Tissue exhibits ischemia
Tender
When compressed – refers pain in a specific and predictable pattern
Pain felt with active and passive stretch
–> Protected from further lengthening by a muscle spasm
active Trp palpation
Palpation produces a local twitch response and possible referred autonomic phenomena
latent TrP
Produces pain only when palpated**
–> Same characteristics as active TrP
More common that active TrPs and can persist for years after initial injury
May revert to an active state by any referred pain, overuse, overstretching or chilling of the muscle containing it
how does latent TrP become active?
referred pain,
overuse,
overstretching or
chilling of the muscle
Trp other types, primary vs secondary, vs satellite
.
primary trp
Directly activated by acute or chronic mechanical strain or overload of the affected muscle
secondary trp
Activated VIA the overworked synergist or antagonist muscles
satellite trp
Found in muscle that lies within the referral pattern of another trigger point
myopathy
Any disease or disorder where the muscles do not work properly leading to muscular weakness
myopathy, characteristic
muscle weakness
inflammatory myopathy
Can include inflammatory myopathies (myositis), dystrophies, etc.
congenital myopathy
A group of rare diseases that caues general muscle weakness and are seen from birth
acquired myopathy
Non-specific muscle weakness secondary to some identifiable disease
myalgia
muscle pain
A symptom of a variety of disorders that could lead to muscle pain
E.g. trauma, infection, metabolic disease, nutritional defect, etc.
myotonia
Slow relaxation of muscles after contraction or electrical stimulation
Due to neurological pathologies
myositis
inflammation of muscle
infectious myositis
May be caused by bacteria, viruses, protozoa or worms
immune myositis
Is myositis that is caused by immune mechanisms
atrophy
atrophy
disuse atrophy
denervation atrophy
atrophy?
decrease in size of body organ, tissue or part
disuse atrophy
occurs because muscles are not being used
denervation atrophy
occurs because the nerve supply to the muscle is disrupted or cut
..
..
bursiits
Inflammation of a bursa
bursa
A small, flat sac lined with synovium
Reduces friction
Found between
skin and bone,
muscle and bone,
tendon and bone,
ligament and bone
buritistis cause
Overuse of structures surrounding the bursa
Leads to excessive friction and inflammation of the bursa wall
Secondary to
Acute trauma, infection, OA, RA, gout
Contributing Factors
Muscle imbalances
Poor mechanics
Postural dysfunction (scoliosis)
Lack of flexibility
contributing factors
Muscle imbalances (E.g. antagonists weaker than agonist)
Poor mechanics
Postural dysfunction (e.g. scoliosis)
Lack of flexibility
bursitis lcoations
Subacromial (subdeltoid) bursa
Subscapular Bursa
elbow burisitis
Olecranon Bursa
“student’s elbow”
hip bursa
Trochanteric bursa
Iliopectineal bursa
Ischial busa
knee bursae
Pes anserine bursa
Infrapatellar bursa
Prepatellar burse
ankle bursa
Retrocalcaneal bursa
(“to reduce friction between the heel bone and the Achilles tendon”)
bunion
.first MTP joint capsule
Formed by excessive bone growth (exostosis) (osteophytes)
a callus and an inflamed, thickened bursa developing over the joint
bone spur, aka
exostosis –>ex, ostosis
aka OSTEOPHYTES
bunion risk factor
Joint hypermobility
Poor biomechanics of first MTP joint
bunion treatment
orthotics
changing footwear
surgery if severe
baker’s cyst (other bursal injuries)
“Synovial cyst that usually appears at the lateral side of the popliteal space”
posterior knee –> lateral side (popliteal space)
bursitis management
diagnosis:
Palpation,
ROM
(Special tests)
Ober’s test,
Faber test,
painful arc,
neer impingement tests
bursitis acute, amnagement
rest
NSAIDs
ice (acute and subacute)
preventative
Protections to more superficial bursa
Stretching and Strengthening of muscles crossing bursa
tendinitis
inflammation of tendon
Is inflammation of a tendon
Resulting from mircoscopic tearing of the tendon fascicles due to overloading of the tendon
tendinitis mechanism?
mircoscopic tearing of the tendon fascicles due to overloading of the tendon
tendon shapes
Cord-like
Broad sheet – aponeuroses
paratendon
Surrounds a tendon that moves in a straight line, houses blood vessels
“vascular”
tendon sheath
Surrounds a tendon that crosses a bony prominence
Double layered, filled with synovial fluid
“avascular”
why tendon sheath?
Surrounds a tendon that crosses a bony prominence
tendon sheath synovial layer/fluid
Double layered, filled with synovial fluid
tendinitis risk factors, cause
Chronic overload of the tendon
Leading to microtearing and an inflammatory response
other risk factors, contributing factors
Muscle imbalances
Poor biomechanics
Lack of flexibility
Chronic degenerative changes in the tendon
Poor blood supply
Improper equipment or training errors
tendinitis grade 1-4
Grade 1
Pain after activity only
Grade 2
Pain at the beginning of activity which disappears during activity
Grade 3
Pain at the beginning of activity, during activity and after activity
Grade 4
Pain with ADLs, pain continues to get worse
paratendinitis
Inflammation of the paratendon or the tendon sheath
paratendinitis aka
Tenosynovitis – inner surface irritation
Tenovaginitis – irritation and thickening of tendon
tendinosis
Degenerative changes occurring with chronic overuse tendon injuries
No inflammation
calcific tendinitis
aged 30-60
Esp @ ROTATOR CUFF MUSCLES –> E.g. esp SUPRASPINATUS
calcific tendinitis mechanism
Tendon’s fibrocytes change to chondrocytes,
collagen disintegrates and calcific deposits accumulate in the cells
Deposits can be soft or hard
calcific tendinitis locaitons (& tendinitis in general?)
Shoulder:
Supraspinatus tendon (MOST COMMON, b/c overhead activities)
Infraspinatus tendon
Subscapularis tendon
tendinitis other locaitons
Biceps Long Head (just like strain)
tendinitis vs strain (?)
“The way to distinguish between the two is that with a muscle strain, the pain is felt in the muscle itself, whereas in tendonitis, the pain is felt near where the muscle attaches to the bone.”
what if strain is near tendon??
strain may be referring to more substantial tearing/damage
vs.
microtearing of tendinitis
maybe repetitive use strains are structurally similar to tendinitis in some occasions (??)
forearm tendinitis
common extensor tendon
(tennis elbow?)
common flexortendon (golfers elbow?)
repetitive use strain @ tendon can include tendinitis, or tendinosis (?)
chatgpt
wrist, tendinitis
abductor pollicis longus
extensor pollicis brevis
same tendons of DeQuervain’s Tenosynovitis
knee, tendintiis
tibialis posterior tendon
Calcaneal tendon
tendinitis management
rest, ice, NSAIDs (acute)
stretch, strengthen, modify activities/form/technique
Braces/taping
Steroid injections
Ultrasound
Laser therapy
Surgical repair (if severe)
subluxation, dislocation
Dislocation
The complete dissociation of the articulating surfaces of a joint
Subluxation
is when the articulating surfaces of a joint remain in partial contact with each other
about subluxation and dislocaiton
May occur at any joint
However some joints are more unstable due to their anatomical configuration\
most frequently dislocation
GH
shallow glenoid fossa (despite glenoid labrum)
other joints
AC joint (separated shoulder, esp advanced levels)
MCP joints, IP joints
dislocations, complications, other damage
damage of:
Joint capsule,
surrounding ligaments,
tendons,
synovial sheaths,
articular cartilage,
contusion
nerves
bv
(bone) fractures
sublux, dislocation, cause
Trauma – related sudden twist or wrench of the joint beyond its normal range of motion
direct vs idnirect “
Direct – force to joint itself
Indirect – joint is the weak link in a closed kinetic chain
” contributing factors
Pathologies:
RA, paralysis
Congenital ligamentous laxity
Previous dislocations (ligament and joint capsule structures become weaker)
joint reduction
Tractioning of bones to bring surfaces back in contact
why no popping joint back in place?
can damage nerve/bv/other joint structures if is not tractioned first
other treatment?
surgery if severe
brace/support
PT exercises:
ROM,
strengthening surrounding musclature to partially compensate for weakened joint capsule, and ligament structures (ease the load off those structures)
ice if acute/subacute (?)
NSAIDs “
increase circulation/hormones for healing maximum capacity via exercise however possible
GH dislocation
most common anterior dislcation
anterior GH dislocaiton AKA
subcoracoid disloaction
because GH head moves anterior and inferior, below where coracoid process is situated
anterior dislocaiton mechanism
hyperextension (note anterior glide, posterior roll)
excess abduction with external rotation (again note anterior glide for ER)
posteior dislocation GH
mechniams
flexion (p roll), adduction, and internal rotation (p roll)
patella dislocaiton
esp laterally
mechanism?
external rotation of tibia/foot when knee is flexed
lunate dislocation
FOOSH, wrist hyperextension
elbow “
usually w/ fracture (of coronoid process?)
b/c HU jt is strong
ulna/radius displaced posteriorly
MOI
FOOSH
esp MVA (lots of force required for fracture)
hip “
Femur is forced posteriorly by a direct impact to the knee
MOI
MVA
if accompanied by fracture, can be life-threatening (RBM, site of blood cell production)
edema
Is a local or general accumulation of fluid in the interstitial tissue spaces
Result of altered physiological function in the body, not a disease itself
Used to describe the physical sign commonly linked to swelling or increased girth that accompanies the accumulation of fluid in a body part
fibrosis
The formation or development of excess fibrous CT in an organ or tissue as a reparative or reactive process
fibrositis
Inflammatory hyperplasia of white fibrous connective tissue, especially surrounding muscles, causing pain and stiffness
hypermobility
Is an increased degree of motion at a joint
Can occur at one joint or several
Range from mild joint laxity to extreme mobility or even joint instability
Females>males
Children>adults
Asian>Africans>Caucasians
hypermobility..
If one joint is hypermobile
It can result in compensatory weakness or hypomobility in another joint
joint laxity, risk factor
Joint laxity may increase risk for
Sprains, tendinitis, osteoarthritis and entrapment neuropathies
hypermobility causes, risk factors
Compensation due to hypomobility
Increased flexibilty
Hormonal influences
Joint trauma
Pathologies
Ehlers-Danlos Syndrome
Marfans Syndrome
RA
hypermobility scale
Beighton scale
–> general measuring tool, diagnosis tool for hypermobility
getting 5 positives on a list of joints via measurement of ROM @ those joints
= positive for generalized hypermobility
hypomobility
Is loss of motion at a joint, including the loss of normal joint play movements
Can be local or generalized
Joints on the dominant side of the body tend to be more hypomobile than those on the non-dominant side (e.g. Right?)
hypomobility risk factor for
strained muscles,
nerve compression,
tendinitis
hypomobility cause
Compensation due to hypermobility
Decreased flexibilty (no stretching with weightlifting, not moving joints through entire ROM on daily basis)
Intra-articular and extra-articular adhesions
Surgical fixations
hypomobility via adhesions
Intra-articular and extra-articular adhesions
hypomobility pathologies
Dupuytren’s contractures,
frozen shoulder
hypertrophy
General increase in bulk of a part or organ, not due to tumor formation
Greater bulk through increase in size but not number of cells or other individual tissue elements
muscle hypertrophy
The growth and increase of size of muscle cells
muscle hyperplasia
Formation of new muscle cells
